Nasa Khan MRCS A Notes 2018 PDF

MRCS NoTes
NASA KHAN
2018
ANATOMY
© Notes by Dr. Sakib (MRCS Online Preparatory Course By Nasa Khan)
SUPERIOR EXTREMITY
IMPORTANT MUSCLE ATTACHMENT AND RELATED INFORMATION
● 7 muscles attach the Scapula to the chest wall: PORTaLS

- P.Minor - Trapezius
- Omohyoid - L. Scapulae
- Rhomboids (Major +Minor) - S. Ant.
● 6 muscles originates from Scapula & inserted @ Humerus: Cuff Muscles (TISS) +TD
- T. Minor - T. Major
- Infraspinatous - Deltoid
- Supraspinatous.MEN
- Subscapularis
● MUSCLES OF F.ARM: (Med. to Lat.) (N-416)

**Superficial Layer (above downwards) Deep Layer
- P.Teres - F.D.Sup. - F.P. Longus
- F.C.Radialis - F.C.Ulnaris - F.D. Profundus
- P. Longus - P. Quadratus
[**muscles of Common Flexor Origin ]
● COMMON EXTENSOR ORIGIN (N-411) : ECRL; ECRB; ED; EDM; ECU; BRD
© Notes by Dr. Sakib (MRCS Online Preparatory Course By Nasa Khan) Page | 1
● COMMON FLEXOR ORIGIN (N-416) : PT; PL; FCU; FCR; FDS

● THUMB EXTENSORS (N-412) : ABPL; EPL; EPB
● WRIST ABDUCTORS (N-412) : ECRB; FCR
● WRIST FLEXORS (N-412) : FCR; FCU; PL
● DIGIT FLEXORS (N-413) : FDS; FDP; FPL
● FDP is tested by holding PIP joint. Straight & instructing patient to bend distal joint.
● FDS is tested by holding all fingers straight, then releasing one & asking pt. to bend the proximal jt. Holding fingers
straight immobilizes all the deep flexors(including that of the finger being tested), which have a common muscle belly
● Pectoralis Minor depresses the point of the shoulder, (glenoid fossa) directly.
● BRACHIORADIALIS: function, innervation, one relation, one attachment
BrachioRadialis:
Function: Its the Beer Raising muscle, flexes elbow, strongest when wrist is oriented like holding a beer.
Innervation: Breaks Rule: it’s a flexor muscle, But Radial.(Radial nerve usually is for extensors: Recall
BEST rule: B was for brachioradialis).
Important relation: Behind it is the Radial nerve in the cubital fossa.
Attachment: Attaches to Bottom of Radius.
● SERRATUS ANTERIOR: INNERVATION AND ACTION: SALT- 567

• Serratus Anterior is innervated by Long Thoracic nerve which arises from the roots- C5, C6, and C7.
● Deltoid: Proximal attachments CLASs:

• CL avicle
• A cromion
• S pine of the s capula.
● PALMARIS LONGUS: LOCATION, RELATIVE TO WRIST NERVES "The Palmaris between two Palmars"
Palmaris longus is between Palmar cutaneous branch Ulnar nerve and Palmar cutaneous branch Median nerve.
Important Nerve and related infos
● MOVEMENT SEGMENTAL INNERVATION
Shoulder Abduction - C5
Shoulder Adduction - C7
Elbow Flexion - C5
Elbow Extension - C7
Supination/Pronation C6
Wrist flexion/extension C6/C7 extension C6

Finger flexion/extension C7/C8
Small muscles of hand T1
Brachial Plexus (Also see the Chart Note)
Divisions located at Axilla

Cords are related to Axillary Artery
Brachial Plexus ends with a total of 15 nerves. Of these 5 are main nerves to the upper limb (Axillary, Radial, Ulnar,
Median and Musculocutaneous)
Flial Upper Limb – Brachial Plexus injury followed by Horner’s Syndrome (if sympathetic chain involved)
Axillary Surgery: Chance of injury - Thoracodorsal Nerve / Middle Subscapular / Nerve to Latissimus Dorsi.
After Breast surgery, patient can't touch Scapula with hand. Answer: Thoracodorsal Nerve Lesion
nd nd
Mastectomy: Chance of injury - Long Thoracic N.+ Lateral Thoracic Artery(2 branch of Axillary Artery 2 part) as
both accompany to the Serratus Anterior Muscle.
Axillary Dissection: Intercostobrachial Nerves are frequently injured. These nerves traverse the axilla and
supply cutaneous sensation
Erb’s Palsy
Accidental C5,6 root tear → Shoulder Joint Abduction totally lost → Called Erb’s Palsy / “Waiter’s Tip”
Main paralysed:
o Biceps
o Brachio Radialis
o Deltoid
Partial paralysed:
o Supraspinatous
o Infraspinatous
o Supinator
Features of Erbs Palsy

• Waiter's tip position
• Loss of shoulder abduction (Deltoid and Supraspinatus paralysis)
• Loss of shoulder external rotation (Infraspinatus & Teres Major paralysis)
• Loss of elbow flexion (Biceps, Brachialis & Brachioradialis paralysis)
• Loss of forearm supination (Biceps paralysis)
Klumpke’s Palsy
During Child birth Lower trunk (C7,8, T1 ) injured.

Features of Klumpkes Paralysis Lower trunk (C7,8, T1)
• Claw hand (MCP joints extended and IP joints flexed)
• Loss of sensation over medial aspect of forearm and hand
• Horner's syndrome C8, T1
• Loss of flexors of the wrist
● “Stabbed in the neck & inferior trunk of brachial plexus is injured” - Lower trunk of the brachial plexus is
injured (though its a rare injury !!!). Nerve roots C8 and T1 will be injured. Therefore this will most consistently affect
Ulnar Nerve & Median Nerve which will effect in:
Abduction of the fingers
Flexion of the little finger
Sensation on the palmar aspect of the little finger
Gripping a screwdriver
● Axillary Nerve passes directly under Subscapularis muscle, when it passes out from axilla. Subscapularis is the
main muscle of Medial Rotation.
Sample theme:
A 30 year-old male presents with a week history of right arm weakness. Originally the problem began with severe pain in
the neck which radiated into the right shoulder, which was followed by weakness. Examination revealed winging of the
right scapula with weakness of right shoulder abduction and elbow extension. There was some sensory loss over the
lateral aspect of the right shoulder and right triceps reflex was absent.What is the most likely diagnosis?
ANS: NEURALGIC AMYOTROPHY. it is a brachial plexopathy (usually upper brachial plexus) usually preceded by an
infective picture.It usually presents with severe pain for days to weeks followed by weakness and sensory loss over the
corresponding territory of the brachial plexus (more commonly C5-7). It is self-limiting condition but recovery may be slow
(years)
Radial nerve C5-8 + T1(N-446-47)
Continuation of posterior cord of the brachial plexus (root values C5 to T1)
● RADIAL NERVE: MUSCLES SUPPLIED (SIMPLIFIED)

"BEST muscles": Brachioradialis; Extensors; Supinator; Triceps
● RADIAL NERVE PATH

• @ Axilla: lies posterior to Axillary Artery and lies on Subscapularis, Latissimus Dorsi & Teres Major.
• Enters the arm: between the Brachial Artery and Long Head Triceps (medial to humerus).(N-446)
• Spirals around post. surface of humerus in the groove for radial nerve between lateral & medial heads
• @ distal third of the lateral border of humerus it pierces intermuscular septum & descends in front of lateral
epicondyle.
• @ Lateral Epicondyle lies deeply between Brachialis & Brachioradialis where it divides into superficial & deep
terminal branch
• Deep branch crosses the Supinator to become the Posterior Interosseous Nerve
PATTERNS OF DAMAGE
At Axilla
- Loss of Elbow Extension
- Loss of Sensation in the lateral and posterior Part of Arm
- Loss of Wrist Extension - Wrist Drop
- Loss of Thumb Extension - Thumb drop
- Loss of Finger Extension - Finger drop
- Loss of Sensation in the first dorsal web space
At the Spiral Groove

- Loss of Wrist Extension - Wrist Drop
After Spiral Groove Before Piercing the Supinator and before the origin of sensory branch
- Diminished Wrist Extension - Radial Deviation of wrist

After Piercing the Supinator (Posterior Interosseus Nerve)

(Posterior Interosseous Neuropathy is a motor syndrome results - Finger drop & radial wrist deviation on extension)
Superficial Branch
● Radial Nerve may become entrapped in the "Arcade of Frohse" which is a superficial part of the supinator muscle
which overlies Posterior Interosseous Nerve. On emerging from Supinator, Posterior Interosseous Nerve lies
between superficial extensor muscles and lowermost fibres of Supinator. It then gives branches to extensors.
● Gantzer Muscle is an aberrant accessory of Flexor Pollicis Longus & is risk factor for Anterior Interosseous Nerve
compression
Ulnar nerve C7- 8 + T1 (N-445)
Path
• Posteromedially of ulna → flexor compartment forearm→Passes under Flexor Carpi Ulnaris → superficially
through Flexor Retinaculum → palm.
st
• Ulnar nerve eventually passes between two heads of Adductor Pollicis →Ends in 1 Dorsal Interosseous
• Ulnar nerve has no branches @ Arm and lies anterior to the medial head of Triceps
Effects of injury
Damage at the wrist • Wasting and paralysis of intrinsic hand muscles (claw hand)
• Wasting and paralysis of hypothenar muscles
• Loss of sensation medial 1½ fingers
Damage at the elbow • Radial deviation of the wrist

• Clawing less in 3rd and 4th digits
● “True claw hand caused by injury to Ulnar Nerve @ wrist rather than elbow” as Proximal Interphalangeal &
Distal Interphalangeal joints are flexed mentioned, – due to Flexor Digitorum Profundus being intact & there is no
radial deviation. Radial deviation is expected if Ulnar Nerve is injured @ elbow due to paralysis of Flexor Carpi Ulnaris.
● 'Ulnar Paradox': Due to more proximal level of transaction – the hand will typically have a claw and a claw like
appearance may be seen following a more distal injury.
ULNAR NERVE PALSY TESTS

• Card test (to check out palmer interossei, adductors of fingers) (injury @ elbow)
Inability to hold a card in between fingers due to loss of adduction by the palmar interossei
• Egawa test (to check dorsal interossei of middle finger)

With palm flat on the table the patient is asked to move the middle finger sideways.
• Foment’s sign / Book test (to check out Adductor Pollicis – Deep branch of Ulnar Nerve )
Hold a piece of paper or a book between the thumb and index finger. The object is then pulled
away. If Ulnar Nerve palsy, unable to hold the object and will flex the Flexor Pollicis Longus to
compensate (flexion of thumb at interphalangeal joint).
• 1st dorsal interossei is also tested by applying force on index finger by index finger.
● Think "peripheral nerves": ulnar nerve is "ulnar" to ulnar artery. Radial nerve is "radial" to radial artery.
● Ulnar nerve is called Musicians’ nerve as it controls all fine movements of hand.
● Laceration between Little finger base and wrist. Several weeks later, complains, “Loss of thumb adduction power” –
Deep Ulnar Nerve Injury - will be the correct answer
Median nerve (C5-8 + T1)
Path
Relations of Median Nerve to the Brachial Artery: L-ateral → A-nterior→ Me-dial = LAMe
@ Upper Arm Median Nerve starts descend lateral to Brachial Artery →Then passes anterior to Brachial Artery →
Then lie on medial side of Brachial Artery → Then passes deep to Bicipital Aponeurosis and Median Cubital Vein @
Elbow → enters forearm between the two heads of Pronator Teres → runs within deep fascial sheath of Flexor
Digitorum Superficialis → @ Wrist becomes superficial between tendons of Flexor Digitorum Superficialis & Flexor
Carpi Radialis → passes deep to Flexor Retinaculum to enter palm.
PATTERNS OF DAMAGE (DR. CUMA: Drop=Radial N; Claw=Ulnar N; Median =Ape or Apostol or preacher hand)
Damage at wrist ( e.g. Carpal tunnel syndrome)

• Paralysis and wasting of thenar eminence muscles and Opponens Pollicis (ape hand deformity)
• Sensory loss to palmar aspect of lateral (radial) 3 ½ fingers
Damage at elbow, as above plus:

• Unable to pronate forearm
• Weak wrist flexion
• Ulnar deviation of wrist
Anterior interosseous nerve (Motor branch of Median Nerve)

• Leaves just below the elbow
When damaged it classically causes:
• Pain in the forearm
• Loss of pincer movement of the thumb and index finger (innervates the long flexor muscles of Flexor Pollicis
Longus & Flexor Digitorum Profundus of the index and middle finger)
• Minimal loss of sensation due to lack of a cutaneous branch
• Results in loss of pronation of forearm
● Named tests for Median nerve:

PEn test (OPPOnens test) and POinting index test MEdian nerve. (Remember OPPOsite ME)
Phalen's test
• Assess carpal tunnel syndrome
• More sensitive than Tinel's sign
• Hold wrist in maximum flexion and the test is positive if there is numbness in the median nerve distribution.
Tinel's Sign
• Assess for carpal tunnel syndrome
• Tap the median nerve at the wrist and the test is positive if there is a tingling/electric-like sensation over the
distribution of the median nerve.
● MEDIAN AND ULNAR NERVES: COMMON FEATURES
Each supply 1/2 of FDP [ulnar: Medial Half; median: Lat. half]
Each supplies 2 lumbricals.
Each has a palmar cutaneous nerve that pops off prematurely.
Each supplies an eminence group of muscles [ulnar: Hypothenar. median: Thenar].
Each enters forearm through two heads [ulnar: heads of FCU. median: heads of PT].
Each has no branches in upper arm.
Each makes two fingers claw when cut at wrist.
Each supplies a palmaris [median: PL; ulnar: PB].
Musculocutaneous nerve C5-7

• Branch of lateral cord of brachial plexus
● Path
• Arises @ lower border of Pectoralis Minor
• It penetrates the Coracobrachialis muscle in front of arm
• Runs obliquely between the Biceps brachii and the Brachialis to the lateral side of arm
• Above the elbow it pierces the deep fascia lateral to the tendon of the Biceps brachii
• Continues into the forearm as the lateral cutaneous nerve of the forearm
● Innervates BBC
• Coracobrachialis
• Biceps brachii
• Brachialis
● if damaged then elbow flexion will be impaired due to defect of Biceps
IMPORTANT VESSELS AND RELATED INFORMATION
AX.A. BRANCH: “Some Times Life Seems A Pain”

st
1 Part : (1br.): S uperior Thoracic.
nd
2 Part : (2br.): T horaco Acromial [4 br. ABCD: Acromial, Breast-(Pectoral) Clavicular, Deltoid]; Lat. Thoracic
rd
3 Part : (3br.): S ubscapular; Ant. Circumflex Humeral; Post. Circumflex Humeral
Clinical Note: Compound fracture of distal third of clavicle, there is evidence of arterial hemorrhage. Thoraco Acromial
Artery is most likely to be encountered first during the subsequent surgical exploration.
Brachial artery (fig with Median nerve page)
● Brachial artery begins at the lower border of Teres Major.

● It terminates in Cubital Fossa @ level of the neck of the Radius → divides into radial & ulnar arteries.
Relations
● Posteriorly : Long head of Triceps; Radial Nerve; Profunda Vessels.
● Anteriorly : Medial Border of Biceps. ("BAMBI": Brachial Artery is Medial to Biceps In elbow)
● Laterally : Accompanied by two Brachial veins on each sides
● It is crossed by the Median Nerve in the middle of the arm. (v.v.v.imp.)
● Branches
- Deep Artery or Profunda Brachii Artery
- Recurrent and Collateral branches : "I Am Sexy Pretty ".
● I nferior ulnar collateral artery gives continution named A nterior ulnar recurrent artery.
● S uperior ulnar collateral artery gives continution named P osterior ulnar recurrent artery.
** Superior Ulnar Collateral Artery & Ulner Nerve lies back of Medial Epicondyle, **
Clinical note: Median Nerve lies close to Brachial Artery in the antecubital fossa. This is the usual site of surgical
access to Brachial Artery for an embolectomy procedure. Median Nerve may be damaged during clumsy application of
vascular clamps to the artery
Ulnar artery (fig with Median nerve page)
Path
• Starts @ middle of antecubital fossa
• It follows the ulnar border to the wrist
• Crosses over the Flexor Retinaculum.*
• Lastly divides into the superficial and deep volar arches.
Relations
• Lies deep to 3 muscles : Pronator Teres,
Flexor Carpi Radialis,
Palmaris Longus
• Lies on 2 muscles : Brachialis,
Flexor Digitorum Profundus,
• At The Wrist: Superficial to the Flexor Retinaculum or Crosses over the Flexor Retinaculum
• Median Nerve is in Medial Side of the artery → And then crosses the vessel, then separated from Ulnar
Artery by ulnar head of Pronator Teres
• Ulnar Nerve lies medially to the lower two-thirds of the artery
Branch
• Anterior interosseous artery
Radial artery (fig with Median nerve page)
● Radial artery passes under Brachioradialis

● Radial Recurrent Artery lies on Supinator muscle (N-417)
Basilic vein
● Path
• Originates on the medial side of the dorsal venous network.
• Near the region anterior to the cubital fossa it joins Cephalic Vein through Median Cubital Vein.
• Midway up the humerus, Basilic Vein passes deep under the muscles.
• At the lower border of Teres Major, the Anterior & Posterior Circumflex Humeral Vein feed into it.
• Joins Brachial Vein to form Axillary Vein.
● PICC (Peripherally Inserted Central Catheter) line for long term venous acces: inserted into the Basilic Vein at
the region of the elbow. As the catheter is advanced, the tip is likely to pass from Basilic Vein to Axillary Vein
Cephalic vein
● Path
• Dorsal venous arch drains laterally into the Cephalic Vein
• Crosses the anatomical snuffbox and travels laterally up the arm
• At the antecubital fossa connected to the Basilic Vein by the Median Cubital Vein
• Pierces deep fascia (coracoid membrane – continuation of Clavipectoral) of deltopectoral groove to join Axillary
Vein
Axillary Vein Thrombosis
• 1-2% of all deep venous thrombosis

• Primary cause:
Trauma
Thoracic Outlet Obstruction (TOO)
Repeated effort in a dominant arm (badminton, tennis player)
• Secondary cause:
Central line insertion
Malignancy
Pacemakers
Clinical features
• Pain and swelling (non pitting)
• Numbness
• Discolouration: mottling, dusky
• Pulses present
• Congested veins
Investigations
• FBC: viscosity, platelet function
• Clotting
• Liver function tests
• D-dimer
• Duplex scan: investigation of choice
• CT scan: in case of TOO
Treatment
st
• Local catheter directed tPA(Tissue Plasminogen Activator) - 1 choice
• Heparin
• Warfarin
**Heparin and warfarin prevent propagation / spread of the clot.
Shoulder joint
• Shallow synovial ball and socket type of joint.

• Stability is provided by muscles of the rotator cuff that pass from the scapula to insert in the Greater Tuberosity
(all except sub scapularis-lesser tuberosity).
Glenoid Labrum
• Fibrocartilaginous rim
• The long head of biceps arises from within the joint from the supraglenoid tubercle
• The long head of triceps attaches to the infraglenoid tubercle
Fibrous Capsule
• Attaches to the humerus at the level of the anatomical neck superiorly and the surgical neck inferiorly
• The capsule is in contact with
Anteriorly - tendon of Subscapularis,
Posteriorly - tendons of Infraspinatus & Teres Minor.
Superiorly - tendon of Supraspinatus
• Two defects in the fibrous capsule
Superiorly for the tendon of Biceps.
Anteriorly there is a defect beneath the Subscapularis tendon.
Important Anatomical Relations
Anteriorly Brachial plexus
Axillary artery and vein
Posterior Suprascapular nerve

Suprascapular vessels
Inferior Axillary nerve
Structures @ risk during Anterior approach of the shoulder joint are:

Cephalic Vein
Short head of Biceps
Subscapularis
Musculocutaneous nerve
Axilla
Boundaries of the axilla (N-399)
st
Medially 1 four ribs & their corresponding intercostals;
Serratus anterior
Laterally Humeral head mainly.

Coracobrachialis;
Biceps brachii.
Posteriorly Subscapularis;
Teres Major;
Latissimus Dorsi
Anteriorly Pectoralis major;

Pectoralis minor
Fascia Clavipectoral fascia
Contents:
Long thoracic nerve Passes behind the brachial plexus to enter the axilla.
(of Bell) C5-7 Lies on the medial chest wall and supplies Serratus Anterior.
Location puts it at risk during axillary surgery.
SALT – 567 Damage will lead to winging of the scapula.
Thoracodorsal nerve C6-8 Innervate and vascularise Latissimus orsi. (LAT)

And vessel
Intercostobrachial nerves Traverse the axillary LN & are often divided during axillary surgery.
They provide cutaneous sensation to axillary skin.
Axillary vein Lies @ apex of axilla,

It is the continuation of the Basilic Vein. Becomes the Subclavian Vein
@ outer border of 1st rib.(Basilic→Axillary→Subclavian)
Lymph nodes The axilla is the main site of lymphatic drainage for the breast.
Axillary LN Stations
Level 1 : Inferior to P.minor
Level 2 : Behind the P.minor
Level 3 : Above the P.minor
Muscles of the rotator cuff
Muscle Innervation
Supraspinatus muscle Suprascapular nerve
Infraspinatus muscle Suprascapular nerve
Teres minor muscle Axillary nerve
Subscapularis muscle Superior and inferior subscapular nerves
Rotator cuff
Greater Tubercle insert 3 muscles – S upraspinatus, I nfraspinatus, T eres Minor→
→ SIT,
Lesser Tubercle insert 1 muscle – Subscapularis
● Greater Tubercle & Lesser Tubercle contains inter-tubercular groove which passes the tendon of Long head Biceps
& a branch of Ant. Humeral Artery to shoulder joint (N-394)
Rotator cuff tears

- Common in elderly people and may occur following minor trauma or as a result of long standing impingement.
- Supraspinatus tear is the most common of rotator cuff tears.
- It occurs as a result of degeneration and is rare in younger adults
- Tears greater than 2cm should generally be repaired surgically
Shoulder disorders
Proximal humerus fractures

• Very common. Usually through the surgical neck.
• It is rare to have fractures through the anatomical neck.
• Anatomical neck fractures displaced by >1cm carry a risk of AVN to the humeral head.
• In children commonest injury is greenstick fracture through the surgical neck.
• Impacted fractures of the surgical neck are usually managed with a collar and cuff for 3 weeks followed by
physiotherapy.
• More significant displaced fractures may require ORIF or use of an intramedullary device.
Neer’s classification of proximal humerus fractures

• Group I: All fractures with displacement <1 cm, angulation 45°
• Group II: Anatomical neck fractures displaced >1 cm (can be complicated by AVN)
• Group III: Surgical neck fracture + displacement or angulation (can be complicated by axillary nerve injury)
• Group IV: Greater tuberosity fracture, displaced by pull of supraspinatus (can be complicated by painful arc
syndrome due to impingement of the greater tuberosity on the acromion process and coracoacromial ligament)
• Group V: Lesser tuberosity fractures
• Group VI: Fracture dislocations
Groups II–VI may be subdivided according to the number of ‘parts’ (eg two-part fracture).
Types of shoulder dislocation

• Glenohumeral dislocation (commonest): anterior shoulder dislocation most common
• Acromioclavicular dislocation (12%): clavicle loses all attachment with the scapula
• Sternoclavicular dislocation (uncommon)
Types of glenohumeral dislocation:
Anterior shoulder dislocation • External rotation and abduction

• 35-40% recurrent (it is the commonest disorder)
Assocociated with
• Greater tuberosity fracture,
• Bankart lesion,
• Hill-Sachs defect
Inferior shoulder dislocation Luxatio erecta
Posterior shoulder dislocation • Rim's sign,

• Light bulb sign.
• Trough sign
Superior shoulder dislocation Rare and usually follow major trauma.
Bankart lesion
Its an injury of the anterior (inferior) glenoid labrum of the shoulder due to repeated anterior shoulder dislocation.
When this happens, a pocket at the front of the glenoid forms that allows the humeral head to dislocate into it. It is an
indication for surgery and often accompanied by a Hill-Sachs lesion, damage to the posterior humeral head
Hill-Sachs lesion, also Hill-Sachs

Sachs fracture
It’s a cortical depression in the posterolateral head of thehumerus
the bone. The cartilage surface of the humerus is in
contact with the rim of the glenoid
● Treatment
- In recurrent anterior dislocation there is usually a Bankart lesion and this may be repaired surgically.
- Recurrent posterior dislocations may be repaired in similar manner using posterior (or arthroscopic) approach
Sample Theme:
A 28 year old man complains of pain and weakness in the shoulder. He has recently been unwell with glandular fever
from which he is fully recovered. On examination there is some evidence of muscle wasting and a degree of winging of
the scapula. Power during active movements is impaired.
Answer: Parsonage - Turner syndrome
This is a peripheral neuropathy that may complicate viral illnesses and usually resolves spontaneously.
Car accident + unable to raise arm easily + spontaneous multiple dislocation history – Ans: Suprascapular nerve injury
Hand, Wrist joint and Clinicals
Anatomy of the hand
Bones • 8 Carpal bones

• 5 Metacarpals
• 14 phalanges
Intrinsic 7 Interossei - Supplied by Ulnar Nerve "3 on the P, 4 on the Dor":

Muscles • 3 Palmars – Adduct – PAD – Unipennate. Middle finger has no attachment with palmer interossi
interossi.
• 4 Dorsals – Abduct – DAB – Bipennate
Intrinsic Lumbricals
muscles • Origin: Deep Flexor Tendon
• Insertion: dorsal extensor hood mechanism; medially directed
st nd rd th
• Innervation: 1 & 2 (Unipennate) – Median N.; 3 & 4 (Bipennate) – deep branch Ulnar N.
• Action: Flex MCPJ and extend the IPJ. Remember– to hold a pea, When look at this hand in this
position, can see this makes an "L" shape, since L is for Lumbical
● INTRINSIC MUSCLES OF HAND For thenar and hypothenar muscles, think: "A OF A OF A"
Thenar eminence (lateral to medial on palmar surface):

• Abductor PB
• Opponens pollicis
• Flexor pollicis brevis
• Adductor pollicis.
Hypothenar eminence (lateral to medial on palmar surface):

• Opponens digiti minimi
• Flexor digiti minimi
• Abductor digiti minimi
Anatomical snuffbox (N-436)
Posterior border Tendon of Extensor Pollicis Longus
Anterior border Tendons of Extensor Pollicis Brevis and Abductor Pollicis Longus
Proximal border/ Styloid process of the radius

Limited Above
Distal border Apex of snuffbox triangle
Floor Trapezium; Scaphoid; ECRL; ECRB; Crossed by Radial artery
Roof Skin & Fascia; Beginning of Cephalic Vein; Superficial Branch of Radial nerve
Content Radial artery
Extensor retinaculum (N-439)
The Extensor Rentinaculum is a thickening of the deep fascia that stretches across the back of the wrist and holds the
long extensor tendons in position. Its attachments are:
• The Pisiform and hook of Hamate Medially

• The end of the Radius Laterally
● Structures related to the extensor retinaculum
Structures superficial • Basilic vein
to retinaculum • Dorsal cutaneous branch of ulnar nerve

• Cephalic vein
• Superficial branch of radial nerve
Structures passing deep Compartment 1 : EPB; APL

to extensor retinaculum – Extensor Compartment 2 : ECRL; ECRB
Compartments ē extensor Compartment 3 : EPL
muscle tendons Compartment 4 : ED; EI
Compartment 5 : EDM
Compartment 6 : ECU
Beneath the extensor retinaculum fibrous septa form six compartments that contain the extensor muscle tendons. Each
compartment has its own synovial sheath.
Flexor retinaculum (Transverse Carpal Ligament, or Anterior Annular Ligament)
Its a strong, fibrous band that arches over the carpus converting the deep groove on the front of the carpal bones into a
tunnel, the carpal tunnel, through which the Flexor tendons of the digits and the median nervepass. Its attachments are:
• The Pisiform and hamulus of Hamate – Medially
• The Scaphoid tubercle and medial part of the volar surface & ridge of Trapezium – Laterally
● Structures passing through the carpal tunnel

Median Nerve
Flexor Policis Longus
FDS, FDP
Radial & Ulnar Bursa
● Structures passing superficial to carpal tunnel

Palmaris longus
Ulnar Nerve
Cutaneous Branch of Ulnar nerve
Cutaneous Branch of Median
● The 5th tendon sheath extends from the little finger to the proximal aspect of the carpal tunnel. This carries a
significant risk of allowing infections to migrate proximally
ulnar side or medial side

MediAN nerve (policeMAN) - Compression causes carpal tunnel syndrome
Flexor POLICis longus (POLICe jeep)
FDS, FDP (FD = Fixed Deposit in piggy bank)
Radial & ulnar Bursa (piggy Bank)
●Structures passing superficial to carpal tunnel:

PALMaris LONGus (LONG
LONG PALM tree)
Cutaneous branch of MediAN Nerve (boy = small MAN;; Big policeMAN was MediAN nerve, so small man
represents cutaneous branch)
UlNar nerve (Umen = woman)
Cutaneous br. of UlNar
ar nerve (small Umen = small woman = represented by girl in the picture)
GUYON'S CANAL
- Wrist space between Flexor Retinaculum and Palmar Carpal Ligament (Runs between pisiform and hamate),
- Through this canal Ulnar Artery and Ulnar Nerve travel into the hand.
● Radial Artery passes between the lateral collateral ligament of the wrist joint and the tendons of the abductor pollicis
longus and extensor pollicis brevis.
Capitate bone
- This is the largest of the carpal bones.

- Has articular surfaces for 5 bones : Scaphoid; Lunate; Hamate; Trapezoid; Middle metacarpal
Pisiform bone
Has a single articular facet.

It projects from the triquetral bone at the ulnar aspect of the wrist.
wrist
It is a sesamoid bone
Lying within the tendon of Flexor Carpi Ulnaris

Articulates with only 1 bone – Triquetral
Immediately lateral to Pisiform bone structures are : Ulnar Nerve & Ulnar Artery
● CARPAL BONES: TRAPEZIUM VS. TRAPEZOID LOCATION

● TrapeziUM is by the thUMb, TrapezOID is by its siDE.
● Remember : No tendons are attached with Scaphoid; Lunate; Triquetrum

● Remember : Distal end of Radius articulates primarily with 2 bones – Scaphoid and Lunate
Scaphoid bone
- The Scaphoid has articular surfaces for 5 bones : Lunate; Capitate; Trapezoid; Trapezium; Radius
- Blood supply to the scaphoid enters from a small non articular surface near its distal end. Transverse fractures through
the scaphoid therefore carry a risk of non union.
Hand Diseases
Dupuytrens contracture
• Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.
• Caused by underlying Contractures of The Palmar Aponeurosis .
• The Ring Finger and Little Finger are the fingers most commonly affected. The Middle Finger may be affected
in advanced cases, but the Index Finger And The Thumb are nearly always spared.
• Association with liver cirrhosis and alcoholism. However, many cases are idiopathic.
• Treatment is surgical and involves fasciectomy.
CARPEL TUNNEL SYNDROME

Idiopathic median nerve neuropathy due to compression, at the carpal tunnel
History
• Altered sensation - pain/pins and needles in lateral 3 fingers thumb, index, middle finger
• Symptoms occur mainly at night
• Patient flicks hand to obtain relief
• Commoner in females
• Associated with Dupuytren’s contracture
• Associated with other connective tissue disorders such as rheumatoid disease. It may also occur in pregnancy
and following trauma to the distal radius.
Examination
• Weakness of thumb abduction
• Wasting of thenar eminence (NOT hypothenar)
• Tinel's sign (compression of the contents of the carpal tunnel): tapping causes paraesthesia
• Phalen's sign: flexion of wrist causes symptoms
• Formal diagnosis is usually made by electrophysiological studies.
Causes of carpal tunnel syndrome MEDIAN TRAP

• Myxoedema
• Edema premenstrually
• Diabetes
• Idiopathic
• Agromegaly
• Neoplasm
• Trauma
• Rheumatoid arthritis
• Amyloidosis
• Pregnancy
Management
Non surgical treatment Surgery
May resolve spontaneously Complete division of the flexor retinaculum and decompression of the tunnel
Avoid precipitants and reassurance (successful in approximately 80% of patients)

Night-time splints Incision is given distal to the distal skin crease of the wrist
Local steroid injections
MISCELLANEOUS HAND LUMPS
Osler's Painful, red, raised lesions with a pale centre found on the hands and feet.
nodes Occur as a result of immune complex deposition.
Often association with Endocarditis. Other causes SLE, Gonorrhoea, Typhoid, Haemolytic Anaemia.
Bouchards Hard, bony outgrowths or gelatinous cysts on Proximal Interphalangeal Joints

nodes Sign of osteoarthritis, and caused by formation of calcific spurs of the articular cartilage.
Heberdens Distal Interphalangeal Joint Involved

nodes Typically develop in middle age
Beginning either with a chronic swelling of the affected joints or the sudden painful onset of redness,
numbness, and loss of manual dexterity. This initial inflammation and pain eventually subsides, and
the patient is left with a permanent bony outgrowth that often skews the fingertip sideways.
Ganglion Swelling in association with a tendon sheath commonly near a joint.

Common lesions in the wrist and hand.
Usually they are asymptomatic and cause little in the way of functional compromise. T
Fluid filled although the fluid is similar to synovial fluid it is slightly more viscous.
When the cysts are troublesome they may be excised.
● Sites of Avascular Necrosis : Humeral Head

Femoral Head
Scaphoid
Talus
Lunate
● ELBOW OSSIFICATION CENTERS: "Come, Rub My Tree Of Love !!! "

C apitullum
R adial head
M edial epicondyle
T rochlea
O lecranon
L ateral epicondyle
These appear at 2, 4, 6, 8, 10, and 12 years of age, respectively, and disappear two years later.
st
● Sentinel LN is the 1 LN in Axilla to receive drainage from Breast.
● Tourniquet should be released in every 90mins in SupEx & every 120mins in InfEx.
● Child + Suprachondylar fracture Humerus = Neuropraxia of Median Nerve (Transient episode motor paralysis ē little
/no sensory/autonomic dysfunction) First to think as diagnosis
st
● Child + Suprachondylar fracture Humerus + cold periphery+ no pulse palpable = 1 treatment Manipulation Under
Anaesthesia - If unkinking of Brachial Artery occurs and restoration of distal flow achieved, then ok. Otherwise surgical
exploration is the next TREATMENT of choice.
● NERVES & ARTERIES AFFECTED BY HUMERUS FRACTURE LOCATION From superior to inferior:
Axillary N.& Ant+Post Circumflex Humeral Art. : Humerus Head; Surgical neck
Radial N. & Prfunda Brachii Art. : Humerus mid shaft
rd
Radial N. : Humerus shaft distal 3 / Holstein – Lewis
Median N. (→ Ant. Interosseus N.) : Supracondylar(Ok sign not possible; unable to flex index finger)
Ulnar N. & Sup. Ulnar collateral artery : Medial Epicondylar
● ELBOW: MUSCLES THAT FLEX IT

3 B's Bend the elBow: Brachialis, Biceps, Brachioradialis
● ELBOW JOINT:
Radius vs. Ulna ends CRAzy TULips: OR CUTER: Capitalum = ULnar; Trochlear = Radius
Cubital Fossa
Boundary
• Base : Imaginary Connecting Line between two Epicondyles
• Medially : Pronator Teres lateral border
• Laterally : Brachioradialis medial border
• Apex : Downward meeting point of medial and lateral border.
• Floor : Brachiallis and Supinator
• Roof : Skin
Superficial Fascia (containing Median Cubital Vein + Med. and Lat. Cutaneous Nerve of fore arm)
Deep Fascia
Bicipital Aponeurosis
Contents: "Navy-MAN": Lateral to medial.: Nerve Muscle Artery Nerve.

• Radial Nerve
• Tendon of Biceps (Muscle)
• Brachial Artery
• Median Nerve
BRACHIAL PLEXUS BRANCHES (Robert Taylor Drinks Cold Beer : Root; Trunk; Division; Cord; Branch)
ROOTS TRUNKS CORDS TERMINAL BR.
(Ventral Rami of Spinal.Nerve) Upper C5-6. ; Middle C7; Lower C8,T1
- Begins at C5 & total 5 roots - Located post.to middle third of
LAT.CORD MED.CORD POST. CORD
- Located in posterior triangle clavicle
- Pass betn Scalenus ant. & medius - Upper & middle trunk related sup. C5-7 C8-T1 C5-T1
to Subclavian Artery Ant. Divisn- upper & middle Ant. divisn- lower trunk Post. Divisn - all 3 trunks
- Lower trunk passes over 1st rib trunks
post. to Subclavian Art.
DOLLPHinS 2S (only comes from upper part) LaaL Musa M4 U ULNAR MARMU
Do rsal Scapular C5 (N2Rh.) S upra - Scapular C5-6 L at.Pect. C5-7 M ed.Pect. U pper Subscapular C5-6 M usculocut C5-7
L. Thoracic C5-7 S ubclavius C5-6 L at.Root Median M ed.Root Median L ower Subscapular C5-6 A xillary. C5-6
(Nerve to S.A.; Nerve.of Bell) Musculocut. C5-7 M ed.Cut. Arm N. to L.Dorsi C6-8 R adial C5-8 T1
L ongus Colli M ed.Cut. F.Arm. (Thoracodorsal/Middle.Sub M edian C5-8 T1
To Ph renic N. U lnar C7 C8 + T1 Scapular) U lnar C7 C8 + T1
S calene A xillary. C5-6
R adial C5-8 + T1
Nerves Muscular Articular Cutaeneous Applied Special Notes

Branches Anatomy
Ulnar ● F.Carpi Ulnaris ● Elbow ● Wrist ● Hypothenar eminence Skin ● Loss hypothenar ● Ulnar Artery
● F. Dig. Profundus. (Med. Half) ● Med. 1½ finger dorsum, adjoining & its eminence.
● Hypothenars proximal parts ● Interossi paralysis →
M. cord
(F.D.M.+ Abd.D.M.+ O.D.M.) Prominent metacarpals ●Complete claw =
● Palmaris Brevis ● Partial claw U+M nerve palsy
OftenC7 ● Adductor Pollicis
C8 + T 1 ● Medial 2 Lumbricals
● All Interossi
st nd
Median ● Lumbricals(1 , 2 ) ● Elbow ● Wrist ● Lateral 3½ digits (Palmar part) ● Labourers' Nerve Radial + Brachial +
● Thenars: ● Rad-Ulnar Prox & 2
● Skin- Lateral γ /3 of Palmar Part; Thenar ● PointingIndex Ulnar Artery
( F.P.B.+ Abd.P.B.+ Op.Pol.) Dist. Eminence
● Communicating
M+L Cord ● All Flexors except Branch to Ulnar nerve
- F.Carpi Ulnaris
- F. Dig. Profundus (Med. Half)
● F. Dig. Profundus(Lat. Half)
● P. Teres+ P. Quadratus
C5-8 T1
● Palmaris Longus
Radial ● Abd. Policis Longus ● Elbow ● Lat. 3½ fingers dorsum ● Wrist Drop
● All E-xtensors ● Lat.+ Post cut. Branch arm
● T riceps ● Post. Cut. Branch F.arm
P. cord
● B rachialis
● B rachioradialis
● S upinator
C5-8 T1 In a word- back of Upper limb
all muscles- (BEST)
M.Cut ● Elbow ● Lat. Cut. Branch F.arm from Communicating. Br. To
● C.brachialis ● Humerus elbow to wrist ● Superficl. Br.radial N.
L ● Brachialis ● Post.cut. N. F.arm
● Palmar. cut. Br.of
C5-7 ● Biceps med. nerve
SHOULDER JOINT HIP JOINT KNEE JOINT

MOVMENT CHIEF ACCESSORY CHIEF ACCESSORY CHIEF ACCESSORY
● Deltoid (Main abductor)
N
ABDUCT ● Supra Spinatous ● G. Med.+ Min. ● Sartorius LOCK
0 0
(Initiates+abduct 90 -120 ) ● T.F.L. ● Quadriceps Femoris
● Trapezius (upper+lower
fibres)
● Serratus.Ant.(Trap + S.Ant.
→Scapula rotation)
● Lat. Dorsi ● T. Major
N
ADDUCT ● P. Major ● Choraco ● Adductors. ● Pectineus. UNLOCK
2 Majors Addicted to LaDy ● Biceps(short) ● Gracilis. ● Popliteus
● Triceps(long)
Pet Major of Delta Force ● Pectineus. ● SM(Semi Membranosus) ● Gracilis.
N
FLEX ● Delt oid (Ant. Fibre) ● P. Major ● Ilio-Psoas(Maj.) ● Sartorius ● ST(Semi Tendinosus) ● Sartorius
● P. Major ● Choraco ● Adductors. ● BF(Biceps Femoris) ● Popliteus.
● Biceps(short) ● R. Femoris. ● Gastrocnemious
● G. Max.
N
EXTENT ● Deltoid (Post. Fibre) ● T. Major ● Hamstring :( S. M. + S.T. + ● Quadricep Femoris ● T.F.L.(Tensor
● Lat. Dorsi ● Triceps(long) B.F. + Ischial head Ad.Mag.) Fascia Lata)
● Deltoid (Ant. Fibre) ** ● SM

MED. ● P. Major ● Subscapularis ● G. Med + Min. ● ST ● Gracilis.
N
ROT ● Lat. Dorsi ● T.F.L ● Popliteus ● Sartorius
● T. Major
● D eltoid (Post. Fibre) ● 2 Obturators ● G. Max. ● BF
N
LAT. ROT ● I nfraspinatous ● 2 Gamelli ● Sartorius
● T . Minor………… DIT ● Quadretus Femoris ● Piriformis
● DELTOID is responsible for all mvements of shoulder joint except Adduction.
● L at. dorsi (supplied by – Thoracodorsal Nerve) involved in 3 movements of shoulder : A dduction + E xtention+ M ed. Rotation → LAME
●SUBSCAPULARIS is the main muscle of Medial Rotation although here its mentioned as accessory.
" 2 M ajors Drooling on L ady's S houlder Medially" → medial rotation of shoulder joint mnemonic
● TRENDELENBURG GAIT is caused by weakness of the hip abductors. A superior gluteal nerve injury would paralyse the gluteus medius causing a Trendelenburg gait.
● During knee extention Patella moves upwards and Laterally. Also Medial rotation of femur occurs.
MOVEMENT ANKLE JOINT

CHIEF ACCESS
DORSIFLEX ● TA ● EDL ● EHL ● P.Tertius
PLANTER FLEX ● Gastrocnemius ● FHL ● FDL
● Soleus ● TP ● Plantaris
(I)NVERTION ● t(I)bialis anterior ● t(I)bialis posterior
(E)VERTION ● p(E)roneus muscles
SHOULDER JOINT SPACES’ BOUNDARIES , CONTENTS

SPACES SUPERIOR INFERIOR MEDIAL LATERAL CONTENTS
QUADRANGULAR ● Subscap.(front) ● T. Major ● Triceps (long) ● Surg. Neck ● AxN
● T. Minor(back) ● Post.Cir. Vessels
● Jt. Capsule
UPPER ● T. Major ● T. Minor ● Triceps (long) ● Cir. Scapular Art.
TRIANGULAR ● Lower Subscapular N.
LOWER ● T. Major ● Triceps (long) ● Med. Border ● Radial N.
TRIANGULAR Humerus ● Deep artery of arm
INFERIOR EXTREMITY
IMPORTANT MUSCLE ATTACHMENT AND RELATED INFORMATION
Fascial Compartments of The Lower Limb
● Compartments of the thigh Formed by 3 septae passing from the femur to the fascia lata.
Compartment Nerve Muscles Blood supply
Anterior compartment Femoral • Iliacus Femoral artery
• Tensor fasciae latae

• Sartorius
• Quadriceps femoris
Medial compartment Obturator • Adductor longus/magnus/brevis Profunda femoris artery and
• Gracilis obturator artery
• Obturator externus
Posterior compartment Sciatic • Semimembranosus Branches of Profunda
• Semitendinosus femoris artery
• Biceps femoris
● Compartments of the lower leg
Separated by the interosseous membrane (anterior and posterior compartments), anterior fascial septum (separate
anterior and lateral compartments) and posterior fascial septum (separate lateral and posterior compartments)
Compartment Nerve Muscles Blood supply
Anterior compartment Deep • Tibialis anterior Anterior tibial artery

peroneal • Extensor digitorum longus
nerve
• Extensor digitorum Brevis
• Extensor hallucis longus
• Peroneus tertius
Posterior compartment Tibial • Muscles: deep and superficial compartments Posterior tibial
(separated by deep transverse fascia)
• Deep: Flexor hallucis longus, Flexor digitalis
longus, Tibialis posterior, Popliteus
• Superficial: Gastrocnemius, Soleus, Plantaris
Lateral compartment Superficial • Peroneus longus/brevis Anterior tibial

peroneal
Lower limb- Muscular compartments
● Anterior compartment
Muscle Nerve Action
Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot
Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint
Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot
Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe
● Peroneal compartment
Muscle Nerve Action
Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion
Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint
● Superficial posterior compartment
muscle Nerve Action
Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee
Soleus Tibial nerve Plantar flexor
● Deep posterior compartment
Muscle Nerve Action
Flexor digitorum longus Tibial Flexes the lateral four toes
Flexor hallucis longus Tibial Flexes the great toe
Tibialis posterior Tibial Plantar flexor, inverts the foot
● THE HAMSTRINGS MUSCLES ARE : Biceps Femoris (both heads), Semitendinosus & Semimembranosus.
All are supplied by Sciatic Nerve (tibial part) except Short head of Biceps (supplied by Common Peroneal Nerve).
* Biceps Femoris is commonly injured in sports where explosive bending of knee is required e.g. Sprint,
especially if the athlete has not warmed up first
* Ischial Head of Adductor Magnus is sometimes considered as one of Hamstring muscles
● MUSCLES ATTACHED TO G. TROCHANTER:

- G. Med. +Min. - Piriformis - Qtus. F. (Insert to Quadrate tubercle on the
inter-trochenteric crest)
- O. Ext. +Int. - Gamelli
** O. Int. emerges from the pelvis through the L.S. Foramen
● MUSCLES ATTACHED TO L.TROCHANTER: (N-469)

- Ilio-Psoas
● MUSCLES ATTACHED TO THE LINEA ASPERA: (N-481)

- G. Max. - V. Med+Lat.
- Adductors - Short Head B. F.
● Muscles of Pes Anserinus (The Muscles Attached To Tibia's Medial Side) (N-459)
"A Girl between Two Sargeants":
Gracilus is between Sartorius and Semitendonosus
* Pes Anserinus Bursitis / GOOSE’s FOOT is common in sportsmen due to overuse injuries. The main sign is of pain
in the medial proximal tibia. Here the McMurray test is negative, so medial meniscal injury is excluded.
nd
● INVERSION VS. EVERSION MUSCLES IN LEG: 2 letter rule for Inversion/Eversion
(E)version muscles: p(E)roneus longus, p(E)roneus brevis, p(E)roneus terius
(I)nversion muscles: t(I)bialis anterior t(I)bialis posterior
IMPORTANT NERVE AND RELATED INFORMATION
● MAIN LIMB REFLEXES: 1, 2, 3, 4, 5, 6, 7, 8

- Ankle (S1,2) - Biceps + Supinator (C5,6)
- Knee (L3,4) - Triceps (C7,8)
● OTHER REFLEXES:
- Anal (S3,4) - Abdominal (T7-12) - Deltoid (C7)
- Cremasteric (L1,2) - Hamstrings + Planter (L5,S1) - Hoffmann (C7,8 T1)
● MOVEMENT SEGMENTAL INNERVATION (N-507)

hip flexn (L2,3); knee extentn (L3,4); foot dorsiflexed (L4,5) & inverted (L4,5)
n n
hip extent (L5, S1); knee flex (L5, S1); foot planterflexed (S1,2) & everted (L5, S1)
or
n
- Hip Flex L2,3
- Hip Extn L4,5
n
- Knee Ext L3,L4
n
- Knee Flex L5, S1
- Ankle Dorsifln L4, L5

n
- Ankle Plantarflex S1, S2
n
- Ankle invers L4
n
- Ankle evers L5, S1
- Great toe extention: L5
● Compression of L5 root may be associated with : Paraesthesia over outer leg

Difficulty in walking on heels
Foot- Cutaneous sensation
Region Nerve
Lateral plantar Sural
Dorsum (not 1st web space) Superficial peroneal
1st Web space Deep peroneal
Extremities of toes Medial and lateral plantar nerves
Proximal plantar Tibial
Medial plantar Medial plantar nerve
Lateral plantar Lateral plantar nerve
● Sperior Gluteal Nerve L4, 5; S1 Inferior Gluteal Nerve L5; S1, 2
Lumbar Plexus
Interested In Getting Laid On Fridays?
I liohypogastric [L1]
I lioinguinal [L1]
G enitofemoral [L1, L2]
L ateral femoral cutaneous [L2, L3]
O btruator [L2, L3, L4]
F emoral [L2, L3, L4]
● Obturator nerve, lies immediate medially to Psoas Major musc
● LUMBAR PLEXUS ROOTS "2 FROM 1, 2 FROM 2, 2 FROM 3":

2 nerves from 1 root: Ilioinguinal (L1), Iliohypogastric (L1).
2 nerves from 2 roots: Genitofemoral (L1, L2), Lateral Femoral (L2, L3).
2 nerves from 3 roots: Obturator (L2, L3, L4), Femoral (L2, L3, L4)
Ilioinguinal Nerve - L1 Ventral ramus of spinal nerve (N- 250, 464)
- It passes inferolaterally.
- Pierces Psoas Major and passes over the anterior surface of Quadratus Lumborum.
- Pierces the Internal Oblique and passes deep to the aponeurosis of External Oblique.
- Enters Inguinal Canal; continue outside the Spermatic Cord and passes through Superficial Inguinal Ring and
then reach the skin
● Ilioinguinal nerve is most commonly identified during Inguinal Hernia Surgery as it passes through Inguinal Canal
● Ilioinguinal nerve is at greatest risk of injury during appendicectomy with Lanz Incision
● Branches
• To supply those muscles of the abdominal wall through which it passes.
• Skin and fascia over the pubic symphysis,
• Superomedial part of the femoral triangle
• Surface of the scrotum
• Root and dorsum of penis or labia majora in females.
● Ilioinguinal nerve entrapment may be a cause of neuropathic pain following inguinal hernia surgery
Genitofemoral Nerve L1, L2
- Passes obliquely through Psoas Major, and emerges from its medial border opposite the fibrocartilage between
rd th
3 and 4 lumbar vertebrae
- Descends on the surface of Psoas Major, under cover of the peritoneum
- Divides into Genital and Femoral branches.
- Genital Branch enters into Inguinal Canal thru’ Deep Inguinal Ring & continue within spermatic cord structures
→ supply overlying skin & fascia of scrotum.
- Femoral Branch enters thigh posterior to Inguinal Ligament, lateral to Femoral Artery → supplies skin & fascia
over Femoral Triangle.
● Genitofemoral Nerve may be injured during abdominal or pelvic surgery, or during Inguinal Hernia repairs.
● Genitofemoral Nerve is responsible mainly for the cremasteric reflex (both motor & sensory fibres are tested). A small
contribution is also played by the Ilioinguinal Nerve and thus the reflex may be lost following inguinal hernia repair
● Genitofemoral Nerve – Genital branch passes anterior to External Iliac Artery
Lateral Cutaneous Nerve of Thigh L 2, 3
- Supplies the antero-lateral aspect of the thigh.

- Has no motor branches.
- Meralgia Paraesthetica is a condition which where there is irritation of the nerve causing sensory changes in
the distribution of Lateral Cutaneous Nerve of The Thigh without any motor changes.
Obturator Nerve L 2, 3, 4 Ventral division
- The Obturator Nerve emerges from medial border of Psoas Major at the lateral margin of the Sacrum.
- It then crosses the sacroiliac joint and enters Lesser Pelvis
- Descends on Obturator Internus to enter the obturator groove.
- In the Lesser Pelvis Obturator Nerve lies lateral to the Internal Iliac vessels and Ureter, and is joined
by the Obturator vessels lateral to the Ovary or Ductus Deferens.
● Supplies
Medial compartment of thigh. Muscles supplied are :

Anterior Part Posterior Part
- Adductor Longus - Adductor Magnus (except: lower part - Sciatic Nerve)
- Adductor Brevis - Obturator Externus
- Gracilis
The cutaneous branch supplies distal ⅔ of medial aspect of thigh
● Obturator Canal
• Connects the pelvis and thigh: contains the obturator artery, vein, nerve. This nerve supplies O. externus
Femoral Nerve L 2, 3, 4
- Penetrates Psoas Major

- Exits the pelvis by passing under the Inguinal Ligament to enter the Femoral Triangle, lateral to the femoral
artery and vein.
● Mnemonic for Femoral Nerve supply (don't) M I S V Q Scan for PE
M edial cutaneous nerve of the thigh
I ntermediate cutaneous nerve of the thigh
S aphenous nerve
V astus
Q uadriceps femoris
S artorius
PE ectineus
● The Iliacus muscle lies posterior to the Femoral Nerve in the Femoral Triangle
Sciatic Nerve L4-S3 (Both Ventral And Dorsal Divisions)
Articular Branches Hip joint
Muscular branches in upper leg • Semitendinosus

• Semimembranosus
• Biceps femoris
• Part of Adductor Magnus
Cutaneous sensation • Posterior aspect of thigh

• Gluteal region
• Entire lower leg (except the medial aspect)
Terminates At the upper part of the popliteal fossa by dividing into tibial and peroneal nerves
• The nerve to the short head of the biceps femoris comes from the common peroneal part of the sciatic and the
other muscular branches arise from the tibial portion.
• The tibial nerve goes on to innervate all muscles of the foot except the extensor digitorum brevis (which is
innervated by the common peroneal nerve).
Tibial nerve – Ventral Divisions (L4,5; S1,2,3)
● Begins at the upper border of Popliteal Fossa and is a branch of the sciatic nerve.
● Muscles innervated
• Popliteus
• Gastrocnemius
• Soleus
• Plantaris
• Tibialis posterior
• Flexor hallucis longus
• Flexor digitorum brevis
● Terminates by dividing into the medial and lateral plantar nerves.

● Tibial Nerve at its origin lies medial to and then lateral to Posterio Tibial Artery after it crosses the vessel. (N- 483)
Common peroneal nerve – Dorsal Divisions (L4,5; S1,2)
● Path
- It is laterally placed within the Sciatic Nerve.
- From the bifurcation of the Sciatic Nerve it passes inferolaterally in the lateral and proximal part of the
Popliteal Fossa,
- It lies under the cover of Biceps Femoris and its tendon.

- It ends by dividing into the deep and superficial peroneal nerves at the point where it winds around the
lateral surface of the neck of the fibula in the body of Peroneus Longus, approximately 2cm distal to
the apex of head of the Fibula.
● Branches
In the thigh Nerve to the short head of biceps

Articular branch (knee)
In the popliteal fossa Lateral cutaneous nerve of the calf
Neck of fibula Superficial and deep peroneal nerves
● Common Peroneal Nerve lies @ medial aspect of Biceps Femoris under its cover & is therefore at greatest risk of
injury. The Tibial Nerve may also be damaged in such an injury
● Unable to Dorsiflex & Evertion of foot = Common Peroneal nerve injury
Superficial peroneal nerve (L4,5; S1)
● Path
• Passes between Peroneus Longus and Peroneus Brevis
• 6-7 cm distal to fibula, Superficial Peroneal Nerve bifurcates into intermediate & medial dorsal cutaneous nerve
● Supplies
• Lateral compartment of leg: Peroneus Longus, Peroneus Brevis (action: eversion and plantar flexion)
• Sensation over dorsum of the foot (except the first web space, which is innervated by the deep peroneal nerve)
● Action: Eversion and Plantar Flexion
Deep peroneal nerve (L4,5; S1,2)
Origin From common peroneal nerve,@ lateral aspect of fibula, deep to Peroneus Longus
Course and relation • Pierces the anterior intermuscular septum to enter the anterior compartment
• Passes anteriorly down to the ankle joint, midway between the two malleoli
Terminates In the dorsum of the foot
Muscles innervated • Tibialis anterior

• Extensor hallucis longus
• Extensor digitorum longus
• Extensor digitorum brevis
• Peroneus tertius
Cutaneous supply Web space of the first and second toes
Actions • Eversion and Dorsiflexion (deep cz dorsiflexion)

• Extension of all toes (Extensor Hallucis Longus & Extensor Digitorum Longus)
● After bifurcation past the ankle joint, the lateral branch of Deep Peroneal Nerve innervates the EDB and EHB
The medial branch supplies the web space between the first and second digits
Pudendal nerve S2, 3, 4
- The pudendal nerve exits the pelvis through the greater sciatic foramen.
- Re-enters the pelvis through the lesser sciatic foramen.
- 3 divisions of the pudendal nerve:
• Rectal nerve
• Perineal nerve
• Dorsal nerve of penis/ clitoris
All these pass through the greater sciatic foramen. Pudendal Nerve passes between Piriformis & Coccygeus
medial to Sciatic Nerve and exits the pelvis through the Greater Sciatic Foramen. It crosses the spine of the
Ischium and reenters the pelvis through the Lesser Sciatic Foramen. It passes through the pudendal canal.
- Give supply to Anal Sphincters and External Urethral Sphincter. Also provides cutaneous innervation to the
region of perineum surrounding the anus and posterior vulva.
● Traction and compression of Pudendal Nerve by the foetus in late pregnancy may result in late onset Pudendal
Neuropathy which causes Faecal Incontinence.
IMPORTANT VESSELS AND RELATED INFORMATION
Femoral Artery
● Branches :
Superficial 3Br. Deep 3Br.

- Sup. Ext. Pudendal (SEPA) - Deep Ext. Pudendal (DeEPA)
- Sup. Epigastric (SEA) - Deep Art. Thigh/ Profunda Femoris A. (DeTa)
- Superficial Circum. Iliac (SeCa) - Muscular branches
Remember: Deep Circumflex Iliac Artery arises from External Iliac Artery
● PROFUNDA FEMORIS ARTERY BRANCHES: "Put My Leg Down Please"
- Profundus femoris (deep femoral artery) branches

- Medial circumflex femoral artery
- Lateral circumflex femoral artery
- Perforating arteries
- Descending genicular arteries
● Between Pectineus and iliopsoas muscle 1 artery passes---- Medial circumflex femoral (branch of profunda femoris/
deep artery of thigh). It supplies head & neck of the Femur
● There is a fibrous canal between TP & FHL; It contains 1 artery---- Peroneal artery or Fibular artery
Anterior Tibial Artery (ATA)

• Artery of the anterior compartment
• Begins opposite the distal border of Popliteus; terminates in front of ankle, continuing as Dorsalis Pedis Artery
• Deep Peroneal Nerve, lies Anterior to ATA @ middle ⅓ and Lateral to ATA @ lower ⅓
• Tibialis Anterior lies medial to ATA
Posterior Tibial Artery (PTA) (N- 483, 499)
• Terminal branch of the Popliteal Artery

• Terminates by dividing into Medial and Lateral Plantar Arteries
• Accompanied by two veins throughout its length
Relations Proximal to distal
Anteriorly Tibialis posterior

Flexor Digitorum Longus
Posterior surface of Tibia and Ankle Joint
Posterior Tibial nerve 2.5 cm distal to its origin

Proximal part covered by Gastrocnemius and Soleus
Distal part covered by skin and fascia
● Tibial Nerve at its origin lies medial to and then lateral to PTA after it crosses the vessel. (N- 483)
● Post Tibial A. passes deep to the F.Retinaculum; divides into Med. & Lat. Planter A. - supplies posterior Compartment
of leg.
Saphenous Vein (N-508)
● LSV/GSV Tributaries to be divided B4 Entering Into SFJ :
- Superficial External Pudendal Vein

- Deep External Pudendal Vein
- Superficial Circumflex Iliac Vein
- Superficial Epigastric Vein
- Postero – Medial Thigh branch
● SFJ opening (3cm below & lateral to P. tubercle) may cause Deep External Pudendal Artery (DeEPA – injury) is at
greatest risk of injury as it runs under the LSV close to its origin.(Ref: www.emrcs.com)
● During SFJ exposing--- (Superficial External Pudendal Artery(SEPA) is most likely to seen passing through the
saphenous opening (ref: 500 Anatomy Infex Q no. 2.48) CONFUSED !!!
● Short Saphenous Vein

• Originates at the 5th digit
• It passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along
the posterior aspect of the leg (with the sural nerve – which is purely sensory)
• Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein, approximately at or
above the level of the knee joint.
• Has got 9-12 valves.
GENERAL DISCUSSION
Hip joint (N- 454, 470)
• The acetabulum holds the femoral head by the acetabular labrum

• Normal angle between femoral head and femoral shaft is 130o
● Ligaments
• Transverse ligament: joints anterior and posterior ends of the articular cartilage
• Head of femur ligament (ligamentum teres): acetabular notch to the fovea.
Extracapsular ligaments
• Iliofemoral ligament
• Pubofemoral ligament
• Ischiofemoral ligament
● Blood supply
Medial Circumflex Femoral (Branches of Profunda Femoris)
Lateral Circumflex Femoral (Branches of Profunda Femoris)
And also Obturator , Sup. & Inf. Gluteal
● 2 anastomoses
Cruciate anastomosis
Trochanteric anastomosis… (both provide most of the blood to the head of the femur)
● STRUCTURES PASSES THRU’ THE G.S. FORAMEN:

Above Piriformis: Sup. Gluteal Nerve + Vessels
Below Piriformis:
- Inf. Gluteal Nerve + Vessels
- Internal Pudendal Vessels ← IIA
- Pudendal Nerve
- Sciatic Nerve
- Posterior Cutaneous.Nerve of Thigh
- Nerve to Quadratus.Femoris
- Nerve to Obturator Internus
● STRUCTURES PASSES THRU’ THE L.S. FORAMEN:

- Internal Pudendal Vessels
- Pudendal Nerve
- Nerve to Obturator Internus
- Tendon to Obturator Internus
- Upper & Lower part Filled up by 2Gamelli muscles.
● Structures passing through both the lesser and greater sciatic foramina (medial to lateral):PIN
• P udendal nerve
• I nternal pudendal artery
• N erve to obturator internus
Hip fractures
● Marked lateral rotation of the thigh is a sign of fractured neck of Femur
Classification (Intracapsular)
Chance of AVN is more in elderly as it will disrupt retinacular vessels & only artery in Ligamentum Teres works
The Garden system is one classification system in common use.
• Type I : Unicortical, Stable, Undisplaced fracture with impaction in valgus.
• Type II : Bicortical, Complete, Undisplaced fracture
• Type III : Head is partially displaced, usually rotated and angulated, but still has bony contact – trabeculae
unaligned across the fracture site
• Type IV : Complete bony disruption – trabeculae disrupted
**Blood supply disruption is most common following Types III and IV.
Classification (Extracapsular) usually occurs from basal part of neck to 5cm below the Lesser Trochanter
• Inter – trochanteric
• Basal
• Sub – trochanteric
Classification based on fragments :
• Undisplaced (2 parts)
• Displaced (2 parts)
• Involving G. trochanter (3parts)
• Involving L. trochanter (3parts)
• 4 parts
• Reverse obliquity
Management of hip fractures in older adults SIGN (Scottish Intercollegiate Guidelines Network) Guidelines
(some addition by Dr. Sakib, ITALIC lines)
Fracture type Patient co-morbidities Management
INTRACAPSULAR FRACTURE
Undisplaced Nil Internal fixation (especially if

young)
Undisplaced Nil age <70, leading active life,

Percutaneous Fixation is
reasonable
Undisplaced Major illness or advanced organ Hemiarthroplasty

specific disease
Displaced Displace Nil If age <70 then Internal fixation

always THR. (if possible),
In >70yrs THR, if not possible
cases if
Displaced Nil Age >70 THR
possible u
Displaced can try IF pre-existing joint disease, good level of Age >70 THR
otherwise activity, high life expectency
THR
Displaced Major/ immobile Hemiarthroplasty; (in most
cases non-cemented prosthesis
is used)
EXTRACAPSULAR FRACTURE
Extracapsular fracture (non special type) Only major co-morbidities affect Dynamic hip screw
management
Extracapsular fracture Only major co-morbidities affect Usually intramedullary device

(reverse oblique, transverse or sub management
trochanteric)
** Sub – Trochanteric Fracture management: ORIF (ref: PP – 3 Q-109)
Remember the following rhyme to memorize treatment

“Garden one & two
Cannulated screw
Garden three & four
Austine – Moore (Hemiarthroplasty)”
● SURGICAL APPROACHES FOR THE HIP

Anterior (Smith–Petersen) Approach
- Structures @ risk : Lat. Cutaneous N.; FN; Lat. Fem.circumflex Artery (ascending branch)
- Rectus Femoris detached must
- but for better exposure some times TFL & ant. Part of G.Med. is detached
Antero-lateral (Watson-Jones / Hardinge) Approach (Recommended in the SIGN guidelines)

- Structures @ risk : Femoral Nerve
- Usually enters between TFL & G.Med joint, for better exposure, ant. Part of G.Med. is Detouched
-
Direct lateral (modified Hardinge) Approach**
- Structures @ risk : Superior Gluteal Nerve
- TFL incised & split in the line of its fibre (later G.med is encountered )
- Anterior Tendon of G.med & V.Lat. is divided.
- The transverse branch of the Lateral Circumflex Femoral Artery is divided to gain access.
Posterior (Moore or Southern) Approach**

- Structures @ risk : Sciatic Nerve
- TFL incised & split in the line of its fibre
- Middle of G.max split in the line of its fibre
- Short ext.rotators (piriformis, OI & gamelli) are divided (** most important**)
- There is a increased risk of dislocation with this method
Femoral triangle anatomy
● Boundaries "So I May Always Love Sally":
Superiorly : Inguinal ligament;

Medially : Adductor longus;
Laterally : Sartorius.
Floor : Iliopsoas, adductor longus and pectineus
Roof : Fascia lata and Superficial fascia
Superficial inguinal lymph nodes (palpable below the inguinal ligament)
Great saphenous vein
● Contents
NAVY: In order from lateral to medial: Nerve Artery Vein Y of the groin ·
Alternatively: Y = Y-fronts [male underwear].
long saphenous vein, lies lat. To FV. Structures lie more laterally are:
• Deep and superficial inguinal lymph nodes
• Lateral cutaneous nerve

• Great saphenous vein
• Femoral branch of the genitofemoral nerve
Femoral Sheath (Crural Sheath)
Anterior wall : Continuous above with Fascia Transversalis

Posterior wall : Continuous with Psoas Fascia or Fascia Iliacus
● Femoral branch of GFN pierce the anterior wall of Femoral Sheath running on anterior surface of Ext. Iliac Artery
● Septate into 3 compartments containing lateral to medial is : Artery →Vein → Lymphatics
Femoral canal
● Lies at medial aspect of the Femoral Sheath i.e. medial to the vein.
● Borders
Laterally Femoral vein
Medially Lacunar ligament
Anteriorly Inguinal ligament
Posteriorly Pectineal ligament - PP
● Contents
• Lymphatic vessels
• Cloquet's lymph node
● Physiological significance : Allows Femoral Vein to expand to allow for increased venous return from lower limbs.
● Pathological significance : Site of femoral hernias. Relatively tight neck places these at high risk of strangulation.
Adductor canal or Hunter's or subsartorial canal
• Immediately distal to the apex of the femoral triangle,

• Lying in the middle third of the thigh.
• Canal terminates at the adductor hiatus.
Borders Contents
Laterally Vastus medialis ● Saphenous nerve

Posteriorly Adductor longus & magnus ● Femoral vessels
Roof Sartorius ● Nerve to Vastus
medialis
● Adductor canal compression syndrome

- Commonly presents in young males
- Caused by compression of the femoral artery by the musculotendinous band from Adductor Magnus
Treatment: Division of the abnormal band and restoration of the arterial circulation
Differential diagnosis:
- Popliteal fossa entrapment is the main D/D – here popliteal pulse disappears when knee is fully extended
- Important differential diagnosis in men presenting with symptoms of acute limb ischaemia on exertion.
Popliteal fossa
Boundaries of the popliteal fossa
Supero Laterally Biceps femoris
Supero Medially Semimembranosus

Semitendinosus
Gracilis
Sarorius
Adductor Magnus
Infero Laterally Gastrocnemius (lateral head)

Plantaris
Infero Medially Gastrocnemius (medial head)
Floor Popliteal surface of the femur,

N-476 Posterior ligament of knee joint
Popliteus muscle and ligament
Popliteal fascia
Roof Superficial and deep fascia / popliteal fascia/ Fascia lata

N-509 Contents are : - SSV
- Post. Cut. Nerve of thigh
- Med. Cut. Nerve of thigh (post. Div.)
- Sural / Peroneal Common nerve
Contents
• Popliteal vessels and Lymph nodes
• Fat
• Common peroneal nerve & branches
• Tibial nerve & branches
• Posterior cutaneous nerve of the thigh
• Genicular branch of the obturator nerve
• SSV
Some key points

• Sciatic nerve divides within apex
• Tibial nerve is the superficial most structure
• Popliteal vein lies deep to the Tibial nerve
• Popliteal artery is the deepest structure
• Upper part of the fossa (med. → lat.) : AVN
• Middle part of the fossa (forward → behind) : AVN

• Lower part of the fossa (lat. → med.) : AVN
• Common peroneal nerve lies in the same plane of Tibial nerve; crosses the fossa obliquely from superior to
lateral angle along the medial border of the Biceps Femoris
• PCL is seperated from the popliteal vessels by oblique Popliteal ligament
Knee joint
● During full extension all ligaments are taut and the knee is locked.
● Both ACL & PCL are intracapsular but Extrasynovial
● ACL does not allow Femur to ga backward and PCL does not allow Femur- to go forward--- remember this rhyme
● ACL is attached to anterior intercondylar area of tibia on the tibial spine then passes postero-laterally to insert into
posteromedial aspect of lateral femoral condyle – ABUL – ACL goes Backward, Upward & Laterally
● ACL is Taut in Knee extention;
● PCL is separated from the popliteal vessels at its origin by Popliteal Ligament
● PCL is Taut in Knee Flexion
● ACL Injury :
• Typically presents with: POP sound while playing + foot got stucked at
mud; loud crack, pain and RAPID swelling knee (haemoarthrosis)
• Sport injury
n
• Mechanism: Hyper extent injury; high twisting force applied to a bent knee
• Poor healing
● Medial ligament Injury :Funny Angle during play,

Knee feels Unsafe,

Significant laxity in Valgus stress,
unable to fully extend the kneedue to pain
● Meniscus Tear : Twisting injury to flexed knee,

Delayed swelling
Joint locking (Patient may develop skills to "unlock" the knee)
Recurrent episodes of pain & effusion are common, often following minor trauma
Scenario : 1st time tackle → Swelling @ night → Ice compression → Pain↓ →
Again played → Re-injury → Immediate swelling
Lateral Menisci is attached to Popliteus tendon & its free to move.
Medial Menisci is fixed as its adherent to the deep part of Medial Collateral Ligament.(N-474)
● Car Hit --- Valgus Hit , Then think # or Bony damage

if Vulgas Hit during play ---- MCL Injury is the common answer.
● Chondromalacia : Softening of articular cartilage of patella

Patellae
• Teenage girls, following an injury to knee e.g. Dislocation patella
• Typical history of pain on going downstairs or at rest
• Tenderness, quadriceps wasting
● Dislocation of patella :
• Most commonly occurs as a traumatic primary event, either through direct trauma or through
severe contraction of quadriceps with knee streched in valgus and external rotation
• Genu valgum, tibial torsion and high riding patella are risk factors
• Skyline x-ray views of patella are required, although displaced patella may be clinically obvious
● Osgood-Schlatter : Pain knee after activity and settles with rest; no h/o trauma;
Tender palpable lump over prox.tibia;
Painful tibial tubercle
● Osteochondritis : Small Osteocartilagenous fragment separates from one of the femoral condyle (usually
Dessicans medial), and is rendered avascular. If loose body becomes trapped betn joint surface then
locking occurs. If it occurs at Elbow Capitulum– PANNER’S DISEASE.
Ankle joint
● Structures passes thru’ F. Retinaculum/ Tarsal Tunnel(Ant. To Post): (N-493) Tall Doctors Are Never Hungry
- TP - T-VAN
- FDL - FHL
● The Flexor Hallucis Longus tendon is the most posterior structure at the medial malleolus
● Inversion & Eversion of Ankle takes place mainly @ Subtalar & Talocalcaneonavicular joint
partly @ Transverse Tarsal Joint
st
● Most common & 1 ligament to be ruptured with a planter flexion-inversion ankle sprain is Anterior Talofibular
Ligament
n
● Ankle joint is best aspirated bet TA & EHL
● TARSAL BONES : "Tall Californian Navy Medcial Interns Lay Cuties": (rt. foot, superior to inferior, medial to lateral):
T alus; C alcanous; N avicular; M edial cuneiform; I ntermediate cuneiform; L ateral cuneiform; C uboid
● Cuboid is located @ lateral aspect of foot between calcaneus posteriorly and 4th and 5th metatarsals distally
● Tuberosity of Navicular bone gives attachment to Tibialis Posterior. This Bone articulates with 4 bones : Talus, 3
th
Cuneiforms (& occasionally with a 5 – Cuboid)
● Planter Fascitis : Pain under ball of feet,

Tenderness along the distal edge of heel contact area
● Kohler’s Disease : Osteochondritis of Navicular

● Severe’s Disease : Osteochondritis of Calcaneum
nd
● Freidberg’s Dis. : Osteochondritis (crushing type) of 2 Meta Tarsal head
th
● Jones Fracture : # of 5 metatarsal – effects the insertion of P. brevis and P. tertius muscles
● Metatarsalgia : Any painful foot condition affecting the metatarsal region of foot
n n
● Charcot’s Joint : Progressive degenerat of a wt. bearing joint – a process, marked by body destruct ,
n
bone resorpt & eventual deformity (Neurotrauma or Neurovascular cz, e.g. DM)
Trendelenberg Test
Injury or division of the superior gluteal nerve results in a motor deficit that consists of weakened abduction of the thigh
by gluteus medius, a disabling gluteus medius limp and a compensatory list of the body weakened gluteal side. The
compensation results in a gravitational shift so that the body is supported on the unaffected limb.
When a person is asked to stand on one leg the gluteus medius usually contracts as soon as the contralateral leg leaves
the floor, preventing the pelvis from dipping towards the unsupported side. When a person with paralysis of the superior
gluteal nerve is asked to stand on one leg, the pelvis on the unsupported side descends, indicating that the gluteus
medius on the affected side is weak or non functional ( a positive Trendelenberg test).
● Trendelenburg gait is czed by weakness of hip abductors. Superior Gluteal Nerve(L5, S1 ) injury paralyse Gluteus
Medius causing this gait. Buttock muscle wasting can also be found
● Gerdy's tubercle is a lateral tubercle of the tibia, where the Iliotibial Tract inserts.
Pilonidal sinus
• Occur as a result of hair debris creating sinuses in the skin (Bascom theory). extremely common in hirsute
individuals
• Usually in the natal cleft of male patients after puberty – most commonly located in the midline
• The opening of the sinus is lined by squamous epithelium, but most of its wall consists of granulation tissue.
• Squamous cell carcinoma can occur with chronic pilonidal sinus.
• Clinically the sinus presents when acute inflammation occurs, leading to an abscess.
• Patients may describe being asymptomatic and periods of pain and discharge from the sinus.
• Definitive treatment should never be undertaken when acute infection or abscess is present as this will result in
failure.
• Definitive treatments include Bascom procedure with excision of the pits and obliteration of the underlying
cavity.
• The Karydakis procedure involves wide excision of the natal cleft such that the surface is recontoured once
the wound is closed. This avoids the shearing forces that break off the hairs and has reasonable results.
• When performing incision and drainage for pilonidal abscess try to avoid making the incision in the midline
of the natal cleft
THORAX
● Line drawn between tips of scapulae corresponds the body of T7 vertebra

between superior margin of iliac crests corresponds the body of L4 vertebra
● Most prominent vertebral spinous process is C7
st
● 1 Rib Neck Ant. Relation (From Med. to Lat) SVAN
- Symp. Chain
- 1st post. Intercostals vein
- Superior intercostal artery
- T1 nerve
● Subclavian Vein, passes in front of Scalene Tubercle. Subclavian Art.& Lowest trunk Br.plexus passes back of it
● Intervertebral discs
• The posterior longitudinal ligament overlies the posterior aspect of the vertebral bodies. It also overlies the
posterior aspect of the intervertebral disks.
• Consist of an outer annulus fibrosus and an inner nucleus pulposus.
• The anulus fibrosus consists of several layers of fibrocartilage.
• The nucleus pulposus contains loose fibres suspended in a mucoprotein gel with the consistency of jelly. The
nucleus of the disc acts as a shock absorber.
• Pressure on the disc causes posterior protrusion of the nucleus pulposus. Most commonly in
lumbrosacral and lower cervical areas.
• The discs are separated by hyaline cartilage.
• There is one disc between each pair of vertebrae, except for C1/2 and the sacrococcygeal vertebrae.
• Acute Disc prolapse → Hip extension pain → Femoral stretch(L2 - 4) → cause Scoliosis as a result
CLINICAL SIGNIFICANCE OF THE STERNAL ANGLE

Sternal Angle of Louis or Ludwig’s plane
2nd costal cartilage anteriorly and between T4-5 vertebra posteriorly.
It is a significant landmarks as –
1. Ribs are counted from this level to downwards. 2nd rib lies at sternal angle.
2. It marks the plane of sepraration of superior and inferior mediastinum.
3. Ascending aorta ends, arch of aorta starts and ends and descending aorta starts.
4. Trachea divides into 2 principle bronchi.
5. Azygous vein arches over the root of the Rt. Lung and opens in SVC.
6. Pulmonary trunk divides into 2 pulmonary arteries below this level.
7. Thoracic duct crosses from right to left side and reaches left side at the level of sterna angle.
8. It marks the upper limit of the base of the heart.
9. Cardiac plexus are situated at the same level.
● Anatomical structures at the level of the manubrium and upper sternum
Upper part of the manubrium • Left brachiocephalic vein

• Brachiocephalic artery
• Left common carotid
• Left subclavian artery
Lower part of the manubrium/ manubrio-sternal • Costal cartilages of the 2nd ribs
angle • Transition point between superior and inferior
mediastinum
• Arch of the aorta
• Tracheal bifurcation
• Union of the azygos vein and superior vena cava
• The thoracic duct crosses to the midline
The Thoracic Wall
● The thoracic wall is innervated by the Intercostal nerves – the ventral primary rami of spinal nerves T1 – T11
● Remember:
Winging of scapula laterally indicates Trapezius muscle weakness. Innervated by Spinal Accessory Nerve
Winging of scapula medially indicates Serratus Anterior muscle weakness. Innervated by Long Thoracic
Winging of scapula may be produced by Damage to rhomboids. Innervated by Dorsal Scapular. But its rare.
st
● During surgery if 1 aortic intercostal artery is injured then right bronchus might be deprived of main source blood
supply.
Pectoralis major muscle
Origin From the medial two thirds of the clavicle,

manubrium and sternocostal angle
Insertion Crest of the greater tubercle
Nerve supply Lateral pectoral nerve
Actions Adductor and medial rotator of humerus
Clavipectoral Fascia
Components
- Subclavius muscle & its investing fascia
- Costocoracoid ligament
- Costocoracoid membrane
- Pectoralis minor muscle & its investing fascia
- Suspensory ligament of axilla
Pierced By
- Thoraco-acromion Vessels
- Cephalic Vein
- Lat. Pect. N.
- Lymphatics from Breast & pect. region to Apical nodes.
● A man has an incision sited than runs 8cm from the deltopectoral groove to the midline. Which of the following is not at
risk of injury? (April’2012)
A. Cephalic vein;
B. Shoulder joint capsule; Ans.
C. Axillary artery;
D. Pectoralis major;
E. Pectoralis major
● Scapula protracts SA --- Long thoracic nerve

Scapula retracts Trapezius (accessory nerve) & Rh. Major (dorsal scapular nerve)
Antagonistic 2group muscles
Mediastinum
Region between the pulmonary cavities.
It is covered by the mediastinal pleura. It does not contain the lungs.
It extends from the thoracic inlet superiorly to the diaphragm inferiorly.
● Contents Middle Mediastinum MAAPH

• P ericardium
• H eart
• A ortic root
• A rch of azygos vein
• M ain bronchi
● Contents Posterior Mediastinum : DATES

D escending aorta
A zygous and hemiazygos vein
T horacic duct
E sophagus
S ympathetic trunk/ganglia; splanchnic nerves
Vagus nerve
● Anterior Mediastinum may contain germ cell tumor
● 4 collateral venous systems exists for SVC obstruction:

• Azygos venous system
• Internal mammary venous pathway
• Long thoracic venous system with connections to the femoral and vertebral veins (2 pathways)
Blood supply of the Heart
● Right Coronary Artery Supplies: (Arises from Anterior Aortic Sinus)

• Right atrium
• Diaphragmatic part of the Left Ventricle
• Usually the posterior third of the inter ventricular septum
• The SA node (60% cases)
• The AV node (80-90% cases)
● Left Coronary Artery Supplies: (Arises from Left Posterior Aortic Sinus)
• Left atrium
• Most of Left Ventricle
• Part of the Right Ventricle
• Anterior two thirds of the inter ventricular septum
• The SA node (remaining 40% cases)
Venous Drainage of the Heart
Cardiac veins ultimately join to form an enlarged vessel known as the Coronary sinus
lies @ posterior part of the coronary sulcus.
The sinus opens into the right atrium between the opening of the inferior vena cava and the tricuspid valve. The
opening of the sinus is guarded by a semilunar valve which is also called Thebesian valve.
Tributaries of coronary sinus are :
• Great Cardiac Vein: Begins at the cardiac apex
Runs in the anterior interventricular sulcus with LAD
Drains both ventricles and left atrium – to Left extremity of coronary sinus
• Middle Cardiac Vein: Begins at the cardiac apex

Runs in the posterior interventricular sulcus with PDA
Drains the areas supplied by PDA – to Right extremity of coronary sinus
• Small Cardiac Vein: Runs in the right posterior atrioventricular (AV) groove
Drains the posterior part of right atrium & ventricle – to Right extremity of coronary
sinus near its atrial end.
• Oblique Vein Lt. Atr. : Descends obliquely on the back of the left atrium to join the Left extremity of
coronary sinus near its end. Also known as Oblique Vein of Marshall
• Post. Vein of Lt. Vent: Runs on the diaphragmatic surface of left ventricle
Drains to Left extremity of coronary sinus & sometimes to Great cardiac vein
OTHER CARDIAC VEINS DRAINING INDEPENDENTLY INTO THE RIGHT ATRIUM
Anterior Cardiac Veins: Arise on the anterior surface of the right ventricle.
Drain the anterior portion of the right ventricle & open into the right atrium.
Venae cordis minimae, or Veins of Thebesius, or Smallest Cardiac Veins:

Arise in the muscular wall of the heart. Numerous in the right atrium and ventricle.
Drain directly into the chambers of the heart (majority in atria).
Innervation of the Heart
Autonomic nerve fibres: - From superficial and deep cardiac plexus – send small branches to the heart along the
major vessels, continuing with the right and left coronary arteries
- These lie Anterior to bifurcation of trachea,
Posterior to ascending aorta
Superior to bifurcation of pulmonary trunk.
Parasympathetic supply: From presynaptic fibres of the Vagus Nerves.
** The background vagal discharge serves to limit heart rate, and loss of this background vagal tone accounts for the
higher resting heart rate seen following cardiac transplant**
● Receptors on Heart:
The ventricles: beta-1 adrenoceptors
The atria: cholinergic receptors.
The aortic arch: contains baroreceptors.
The carotid body: contains baroreceptors
● Structures within the Right Atrium:

• Musculi pectinati (unique feature!!)
• Crista terminalis
• Opening of the coronary sinus (Thebesian valve)

• Opening of IVC (Eustachian valve)
• Fossa ovalis
• Tricuspid valve
** The trabeculae carnae are located in the right ventricle**
● Stroke volumes range from 55 -100ml. avg. 70ml
● ABC'S
*A*ortic arch gives off *B*racheiocephalic trunk (innominate artery), left *C*ommon Carotid & left *S*ubclavian artery
Electrical activity of the heart
Myocardial action potential
Phase Description Mechanism
0 Rapid Rapid Na+ influx

depolarisation These channels automatically deactivate after a few ms
1 Early repolarisation Efflux of K+
2 Plateau Slow influx of Ca
3 Final repolarisation Efflux of K+
4 Restoration of ionic Resting potential is restored by Na+/K+ ATPase

concentrations There is slow entry of Na+ into the cell decreasing the potential difference
until threshold potential is reached, triggering a new action potential
NB: cardiac muscle remains contracted 10-15 times longer than skeletal muscle
● Starlings law
• Increase in end diastolic volume will produce larger stroke volume.
• This occurs up to a point, beyond which cardiac fibres are when excessively stretched then stroke volume will
fall.
• It is important for regulation of cardiac output in cardiac transplant patients who need to increase cardiac output.
● Baroreceptor reflexes
• Baroreceptors located in Aortic Arch And Carotid Sinus.
• Aortic baroreceptor impulses travel via the Vagus
• Carotid baroreceptor impulses travel via the Glossopharyngeal Nerve.
• They are stimulated by arterial stretch.
• Even at normal blood pressures they are tonically active.
• Increase in baroreceptor discharge causes:
*Increase parasympathetic discharge to the SA node.
*Decrease sympathetic discharge to ventricular muscle causing decrease contractility & fall strokevol.
*Decrease sympathetic discharge to venous system causing increased compliance.
*Decrease peripheral arterial vascular resistance
● Atrial stretch receptors

• Located in atria at junction between pulmonary veins and vena cava.
• Stimulated by atrial stretch and are thus low pressure sensors.
• Increased blood volume will cause increased parasympathetic activity.
• Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors: the Bainbridge
reflex.
• Decreases in receptor stimulation → increased sympathetic activity → decrease renal blood flow → decreases
GFR → decreases urinary sodium excretion → renin secretion by juxtaglomerular app.→ raise angiotensin II.
• Increased atrial stretch will also result in increased release of Atrial Natriuretic Peptide.
● CVP LINE POINT

Obese Patients : 2 cm under the mid-point of the clavicle and 1 cm laterally.
Thin Patients : 1 cm under the mid-point of the clavicle and 0.5 cm laterally.
2days after CVP line given patient complains pleuritic chest pain. O/E CXR P/A shows – Radio-opaque density
@ left hilum. Answer- Embolisation of Broken Catheter tip
Auscultatory Areas
Auscultatory areas starting from left 2nd intercostal space: Remember: All Patients Take Medicines
Aortic - Pulmonary - Tricuspid - Mitral
• Only Aortic area is on right ; Remember that All stands for aortic area - read as Aortic ll (Second)
• Remember " Lot no.245 " - Left 2, 4, 5 IC spaces in that order for Pulmonary, Tricuspid, Mitral
Valve Site
Pulmonary valve Left second intercostal space, at the upper sternal border
Aortic valve Right second intercostal space, at the upper sternal border
Mitral valve Left fifth intercostal space, just medial to mid clavicular line
Tricuspid valve Left fifth intercostal space, at the lower left sternal border
● CARDIAC MURMUR
Diastolic(D) → (MS, TS)
Systolic (mid/ejection) → (AS, PS)
Systolic (pan) → (MR, TR)

Diastolic(early) → (AR, PR)
Regarding cardiac murmurs :
- Mid diastolic murmur @ apex; enhanced in left lateral position: MS
- Ejection systolic murmur loudest @ aortic region, no radiation to carotid arteries, ECG normal → Aortic
Sclerosis not AS, because AS confirms above features
● Prosthetic valve endocarditis 2 types–

st st
1 type occurs within 1 yr of surgery cz --- Staphylococci
nd nd
2 type occurs after 2 yr of surgery cz ----- group A haemolytic streptococci (otherwise known as strep. viridans)
● Prosthetic heart valves on Chest X-rays

Aortic : Usually located medial to the 3rd ICS on the right.
Mitral : Usually located medial to the 4th ICS on the left.
Tricuspid : Usually located medial to the 5th ICS on the right.
Congenital heart disease

Acyanotic - most common causes
Ventricular septal defects (VSD) - most common, accounts for 30%
Atrial septal defect (ASD) - due to incomplete closure of Foramen Ovale
Patent ductus arteriosus (PDA)
Coarctation of the aorta
Aortic valve stenosis
VSDs are more common than ASDs. However, in adult patients ASDs are the more common new
diagnosis as they generally presents later
Cyanotic - most common causes

Tetralogy of Fallot
Transposition of the great arteries (TGA)
Tricuspid atresia
Pulmonary valve stenosis
Fallot's is more common than TGA. However, at birth TGA is the more common lesion as patients with
Fallot's generally presenting at around 1-2 months
● ASD = split fixed S2 (sometimes ejection systolic)

● VSD = Pansystolic murmur
● PDA = Continuous machinery murmur (systolic+diastolic)
(Weak arm pulse, radio-femoral delay)
● COA = Late systolic murmur (systolic+diastolic)
● TOF = Ejection systolic murmur (systolic+diastolic)
th
(Systolic murmur loudest @posterior aspect of 4 ICS)
** Almost All CHD shows systolic murmur **
● Structure @ risk during PDA ligation is Lt. recurrent Laryngeal nerve, which lies dorsally to ductus arteriosus.
● Infective endocarditis is the complication of untreated VSD, commonly found in IV drug users, rarely occurs in MS,
TOF
Jugular Venous Pressure

Provides information on right atrial pressure,
Provides clues to underlying valvular disease.
A non-pulsatile JVP is seen in SVC obstruction.
Kussmaul's sign: paradoxical rise in JVP during inspiration in constrictive pericarditis
'a' wave = atrial contraction

• Large if atrial pressure raised e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
• Absent if there is atrial fibrillation
Cannon 'a' waves

• Caused by atrial contractions against a closed tricuspid valve
• Are seen in complete heart block, VT/ ectopics, nodal rhythm, single chamber ventricular pacing
'c' wave
• Closure of tricuspid valve
• Not normally visible
JVP: {C} wave - {c}losure of the tricuspid valve
'v' wave
• Due to passive filling of blood into the atrium against a closed tricuspid valve
• Giant v waves in tricuspid regurgitation
'x' descent = fall in atrial pressure during ventricular systole
'y' descent = opening of tricuspid valve
● Fixed raised JVP : SVC obstruction

Rising JVP ē normal breath sound : Cardiac temponade (muffled heart sound, pulse fade on inspiration)
The ECG
P wave
• Represents Atrial Depolarization
• Duration 0.08 to 0.1 seconds (80-100 ms)
• Electrical vector is directed from SA to AV node, and spreads from right atrium to left atrium. This create P
wave.
QRS complex
• Represents Ventricular Depolarization
T wave
• Represents Ventricular Repolarization
• Duration 160ms
• The interval from the beginning of QRS complex & the apex of T wave is called Absolute Refractory Period.
• The last half of the T wave is called Relative Refractory Period (or vulnerable period)
• A small positive U wave may follow the T wave which represents the last remnants of ventricular repolarization.
P-R interval
• Time from the onset of the P wave to the beginning of the QRS complex
• Duration 0.12 to 0.20 seconds (120 to 200 ms)
• Represents the time between the onset of atrial depolarization and the onset of ventricular depolarization
ST segment
• Isoelectric period following the QRS
• Duration 320 ms
• Represents period, in which the entire ventricle has been depolarized.
• It corresponds to the plateau phase of the ventricular action potential
Q-T interval
• Represents both Ventricular Depolarization and Repolarization
• Estimates the duration of an average ventricular action potential.
• Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
● ECG FINDINGS & CULPRIT VESSEL
Reciprocal
Wall Affected ST Elevatn n
Culprit Artery
ST Depres
Septal V1-2 None LAD
Anterior V3-4 None LAD
Anteroseptal V1-4 None LAD
Anterolateral V3-6, I, aVL II, III, aVF LAD, LCX / OM
Ext. anterior
V1-6, I, aVL II, III, aVF LM
(or Ant.sept.ē Lat.extn)
Inferior II, III, aVF I, aVL RCA/ LCX
Lateral I, aVL, V5-6 II, III, aVF LCX / OM
Post.(assoc.ē Inf.
V7-9 V1-4 PDA / LCX
or Lat. bt can isolated)
Rt ventricular
II, III, aVF, V1, V4R I, aVL RCA
(assoc. ē Inf.)
● ECG changes for thrombolysis or percutaneous intervention:

- ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR
- ST elevation > 1mm (1 small square) in > 2 consecutive inferior leads (II, III, avF, avL) OR New LBBB
- ST elevation of 1mm in leads II, III and aVF reflects significant cardiac ischaemia due to RCA occlusions
which puts the patient @ risk of cardiac arrhythmias (due to blood supply to the SA node).
● ECG: left vs. right bundle block "WiLLiaM MaRRoW":

W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W pattern in V3-V6 is Right bundle block.
[ Note: consider bundle branch blocks when QRS complex is wide.]
● ECG FINDINGS
n
Hypokalaemia : Prolong P-R S-T depres flattened / inverted T U- waves
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!!!
Hyperkalaemia : Small P tall, tented T Wide QRS

More Pot more T, no P, broad QRS +(irregular pulse**)
PE : P pulmonale(peaked P) tall R in V1 inverted T in V1-4 S 1 Q 3 T3

+ (atrial arrhythmias, tachycardia, right ventricular strain pattern, RBBB, right axis deviation)
Hypercalcaemia : Short QT
Hypocalcaemia : Long QT
Other cz of long QT are Hypomagnesaemia & β-blocker, Amiodarone therapy
WPW : δ-wave
Pericarditis : Concave upward S-T elevation- cave upward !!!
MI : Convex upward S-T elevation
Hypothermia : J- wave
Arterial line in situ : On studying trace, the incisura can be found – the elastic recoil of the aorta is the
physiological event, which cause this process.
Ventricular Tachycardia – VT
Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus. Two main types of
VT:
• Monomorphic VT: most commonly caused by myocardial infarction
• Polymorphic VT: A subtype of polymorphic VT is Torsades De Pointes which is precipitated by prolonged QT
interval. The causes of a long QT interval are listed below
Causes of a prolonged QT interval
Congenital Drugs Other

• Jervell-Lange-Nielsen syndrome • Amiodarone, sotalol, class • Hypocalcaemia,
(includes deafness and is due to 1a antiarrhythmic drugs Hypokalaemia,
an abnormal potassium channel) • TCA, fluoxetine Hypomagnesaemia
• Romano-Ward syndrome (no • Chloroquine • Acute MI
deafness) • Terfenadine* • Myocarditis
• Erythromycin • Hypothermia
• SA haemorrhage
Ventricular tachycardia – Verapamil is contraindicated

Torsades de pointes – Treatment IV magnesium sulphate
n
● Thymus op =Risk of left brachiocephalic vein injury, cz it lies immediate posteriorly
● During esophagectomy while mobilizing esophagus, surgeon must be careful of avoiding injury to Thoracic duct.
Lung Relations (some key points)
– The apex extends about 4 cm above the medial one-third of the clavicle.
– Suprapleural fascia (Sibson's fascia) runs from C7 to 1st rib and overlies the apex. It lies between
parietal pleura and the thoracic cage
– The oblique fissure corresponds closely to medial border of scapula when the arm is fully abducted.
– The transverse fissure of the right lung corresponds to the level of the fourth rib.
– The lower border on each side corresponds to 8th rib in mid-axillary line and the 10th rib posteriorly
– At the mid-clavicular line, the costodiaphragmatic recess is between ribs 6 and 8;
– At the mid-axillary line the costodiaphragmatic recess is between ribs 8 and 10;
– At the paravertebral line the costodiaphragmatic recess is between ribs 10 and 12.
– Phrenic nerve is the most anteriorly located structure in the lung root
– Vagus nerve is the most posteriorly located structure in the lung root
th
● Safety Triangle for ICD: (N-395) 5 ICS Anterior To the mid Axillary line
Anterior edge of latissimus dorsi,
The lateral border of pectoralis major,
A line superior to the horizontal level of the nipple, and the apex below the axilla.
Alveolar Ventilation
n
• Minute ventilat is total vol.of gas ventilated per min.i.e. MV (ml/min) = tidal volume x Respiratory rate
(resps/min).
• Dead space ventilation describes the volume of gas not involved in exchange in the blood.
1. Anatomical dead space: 150ml

• Volume in conducting airways not involved in gaseous exchange: mouth to terminal bronchioles
• Measured by Fowlers method
• Increased by : Standing,
Increased size of person,
Increased lung volume
Drugs causing bronchodilatation e.g. Adrenaline
2. Physiological dead space: normal 150 ml,

Increases in ventilation/perfusion mismatch e.g. PE, COPD, Hypotension
• Volume of gas in the alveoli and anatomical dead space not involved in gaseous exchange.
• Alveolar ventilation: vol. of fresh air entering alveoli per min.i.e. Alveolar ventilation = minute ventilation –
Dead space volume
Control of Ventilation
• Control of ventilation is coordinated by the respiratory centres, chemoreceptors, lung receptors and muscles.
• Automatic, involuntary control of respiration occurs from the medulla.
• The respiratory centres control the respiratory rate and the depth of respiration.
Respiratory centres
Medullary respiratory centre: Inspiratory and expiratory neurones.
• Has ventral group which controls forced voluntary expiration
• Has dorsal group which controls inspiration.
• Depressed by opiates.
Apneustic centre: Lower pons

• Stimulates inspiration - activates and prolongs inhalation
• Overridden by pneumotaxic control to end inspiration
Pneumotaxic centre: Upper pons

• Inhibits inspiration at a certain point.
• Fine tunes the respiratory rate.
• Levels of PCO2 most important in ventilation control
• Levels of O2 are less important.
Peripheral chemoreceptors:
• Located in the bifurcation of carotid arteries and arch of the aorta.
+
• They respond to changes in reduced pO2, increased H and increased pCO2 in ARTERIAL BLOOD.
• During acute hypercapnia the carotid receptors will be stimulated first
Central chemoreceptors:
• Located in the medulla.
• Stimulated by arterial CO2 therefore respond to raised H+ in Brain Interstitial Fluid to increase
ventilation.
• Are NOT influenced by O2 levels therefore insensitive to hypoxia
Lung receptors:
• Stretch receptors : respond to lung stretching causing a reduced respiratory rate
• Irritant receptors : respond to smoke etc causing bronchospasm

• J (juxtacapillary) receptors
● Apex - ventilation (V) more, perfusion (Q) less, So, Apex – V / Q = more
Base - perfusion (Q) more ventilation (V) less, So, Base – V / Q = less
Lung Compliance
– Lung compliance is a measure of the ease of expansion of the lungs and thorax.
– Determined by pulmonary volume and elasticity
– Increased Compliance means – loss of elastic recoil of lungs. This is due to loss of supportive tissue around the
airways e.g.: old age or emphysematous COPD
– Decreased Compliance means – greater change in pressure is needed for a given change in volume e.g.
atelectasis, pulmonary oedema+ fibrosis, pneumonia, pneumonectomy, kyphosis lack of surfactant
● LUNG VOLUMES AND CAPACITIES
Tidal Volume (TV/ VT) : 500; Inspired/expired in each breath; 340mls in females.
Inspiratory Reserve Volume (IRV) : 3000; Extra volume that can be inspired above Tidal volume.
Expiratry Reserve Volume (ERV) : 1300; Forceful volume that can be expired after expiration of Tidal volume
Residual Volume (RV) : 1200; remains in the lungs after a most forceful expiration.
Inspiratory Capacity ( IC) : IRV + TV= 3000+500=3500; Volume of maximal inspiration
Functional Residual Capacity (FRC) : ERV+ RV= 1300+1200= 2500; Air remaining after normal expiration
Vital Capacity (VC) : TV +IRV + ERV = 500+3000+1300= 4800; Maximum amount that
can be expired by forced expiration after a forceful inspiration
Total Lung Capacity (TLC) : VC+ RV = 4800+1200=6000; Max. Amount to which lung can be
expanded
[** Not measurable by spirometry: RV; FRC; TLC – They can only be measured by helium dilution]
● The Vital Capacity is Reduced in:

1. Pulmonary fibrosis / infiltration / oedema / effusions
2. Weak respiratory muscles e.g. MG, GBS, myopathies
3. Skeletal abnormalities e.g. chest wall abnormalities
● The Functional Residual Capacity (FRC) is increased in:

• Erect position
• Emphysema
• Asthma
● Flow volume loop is the investigation of choice for upper airway compression.
● ALVEOLAR MACROPHAGE
- Derived from monocyte of bone marrow
- Found in the surface of the alveolus and interior of alveolar septum
- Are called dust cells
● FEV1 : Volume expired in 1 second after a maximal inspiration. 80% of the forced vital capacity, expressed as
FEV1/FVC.
FEV1 <1.5 L persons are not allowed for pneumonectomy
Obstructive lung disease Restrictive lung disease
FEV1 is reduced more than FVC, both FEV1 and FVC decrease
thus the FEV1/FVC ratio কমে < 0.8. so ratio ≥ 0.8
Asthma Pulmonary fibrosis

COPD Asbestosis
Bronchiectasis Sarcoidosis
Bronchiolitis obliterans Acute respiratory distress syndrome
Laryngeal malignancy Infant respiratory distress syndrome
Kyphoscoliosis
Neuromuscular disorders
● RESPIRATORY FAILURE
H
p : 7.35 – 7.45; pCO2 : 4-6 KPa (35 – 45) mmHg; pO2 : 10 – 14 KPa (75-105) mmHg, HCO3 : 22 -26;
- Type-I causes that impairs gas exchange; (Hypoxia + )

- Type-II causes that creates alveolar hypoventilation; (Hypoxia ē Hypercapnia – RR ↑)
- Type-I Acute + Chronic pCO2 Normal

- Type-II Acute + Chronic pCO2 Increased
- Type-II Chronic HCO3 Increased but Normal in others
H
- p usually normal in all 4 but in some cases- Type-I Acute & Type-II Chronic show reduction
H
- Type-II chronic --- ↑ pCO2; ↑HCO3; ↓p
- COPD – only TLC & FRC raised and rests are reduced
● Bed ridden pt.+ lung abscess = gravitates at superior segment of lower lobe
● The hilar LN is not accessible ē mediastinoscope.
● Mnemonic of right shift of oxyhemoglobin dissoc. Curve : CADET face RIGHT

C O2
A cidosis
2,3-DPG
E xercise
T emperature
● STORED BLOOD has less 2,3 DPG and therefore has a higher affinity for oxygen, So this blood has reduced
ability to release oxygen at metabolising tissues
Adult respiratory distress syndrome
– Bilateral pulmonary infiltrates and severe hypoxemia (PaO2/FiO2 ratio < 200)
– No cardiogenic pulmonary edema (clinically or pulmonary capillary wedge pressure or CVP < 18 mm Hg).
– In is subdivided into two stages: Early stages consist of an exudative phase of inury ē associated edema.
– Later stage is of repair & consists of fibroproliferative changes.
– Subsequent scarring may result in poor lung function.
Causes
• Sepsis
• Direct lung injury
• Trauma
• Acute pancreatitis
• Long bone fracture or multiple fractures (through fat embolism)
• Head injury (causes sympathetic nervous stimulation which leads to acute pulmonary hypertension)
Clinical features
• Acute dyspnoea and hypoxaemia hours/days after event

• Multi organ failure
Management
• Treat the underlying cause
• Antibiotics
• Negative fluid balance i.e. Diuretics
• Mechanical ventilation strategy using low tidal volumes as conventional tidal volumes may cause lung injury
(only treatment found to improve survival rates)
Pulmonary embolism: investigation
• CTPA is the first line investigation for PE according to current BTS guidelines
• If CTPA is negative then patients do not need further investigations or treatment for PE
• Ventilation-perfusion scanning may be used initially if –
Appropriate facilities exist,
Chest x-ray is normal
No significant symptomatic coexisting cardiopulmonary disease
{Some other points}
● D-dimers
• sensitivity = 95-98%, but poor specificity
● V/Q scan
• Sensitivity = 98%; specificity = 40% - high negative predictive value, i.e. if normal virtually excludes PE
• Other causes of mismatch in V/Q include
Old pulmonary embolisms,
AV malformations,
Vasculitis,
Radiotherapy
• COPD gives matched defects
● CTPA
• Peripheral emboli affecting subsegmental arteries may be missed
● Pulmonary Angiography
• Gold standard
● ECG changes
• No changes
• S1, Q3, T3
• Tall R waves: V1
• P pulmonale (peaked P waves): inferior leads
• Right axis deviation, Right bundle branch block
• Atrial arrhythmias
• T wave inversion: V1, V2, V3
• Right ventricular strain
Pulmonary embolism: management
● A summary of the British Thoracic Society guidelines

• Heparin should be given if intermediate or high clinical probability before imaging.
o Unfractionated heparin (UFH) should be considered

(a) As a first dose bolus,
(b) In massive PE,
(c) Where rapid reversal of effect may be needed.
o Otherwise, low molecular weight heparin (LMWH) should be considered as preferable to UFH, having
equal efficacy and safety and being easier to use.
• Oral anticoagulation should be used when Venous Thrombo Embolism (VTE) has been reliably confirmed.
• The target INR should be 2.0-3.0; when this is achieved, heparin can be discontinued.
• The standard duration of oral anticoagulation is: 46 weeks for temporary risk factors,
3 months for first idiopathic,
At least 6 months for other;
● Massive PE
• CTPA or echocardiography will reliably diagnose clinically massive PE.
• Thrombolysis is 1st line for massive PE (ie circulatory failure) and may be instituted on clinical grounds alone if
cardiac arrest is impending; a 50 mg bolus of Alteplase is recommended.
• Invasive approaches (thrombus fragmentation and IVC filter insertion) should be considered where facilities and
expertise are readily available.
● CXR shows Kerley B lines ---- interstitial oedema

● CXR shows Azygous Lobe is in normal variant – as ‘Reverse Comma Sign’ behind medial end of right clavicle
● CXR shows Coin Shadow ----- Hamartoma ; u can give answer granuloma also which can be differentiated by
uncontrolled growth.
● CXR shows Rib Notching ------ Coarctation of aorta. Due to enlarged intercostals arteries
Lung Cancer
Classified according to histological subtypes- small cell and non small cell lung cancer.
Small cell lung carcinoma

- Strongly associated with smoking
- Typically arise in the larger or main airways; centrally located
- Most aggressive, rapid grower, early metastaser;

- Frequent associated with Para-Neoplastic.synd.
- It presents in disseminated form
- Usually chemosensitive
Non Small Cell Lung Cancer

Most common variant and accounts 80% of all lung cancers.These share common features of prognosis and
management. Paraneoplastic features and early disease dissemination are less likely among these.They comprises:
• Squamous cell carcinoma (25% cases)

- Best prognosis (Sq > Large > Adeno > Small = SLAM)
- Most associated ē Smoking
- More slow growing and are typically centrally located
- Polygonal pink cells with dark angular nuclei
- Associated with a survival of a year without treatment
• Adenocarcinoma (40% cases)

- most common lung cancer among never-smokers
- Usually found in the periphery of lung
• Large Cell Carcinoma (10% Cases)
Non Small Cell Ca Management

Only 20% suitable for surgery
Mediastinoscopy performed prior to surgery as CT not always show mediastinal LN involvement
Curative or palliative radiotherapy ( usually poor response to chemotherapy)
Surgery contraindications
• Assess general health
• Stage IIIb or IV (i.e. metastases present)
• FEV1 < 1.5 litres is considered a general cut-off point*
• Malignant pleural effusion
• Tumour near hilum
• Vocal cord paralysis (it implies extracapsular spread to mediastinal nodes and is an indication of inoperability)
• SVC obstruction
Thoracic duct
• Begins as the continuation of cisterna chyli in abdomen in front of L2 body & Enters the thorax at T12
• 38 – 45 cm in length
• @ starting its @ right side of & behind the Aorta by the side of right crus.
• @ thoracic cavity it ascends thru’ the posterior mediastinal cavity between Aorta & Azygos Vein
• Lies posterior to the oesophagus for most of its intrathoracic course – Crosses from right to left side and
reaches left side at the level of sternal angle T5
• Drains all lymphatics except Right side of head, neck, thorax, upper rt. extremity, rt.lung, rt.side of heart &
convex surface of liver – and all below diaphragm
• Lymphatics draining the left side of head & neck → thoracic duct prior to its entry to left brachiocephalic vein.
• Lymphatics draining the right side of head & neck → subclavian and jugular trunks → right lymphatic duct → the
mediastinal trunk → the right brachiocephalic vein.
• Its location in the thorax makes it prone to injury during oesophageal surgery. Some surgeons administer cream
to patients prior to oesophagectomy so that it is easier to identify the cut ends of the duct.
Diaphragm
● Embryology
• Septum transversum - Central tendon

• Pleuroperitoneal membranes - Parietal membranes surrounding viscera
• Cervical somites C5 to C7 - Muscular component of the diaphragm
● Apertures Memory aid:

T8 (8 letters) = vena cava = IVC + Inf. Phrenic nerve (Rt.)
T10 (10 letters) = oesophagus = O esophagus + V agus nerve + Ga stric artery (Lt.) = OVaGa
T12 (12 letters) = aortic hiatus = A orta + T horacic duct + A zygos vein = ATA
● Hernia
Type of hernia Features
Morgagni Anteriorly located

Minimal compromise on lung development
Minimal signs on antenatal ultrasound
Usually present later
Usually good prognosis
Bochdalek hernia Posteriorly located; Larger defect

Often diagnosed antenatally
Associated with pulmonary hypoplasia
associated with chromosomal abnormalities -Trisomy 21,18
Poor prognosis
Phrenic Nerve
Origin
• C3, 4, 5
• Have both motor and sensory functions. For this reason sub diaphragmatic pathology may cause referred pain
to the shoulder
Supplies
• Diaphragm, sensation central diaphragm and pericardium
Path
• The Phrenic Nerve passes with the Internal Jugular Vein across Scalenus Anterior.
• It passes deep to Pre-vertebral Fascia (of Deep Cervical Fascia).
• Left: crosses anterior to the 1st part of the Subclavian Artery.
• Right: Anterior to Scalenus Anterior and crosses anterior to the 2nd part of the Subclavian Artery.
• On both sides, the phrenic nerve runs posterior to the Subclavian Vein and posterior to the Internal Thoracic
Artery as it enters the thorax.
• They both lie anterior to the hilum of the lung
Right phrenic nerve

• In the superior mediastinum: anterior to Right Vagus and laterally to SVC
• Middle mediastinum: right of Pericardium
• It passes over the Right Atrium to exit the diaphragm at T8
Left phrenic nerve

• Passes lateral to the Left Subclavian Artery, Aortic Arch and Left Ventricle
• Passes anterior to the root of the lung
• Pierces the diaphragm alone
GROIN SPACES’, TRIANGLES, CANALS BOUNDARIES, CONTENTS

SUP INF ANT POST MED LAT CONTENTS
INGUINAL Lat→→Med ● IL (mostly) ● EO (mostly) ● FT (mostly) ● Vas
CANAL TA-IO-CT ● LL (medially) ● IO (laterally) ● CT (medially) ● Artery 2Vas, Testicular, Cremasteric
Conjoint Superficial ring ● Pampiniform plexus of veins
Tendon is a defect in ● Lymphatic vessels
formed by Ant. Wall – a ● Nerves: genital Br. GFN,
the fusion triangular ileoinguinal, Sypm. Nerve to Arteries
of opening @ ● Processus Vaginalis
aponeuro EOA
sis of IO &
TA
FEMORAL ● IL ● Pectineus ē covering ● LL ● FV separating ● Fatty connective tissues
CANAL fascia ● Efferent vessels from deep nodes
● Cloquet node
FEMORAL ● IL ● Superior pubic ramus ● LL ● FV These are also the margins of neck of
● PL ● IPT Femoral Hernia. As 3 of 4 of these
RING *** boundaries are rigid, so this hernia is
prone to strangulation more
FEMORAL ● FT ● Fascia iliacus/ psoas fascia A-V-Lymphatic ( Lat→ → Med)
SHEATH Femoral Br. GFN (pierce ant wall)
(CRURAL)
FEMORAL ● IL ● AL ● Sartorius
TRIANG.
IL: Inguinal Ligament (Poupart). LL: Lacunar Ligament (Gimbernat). PL: Pectineal Ligament (Cooper) FT: Fascia Transversalis. CT: Conjoint tendon(inguinal falx). EO: External
Oblique. IO: Internal Oblique. TA: Transversus Abominis FV: Femoral Vein; AL: Adductor Longus IPT: Ileopubic tract
*** These are also MARGINS OF NECK OF FEMORAL HERNIA. As 3 of 4 of these boundaries are rigid, Femoral hernia is prone to strangulation most of all hernias.
● MPI : ASIS & PT; MIP : ASIS & PS; MIPS: Femoral pulse MPI : Deep Inguinal Ring
● DEEP INGUINAL RING :

- F. transversalis – oval opening
- The transversalis fascia forms the superolateral edge of the deep inguinal ring. The epigastric vessels form its inferomedial wall.
- 1.3 cm above ing. Ligament. @ MPI
- Lat. To MIP
● The pubic tubercle marks the site of the superficial inguinal ring.
Structures Associated with the Umbilical Cord and Umbilicus
In the Primitive Body At the Umbilicus at In the Neonatal Abdomen Pathology

Stalk Term
Yolk stalk (vitelline Absent or vestigial Absent Meckel's diverticulum or

duct) umbilical sinus or fistula
Extraembryonic Absent None

coelom
Herniated intestine Returned to abdomen Returned to abdomen Failure of return:

omphalocele
Vitelline arteries Absent Celiac, superior, and inferior

mesenteric arteries
Vitelline veins Absent Part of portal vein
Allantois Absent or vestigial Urachus (median umbilical Patent urachus;

ligament) undescended bladder
Umbilical arteries Both present Medial umbilical ligaments Single umbilical artery (1%)
Umbilical veins Only left vein present Round ligament in falciform

ligament
Undifferentiated Embryonic connective None

mesenchyme tissue at cord
HEAD-NECK, NEURO, EYE, ENT PART-1
Important Muscle Attachment And Related Infos
● STRAP / INFRA HYOID MUSCLES

These muscles depress the hyoid bone i.e. infrahyoid muscles - TOSS
S ternothyroid
S ternohyoid
T hyrohyoid
O mohyoid
● Digastric Muscle bellies develop from 2 separate Pharyngeal Arches. 1st arch -- Ant. Belly; 2nd arch --- Post. Belly
● Digastric muscle (posterior belly )crosses the carotid artery superiorly (N-29)
● Digastric muscle is the only muscle which lies exclusively in Anterior Triangle
● Pterygomedibular Raphe’ serves as point of attachment of Superior Pharyngeal Constrictor & Buccinator
nd
● Muscles of facial expression developed from mesoderm 2 branchial arch
● Muscles of facial expression are the remnants of Panniculus Carnosus(a continuous subcutaneous muscle sheet)
● Inferior Belly Omohyoid divides posterior triangle further into an upper and lower triangle (Fig. later page)
th
● Palatoglossus muscle contained in palatoglossal arch & is supplied by 10 CN
th
● Levator Veli Palatini muscle supplied by 10 CN
● Tensor Veli Palatini muscle
Tense Palate
th
Opens Auditory Tube supplied by 5 CN
● Tensor veli palatini muscle hooks around the medial pterygoid hamulus
th
● Tensor tympani tense tympanic membrane supplied by 5 CN
● Lateral Pterygoid Muscle Action
Protrude mandible (main function)
Depresses mandible,
Side to side movement of mandible

● Rectus capitis anterior muscle is innervated by ventral rami of C1 & C2
Sternocleidomastoid
Anatomy
Origin Rounded tendon attached to upper manubrium sterni

Muscular head attached to medial third of the clavicle
Insertion Mastoid process of the temporal bone and lateral area of the superior nuchal line of
the occipital bone
Innervation The motor supply to the sternocleidomastoid is from the accessory nerve. The ansa
cervicalis supplies sensory information from the muscle - anterior rami of C2 and C3
(proprioception)
Action • Both: extend the head at atlanto-occipital joint and flex the cervical vertebral
column. Accessory muscles of inspiration.
• Single: lateral flexion of neck, rotates head so face looks upward to the
opposite side
Sternocleidomastoid divides the anterior and posterior triangles of the neck.
Important Vessels And Related Infos
Cerebral blood flow
• CNS autoregulates its own blood supply

• Factors affecting the cerebral pressure include: Systemic CO2 levels, CNS metabolism, CNS trauma, CNS
pressure
• The PaCO2 is the most potent mediator
• Acidosis and hypoxaemia will increase cerebral blood flow but to a lesser degree
• Cerebral perfusion pressure may increase in patients with head injuries and this can result in impaired blood
flow
• ICP governed by Monroe-Kelly Doctrine: which considers brain as closed box, changes in pressure are offset
by loss of CSF. When this is no longer possible ICP rises
Source: Netter Clinical Anatomy 2nd Edition

Circle of Willis
May also be called the Circulus Arteriosus

• Inferior surface of brain. Supplied by the Internal Carotid Arteries and Vertebral Arteries
• If artery is occluded, collaterals may be able to compensate
• Components include:
1. Anterior Communicating Arteries
2. Anterior Cerebral Artery-Supply: Olfactory Bulb, Frontal Lobe Med.& Inf.surface, Corpus Callosum
3. Internal Carotid Arteries

4. Posterior Communicating Arteries
5. Posterior Cerebral Arteries
6. Termination of Basilar Artery
• Supply: Corpus striatum, Internal Capsule, Diencephalon, Midbrain
• Middle Cerebral Artery (←
← ICA) largest part of circle of Willis(contained in cisterna basalis), passes thru’
lateral sulcus of cerebrum between temporal & frontal lobe; Here lesion causes Contralateral hemiplegia.
• Left sided Lesion is worse because Broca’s Speech Area situated here
● Posterior Cerebral Artery is well visualized in Vertebral Angiogram
Vertebral Arteries
• Enter the cranial cavity via foramen magnum
• Lie in the subarachnoid space
• Ascend on anterior surface of medulla oblongata
• Unite to form the basilar artery at the base of the pons
Branches:
• Posterior spinal artery
• Anterior spinal artery
• Posterior inferior cerebellar artery (largest of the cerebellar arteries arising from vertebral artery)
The Vertebral Artery is the first branch of the subclavian artery. Anatomically it is divisible into 4 regions:
• The first part runs to the foramen in the transverse process of C6. Anterior to this part lies the vertebral and
internal jugular veins. On the left side the thoracic duct is also an anterior relation.
• The second part runs superiorly through the foramina of the the transverse processes of the upper 6 cervical
vertebrae. Once it has passed through the transverse process of the axis it then turns superolaterally to the
atlas. It is accompanied by a venous plexus and the inferior cervical sympathetic ganglion.
• The third part runs posteromedially on the lateral mass of the atlas. It enters the sub occipital triangle, in the
groove of the upper surface of the posterior arch of the atlas. It then passes anterior to the edge of the posterior
atlanto-occipital membrane to enter the vertebral canal.
• The fourth part passes through the spinal dura and arachnoid, running superiorly and anteriorly at the lateral
aspect of the medulla oblongata. At the lower border of the pons it unites to form the basilar artery.
Basilar artery Branches:

• Anterior inferior cerebellar artery
• Labyrinthine artery
• Pontine arteries
• Superior cerebellar artery
• Posterior cerebral artery
Common Carotid Artery
● CCA lies lateral to Inferior Parathyroid
- RCCA arises at the bifurcation of the brachiocephalic trunk,

- LCCA arises from the arch of aorta.
- Both terminate @ upper border of thyroid cartilage (lower border, C3 vertebra) by dividing into ICA and ECA
● Left Common Carotid Artery

- Arises immediately to the left and slightly behind the origin of the brachiocephalic trunk.
- Thoracic portion is 2.5- 3.5 cm in length and runs superolaterally to the sternoclavicular joint.
In the thorax, The vessel is in contact,

- From below upwards: Trachea, left RLN, left margin of oesophagus.
- Anteriorly: Left Brachiocephalic Vein runs across the artery, the cardiac branches from the left
vagus descend in front of it.
- These structures together with thymus and anterior margins of left lung and pleura separate the
artery from manubrium.
In the neck, The artery

- Runs superiorly deep to sternocleidomastoid and then enters the anterior triangle.
- At this point it lies within the carotid sheath with the vagus nerve and the internal jugular vein.
- Posteriorly the sympathetic trunk lies between the vessel and the prevertebral fascia.
- At the level of C7 the vertebral artery and thoracic duct lie behind it.
- The anterior tubercle of C6 transverse process is prominent and the artery can be compressed
against this structure (it corresponds to the level of the cricoid).
- Anteriorly at C6 the omohyoid muscle passes superficial to the artery.
- Within the carotid sheath the jugular vein lies lateral to the artery.
● Right Common Carotid Artery

- Arises from the brachiocephalic artery.
- Corresponds with cervical portion of LCCA, except that there is no thoracic duct on right.
- Oesophagus is less closely related to RCCA than LCCA.
Summary points about the carotid anatomy - Path

Passes behind the sternoclavicular joint (12% patients above this level) to the upper border of the thyroid cartilage, to
divide into the external (ECA) and internal carotid arteries (ICA).
Relations
• At the level of C6 crossed by Omohyoid
• Then passes deep to the thyrohyoid, sternohyoid, sternomastoid muscles.
• Passes behind carotid tubercle (transverse process C6 vertebra)- (compression here stops haemorrhage).
• The inferior thyroid artery passes posterior to CCA.
• Then : LCCA crossed by thoracic duct, RCCA crossed by RLN
Contents of carotid sheath: CCA; ICA; IJV; Vagus
External Carotid Artery
● Path
• Upper border of thyroid cartilage to pass in between the angle of the mandible and mastoid process
• Initially anteromedial to the ICA, then becomes lateral
• Lower ECA covered by sternomastoid, passed by hypoglossal nerve/lingual & facial vein
• Then deep to digastric and stylohyoid, eventually passes into the parotid gland where it divides into the
superficial temporal and maxillary branches
● ECA BRANCHES: Some Aggressive Ladies Find Odd Positions More Stimulating!!!
Susan Always Lays Flat On Pillows Making Sex Terrific !!!
st
• S uperior thyroid (1 br. of ECA)
• A scending pharyngeal
• L ingual
• F acial
• O cciptal
• P osterior auricular
• M axillary
• S uperficial T emporal
or
• Anterior branches : Superior thyroid (1st br. of ECA)
Lingual
Facial
• Posterior branches : Occiptal

Posterior auricular
• Medial branches : Ascending pharyngeal
• Terminal branches : Maxillary

Superficial temporal
th
● 12 Nerve crosses the ECA 1cm superior to carotid bifurcation. @ that point it also cross Lingual artery (N-29)
Middle meningeal artery
• Middle meningeal artery is typically the third branch of the first part of the maxillary artery, one of the two
terminal branches of the External Carotid Artery. After branching off the maxillary artery in the infratemporal
fossa, it runs through the foramen spinosum to supply the dura mater (the outermost meninges) .
• The middle meningeal artery is the largest of the three (paired) arteries which supply the meninges, the
others being the anterior meningeal artery and the posterior meningeal artery.
• The middle meningeal artery runs beneath the Pterion. It is vulnerable to injury at this point, where the skull is
thin. Rupture of the artery may give rise to an extra dural hematoma.
• In the dry cranium, the middle meningeal, which runs within the dura mater surrounding the brain, makes a
deep indention in the calvarium.
• The middle meningeal artery is intimately associated with the auriculotemporal nerve which wraps around
the artery making the two easily identifiable in the dissection of human cadavers and also easily damaged in
surgery.
• Middle meningeal artery hemorrhage: To stop, sometimes ligation done near its origin→
→ Auriculotemporal
Nerve damage may occur→
→ Parasthesia of ipsilateral External ear and outer most part of Tympanic Membrane
● Pterion is the important landmark---- Middle meningeal artery(←Mx A← ECA) (N-2)

mainly vault bones supplier, but never supply brain – hemorrhage from it can cz pressure over the motor area.
Internal carotid artery
- Formed from the common carotid opposite the upper border of the thyroid cartilage.
- It extends superiorly to enter the skull via the carotid canal.
- From the carotid canal it then passes through the cavernous sinus, above which it divides into the anterior
and middle cerebral arteries.
Relations in the neck
Posterior • Longus capitis

• Pre-vertebral fascia
• Sympathetic chain
• Superior laryngeal nerve
Medially • External carotid (near origin)

• Wall of pharynx
• Ascending pharyngeal artery
Laterally • Internal jugular vein (moves posteriorly at entrance to skull)

• Vagus nerve (most posterolaterally)
Anteriorly • Sternocleidomastoid
• Lingual and facial veins
• Hypoglossal nerve
Relations in the carotid canal

• Internal carotid plexus
• Cochlea and middle ear cavity
• Trigeminal ganglion (superiorly)
• Leaves canal lies above the foramen lacerum
Path and relations in the cranial cavity

- The artery bends sharply forwards in the cavernous sinus,
- Abducens nerve lies close to its inferolateral aspect.
- Oculomotor, trochlear, opthalmic and, usually, the maxillary nerves lie in the lateral wall of the sinus.
- Near the superior orbital fissure it turns posteriorly and passes postero-medially to pierce the roof of the
cavernous sinus inferior to the optic nerve.
- It then passes between the optic and oculomotor nerves to terminate below the anterior perforated substance
by dividing into the anterior and middle cerebral arteries.
Branches
• Anterior and middle cerebral artery
• Ophthalmic artery
• Posterior communicating artery
• Anterior choroid artery
• Meningeal arteries
• Hypophyseal arteries
● Structures passing betn ICA & ECA
- 2 Muscles : Styloglossus
Stylopharyngeus
th
- 2 Nerves : 9 CN
th
10 CN, pharyngeal branch
- Gland : Parotid
- Styloid process
● Superior Thyroid Artery Br. : May I Softly Squeeze Charlie's Girl?

• M uscular
• I nfrahyoid
• S uperior laryngeal
• S ternomastoid
• C ricothyroid
• G landular
● Thyroidea ima artery, supplies lower part of thyroid. Usually not found; if found, may be found to arise from
Brachiocephalic Trunk usually. Beside this it can be arise from RCC, Subclavian, Aorta or Int. Mammary Artery
Subclavian Artery Branches ViT CD
V ertevral
i nternal thoracic
T hyrocervical trunk (Inf.thyroid + Transverse cervical + Suprascapular)
st
**Inf. thyroid Artery passes medially over 1 part of Vertebral Art. & longus coli**
**Suprascapular + Transverse cervical artery passes over phrenic nerve to enter to
post triangle**
nd
C ostocervical trunk (2 prt Deep cervical+Supreme intercostal )
rd
D orsal scapular(3 part)
● Subclavian Artery becomes Axillary artery from outer border of 1st rib
st nd rd
● Subclavian Artery 1 part medial to, 2 part behind & 3 part lateral to Anterior Scalene
● Ophthalmic Artery Branches

1. Central artery of retina (smallest & 1st branch)
2. Main trunk branches
Post. Ciliary
Supra-orbital
Supra-trochlear
Ant. & post. Ethmoidal
Medial palpebral
Dorsal nasal
3. Lacrimal branch
Cavernous Sinus
● Floor is formed by Endosteal layer of dura & other walls or boundaries by meningeal layer of dura
Vertically, From Superior To Inferior (structuresw within lateral wall) O, TOM CAT
rd
• O culomotor nerve (3 CN)
• T rochlear nerve (4th CN)
th
• O phthalmic branch of 5 nerve (V1)
th
• M axillary branch of 5 nerve ( V2)
• T rigeminal ganglion
Structures passing thru’

• I C A ē venous & sympathetic plexus around it
th
• A bducent (6 CN)
Draining channel
• Into transverse sinus thru’ superior petrosal sinus
• Into IJV thru’ inferior petrosal sinus
• Into pteryghoid plexus of vein thru’ emissary veins

• Rt. & Lt. C.sinus thru’ ant & post intercavernous sinus & basilar plexus of vein
Cavernous Sinus Lesion

• Cavernous sinus Thrombosis
• Extending Pituitary tumor
• ICA Aneurysm
• Secondary deposit
● Inferior Sagittal Sinus is enclosed in posterior half or two thirds of the free margin of falx cerebri (N-97)
● Superior Petrosal Sinus connects two sinuses – Cavernous & transverse
IJV and EJV
● IJV: TRIBUTARIES: Medical Schools Let Confident People In (inferior to superior)

• M iddle thyroid
• S uperior thyroid
• L ingual
• C ommon facial
• P haryngeal
• I nferior petrosal sinus
● EJV: TRIBUTARIES: PAST

P osterior external jugular vein
A nterior jugular vein
S uprascapular vein
T ransverse cervical vein
Facial Artery and Vein
● Facial vein crosses the carotid bifurcation

● Facial Vein is the usual superficial venous connection thru’ which infection courses towards cavernous sinus.
Beside this veins of face, scalp, diploic bone have no valve, so infection can easily pass to dural venous sinus.
● Facial artery :--- imp. Landmark, anterior Border of masseter muscle

● Facial artery arises @ Carotid Triangle, a little above the Lingual Artery
● Facial artery is crossed by the branches of Facial nerve from behind forward
● Great cerebral vein (of Galen), formed by union of two internal cerebral veins and ends in straight sinus(N-137)
● Great cerebral vein (of Galen) aneurysmal dilatation effect optic radiation → Homonymous Hemianopia
Little’s Area / Kisselbach’s Area (N-35)
Anastomosis among
• Septal branch of Superior Labial Artery (←
← FA ← MXA)
• Branch of Sphenopalatine Artery (←
← MXA)
• Branch of Greater Palatine Artery (←
←MXA)
• Anterior and Posterior Ethmoidal Artery (←
← Ophthalmic artery)
● Anterior bleed refers Little’s area and posterior bleed refers bleeding point @ post. end of inferior turbinate
Epistaxis (N-36)
Usually trivial and insignificant but severe haemorrhage may compromise airway and pose a risk to life.
Anatomy:
Arterial supply
• From internal and external carotid
• An arterial plexus exists at Little's area and is the source of bleeding in 90% cases
• Major arterial supply is from the sphenopalatine and greater palatine arteries (branches of the maxillary artery)
• The facial artery supplies the more anterior aspect of the nose
• Ethmoidal arteries are branches of the ophthalmic artery. They supply the posterosuperior nasal cavity
Venous drainage follows the arterial pattern
Classification
• Primary idiopathic epistaxis accounts for 75% of all cases
• Secondary cases arise as a result of events such as anticoagulants, trauma and coagulopathy
• Classification into anterior and posterior epistaxis may help to locate the source and becomes more important
when invasive treatment is required
Management
• Resuscitate if required
• Subject should sit upright and pinch nose firmly
• Nasal cavity should be examined using a headlight
• Simple anterior epistaxis may be managed using silver nitrate cautery. If difficult to manage then custom
manufactured packs may be inserted
• Posterior packing or tamponade may be achieved by passing a balloon tamponade device and inflating it. This
is indicated where anterior packing along has failed to achieve haemostasis.
• Post nasal pack patients should receive antibiotics
• Failure of these methods will require more invasive therapy. Where a vascular radiology suite is available
consideration may be given to angiographic techniques. Direct ligation of the nasal arterial supply may also be
undertaken. Of the arterial ligation techniques available the endo nasal sphenopalatine arterial ligation
procedure is most popular.
● To expose Lingual Artery, Hyoglossus muscle is to be exposed

● Descending palatine Artery arises within pterygopalatine fossa (N-35)
● Pterygoid plexus drains via Maxillary vein @ infratemporal foss (N-64)
Important Nerve And Related Infos
● Important Informations
All post - ganglionic fibers of sympathetic are adrenergic (except sweat gland, piloerector -colenergic)
All pre - ganglionic fibers of sympathetic are cholinergic
All pre & post - ganglionic fibers of p. sympathetic are cholinergic
A preganglionic fibre is always cholinergic
Sympathetic nervous system- anatomy
The cell bodies of the pre-ganglionic efferent neurones lie in the lateral horn of the grey matter of the spinal cord in the
thoraco-lumbar regions.
The pre-ganglionic efferents leave the spinal cord at levels T1-L2. These pass to the sympathetic chain.
Lateral branches of the sympathetic chain connect it to every spinal nerve. These post ganglionic nerves will pass to
structures that receive sympathetic innervation at the periphery.
Sympathetic chains
These lie on the vertebral column and run from the base of the skull to the coccyx.
Cervical region Lie anterior to the transverse processes of the cervical vertebrae and
posterior to the carotid sheath.
Thoracic region Lie anterior to the neck of the upper ribs and and lateral sides of the lower
thoracic vertebrae.They are covered by the parietal pleura
Lumbar region Enter by passing posterior to the median arcuate ligament. Lie anteriorly
to the vertebrae and medial to psoas major.
Sympathetic ganglia
• Superior cervical ganglion lies anterior to C2 and C3.
• Middle cervical ganglion (if present) C6
• Stellate ganglion- anterior to transverse process of C7, lies posterior to the subclavian artery, vertebral artery
and cervical pleura.
• Thoracic ganglia are segmentally arranged.
• There are usually 4 lumbar ganglia.
Clinical importance
• Interruption of the head and neck supply of the sympathetic nerves will result in an ipsilateral Horners
syndrome.
• For treatment of hyperhidrosis the sympathetic denervation can be achieved by removing the T2 and T3 ganglia
with their rami. Removal of T1 will cause a Horners syndrome and is therefore not performed.
In patients with vascular disease of the lower limbs a lumbar sympathetomy may be performed, either radiologically or
(more rarely now) surgically. The ganglia of L2 and below are disrupted. If L1 is removed then ejaculation may be
compromised (and little additional benefit conferred as the preganglionic fibres do not arise below L2.
Nerve Injury
Neuropraxia • Nerve intact but electrical conduction is affected

• Full recovery
• Autonomic function preserved
• Wallerian degeneration does not occur
Axonotmesis • Axon is damaged and the myelin sheath is preserved. The

connective tissue framework is not affected.
• Wallerian degeneration occurs.
Neurotmesis • Disruption of the axon, myelin sheath and surrounding

connective tissue.
• Wallerian degeneration occurs.
Wallerian Degeneration
• Axonal degeneration distal to the site of injury.
• Is the process that occurs when a nerve is cut or crushed.
• Typically begins 24-36 hours following injury neuronal injury and the distal axon remains excitable up until this
time.
• Axons are excitable prior to degeneration occurring.
• Myelin sheath degenerates and is phagocytosed by tissue macrophages.
• Eventually regeneration of the nerve may occur although recovery will depend on the extent and manner of
injury
Nerve repair
• Neuronal repair may only occur physiologically where nerves are in direct contact. Where a large defect is
present the process of nerve regeneration is hampered and may not occur at all or result in the formation of a
neuroma. Where nerve regrowth occurs it typically occurs at a rate of 1mm per day.
Cranial nerves
● Sensory : 128; Motor: 346 11 12; Mixed: 579 10

● Cranial Nerve Lesions
Olfactory nerve May be injured in basal skull fractures or involved in frontal lobe tumour extension.
Loss of olfactory nerve function in relation to major CNS pathology is seldom an isolated event.
Optic nerve ● Problems with visual acuity may result from intra ocular disorders.
● Problems with the blood supply such as amaurosis fugax may produce temporary visual
distortion.
● Pretectal nucleus resizes the pupil connect, bypassing the lateral geniculate nucleus and the
primary visual cortex.
● Pretectal nucleus neurones pass to the Edinger - Westphal nucleus, motor axons from here
pass along with the oculomotor nerve. They synapse with ciliary ganglion neurones;
Parasympathetic axons from this then innervate the iris and produce miosis.
● The miotic pupil is seen in disorders such a Horner's syndrome or opiate overdose.
● Mydriasis is the dilatation of the pupil in response to disease, trauma, drugs (or the dark!). It
is pathological when light fails to induce miosis. The radial muscle is innervated by
sympathetic nervous system. Because the parasympathetic fibres travel with the oculomotor
nerve they will be damaged by lesions affecting this nerve (e.g. cranial trauma).
● The response to light shone in one eye is usually a constriction of both pupils – This
indicates intact direct and consensual light reflexes.
● When the optic nerve has an Afferent Defect the light shining on the affected eye will
produce a diminished pupillary response in both eyes. Whereas light shone on the
unaffected eye will produce a normal pupillary response in both eyes. This is referred to as
the Marcus Gunn pupil and is seen in conditions such as Optic Neuritis.
nd
● In a total 2 CN lesion, shining the light in the affected eye will produce no response.
Oculomotor nerve ● The pupillary effects are described above. In addition it supplies all ocular muscles apart
from lateral rectus and superior oblique(LR6 SO4). Thus the affected eye will be deviated
inferolaterally.
● Levator palpebrae superioris also impaired resulting in impaired ability to close the eye.
- Dilated unreactive pupil

- Typically ptosis – divergent squint
- Eyeball is displaced downwards and outwards – affected eye deviated 'down and out’
Trochlear nerve The eye will not be able to look down.
Trigeminal nerve ● Largest cranial nerve.
● Exits the brainstem at the pons.
● Branches are – Ophthalmic, Maxillary and Mandibular.
● Only the Mandibular branch has both sensory and motor fibres.
● Branches converge to form the Trigeminal Ganglion (located in Meckels Cave).
● It supplies Muscles Of Mastication and also Tensor Veli Palatine, Mylohyoid, Anterior Belly
of Digastric and Tensor Tympani.
● The corneal reflex is mediated by:- Naso–ciliary branch of Ophthalmic Division of

Trigeminal
(sensory component) and the Facial Nerve producing the motor response.
● Lesions of the afferent arc will produce bilateral absent blink

Lesions of the efferent arc will produce unilateral absent blink.
● PALSY
- Complete palsy cause unilateral sensory loss of face, tongue & buccal mucosa as it
is the major sensosory nerve of face except over the angle of the jaw – which is
innervated by Greater Auricular Nerve (C2, 3)
- Corneal reflex loss is the early indication of the palsy
- Trigeminal neuralgia is treated by Carbamazepine
Abducens nerve ● The affected eye will have a deficit of abduction.
● This cranial nerve exits the brainstem between the pons and medulla.
● It thus has a relatively long intra cranial course which renders it susceptible to damage in
raised intra cranial pressure.
Facial nerve ● Emerges from brainstem between pons and medulla.
● It controls muscles of facial expression and taste from the anterior 2/3 of the tongue.
● Facial nerve has no sensory coetaneous supply

● The nerve passes into the petrous temporal bone and into the internal auditory meatus.
Then passes through the facial canal and exits @ stylomastoid foramen. It passes through
parotid gland and divides at this point. It does not innervate the parotid gland.
● Its motor fibres innervate orbicularis oculi to produce the efferent arm of the corneal reflex.
● It may be injured during parotid gland surgery or invaded by malignancies of the gland and a
lower motor neurone on the ipsilateral side will result.
Vestibulo-cochlear ● Exits from the pons and then passes through the internal auditory meatus.
nerve
● It is implicated in sensorineural hearing loss.
● Individuals with sensorineural hearing loss will localise the sound in webers test to normal
ear. Rinnes test will be reduced on affected side but should still work. These two tests will
distinguish sensorineural hearing loss from conductive deafness. In the latter condition
webers test will localise to affected ear and Rinnes test will be impaired on affected side.
● Surgical lesions affecting this nerve include CNS tumours and basal skull fractures. It may
also be damaged by the administration of ototoxic drugs (of which gentamicin is the most
commonly used in surgical practice).
Glossopharyngeal ● Exits the pons just above the vagus.

nerve
● Receives sensory fibres from posterior 1/3 tongue, tonsils, pharynx and middle ear (otalgia
may occur following tonsillectomy).
● It receives visceral afferents from the carotid bodies.
● It supplies parasympathetic fibres to parotid gland via otic ganglion and motor function
to stylopharyngeaus muscle.
● It supplies the interior of Tympanic membrane
●The sensory function of the nerve is tested using the gag reflex.
Vagus nerve ● Leaves the medulla between the olivary nucleus and the inferior cerebellar peduncle.
● Passes through the jugular foramen and into the carotid sheath.
● Vagus Nerve supplies sensation to inferior external auditory canal &responsible forcough
when ear is suctned for wax
Accessory nerve ● Exists from the caudal aspect of the brainstem (multiple branches) supplies trapezius and
sternocleidomastoid muscles.
● The distal portion of this nerve is most prone to injury during surgical procedures.
Hypoglossal nerve ● Emerges from the medulla at the preolivary sulcus, passes through the hypoglossal canal.
● It lies on the carotid sheath and passes deep to the posterior belly of digastric to supply
muscles of the tongue (except palatoglossus).
● Its location of the carotid sheath makes it vulnerable during carotid endarterectomy surgery
and damage will produce ipsilateral defect in muscle function.
● It crosses the ECA 1cm superior to carotid bifurcation. At that point it also crosses the
Lingual artery (N-29)
● Supratrochlear nerve, smaller of two branches of frontal nerve, passes above the pulley of the superior oblique. (N-
18, 20, 40, 81)
Cranial Nerves Ganglia

(Both peripheral sensory and peripheral autonomic ganglia)
● Ciliary
Autonomic preganglionic neurons in the Edinger-Westphal nucleus synapse on postganglionic neurons via CN
3 in the ciliary ganglion
P.symp. ganglion @post.part of orbit lat. Side of ophthalmic artery
Innervate constrictor muscles of the iris and the ciliary muscle
** Postganglionic sympathetic fibers innervating the dilator pupillae muscle begin in Superior cervical
ganglion **
● Trigeminal (Gasserian or semilunar)

Sensory ganglion to the spinal nucleus, main sensory nucleus, and mesencephalic nucleus of CN 5
From face, muscle receptors and meninges;
Contains pseudounipolar ganglion cells similar to those found in the dorsal root ganglia
● Pterygopalatine
Autonomic ganglia of CN 7
Innervate lacrimal glands and glands of nasal mucosal from the superior salivatory nucleus
● Submandibular
Autonomic ganglia of CN 7
Innervate salivary glands from the superior salivatory nucleus
● Geniculate
Sensory ganglia of CN 7
rd
Innervates anterior 2/3 of tongue and palate (via chorda tympani) as well as the skin of the external
ear from the solitary nucleus and the spinal nucleus of CN 5
● Vestibular
Sensory ganglia of CN 8 from the vestibular nuclei going to the hair cells of the vestibular labyrinth
● Spiral
Sensory ganglia of CN 8 from the cochlear nuclei going to the hair cells in the organ of Corti
● Otic
Autonomic ganglia of CN 9 that innervate parotid gland from the inferior salivatory nucleus
Found in medial side of V3
th
Receives preganglionic symp. Fibers from 9 CN
● Inferior (petrosal) ganglia of glossopharyngeal

Sensory ganglia of CN 9 going from solitary nucleus
Mucous membranes of pharynx, middle ear, carotid body and sinus

rd
Taste sensor on the posterior 1/3 of the tongue
● Superior (jugular) ganglia of glossopharyngeal

Sensory ganglia of CN 9 from the spinal nucleus of CN 5 to the skin of the external ear
middle ear is innervated by Jacobsen’s nerve which is a branch off of CN 9
● Superior (rostral) ganglion of vagus nerve

Sensory ganglia of CN 10 going from spinal nucleus of CN 5 to skin of external ear and meninges
● Inferior (nodose) ganglion of vagus nerve
Sensory ganglia of CN 10 going from solitary nucleus (caudal) to larynx, trachea, gut, and aortic arch receptors
Sensory ganglia of CN 10 going from solitary nucleus (rostral) to taste receptors of the posterior oral cavity
● Peripheral autonomic ganglia
Autonomic ganglia of CN 10 going from dorsal motor nucleus of CN 10 to gut, respiratory structures and heart.
Third nerve palsy
Features
• Eye is deviated 'down and out'
• Ptosis
• Pupil may be dilated (sometimes called a 'surgical' third nerve palsy)
Causes
• Diabetes mellitus
• Vasculitis e.g. temporal arteritis, SLE
• False localizing sign** due to uncal herniation through tentorium if raised ICP
• Posterior communicating artery aneurysm (pupil dilated)
• Cavernous sinus thrombosis
• Weber's syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain strokes
• Other possible causes: amyloid, multiple sclerosis
th
**this term is usually associated with 6 nerve palsies but it may be used for a variety of neurological presentations
Facial nerve
- Main nerve supplying the structures of the second embryonic branchial arch.
- Efferent nerve to the muscles of facial expression, digastric muscle and also to many glandular structures.
- Afferent fibres are few – which originate in the cells of its genicular ganglion and are concerned with taste.
Supply - 'face, ear, taste, tear'

• Face: muscles of facial expression
• Ear: nerve to stapedius
• Taste: supplies anterior two-thirds of tongue
• Tear: parasympathetic fibres to lacrimal glands, also salivary glands
Path- Subarachnoid path

• Origin: motor- pons, sensory- nervus intermedius
• Pass through the petrous temporal bone into the internal auditory meatus with the vestibulocochlear nerve.
Here they combine to become the facial nerve.
Facial canal path

• The canal passes superior to the vestibule of the inner ear
• At the medial aspect of the middle ear, it becomes wider and contains the geniculate ganglion.
3 branches: 1. greater petrosal nerve ; 2. nerve to stapedius; 3. chorda tympani
● Stylomastoid foramen
• Passes through the stylomastoid foramen (tympanic cavity anterior and mastoid antrum posteriorly)
• Posterior auricular nerve and branch to Posterior belly of Digastric and Stylohyoid muscle
Face Enters parotid gland and divides into 5 branches:

• Temporal branch
• Zygomatic branch
• Buccal branch
• Marginal mandibular branch
• Cervical branch
Upper Vs Lower motor neurone lesions - Facial nerve
- The nucleus of the facial nerve is located in the caudal aspect of the ventrolateral pontine tegmentum.
- Axons exit the ventral pons medial to the spinal trigeminal nucleus.
- Any lesion occurring within or affecting the corticobulbar tract is known as an upper motor neuron lesion.
- Any lesion affecting the individual branches (temporal, zygomatic, buccal, mandibular and cervical) is
known as a lower motor neuron lesion.
- Branches of the facial nerve leaving the facial motor nucleus (FMN) for the muscles do so via both left and
right posterior (dorsal) and anterior (ventral) routes. In other words, this means LMN of facial nerve can
leave either from the left anterior, left posterior, right anterior or right posterior facial motor nucleus.
- The temporal branch travels out from the left and right posterior components. The inferior four branches do
so via the left and right anterior components.
- The left and right branches supply

supply their respective sides of the face (ipsilateral innervation).
- Accordingly, the posterior components receive motor input from both hemispheres of the cerebral cortex
(bilaterally).
- Anterior components receive strictly contralateral input. This means that
that the temporal branch of the facial
nerve receives motor input from both hemispheres of the cerebral cortex.
- Whereas the zygomatic, buccal, mandibular and cervical branches receive information from only
contralateral hemispheres.
- Anterior facial motor nucleus
cleus (FMN) receives only contralateral cortical input whereas the posterior receives
that which is bilateral.
- A corticobulbar lesion (UMN lesion) occurring in the left hemisphere would eliminate motor input to the right
anterior FMN component, thus removing
removing signaling to the inferior four facial nerve branches, thereby
paralyzing the right mid- and lower-face.
lower
- The posterior component, however, although now only receiving input from the right hemisphere, is still
able to allow the temporal branch to sufficiently
suffici innervate the entire forehead. This means that the
forehead will not be paralyzed.
- The same mechanism applies for an UMNL in the right hemisphere. The left anterior FMN component no
longer receives cortical motor input due to its strict contralateral innervation, whereas the posterior
component is still sufficiently supplied by the left hemisphere. The result is paralysis of the left mid
mid- and
lower-face
face with an unaffected forehead.
- On the other hand, a LMN lesion is a bit different.
different
A lesion on either the left or right side would affect both the anterior and posterior routes on that side
because of their close physical proximity to one another. So, a lesion on the left side would inhibit muscle
innervation from both the left posterior and anterior routes, thus paralyzing the whole left side of the face
(Bells Palsy).
- With this type of lesion, the bilateral and contalateral inputs of the posterior and anterior routes,
respectively, become irrelevant because the lesion is below the level
level of the medulla and the facial motor
nucleus (FMN). Whereas at a level above the medulla a lesion occurring in one hemisphere would mean
that the other hemisphere could still sufficiently innervate the posterior facial motor nucleus, a lesion
affecting a LMN would eliminate innervation altogether because the nerves no longer have a means to
receive compensatory contralateral input at a downstream decussation.
Facial nerve lesion
Upper motor neuron lesion
Contralateral lower quadrant weakness

Angle of the mouth
Opposite side
Lower motor neuron lesion

Ipsilateral orbicularis oculi muscle and facial muscles involved
Half of face
Unable to close eyes
Weakness of angle of the mouth
Cannot elevate eyebrows
Same side
Facial nerve palsy
Sarcoid ● most frequent neurological manifestation of sarcoid

● Affects right and left side with equal frequency, may be bilateral
● Typically resolves in up to 80% of cases
Cholesteatoma ● Destructive and expanding growth of keratinised squamous epithelium

● Patients often complain of chronic ear discharge
● nfection with Pseudomonas may occur resulting in foul smell to discharge
● Aquired lesions usually arise from the Pars flaccida region of the tympanic membrane
● Surgical removal and mastoidectomy may be needed
● Recurrence rates of 20% may be seen following surgery
Basal skull fracture ● History of head injury

● Presence of features such as Battles sign on examination
● Clinical presence of CSF leak strongly supports diagnosis
● Assessment is by CT and MRI scan
● Prophylactic antibiotics should be given in cases of CSF leak
● The corneal reflex is mediated by the opthalmic branch of the trigeminal nerve sensing the stimulus on the cornea, lid
or conjunctiva; the facial nerve initiates motor response of reflex
● Inferior alveolar nerve (br. of V3) LA দিলে all teeth of that hemimandible anaesthetized হয় আর lower lip numbness হয়
Recurrent laryngeal nerve

• Branch of the vagus nerve
Path
Right
• Arises anterior to the subclavian artery and ascends obliquely next to the trachea, behind the common carotid
artery
• It is either anterior or posterior to the inferior thyroid artery
Left
• Arises left to the arch of the aorta
• Winds below the aorta
• Ascends along the side of the trachea
Then both
• Pass in a groove between the trachea and oesophagus
• Enters the larynx behind the articulation between the thyroid cartilage and cricoid
• Distributed to larynx muscles
Branches to
• Cardiac plexus
• Mucous membrane and muscular coat of the oesophagus and trachea
Innervates
• Intrinsic larynx muscles (excluding cricothyroid)
● Ansa Cervicalis Nerves: GHost THought SOmeone STupid SHot Irene

• G eniohyoid
• T hyrohyoid
• S uperior Omohyoid
• S ternothyroid
• S ternohyoid
• I nferior omohyoid
N.B. All the infrahyoid strap muscles are innervated by the Ansa Cervicalis
● Cervical Plexus: Arrangement of the Important Nerves:

GLAST: 4 compass points: clockwise from north on the right side of neck:
• G reat auricular
• L esser occipital
• A ccessory nerve pops out between L and S
• S upraclavicular
• T ransverse cervical
● Shrugging of shoulder is done by Spinal Accessory nerve

● Corticospinal / Pyramidal fibres aggregated to form the elevation of Pyramid (N-108)
th
● CAROTID BODY is innervated by 9 CN
GENERAL DISCUSSION
● BASE OF SKULL
- Carotid canal : ICA

Internal carotid nerve plexus
- Caecum : Emissary veins to Superior Saggital Sinus
- Hypoglossal : 12 nerve
- Jugular**** : 9 10 11 nerves
IJV
Inferior petrosal sinus
Posterior Meningeal Artery
****
- Lacerum : Meingeal br.ascending pharyngeal art.

ICA
- Olfactory foramina is Cribriform Foaramina,

Foaramina lies at Anterior Cranial Fossa
- Optic canal : 2 Nerve

Ophthalmic artery
- Ovale** : M andibular Division Trigeminal Nerve (V3)

A ccessory meningeal artery
L esser petrosal nerve
E missary veins
+ Otic ganglia
- Spinosum** : Middle meningeal vessels(←

vessels ←Max. Artery←
←ECA)
Meningeal branch mandibular division
div Trigeminal Nerve (V3);
- St.mastoid/IAM*: 7, 8 nerves
Labyrithine Artery
A
- Sup.Orb. fissure: 346 nerves

Frontal, Lacrimal & Nasociliary branch of Ophthalmic Division Of Trigeminal ((V1)
Superior ophthalmic Vein
- Rotundum** : Maxillary div. trigeminal n. (V2)
- Magnum : Anterior and posterior Spinal arteries

Vertebral artery
Medulla oblongata
● Exit of 5th CN : S tanding R oom O nly

V1 : S uperior Orbital fissure (Sensory)
V2 : R otundum (Sensory)
V3 : O vale (Mixed)
● Nerves pass through the Supraorbtal Fissure: Live Frankly To See Absolutely No Insult
L acrimal
F rontal
T rochlear
S uperior Division of Oculomotor
A bducens
N asociliary
I nferior Division of Oculomotor nerve
● Inernal Acoustic Meatus compression → Facial nerve involved → Sympathetic innervation hampered → dry eye
● After Inernal Acoustic Meatus compression → Facial nerve involved → Facial expression effected
● Pterygoid Canal or Vidian Canal – transmits nerve of preganglionic parasymp. & post ganglionic symp.fibers.
● Bone Wise Foramen Distribution

Sphenoid Bone: - L acerum Sexy LOSS eR
O vale
S pinosum
S uperior Orbital Fissure
R otundum
Temporal Bone: - J ugular Temporary Jatiyo Sangshad

S tylomastoid
Occipital Bone: - Magnum
Tongue
● Muscles (N-54) (Developed from occipital myotome)

Intrinsic
Sup. & inf. Longitudinal
Transverse
Vertical
Extrinsic
Genioglossus
Hyoglossus
Styloglossus
Palatoglossus
● Nerve Supply (N-41,125)
MOTOR
• All muscles by XII (Hypoglossal)
• Only Palatoglossus by XI (Accessory-cranial part thru’ pharyngeal plexus)
SENSORY
rd st
Anterior 2/3 (developed from lingual swelling of 1 arch)
• General : Lingual ←V3 (mandibular div. trigeminal)
• Taste : Chorda tympani ←VII (pass from Lingual nerve to facial nerve just below the skull)
Posterior 1/3rd (developed from 3rd arch – Forms large ventral part of hypobranchial eminence)
• General : IX (Glossopharyngeal)
• Taste : IX (Glossopharyngeal)
th
Posterior most : (developed from 4 arch – Forms small dorsal part of hypobranchial eminence)
X (vagus) thru’ Int. Laryngeal nerve.
important: Special visceral sensation for taste is carried out by Facial, Glossopharyngeal & Vagus nerve(7,9,10)
Lymphatic Drainage
• Anterior 2/3rd → ipsilateral nodes.
rd
• Posterior 1/3 → have communicating networks, so early bilateral nodal metastases are more common in this
area.
• Tip → sub mental nodes → deep cervical nodes.
• Mid portion →submandibular nodes → deep cervical nodes.
(Mid tongue tumours laterally drain to ipsilateral deep cervical nodes, those from more central regions may have
bilateral deep cervical nodal involvement.)
n
● Perforated Tympanic Membrane repair → Chance of Chorda Tympani Nerve injury→ altered taste sensat
Salivary Glands
● Aldosterone is responsible for regulating ion exchange in salivary glands
● Para.sympathetic stimulation produces – water rich, serous saliva.

Sympathetic stimulation produces – low vol., enzyme-riched saliva.
● Submandibular contribute 70% saliva,

Sublingual contribute 5% and the remainder 25% from the parotid.
Submandibular Gland (N-54,55)
● Relations
Superficial - Platysma, deep fascia and mandible

- Submandibular lymph nodes
- Facial vein (facial artery near mandible)
- Marginal mandibular nerve
- Cervical branch of the facial nerve
Deep - Facial artery (inferior to the mandible)

- Mylohoid muscle
- Sub mandibular duct
- Hyoglossus muscle
- Lingual nerve
- Submandibular ganglion
- Hypoglossal nerve
Divided into superficial & deep part by mylohyoid. Secrets both mucous & serous saliva.
Blood supply from facial vessels. (N-55),
Which important structure lies at medial relation of Submandibular Gland?--- mylohyoid muscle
Submandibular duct (Wharton's duct)

• Opens lateral to the lingual frenulum on the anterior floor of mouth.
• 5 cm length
• Lingual nerve wraps around Wharton's duct. As the duct passes forwards it crosses medial to the nerve to
lie above it and then crosses back, lateral to it, to reach a position below the nerve.
Innervation
• Sympathetic - Superior Cervical ganglion via the Lingual nerve
• Parasympathetic - Submandibular ganglion
Arterial supply
Branch of the Facial artery. The facial artery passes through the gland to groove its deep surface. It then
emerges onto the face by passing between the gland and the mandible.
Venous drainage
Anterior Facial vein (lies deep to the Marginal Mandibular nerve)
Lymphatic drainage
Deep cervical and jugular chains of nodes
Submandibular glands- disease
Physiology
The submandibular glands secrete approximately 800- 1000ml saliva per day. They typically produce mixed
seromucinous secretions. When paraympathetic activity is dominant the secretions will be more serous. The
parasympathetic fibres are derived from the chorda tympani nerves and the submandibular ganglion, they travel to the
glands via the lingual nerves.
Sialolithiasis
• 80% of all salivary gland calculi occur in the submandibular gland

• 70% of the these calculi are radio-opaque
• Stones are usually composed of calcium phosphate or calcium carbonate
• Patients typically develop colicky pain and post prandial swelling of the gland
• Investigation involves sialography to demonstrate the site of obstruction and associated other stones
• Stones impacted in the distal aspect of Whartons duct may be removed orally, other stones and chronic
inflammation will usually require gland excision
Sialadenitis
• Usually occurs as a result of Staphylococcus aureus infection

• Pus may be seen leaking from the duct, erythema may also be noted
• Development of a sub mandibular abscess is a serious complication as it may spread through the other deep
fascial spaces and occlude the airway
Submandibular tumours
• Only 8% of salivary gland tumours affect the sub mandibular gland

• Of these 50% are malignant (usually adenoid cystic carcinoma)
• Diagnosis usually involves fine needle aspiration cytology
• Imaging is with CT and MRI
• In view of the high prevalence of malignancy, all masses of the submandibular glands should generally be
excised.
● Submandibular Gland Excision

- A transverse incision 4cm below the mandible to save Marginal Mandibular Nerve → Branch of Facial Nerve
- Layers: Skin → Platysma muscle → Deep fascia → Facial Vein
- Facial Artery and Facial Vein injury chance (+)ve
3 CN injury chance : 7,5,12
- Mandibular division of Facial nerve (injury causes Difficulty of sipping water and lower lip drooping)
- Lingual nerve, branch of V3
th
- Hypoglossal Nerve (12 nerve)
● Submandibular Fossa Contents

- Submandibular gland
- Inf. Alveolar vessels
- Facial artery submental branch
- Submental & Submandibular LN
Parotid gland
Anatomy of the parotid gland
Location Overlying the mandibular ramus; anterior and inferior to the ear.
Salivary duct Crosses the masseter, pierces the buccinator and drains adjacent to the 2nd upper molar tooth
(Stensen's duct).
Structures passing • Facial nerve (Mnemonic: The Zebra Buggered My Cat)

through the gland Temporal
Zygomatic,
Buccal,
Mandibular (is well separated from the parotid gland)
Cervical
• External Carotid Artery
• Retromandibular vein (The maxillary vein joins to the superficial temporal vein and they
form the retromandibular vein which then runs through the parotid gland)
• Auriculotemporal nerve – Following parotidectomy, this nerve may be damaged and
during neuronal regrowth may then attach to sweat glands in this region. This can then
cause gustatory sweating (Freys Syndrome)
Relations • Anterior: masseter, medial pterygoid, superficial temporal and maxillary artery, facial
nerve, stylomandibular ligament
• Posterior: posterior belly digastric muscle, sternocleidomastoid, stylohyoid, internal
carotid artery, mastoid process, styloid process
Arterial supply Branches of external carotid artery
Venous drainage Retromandibular vein
Lymphatic drainage Deep cervical nodes
Nerve innervation • Parasympathetic – Secretomotor(produces water rich, serous saliva)

• Sympathetic – Superior cervical ganglion (produces low volume, enzyme-rich saliva)
• Sensory – Greater auricular nerve
Secretion of saliva by the parotid gland is controlled by postsynaptic parasympathetic fibres
originating in the inferior salivatory nucleus; these leave the brain via the tympanic nerve (branch
of glossopharyngeal nerve (CN IX), travel through the tympanic plexus (located in the middle
ear), and then form the lesser petrosal nerve until reaching the otic ganglion. After synapsing in
the Otic ganglion, the postganglionic (postsynaptic) fibres travel as part of the auriculotemporal
nerve (a branch of the mandibular nerve (V3) to reach the parotid gland.
● Arteries enters : ECA (thru’ posteromedial border)
● Arteries exits : Maxillary (thru’ anteromedial surface)

Trnsverse Facial (thru’ anteromedial surface)
Superficial Temporal (thru’ superior surface)
Post.auriculur (arise within gland)
● Veins forms : Retromandibular (within gland by sup.temporal & maxillary)
● Nerve enters : Facial (thru’ posteromedial surface)
● Nerves exit : Terminal br. Facial (thru’ anteromedial surface)
● Causes of bilateral parotid enlargement

• Mumps: Associated with meningoencephalitis, pancreatitis, orchitis, or deafness
• Parotitis
• Sialectasis - especially if related to eating

• Sjogren's syndrome: dry eyes or mouth, connective tissue disease
• Sarcoidosis
• Tuberculosis
• Alcoholism
• Myxoedema
• Cushing's disease
• Diabetes/insulin resistance
• Liver cirrhosis
• Gout
• Bulimia nervosa
• Drugs
• Severe dehydration
• Malnutrition
● Causes of unilateral parotid enlargement
• Salivary calculus
• Tumour
● Parotid gland tumours

• Parotid tumours may present at any region in the gland. However, most lesions will be located behind the angle
of the mandible, inferior to the ear lobe. Tumours of the deep lobe of the parotid may present as a
parapharyngeal mass and large lesions may displace the tonsil
• Pleomorphic adenomas are the most common.
• Incisional biopsy of parotid masses is not recommended, so superficial parotidectomy is the usual procedure of
choice.
• Signs of facial nerve palsy and a parotid mass should raise suspicion of malignancy.
• Warthins tumours are relatively benign lesions that are slow growing and occur most commonly in elderly
male smokers.
• Adenoid cystic carcinoma has a tendency for perineural invasion.
● Parotid Gland Malignancy

• Most parotid neoplasms (80%) are benign lesions
• Most commonly present with painless mass in cheek region
• Up to 30% may present with pain, when this is associated with a discrete mass lesion in the parotid it usually
indicates perineural invasion.
• Perineural invasion is very unlikely to occur in association with benign lesions
• 80% of patients with facial nerve weakness caused by parotid malignancies will have nodal metastasis and a 5
year survival of 25%
Types of malignancy
Mucoepidermoid - 30% of all parotid malignancies

carcinoma - Usually low potential for local invasiveness and metastasis (depends mainly on grade)
Adenoid cystic - Unpredictable growth pattern

carcinoma - Greatest tendency for perineural spread
- Nerve growth may display skip lesions resulting in incomplete excision
- Distant metastasis more common (visceral rather than nodal spread)
- 5 year survival 35%
Mixed tumours Often a malignancy occurring in a previously benign parotid lesion
Acinic cell ca. - Intermediate grade malignancy

- May show perineural invasion
- Low potential for distant metastasis
- 5 year survival 80%
Adenocarcinoma - Develops from secretory portion of gland

- Risk of regional nodal and distant metastasis
- 5 year survival depends upon stage at presentation, may be up to 75% with small lesions
with no nodal involvement
Lymphoma - Large rubbery lesion, may occur in association with Warthins tumours
- Diagnosis should be based on regional nodal biopsy rather than parotid resection
- Treatment is with chemotherapy (and radiotherapy)
● Sialosis Features
Recurrent swelling of salivary gland in the absence of neoplasia / inflammation
Swelling is typically painless & bilateral; soft & not indurated
Associated ē endocrine dis.; metabolic dis.; drugs
● Sjögren’s Syndrome Triad:

Keratoconjunctivitis sicca / Xerophthalmia (dry eyes)
Xerostomia (dry mouth); gland enlargement (±)
Rheumatoid arthritis or other connective tissue disorder (eg scleroderma, SLE, polyarteritis nodosa).
** May be Connective tissue dis. Involve or not. If not involve -- primary and if involved : secondary**
● Mikulicz’s Syndrome (autoimmune syndrome):

Salivary glands enlargement (parotid, submandibular, sublingual)
Lacrimal glands enlargement – cz a bulge below eyelids outer end & narrowing palpebral fissures.
Xerostomia
**associated lymphosarcoma, leukaemia, TB, sarcoidosis, syphilis may present**
● Pleomorphic Adenoma Features

- Most common benign salivary tumor; Mixed type
- Young pt 30-40 yrs
- Slow growing, farm, smooth, movable; contains myoepithelial cells
- Usually @ the tail of parotid gland
- Recurrence may occur
● Warthin’s Tumor Features (Adenolymphoma of Parotid)

- Benign cystic tumor
- Contains epithelial lymphoid elements – multiple cyst & solid component consists of lymphoid tissue
- Old pt.; male dominant

- Slow growing, Soft & well defined
- Recurrence rare
Carotid Sheath
● Content:s: I See 10 CC's in the IV

• I See (I.C.) = Internal Carotid artery
• 10 = CN 10 (Vagus nerve)
• CC = Common Carotid artery
• IV = Internal Jugular Vein
● Carotid Sheath :- anteriorly-- Ansa cervicalis embedded (Exposed by division of pretracheal fascia)
Posteriorly-- Cervical sympathetic trunk plastered to prevertebral fascia
● Carotid Triangle Operation Risk:

Loss of sense of skin of left side of neck and difficulty in swallowing → Transeverse cervical nerve injury→
Hyoid bone deviated to right side
● Supraclavicular LN palpable+ TB features + Caucasian = Lymphoreticular dis.
Carotid Endarterectomy
During a carotid endarterectomy the sternocleidomastoid muscle is dissected, with ligation of the common facial vein and
then the internal jugular is dissected exposing the common and the internal carotid arteries. The nerves at risk during the
operation include:
• Hypoglossal nerve
• Greater auricular nerve
• Superior laryngeal nerve
The sympathetic chain lies posteriorly and is less prone to injury in this procedure
● Nerves @ risk during Carotid Endarterectomy : 5,7 (9) 10 12
V (cutaneous br.); VII (mandibular br.); IX(mainly); X; XII
● Carotid Endarterectomy monitoring is done by Transcranial Doppler ultrasound
Root of the neck
Thoracic Outlet
• Where the subclavian artery and vein and the brachial plexus exit the thorax and enter the arm.
• They pass over the 1st rib and under the clavicle.
• The Subclavian Vein is the most anterior structure and is immediately anterior to scalenus anterior and its
attachment to the first rib.
• Scalenus anterior has 2 parts; the Subclavian Artery leaves the thorax by passing over the first rib and between
these 2 portions of the muscle.
• At the level of the first rib, the lower cervical nerve roots combine to form the 3 trunks of the brachial plexus. The
lowest trunk is formed by the union of C8 and T1, and this trunk lies directly posterior to the artery and is in
contact with the superior surface of the first rib.
• Thoracic outlet obstruction causes neurovascular compromise.
Anterior triangle of the neck (N-23, 28, 164)
Boundaries
• Anterior border of the Sternocleidomastoid
• Lower border of mandible
• Anterior midline
Sub triangles (divided by Digastric above and Omohyoid)

• Muscular triangle: Neck strap muscles
• Carotid triangle: Carotid sheath
• Submandibular Triangle (digastric)
Contents of the anterior triangle
Digastric triangle - Submandibular gland

- Submandibular nodes
- Facial vessels
- Hypoglossal nerve
Muscular triangle - Strap muscles

- External jugular vein
Carotid triangle - Carotid sheath (CCA, Vagus & IJV)

- Ansa cervicalis
Nerve supply to digastric muscle

• Anterior: Mylohyoid nerve
• Posterior: Facial nerve
Posterior triangle of the neck
Boundaries
Apex Sternocleidomastoid and the Trapezius muscles at the Occipital bone
Anterior Posterior border of the Sternocleidomastoid
Posterior Anterior border of the Trapezius
Base Middle third of the clavicle
Contents
Nerves • 11th CN
• Phrenic nerve
• Three trunks of the brachial plexus
• Cervical plexus branches: Supraclavicular, transverse cervical,
great auricular, lesser occipital
Vessels • EJV
• Subclavian Artery
• Occipital Artery (@ post. triangle, 12th CN lies laterally of this)
• Transverse cervical and suprascapular vessels
Muscles • Inferior belly of omohyoid

• Scalene
Lymph nodes • Supraclavicular
• Occipital
**Posterolateral aspect injury scenario, ans will be 11th CN injury

● Posterolateral injury+ Unable to raise shoulder tip = ans -Trapezius muscle injury or 11th CN injury.
● Nerves @ risk during Branchial cyst excision:

• Mandibular branch of 7th CN
th
• 11 CN
• Greater auricular nerve
Neck lumps
Reactive lymphadenopathy – Most common cause of neck swellings.

– There may be a history of local infection or a generalised viral illness
Lymphoma – Rubbery, painless lymphadenopathy

– The phenomenon of pain whilst drinking alcohol is very uncommon
– There may be associated night sweats and splenomegaly
Thyroid swelling – May be hypo-, eu- or hyperthyroid symptomatically

– Moves upwards on swallowing
Thyroglossal cyst – More common in patients < 20 years old

– Usually midline, between the isthmus of the thyroid and the hyoid bone
– Moves upwards with protrusion of the tongue
– May be painful if infected
Pharyngeal pouch – More common in older men

n
– Represents a posteromedial herniation bet Thyropharyngeus & Cricopharyngeus
– Usually not seen, but if large then a midline lump in neck that gurgles on palpation
– Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough
Cystic hygroma – Congenital lymphatic lesion (lymphangioma) typically found in neck, classically on left
– Most are evident at birth, around 90% present before 2 years of age
Branchial cyst – Oval, mobile cystic mass that develops between sternocleidomastoid and pharynx
– Develop due to failure of obliteration of 2nd branchial cleft in embryonic development
– Usually present in early adulthood
Cervical rib – More common in adult females

– Around 10% develop thoracic outlet syndrome
Carotid aneurysm – Pulsatile lateral neck mass which doesn't move on swallowing
Neck Masses in Children
Thyroglossal cyst • Located in the anterior triangle, usually in the midline and below the hyoid (65%
cases)
• Derived from remnants of the thyroglossal duct

• Thin walled and anechoic on USS (echogenicity suggests infection of cyst)
Branchial cyst • Six branchial arches separated by branchial clefts

• Incomplete obliteration of the branchial apparatus may result in cysts, sinuses or
fistulae
• 75% of branchial cysts originate from the second branchial cleft
• Usually located anterior to sternocleidomastoid near the angle of mandible
• Unless infected the fluid of the cyst has a similar consistency to water and is
anechoic on USS
Dermoids • Derived from pleuripotent stem cells and are

• Soft, fluctuant
• Most commonly located in midline in a suprahyoid location
• They have heterogeneous appearances on imaging and contain variable amounts of
calcium and fat
Thyroid gland • True thyroid lesions are rare in children and usually represent thyroglossal cysts or
tumours like lymphoma
Lymphatic • Usually located posterior to the sternocleidomastoid

malformations • Cystic hygroma result from occlusion of lymphatic channels
• The painless, fluid filled, lesions usually present prior to the age of 2
• They are typically hypoechoic on USS
Infantile haemangioma • May present in either triangle of the neck

• Grow rapidly initially and then will often spontaneously regress
• Plain x-rays will show a mass lesion, usually containing calcified phleboliths
• As involution occurs the fat content of the lesions increases
Lymphadenopathy • Located in either triangle of the neck

• May be reactive or neoplastic
• Generalised lymphadenopathy usually secondary to infection in children (very
common)
● Cystic Hygroma : sternomastoid muscle along the ant. Border, any soft cystic swelling
● Sternomastoid Tumor : Baby turns head on the side of the tumor
● Ramsay Hunt Syndrome: Occurs among children; pain, facial nerve palsy, ear canal shows visible vesicles
HEAD-NECK, NEURO, EYE, ENT PART-2
Vertebral column
• There are 7 cervical, 12 thoracic, 5 lumbar, and 5 sacral vertebrae.
• The spinal cord segmental levels do not necessarily correspond to the vertebral segments. For example, while
the C1 cord is located at the C1 vertebra, the C8 cord is situated at the C7 vertebra. While the T1 cord is
situated at the T1 vertebra, the T12 cord is situated at the T8 vertebra. The lumbar cord is situated between T9
and T11 vertebrae. The sacral cord is situated between the T12 to L2 vertebrae.
Cervical vertebrae
The interface between the first and second vertebra is called the atlanto-axis junction. The C3 cord contains the phrenic
nucleus. The cervical cord innervates the deltoids (C4), biceps (C4-5), wrist extensors (C6), triceps (C7), wrist extensors
(C8), and hand muscles (C8-T1).
Thoracic vertebrae
The thoracic vertebral segments are defined by those that have a rib. The spinal roots form the intercostal nerves that
run on the bottom side of the ribs and these nerves control the intercostal muscles and associated dermatomes.
Lumbosacral vertebrae
Form the remainder of the segments below the vertebrae of the thorax. The lumbosacral spinal cord, however, starts at
about T9 and continues only to L2. It contains most of the segments that innervate the hip and legs, as well as the
buttocks and anal regions.
Cauda Equina
The spinal cord ends at L2 vertebral level. The tip of the spinal cord is called the conus. Below the conus, there is a
spray of spinal roots that is called the cauda equina. Injuries below L2 represent injuries to spinal roots rather than the
spinal cord proper.
Diseases affecting the vertebral column
Ankylosing • Chronic inflammatory disorder affecting the axial skeleton

spondylitis • Sacro-ilitis is a usually visible in plain films
• Up to 20% of those who are HLA B27 positive will develop the condition
• Affected articulations develop bony or fibrous changes
• Typical spinal features include loss of the lumbar lordosis and progressive kyphosis of
the cervico-thoracic spine
Scheuermann's • Epiphysitis of the vertebral joints is the main pathological process

disease • Predominantly affects adolescents
• Symptoms include back pain and stiffness
• X-ray changes include epiphyseal plate disturbance and anterior wedging
• Clinical features include progressive kyphosis (at least 3 vertebrae must be involved)
• Minor cases may be managed with physiotherapy and analgesia, more severe cases
may require bracing or surgical stabilisation
Scoliosis • Consists of curvature of the spine in the coronal plane

• Divisible into structural and non structural, the latter being commonest in adolescent
females who develop minor postural changes only. Postural scoliosis will typically
disappear on manoeuvres such as bending forwards
• Structural scoliosis affects > 1 vertebral body and is divisible into idiopathic, congential
and neuromuscular in origin. It is not correctable by alterations in posture
• Within structural scoliosis, idiopathic is the most common type
• Severe, or progressive structural disease is often managed surgically with bilateral rod
stabilisation of the spine
Spina bifida • Non fusion of the vertebral arches during embryonic development
• Three categories; myelomeningocele, spina bifida occulta and meningocele
• Myelomeningocele is the most severe type with associated neurological defects that may
persist in spite of anatomical closure of the defect
• Up to 10% of the population may have spina bifida occulta, in this condition the skin and
tissues (but not not bones) may develop over the distal cord. The site may be identifiable
by a birth mark or hair patch
• The incidence of the condition is reduced by use of folic acid supplements during
pregnancy
Spondylolysis • Congenital or acquired deficiency of the pars interarticularis of the neural arch of a
particular vertebral body, usually affects L4/ L5
• May be asymptomatic and affects up to 5% of the population
• Spondylolysis is the commonest cause of spondylolisthesis in children
• Asymptomatic cases do not require treatment
Spondylolisthesis • This occurs when one vertebra is displaced relative to its immediate inferior vertebral
body
• May occur as a result of stress fracture or spondylolysis
• Traumatic cases may show the classic "Scotty Dog" appearance on plain films
• Treatment depends upon the extent of deformity and associated neurological symptoms,
minor cases may be actively monitored. Individuals with radicular symptoms or signs will
usually require spinal decompression and stabilisation
● Intervertebral discs
• The posterior longitudinal ligament overlies the posterior aspect of the vertebral bodies. It also overlies the
posterior aspect of the intervertebral disks.
• Consist of an outer annulus fibrosus and an inner nucleus pulposus.
• The anulus fibrosus consists of several layers of fibrocartilage.
• The nucleus pulposus contains loose fibres suspended in a mucoprotein gel with the consistency of jelly. The
nucleus of the disc acts as a shock absorber.
• Pressure on the disc causes posterior protrusion of the nucleus pulposus. Most commonly in
lumbrosacral and lower cervical areas.
• The discs are separated by hyaline cartilage.
• There is one disc between each pair of vertebrae, except for C1/2 and the sacrococcygeal vertebrae.
• Acute Disc prolapse → Hip extension pain → Femoral stretch(L2 - 4) → cause Scoliosis as a result
Prolapsed disc
A prolapsed lumbar disc usually produces clear dermatomal leg pain associated with neurological deficits.
Features
• Leg pain usually worse than back
• Pain often worse when sitting
The table below demonstrates the expected features according to the level of compression:
L3 nerve root compression Sensory loss over anterior thigh

Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L4 nerve root compression Sensory loss anterior aspect of knee

Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L5 nerve root compression Sensory loss dorsum of foot

Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test
S1 nerve root compression Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test
Management
• Similar to that of other musculoskeletal lower back pain: analgesia, physiotherapy, exercises
• Persistent symptoms, muscular weakness, bladder or bowel dysfunction are indications for urgent MRI
scanning to delineate the disease extent to allow surgical planning
• Plain spinal x-rays have no useful role in establishing the extent of disk disease
Lumbar spinal stenosis
Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar
degenerative changes.
Patients may present with a combination of back pain, neuropathic pain and symptoms mimicking claudication. One of
the main features that may help to differentiate it from true claudication in the history is the positional element to the pain.
Sitting is better than standing and patients may find it easier to walk uphill rather than downhill. The neurogenic
claudication type history makes lumbar spinal stenosis a likely underlying diagnosis, the absence of such symptoms
makes it far less likely.
Pathology
Degenerative disease is the commonest underlying cause. Degeneration is believed to begin in the intervertebral disk
where biochemical changes such as cell death and loss of proteoglycan and water content lead to progressive disk
bulging and collapse. This process leads to an increased stress transfer to the posterior facet joints, which accelerates
cartilaginous degeneration, hypertrophy, and osteophyte formation; this is associated with thickening and distortion of the
ligamentum flavum. The combination of the ventral disk bulging, osteophyte formation at the dorsal facet, and
ligamentum flavum hyptertrophy combine to circumferentially narrow the spinal canal and the space available for the
neural elements. The compression of the nerve roots of the cauda equina leads to the characteristic clinical signs and
symptoms of lumbar spinal stenosis.
Diagnosis
MRI scanning is the best modality for demonstrating the canal narrowing. Historically a bicycle test was used as true
vascular claudicants could not complete the test.
Treatment
Laminectomy
Cervical ribs
• 0.2-0.4% incidence
• Consist of an anomalous fibrous band that often originates from C7 and may arc towards, but rarely reaches the
sternum
• Congenital cases may present around the third decade, some cases are reported to occur following trauma
• Bilateral in up to 70%
• Compression of the subclavian artery may produce absent radial pulse on clinical examination and in particular
may result in a positive Adsons test (lateral flexion of the neck away from symptomatic side and traction of
the symptomatic arm- leads to obliteration of radial pulse)
• Treatment is most commonly undertaken when there is evidence of neurovascular compromise. A transaxillary
approach is the traditional operative method for excision
Spinal Cord, Ventricles and CSF
• Rostrally is continues to the medulla oblongata of the brain and caudally it tapers at a level corresponding to the
L1-2 interspace (in the adult),
• A central structure, the filum terminale anchors the cord to the first coccygeal vertebra.
• The spinal cord is characterised by cervico-lumbar enlargements and these, broadly speaking, are the sites
which correspond to the brachial and lumbar plexuses respectively.
There are some key points to note when considering the surgical anatomy of the spinal cord:
- During foetal growth the spinal cord becomes shorter than the spinal canal, hence the adult site of cord termination @
L1 level (lower border); In Newborn @ L3 level (N-150)
- Spinal cord in both adult men and women is 18 inches (45 cm) in length. (N-150)
n
- Dura Mater extends upto S2 lower border(i.e. dural sac ends here) and LP is done bet L3 & L4 (N-150)
- Spinal extradural space contains loose fat (N-150)
- Spinal part of arachnoid invests cauda equina & nerves proceeding from it – separated from dura by subdural space.
n
- In cervical and thoracic regions subarachnoid space is annular, 3 mm – @ terminat @ lower border of L1 (upper
border L2 in some texts) SA space is circular & diameter 15 mm. (N-150)
- Pia mater of the spinal cord has a pair of denticulate ligaments which attach to dura mater (N-155), 21 fibres found.
- Due to growth of the vertebral column the spine segmental levels may not always correspond to bony landmarks as
they do in the cervical spine.
- The spinal cord is incompletely divided into two symmetrical halves by a dorsal median sulcus and ventral
median fissure. Grey matter surrounds a central canal that is continuous rostrally with the ventricular system of
the CNS.
- The grey matter is sub divided cytoarchitecturally into Rexeds laminae.
- Afferent fibres entering through the dorsal roots usually terminate near their point of entry but may travel for varying
distances in Lissauers tract. In this way they may establish synaptic connections over several levels
- At the tip of the dorsal horn are afferents associated with nociceptive stimuli. The ventral horn contains neurones
that innervate skeletal muscle.
The key point to remember when revising CNS anatomy is to keep a clinical perspective in mind. So it is worth
classifying the ways in which the spinal cord may become injured. These include:
• Trauma either direct or as a result of disc protrusion

• Neoplasia either by direct invasion (rare) or as a result of pathological vertebral fracture
• Inflammatory diseases such as Rheumatoid disease, or OA (formation of osteophytes compressing nerve
roots etc.
• Vascular either as a result of stroke (rare in cord) or as complication of aortic dissection
• Infection historically diseases such as TB, epidural abscesses.
● Passing Spinal needle, structures that are penetrated, from superficial to deep:
- Skin
- Subcutaneous connective tissue
- Supraspinous ligament
- Interspinous ligament
- Ligamentum flavum
- Epidural space
- Dura mater (dural sac)
- Subarachnoid space (lumbar cistern with CSF)
Spinothalamic tract
- Transmits impulses from receptors which measure crude touch, pain and temperature.
- Comprises the lateral and anterior spinothalamic tracts,
- Neurones transmitting these signals will typically ascend by one or two vertebral levels in Lissaurs tract prior
to decussating in the spinal cord itself.
- Neurones then pass rostrally in the cord to connect at the thalamus
● Anterior Spinothalamic (AWF) : Crude touch**; Pressure

● Lateral Spinothalamic (LWF) : Pain; Temperature**
● Spinoreticular Tract (LWF) : Conciousness; Awareness

● Spino-Olivery & Spino-Vestibular Tract (LWF) : Proprioception (position / posture sense)
● Spino-Cerebellar (Posterior) Tract : Proprioceptive signals to cerebellum
● Fasciculus Gracilis and
Fasciculus Cunateous (PWF or Dorsal column) : Fine touch, Fine all (Tactile), Pressure,Vibration,
Conscious Kinesthetic (proprioception), Stereognosis
● Anterior corticospinal tract : Conveys motor signal from the precentral gyrus to motor cells
within cord
● Touch Sensation
Crude : Anterior White Funiculous
Fine : Posterior White Funiculous
Discriminative : Tract of Gall
● Fine Touch and Proprioception absent: Lesion at Gracile Nucleus
Effects of Hemisection of Spinal Cord (Brown Sequard Syndrome)
• Brown–Sequard syndrome–Hemisection of the cord producing ipsilateral loss of proprioception and upper
motor neurone signs, plus contralateral loss of pain and temperature sensation. The explanation of this is that
the fibres decussate at different levels.
• Lesions below L1 will tend to present with LMN signs
• A thoracic cord lesion causes – spastic paraperesis, hyperrflexia and extensor plantar responses (UMN
lesion), incontinence, sensory loss below the lesion and 'sensory' ataxia
Site of the lesion Sensory Change Motor Change

Below the lesion ● Crude touch ● UMNL type lesion
(same side) ● Pain ● Spastic paralysis – raised muscle tone
● Temp – intact and Rest lost ● No muscle wasting or skin change
● No superficial reflex but exaggerated
deep reflex (hyperrflexia)
● Babinski’s sign (+) ve; Clonus (+)ve
Below the lesion ● Crude touch
(opposite side) ● Pain No paralysis
● Temp – Lost and Rest intact
At the level of ● Crude touch
lesion (opposite ● Pain No paralysis
side) ● Temp – Lost and Rest intact
At the level of ● LMNL type lesion

lesion (same ● Complete anaesthesia ● Flaccid paralysis – reduced muscle tone
side) ● Muscle wasting – skin cold, shiny or bluish
● All reflex absent
● Vasomotor tone lost
● Clonus (–) ve
** REMEMBER Ipsilateral Motor & Proprioception loss
Contralateral Pain & Temperature loss
Spinal cord injury
C1 – C5
Upper limbs: UMN
Lower limbs: UMN
C6 – T2
Upper limbs: LMN
Lower limbs: UMN
T3 – L3
Upper limbs: normal
Lower limbs: UMN
L4 – S2
Upper limbs: normal
Lower limbs: LMN
Spinal disorders
Dorsal column lesion • Loss vibration and proprioception

• Tabes dorsalis, SACD
Spinothalamic tract • Loss of pain, sensation and temperature

lesion
Syringomyelia • Selectively affects the spinotholamic tracts with loss of

pain and temperature sensation.
• Bilateral distribution of symptoms present
• A cystic cavity forms within the spinal cord.
• The commonest variant is the Arnold- Chiari
malformation in which the cavity connects with a
congenital malformation affecting the cerebellum.
• Acquired forms of the condition may occur as a result
of meningitis, surgery or tumours.
Osteomyelitis • Normally progressive

• Staph aureus in IVDU, normally cervical region
affected
• Fungal infections in immunocompromised
• Thoracic region affected in TB
Infarction spinal cord • Dorsal column signs (loss of proprioception and fine
discrimination
Cord compression • UMN signs

• Malignancy
• Haematoma
• Fracture
Brown-sequard • Hemisection of the spinal cord

syndrome • Ipsilateral paralysis
• Ipsilateral loss of proprioception and fine discrimination
• Contralateral loss of pain and temperature
● Central Cord Syndrome

n nd
- Usually hyperextens injury cervical spine in pt ē pre-existing cervical canal stenosis, 2 ary to osteoarthritis.
- Thought to arise as a result of vascular compromise of the cord in the distribution of the anterior spinal artery
- Disproportionately greater loss of motor power in supex–more distal than proximal; compared to infex
- Weakness more in arms, Flaccid paralysis of the upper limbs
- Varying degrees of sensory loss specially affecting cervical dermatomes
- Pt becomes quadriplegic after trauma, and regains strength in hours even in minutes
- Urinary retention
● Anterior Cord Syndrome
- Severe injury to most of the cord, with dorsal column sparing

- Spastic paraplegia
- Proprioception and deep pressure sensation remains intact
● Posterior Cord Syndrome

- Light touch, two-point discrimination and proprioception loss
- Normal pain and temperature sensation
- Normal motor function.
● Conus Lesions
- Damage to the sacral cord/lumbar nerve roots
- Produce reflex bowel and bladder function – Autonomous neurogenic bladder
- Constipation, impaired ejaculation and erection
- UMN signs, early sphincter dysfunction
- Pelvic floor weakness
- Cutaneous manifestations of spinal dysraphism
● Cauda Equina Lesion

- Compression lumbar sacral roots below L3 vertebra
- Early radicular pain, worse at night
- LMN signs; late sphincter dysfunction
- Areflexic paralysis producing peripheral paraplegia
- Asymmetrical sensory loss in saddle area
- Ankle reflex ↓↓
Dermatomes
• C2 to C4 The C2 dermatome covers the occiput and the top part of the neck. C3 covers the lower part of the
neck to the clavicle. C4 covers the area just below the clavicle.
• C5 to T1 Situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers the forearm and the
radial (thumb) side of the hand. C7 is the middle finger, C8 is the lateral aspects of the hand, and T1 covers the
medial side of the forearm.
• T2 to T12 The thoracic covers the axillary and chest region. T3 to T12 covers the chest and back to the hip
girdle. The nipples are situated in the middle of T4. T10 is situated at the umbilicus. T12 ends just above the hip
girdle.
• L1 to L5 The cutaneous dermatome representing the hip girdle and groin area is innervated by L1 spinal cord.
L2 and 3 cover the front part of the thighs. L4 and L5 cover medial and lateral aspects of the lower leg.
• S1 to S5 S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs. S3 cover the
medial side of the buttocks and S4-5 covers the perineal region. S5 is of course the lowest dermatome and
represents the skin immediately at and adjacent to the anus.
Myotomes Upper limb Myotomes Lower limb
Hip flexors (psoas) L1 and L2
Knee extensors (quadriceps) L3

Elbow flexors/Biceps C5
Ankle dorsiflexors (tibialis anterior) L4 and L5
Wrist extensors C6
Toe extensors (hallucis longus) L5
Elbow extensors/Triceps C7
Ankle plantar flexors (gastrocnemius) S1
Long finger flexors C8
Small finger abductors T1
The anal sphincter is innervated by S2, 3, 4

rd
● 3 & Lat. ventricle in between Interventricular foramina (of Monro)
rd th
● 3 & 4 ventricle in between Cerebral Aqueduct (of Sylvius)
th
● 4 ventricle’s L ateral aperture is Foramen L uschka; which allow CSF to L eave ventricular system
M edian aperture is Foramen M agendie; which allow CSF to Enter subarachnoid space
● CSF replaces the lymph of the CNS. The total volume is approximately 150ml. Approximately 500 ml is produced by
the ependymal cells in the choroid plexus (70%), or blood vessels (30%).
th
● Central canal is continuous with 4 ventricle; it’s the place where CSF flows through the spinal cord.(N-150)
● CSF reabsorbed into venous system via arachnoid granulations in Superior Sagittal Sinus
● Cob web coagulation of CSF is found in Tubercular meningitis
● Mass in the Lateral Ventricles

@ Roof of post.horn : Compresses Corpus Callosum fiber
@ Medial wall of body : Compresses Septum Pellucidum posterior part
@ Floor of inferior cornu : Compresses Hippocampus / Caudate Nucleus, Stria terminalis, Terminal Vein
● MASS IN THE 4th VENTRICLE

th
@ Floor : Compresses 6 CN Nuclei
● C/F of cervical spinal injury of unconscious pt:

Flaccid aereflexia
Elbow flexion without extention
Abdominal breathing (using of accesspry muscles of respiration)
Reduced BP, HR, Vol.(euvolaemia)
Grimace to pain above clavicle (not to below clavicle)
Priapism
Intracranial Pressure
(normal = 7-15 mmHg - avg.10mmHg ; abnormal >20mmHg; The brain can accommodate increases up to 24 mm Hg,
thereafter clinical features will become evident)
● ICP rise cause Cushing’s response

- RR & HR decreases
- Systolic BP & PP increases
rd
- Pupillary dilatation as a result of 3 CN palsy
- Cushings triad
• Widening of the pulse pressure
• Respiratory changes (Cheyne Stokes style)
• Bradycardia
● Raised ICP 1st plan of management – sedate & intubate.
Applied neurophysiology
• Pressure within the cranium is governed by the Monroe-Kelly doctrine. This considers the skull as a closed box.
Increases in mass can be accommodated by loss of CSF. Once a critical point is reached (usually 100- 120ml
of CSF lost) there can be no further compensation and ICP rises sharply. The step is that pressure will begin to
equate with MAP and neuronal death will occur. Herniation will also accompany this process.
• The CNS can autoregulate its own blood supply. Vaso constriction and dilatation of the cerebral blood vessels is
the primary method by which this occurs. Extremes of blood pressure can exceed this capacity resulting in risk
of stroke. Other metabolic factors such as hypercapnia will also cause vasodilation, which is of importance in
ventilating head injured patients.
• The brain can only metabolise glucose, when glucose levels fall, consciousness will be impaired.
Coning
• The cranial vault is a confined cavity apart from infants with a non fused fontanelle.
• Rises in ICP may be accommodated by shifts of CSF.
• Once the CSF shifting has reached its capacity ICP will start to rise briskly.
• The brain autoregulates its blood supply, as ICP raises the systemic circulation will display changes to try and
meet the perfusion needs of the brain. Usually this will involve hypertension.
• As CSF rises further, the brain will be compressed, cranial nerve palsies may be seen and compression of
essential centres in the brain stem will occur. When the cardiac centre is involved bradycardia will often
develop.
Traumatic Brain Injury
Extradural ● Bleeding into the space between the dura mater and the skull.
haematoma ● Results from acceleration-deceleration trauma or a blow to the side of the head.
● Majority occur in temporal region where skull fractures cause rupture of middle meningeal artery.
Features
• Raised intracranial pressure
• Some patients may exhibit a lucid interval
Subdural ● Bleeding into the outermost meningeal layer due to :

haematoma - Laceration of Middle Meningeal Vein
- Leakage from Cerebral vein
- Leakage from Dural bridging vein
● Occurs due to Fracture in diploic space
● Most commonly occur around frontal and parietal lobes.
● Risk factors include old age and alcoholism.
● Slower onset of symptoms than a extradural haematoma.
Subarachnoid ● Sudden collapse and loss of consciousness is most likely - commonly among youngs
haemorrhage ● Usually occurs spontaneously due to ruptured cerebral aneurysm but may be seen in association
with other injuries when a patient has sustained a traumatic brain injury
Intracerebral ● Usually hyperdense lesions on CT scanning.

haematoma ● Arise in areas of traumatic contusion with fuse to become a haematoma.
● Areas of clot and fresh blood may co-exist on the same CT scan (Swirl sign).
● Large haematomas and those associated with mass effect should be evacuated.
Intraventricular ● Haemorrhage that occurs into the ventricular system of the brain.
haemorrhage ● It is relatively rare in adult surgical practice and when it does occur, it is typically associated
with severe head injuries.
● In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow,
hydrocephalus may result.
● In neonatal practice the vast majority of IVH occur in the first 72 hours after birth and it occurs as a
result of birth trauma combined with cellular hypoxia, together the with the delicate neonatal CNS.
Treatment
- Largely supportive, therapies such as intraventricular thrombolysis and prophylactic CSF drainage
have been trialed and not demonstrated to show benefit. Hydrocephalus and rising ICP is an
indication for shunting
● Hunt and Hess Scale Grades SAH

1. Asymptomatic or minimal headache + slight neck stiffness
2. Moderate or severe headache ē neck stiffness, but no neurological deficit other than cranial nerve palsy.
3. Drowsiness with confusion or mild focal neurology
4. Stupor with moderate to severe hemi paresis or mild decerebrate rigidity
5. Deeply comatose with severe decerebrate rigidity.
(Severity and mortality increase with grade).
● Intracerebral hemorrhage is the worst among all

● Hypercapnia will tend to produce cerebral vasodilation. It is important in patients with cranial trauma as it cz ↑ ICP
● INTERPRETATION OF PUPILLARY FINDINGS IN HEAD INJURIES

th st
6 nerve (Abducent) is usually 1 to be affected by raised intracranial pressure
6th nerve (Abducent) innervates LR muscle; effect of damage of this nerve - unability to abduct (laterally deviate)
rd n
3 nerve (Oculomotor) is affected by ↑ ICP, cz pupillary dilatat (ptosis,unability to adduct,eye displacement
outwards & downwards)
Pupil size Light response Interpretation
Unilaterally dilated Sluggish or fixed 3rd nerve compression secondary to tentorial herniation
Bilaterally dilated Sluggish or fixed • Poor CNS perfusion

• Bilateral 3rd nerve palsy
Unilateral dilated or equal Cross reactive (Marcus - Gunn) Optic nerve injury
Bilaterally constricted May be difficult to assess • Opiates

• Pontine lesions
• Metabolic encephalopathy
Unilaterally constricted Preserved Sympathetic pathway disruption
● Head Injury Management- NICE Guidelines
Summary of guidelines
• All patients should be assessed within 15 minutes on arrival to A&E
• Document all 3 components of the GCS
• If GCS <8 or = to 8, - consider stabilising the airway
• Treat pain with low dose IV opiates (if safe)
• Full spine immobilisation until assessment if:
- GCS < 15
- neck pain/tenderness
- paraesthesia extremities
- focal neurological deficit
- suspected c-spine injury
• If a c-spine injury is suspected a 3 view c-spine x-ray is indicated. CT c-spine is preferred if:
- Intubated
- GCS <13
- Normal x-ray but continued concerns regarding c-spine injury
Immediate CT head (within 1h) if

• GCS < 13 on admission
• GCS < 15 2h after admission
• Suspected open or depressed skull fracture
• Suspected skull base fracture (panda eyes, Battle's sign, CSF from nose/ear, bleeding ear)
• Focal neurology
• Vomiting > 1 episode
• Post traumatic seizure
• Coagulopathy
Contact neurosurgeon if:

• Persistent GCS < 8 or = 8
• Unexplained confusion > 4h
• Reduced GCS after admission
• Progressive neurological signs
• Incomplete recovery post seizure
• Penetrating injury
• Cerebrospinal leak
Observations
• 1/2 hourly GCS until 15
● Head injury paediatrics

Criteria for immediate request for CT scan of the head (children)
* Loss of consciousness lasting more than 5 minutes (witnessed)
* Amnesia (antegrade or retrograde) lasting more than 5 minutes
* Abnormal drowsiness
* Three or more discrete episodes of vomiting
* Clinical suspicion of non-accidental injury
* Post-traumatic seizure but no history of epilepsy
* GCS <14, or for a baby under 1 year GCS (paediatric) <15, on assessment in the emergency department
* Suspicion of open or depressed skull injury or tense fontanelle
* Sign of basal skull fracture (haemotympanum, ‘panda' eyes, CSF leakage from the ear or nose, Battle's sign)
* Focal neurological deficit
* If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head
* Dangerous mechanism of injury
- High-speed RTA
- Fall from height >3m
- High-speed injury from a projectile or an object
● CLASSICAL SIGNS AND SYMPTOMS BASAL SKULL #

- Periorbital haematoma (Raccoon eyes),
- Subconjunctival haemorrhage
- Battles sign
- Rhinorrhoea / otorrhoea (blood mixed with CSF,doesn't clot due 2damage2cribriform plates).
● Racoon-eye or Panda sign found in Basal skull # or Subgaleal (subaponeurotic) Haematoma
● SCALP NERVE SUPPLY:: GLASS

• G reater occipital/ Greater auricular
• L esser occipital
• A uriculotemporal
• S upratrochlear
• S upraorbital
● Subgaleal (subaponeurotic) Haematoma and Localized Scalp Hematoma - difference
Subgaleal (subaponeurotic) Haematoma shows
Diffuse, large, fluctuant hematoma extending from the frontal region to occiput হয়,
May be associated ē swollen eyelid;
Usually occurs a few days after the head injury
Stroke: Types
Primary intracerebral haemorrhage • Presents with headache, vomiting, loss of consciousness

(PICH, c. 10%)
Total anterior circulation infarcts (TACI, • Involves middle and anterior cerebral arteries
c. 15%) • Hemiparesis/hemisensory loss
• Homonymous hemianopia
• Higher cognitive dysfunction e.g. Dysphasia
Partial anterior circulation infarcts (PACI, • Involves smaller arteries of anterior circulation e.g. upper or lower
c. 25%) division of middle cerebral artery
• Higher cognitive dysfunction or two of the three TACI features
Lacunar infarcts (LACI, c. 25%) • Involves perforating arteries around the internal capsule,
thalamus and basal ganglia
• Present with either isolated hemiparesis, hemisensory loss or
hemiparesis with limb ataxia
Posterior circulation infarcts (POCI, c. • Vertebrobasilar arteries

25%) • Presents ē features of brainstem damage – vertigo & dysarthria
• Ataxia, disorders of gaze and vision, cranial nerve lesions
Lateral medullary syndrome (posterior • Wallenberg's syndrome

inferior cerebellar artery) (N-132) • Infarcts entire dorsolateral part of rostral medulla
• Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness,
cranial nerve palsy e.g. Horner's
• Contralateral: limb sensory loss
Weber's syndrome • Ipsilateral III palsy

• Contralateral weakness
Anterior cerebral artery

• Contralateral hemiparesis and sensory loss, lower extremity > upper
• Disconnection syndrome
Middle cerebral artery

• Contralateral hemiparesis and sensory loss, upper extremity > lower
• Contralateral hemianopia
• Aphasia (Wernicke's)
• Gaze abnormalities
Posterior cerebral artery

• Contralateral hemianopia with macular sparing
• Disconnection syndrome
Lacunar
• Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
Lateral medulla (posterior inferior cerebellar artery)

• Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g.
Horner's
• Contralateral: limb sensory loss
Pontine
• VI nerve: horizontal gaze palsy
• VII nerve
• Contralateral hemiparesis
● Indications for hemicraniectomy include:

• Age under 60 years
• Clinical deficit in middle cerebral artery territory
• Decreased consciousness
• >50% territory infarct
● SCHEUERMANN’S DISEASE: vertebrae grow unevenly; that is the ant. Angle > post.angle – resulting wedge shaping
of vertebra czing kyphosis
Brain Pathology
● CNS tumours
• 60% = Glioma and metastatic disease

• 20% = Meningioma
• 10% = Pituitary lesions
• In paediatric, Medulloblastomas (Neuroectodermal Tumours) are commonest lesion, but very rare in adults.
• Tumours arising in right temporal and frontal lobe may reach considerable size before becoming
symptomatic. Whereas tumours in the speech and visual areas will typically produce early symptoms.
• Diagnosis
MRI Scanning provides the best resolution.
• Treatment
- Usually surgery, even if tumour cannot be completely resected conditions such as rising ICP can be
addressed with tumour debulking and survival and quality of life prolonged.
- Curative surgery can usually be undertaken with lesions such as meningiomas. Gliomas have a marked
tendency to invade normal brain and resection of these lesions is nearly always incomplete
● Glioma
– Glioma is a tumour that is typically found in the CNS.
– These tumours arise from Glial Cells ((otherwise known as neuroglial cells)
– They are sub categorised according to the cell type they most closely resemble.
Glioma sub types

• Ependymomas- Ependymal cells
• Astocytomas- Astrocytes (including glioblastoma)
• Oligodendrogliomas- Oligodendrocytes
• Mixed- e.g. oligoastrocytomas
– Gliomas are categorised as being either high or low grade lesions (the former has the worse prognosis).
– They may be either supra or infra tentorial.
– Their symptoms will typically reflect their site of origin.
– Glioblastoma multiforme has the worst prognosis and few patients will survive beyond 12 months.
NAME C/F PATHOLOGY POINTS

Meningioma - H/O long time headache
- Weakness of limbs - Well-circumscribed lesion @
frontoparietal junction
Glioblastoma - H/O grand mall seizure - Poor prox.
multiforme - Either @ grey or white but mainly - Large, poorly demarcated mass - Survival
occurs at deep white matter with central necrosis surrounded beyond 1yr is
- Most common intrinsic brain tumour by highly anaplastic cells rare
accounting between 30-50% in adult - Enhancing ring around an area
peak incidence between 55-65yrs of necrosis
Cerebral
abscess - Short h/o headache - Ring enhancing mass
- Fever - Gliosis, fibrosis ē necrosis,
- Confused state neutrophils & lymphocytes
Chr. Cerebral
abscess - Ring enhancing mass
- Granulation tisuue ē adjacent
Collagenisation, gliosis & edema
Vestibular - Sudden onset of dizziness ē nausea
neuronitis & vomiting, headache
- Nystagmus towards affected side - Symptom disappear ē in 7-10day
- Absence of concomitant tinnitus or
hearing loss is a hallmark
Shwannoma Best Prox
- Benign & arise from nerve sheath following
- Most commonly from sensory nerve surgery
root
Astrocytoma - Common in children - Glial Fibrillary Acidic Protein
- Sudden onset of generalised seizure (GFAP)
- Solid mass
- Noncavitating
- Almost undistinguishable from white
matter
Brain abscess
• Causes : Extension of sepsis from middle ear or sinuses,

Trauma or surgery to the scalp,
Penetrating head injuries
Embolic events from endocarditis.
• Symptoms : Depend on the site of abscess (those in critical areas e.g.motor cortex) will present earlier.
Raised intra cranial pressure
Fever (not the swinging pyrexia seen with abscesses at other sites),
Headache and focal neurology
• Assessment : CT (ring enhancing lesion found – as i/v contrast can’t enter the centre of abscess cavity)
• Treatment : Craniotomy and the abscess cavity debrided.

Abscess may reform because the head is closed following abscess drainage
● Cerebellopontine angle lesions are

- Meningioma;
th
- Acoustic neuroma (5 CN palsy )
- 2nd ary tumor deposits
- Epidermoid
- Arachnoid cyst
- Paraganglioma
● Hemorrhagic lesion of Temporal lobe is typical of Herpes Simplex Virus (HSV). HSV encephalitis occurs @ anytime of
the year – has bimodal age distribution.
Trachea
Location ● Trachea Commences @ C6

Trachea bifurcates @ T5
The right main bronchus @ T5
The left main bronchus @ T6
Arterial and venous supply Inferior thyroid arteries and the thyroid venous plexus.
Nerve Branches of vagus, sympathetic and the recurrent nerves
● Relations in the neck
Anterior(Superior to inferior) • Isthmus of the thyroid gland

• Inferior thyroid veins
• Arteria thyroidea ima (when that vessel exists)
• Sternothyroid
• Sternohyoid
• Cervical fascia
• Anastomosing branches between the anterior jugular veins
Posterior Oesophagus.
Laterally • Common carotid arteries

• Right and left lobes of the thyroid gland
• Inferior thyroid arteries
• Recurrent laryngeal nerves
● Relations in the thorax
Anterior
• Manubrium sterni, the remains of the thymus, the aortic arch, left common carotid arteries, and the deep cardiac
plexus
Lateral
• In the superior mediastinum, on the right side is the pleura and right vagus; on its left side are the left recurrent
nerve, the aortic arch, and the left common carotid and subclavian artery
Larynx and Pharynx
● Hyoid bone is @ C3
● Thyroid cartilage is @ C4 & C5
● Cricoid cartilage is @ C6
● Trachea commences @ C6 and Bifurcates @ T5 (tall person or during deep inspiration @ T6)
● C7 vertebra has the most prominent spinous process
● Scapular spine – dermatome C7 (Dorsal Primary Ramus)
The larynx lies in the anterior part of the neck at the levels of C3 to C6 vertebral bodies. The laryngeal skeleton consists
of a number of cartilagenous segments. Three of these are paired; arytenoid, corniculate and cuneiform. Three are
single; thyroid, cricoid and epiglottic. The cricoid cartilage forms a complete ring (the only one to do so).
The laryngeal cavity extends from the laryngeal inlet to the level of the inferior border of the cricoid cartilage.
Divisions of the laryngeal cavity
Laryngeal vestibule Superior to the vestibular folds
Laryngeal ventricle Lies between vestibular folds and superior to the vocal cords
Infraglottic cavity Extends from vocal cords to inferior border of the cricoid cartilage
● Blood supply
Arterial supply : - Laryngeal arteries← superior and inferior thyroid arteries.
- Superior laryngeal artery is closely related to the internal laryngeal nerve.
- Inferior laryngeal artery is related to the inferior laryngeal nerve.
Venous drainage: - Via superior and inferior laryngeal veins,

- Superior laryngeal vein drains into Superior Thyroid Vein
- Inferior laryngeal vein drains into Middle thyroid vein, or thyroid venous plexus.
● Lymphatic drainage
The vocal cords have no lymphatic drainage and this site acts as a lymphatic watershed.
Supraglottic part : Upper deep cervical nodes

Subglottic part : Prelaryngeal and pretracheal nodes and inferior deep cervical nodes
The aryepiglottic fold and vestibular folds have a dense plexus of lymphatics associated with them and
malignancies at these sites have a greater propensity for nodal metastasis.
● Piriform fossa or recess is located on either side of the larynx within laryngopharynx(N-60)
● Thyroepiglotticus : only muscle that opens Larynx inlet (N-72)

● Post. Cricoarytenoids : only muscle that abducts or opens Vocal cords (N-72)
● Cricothyroid : only muscle that tense Vocal cords (N-72)

● Thyroarytenoid + vocalis : relax Vocal cords (N-72)
● 2 Muscles Have 2 Functions Each
Cricothyroid : - Tense vocal cord

- Close glottis
Thyroarytenoid : - Close glottis

- Relax vocal cord (+ Vocalis)
● The vocal folds (true vocal cords) control sound production. The apex of each fold projects medially into the laryngeal
cavity. Each fold includes:
• Vocal ligament – formed by superior free edge of the Conus Elasticus (N-72)
• Vocalis muscle (most medial part of Thyroarytenoid Muscle)
● The Glottis is composed of the vocal folds, processes and Rima Glottidis.
● The Rima Glottidis is the narrowest potential site within the larynx
Voice production
There are 2 main nerves involved:
Superior laryngeal nerve (SLN)
• Innervates the cricothyroid muscle, No vocal cord paralysis
Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high notes during singing, SLN
paresis and paralysis result in:
a. Abnormalities in pitch
b. Inability to sing with smooth change to each higher note (glissando or pitch glide)
Recurrent laryngeal nerve (RLN)/Inferior laryngeal nerve
• Innervates intrinsic larynx muscles
a. Opening vocal folds (as in breathing, coughing)

b. Closing vocal folds for vocal fold vibration during voice use
c. Closing vocal folds during swallowing
● All muscles of larynx is supplied by R.L.N. except -

Cricothyroid which is supplied by External branch of Superior Laryngeal Nerve (N-72). Any lesion of this nerve:-
- Can effect High Pitched Voice
- Cause Incomplete paralysis of vocal cord
- Can go un-noticed but patients can complain of a weak voice when trying to sing or shout
● R.L.N. injury causes paralysis of vocal cord of corresponding side. Followings are various types of lesions:
Unilateral Complete paralysis:

- Weak and Hoarse voice, bovine cough
- Paralysis of Cricopharyngeus and Adductor muscles
- Liquid swallowing difficulty due to Cricopharyngeus paralysis
- Effected vocal cord lies further away from midline than in an incomplete paralysis
- Adductor muscles paralysis
- It is still possible to see some compensation by the Unaffected cord
Unilateral Incomplete paralysis:

- Weak and Hoarse voice but satisfactory
- Effected vocal cord is paralysed
- Effected vocal cord lies away from midline or near the midline (At rest)
- Effected vocal cord retains some Adductor function(Cricothyroid)
- Unaffected vocal cord crosses the midline to compensate the effected one
Treatment of unilateral RLN injuries(Complete or Incomplete )

- Speech therapy or Surgery
- Type – I Thyroplasty surgery (procedure: under LA, a silastic wedge is inserted through a window in
Alar cartilage overlying affected cord. The effect is tested by asking the patient to speak during the
procedure )
- Another option is vocal cord injection with synthetic material to cause vocal cord medialisation.
Bilateral Complete paralysis :

- Dire long-term sequelae with regard to loss of voice
- Phonation is lost but respiration is possible

- Patients may be dyspnoeic on exertion and cold can cause critical narrowing of the glottis
- The cords are completely immobile and lie in the cadaveric position
Bilateral Incomplete paralysis :

- The voice can be surprisingly good but this is very serious
- There is unopposed adductor action of the Cricothyroid muscle which leads to closure of the glottis.
- Patients presents by inspiratory stridor or airway obstruction immediately post-operatively
- Tracheostomy required.
Treatment of bilateral RLN injuries (Complete or Incomplete)

- Laser Arytenoidectomy to enlarge to glottic airway (this improves the airway but impairs the voice)
- Tracheostomy with speaking valve (popular method)
● Inspiratory stridor occurs due to Laryngeal narrowing

Expiratory stridor occurs due to Bronchial tree narrowing
Inspiratory+ Expiratory stridor occurs due to Subglottic Ca
● Laryngeal Carcinoma Treatment

- Glottic ca + Ant. Commissure involved : Radio
- Glottic ca + T3 & T4 stage : Elective neck dissection
- Vocal cord ca T1 + Ant. Commissure not involved : Radio
- Vocal cord ca in situ : excision of mucosa
- Vocal cord ca + neck LN involve : Total laryngectomy + neck dissection
- Supraglottic ca : Total laryngectomy + neck dissection
- Supraglottic all disease – bilateral neck dissection is done due2 chance of metastasis
- Supraglottic is worse than glottic
● Laryngomalacia occurs in newborn baby. Soft & immature cartilage of upper larynx collapse inward during
inhalation. Which cause loud noises by certain position in sleep.
● Pharyngeal pouch is also called Zenker’s diverticulum.
● Although squamous ca common in head neck region, But who works with hard wood (carpenter, cabinet maker),
among them adenocarcinoma is the commonest findings (confusing???? )
● Reinke’s Oedema / Polypoid Degeneration : swelling of vocal cord due to fluid collection.
Tonsil
● Tonsil Bed Formation (N-59)

- Pharyngobasilar fascia
- Buccopharyngeal fascia
- Sup. Constrictor + Palatopharyngeus + Styloglossus
th
- 9 CN
Anatomy
• Each palatine tonsil has two surfaces, a medial surface which projects into the pharynx and a lateral surface
that is embedded in the wall of the pharynx.
• They are usually 25mm tall by 15mm wide, although this varies according to age and may be almost completely
atrophied in the elderly.
• Their arterial supply is from the tonsillar artery, a branch of the facial artery.
• Its veins pierce the constrictor muscle to join the external palatine or facial veins. The external palatine vein is
immediately lateral to the tonsil, which may result in haemorrhage during tonsillectomy.
• Lymphatic drainage is the jugulodigastric node and the deep cervical nodes.
Tonsillitis
• Usually bacterial (50%) - group A Streptococcus - Streptococcus pyogenes the most common organism.
Remainder viral.
• Characterised by pharyngitis, fever, malaise and lymphadenopathy.
• The tonsils are typically oedematous and yellow or white pustules may be present
• Infectious mononucleosis may mimic the condition.
• Treatment with penicillin type antibiotics is indicated for bacterial tonsillitis.
• Bacterial tonsillitis may be complicated by development of abscess (Quinsy). This may distort the uvula result
in local abscess formation
- Indications tonsillectomy includes recurrent tonsillitis, suspected malignancy, and enlargement czing sleep apnoea.
- Dissection tonsillectomy is the preferred technique with haemorrhage being the commonest complication. Delayed
otalgia may occur owing to irritation of the glossopharyngeal nerve.
Secondary haemorrhage after tonsillectomy
- Primary or reactionary hemorrhage most commonly occurs in the first 6-8 hours following surgery. It is
managed by immediate return to theatre.
- Secondary haemorrhage occurs between 5 and 10 days after surgery, it is often associated with a
wound infection.
- Treatment is usually with admission and antibiotics. Severe bleeding may require surgery. Secondary
haemorrhage occurs in 3% of all tonsillectomies.
● Tonsillitis otalgia --- cause neuralgia of the glossopharyngeal (IX) nerve.
● External Palatine Vein lies immediate lateral to the tonsil and may cause reactionary hemorrhage followimg
tonsillectomy
● Cochlear implant bypasses mechanical structures of normal hearing pathway & provides direct electrical stimulus
2spiral ganglion cells of auditory nerve.
Choanal atresia
• Congenital disorder with an incidence of 1 in 7000 births.

• Posterior nasal airway occluded by soft tissue or bone.
• Associated with other congenital malformations e.g. coloboma
• Babies with unilateral disease may go unnoticed.

• Babies with bilateral disease will present early in life as they are obligate nasal breathers.
• Treatment is with fenestration procedures designed to restore patency.
Eye
● Iris separates the anterior and posterior chambers in the eyeball
● External oblique muscle
External oblique forms the outermost muscle of the three muscles comprising the anterolateral aspect of the abdominal
wall. Its aponeurosis comprises the anterior wall of the inguinal canal.
Origin Outer surfaces of the lowest eight ribs
Insertion • Anterior two thirds of the outer lip of the iliac crest.
• The remainder becomes the aponeurosis that fuses with the
linea alba in the midline.
Nerve supply Ventral rami of the lower six thoracic nerves
Actions Contains the abdominal viscera, may contract to raise intra

abdominal pressure. Moves trunk to one side.
● Lacrimal system
Lacrimal gland
Consists of an orbital part and palpebral part. They are continuous posterolaterally around the concave lateral edge of
the levator palpebrae superioris muscle.
The ducts of the lacrimal gland open into the superior fornix. Those from the orbital part penetrate the aponeurosis of
levator palpebrae superioris to join those from the palpebral part. Therefore excision of the palpebral part is functionally
similar to excision of the entire gland.
Blood supply
Lacrimal branch of the opthalmic artery. Venous drainage is to the superior opthalmic vein.
Innervation
The gland is innervated by the secretomotor paraympathetic fibres from the pterygopalatine ganglion which in turn may
reach the gland via the zygomatic or lacrimal branches of the maxillary nerve or pass directly to the gland. The
preganglionic fibres travel to the ganglion in the greater petrosal nerve (a branch of the facial nerve at the geniculate
ganglion).
Nasolacrimal duct
Descends from the lacrimal sac to open anteriorly in the inferior meatus of the nose.
Lacrimation reflex
Occurs in response to conjunctival irritation (or emotional events). The conjunctiva will send signals via the opthalmic
nerve. These then pass to the superior salivary centre. The efferent signals pass via the greater petrosal nerve
(parasympathetic preganglionic fibres) and the deep petrosal nerve which carries the post ganglionic sympathetic fibres.
The parasympathetic fibres will relay in the pterygopalatine ganglion, the sympathetic fibres do not synapse. They in turn
will relay to the lacrimal apparatus.
Disorders of the oculomotor system
Nerve Path Nerve palsy features
Oculomotor nerve • Large nucleus at the midbrain – Ptosis
• Fibres pass through the red nucleus and the – Eye down and out
pyramidal tract; through the cavernous sinus – Unable to move the eye superiorly,
into the orbit inferiorly, medially

– Pupil fixed and dilated
Trochlear nerve • Longest intracranial course – Vertical diplopia (diplopia on descending
• Only nerve to exit the dorsal aspect of the stairs !!! )
brainstem – Unable to look down and in
• Nucleus at midbrain, passes between the

posterior cerebral and superior cerebellar
arteries, through the cavernous sinus into the
orbit
Abducens nerve Nucleus lies in the mid pons – Convergence of eyes in primary position
– Lateral diplopia towards side of lesion
– Eye deviates medially
Visual field defects

• left homonymous hemianopia means visual field defect to the left, i.e. Lesion of right optic tract
• homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
• incongruous defects = optic tract lesion; congruous defects = optic radiation lesion or occipital cortex
Homonymous hemianopia
• Incongruous defects: lesion of optic tract
• Congruous defects: lesion of optic radiation or occipital cortex
• Macula sparing: lesion of occipital cortex
Homonymous quadrantanopias
• Superior: lesion of temporal lobe
• Inferior: lesion of parietal lobe
• Mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
Bitemporal hemianopia
• Lesion of optic chiasm
• Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
• Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a
craniopharyngioma
Superior quadranopia = temporal lobe lesion

Inferior quadranopia = parietal lobe lesion
Horners syndrome
– Clinical features:
• Ptosis
• Miosis
• Endopthalmos
• Anhydrosis
– Primarily a disorder of the sympathetic nervous system.

– Extent of symptoms depends upon the anatomical site of the lesion.
– Proximal lesions occur along the hypothalamospinal tract
– Distal lesions are usually post ganglionic e.g. at level of internal carotid artery or beyond.
In contrast to a 3rd nerve palsy the ptosis is more mild and the pupil constricted rather than dilated.
Facial development
• Frontonasal prominence : Fore head; Nose bridge; Medial and lateral Nasal prominence
• Medilal nasal prominence : Philtrum; Crest and tip of nose
• Lateral nasal prominence : Alae of nose
• Maxillary prominence : Cheeks and lateral portion of upper lip
• Mandibular prominence : Lower lip
Cleft lip and palate
Cleft lip and palate are the most common congenital deformity affecting the orofacial structures. Whilst they may be an
isolated developmental malformation they are also a recognised component of more than 200 birth defects. The
incidence is as high as 1 in 600 live births. The commonest variants are:
• Isolated cleft lip (15%)
• Isolated cleft palate (40%)
• Combined cleft lip and palate (45%)
Cleft lip
• ICleft lip occurs as a result of disruption of the muscles of the upper lip and nasolabial region.
• These muscles comprise a chain of muscles viz; nasolabial, bilabial and labiomental.
• Defects may be unilateral or bilateral.
Cleft palate
• The primary palate consists of all anatomical structures anterior to the incisive foramen.
• The seconday palate lies more posteriorly and is sub divided into the hard and soft palate.
• Cleft palate occurs as a result of non fusion of the two palatine shelves.
• Both hard and soft palate may be involved.
• Complete cases are associated with complete separation of the nasal septum and vomer from the palatine
processes.
Treatment
• Surgical reconstruction is the mainstay of management.
• Simple defects are managed as a single procedure. Complex malformations are usually corrected in stages.
• Affected individuals have a higher incidence of hearing and speech problems
Nose and Nasal sinuses
● Nasolacrimal duct empties into inferior meatus by an imperfect valve, plica lacrimalis (Hasner’s fold) (N-32)
● Middle Meatus Opening(N-32)

Ethmoidal bula : Middle ethmoidal sinus opening
Hiatus semilunaris : Frontal & Maxillary sinus opening
Infundibulum
● Sphenoidal sinus opens at spheno – ethmoidal recess

● Mastoid air cell infection goes via Epitympanic Recess
Diseases of nose and sinuses
● Benign Tumours
• Simple papilloma
o Incidental finding
o Present with obstructive symptoms.
o Treatment : Excision under GA
• Transitional cell papilloma

o More extensive
o Produce obstructive symptoms.
o Erosion of local structures is a recognised complication.
o Treatment: Careful and complete excision as these lesions may rarely undergo malignant
transformation. Some cases may require partial or total maxillectomy.
• Pleomorphic adenomas of Maxillary sinus

o Extremely rare,
o Nasal obstruction and pain if the sinus is obstructed.
o Treatment: Complete surgical excision.
• Benign osteomas
o Develops in paranasal sinuses, the frontal sinus is the most frequent location of such lesions.
o Pain, rhinorrhoea and anosmia.
o Treatment: Observation, if asymptomatic.
Sphenoid osteomas should be resected completely soon after diagnosis as enlargement
may compromise visual fields. Many sinus osteomas can now be resected endoscopically.
• Nasal polyps
o Benign lesions of ethmoid sinus mucosa. rare in childhood
o Many patients may also have asthma, cystic fibrosis and a sensitivity to aspirin.
o Watery rhinorrhoea, infection and anosmia.
o The polyps are usually a semi transparent grey mass.
o Treatment: Either with systemic steroids or surgical resection. The latter should be combined with
antral washout. Low dose nasal, steroid drops may reduce the risk of recurrence.
● Malignant disease
• Malignancies encountered in the nose and paranasal sinuses include,
o Adenoid cystic carcinoma,
o Squamous cell carcinoma
o Adenocarcinoma.
• Adenocarcinoma of the paranasal sinuses and nasopharynx is strongly linked to exposure to hard wood dust
(after >10 years exposure)
• Adenoid cystic carcinoma usually originates in the smaller salivary glands.
• The majority of cancers (50%) arise from the lateral nasal wall, a smaller number (33%) arise from the maxillary
antrum, ethmoid and sphenoid cancers comprise only 7%.
• Signs of malignancy include
o Loose teeth,
o Cranial nerve palsies and lymphadenopathy.
• Nasopharyngeal cancers
o Most common in individuals presenting from China and Asia. Linked to infection with EBV
o Strongly associated with wood work. Most cases require occupational exposure > 10 years
o Most cases are ethmoidal in origin
o Squamous Cell Carcinoma of the nasopharynx. Are Adenocarcinomas on histology(?!)
o Presenting Features:
Cervical lymphadenopathy
Otalgia
Unilateral Serous Otitis Media
Nasal obstruction, discharge and/ or epistaxis
Cranial nerve palsies e.g. III-VI
o Imaging: Combined CT and MRI.

st
o Radiotherapy is the 1 line therapy and chemotherapy also used.
● Maxillary sinusitis
• Common symptoms include
o Post nasal discharge,
o Pain,
o Headache
o Toothache.
• Imaging may show a fluid level in the antrum.
• Common organisms
o Haemophilus influenzae
o Streptococcus pneumoniae.
• Treatment
o Antral lavage may facilitate diagnosis and relieve symptoms.
o Antimicrobial therapy has to be continued for long periods.
o Antrostomy may be needed.
● Frontoethmoidal sinusitis
• Usually presents
o Frontal headache,
o Nasal obstruction
o Altered sense of smell.
o Inflammation may progress to involve periorbital tissues.
o Ocular symptoms may occur and secondary CNS involvement brought about by infection entering via
emissary veins.
• CT scanning is the imaging modality of choice.
• Early cases may be managed with antibiotics. More severe cases usually require surgical drainage
Ear
External ear
- Auricle is composed of elastic cartilage covered by skin.
- The lobule has no cartilage and contains fat and fibrous tissue.
- External auditory meatus is approximately 2.5cm long. Lateral third of the external auditory meatus is cartilaginous and
the medial two thirds is bony.The region is innervated by the greater auricular nerve. The auriculotemporal branch of
the trigeminal nerve supplies most of external auditory meatus and the lateral surface of the auricle.
Middle ear
- Space between the tympanic membrane and cochlea.
- The aditus leads to the mastoid air cells is the route through which middle ear infections may cause mastoiditis. ---
- Anteriorly the eustacian tube connects the middle ear to the naso pharynx.
- The middle ear is innervated by the glossopharyngeal nerve and pain may radiate to the middle ear following
tonsillectomy.
The Tympanic Membrane consists of:
• Outer layer of Stratified Squamous Epithelium.
• Middle layer of Fibrous Tissue.
• Inner layer of Mucous Membrane continuous with the middle ear.

• The tympanic membrane is approximately 1cm in diameter.
• The chorda tympani nerve passes on the medial side of the pars flaccida..
Ossicles
- Malleus attaches to the tympanic membrane (the Umbo).
- Malleus articulates with the incus (synovial joint).
- Incus attaches to stapes (another synovial joint).
Internal ear
- Cochlea, semi circular canals and vestibule
- Organ of Corti is the sense organ of hearing and is located on the inside of the Cochlear Duct on basilar membrane.
- Vestibule accommodates the utricule and the saccule. These structures contain endolymph and are surrounded by
perilymph within the vestibule.
- The semicircular canals lie at various angles to the petrous temporal bone. All share a common opening into the
vestibule.
● Osteosclerosis of ear- hearing is often improved in background noisy places: so-called Paracusis Willisii.
Disorders affecting the ear
Otitis externa
Variant Cause Features Treatment
Acute otitis Boil in external auditory meatus Acute pain on moving the Ear packs may be used
externa pinna Topical antibiotics
Conductive hearing loss if Operative debridement may be
lesion is large needed in severe cases
When rupture occurs pus
will flow from ear
Chronic Chronic combined infection in the external Chronic discharge from Cleansing of the external ear and
otitis auditory meatus usually combined affected ear, hearing loss treatment with antifungal and
media staphylococcal and fungal infection and severe pain rare antibacterial ear drops
Otitis media
Variant Cause Features Treatment
Acute Viral induced middle ear Most common in children and Antibiotics (usually amoxycillin)
suppurative effusions secondary to rare in adults
otitis media eustacian tube dysfunction May present with symptoms
elsewhere (e.g. vomiting) in
children
Severe pain and sometimes
fever
May present with discharge is
tympanic rupture occurs
Chronic May occur with or without Those without cholesteatoma Simple pars tensa perforations may be
suppurative cholesteatoma may complain of intermittent managed non operatively or a
otitis media Those without discharge (non offensive) myringoplasty considered if symptoms
cholesteatoma have a Those with cholesteatoma troublesome.
perforation of the pars tensa have impaired hearing and foul Pars flaccida perforations will usually
Those with cholesteatoma smelling discharge require a radical mastoidectomy
have a perforation of the
pars flaccida
Otosclerosis
• Progressive conductive deafness
• Secondary to fixation of the stapes in the oval window
• Treatment is with stapedectomy and insertion of a prosthesis
Acoustic neuroma
• Symptoms of gradually progressive unilateral perceptive deafness and tinnitus
• Involvement of the vestibular nerve may cause vertigo
• Extension to involve the facial nerve may cause weakness and then paralysis.
Pre auricular sinus

• Common congenital condition in which an epithelial defect forms around the external ear
• Small sinuses require no treatment
Deeper sinuses may become blocked and develop episodes of infection, they may be closely related to the facial nerve
and are challenging to excise
Hearing Loss
Hearing loss may be conductive or sensorineural. To determine which is present patients will often require a formal
assessment with pure tone audiometry. In the clinical setting Webers and Rinnes tests may be helpful in categorising
various types of hearing loss.
Rinne Test Weber without Weber lateralises to left Weber lateralises to right
lateralisation
Both ears Air>Bone Normal Sensorineural loss on right Sensorineural loss on left
Left Bone > Air Conductive loss on left Combined loss on left
Right Bone> Air Combined loss on right Conductive loss on right
Both Bone > Air Combined loss on right and Combined loss on left and
conductive on left conductive on right
Thermoregulation
• The hypothalamus is the main centre for thermoregulation. Peripheral and central thermoreceptors relay to this
region.
• Central chemoreceptors play the main role in maintenance of core temperature.
• Hypothalamus may initiate involuntary motor responses to raise body temperature (e.g.shivering). It will also
stimulate the sympathetic nervous system to produce peripheral vasoconstriction and release of adrenaline
from the adrenal medulla
• Heat loss is governed by behavioural responses and by autonomic responses including peripheral vasodilation
• Heat loss can be maintained within the thermoneutral zone (25 to 30 degrees) although the absolute value
depends upon atmospheric humidity.
• Sepsis results in the release of cytokines that reset the thermoregulatory centre resulting in fever.
Von Hippel-Lindau syndrome
- Autosomal Dominant condition
- Predisposing to neoplasia.
- It is due to an abnormality in the VHL gene located on short arm of chromosome 3
Features
• Cerebellar haemangiomas
• Retinal haemangiomas: vitreous haemorrhage
• Renal cysts (premalignant)
• Phaeochromocytoma
• Extra-renal cysts: epididymal, pancreatic, hepatic
• Endolymphatic sac tumours
Temporal artery biopsy in temporal arteritis
• Superficial temporal artery is a terminal branch of the external carotid artery
Main indication
• Temporal arteritis
American College of Rheumatology guidelines recommend a temporal artery biopsy if:
• Age of onset older than 50 years

• New-onset headache or localized head pain
• Temporal artery tenderness to palpation or reduced pulsation
• ESR > 50 mm/h
Histopathology
• Vessel wall granulomatous arteritis with mononuclear cell infiltrates and giant cell formation
Procedure
• Position: supine, head 45 degrees

• USS doppler to locate the superficial temporal artery or palpate
• Local anaesthetic
• Artery within temporoparietal fascia
• Clamp and ligate the vessel
• Cut 3-5cm
• Ligate the remaining ends with absorbable suture
• Close the skin
Contraindication: Glucocorticoid therapy > 30 days
Risks: Injury to facial or auriculotemporal nerve
Nerves @ Risk Very important for exam … must get at least 2 question
• Carotid Endarterectomy : 5,7 (9) 10 12

o Glossopharyngeal (mainly)
o Trigeminal (cutaneous br.);
o Facial (mandibular br.);
o Vagus
o Hypoglossal
• Branchial cyst excision 7, 11
o Mandibular branch of Facial nerve
o Accessory Nerve
o Greater auricular nerve
• Submandibular Gland Excision 7,5,12
o Mandibular division of Facial nerve (injury causes Difficulty of sipping water and lower lip drooping)
o Lingual nerve, branch of mandibular division of Trigeminal nerve
th
o Hypoglossal Nerve (12 nerve)
ARCHES NERVE MUSCLES SKELETON ARTERY

Max. process 1st aortic arch
Chordatympani –pretrematic Muscles of mastication
Mandibular –post trematic Mylohyoid - Premaxilla Maxillary Artery
Digastric – ant. Belly - Maxilla
Tensor veli palatine - Zygomatic part of temporal
Tensor tympani
1st Mand. Process - Meckel’s cartilage
Mandibular
- Malleus
- Ant.ligament malleus
- Incus
- Sphenomand.ligament
- Lingual of mandible
Muscles of facial
nd th nd
2 Arch Facial 7 Expression Reichert’s cartilage 2 Aortic Arch
Hyoid - Stapes
Digastric – post. Belly - Styloid process temporal Stapedial artery
Stapedius - Stylohyoid ligament Hyoid artery
Stylohyoid - Lesser horn & upper part of body of hyoid
3rd Aortic Arch

rd th
3 Arch Glossopharyngeal 9 Stylopharyngeus Greater cornu & lower part of body of hyoid
Ventral part - CCA
Dorsal part - stem of ICA
4th Aortic Arch
th
Vagus 10 Cricothyroid Lamina of thyroid cartilage
th
4 Arch Sup. Laryngeal branch Levator palatini Right – Rt. Subclavian A. prox.part
Constrictor of pharynx Left – Part of Arch of aorta
6th Aortic Arch
th
Vagus 10 Intrinsic muscles of larynx Cricoid cartilage
R. Laryngeal branch Arytenoids cartilage Right Ventral – Right PA
th
6 Arch Right Dorsal – disappears
Left Ventral – Left. PA

Left Dorsal – Ductus arteriosus
Young man ē halitosis, regurgitation & flatulence is most likely to have hiatus hernia. These are also found in pharyngeal pouch, but this is more commonly found in elderly
patients,
POUCH DERIVATIVES
Middle ear cavity
st
1 Pouch Auditory tube
Endoderm lining of tympanic membrane
2nd Pouch Palatine tonsil
rd
3 Pouch Inf. P.thyroid gland- From dorsal part
Thymus- From ventral part
4th Pouch Sup. P.thyroid gland

Lat. Thyroid element
5th Pouch Ultimobranchial body which later forms

parafollicularcells of thyroid gland
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PHYSIOLOGY
H
p pCO2 HCO3 DISORDERS
↑ (↑
↑∕↨) ↑ MAL
>7.4 ↑ ↑ CMAL
↓ (↓
↓ ∕ ↨) ↓ MAC
<7.4 ↓ ↓ CMAC
↑ ↓ (↓
↓ ∕ ↨) RAL
>7.4 ↓ ↓ CRAL
↓ ↑ (↑
↑∕↨) RAC
<7.4 ↑ ↑ CRAC
1KPa = 7.5mmHg; 1mmHg = 0.1333 KPa; followings are normal value :

pH : 7.35 – 7.45; pCO2 : 4 – 6 KPa (35 – 45) mmHg;
pO2 : 10 – 14 KPa (75-105) mmHg, HCO3 : 22 – 26 mEq/L (24 mEq/L)
● COMPENSATION
Acute RAC : 1 for 10 : 10 mmHg pCO2 rise causes HCO3 rise 1 mEq/L(compensesn limit 32)
n
Chronic RAC : 4 for 10 : 10 mmHg pCO2 rise causes HCO3 rise 4 mEq/L (compenses limit 45)
n
Acute RAL : 2 for 10 : 10 mmHg pCO2 reduction causes HCO3 reduction 2 mEq/L (compenses limit 12-20)
Chronic RAL : 5 for 10 : 10 mmHg pCO2 reduction causes HCO3 reduction 5 mEq/L (compensesn limit 12-15)
n
MAC : HCO3 compensating pCO2 amount : 1.5 X HCO3 + 8 = ± 2 (pO2 compenses limit 12)
n
MAL : HCO3 compensating pCO2 amount : 0.7 X HCO3 + 20 = ± 5 (pO2 compenses limit 55)
● COPD collapse / Perforation / Laparotomy → Pain → Respiration restricted → CO2 Retention → RR↓
↓ = RAC
● A patient with chronic COPD will have chronic RAC
● Pulmonary Embolus → Hypoxia → SOB → RR ↑ → CO2 ↓ = RAL (due to hyperventilation)

● Aspirin Overdose: usually presents ē RAL featuring a low pCO2 but not a low pO2
● Low-lander staying @ high altitude for 2 weeks: will have both low pCO2 and low pO2; low HCO3; nearly normal
pH due to recompensation in the form of HCO3 secretion.
● A pCO2 < 40 mm Hg always implies a RAL (*True in 90% cases) !!!
● Diarrhoea / Fluid Loss / Vol. Loss / Pancreatitis* / Peritonitis* / Septic Condition = MAC
● Pancreatitis ; Peritonitis- MAC
● Vomiting / Milk Alkali Syndrome = MAL *Here though Vomiting is Fluid Loss, but its MAL
● Salicylate overdose leads mixed RAL & MAC. Early stimulation of respiratory centre leads to RAL whilst later the
direct acid effects of salicylates (combined with ARF) may lead to an acidosis
● A HCO3 ≤ 18 always implies a MAC (and in Diabetic Ketoaccidosis its ≤ 12)

● Anion gap 12-16 mmol is normal (avg 12); 20-30 range shows MAC in 70 % cases !!! ; >30 always implies a MAC
● In MAC how much will be the pCO2 ? last 2 digits of pH - in maximum cases !!!
● MAC will have a low HCO3 level and a low base excess (< -2 mmol)
● MAL will have a high HCO3 and a high base excess (> +2 mmol)
● A pt. can’t have a MAC and a MAL simultaneously

● A pt. can have a MAC with a compensatory RAL
● SAMPLE QUESTION Theme from April 2012 exam
A 67 year old male is admitted to the surgical unit with acute abdominal pain. He is found to have a right sided
pneumonia. The nursing staff put him onto 15L O2via a non rebreathe mask. After 30 minutes the patient is found
moribund, sweaty and agitated by the nursing staff. An arterial blood gas reveals:
pH 7.15
pCO2 10.2
pO2 8
Bicarbonate 32
Base excess 5.2
What is the most likely cause for this patients deterioration?

A. Acute respiratory alkalosis secondary to hyperventilation
B. Over administration of oxygen in a COPD patient ← ans
C. Metabolic acidosis secondary to severe pancreatitis
D. Metabolic alkalosis secondary to hypokalaemia
E. Acute respiratory acidosis secondary to pneumonia
This patient has an acute respiratory acidosis, however this is on a background of chronic respiratory acidosis (due to
COPD) with a compensatory metabolic alkalosis (the elevated bicarbonate is the main clue to the chronic nature of the
respiratory acidosis). This blood gas picture is typical in a COPD patient who has received too much oxygen; these
patients lose their hypoxic drive for respiration, therefore retain CO2 and subsequently hypoventilate leading to
respiratory arrest. If the bicarbonate was normal, then the answer would be acute respiratory acidosis secondary to
pneumonia.
● ANION GAP MNEMONICS

• Increased Anion gap Acidosis causes : MUDPILES
M ethanol,
U remia,
D iabetic ketoacidosis,
P ropylene glycol / paraldehyde / phenformin
I soniazid, iron
L actic acidosis,
E thylene glycol,
S alicylates
• Normal Anion Gap Acidosis: HARDUP
H - Hyper alimentation/hyperventilation
A - Acetazolamide
R - Renal tubular acidosis
D - Diarrhoea
U - Ureteral diversion
P - Pancreatic fistula/parenteral saline
• Anion gap is DECREASED in conditions associated with HYPOalbuminemia (Causes of which are Hemorrage
and NIL – N ephrotic syndrome, I ntestinal obstruction, L iver cirrhosis)
Hyper calcaemia
Hyper magnesaemia
Hyper γ-globulinaemia
Hyper viscosity
Halide intoxication
Lithium intoxication
Fluid compartment physiology
Body fluid compartments comprise intracellular and extracellular compartments. The latter includes interstitial fluid,
plasma and transcellular fluid.
Typical figures are based on the 70 Kg male.
The 60-40-20 rule:

60% total body weight is water
40% of total body weight is ICF
20% of body weight is ECF
Plasma typically accounts for 4-6% of body weight in healthy individuals
Body fluid volumes
Compartment Volume in litres Percentage of total volume
Intracellular 28 L 60-65%
Extracellular 14 L 35-40%
Plasma 3L 8%
Interstitial 10 L 24%
Transcellular 1L 3%
MEASUREMENT OF BODY WATER VOLUME

Plasma volume
Evan’s blue(T-1284) / protein bound dye dilution technique
RISA (radio-iodinated human serum albumin)
Radio-iodinated γ globulin & Fibrinogen
RBC volume (all are radioactives)

55
Fe, 59Fe
32
P
51
Cr
ECF volume STIMaR

S ucrose
T hiocyanate Ion
I nulin
Ma nnitol
R adioactive Na
Total body H2O DATe

D 2O
A mynopyrine
T ritiated water
● ISF = ECF – plasma

● ICF = TBW – ECF
Feature Cushing’s synd. / Hypercortisolism Addison’s / Adrenocortical insufficiency Conn’s / Primary Aldosteronism Phaeochromocytoma
Cause - Raised Cortisol level - Decrease Cortisol level - Raised Aldosterone level cause - Raised Catecholamines due to medulla tumor
- Increase Steroid use - Steroid withdraw o K+ & H+ loss; Na+ & H2O retention arising from chromaffin cells
- Non-iatrogenic → Due to pituitary - Post adrenalectomy → ↑ Vol → ↑BP - Disease of 10%
tumor →Cushing’s Disease(CD) - TB, HIV - Unilateral adenoma of adrenal o 10% Extraadrenal
● Within Cortex causes - Sarcoidosis, Amyloidosis cortex(75% cases) o 10% Bilateral
- Adrenal hyperplasia, Adenoma, Carcinoma - Drugs - Rest cases related to Bilateral o 10% Multiple
● Outside Cortex causes o Ketoconazole adenocortical hyperplasia & adrenal o 10% Malignant
- Iatrogenic o Rifampicin adenocarcinoma o 10% Familial
- Pituitary adenoma causing ↑ACTH o Phenytoin
- Ectopic ACTH secn
○ Oat cell Ca **Uncontrolled hypertension; Sweating; Flushing**
○ Bronchial adenoma; Bronchial Ca * Hypotension, Profound generalized weakness, **Weakness, Hypertension**
○ Thymic tumor Generalized pigmentation*
○ Medullary Ca
○ Islet cell tumor ** Among 4 only this causes Hypotension **
C/F - Raised BP, DM - Low BP - Raised BP due to Na+ & H2O retention - Raised BP & HR
- Metabolic Alkalosis occurs - Low Na+, Dehydration - Metabolic Alkalosis occurs - DM; sweating; SOB
- Truncal obesity; Buffalo hump - Weight loss, Anorexia - Polyuria, polydipsia, nocturia - Headache, anxiety, tremor
- Moon face(plethoric cheek) - Pernicious anaemia - Thirst, tiredness, palpitation - Associated with
- Hirsutism - Muscle wasting - Headache, o Neurofibrosarcoma
- Muscle wasting - Circum oral & skin pigmentation due to - Muscle weakness(tetany) o Osteomalacia
- Striae, bruising, pigmentation ↑ACTH as it cause MSH(+) - ECG shows o Acoustic neuroma
- Osteoporosis, kyphosis o Prolonged PR interval
- Na+↑ o Arrhythmia due to
-
K+↓ hypokalaemia
Dx - Plasma cortisol (raised) - Plasma cortisol (reduced) - Aldosterone (raised) - Blood picture shows
- 24hrs urine cortisol (raised) - ACTH (raised) - Plasma Renin (reduced) o Raised Adrenalin
- Dexamethasone suppression test is - Hyponatremia - Hypernatremia o Raised Noradrenalin
diagnostic - Hyperkalaemia - Hypokalaemia
o 2mg oral dexa given at midnight - Synacthen test(ACTH analogue) - Adrenal CT or MRI - 24 hrs urine shows
and shows no change in morning o Addison’s patient doesn’t show the rise o Raised VMA
cortisol level of Cortisol after admin. of Synacthen o Raised Meta-adrenalin
- Plasma ACTH o Raised Nor meta-adr.
o Raised, following CRH - I131 labeled MIBG scan to see the extra adrenal
administration in CD but lesion
not, if source is ectopic - Adrenal CT or MRI
- Pituitary & Adrenal CT or MRI
- Thracic CT
- CXR P/A view
Rx - Trans-sphenoidal pituitary excision - In acute patient: fluid resuscitation - Adrenalectomy for adenoma or ca. - Adrenalectomy. Preoperatively
- Bilateral adrenalectomy o ± Ionotropic support - Spironolactone(aldosterone antagonist) o α-block ē tds 20mg Phenoxybenzamine1 week
- Surgical resection of ectopic tumor o Hydrocortisone 100mg 6hrly for adrenocortical hyperplasia – 300 mg o β-block ē propranolol 40 mg tds for 4 weeks
per day for 4weeks preoperatively o Sliding scale insulin- if patient is DM
BIOPHYSICS IMPORTANT INFORMATION
Gray - SI unit of absorbed dose of ionising radiation

Sievert - SI unit of equivalent dose of ionising radiation
Becquerel - SI unit of radioactive decay
Tesla - SI unit of magnetic field strength
Hertz - Frequency
The ECG
P wave
• Represents Atrial Depolarization
• Electrical vector is directed from SA to AV node, and spreads from right atrium to left atrium. This create P wave.
QRS complex
• Represents Ventricular Depolarization
T wave
• Represents Ventricular Repolarization
• Duration 160ms
• The interval from the beginning of QRS complex & the apex of T wave is called Absolute Refractory Period.
• The last half of the T wave is called Relative Refractory Period (or vulnerable period)
• A small positive U wave may follow the T wave which represents the last remnants of ventricular repolarization.
P-R interval
• Time from the onset of the P wave to the beginning of the QRS complex
• Duration 0.12 to 0.20 seconds (120 to 200 ms)
• Represents the time between the onset of atrial depolarization and the onset of ventricular depolarization
ST segment
• Isoelectric period following the QRS
• Duration 320 ms
• Represents period, in which the entire ventricle has been depolarized.

• It corresponds to the plateau phase of the ventricular action potential
Q-T interval
• Represents both Ventricular Depolarization and Repolarization
• Estimates the duration of an average ventricular action potential.
• Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
● ECG FINDINGS & CULPRIT VESSEL
n
Reciprocal
Wall Affected ST Elevat Culprit Artery
ST Depresn
Septal V1-2 None LAD
Anterior V3-4 None LAD
Anteroseptal V1-4 None LAD
Anterolateral V3-6, I, aVL II, III, aVF LAD, LCX / OM
Ext. anterior
n
V1-6, I, aVL II, III, aVF LM
(or Ant.sept.ē Lat.ext )
Inferior II, III, aVF I, aVL RCA/ LCX
Lateral I, aVL, V5-6 II, III, aVF LCX / OM
Post.(assoc.ē Inf.
V7-9 V1-4 PDA / LCX
or Lat. bt can isolated)
Rt ventricular
II, III, aVF, V1, V4R I, aVL RCA
(assoc. ē Inf.)
● ECG: left vs. right bundle block "WiLLiaM MaRRoW":

W pattern in V1-V2 and M pattern in V3-V6 is Left bundle block.
M pattern in V1-V2 and W pattern in V3-V6 is Right bundle block.
[ Note: consider bundle branch blocks when QRS complex is wide.]
● ECG FINDINGS
Hypokalaemia : Prolong P-R S-T depresn flattened / inverted T U- waves
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!!!
Hyperkalaemia : Small P tall, tented T Wide QRS

More Pot more T, no P, broad QRS +(irregular pulse**)
PE : P pulmonale(peaked P) tall R in V1 inverted T in V1-4 S 1 Q 3 T3

+ (atrial arrhythmias, tachycardia, right ventricular strain pattern, RBBB, right axis deviation)
Hypercalcaemia : Short QT
Hypocalcaemia : Long QT
Other cz of long QT are Hypomagnesaemia & β-blocker, Amiodarone therapy
( For Deatils see below)
WPW : δ-wave
Pericarditis : Concave upward S-T elevation- cave upward !!!
MI : Convex upward S-T elevation
Hypothermia : J- wave
Arterial line in situ : On studying trace, the incisura can be found – the elastic recoil of the aorta is the
physiological event, which cause this process.
ECG Features of Hypocalcaemia:
• Narrow QRS complex
• Reduced PR interval
• T wave flattening and inversion
• Prolongation of the QT-interval
• Prominent U-wave
• Prolonged ST and ST-depression
Jugular Venous Pressure

Provides information on right atrial pressure,
Provides clues to underlying valvular disease.
A non-pulsatile JVP is seen in SVC obstruction.
Kussmaul's sign: paradoxical rise in JVP during inspiration in constrictive pericarditis
'a' wave = atrial contraction

• Large if atrial pressure raised e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
• Absent if there is atrial fibrillation
Cannon 'a' waves

• Caused by atrial contractions against a closed tricuspid valve
• Are seen in complete heart block, VT/ ectopics, nodal rhythm, single chamber ventricular pacing
'c' wave
• Closure of tricuspid valve
• Not normally visible
JVP: {C} wave - {c}losure of the tricuspid valve
'v' wave
• Due to passive filling of blood into the atrium against a closed tricuspid valve
• Giant v waves in tricuspid regurgitation
'x' descent = fall in atrial pressure during ventricular systole
'y' descent = opening of tricuspid valve
● Fixed raised JVP : SVC obstruction

Rising JVP ē normal breath sound : Cardiac temponade (muffled heart sound, pulse fade on inspiration)
IMPORTANT: The JVP a-wave corresponds to the P wave on an ECG i.e. atrial contraction.
In Atrial fibrillation there are no P waves and therefore on the JVP waveform there are absent a waves
ULTRASOUND
• Ultrasound frequencies are those above the range detectable by the human ear.
• The human ear can detect frequencies from 20Hz to 20 kHz typically.
• Ultrasound frequencies are those above 20 kHz.
• In medical imaging ultrasound frequencies range from 2 MHz to 15 MHz
• Transabdominal 3 - 3.5 MHz; Transvaginal 5 - 7.5 MHz (post bladder void)
Radiotherapy Key Points

• Ionizing radiation
• Causes DNA damage leading to cellular death
• DNA damage caused by ionisation leading to free radical formation
• Can be locally placed i.e Brachythrapy or external beam
• To reduce damage to normal tissue shaped and multiple beams are used with a higher absorbed dose at the point of
convergence
• Radiosensitizers increase the effect of a given dose of radiation
• Radiosensitisers fall into 4 main groups:
1. Oxygen
2. Hypoxic cell sensitizers
3. Halogenated Pyrimidines
4. Bioreductive Agents
• Radioprotectors are agents that reduce the effects of radiation. Their role is limited in clinical practice due to possible
protection of tumours
• Radiotherapy dosing is in Gray (Gy).
• Total dose varies between tumour type and stage but typical regimes involve 1.8-2.0 Gy fractions delivered over a
number of weeks with total dose accumulating to reach around 50 Gy
• SIDE EFFECTS: vary significantly from site to site. Some side effects such as dry mouth may be acute or late.
Moist skin desquamation is an acute side effect of radiotherapy.
Epilation is more likely to occur in fields targeted by radiotherapy with cumulative dose of 45 Gy.
Myelodysplastic syndromes (MDS )can develop years after radiotherapy. It is thought about 10% of MDS are
secondary, most often due to radiotherapy or chemotherapy for cancer. Some MDS remain indolent whilst others
transform to aggressive forms such as AML.
Fibrosis and lymphoedema are other late complications
LASER
LASER stands for light amplification by the stimulated emission of radiation. There are multiple types.
X-RAYS
• Ionising electromagnetic radiation
• Frequency 30 petahertz to 30 exahertz (10 to the power 16 to 10 to the power 19)
• Typical Energy100 eV to 100 keV
• Chest XRAY equivalent to 2.4 days natural background radiation
• CT abdomen by comparison is equivalent to 2.7 years natural background radiation
MRI Key Points
• Non-ionising form of radiation

• Use strong magnetic fields that cause protons to align with the magnetic field
• Radiofrequency pulses then causes the protons to excite or "spin", when they relax back into alignment of the field they
release radio waves which are detected by the MRI sensors
• Computers use the radio wave emissions to construct an image
• Images are often described as T1 or T2 weighted
• T1 weighted fluid appears dark
• T2 weighted fluid appears bright
• MRI magnets typically generate fields of 0.5 to 3.0 Tesla
• Tesla (T) is the SI unit for magnetic field
• Weber (Wb) is the SI unit for magnetic flux
DEXA Key Points

• 2 low dose XRAY beams used at each site
• XRAY absorption measured by detectors
• Soft tissue absorption subtracted to give BMD measurment
• T-score is standard deviation score when compared to a young healthy adult
• T-score < -2.5 confirms osteoporosis
COMPARE MRI, CT, USG, PET
MRI
• Utilises a strong magnetic field that causes protons to align with the field
• Radiofrequency is then applied to disrupt the proton alignment. When the radio frequency is stopped the protons return
to their axis of equilibrium but release energy in the process.
• This energy release is detected by the scanner
• Non-ionising
CT
• Utilises Multiple X-Rays that are then analysed by computer and create 3D images.
• Potential for high dose of ionisng radiation
• A CT abdomen is equivalent to 400 chest X-rays or 2.7 years background radiation
PET
• PET CT uses a radioactive tracer, usually fluorodeoxyglucose (FDG), an analogue of glucose. Which is given to the
patient and is taken up in areas of high metabolism (e.g. cancer mets)
• The tracer emits gamma rays which are detected by the scanner.
• ionising
Ultrasound
• Non-ionising
• Utilises high frequency sound waves
• Produced by applying voltage across a piezoelectric crystal. Crystal resonance prodiuces sound waves which are then
directed by the transducer.
• Different tissues reflect varying amounts of the beam depending on their density (or acoustic impedance). The
reflected beam is measured by the receiver and used to generate an image.
• Doppler utilises the Doppler principle and can be used to measure flow. This creates a duplex image where flow
towards is coloured red and flow away blue.
DIATHERMY BASICS
In surgical diathermy (or electrosurgery) AC current is passed through a conductor with some energy appearing as heat.
There are 2 types of Diathermy

• Monopolar Current passed from small electrode held by surgeon and returned to a large area plate via patients
tissues. The concentrated current at the electrode tip produces a lot of heat whereas the current is dissipated over a
large area at the plate. It is important the plate is properly attached as if the plate area is reduced the current
concentrates and can cause tissue burns
• Bipolar Current passes between two electrodes held by surgeon as forceps.
Diathermy can be used for cutting or coagulating. Bipolar is used to coagulate not cut. In cutting (monopoly) the waveform can
be varied. A continuous single frequency sine wave is often used. Pulsed waves can reduce local thermal tissue damage.
To prevent cell deploarisation (especially in cardiac tissue) the frequency must be over 100 kHz. Below this electric shock or
even electrocution could occur. In surgical practice frequencies of around 500KHz are used.
ENDOCRINE
Pituitary Gland
- Located within the sella turcica within the sphenoid bone in the middle cranial fossa.
- Covered by a dural fold and weighs around 0.5g.
- Attached to the hypothalamus by the infundibulum.
- The anterior pituitary receives hormonal stimuli from the hypothalamus by way of the
hypothalamo-pituitary portal system. It develops from a depression in the wall of the pharynx
(Rathkes pouch). It is one of only a few portal system of circulation in the body, that is, it involves
two capillary beds connected by venules rather than arterioles.
- The hypothalamaic-hypophyseal venous portal system carries prolactin inhibitory hormone
from the hypothalamus to the anterior pituitary gland. In the absence of this hormone,
prolactin secretion increases to about 3 times normal level.
● Anterior pituitary hormones (receives hormonal stimuli hypothalamus by hypothalamo-pituitary portal system)
• Growth hormone
• Thyroid stimulating hormone
• ACTH
• Prolactin
• LH and FSH
• Melanocyte releasing hormone
● Posterior pituitary hormones (synthesized by hypothalamus)

• Oxytocin
• Anti diuretic hormone
● Sheehan’s Syndrome
- Post – partum hypo-pituitarism caused by necrosis due to blood loss & hypovolaemic during & after childbirth
- Rare complication in pregnancy
RECEPTORS
- α1 (Smooth M.) - β2 (Blood vessels, Bronchioles)
- α2 (Smooth M., Fat, Platelets) - β3 (Fat)
- β1 (Cardiac tissue)
Dopamin → (+) β1, D1, 2 → (+) Ionotropic Action → ↑ CO; Dobutamin → (+) β1, 2
Inotrope Cardiovascular receptor action
Adrenaline α-1, α-2, β-1, β-2
Noradrenaline α-1,( α-2), (β-1), (β-2)
Dobutamine β-1, (β 2)
Dopamine (α-1), (α-2), (β-1), D-1, D-2
** Minor receptor effects in brackets

● Stimulation of either β-1 & β-2 receptor activates Adenylate Cyclase
● Stimulation of α-1 receptor inhibits Adenylate Cyclase
Effects of receptor binding
α-1, α-2 Vasoconstriction
β-1 Increased cardiac contractility and HR
β-2 Vasodilatation
D-1 Renal and spleen vasodilatation
D-2 Inhibits release of noradrenaline
Adrenal gland anatomy

Anatomy (N-314)
Location Superomedially to the upper pole of each kidney
Relationships of the right Diaphragm-Posteriorly, Kidney-Inferiorly, Vena Cava-Medially, Hepato-renal pouch and
adrenal bare area of the liver-Anteriorly
Relationships of the left Crus of the diaphragm-Postero- medially, Pancreas and splenic vessels-Inferiorly, Lesser
adrenal sac and stomach-Anteriorly
Superior adrenal arteries- from inferior phrenic artery, Middle adrenal arteries - from
Arterial supply aorta, Inferior adrenal arteries -from renal arteries
Venous drainage of the Via one central vein directly into the IVC
right adrenal
Venous drainage of the left Via one central vein into the left renal vein
adrenal
Adrenal physiology
Adrenal medulla
- The chromaffin cells of the adrenal medulla secrete catecholamines – noradrenaline, adrenaline, dopamin.
- The medulla is innervated by the splanchnic nerves; the preganglionic sympathetic fibres of the nerve secrete
acetylcholine causing chromaffin cells to secrete their contents by exocytosis.
Phaeochromocytomas are derived from these cells and will secrete both adrenaline and nor adrenaline.
Adrenal cortex – Three histologically distinct zones are recognised: (mnemonic GFR - ACD)
Zone Location Hormone Secreted
Zona Outer zone MinerALoCOrtiCOids(A ldosterone mainly; Cortisone; Deoxy Corticosterone,

Glomerulosa Corticosterone)
Zona F asiculata Middle GluCO COrtiCOids (C ortisol mainly, Cortisone; Corticosterone)

zone
Zona R eticularis Inner zone D ehydroepiandrosterone (DHEA) mainly, Androgens
Glucocorticoids and aldosterone are mostly bound to plasma proteins in the circulation. Glucocorticoids are inactivated
and excreted by the liver.
● Beta – endorphin is a cleavage product of pro-opiomelanocortin(POMC) which is the precursor hormone for ACTH.
Cortisol
• Glucocorticoid; Released by zona fasiculata
• 90% protein bound; 10% active
• Shows Circadian or Diurnal rhythm: High in the morning
• Negative feedback via ACTH
Actions
• Glycogenolysis + Glucaneogenesis
• Protein catabolism + Decrease protein in bones
• Lipolysis
• Stress response + Anti-inflammatory response
• Increase gastric acid
• Increases all blood cells ( neutrophils/platelets/RBC)
• Inhibits fibroblastic activity
Addisonian crisis
Causes
• Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's, Hypopituitarism)
• Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
• Steroid withdrawal
Features of an addisonian crisis:

• Hyponatraemia
• Hyperkalaemia
• Hypoglycaemia
• Hypotension
Management
• Hydrocortisone 100 mg im or iv 6hrly
• 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
• Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol
exerts weak mineralocorticoid action
• Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
● Adrenaline
• Fight or Flight response
- Catecholamine (from phenylalanine and tyrosine); Neurotransmitter and hormone released by adrenal gland
- Effects on α 1 and 2, β 1 and 2 receptors
- Main effect on α 1 receptors in skeletal muscle-causing vasodilation - Increase CO and total peripheral
resistance- This leads to vasoconstriction in the skin and kidneys causing a narrow pulse pressure
Actions
α adrenergic receptors:
• Inhibits insulin
• Stimulates glycogenolysis in the liver and muscle
• Stimulates glycolysis in muscle
β adrenergic receptors:
• Stimulates glucagon secretion
• Stimulates ACTH
• Stimulates lipolysis by adipose tissue
● Adrenaline
• Anaphylactic shock –used as bronchodilator --it has the most Bronchodilator effect among all.
• Cardiac arrest-used to convert non-shockable rhythm to VF- which is suscceptible to shock
● Nor Adrenaline used mainly in shock to raise BP beside this it also reduce renal blood flow
INOTROPES
In patients with an adequate circulating volume but on-going circulatory compromise a vasoactive drug may be
considered. These should usually be administered via the central venous route. Commonly used inotropes include:
• Noradrenaline- A vasopressor with little effect on cardiac output. Acts as an α agonist.

• Adrenaline-Acts on both α and β thereby increasing CO and increasing systemic vascular resistance.
• Dopamine- Acts as a β 1 agonist and increases contractility and rate. Some key points:
+
@ Very low dose (<4µgm/kg/min) rises GFR & Na excretion (Renal dose is an obsolete concept)
@ Higher dose cz - β1 (+) - thus rises HR & contractility
@ Very high dose (>10 µgm/kg/min) cz α1(+) thus reduces tissue perfusion & GFR
• Dobutamine- Has both β 1,β 2 effects & will increase CO & cause decrease in systemic vascular resistance.
• Milrinone- Phosphodiesterase inhibitor with a positive inotropic effect. It has a short half-life (1-2 hours) and
may precipitate arrhythmias. Vasopressors often co-administered as it is a vasodilator.
● Aldosterone is responsible for regulating ion exchange in salivary glands

● Cortisol & adrenal androgens are synthesized from cholesterol. The intermediary in the metabolism of cortisol and
androgens is Pregnolone
Renin-angiotensin-aldosterone system
Adrenal cortex (mnemonic GFR - ACD)
• Zona glomerulosa (on outside): mineralocorticoids, mainly aldosterone
• Zona fasciculata (middle): glucocorticoids, mainly cortisol
• Zona reticularis (on inside): androgens, mainly dehydroepiandrosterone (DHEA)
Renin
• Released by JGA cells in kidney in response to reduced renal perfusion, low sodium
• Hydrolyses angiotensinogen to form angiotensin I
Factors stimulating renin secretion

• Low BP
• Hyponatraemia
• Sympathetic nerve stimulation
• Catecholamines
• Erect posture
Factors reducing renin secretion: drugs: beta-blockers, NSAIDs
Angiotensin
• ACE in lung converts angiotensin I --> angiotensin II
• Vasoconstriction leads to raised BP
• Stimulates thirst
• Stimulates aldosterone and ADH release
Aldosterone
• Raised angiotensin II, potassium, and ACTH levels → Release of Aldosterone
• Secretion is regulated by the renin- angiotensin system and by plasma levels of sodium and potassium
+ + +
• Release of Aldosterone → Retention of Na in exchange for K /H in DCT.
+ + +
“Aldosterone conserves Na by stimulating the reabsorption of Na in distal nephron in exchange for K ”
• Lack of aldosterone release will result in hyperkalaemia and hyponatraemia
A summary of the hormonal changes associated with the stress response
Increased Decreased No Change
ACTH Insulin TSH
Cortisol Testosterone LH
Aldosterone Oestrogen FSH
Renin ITO
ADH
GH
Glucagon
PL
Pancreas endocrine physiology

Hormones released from the islets of Langerhans
Beta cells Insulin (70% of total secretions)
Alpha cells Glucagon
Delta cells Somatostatin
F cells Pancreatic polypeptide
● Secretin causes secretion of water and electrolytes of pancreatic juice

Cholecystokinin causes increase volume of enz. Secretion of pancreatic juice
Somatostatin causes decrease the volume of secretions of pancreatic juice
Aldosterone conserves electrolytes of pancreatic juice
● PANCREATIC TUMORS SYMPTOMS

Gastrinoma : PUD; ulceration; haematemesis
Insulinoma :
Glucagonoma : Diarrhoea; Wt.loss; Anaemia; Necrolytic migratory erythema, Raised RBS
Somatostatinoma : Obstructive jaundice; gallstones; raised RBS
VIPoma :
Insulin
• Anabolic hormone; is degraded by enzymes in the circulation. It typically has a half life of < 30 minutes
Structure
• and chain linked by disulphide bridges
Synthesis
• Pro-insulin is formed by the rough endoplasmic reticulum in pancreatic beta cells. Then pro-insulin is cleaved to
form insulin and C-peptide. Insulin is stored in secretory granules and released in response to Ca.
Function
• Increased Glucose utilisation and glycogen synthesis
• Increased Fatty acid synthesis & increased esterification of fatty acid
• Decrease lipolysis by inhibiting hormone – sensitive lipase (to impair hydrolysis of triglyceride)
• Decreased Gluconeogenesis
• Decrease Proteolysis → Decreases muscle protein loss
• Increased Potassium uptake
● Inhibitor of insulin release are:

Beta blockers; Alpha adrenergic drugs; Sympathetic nerves
● Stimulation of insulin release are:
Glucose; Amino acid; Fatty acids; Secretin / Gastrin / CCK; Beta adrenergic drugs; Vagal cholinergic action;
● Intracellular domain of the insulin receptors has Tyrosine kinase enzyme activities
● After Head injury Diabetes Insipidus may occur ----confirmation test water deprivation test
Glucagon
- Glucagon, the hormonal antagonist to insulin, released from α – cells of Islets of Langerhans in pancreas.
- Glucagon is a protein comprised of a single polypeptide chain
- It will result in an increased plasma glucose & ketone level.
Stimulation Inhibition
Decrease plasma glucose Somatostatin
Increased plasma amino acids Insulin
Increased catecholamines Increased free fatty acid
Sympathetic nervous system Increased urea
Acetylcholine Increased keto acids
CCK
Glucagonoma
• Rare pancreatic tumours arising from the α – cells of the pancreas.
• Glucagon levels markedly elevated. A serum level of glucagon >1000pg/ml usually suggests the diagnosis,
imaging with CT scanning is also required
• Symptoms include diarrhoea, weight loss and necrolytic migratory erythema (very important for exam !!!)
• Treatment is with surgical resection.
Multiple Endocrine Neoplasia (MEN)

Inherited as an autosomal dominant disorder
MEN type I – Werner Syndrome MEN IIa – Sipple Syndrome MEN IIb –Gorlin’s Syndrome
Mnemonic 'three P's': Phaeochromocytoma MEN IIa + addition of:

Medullary thyroid cancer (70%) Marfanoid body habitus
Parathyroid (95%): Parathyroid adenoma Hyperparathyroidism (60%) Mucosal & ganglioneuromas
Pituitary (70%): Prolactinoma/ACTH/Growth Hormone
secreting adenoma
Pancreas (50%): Insulinoma, PP-oma(pancreatic
polypeptide) /Zollinger Ellison syndrome
Gastrinoma
also: Adrenal (adenoma or CA) and thyroid (adenoma)
Fore-gut or mid-gut carcinoid
Lipoma
MENIN gene (chromosome 11) RET oncogene (chromosome 10) RET oncogene (chromosome
Most common presentation = hypercalcaemia 10)
** Screening for MEN – I is biochemical and MEN – II is genetic. The tests in suspected of MEN – I pts should
start @ age 15 & should be repeated in every 3yrs. Tests are :
S. Albumin
S. PTH
S. PL
S. Pancreatic polypeptide
S. Gastrin
FBS
Plasma chromoglycan A
HEMATOLOGY
Coagulation cascade
Intrinsic pathway (components already present in the blood)

• Minor role in clotting
• Subendothelial damage e.g. collagen
• Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and
Factor 12
• Prekallikrein is converted to kallikrein and Factor 12 becomes activated
• Factor 12 activates Factor 11
• Factor 11 activates Factor 9, which with its co-factor Factor 8a form the tenase complex which activates Factor
10
Extrinsic pathway (needs tissue factor released by damaged tissue)

• Tissue damage
• Factor 7 binds to Tissue factor
• This complex activates Factor 9
• Activated Factor 9 works with Factor 8 to activate Factor 10
Common pathway
• Activated Factor 10 causes the conversion of prothrombin to thrombin
• Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form links between
fibrin molecules
Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption
Intrinsic pathway Increased APTT Factors 8,9,11,12
Extrinsic pathway Increased PT Factor 7
Common pathway Increased APTT & PT Factors 2,5,10
Vitamin K dependent Factors 2,7,9,10
● Coagulation factors are generally serine proteases. But some are
Glycoproteins – V & VIII

Transglutaminase – XIII
● Hageman factor (XII), on contact ē injured vascular basement membrane, activates both collagen sequence &
kinin system.
Abnormal coagulation
Cause Factors affected
Heparin Prevents activation factors 2,9,10,11
Warfarin Affects synthesis of factors 2,7,9,10
DIC Factors 1,2,5,8,11
Liver disease Factors 1,2,5,7,9,10
Von Willebrand Disease (clinically resembles hemophilia)
RX : Desmopressin (DDAVP-RX of choice) Cryoprecipitate (I, VIII, XIII, vWF); VIII conc.; Desmopressin. The most useful
test in practice is to do the VwB Antigen and activity(RICOF)
Disseminated intravascular coagulation
Simultaneous coagulation and haemorrhage caused by initially formation of thrombi which consume clotting factors
(factors 5,8) and platelets, ultimately leading to bleeding
Causes include:
• Infection
• Malignancy
• Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm
• Liver disease
• Obstetric complications
Key points
• Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure
• Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased fibrinogen
degradation products
• Treat the underlying cause and supportive management
D-I-S-S-E-M-I-N-A-T-E-D
D - Dx: D dimer
I - Immune complexes
S - Snakebite, shock, heatstroke
S - SLE
E - Eclampsia, HELLP syndrome
M - Massive tissue damage
I - Infections: viral and bacterial
N - Neoplasms
A - Acute promyelocytic leukemia
T - Tumor products: Tissue Factor (TF) and TF-like factors released by carcinomas of pancreas, prostate, lung,
colon, stomach
E - Endotoxins (bacterial)
D - Dead fetus (retained)
● Platelet function disorder : All (N)

● Extrinsic Pathway; Warferin Rx; VII deficiency : All (N), PT rises
● Intrinsic Pathway; Heparin; Haemophilia; (VIII, IX,XII) deficiency : All (N), APTT rises
● VWD : All (N), APTT, BT rise (F VIIIc abnormal)
● Vitamin K deficiency : All (N), APTT, PT rise
● Common Pathway; DIC; Acute liver disease : All rises, Platelet, Hb reduce (Initially
factor V & VIII are consumed, then platelets)
* DIC : D – dimer may be elevated due to endothelial cell injury *; (And also in PE)
** DIC shows rise of all except Platelet + fibrinogen**
*** APTT indicate intrinsic pathway and PT indicate extrinsic pathway***
● DVT pt. + anticardiolipin & lupus anticoagulant ab (+)ve = underlying cz antiphospholipid syndrome.
● Recurrent DVT = Factor V Leiden, Protein C, Protein S test to be done
Heparin
● LMWH (and also Fondaperinux) :- (-) Xa (indirect inactivn of Xa)

● HMWH: - binds ē antithrombin→Heparin-antithrombin complex → (-) IIa, IXa, Xa (indirect inactivn of thrombin)
n
● Both unfractionated and low-molecular weight heparin can cz hyperkalaemia. It caused by inhibit of aldosterone
n
secret
WARFERIN ALL
● Warferin, inhibit vitamin K –to become active hydroquinone form (hydroquinone form acts as co-factor in the
formation of factor II, VII, IX and X (mnemonic = 1972) and protein C)
Factors that may potentiate warfarin

• Liver disease
• P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
• Cranberry juice
• Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
• Inhibit platelet function: NSAIDs
Side-effects
• Haemorrhage
• Teratogenic
• Skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary
procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration.
Thrombosis may occur in venules leading to skin necrosis…
● Protein-C is used as co-factor in activation of thrombomodulin

● Blood products used in warfarin reversal
Immediate or urgent surgery in patients taking warfarin(steps 1 & 2):
1. Stop warfarin
2. Vitamin K (reversal within 4-24 hours)
-IV takes 4-6h to work (at least 5mg)
-Oral can take 24 hours to be clinically effective
3. Human Prothrombin Complex Concentrate (reversal within 1 hour)

-Bereplex 50 u/kg
-Rapid action but factor 6 short half life, therefore give with vitamin K
4. Fresh frozen plasma

…Used less commonly now as 1st line warfarin reversal
-1
-30ml/kg
-Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid overload)
-Need blood group
-Only use if human prothrombin complex is not available
4. Human Prothrombin Complex (reversal within 1 hour)

-Bereplex 50 u/kg
**Massive bleeding= stop warin, IV vitamin K & either PCC or FFP (PCC preferable, if available),
**If question says Bleeding due to Excessive Warferinisation then Factor IX concentrate (IX, X, XI ) to be given
● Antistatin: direct factor Xa inhibitor
● Hirudin+ Argatroban: Direct inactivation of thrombin
Anaemias
Chr.dis : S. Fe low; SpO2 low. S.ferritin raised TIBC low

Haemolytic : S. Fe not low
Chr. Blood loss : S. Fe low S. ferritin low; TIBC high
Fe deficiency : S. ferritin low; TIBC high
Megaloblastic : Not assoc. with Fe metabolism (gastritis; pernicious, B12 def.)
Autoimmune haemolytic : Direct coomb’s test positive (& also in Reynaud’s disease)
● Vit B12 deficiency cause macrocytic anaemia and thrombocytopenia
Sickle cell anaemia
Disorder of varying degrees. It may present in childhood with anaemia and mild jaundice. In the older patient, vaso-
occlusive problems occur due to sickling in the small vessels of any organ, mimicking many medical and surgical
emergencies.
Typical infarctive sickle crises (Vasoactive crisis; aplastic crisis; sequestration crisis) includes bone pain,
pleuritic pain, hemiparesis, fits, splenic infarcts, and priapism, Autosplenectomy occurs
• Autosomal recessive
• Single base mutation
• Deoxygenated cells become sickle in shape
• Causes: short red cell survival, obstruction of microvessels and infarction
• Sickling is precipitated by: dehydration, infection, hypoxia
• Manifest at 6 months age
• Africans, Middle East, Indian
• Diagnosis: Hb electrophoresis
Sickle crises
• Bone pain
• Pleuritic chest pain: acute sickle chest syndrome commonest cause of death
• CVA, seizures
• Papillary necrosis
• Splenic infarcts
• Priapism
• Hepatic pain
Long-term complications
• Infections: Streptococcus pnemoniae
• Chronic leg ulcers

• Gallstones: haemolysis
• Aseptic necrosis of bone
• Chronic renal disease
• Retinal detachment, proliferative retinopathy
Surgical complications
• Bowel ischaemia
• Cholecystitis
• Avascular necrosis
Management
• Supportive
• Hydroxyurea
• Repeated transfusions pre operatively
• Exchange transfusion in emergencies
Sickle cell trait

• Heterozygous state
• Asymptomatic
• Symptoms associated with extreme situations ie anaesthesia complications
• Protective against Plasmodium falciparum
Drugs causing Aplastic Anaemia

Indomethacin
Sulphonamides
Penicillamine
● Chronic Alcoholic develops Megalolblastic Anaemia (↓Hb & ↑MCV)
Thrombocytopenia
Causes of severe thrombocytopenia

• ITP
• DIC
• TTP
• haematological malignancy
Causes of moderate thrombocytopenia

• heparin induced thrombocytopenia (HIT)
• drug-induced (e.g. quinine, diuretics, sulphonamides, aspirin, thiazides)
• alcohol
• liver disease
• hypersplenism
• viral infection (EBV, HIV, hepatitis)
• pregnancy
• SLE/antiphospholipid syndrome
• vitamin B12 deficiency
Hereditary Spherocytosis
Most common disorder of the red cell membrane, it has an incidence of 1 in 5000. The abnormally shaped erythrocytes
are prone to splenic sequestration and destruction. This can result in hyperbilirubinaemia, jaundice and splenomegaly. In
older patients an intercurrent illness may increase the rate of red cell destruction resulting in more acute symptoms.
Severe cases may benefit from splenectomy
Some PBF Findings
AML : Blast cells with Auer bodies
CML, Myelofibrosis : Philadelphia chromosome (due to long arm deletion in chr-22)
CLL : Numerous small, mature lymphocytes
Infectious Mono. : Atypical Lymphocytosis; (Monospot test +ve)
DIC : Schistocyte(RBCs undergoing fragmentation)
Splenectomy** : Howell-Jolly bodies;

Pappenheimer bodies;
Poikilocytes (Target cells);
Irregular contracted erythrocytes(siderotic granules)
Hairy Cell Leukaemia : Hairy cell
Pb poison; Anaemia; Septicaemia : Basophilic Stippling; Clover leaf morphology(Pb poisoning)
Sickle cell; Thalassemia; Hemolytic : Traget cell
st
** In 1 few days after splenectomy target cells, siderocytes and reticulocytes will appear in circulation. Immediately
following splenectomy a granulocytosis (mainly neutrophils) is seen, it is replaced by lymphocytosis & monocytosis over
following weeks. Platelet count is usually raised & this may b persistent, oral antiplatelet agents may b needed.
● XI deficiency is called Haemophilia – C. Ashkenazi Jews are sufferer

● Presence of Lupus anticoagulant: Antiphospholipid Syndrome
WHOLE BLOOD FRACTIONS
Fraction Key points
Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large volumes of fluid may result
in cardiovascular compromise. Product obtained by centrifugation of whole blood.
Platelet rich Usually administered to patients who are thrombocytopaenic and are bleeding or require surgery. It is
plasma obtained by low speed centrifugation.
Platelet Prepared by high speed centrifugation and administered to patients with thrombocytopaenia.
concentrate
Fresh frozen • Prepared from single units of blood.

plasma • Contains clotting factors, albumin and immunoglobulin.
• Unit is usually 200 to 250ml.
• Usually used in correcting clotting deficiencies in patients with hepatic synthetic failure who
are due to undergo surgery.
-1
• Usual dose is 12-15ml/Kg .
• It should not be used as first line therapy for hypovolaemia.
Cryoprecipitate • Formed from supernatant of FFP.

• Rich source of Factor VIII and fibrinogen.
• Allows large concentration of factor VIII to be administered in small volume.
SAG-Mannitol Removal of all plasma from a blood unit and substitution with:
Blood • Sodium chloride
• Adenine
• Anhydrous glucose
• Mannitol
Up to 4 units of SAG M Blood may be administered. Thereafter whole blood is preferred. After 8 units,
clotting factors and platelets should be considered.
● BAINBRIDGE REFLEX release Aldosterone to increase HR mediated via atrial stretch receptors that occurs following
rapid infusion of blood.
METABOLISM, VITAMINS AND MINERALS RELATED DISCUSSION
Ferritin
Ferritin is an intracellular protein that binds iron and stores it to be released in a controlled fashion at sites where iron is
required. Because iron and ferritin are bound the total body ferritin levels may be decreased in cases of iron deficiency
anaemia. Measurement of serum ferritin levels can be useful in determining whether an apparently low haemoglobin and
microcytosis is truly caused by an iron deficiency state.
Ferritin is an acute phase protein and may be synthesised in increased quantities in situations where inflammatory
activity is ongoing. Falsely elevated results may therefore be encountered clinically and need to be taken in context of
the clinical picture and full blood count results.
Iron metabolism
Absorption • Duodenum and upper jejunum

• About 10% of dietary iron absorbed
2+ 3+
• Fe (ferrous iron) much better absorbed than Fe (ferric iron)
• Ferrous iron is oxidized to form ferric iron, which is combined with apoferritin to form ferritin
• Absorption is regulated according to body's need
• Increased by vitamin C, gastric acid
• Decreased by proton pump inhibitors, tetracycline, gastric achlorhydria, tannin (found in tea)
3+
Transport In plasma as Fe bound to transferrin
Storage Ferritin (or haemosiderin) in bone marrow
Excretion Lost via intestinal tract following desquamation
Distribution in body
Total body iron 4g
Haemoglobin 70%
Ferritin and haemosiderin 25%
4%
Myoglobin
Plasma iron 0.1%
Vitamin deficiency
Vitamin Effect of deficiency
A Night blindness
Epithelial atrophy
Infections
C Poor wound healing

Impaired collagen synthesis
D Rickets (Children)
Osteomalacia (Adults)
K Clotting disorders
Vitamin C deficiency
Vitamin C deficiency (scurvy) leads to defective synthesis of collagen resulting in capillary fragility (bleeding tendency)
and poor wound healing
Features
• gingivitis, loose teeth
• poor wound healing
• bleeding from gums, haematuria, epistaxis
• general malaise
B Vitamin Deficiency
Vitamin B12 deficiency

Vitamin B12 is mainly used in the body for red blood cell development and also maintenance of the nervous system. It is
absorbed after binding to intrinsic factor (secreted from parietal cells in the stomach) and is actively absorbed in the
terminal ileum. A small amount of vitamin B12 is passively absorbed without being bound to intrinsic factor.
Causes of vitamin B12 deficiency

• pernicious anaemia
• post gastrectomy
• poor diet
• disorders of terminal ileum (site of absorption): Crohn's, blind– loop etc
Features of vitamin B12 deficiency

• macrocytic anaemia
• sore tongue and mouth
• neurological symptoms: e.g. Ataxia
• neuropsychiatric symptoms: e.g. Mood disturbances
Management
• if no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3
months
• if a patient is also deficient in folic acid then it is important to treat the B12 deficiency first to avoid precipitating
subacute combined degeneration of the cord
Vitamin Name DEFICIENCY EFFECTS
Beriberi.
Wernicke's encephalopathy
Korsakoff's syndrome,
B1 Thiamine
( irreversible psychosis
characterized by amnesia
n
confabulat
Cheilosis (cracks in the lips),

Hgh sensitivity to sunlight,
Agular cheilitis,
B2 Riboflavin n
Gossitis (inflam of tongue),
Sborrheic dermatitis
Paryngitis (sore throat),
B3 Niacin Pellagra.
B5 Pantothenic acid Acne & paresthesia,
B6 Pyridoxine Microcytic anemia ,
Multiple carboxylase deficiency,(Inorn

error of metabolism, can lead 2iotin
B7 Biotin
deficiency even when dietary intake
normal)
Macrocytic anemia,
Eevated levels of homocysteine.
B9 Folic acid
Deficiency in pregnant women can
lead to birth defects.
Pernicious anemia.
Macrocytic anemia,
B12 Cobalamin Eevated homocysteine,
Pripheral neuropathy, memory loss &
other cognitive deficits.
Malabsorption
Malabsorption is characterised by diarrhoea, steatorrhoea and weight loss. Causes may be broadly divided into intestinal
(e.g. villous atrophy), pancreatic (deficiency of pancreatic enzyme production or secretion) and biliary (deficiency of bile–
salts needed for emulsification of fats)
Intestinal causes of malabsorption

• coeliac disease
• Crohn's disease
• tropical sprue
• Whipple's disease
• Giardiasis
• brush border enzyme deficiencies (e.g. lactase insufficiency)
Pancreatic causes of malabsorption

• chronic pancreatitis
• cystic fibrosis
• pancreatic cancer
Biliary causes of malabsorption

• biliary obstruction
• primary biliary cirrhosis
Other causes
• bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
• short bowel syndrome
• lymphoma
Water absorption
During a 24 hours period the average person will ingest up to 2000ml of liquid orally. In addition a further 8000ml of fluid
will enter the small bowel as gastrointestinal secretions. Intestinal water absorption is a passive process and is related to
solute load. In the jejunum the active absorption of glucose and amino acids will create a concentration gradient that
water will flow across. In the ileum most water is absorbed by a process of facilitated diffusion (with sodium).
Approximately 150ml of water enters the colon daily, most is absorbed, the colon can adapt to, and increase this amount
following resection.
Collagen
One of the major connective tissue proteins

• Composed of 3 polypeptide strands that are woven into a helix
• Numerous hydrogen bonds exist within molecule to provide additional strength
• Many sub types but commonest sub type is I (90% of bodily collagen)
• Vitamin c is important in establishing cross links
Collagen Diseases
• Osteogenesis imperfecta
• Ehlers Danlos
Osteogenesis imperfecta:
– 8 Subtypes
– Defect of type I collagen
– In type I the collagen is normal quality but insufficient quantity
– Type II– poor quantity and quality
– Type III– Collagen poorly formed, normal quantity
– Type IV– Sufficient quantity but poor quality
Patients have bones which fracture easily, loose joint and multiple other defects depending upon which sub type they
suffer from
Ehlers Danlos:
– Multiple sub types
– Abnormality of types 1 and 3 collagen
– Patients have features of hypermobility.
– Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other
diseases related to connective tissue defects
Malabsorption
Malabsorption is characterised by diarrhoea, steatorrhoea and weight loss. Causes may be broadly divided into intestinal
(e.g. villous atrophy), pancreatic (deficiency of pancreatic enzyme production or secretion) and biliary (deficiency of bile–
salts needed for emulsification of fats) Intestinal causes of malabsorption
• Coeliac disease
• Crohn's disease
• tropical sprue
• Whipple's disease
• Giardiasis
• brush border enzyme deficiencies (e.g. lactase insufficiency)
Pancreatic causes of malabsorption

• chronic pancreatitis
• cystic fibrosis
• pancreatic cancer
Biliary causes of malabsorption

• biliary obstruction
• primary biliary cirrhosis
Other causes
• bacterial overgrowth (e.g. systemic sclerosis, diverticulae, blind loop)
• short bowel syndrome
• lymphoma
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PATHOLOGY
GENERAL PATHOLOGY
Phases of Cell Cycle
G0 : Quiescent (resting phase)

G1 : Pre – synthetic ;
Gap phase under the influence of the p53 gene;
In Normal tissues, cells ē significant damage 2 DNA are arrested @ this phase
S : S ynthesis of DNA (chromosome replication)

G2 : Pre-mitotic;
Gap phase when cells contain twice amount DNA as non-dividing cells
M : M itotic (cell division)
CELLULAR ADAPTATION
Cellular adaptation refers to cellular changes that occur in response to environmental changes. The may be physiological or
pathological. There are 5 types:
Atrophy
• Decrease in cell size.
• May be physiological such as thymus atrophy in childhood or pathological such as disuse atrophy in neurological injury.
Hypertrophy
• Increase in cell size
• Typically result of increased intracellular protein rather cytosol
• May be physiological such as muscle hypertrophy in weightlifters or pathological such as cardiac hypertrophy following MI.
Hyperplasia
• Increase in cell number
• Physiological endometrial hyperplasia occurs in pregnancy whereas pathological hyperplasia occurs in endometriosis
Metaplasia
• Reversible change of one differentiated cell type with another
• One example is cervical metaplasia where glandular epithelium is replaced by stratified squamous epithelium.
Dysplasia
• Abnormal change to cellular size, shape and/or organisation
• Sometimes referred to as atypical hyperplasia
• Can progress to cancer
• Cervix tissue is prone to dysplasia
Note: neoplasia refers to abnormal growth of cells typically resulting in tumour formation and may comprise a number of the cellular
adaptations referred to above
Apoptosis
Necrosis Type Organ(s)/Environment
Coagulative Kidney
Heart
Adrenals
Hypoxic
Liquefactive (colliquative) Brain
Fat Pancreas
Gangrenous GI tract
Peripheral limb
Caseous (granulomatous) TB infection

INFLAMMATIONS
Acute inflammation
Inflammation is the reaction of the tissue elements to injury. Vascular changes occur, resulting in the generation of a
protein rich exudate. So long as the injury does not totally destroy the existing tissue architecture, the episode may
resolve with restoration of original tissue architecture.
Vascular changes
• Vasodilation occurs and persists throughout the inflammatory phase.
• Inflammatory cells exit the circulation at the site of injury.
• The equilibrium that balances Starlings forces within capillary beds is disrupted and a protein rich exudate will
form as the vessel walls also become more permeable to proteins.
• The high fibrinogen content of the fluid may form a fibrin clot. This has several important immunomodulatory
functions.
Sequelae
Resolution • Typically occurs with minimal initial injury

• Stimulus removed and normal tissue architecture results
Organisation • Delayed removed of exudate

• Tissues undergo organisation and usually fibrosis
Suppuration • Typically formation of an abscess or an empyema

• Sequestration of large quantities of dead neutrophils
Progression • Coupled inflammatory and reparative activities

to chronic • Usually occurs when initial infection or suppuration has
inflammation been inadequately managed
Causes
• Microbacterial infections e.g. Viruses, exotoxins or endotoxins released by bacteria
• Chemical agents
• Physical agents e.g. Trauma
• Hypersensitivity reactions
• Tissue necrosis
Presence of neutrophil polymorphs is a histological diagnostic feature of acute inflammation
● CELLS OF ACUTE INFLAMMATION BE MaN

B asophil
E osinophil
Ma crophage
N utrophil
● CELLS OF CHRONIC INFLAMMATION LMP (Last Menstrual Period)

L ymphocytes
M onocytes (large bilobed nucleus)
P asma cell
Chronic inflammation
Overview
Chronic inflammation may occur secondary to acute inflammation.In most cases chronic inflammation occurs as a
primary process. These may be broadly viewed as being one of three main processes:
• Persisting infection with certain organisms such as Mycobacterium tuberculosis which results in delayed type
hypersensitivity reactions and inflammation.
• Prolonged exposure to non-biodegradable substances such as silica or suture materials which may induce an
inflammatory response.
• Autoimmune conditions involving antibodies formed against host antigens.
Acute vs. Chronic inflammation
Acute inflammation Chronic inflammation
Changes to existing vascular structure and increased permeability of Angiogenesis predominates

endothelial cells
Infiltration of neutrophils Macrophages, plasma cells and lymphocytes

predominate
Process may resolve with: Healing by fibrosis is the main result

Suppuration
Complete resolution
Abscess formation
Progression to chronic inflammation
Healing by fibrosis
Granulomatous inflammation
A granuloma consists of a microscopic aggregation of macrophages (with epithelial type arrangement =epitheliod). Large
giant cells may be found at the periphery of granulomas.
Mediators
Growth factors released by activated macrophages include agents such as interferon and fibroblast growth factor (plus
many more). Some of these such as interferons may have systemic features resulting in systemic symptoms and signs,
which may be present in individuals with long standing chronic inflammation.
Granuloma Histological Classification
Non caseating : Hard tubercle of TB

Hard tubercle of tuberculoid leprosy
FB garnuloma
Sarcoidosis (associated hypercalcaemia may present)**
Schistosomiasis
Caseating : Soft tubercle of Tuberculosis
Suppurative : Lymphogranuloma Venereum

Cat-scratch disease
Diffuse granulomatous : Lepromatous leprosy
Giant cells
• A giant cell is a mass formed by the union of several distinct types of cells
• They are most commonly comprised of macrophages
• They are different to granulomas although causative agents may overlap
● COMPLEMENT SYSTEM
Anaphylatoxin : C3a, C4a (small extent), C5a
Opsonin : C3b, C3bi
MAC : C5b-9 (MAC = Membrane Attack Complex; czes lysis of cell)
● INTERLEUKINS
IL1 : Activates T-cell, B-cell, It is the endogenous pyrogen
IL3 : Secreted by T-cell to stimulate the proliferation of haemopoietic progenitor cells
IL4 : Enhances synthesis of IgE; Helper T-cell proliferation
IL5 : Activation of Eosinophil ; Enhances synthesis of IgA
IL6 : Known as Myokine as secreted by muscles (also by T-cell & macrophage)

Most influential cytokine involved in coagulation activation (+TNF)
Pro-inflammatory
Mucous secretion
IL10 : Anti inflammatory; CSIF (Cytokine Synthesis Inhibitory Factor)
● Pro-inflammatory cytokines are IL2, IL3, IL6, TNF
● Cyclosporin; Tacrolimus : Inhibit IL-2 production in an activated T-cell

● Rapamycin (Sirolimus) : Inhibit IL-2 action
● NK & CD8 T-cells has perforin in its granules
Difference Between Exudate & Transudate
EXUDATE TRANSUDATE
↑Permeability ↑ Hydrostatic pr./
colloidal osmotic
pr.↓
Protein 1-6gm% <1gm %
Alb, Glb, Fibrinogen All Albumin
Sp.Gr. >1020 <1012
Clotts Doesn’t clot
Cell: plenty All mesothelial cells

polymorph;
lymphocytes
Inflammation & Non- inflammatory
malignancy
● All inflammatory & malignanat czes of pleural effusions are transudate
Phases of Wound Healing
Phase Key features Cells Timeframe
Haemostasis • Vasospasm in adjacent vessels Erythrocytes Seconds/
• Platelet plug formation and generation of fibrin rich Minutes
clot
Inflammation • Neutrophils migrate into wound (function impaired in Neutrophils, fibroblasts Days
diabetes). and macrophages
• Growth factors released, including basic fibroblast

growth factor and vascular endothelial growth factor.
• Fibroblasts replicate within the adjacent matrix and
migrate into wound.
• Macrophages and fibroblasts couple matrix
regeneration and clot substitution.
Regeneration • Platelet derived growth factor and transformation Fibroblasts, endothelial Weeks
growth factors stimulate fibroblasts and epithelial cells, macrophages
cells.
• Fibroblasts produce a collagen network.
• Angiogenesis occurs and wound resembles
granulation tissue.
Remodelling • Longest phase of the healing process and may last Myofibroblasts 6 weeks to 1
up to one year (or longer). year
• During this phase fibroblasts become differentiated

(myofibroblasts) and these facilitate wound
contraction.
• Collagen fibres are remodelled.
• Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may distort this process. It is obvious that
one of the key events is the establishing well vascularised tissue. At a local level angiogenesis occurs, but if arterial
inflow and venous return are compromised then healing may be impaired, or simply nor occur at all. The results of
vascular compromise are all too evidence in those with peripheral vascular disease or those poorly constructed bowel
anastomoses.
Conditions such as jaundice will impair fibroblast synthetic function and overall immunity with a detrimental effect in most
parts of healing.
Problems with scars:
Hypertrophic scars
– Excessive amounts of collagen within a scar.
– Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on
the surface.
– The tissue itself is confined to the extent of the wound itself and is usually the result of a full thickness
dermal injury.
– They may go on to develop contractures.
Keloid scars
– Excessive amounts of collagen within a scar.
– Typically a keloid scar will pass beyond the boundaries of the original injury.
– They do not contain nodules and may occur following even trivial injury.
– They do not regress over time and may recur following removal.
Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue
becomes macroscopically evident.
Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.
● Mnemonic to remember factors affecting wound healing: DIDNT HEAL

D iabetes
I nfection, irradiation
D rugs eg steroids, chemotherapy
N utritional deficiencies (vitamin A, C & zinc, manganese), Neoplasia
T issue necrosis
H ypoxia
E xcess tension on wound
A nother wound
L ow temperature, Liver jaundice
● Vasculogenesis vs Angiogenesis : Vascu is new. Angi is pre
Vasculogenesis is new vessels developing in situ from existing mesenchyme.

Angiogenesis is vessels develop from sprouting off pre-existing arteries.
Fracture healing
Bone fracture
- Bleeding vessels in the bone and periosteum
- Clot and haematoma formation
- The clot organises over a week (improved structure and collagen)

- The periosteum contains osteoblasts which produce new bone
- Mesenchymal cells produce cartilage (fibrocartilage and hyaline cartilage) in the soft tissue around the fracture
- Connective tissue + hyaline cartilage = callus
- As the new bone approaches the new cartilage, endochondral ossification occurs to bridge the gap
- Trabecular bone forms
- Trabecular bone is resorbed by osteoclasts and replaced with compact bone
Factors Affecting Fracture Healing

• Age
• Malnutrition
• Bone disorders: osteoporosis
• Systemic disorders: diabetes, Marfan's syndrome and Ehlers-Danlos syndrome cause abnormal
musculoskeletal healing.
• Drugs: steroids, non steroidal anti inflammatory agents.
• Type of bone: Cancellous (spongy) bone fractures are usually more stable, involve greater surface areas, and
have a better blood supply than cortical (compact) bone fractures.
• Degree of Trauma: The more extensive the injury to bone and surrounding soft tissue, the poorer the outcome.
• Vascular Injury: Especially the femoral head, talus, and scaphoid bones.
• Degree of Immobilization
• Intra-articular Fractures: These fractures communicate with synovial fluid, which contains collagenases that
retard bone healing.
• Separation of Bone Ends: Normal apposition of fracture fragments is needed for union to occur. Inadequate
reduction, excessive traction, or interposition of soft tissue will prevent healing.
• Infection
Fat embolism
Diagnosis and clinical features
System Feature
Cardiothoracic Early persistent tachycardia

Tachypnoea, dyspnoea, hypoxia usually 72 hours following injury
Pyrexia
Dermatological • Red/ brown impalpable petechial rash (usually only in 25-50%)

• Subconjunctival and oral haemorrhage/ petechiae
CNS • Confusion and agitation

• Retinal haemorrhages and intra-arterial fat globules on fundoscopy
Imaging
• May be normal
• Fat emboli tend to lodge distally and therefore CTPA may not show any vascular occlusion, a ground glass
appearance may be seen at the periphery
Treatment
• Prompt fixation of long bone fractures
• Some debate regarding benefit Vs. risk of medullary reaming in femoral shaft/ tibial fractures in terms of
increasing risk (probably does not).
• DVT prophylaxis
• General supportive care
LYMPHOEDEMA
Due to impaired lymphatic drainage in the presence of normal capillary function.

Lymphoedema causes the accumulation of protein rich fluid, subdermal fibrosis and dermal thickening.
Characteristically fluid is confined to the epifascial space (skin and subcutaneous tissues);
Mmuscle compartments are free of oedema. It involves the foot, unlike other forms of oedema. There may be a
'buffalo hump' on the dorsum of the foot and the skin cannot be pinched due to subcutaneous fibrosis.
Causes Of Lymphoedema
Primary
• Congenital < 1 year: sporadic, Milroy's disease
• Onset 1-35 years: sporadic, Meige's disease
• > 35 years: Tarda
Secondary
• Bacterial/fungal/parasitic infection (filariasis)
• Lymphatic malignancy
• Radiotherapy to lymph nodes
• Surgical resection lymph nodes
• DVT
• Thrombophlebitis
Indications For Surgery

• Marked disability or deformity from limb swelling
• Lymphoedema caused by proximal lymphatic obstruction with patent distal lymphatics suitable for a lymphatic
drainage procedure
• Lymphocutaneous fistulae and megalymphatics
Procedures
Homans operation
– Reduction procedure with preservation of overlying skin (which must be in good condition).
– Skin flaps are raised and the underlying tissue excised.
– Limb circumference typically reduced by a third.
Charles operation
– All skin an subcutaneous tissue around the calf is excised down to the deep fascia.
– Split skin grafts are placed over the site.
– May be performed if overlying skin is not in good condition.
– Larger reduction in size than with Homans procedure.
Lymphovenous anastamosis
– Identifiable lymphatics are anastomosed to sub dermal venules.
– Usually indicated in 2% of patients with proximal lymphatic obstruction and normal distal lymphatics.
Lymphadenopathy
• Lymphadenopathy in the neck, axillae, groins and abdomen

• Need to note: solitary/multiple, defined/indistinct, hard/rubbery/soft, tender/painless
Causes of lymphadenopathy Mnemonic: Hodgkins disease
H aematological: Hodgkins lymphoma, NHL, Leukaemia

O ncological: metastases
D ermatopathic lympadenitis
G aucher's disease
K awasaki disease
I nfections: TB, glandular fever, Syphilis
N iemann Pick disease
S erum sickness
D rug reaction (phenytoin)
I mmunological (SLE)
S arcoidosis
E ndocrinological (Hyperthyroidism)
A ngioimmunoplastic lymphadenopathy
S LE
E osinophilic granulomatosis
Para-aortic lymphadenopathy
Organ sites that may metastasise (early) to the para-aortic lymph nodes:
• Testis
• Ovary
• Uterine fundus
Many other organs may result in para-aortic nodal disease. However, these deposits will represent a much later stage of
the disease, since other nodal stations are involved earlier.
Pathological calcification
Dystrophic calcification
– Deposition of calcium deposits in tissues that have undergone, degeneration, damage or disease
– Occurs in the presence of normal serum calcium and phosphate levels

– Common sites :
Necrotic tissues
Caseous necrosis of tubercle
Fat necrosis
Liquefactive necrosis
– Advanced atheromatous lesions
– Haematoma; Thrombus; Infarcts
– Heart valves e.g. subacute infective endocarditis
– Other sites: Uterine fibroids; Meningioma(Psamoma bodies); Constrictive pericarditis; Dead fetus;
Dead parasites
Metastatic calcification
– Deposition of calcium deposits in normal tissues in the presence of increased serum calcium levels
– Causes:
Hyperparathyroidism due to hyperplasia or neoplasm of parathyroid
Vitamin D intoxication
Disseminated bone tumors e.g. metastatic ca; multiple myeloma
Others : Sarcoidosis; Renal tubular acidosis; Milk alkali syndrome
ONCOLOGY, NEOPLASIA AND TUMOR
Dysplasia
• Premalignant condition
• Disordered growth and differentiation of calls
• Alteration in size, shape, and organization of cells
• Features increased abnormal cell growth (increased number of mitoses/abnormal mitoses and cellular
differentiation)
• Underlying connective tissue is not invaded
• Causes include smoking, Helicobacter pylori, Human papilloma virus
• Main differences to metaplasia is that dysplasia is considered to be part of carcinogenesis (pre cancerous) and
is associated with a delay in maturation of cells rather than differentiated cells replacing one another.
• The absence of invasion differentiates dysplasia from invasive malignancy.
• Severe dysplasia with foci of invasion are well recognised.
Metaplasia
• Definition: reversible change of differentiated cells to another cell type.
• May represent an adaptive substitution of cells that are sensitive to stress by cell types better able to withstand
the adverse environment.
• Can be a normal physiological response (ossification of cartilage to form bone)
• Most common epithelial metaplasia occurs with transformation of columnar cells to squamous cells (smoking
causes ciliated columnar cells to be replaced by squamous epithelial cells; Schistosomiasis).
• Metaplasia from squamous to columnar cells occurs in Barrett oesophagus.
• If the metaplastic stimulus is removed, the cells will return to their original pattern of differentiation. However, if
the stimulus is not removed then progression to dysplasia may occur.
• Not considered directly carcinogenic, however the factors which predispose to metaplasia, if persistent may
induce malignant transformation.
• The pathogenesis involves a reprogramming of stem cells that are known to exist in normal tissues, or of
undifferentiated mesenchymal cells present in connective tissue. In a metaplastic change, these precursor cells
differentiate along a new pathway.
Histopathology of malignancy
• Abnormal tissue architecture
• Coarse chromatin
• Invasion of basement membrane*
• Abnormal mitoses
• Angiogenesis
• De-differentiation
• Areas of necrosis
• Nuclear pleomorphism
*= Those features that distinguish invasive malignancy from in situ disease
● Germ-Line Tumor : TESTY

- Teratoma
- Embryonal carcinoma
- Seminoma
- Trophoblastic (Choriocarcinoma)
- Yolk-sac tumor
Tumour grading
Tumours may be graded according to their degree of differentiation, mitotic activity and other features. Grade 1 tumours
are the most differentiated and grade 4 the least. The assessment is subjective, in most cases high grade equates to
poor prognosis, or at least rapid growth.
Tumours of glandular epithelium will tend to arrange themselves into acinar type structures containing a central lumen.
Well differentiated tumours may show excellent acinar formation and poorly differentiated tumours simply clumps of cells
around a desmoplastic stroma. Sometimes tumours demonstrate mucous production without evidence of acinar
formation. Since mucous production is evidence of a glandular function such tumours are often termed mucinous
adenocarcinoma.
Squamous cell tumours will typically produce structures resembling epithelial cell components. Well differentiated
tumours may also produce keratin (depending upon tissue of origin).
Nottingham prognostic index
The Nottingham Prognostic Index can be used to give an indication of survival. In this system the tumour size is weighted
less heavily than other major prognostic parameters.
Calculation of NPI
Tumour Size x 0.2 + Lymph node score(From table below)+Grade score(From table below).
Lymph nodes involved Grade

Score
1 0 1
2 1-3 2
3 >3 3
Prognosis
Score Percentage 5 year survival
2.0 to 2.4 93%
2.5 to 3.4 85%
3.5 to 5.4 70%
>5.4 50%
This data was originally published in 1992. It should be emphasised that other factors such as vascular invasion and
receptor status also impact on survival and are not included in this data and account for varying prognoses often cited in
the literature.
Tumor Markers
Tumour markers may be divided into:
• monoclonal antibodies against carbohydrate or glycoprotein tumour antigens

• tumour antigens
• enzymes (alkaline phosphatase, neurone specific enolase)
• hormones (e.g. calcitonin, ADH)
It should be noted that tumour markers usually have a low specificity
Monoclonal antibodies
Tumour marker Association
CA 125 Ovarian cancer
CA 19-9 Pancreatic cancer
CA 15-3 Breast cancer
NB: The breast cancer tumour marker is not specific or sensitive enough to be used routinely.
Tumour antigens
Tumour marker Association
Prostate specific antigen (PSA) Prostatic carcinoma
Alpha-feto protein (AFP) Hepatocellular carcinoma, teratoma
Carcinoembryonic antigen (CEA) Colorectal cancer
Very Important for Exam
MARKERS ASSOCIATED TUMOR TYPES
Oncofetal antigen
α -fetoprotein (AFP) NSGCT, HCC
Stomach, Colon, Pancreas, urinary tract, breast, cervix,

CEA
ovarian,
Mucins & other glycoproteins
CA15-3 Breast
CA19-9 Pancreatic, colorectal cancer
CA125 Ovarian
Hormones
hCG Gestational trophoblastic disease, NSGCT
Calcitonin Medullary Carcinoma thyroid
Catecholeamines Pheochromocytoma
Isoenz
PSA Prostate
Neuron-specific enolase (NSE) Neuroblastoma, small-cell carcinoma of the lung,
New molecular markers
P53, APC, RAS in stool & serum Colon
P53, RAS in stool & serum Pancreas
P53, APC, RAS in sputum & serum Lung
P53 in urine Bladder
Sarcoma, RCC, endometrial , lung, lymphoma, leukemia,

Vimentin
melanoma
Melanoma, sarcoma (neurosarcoma, lipoma, chondrosarcoma),

astrocytoma, gastrointestinal stromal tumor, salivary gland
S100 protein
cancer, some types of adenocarcinoma, histiocytic tumor
[5]
(dendritic cell, macrophage)
Some extra important points regarding the α-fetoprotein –

Maternal raise : Fetal neural tube defect; Twins; Fetal distress
Amniotic fluid raise : Fetal neural tube defect (e.g. open spina bifida; Enencephaly); Congenital
nephrotic Syndrome; Oesophageal-duodenal atresia
Oncogenes
Oncogenes are cancer promoting genes that are derived from normal genes (proto-oncogenes). Proto-oncogenes play
an important physiological role in cellular growth. They are implicated in the development of up to 20% of human
cancers.
Proto-oncogenes may become oncogenes via the following processes:

• Mutation (point mutation)
• Chromosomal translocation
• Increased protein expression
• Only one mutated copy of the gene is needed for cancer to occur - a dominant effect
● Proto- Oncogenes
RAShed MY ER ToGo ABout with my SIS

ras (signal transducer)
N-my c (transcription factor, TF) Burkitt’s lymphoma
ERB-B1/B2 (GF receptor)
TGF-α
Abl (signal transducer) [anti-apoptosis gene]
SIS gene GF) [osteosarcoma+astrocytoma]
BCL-2 (programmed cell death regulator)
Classification of oncogenes
• Growth factors e.g. Sis
• Transcription factors e.g. Myc
• Receptor tyrosine kinase e.g. RET
• Cytoplasmic tyrosine kinase e.g. Src
• Regulatory GTPases e.g. Ras
Tumour supressor genes

Tumour supressor genes restrict or repress cellular proliferation in normal cells. Their inactivation through mutation or
germ line incorporation is implicated in renal, colonic, breast, bladder and many other cancers. One of the best known
tumour supressor genes is p53. p53 gene offers protection by causing apoptosis of damaged cells. Other well known
genes include BRCA 1 and 2.
● P53 is a tumor suppressor gene and located on chromosome 17; Li-fraumeni Syndrome – এ এটার mutation হয়
Paraneoplastic Syndrome
Thymoma : Pure RBC aplasia, Myasthenia gravis

Small cell Ca Lung : ADH, ACTH secretion; SIAD; Lambert-Eaton myasthenic syndrome
Pancreatic : Trousseau’s superficial migratory thrombophlebitis
Gastric : Acanthosis Nigricans
Breast : Dermatomyocitis
MM : Hypercalcaemia
Secondary malignant tumours of bone
Metastatic lesions affecting bone are more common than primary bone tumours.
The typical tumours that spread to bone include:
• Breast
• Bronchus
• Renal
• Thyroid
• Prostate
75% cases will affect those over the age of 50

The commonest bone sites affected are:
• Vertebrae (usually thoracic)

• Proximal femur
• Ribs
• Sternum
• Pelvis
• Skull
Pathological fracture
Osteolytic lesions are the greatest risk for pathological fracture

The risk and load required to produce fracture varies according to bone site. Bones with lesions that occupy 50% or less
will be prone to fracture under loading (Harrington). When 75% of the bone is affected the process of torsion about a
bony fulcrum may produce a fracture.
The Mirel scoring[1] system may be used to help determine the risk of fracture and is more systematic than Harrington
system described above.
Mirel Scoring system
Score points Site Radiographic appearance Width of bone involved Pain
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by function
Depending upon the score the treatment should be as follows:
Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management
Where the lesion is an isolated metastatic deposit consideration should be given to excision and reconstruction as the
outcome is better [2].
Non operative treatments

Hypercalcaemia- Treat with re hydration and bisphosphonates.
Pain- Opiate analgesics and radiotherapy.
Some tumours such as breast and prostate will benefit from chemotherapy and or hormonal agents.
Chromosome Involvement
Chromosome 1 : Neuroblastoma
Chromosome 11 : Wilm’s tumor

Chromosome 13 : Retinoblastoma
Chromosome 16 : Polycystic kidney disease
Chromosome 17: Neurofibroma; Osteogenic sarcoma
● Common Cancers Among Organ Transplant Recepients

Skin cancer; Kaposi’s; Anogenital ca; Non-Hodgkin’s (large cell & immunoblastic types) – এর মধ্যে Skin cancer, most
common
Extravasation injury
Chemotherapy may be complicated by extravasation reactions in up to 6% of cases. The following chemotherapy agents
are recognised causes of extravasation reactions; doxorubicin, vincristine, vinblastine, adriamycin, cisplatin, mitomycin
and mithramycin.
Up to 30% of extravasation reactions may be complicated by the development of ulceration.
When an extravasation reaction is suspected the infusion should be stopped and the infusing device aspirated. The
extremity should be elevated. As a general rule cold compresses have been shown to reduce the incidence of
subsequent ulceration with doxorubicin. Warm compresses have been found to be beneficial in extravasation of vinca
alkaloids. Dimethylsulfoxide may be infused in some cases, ideally within 5 hours of the event occurring. No conclusive
evidence exists to support the use of corticosteroids or sodium bicarbonate for extravasation injuries
Carcinoid Syndrome
• Systemic symptomps Produced by secretory products of neoplastic enterochromaffin cells (e.g. serotonin,
bradykinin).
• Originate in neuroendocrine cells mainly in intestine (midgut-distal ileum/appendix), but can occur in rectum,
bronchi
• Hormonal symptoms mainly occur when disease spreads outside the bowel i.e. will only occur in the
presence of liver metastasis (as the hormone released from primary lesions will typically be metabolised by
the liver) … Liver metastases is a must for the presence of carcinoid syndrome.
C/F
- Onset: years
- Diarrhoea; flushing; wheezing; Asthma; facial telangiectasia; Palpitation; Pellagra; Cardiac (HF, TR, PS)
Rule of thirds:
1/3 multiple
1/3 small bowel
1/3 metastasize
1/3 second tumour
Investigation : 5-HIAA in 24-hr urine; Scintigraphy; CT scan.
It is important falsely elevate 5-HIAA cz diagnosing carcinoid syndrome incorrectly. These include:
Food: spinach, cheese, wine, caffeine, tomatoes
Drugs: Isoniazid, Monoamine oxidase inhibitors
Treatment
• Drugs : Octreotide (synthetic alternative to somatostatin); Nicotinamide
• RX of HF; wheeze (with bronchodilator); diarrhea
• Avoidance of condition that precipitate flush
• Surgical removal
Carcinoid Tumors
- Of the lung (bronchial adenomas) so called Argentafinomas as they take up Silver are neuroendocrine cells
and are derived from the K cells (kulchitsky) in the lung
- Of appendix :
- Individuals with small carcinoids can be discharged (<2cm and limited to the appendix) as this has
an excellent prognosis.
- Larger tumours should have a radioisotope scan.
- Where the resection margin is positive or where the isotope scan suggests lymphatic metastasis a
right hemicolectomy should be performed.
Peutz-Jeghers syndrome
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous benign hamartomatous polyps
in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Around 50%
of patients will have died from a gastrointestinal tract cancer by the age of 60 years.
Genetics
• Autosomal dominant
• Responsible gene encodes serine threonine kinase LKB1 or STK11
Features
• Hamartomatous polyps in GI tract (mainly small bowel)
• Pigmented lesions on lips, oral mucosa, face, palms and soles
• Intestinal obstruction e.g. intussusception (which may lead to diagnosis)
• Gastrointestinal bleeding
Management
• Conservative unless complications develop
● Most common benign germ cell tumor among pre-menopausal women is Demoid cyst
Sarcomas
• Malignant tumours of mesenchymal origin
Types :
May be either bone or soft tissue in origin.
Bone sarcoma include:
• Osteosarcoma
• Ewings sarcoma (although non bony sites recognised)
• Chrondrosarcoma - originate from Chondrocytes
Soft tissue sarcoma are a far more heterogeneous group and include:
• Liposarcoma-adipocytes
• Rhabdomyosarcoma-striated muscle
• Leiomyosarcoma-smooth muscle
• Synovial sarcomas- close to joints (cell of origin not known but not synovium)
Malignant fibrous histiocytoma is a sarcoma that may arise in both soft tissue and bone.
Features
Certain features of a mass or swelling should raise suspicion for a sarcoma these include:
• Large >5cm soft tissue mass
• Deep tissue location or intra muscular location
• Rapid growth
• Painful lump
Assessment
Imaging of suspicious masses should utilise a combination of MRI, CT and USS. Blind biopsy should not be
performed prior to imaging and where required should be done in such a way that the biopsy tract can be
subsequently included in any resection.
Ewings sarcoma
• Commoner in males
• Incidence of 0.3 / 1, 000, 000
• Onset typically between 10 and 20 years of age
• Location by femoral diaphysis is commonest site
• Histologically it is a small round tumour
• Blood borne metastasis is common and chemotherapy is often combined with surgery
Osteosarcoma
• Mesenchymal cells with osteoblastic differentiation
• 20% of all primary bone tumours
• Incidence of 5 per 1,000,000
• Peak age 15-30, commoner in males
• Limb preserving surgery may be possible and many patients will receive chemotherapy
Liposarcoma
• Malignancy of adipocytes
• Rare approximately 2.5 per 1,000,000. They are the second most common soft tissue sarcoma
• Typically located in deep locations such as retroperitoneum
• Affect older age group usually >40 years of age
• May be well differentiated and thus slow growing although may undergo dedifferentiation and disease
progression
• Many tumours will have a pseudocapsule that can misleadingly allow surgeons to feel that they can 'shell out'
these lesions. In reality tumour may invade at the edge of the pseudocapsule and result in local recurrence if
this strategy is adopted
• Usually resistant to radiotherapy although this is often used in a palliative setting
Malignant Fibrous Histiocytoma

• Tumour with large number of histiocytes
• Most common sarcoma in adults
• Also described as undifferentiated pleomorphic sarcoma NOS (i.e. Cell of origin is not known)
• Four major subtypes are recognised: storiform-pleomorphic (70% cases), myxoid (less aggressive), giant cell
and inflammatory
• Treatment is usually with surgical resection and adjuvant radiotherapy as this reduces the likelihood of local
recurrence
● Sarcomas in which Lymphatic Metastasis is seen: 'RACE For MS'

R : Rhabdomyosarcoma
A : Angiosarcoma
C : Clear cell sarcoma
E : Epithelial cell sarcoma
For : Fibrosarcoma
M : Malignant fibrous histiocytoma
S : Synovial cell sarcoma
Or 'SCARE'
S ynovial sarcoma
C lear cell sarcoma
A ngiosarcoma
R habdomyosarcoma
E pithelioid sarcoma
Occupational cancers
Occupational cancers accounted for 5.3% cancer deaths in 2005.

In men the main cancers include:
• Mesothelioma
• Bladder cancer
• Non melanoma skin cancer
• Lung cancer
• Sino nasal cancer
Occupations with high levels of occupational tumours include:

• Construction industry
• Working with coal tar and pitch

• Mining
• Metalworkers
• Working with asbestos (accounts for 98% of all mesotheliomas)
• Working in rubber industry
Shift work has been linked to breast cancer in women (Health and safety executive report RR595).
The latency between exposure and disease is typically 15 years for solid tumours and 20 for leukaemia.
Many occupational cancers are otherwise rare. For example sino nasal cancer is an uncommon tumour, 50% will be
SCC. They are linked to conditions such as wood dust exposure and unlike lung cancer is not strongly linked to cigarette
smoking. Another typical occupational tumour is angiosarcoma of the liver which is linked to working with vinyl chloride.
Again in the non occupational context this is an extremely rare sporadic tumour
Mesothelioma
Features
• Dyspnoea, weight loss, chest wall pain
• Clubbing
• 30% present as painless pleural effusion
• Only 20% have pre-existing asbestosis
• History of asbestos exposure in 85-90%, latent period of 30-40 years
Basics
• Malignancy of mesothelial cells of pleura
• Metastases to contralateral lung and peritoneum
• Right lung affected more often than left
Management
• Investigation: pleural biopsy, CT Scanning, (PET Scanning if surgery considered)
• Symptomatic
• Industrial compensation
• Chemotherapy, Surgery if operable
• Prognosis poor, median survival 12 months
Palliative care prescribing: pain
SIGN issued guidance on the control of pain in adults with cancer in 2008. Selected points
• the breakthrough dose of morphine is one-sixth the daily dose of morphine
• all patients who receive opioids should be prescribed a laxative
• opioids should be used with caution in patients with chronic kidney disease. Alfentanil, buprenorphine and
fentanyl are preferred
• metastatic bone pain may respond to NSAIDs, bisphosphonates or radiotherapy
When increasing the dose of opioids the dose should be increased by 30-50%.
Conversion between opioids
From To
Oral codeine Oral morphine Divide by 10
Oral tramadol Oral morphine Divide by 5
From To
Oral morphine Oral oxycodone Divide by 2
The BNF states that oral morphine sulphate 80-90mg over 24 hours is approximately equivalent to one '25 mcg/hour'
fentanyl patch, therefore product literature should be consulted.
From To
Oral morphine Subcutaneous diamorphine Divide by 3
Oral oxycodone Subcutaneous diamorphine Divide by 1.5
GENETICS
Genetics and surgical disease
Some of the more commonly occurring genetic conditions occurring in surgical patients are presented here.
Li-Fraumeni Syndrome
• Consists of germline mutations to p53 tumour suppressor gene
• High incidence of malignancies particularly sarcomas and leukaemias
• Diagnosed when:
*Individual develops sarcoma under 45 years

*First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy
under 45 years or sarcoma at any age
BRCA 1 and 2
• Carried on chromosome 17
• Linked to developing breast cancer (60%) risk.
• Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA2).
Lynch Syndrome
• Develop colonic cancer and endometrial cancer at young age

• 80% of affected individuals with get colonic and or endometrial cancer
• High risk individuals may be identified using the Amsterdam criteria
Amsterdam criteria
Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent,
child, sibling) relative of the other two.
Two successive affected generations.
One or more colon cancers diagnosed under age 50 years.
Familial adenomatous polyposis (FAP) has been excluded.
Gardners syndrome
• Autosomal dominant familial colorectal polyposis
• Multiple colonic polyps
• Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts
• Desmoid tumours are seen in 15%
• Mutation of APC gene located on chromosome 5
• Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer
• Now considered a variant of familial adenomatous polyposis coli
Marfan's syndrome
Marfan's syndrome is an autosomal dominant connective tissue disorder. It is caused by a defect in the fibrillin-1 gene on
chromosome 15 and affects around 1 in 3,000 people.
Features
• tall stature with arm span to height ratio > 1.05

• high-arched palate
• arachnodactyly
• pectus excavatum
• pes planus
• scoliosis of > 20 degrees
• heart: dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic
regurgitation, mitral valve prolapse (75%),
• lungs: repeated pneumothoraces
• eyes: upwards lens dislocation (superotemporal ectopia lentis), blue sclera, myopia
• dural ectasia (ballooning of the dural sac at the lumbosacral level)
The life expectancy of patients used to be around 40-50 years. With the advent of regular echocardiography monitoring
and beta-blocker/ACE-inhibitor therapy this has improved significantly over recent years. Aortic dissection and other
cardiovascular problems remain the leading cause of death however
Acute intermittent porphyria
Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in porphobilinogen
deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic accumulation of delta
aminolaevulinic acid and porphobilinogen. It characteristically presents with abdominal and neuropsychiatric symptoms in
20-40 year olds. AIP is more common in females (5:1)
Features
• abdominal: abdominal pain, vomiting
• neurological: motor neuropathy
• psychiatric: e.g. depression
• hypertension and tachycardia common
Diagnosis
• classically urine turns deep red on standing
• raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
• assay of red cells for porphobilinogen deaminase
• raised serum levels of delta aminolaevulinic acid and porphobilinogen
Aggressive fibromatosis
Aggressive fibromatosis is a disorder consisting of desmoid tumours, which behave in a locally aggressive manner.
Desmoid tumours may be identified in both abdominal and extra-abdominal locations. Metastatic disease is rare. The
main risk factor (for abdominal desmoids) is having APC variant of familial adenomatous polyposis coli. Most cases are
sporadic.
Treatment is by surgical excision.
Tuberous sclerosis
Tuberous sclerosis (TS) is a genetic condition of autosomal dominant inheritance. Like neurofibromatosis, the
majority of features seen in TS are neuro-cutaneous
Cutaneous features
• depigmented 'ash-leaf' spots which fluoresce under UV light
• roughened patches of skin over lumbar spine (Shagreen patches)
• adenoma sebaceum: butterfly distribution over nose
• fibromata beneath nails (subungual fibromata)
• café-au-lait spots* may be seen
Neurological features
• developmental delay
• epilepsy (infantile spasms or partial)
• intellectual impairment
Also
• retinal hamartomas: dense white areas on retina (phakomata)
• rhabdomyomas of the heart

• gliomatous changes can occur in the brain lesions
• polycystic kidneys, renal angiomyolipomata
*these of course are more commonly associated with neurofibromatosis. However a 1998 study of 106 children with TS
found café-au-lait spots in 28% of patients
Autosomal dominant
• CNS all (except Friedreich’s ataxia)
• CVS all
• GIT all (except cystic fibrosis)
• Connective tissue all
Autosomal recessive
• Haematological all. (except Haemophilia – X-linked recessive)
• Hepatobiliary all (except PLD, Gilbert’s)
• Metabolic all (except Familial hypercholesterolaemia, Acute intermittent porphyria)
• Respiratory all
• Renal all (except PKD & Benign familial haematuria)
NAME AGE SITE SIGNIFICANT FINDINGS XRAY TREATMENT

OSTEO ● Grow away from joint ● Single or Multiple; bony hard; non tender Mushroom Appearance
CHNDROMA 20yrs around ● Mostly:- Ribs; Scapula; ● Accidentally Discovered; systemically well patient. Calcified Stalk ● Resection
Pelvis; Long Bones Radioluscent Cap
● Hyaline Cartilage within long bone ● Elongated oval lytic Lesion-
● Lobulated Cortex Preseved.
EN ● Cavity of the mass Radioluscent ē ● Currettage or En- Bloc
CHNDROMA 30-50yrs Multiple Enchondromatosis :- OLLIER’S DISEASE areas of calcifican may present. Resection
Multiple Enchondromatosis ē Haemangioma :- MAFFUCCI’S SYND. ● Usual Opacity lost.
● Thinned cortex as mass expands.
JUXTA 20s & 30s ● Buttresses, saucerisation of cortex ● Hyaline Cartilage formed below
CORTICAL periosteum, erodes into cortex
Rare ● Mid Ache + Swelling
CHNDROMA
● Long Bone Shaft, ● Pain worse @ night, might relieved by Aspirin ● Localized osteolytic lesion
OSTEOID 5-30 yrs Mainly Femur Neck ● CT shows Nidus surrounded by a rim of sclerosis ● Excision of nidus
OSTEOMA ● <2cm radioluscent nidus, woven bone ● Radiofrequency ablation
(BONE-FORMING)
OSTEO >40yrs usually ● Only @ Vertebrae & ● Reactive Bone Formation occurs ● Currettage or Excision
BLASTOMA larger
● Long H/O low grade joint pain ● Chicken wire pattern calcification
CHONDRO 20s &30s “Difference with GCT : In GCT Soft Tissue Involved ● Eccentric lesion effect medulla ● Currettage
BLASTOMA ” ● Lytic lesion
● 50% around knee ● Female dominant ● Large radioluscent lesion external to
GCT / ● Metaphyseo- ● 3 type cell:-Mononuclear(Fibroblastic;Fibrohystioytic) subchondral plate
OSTEO Epiphyseal region -Multinucleated(Giant Cell) ● Thinning & fracture of cortex ● Radiotherapy
CLASTOMA ● Below subchondral “MRI: EXTRAOSSEUS SOFT TISSUE MASS” ● Soap Bubble appearance
● Hazy margins, extending to Epiphysis &
plate;Eccentric eroding Articular Cartilage
Defective osteoclast ● Thickening of bone- marrow space replaced ē bone cz
OSTEO function resulting in Anaemia, Infection(Leukoerythroblastic Picture) & death ● Marble Bone Appearance Stem cell transplant and
PETROSIS failure of normal bone ● Thick bone may lead to compression neuropathies(e.g. Also Known as Marble Bone Disease / Interferon-gamma
Autosomal resorption Optic N. or Bell’s palsy) Albers-Schönberg Disease
● Thrombocytopenia may present
Recessive “OSTEOPETROSIS TARDA: Less severe variety; incidental ● Cortex-Medulla differentiation lack
finding”
SIMPLE / 10-20 yrs ● Proximal - Humerus ● Fallen Cresent Sign- well : ● Spontaneous resolve
UNI- 1ST & 2ND - Femur ● Multi-Loculated demarcated radiolucent area in metaphysis ● Tend to heal following fracture
CAMERAL Decade ● New fracture running thru’ it ● Impending fracture consider
BONE CYST Aspiration + Steroid Inj.
● Multiple Blood filled spaces surrounded by thin ● Well-circumscribed; eccentric; expansile;
Aneurysmal <20yrs(75%) layer of bone & periosteum periosteum bulges ● Currettage + Bone graft ē Local
Bone Cyst ● Expanding + Radiolucent Cyst Adjuvant treatment(e.g. Phenol)

PAGET’S >40yrs ● Axial skeleton mostly:- ● Anterior bowing of Femur & Tibia ● Thick Coarse Cortex ● Calcitonin: (-) Osteoclast
DISEASE usually - Skull ● Lion-like facies (Leontiasis ossea) ● Cancellous Bone ● Biphosphonates(either oral
-Thoracic, Lumber, [Excessive osteoclastic resorption followed by increased ● Osteoporosis Circumscripta found Risedronate or IV Zoledronate): (-)Bone
- Disorder of Sacral Spine osteoblastic activity causing areas of sclerosis and deformity] Resorption & Formation
Osteoclasts - Pelvis ● Serum Alk.PO4↑↑ but Serum (Ca & PO4 ) Normal
- Increased but ● Hydroxyprolene (+)ve in Urine Complications
uncontrolled ● Less Commonly ● 3 phases:- Osteolytic, Reparative, Inactive • Deafness (cranial nerve entrapment)
bone turnover. - Humerus, Femur, Tibia ● Malignant change:- Osteosarcoma; Chondrosarcoma; • Sarcoma (1% if affected for > 10 yrs)
- Characterized by Sarcoma; GCT • Fractures
architecturally ● Bone Pain (e.g. Pelvis, femur, Lumbar spine)
abnormal bones ● Deafness:- Nerve Compression / Osteosclerosis
• Skull thickening
● Altered Mental Status:- Skull base causes compression • High-output cardiac failure
over the Posterior Fossa structures
● Kyphosis:- Spinal Cord Injury
● Convex joint mostly:- ● Avascular, never remodel
- Elbow (capitulum) ● Line of Demarcation ● Stable: Actvity Modification
OSTEO - Femoral Head ● Loose Bodies ● Loose or Free fragments
CHONDRITIS - Knee; Patella should be reduced &
DISSECANS - 1st MT Head stabilized ē Biabsorbable
(OCD) pins
● Subchondral bone
tends to micro fracture
● Knock Knees + Hyper Mobile Fingers

● Metabolic Disease of Mutation in gene Coding for Type-1 ● Translucent Bone
Collagen ● Wormian Bone
● Causes imperfect Bone, Teeth; Ligament; Sclera ● Multiple fracture Particularly of Long
OSTEO ● Types: I – Blue Sclera; Early Deafness; Mild bony Bone
GENESIS fragility but No deformity (Dominant)
IMPERFECTA II – Fatal in Perinatal Period (Dominant +Recessive)
III – Intrauterine fracture; White sclera; Very short
stature (Recessive)
IV – Light Sclera; Long Bones Bowing (Dominant)

>50 yrs ● Any Bone ● COMMONEST In Adult
● Monoclonal Ab(+) ● BM Biopsy followed by
● Urine Bence-Jones Protein(+) ● Punched out Lesion Chemotherapy
MULTIPLE ● Serum (Ca & Urea )↑ ● Lytic Lesion ● BM aspiration show plasma
MYELOMA ● Fatigue; Pain; Weakness cells' sheets or clusters
Plasmocytoma ● Generalised Osteoporosis & Crushed Vertebrae
10-25yrs: Usually ● COMMONEST Among Children ● Chemo + Surgery

Adult: Rare; DIST. FEMUR(COMMONLY) ● 2ND COMMONEST in Adult; arise from medullary cavity ● Sun Ray / Sun Burst Effect
OSTEO found ē H/O → Proximal Tibia → ● Painful enlarging Mass, pain worse @ night ● Codman’s Triangle **Vimentin (+) ve spindle shaped
SARCOMA Paget’s Proximal Humerus → ● Pulmonary Metastasis (Cannon-Ball / Nodules) (CXR) ● Bony Destruction; Bony Elevation; cells indicates lung metastases
Proximal Femur → Pelvis ● H/O Retinoblastoma may present in child Sub-periosteal New Bone Formation
“Remember- around knee” ● Pleomorphic spindle shaped cell with malignant Osteoid ● Skip Lesion; Sclerotic Lesion; Chromosome -17 involved
Lytic Lesion
Adult Middle ● 3RD COMMONEST ● Endosteal Scalloping + Cortical ● Radio+ Chemo : Not
aged Flat Bones: ● Cut Lesion is Bluish White [typical feature] Thickening Effective
CHONDRO - Vertebrae; Ribs; ● Pain+ Pathological fracture ● Expansion ē Destruction Surgery is the treatment of
SARCOMA - Girdles; ● H/O multiple Osteochondroma ● Localised Destruction choice
- Proximal Limb Bones ● Pulmonary Metastasis(CXR) may present ● Mottled appearance from
Calcification or Ossification
● Biopsy shows: Numerous
10-20 yrs ● Arise from vascular ● 4TH COMMONEST AMONG ADULT ● Onion Skin (Lamellated Periosteal Small, Round & Blue Cell
EWING’S Peak in 20s endothelium of Bone ● 2ND COMMONEST AMONG CHILDREN Reaction) ● En Bloc Resection +
Onion, moth May mentioned as Marrow ● Chromosomal Translocation Chromosome No. 11 & 22 ● Lytic Lesion ; Moth-Eaten appearance Chemotherapy
Asian in the exam ● Undifferentiated Small, ● Pain + Enlarging mass ± Associated ē Systemic Upset ● Patchy density ● Radiosensitive
paper round tumor of neural crest ● Weight loss; May be febrile ● Wide Zone of transition
origin, flat bones & Diaphysis. ● PAS statin (+) ve
● Biopsy : Blue Cells; Askin Tumor: if arises from chest wall
PNET ALL ARE SAME LIKE EWING’S BUT PRIMITIVE NEURO ECTODERMAL TUMOR SHOWS MORE NEURAL DIFFERENTIATION
Note: Green Coloured are most Important for the Final Exam
Fig: OSTEOCHONDROMA
Fig: ENCHONDROMA
Fig: Aneurysmal Bone Cyst
Fig: Paget's Disease

Fig: Giant Cell Tumor
Fig: Osteosarcoma
© Notes by Dr. Sakib (MRCS Online Preparatory Course By Nasa Khan) Page |
10
Fig: Chondrosarcoma
11
12
Fig: Ewings Sarcoma and Onion skin reaction Periosteum

13
Fig: Ewings Sarcoma and Onion skin reaction Periosteum

EWINGS TUMOR
The above picture gives mnemonic for Ewing's tumor. First let us analyse the picture.
- Note the chick and swelling of Diaphysis of Tibia with the onion.
14
- Chick says VAC VAC VAC VACA, VAC VAC VAC AV / CV.
- The chick has fat and hence PAS stain positive.
- Note the moon and star at the top,
- Radio streaming music & chick fluttering it's wings up & down to the music as represented by 2 arrow marks @ left side.
- See the melted snow below the bone and a blood vessel from the side ( left corner )
Now, this is what the picture says: Ewings –

- The chick with wings; Arises from Diaphysis, most common bone is Tibia.
- Seen in children as represented by the chick.
- Onion represents the onion peel appearance in X-rays.
- The wings going up and down ( arrows ) represent that the size of tumor increases and decreases (H/O Exacerbations &
remissions ). The moon & star represents the clinical feature that pain is worse at night.
- Radio represents that the tumor is extremely radiosensitive - therefore melts like snow.
- Spread is by blood vessels and lymphatics.
- And what the chick says is the chemotherapy regimen - VAC ( Vincristine, Adriamycin, Cyclophosphamide ), VACA ( VAC + Actinomycin ), AV alternating with CV
Brown Tumour
Brown tumors are tumors of bone that arise in settings of excess osteoclast activity, such as Hyperparathyroidism,
Consist of fibrous tissue, woven bone and supporting vasculature, but no matrix.
They are radiolucent on x-ray.
The osteoclasts consume the trabecular bone that osteoblasts lay down and this front of reparative bone deposition followed by additional resorption can expand beyond the
usual shape of the bone, involving the periosteum thus causing bone pain.
They appear brown because haemosiderin is deposited at the site.
This lesion is indistinguishable from a giant cell tumor of bone sharing similar characteristics of a reasonably well-defined expansile lesion in the metaphyseal-epiphyseal
region with destruction down to the articular margin and with a coarse sponge-like appearance due to ridging of the periosteal shell surrounding this
If the radiologist gave the clinician the proper differential diagnosis in this case of giant cell tumor, brown tumor, or aneurysmal bone cyst, a simple lab test confirming high
calcium and low phosphorus levels would lead to the correct nature of underlying hyperparathyroidism in this case.
15
BONE PATHOLOGY- 2
● SERO NEGATIVE SPONDYLO-ARTHROPATHIES ARE: RAP(P)E -
R - Reiters syndrome
A - Ankylosing spondylitis
P - Psoriatic arthropathy
P - Pseudogout
E - Enteropathic arthritis (Chrons Disease, Ulcerative Colitis, Behchets Syndrome)
● Rheumatoid arthritis – stiffness R aises after R est or wo R st @ R est ,
and In Osteoarthritis, stiffness worst @ the end of the day
Inflamed synovium (pannus): this eventually fills the joint space and impinges on joint surfaces.Pannus formation and
release of destructive enzymes and cytokines destroy underlying cartilage
Figures: Osteoarthritis
● Polymyelgia Rheumatica(PMR) all features are like Rheumatoid arthritis, difference is RF, ANA (+)ve
● Frozen Shoulder: FEAR: (The manipulation of shoulder has to be carried out in this sequence)
Flexion
Extension
Abduction, followed by Adduction ( Remember Ab comes before Ad in dictionary)
Rotations (Internal & external)
● Achondroplasia is the commonest cause of short limbed dwarfism. Most cases are autosomal dominant.
● Ankylosing spondylitis kyphosis and HLA – B27 (+)ve
BONE LESIONS (From Netter)
DIAPHYSEAL LESIONS "FEMALE"

• F ibrous dysplasia
• E osinophilic granuloma
• M etastasis
• A damantinoma
• L eukaemia, Lymphoma
• E wing's sarcoma
BONE TUMOURS OF DIAPHYSIS: A LEMON

A -ADMANTINOMA
L-LYMPHOMA
E- EWING SARCOMA
M-MULTIPLE MYELOMA
O-OSTEOID OSTEOMA
N-NEUROBLASTOMA
LYTIC BONE LESIONS: FOG MACHINES

• F ibrous Dysplasia
• O steoblastoma
• G iant Cell Tumor
• M etastasis / Myeloma
• A neurysmal Bone Cyst
• C hondroblastoma / Chondromyxoid Fibroma
• H yperparathyroidism (brown tumors) / Hemangioma
• I nfection
• N on-ossifying Fibroma
• E osinophilic Granuloma / Enchondroma
• S olitary Bone Cyst
MAFFUCCI SYNDROME: BOSE

B = brain gliomas ( increased risk)
O = ovarian carcinomas ( increased risk)
S = soft tissue hemangiomas
E = enchondromatosis
● Supraspinatus tendonitis / Painful Arc Syndrome: Hand movement pain; O/E Tenderness along Anterior Edge of
Acromion
● Acute Calcific Tendinitis : Sudden onset of pain @ shoulder, tenderness but no h/o trauma, arm is held immobile
● Algodystrophy : Also known as CRPS(complex regional pain syndrome)- X-ray shows patchy rarefaction
of bone. Skin may be pale or particular area may be atrophic
● ADAMANTINOMA : Lobulated lytic area of bone(90% Tibia). Mixed Fibrous + Epithelial Stroma found
● CHONDROMALACIA : Softening of Patella articular cartilage,causing pain in ascending+ descending stairs in front
PATELLAE of knee. Also called "Runner's Knee"
● OSTEOCHONDRITIS : Small Osteocartilagenous fragment separates from one of the femoral condyle (usually
DESSICANS medial), and is rendered avascular. If loose body becomes trapped betn joint surface then
locking occurs. If its found @ Elbow Capitulum– then called PANNER’S DISEASE.
● PLANTER FASCITIS : Pain under ball of feet, tenderness along the distal edge of heel contact area
● KOHLER’S DISEASE : Osteochondritis of Navicular

● SEVERE’S DISEASE : Osteochondritis of Calcaneum
nd
● FREIDBERG’S DIS. : Osteochondritis (crushing type) of 2 MetaTarsal head
● JONES FRACTURE : # of 5th metatarsal

● METATARSALGIA : Any painful foot condition affecting the metatarsal region of foot
● CHARCOT’S JOINT : Progressive degeneration of a wt. bearing joint – a process, marked by body destruction,
bone resorption & eventual deformity (Neurotrauma or Neurovascular cause, e.g. DM)
● REITER'S SYNDROME : CUP

C onjunctivitis
U rethritis
P olyarthritis + H/O unprotected sex
● KEINBOCK’S DISEASE : Ischaemic Necrosis of Lunate
● Felty's syndrome is the ARTHRITIS in which the SPLEEN can be felt-y on palpation (splenomegaly) + neutropenia
(low WBCs count).
● RHABDOMYSARCOMA STAGES:
Stage 1 : Eye, head and/or neck, or near the sex organs (but not in bladder,prostate).
Stage 2 : <5 cm ; located not in the areas in Stage 1, not spread 2LN
Stage 3 : Stage 2 tumors >5 cm, ± LN spread
Stage 4 : Metastasis
**Radical excision is the RX of choice
● OSTEOPOROSIS : All (N) Reliable diagnostic tool is Dual Energy Absorptiometry(DEXA).

“The osteoporosis guidelines” state if a postmenopausal woman has a fracture she should be put on
bisphosphonates (there is no need for a DEXA scan).
● OSTEOSCLEROSIS : All (N), PTH raised

● O. IMPERFECTA : All (N), Alk.PO4 raised
● PAGET’S : All (N), Alk.PO4 raises high; [Urine Ca++ raised, Hydroxyprolene (+)ve ]
++
● MULTIPLE MYELOMA : All (N), (Ca + PO4+ Urea) May raised
● OSTEOMALACIA : All reduced; Alk.PO4 and PTH raised; May be mentioned as Asian patient
+
RICKET’S
● METASTASIS : All raised, PTH – Normal or reduced

● P. H. P.THYROIDISM : All raised, PTH – raised
++ ++ ++
● S. H. P.THYROIDISM : All raised, [PTH highly raised], Ca – Normal (Corrected Ca , Urine Ca
raised)
● RENAL OSTEODYSTROPHY : All raised, [PTH highly raised], Ca++ reduced , Alk.PO4 – Normal
● FAMILIAL HYPOCALCIURIC : (Ca++ + PO4) raised, but Slight, Urine Ca++ reduced
HYPER CALCAEMIA
● Mnemonic for the causes of hypercalcaemia: CHIMPANZEES
C alcium supplementation
H yperparathyroidism
I atrogentic (Drugs: Thiazides)
M ilk Alkali syndrome
P aget disease of the bone
A cromegaly and Addison's Disease
N eoplasia
Z olinger-Ellison Syndrome (MEN Type I)
E xcessive Vitamin D
E xcessive Vitamin A
S arcoidosis
● PTH raised in Osteosclerosis, Osteomalacia, Ricket’s, Renal Osteodystrophy, S. H. P.Thyroidism
FIG: RENAL OSTEODYSTRPHY
Fig: Primary Hyperparathyroidism
VILLOUS FAP HAMARTOMAS TUBULAR AD. FIBROMA HYPERPLASTIC /

METAPLASTIC
General
Feature o Familial o If juvenile, occurs <10yrs o Commonly multiple Rare Most common
o >100 in number o P. Jegher’s (no malignant o Usually small- may
o Tubular denomatous potential) co-exist ē carcinoma
is the commonest
Site Rectum o Colon, Rectum . Colon, arise from

submucosal layer
Physical Flat; same color like
structure Carpet like lesion Pedunculated or Hard; mobile; bowel mucosa
sessile Pedunculated
Neoplastic Neoplastic → most

chance of malignany Neoplastic; if Minimal malignant potential Rarely malignant Never undergo
among all untreated, chance of change malignant change
colorectal ca in 20 yrs
Clinical o Diarrhoea ,
Feature o Bright red blood PR bleed or prolapsing thru’
o mucous discharge anus
→ hypokalaemia
Treatment o Panproctocolectomy Only removed if troublesome
+End ileostomy; pain, bleeding /
o Colectomy hypoproteinaemia
+ileorectal
anastomosis;
o Proctocolectomy
+ileal pouch-anal
anastomosis
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Collection
MICROBIOLOGY
Phagocytosis
• Ingestion of pathogens or foreign materials by cells
• First step is opsonisation whereby the organism is coated by antibody
• Second step is adhesion to cell surface
• Third step is pseudopodial extension to form a phagocytic vacuole
• Lysosomes fuse with vacuole and degrade contents
● List of Microbes Which May Not Gm Stain Well (Gm Resistant):" These Microscopic Rascals May Look Colourless
Treponema
Mycobacteria
Rickettsia
Mycoplasma
Legionella
Chlamydia
● All cocci gm(+)ve except : Neisseria; Gono; Meningo
● All rods gm(-)ve except : Bacillus; Clostridia; Coryne-bacterium
● All pathogens are facultative anaerobes except : Clostridiua; Bacteroides (obligate anaerobes)
● Encapsulated bacteria : "Some Killers Have Nice Pretty Capsules"

S treptococcus pneumoniae
K lebsiella pneumoniae
H aemophilus influenzae
N eisseria meningitides
P seudomonas aeruginosa
C ryptococcus neoformans
Difference Between Exotoxins & Endotoxins
EXOTOXIN ENDOTOXIN
Secreted by living cell Dead cell
By both Gm bacteria Only by Gm(-)ve
Polypeptides Lipopolysacchrides; lipid A cz
toxicity
Binds with specific receptor Receptor not required
Highly toxic, enterotoxin Moderately toxic
0 0
Heat labile – destroyed >60 C Stable; not destroyed >60 C for hrs
Highly antigenic Weakly antigenic
Can be convert to toxoid Never
Controlled by xtra-chromosomal By chromosomal gene
gene
Not produce fever Fever produced by IL-1
Modes of actions are various Includes TNF & IL-1
Surgical Microbiology
An extensive topic so an overview is given here. Organisms causing common surgical infections are reasonable topics in
the examination. However, microbiology is less rigorously tested than anatomy, for example.
Staphylococcus aureus
• Facultative anaerobe
• Gram positive coccus
• Haemolysis on blood agar plates
• Catalase positive
• 20% population are long term carriers
• Exo and entero toxin may result in toxic shock syndrome and gastroenteritis respectively
• Ideally treated with penicillin although many strains now resistant through beta Lactamase production. In the UK
less than 5% of isolates are sensitive to penicillin.
• Resistance to methicillin (and other antibiotics) is mediated by the mec operon , essentially penicillin binding
protein is altered and resistance to this class of antibiotics ensues
• Common cause of cutaneous infections and abscesses
Streptococcus pyogenes
• Gram positive, forms chain like colonies, Lancefield Group A Streptococcus
• Produces beta haemolysis on blood agar plates
• Rarely part of normal skin microflora
• Catalase negative
• Releases a number of proteins/ virulence factors into host including hyaluronidase, streptokinase which allow
rapid tissue destruction
• Releases superantigens such as pyogenic exotoxin A which results in scarlet fever
• Remains sensitive to penicillin, macrolides may be used as an alternative.
Escherichia coli
• Gram negative rod
• Facultative anaerobe, non sporing
• Wide range of subtypes and some are normal gut commensals
• Some subtypes such as 0157 may produce lethal toxins resulting in haemolytic-uraemic syndrome
• Enterotoxigenic E-Coli produces an enterotoxin (ST enterotoxin) that results in large volume fluid secretion
into the gut lumen (Via cAMP activation)
• Enteropathogenic E-Coli binds to intestinal cells and cause structural damage, this coupled with a moderate
(or in case of enteroinvasive E-Coli significant) invasive component produces enteritis and large volume
diarrhoea together with fever.
• They are resistant to many antibiotics used to treat gram positive infections and acquire resistance rapidly and
are recognised as producing beta lactamases
Campylobacter jejuni
• Curved, gram negative, non sporulating bacteria
• One of the commonest causes of diarrhoea worldwide
• Produces enteritis which is often diffuse and blood may be passed

• Remains a differential for right iliac fossa pain with diarrhoea
• Self limiting infection so antibiotics are not usually advised. However, the quinolones are often rapidly effective.
Helicobacter pylori
• Gram negative, helix shaped rod, microaerophillic
• Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria
• Flagellated and mobile
• Those carrying the cag A gene may cause ulcers
• It secretes urease that breaks down gastric urea> Carbon dioxide and ammonia> ammonium>bicarbonate
(simplified!) The bicarbonate can neutralise the gastric acid.
• Usually colonises the gastric antrum and irritates resulting in increased gastrin release and higher levels of
gastric acid. These patients will develop duodenal ulcers. In those with more diffuse H-Pylori infection gastric
acid levels are lower and ulcers develop by local tissue damage from H-Pylori- these patients get gastric ulcers.
• Diagnosis may be made by serology (approx. 75% sensitive). Biopsy urease test during endoscopy probably
the most sensitive.
• In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk MALT lymphoma
● Pelvic Inflammatory Disease (PID) is commonly due to Neisseria gonorrhoea;

Post-Hysterectomy sepsis is commonly due to E. coli or Bacteroides fragilis ; if both are present in answer keys
then give e. coli as answer
● E. coli is the most common urinary pathogen

n
● E. coli is the common organism urine C/S iboth hospital & community. However, in hospital, esp. ē instrumenta &
catheters, most likely organism is P. aeruginosa .
● ICU – MDR infection –Acinetobacter common

● Cephalexin commonly associated ē C. difficile diarrhoea. Other agents include Clindamycin, Cephalosporins &
Augmentin. Rx is ē oral metronidazole or vancomycin.
● Any operation in perforated bowel has an high risk of infection commonly by Gm(+)ve bacilli & anaerobes (specially
by E.coli)
● Prosthesis, grafts infection – Staph. epidermidis – common

● rheumatic MS + endocarditis cz = Streptococcus viridans
● Usually after abdominal / gynaecological operation- anaerobic infection occurs by commonly Bacteroids Fragilis
and its β-lactamase producer and penicillin resistant.
● Common organisms responsible for bacterial peritonitis in children include E. coli, K. pneumoniae and
pseudomonas species.
● Large tonsillar infection is also called Vincent’s angina. Two bacteria involved Borrelia vincentii; Fusobacterium
fusiformi s(Gm negative rod)
● Mumps or Acute viral sialadenitis can be distinguished from other forms of acute parotitis by the absence of a
neutrophil Leucocytosis
n
● Commonest organism in acute osteomyelitis > 4 yrs is Staph. aureus. ē immuniozat osteomyelitis due2 H.
influenzae almost eradicated
● Massive Splenomegaly Causes

M alaria
M yelofibrosis
C hronic myeloid leukaemia
K ala-azar
● Following splenectomy a person is at risk of Streptococcus pneumoniae; H. Influenzae; N. Meningitides; E. Coli; P.
aeruginosa. Most common is Streptococcus pneumoniae- which cz life threatening infection.
● Legionella pneumophila occurs in hotels or hospitals where cooling systems or shower facilities contaminated ē
this. 50% of cases gastrointestinal (GI) symptoms; tachypnoea,dry cough that later productive
VACCINE TYPES
Streptococci
Streptococci may be divided into alpha and beta haemolytic types

{Alpha haemolytic streptococci}
The most important alpha haemolytic streptococcus is Streptococcus pneumoniae (pneumococcus). Pneumococcus is a
common cause of pneumonia, meningitis and otitis media. Another clinical example is Streptococcus viridans
{Beta haemolytic streptococci}
These can be subdivided into group A and B
Group A
• most important organism is Streptococcus pyogenes
• responsible for erysipelas, impetigo, cellulitis, type 2 necrotizing fasciitis and pharyngitis/tonsillitis
• immunological reactions can cause rheumatic fever or post-streptococcal glomerulonephritis
• erythrogenic toxins cause scarlet fever
Group B
• Streptococcus agalactiae may lead to neonatal meningitis and septicaemia
MRSA
Methicillin-resistant Staphylococcus aureus (MRSA) was one of the first organisms which highlighted the dangers of
hospital-acquired infections.
Who should be screened for MRSA?

• All patients awaiting elective admissions (exceptions include day patients having terminations of pregnancy and
ophthalmic surgery. Patients admitted to mental health trusts are also excluded)
• In the UK all emergency admissions are currently screened
How should a patient be screened for MRSA?

• nasal swab and skin lesions or wounds
• the swab should be wiped around the inside rim of a patient's nose for 5 seconds
• the microbiology form must be labelled 'MRSA screen'
Suppression of MRSA from a carrier once identified

• nose: mupirocin 2% in white soft paraffin, tds for 5 days
• skin: chlorhexidine gluconate, od for 5 days. Apply all over but particularly to the axilla, groin and perineum
The following antibiotics are commonly used in the treatment of MRSA infections:
• vancomycin
• teicoplanin
Some strains may be sensitive to antibiotics listed below but they should not generally be used alone as
resistance may develop:
• rifampicin
• macrolides
• tetracyclines
• aminoglycosides
• clindamycin
Relatively new antibiotics such as linezolid, quinupristin/dalfopristin combinations and tigecycline have activity
against MRSA but should be reserved for resistant cases
● MRSA Rx Protocol
st
- 1 combination : Rifampicin + Vanco+ Teicoplanin
- Macrolids (Erythro; Azithro; Clarithro; Roxythro)

- Trimethoprim
- Na-fusidate
- Aminoglycoside(Amikacin; Gentamycin; Neomycin; Kanamycin)
- Last combination : Linezolid + Quinopristin / Dalfopristin
Meleney's Gangrene and Necrotising Fasciitis
Necrotising fasciitis
• Advancing soft tissue infection associated with fascial necrosis
• Uncommon, but can be fatal
• In many cases there is underlying background immunosuppression e.g. Diabetes
• Caused by polymicrobial flora (aerobic and anaerobic) and MRSA is seen increasingly in cases of necrotising
fasciitis
• Streptococcus is the commonest organism in isolated pathogen infection (15%)
Meleneys gangrene
• Meleneys is a similar principle but the infection is more superficially sited than necrotising fasciitis and often
confined to the trunk
Fournier gangrene
• Necrotising fasciitis affecting the perineum
• Polymicrobial with E.coli and Bacteroides acting in synergy
Clinical features
Fever, Pain
Cellulitis, Oedema
Induration, Numbness
Late findings
Purple/black skin discolouration
Blistering
Haemorrhagic bullae, Crepitus
Dirty Dishwater fluid discharge
Septic shock
Diagnosis is mainly clinical
Management
• Radical surgical debridement forms the cornerstone of management
• Sterile dressing is used to dress the wound
• Reconstructive surgery is considered once the infection is completely treated
Actinomycosis
- Chronic, progressive granulomatous disease caused by filamentous gram positive anaerobic bacteria from the
Actinomycetaceae family.
- Actinomyces are commensal bacteria that become pathogenic when a mucosal barrier is breached.
- The disease most commonly occurs in the head and neck, although it may also occur in the abdominal cavity
and in the thorax.
- The mass will often enlarge across tissue planes with the formation of multiple sinus tracts.
- Abdominopelvic actinomycosis occurs most frequently in individuals that have had appendicitis (65%) cases.
- The presence of chronic sinuses together with gram positive organisms and sulphur granules is highly
suggestive of Actinomycosis
- Actinomycosis abscess contains sulphur granules
Pathology
• On histological examination gram positive organisms and evidence of sulphur granules.
• Sulphur granules are colonies of organisms that appear as round or oval basophilic masses.
• They are also seen in other conditions such as nocardiosis.
Treatment
• Long term antibiotic therapy usually with penicillin.
Surgical resection is indicated for extensive necrotic tissue, non healing sinus tracts, abscesses or where biopsy is
needed to exclude malignancy.
Bacterial Gastroenteritis
Causative organisms
Campylobacter • Most common cause of acute infective diarrhoea

jejuni • Spiral, gram negative rods
• Usually infects terminal ileum but spreads to involve colon and rectum. Local
lymphadenopathy is common
• May mimic appendicitis as it has marked right iliac fossa pain
• Reactive arthritis is seen in 1-2% of cases
Shigella spp. • Members of the enterobacteriaceae

• Gram negative bacilli
• Clinically causes dysentery
• Shigella soneii is the commonest infective organism (mild illness)
• Usually self limiting, ciprofloxacin may be required if individual is in a high risk group
Salmonella spp • Facultatively anaerobic, gram negative, enterobacteriaceae

• Infective dose varies according to subtype
• Salmonellosis: usually transmitted by infected meat (especially poultry) and eggs
E. coli • Enteropathogenic
• Enteroinvasive: dysentery, large bowel necrosis/ulcers
• Enterotoxigenic: small intestine, travelers diarrhoea
• Enterohaemorrhagic: 0157, cause a haemorrhagic colitis, haemolytic uraemic syndrome
and thrombotic thrombocytopaenic purpura
Yersinia • Gram negative, coccobacilli

enterocolitica
• Enterocolitis, acute mesenteric lymphadenitis or terminal ileitis

• Differential diagnosis acute appendicitis
• May progress to septicaemia in susceptible individuals
• Usually sensitive to quinolone or tetracyclines
Vibrio cholera • Short, gram negative rods

• Transmitted by contaminated water, seafood
• Symptoms include sudden onset of effortless vomiting and profuse watery diarrhoea
• Correction of fluid and electrolyte losses are the mainstay of treatment
• Most cases will resolve, antibiotics are not generally indicated
Helicobacter Pylori
Infection with Helicobacter Pylori is implicated in many cases of duodenal ulceration and up to 60% of patients with
gastric ulceration.
• Gram negative, helix shaped rod, microaerophillic
• Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria
• Flagellated and mobile
• Those carrying the cag A gene may cause ulcers
• It secretes urease that breaks down gastric urea> Carbon dioxide and ammonia> ammonium>bicarbonate
(simplified!) The bicarbonate can neutralise the gastric acid.
• Usually colonises the gastric antrum and irritates resulting in increased gastrin release and higher levels of
gastric acid. These patients will develop duodenal ulcers. In those with more diffuse H-Pylori infection gastric
acid levels are lower and ulcers develop by local tissue damage from H-Pylori- these patients get gastric ulcers.
• Diagnosis may be made by serology (approx. 75% sensitive). Biopsy urease test during endoscopy probably
the most sensitive.
• In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk MALT lymphoma.
Clostridium difficile
Clostridium difficile is a Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes
intestinal damage leading to a syndrome called pseudomembranous colitis. Clostridium difficile develops when the
normal gut flora are suppressed by broad-spectrum antibiotics. Clindamycin is historically associated with causing
Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation
cephalosporins are now the leading cause of Clostridium difficile.
Features
• Diarrhoea
• Abdominal pain
• A raised white blood cell count is characteristic
• If severe, toxic megacolon may develop
Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool
Management
• First-line therapy is oral metronidazole for 10-14 days
• If severe, or not responding to metronidazole, then oral vancomycin may be used
• For life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used
Salmonella
The Salmonella group contains many members, most of which cause diarrhoeal diseases. They are aerobic, Gram
negative rods which are not normally present as commensals in the gut.
Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They
are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia. Features:
• initially systemic upset as above
• relative bradycardia
• abdominal pain, distension
• constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
• rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
Possible complications include:

• osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
• GI bleed/perforation
• meningitis
• cholecystitis
• chronic carriage (1%, more likely if adult females)
Diarrhoea
World Health Organisation definitions
Diarrhoea: > 3 loose or watery stool per day
Acute diarrhoea < 14 days
Chronic diarrhoea > 14 days
Acute Diarrhoea
Gastroenteritis May be accompanied by abdominal pain or nausea/vomiting
Diverticulitis Classically causes left lower quadrant pain, diarrhoea and fever
Antibiotic therapy More common with broad spectrum antibiotics

Clostridium difficile is also seen with antibiotic use
Constipation causing overflow A history of alternating diarrhoea and constipation may be given
May lead to faecal incontinence in the elderly
Chronic Diarrhoea
Irritable bowel Extremely common. The most consistent features are abdominal pain, bloating and change in bowel
syndrome habit. Patients may be divided into those with diarrhoea predominant IBS and those with constipation
predominant IBS.
Features such as lethargy, nausea, backache and bladder symptoms may also be present
Ulcerative Bloody diarrhoea may be seen. Crampy abdominal pain and weight loss are also common. Faecal
colitis urgency and tenesmus may occur
Crohn's disease Crampy abdominal pains and diarrhoea. Bloody diarrhoea less common than in ulcerative colitis.
Other features include malabsorption, mouth ulcers perianal disease and intestinal obstruction
Colorectal Symptoms depend on the site of the lesion but include diarrhoea, rectal bleeding, anaemia and
cancer constitutional symptoms e.g. Weight loss and anorexia
Coeliac disease • In children may present with failure to thrive, diarrhoea and abdominal distension
• In adults lethargy, anaemia, diarrhoea and weight loss are seen. Other autoimmune
conditions may coexist
Other conditions associated with diarrhoea include:

• Thyrotoxicosis
• Laxative abuse
• Appendicitis with pelvic abscess or pelvic appendix
• Radiation enteritis
Diagnosis
Stool culture
Abdominal and digital rectal examination
Consider colonoscopy (radiological studies unhelpful)
Thyroid function tests, serum calcium, anti endomysial antibodies, glucose
Gastro intestinal parasitic infections
Common infections
Enterobiasis • Due to organism Enterobius vermicularis

• Common cause of pruritus ani
• Diagnosis usually made by placing scotch tape at the anus, this will trap eggs that can
then be viewed microscopically
• Treatment is with mebendazole
Ancylostoma • Hookworms that anchor in proximal small bowel

duodenale • Most infections are asymptomatic although may cause iron deficiency anaemia
• Larvae may be found in stools left at ambient temperature
• Infection occurs as a result of cutaneous penetration, migrates to lungs, coughed up and
then swallowed
Ascariasis • Due to infection with roundworm Ascaris lumbricoides

• Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to
lungs, coughed up and swallowed, cycle begins again
• Diagnosis is made by identification of worm or eggs within faeces

Strongyloidiasis • Due to infection with Strongyloides stercoralis

• Rare in west
• Organism is a nematode living in duodenum of host
• Initial infection is via skin penetration. They then migrate to lungs and are coughed up
and swallowed. Then mature in small bowel are excreted and cycle begins again
• An auto infective cycle is also recognised where larvae will penetrate colonic wall
• Individuals may be asymptomatic, although they may also have respiratory disease and
skin lesions
• Diagnosis is usually made by stool microscopy
• In the UK mebendazole is used for treatment
Cryptosporidium • Protozoal infection

• Organisms produce cysts which are excreted and thereby cause new infections
• Symptoms consist of diarrhoea and cramping abdominal pains. Symptoms are worse in
immunosuppressed people
• Cysts may be identified in stools
• Treatment is with metronidazole
Giardiasis • Diarrhoeal infection caused by Giardia lamblia (protozoan)

• Infections occur as a result of ingestion of cysts
• Symptoms are usually gastrointestinal with abdominal pain, bloating and passage of soft
or loose stools
• Diagnosis is by serology or stool microscopy
• First line treatment is with metronidazole
Hydatid cysts
Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm
parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple small daughter cysts. These
cysts are allergens which precipitate a type 1 hypersensitivity reaction.
Clinical features are as follows:

• Up to 90% cysts occur in the liver and lungs
• Can be asymtomatic, or symptomatic if cysts > 5cm in diameter
• Morbidity caused by cyst bursting, infection and organ dysfunction (biliary, bronchial, renal and cerebrospinal
fluid outflow obstruction)
• In biliary ruputure there may be the classical triad of; biliary colic, jaundice, and urticaria
CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts.
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and contents sterilised first).
Wuchereria bancrofti
• Parasitic filarial nematode
• Accounts for 90% of cases of filariasis
• Usually diagnosed by blood smears
• Usually transmitted by mosquitos
• Treatment is with diethylcarbamazine
Trypanosoma Cruzi
• Protozoan
• Causes Chagas disease
• Carried by bugs which infect the skin whilst feeding
• Penetrate through open wounds and mucous membranes
• Intracellular proliferation
• Major infective sites include CNS, intestinal myenteric plexus, spleen, lymph nodes and cardiac muscle
• Chronic disease is irreversible, nifurtimox is used to treat acute infection
Oncoviruses
• Viruses which cause cancer

• These may be detected on blood test and prevented by vaccine
These are the main types of oncoviruses and their diseases:
Oncovirus Cancer
Epstein-Barr virus Burkitt's lymphoma

Hodgkin's lymphoma
Infectious mononeucleosis
Post transfusion lymphoma
Nasopharyngeal carcinoma
Human papillomavirus 16/18 Cervical cancer

Anal cancer
Penile cancer
Vulval cancer
Oropharyneal cancer
Human herpes virus 8 Kaposi's sarcoma
Hepatitis B virus Hepatocellular carcinoma
Hepatitis C virus Hepatocellular carcinoma
Human T-lymphotropic virus 1 Tropical spastic paraparesis

Adult T cell leukaemia
● DNA VIRUSES : PHAPP

P ox
H erpes
H BV
A deno
P apo
P arvo
● ONCOGENIC RNA VIRUS : HCV & Human T-cell virus; rest are oncogenic DNA.
Hepatitis B
Hepatitis B is a double-stranded DNA virus and is spread through exposure to infected blood or body fluids, including
vertical transmission from mother to child. The incubation period is 6-20 weeks.
Immunisation against hepatitis B
• Contains HBsAg absorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using
recombinant DNA technology
• Most schedules give 3 doses of the vaccine with a recommendation for a one-off booster 5 years following the
initial primary vaccination
• At risk groups who should be vaccinated include: healthcare workers, intravenous drug users, sex workers,
close family contacts of an individual with hepatitis B, individuals receiving blood transfusions regularly, chronic
kidney disease patients who may soon require renal replacement therapy, prisoners, chronic liver disease
patients
• Around 10-15% of adults fail to respond or respond poorly to 3 doses of the vaccine. Risk factors include age
over 40 years, obesity, smoking, alcohol excess and immunosuppression
• Testing for anti-HBs is only recommended for those at risk of occupational exposure (i.e. Healthcare workers)
and patients with chronic kidney disease. In these patients anti-HBs levels should be checked 1-4 months after
primary immunization. The table below shows how to interpret anti-HBs levels:
Anti-HBs level Response

(mIU/ml)
> 100 Indicates adequate response, no further testing required. Should still receive booster at 5 years
10 - 100 Suboptimal response - one additional vaccine dose should be given. If immunocompetent no further
testing is required
< 10 Non-responder. Test for current or past infection. Give further vaccine course (i.e. 3 doses again) with
testing following. If still fails to respond then HBIG would be required for protection if exposed to the
virus
Complications of hepatitis B infection

• Chronic hepatitis (5-10%)
• Fulminant liver failure (1%)
• Hepatocellular carcinoma
• Glomerulonephritis
• Polyarteritis nodosa
• Cryoglobulinaemia
Management of hepatitis B
• Pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of
chronic carriers. A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-
Asian, HIV negative, high degree of inflammation on liver biopsy
• However, due to the side-effects of pegylated interferon it is now used less commonly in clinical practice. Oral
antiviral medication is increasingly used with an aim to suppress viral replication (not in dissimilar way to
treating HIV patients)
• Examples include Lamivudine, Tenofovir and Entecavir
Acute infection : HBsAg (+)ve & disaapears after 3 months @ this point anti-HBsAg
Ab(+)ve & indicates immunity
Immunity + previous infection : Anti-HBsAg Ab(+)ve
Carrier status : HBsAg (+)ve in the blood > 6 months from onset of infection
Progression to chronic Infection : HBeAg and HBsAg (+)ve in blood continuously – indicates continuing
infection
Viral Replication & high infectivity : Anti-HBe Ag (+)ve
Seroconverted & infectivity is lower : Anti-HBe Ab (+)ve
**HBeAg will also be seen early, and also disappears by 3 months, after which anti-HbeAg antibodies
will be seen**
Hepatitis C
Hepatitis C is likely to become a significant public health problem in the UK in the decade. It is thought around 200,000
people are chronically infected with the virus. At risk groups include intravenous drug users and patients who received a
blood transfusion prior to 1991 (e.g. haemophiliacs).
Transmission
• the risk of transmission during a needle stick injury is about 2%
• the vertical transmission rate from mother to child is about 6%
• breast feeding is not contraindicated in mothers with hepatitis C
• the risk of transmitting the virus during sexual intercourse is probably less than 5%
Features
• after exposure to the hepatitis C virus less than 20% of patients develop an acute hepatitis
Complications
• chronic infection (80-85%) - only 15-20% of patients will clear the virus after an acute infection and hence the
majority will develop chronic hepatitis C
• cirrhosis (20-30% of those with chronic disease)
• hepatocellular cancer
• cryoglobulinaemia
Management of chronic infection

• currently a combination of pegylated interferon-alpha and ribavirin are used
• up to 55% of patients successfully clear the virus, with success rates of around 80% for some strains
Complications of treatment
• ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of
stopping ribavirin as it is teratogenic
• interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia
HIV testing
HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever type illness.
Increased symptomatic severity is associated with poorer long term prognosis. It typically occurs 3-12 weeks after
infection
Features
• sore throat
• lymphadenopathy
• malaise, myalgia, arthralgia
• diarrhoea
• maculopapular rash
• mouth ulcers
• rarely meningoencephalitis
Diagnosis
• antibodies to HIV may not be present
• HIV PCR and p24 antigen tests can confirm diagnosis
HIV antibody test
• most common and accurate test
• usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory
Western Blot Assay
• most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
p24 antigen test
• usually positive from about 1 week to 3 - 4 weeks after infection with HIV
• sometimes used as an additional screening test in blood banks
Tuberculosis
Tuberculosis (TB) is an infection caused by Mycobacterium tuberculosis that most commonly affects the lungs.
Understanding the pathophysiology of TB can be difficult - the key is to differentiate between primary and secondary
disease.
Primary tuberculosis
A non-immune host who is exposed to M. tuberculosis may develop primary infection of the lungs. A small lung lesion
known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages. The combination of a
Ghon focus and hilar lymph nodes is known as a Ghon complex
In immunocompotent people the intially lesion usually heals by fibrosis. Those who are immunocompromised may
develop disseminated disease (miliary tuberculosis).
Secondary (post-primary) tuberculosis

If the host becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in
the apex of the lungs and may spread locally or to more distant sites. Possible causes of immunocomprise include:
• immunosuppressive drugs including steroids
• HIV
• malnutrition
The lungs remain the most common site for secondary tuberculosis. Extra-pulmonary infection may occur in the following
areas:
• central nervous system (tuberculous meningitis - the most serious complication)
• vertebral bodies (Pott's disease)
• cervical lymph nodes (scrofuloderma)
• renal
• gastrointestinal tract
Tuberculosis pathology
• Is a form of primary chronic inflammation, caused by the inability of macrophages to kill the Mycobacterium
tuberculosis.
• The macrophages often migrate to regional lymph nodes, the lung lesion plus affected lymph nodes is referred
to as a Ghon complex.
• This leads to the formation of a granuloma which is a collection of epithelioid histiocytes.
• There is the presence of caseous necrosis in the centre.
• The inflammatory response is mediated by a type 4 hypersensitivity reaction.
• In healthy individuals the disease may be contained, in the immunocompromised disseminated (miliary TB) may
occur.
Diagnosis
• Waxy membrane of mycobacteria prevents binding with normal stains. Ziehl - Neelsen staining is typically used.
• Culture based methods take far longer.
Risk factors for developing active tuberculosis include:

• silicosis
• chronic renal failure
• HIV positive
• solid organ transplantation with immunosuppression
• intravenous drug use
• haematological malignancy
• anti-TNF treatment
• gastrectomy
IMMUNOLOGY
● GELL & COOMBS CLASSIFICATION OF HYPERSENSITIVITY REACTIONS: ACIDS

Type I : A naphylaxis (Ag reacts ē IgE)
Type II : C ell-bound / Ab mediated; cytotoxic-mediated (IgG/IgM reacts with antigen on cell surface)
Type III : I mmune-complx mediated (free Ag-Ab i.e IgG/IgM combines in presence of complemnt &
precipitate as immune cmplx)
Type IV : D elayed hypersensitivity /cell mediated (sensitized T-lymphocytes stimulated by appropriate Ag)
Type V : S timulatory (some IgG stimulates the cells against which they are directed)
● Examples:
st
Type I : (Ag react ē IgE) Anaphylactic shock occurs (1 line Rx is i/m Inj. Adrenaline 1: 1000 )
Anaphylactic shock(e.g. any type venom)
Atopic disease (e.g. asthma, hay fever, rhinitis);
Drug allergy, food allergy, Latex allergy
Parasitic infestations
All allergy
Type II : My GoD ! Massive Rough TIA ? (Ag react ē IgG/IgM on cell surface) Cytotoxic
My sthenia gravis
Go odpostuer’s Syndrome
D rug induced disease(mainly haematological effects)
M yxoedema
R hesus incompatibility (Ab to Rh groups are IgG)
T ransfusion reation; thyrotoxicosis (Ab to ABO groups are IgM)
I TP
A utoimmune haemolytic anaemia
Type III : SPARS (free Ag & Ab i.e IgG/IgM combines in presence of complemnt & precipitate as
immune complx)
classic pathway of complement system is activated
S LE
P olyarteritis nodosa; post-streptococcal glomerulonephritis
A rthus reaction
R eactive arthritis
S erum sickness
(**Some organic dusts can cause Localised type III reaction)
Type IV : (sensitized T-lymphocytes stimulated by appropriate Ag) Delayed type

CONTACT DERMATITIS;
Graft versus Host reaction;
Tubeculin skin reaction (AFB type All -TB,Leprosy)
** Gloves allergy always type IV** (I don’t know why !!!) several times found in exams
Type V : Grave’s Disease (some IgG stimulates the cells against which they are directed )
Hypersensitivity reactions
The Gell and Coombs classification divides hypersensitivity reactions into 4 types
Type I Type II Type III Type IV
Description Anaphylactic Cytotoxic Immune complex Delayed type
Mediator IgE IgG, IgM IgG, IgM T-cells
Antigen Exogenous Cell surface Soluble Tissues
Response time Minutes Hours Hours 2-3 days
Examples Asthma Autoimmune haemolytic anaemia Serum sickness Graft versus host disease
Hay fever Pemphigus SLE Contact dermatitis
Goodpasture's Aspergillosis
Mnemonic for the reactions and the mediators involved

ACID EGG-T
Type 1 Anaphylactic
Type 2 Cytotoxic
Type 3 Immune complex
Type 4 Delayed type
EGG T (mediators)
IgE
IgG
IgG
T cells
Type 2 hypersensitivity reactions (which includes haemolytic anaemia) are associated with formation of antibody against
cell surface antigens.
● IMMUNOGLOBULINS
- IgM – (Pentamers)
Largest (Macro)
1st line defence
st
initial response to antigen – 1 appears on B lymphocytes
restricted to plasMa;
FATCAt
F irst line defence
A nti-bacterial activity
T oxin neutralization
C omplement fixation
A gglutination
- IgG
Abundant among all (70-80%);
Both intra & extra vascular compartment,
Placenta cross (Go) possible

Longest half life (21days)
ViP CATS
S econdary immune response
A nti-bacterial activity
T oxin neutralization
C omplement fixation
Vi rus neutralization
P rotection of fetus
- IgA (Dimers) – Found in All secretion ; protection of body surface & mucous membrane;
- IgD found in very small amount,, Help in B cell activation
- IgE found in very small amount, Bind with Mast cell; Antihelminthic action
● Structures : Monomer (EDG

EDGe); Dimer (A); Pentamer (M)
● Half life in days : G21 > M10 > A6 > D3 > E2
Q. Whats does monomer,dimer and pentamer mean?

A. The most basic immunoglobulin consists of light and heavy chains to form a "Y" shape as seen by the 1st diagram
below. This is called a monomer. If two of those "Y" shaped immunoglobulins are bound together the complex is called a
dimer and if 5 are stuck together it is a pentamer as illustrated by the second diagram.
The basic immunoglobulin or Monomer
● Plasma cell secretes antibodies
● Recurrent bacterial infections suggests a lack of B-cell immune function with lack of γ-globulin
● Activation of classical complement pathway occurs in SLE due 2large number of double-stranded DNA (dsDNA)
immune complexes that form & able to fix complement.
● CCR-5 has been identified as the co-receptor with CD4 for HIV entry into T cells
Organ transplantation: immunosupressants
A number of drugs are available which help to mitigate the processes resulting in acute rejection. Cyclosporin and
tacrolimus are commonly used drugs.
Example regime
• Initial: ciclosporin/tacrolimus with a monoclonal antibody
• Maintenance: ciclosporin/tacrolimus with MMF or sirolimus
• Add steroids if more than one steroid responsive acute rejection episode
● Mycophenolate
• Organ rejection prophylaxis induction agent
• (-) Purin sythesis → (-) B & T Lymphocyte proliferation
• Side-effects: GI and marrow suppression
● METHOTREXATE
• Antimetabolite
• Interferes with DNA synthesis, repair
• Interferes Cellular replication.
• Can be administered @ prophylaxis of acute graft versus host disease.
● Cyclosporin
• Inhibit IL-2 production in an activated T-cell;
• Nephrotoxic
• Adverse Effect NH4
o N ephrotoxicity
o H epatotoxicity
o H TN
o H irsutism
o H yperplasia Gum
Azathioprine
• Metabolised to form 6 mercaptopurine which inhibits DNA synthesis and cell division
• Side effects include myelosupression, alopecia and nausea
Tacrolimus
• Lower incidence of acute rejection compared to ciclosporin
• Also less hypertension and hyperlipidaemia
• However, high incidence of impaired glucose tolerance and diabetes
Sirolimus (rapamycin)
• Blocks T cell proliferation by blocking the IL-2 receptor
• Can cause hyperlipidaemia
Monoclonal antibodies
• Selective inhibitors of IL-2 receptor
• Daclizumab
• Basilximab
If rejection starts then,

1st line Rx : Methylprednisolone
nd
2 line Rx : Anti-Thrombocyte Globulin(ATG);
Monoclonal Ab
Organ Transplant
A number of different organ and tissue transplants are now available. In many cases an allograft is performed, where an
organ is transplanted from one individual to another. Allografts will elicit an immune response and this is one of the main
reasons for organ rejection.
Graft rejection occurs because allografts have allelic differences at genes that code immunohistocompatability complex
genes. The main antigens that give rise to rejection are:
• ABO blood group
• Human leucocyte antigens (HLA)
• Minor histocompatability antigens
ABO Matching
ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies to other groups.
Group O donors can give organs to any type of ABO recipient whereas group AB donor can only donate to AB recipient.
HLA System
The four most important HLA alleles are:
• HLA A
• HLA B
• HLA C
• HLA DR
● HLA ANTIGEN (located on chromosome 6)

Class I HLA antigen : Cell lysis by CD8 lymphocytes (virtually present all nucleated cell & platelets)
Class II HLA antigen : CD4 lymphocyte activation (present in monocyte, macrophage, B-cell, dendritic &
Langerhans cell)
● No HLA matching is required for Liver, Heart or Heart / Lung transplantation
An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, four each = 8
alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLA mismatching. However,
the greater the number of mismatches the worse the long term outcome will be. T lymphocytes will recognise antigens
bound to HLA molecules and then will then become activated. Clonal expansion then occurs with a response directed
against that antigen.
Surgical overview-Renal transplantation

A brief overview of the steps involved in renal transplantation is given.
Patients with end stage renal failure who are dialysis dependent or likely to become so in the immediate future are
considered for transplant. Exclusion criteria include; active malignancy, old age (due to limited organ availability).
Patients are medically optimised.
Donor kidneys, these may be taken from live related donors and close family, members may have less HLA mismatch
than members of the general population. Laparoscopic donor nephrectomy further minimises the operative morbidity for
the donor. Other organs are typically taken from brain dead or dying patients who have a cardiac arrest and in whom
resuscitation is futile. The key event is to minimise the warm ischaemic time in the donor phase.
The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron immediately prior to
implantation and factors such as accessory renal arteries and vessel length are assessed and managed.
For first time recipients the operation is performed under general anaesthesia. A Rutherford-Morrison incision is made on
the preferred side. This provides excellent extraperitoneal access to the iliac vessels. The external iliac artery and vein
are dissected out and following systemic heparinisation are cross clamped. The vein and artery are anastamosed to the
iliacs and the clamps removed. The ureter is then implanted into the bladder and a stent is usually placed to maintain
patency. The wounds are then closed and the patient recovered from surgery.
In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular necrosis and this tends to
resolve.
Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic twin transplant (live
donor) may survive as long as 25 years.
Types of organ rejection
• Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO incompatibility).
• Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular
lesions.
• Chronic. Occurs after the first 6 months. Vascular changes predominate.
Hyperacute
Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility and HLA Class I
incompatible transplants will all fare worse in long term.
Acute
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of transplanted organ are
susceptible and it may occur in up to 50% cases.
Chronic
Again all transplants with HLA mismatch may suffer this fate. acute rejections and other immunosensitising events all
increase the risk. Vascular changes are most prominent with myointimal proliferation leading to organ ischaemia. Organ
specific changes are also seen such as loss of acinar cells in pancreas transplants and rapidly progressive coronary
artery disease in cardiac transplants.
● TRANSPLANT REJECTION
Hyperacute :- Occurs ē in 24hrs
Antibody mediated
Reaction from pre-existing Ab 2the transplanted tissue
Accelerated :- Upto a week after transplantation

Cell-mediated (Delayed hypersensitivity & Cytotoxicity)
Acute :- Occurs betn a week & 100days

Cellular immunity mediated; a result of HLA type mismatch
Mild : Intensity of infiltrate (+)ve
Moderate: Mild + Severe Tubulitis; Intimal Arteritis
Severe : Moderate + Necrosis of muscle cells
Chronic :- Occurs ē in months to years after transplant

Humoral system mediated.
● GRAFT REJECTION (from eMRCS Notes )

TYPE PATHOLOGY MECHANISM Rx
Hyperacute Thrombosis ; - Recepient’s Preformed None
(mins-hrs) necrosis Ab & complement
n
ē in 24hrs activat (type-II) against
MHC–I or HLA–I -
Expressed by donor ē
IgG
Acute Vasculitis ↑ immunosuppression
vascular(5- T & B lymphocytes & Ab
30days)
If within
6months
Acute Cellular CD4 & CD8 cells (type-IV) ↑Immunosuppression
n
cellular (5- infiltrat
30days)
If within
6months
Chronic Fibrosis & Immune & non-immune Minimize drug toxicity,
allograft scarring mechanism or control of HTN &
failure Ab & cell-mediated hyperlipidaemia
(>30days) effector mechanism
● Post renal transplant Acute rejection + hypoalbuminaemia, proteinria, genertalised edema + biopsy shows IgM
deposits in glomerulus = Dx is Focal segmental glomerulosclerosis,Usually found within 1wk
Renal transplant:HLA typing and graft failure
The human leucocyte antigen (HLA) system is the name given to the major histocompatibility complex (MHC) in humans.
It is coded for on chromosome 6.
Some basic points on the HLA system

• class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
• when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR >
B>A
Graft survival
1 year = 90%, 10 years = 60% for cadaveric transplants
1 year = 95%, 10 years = 70% for living-donor transplants
Tumour necrosis factor
Tumour necrosis factor (TNF) is a pro-inflammatory cytokine with multiple roles in the immune system
TNF is secreted mainly by macrophages and has a number of effects on the immune system, acting mainly in a
paracrine fashion:
• activates macrophages and neutrophils
• acts as costimulator for T cell activation
• key mediator of bodies response to Gram negative septicaemia
• similar properties to IL-1
• anti-tumour effect (e.g. phospholipase activation)
TNF-alpha binds to both the p55 and p75 receptor. These receptors can induce apoptosis. It also cause activation of
NFkB
Endothelial effects include increase expression of selectins and increased production of platelet activating factor, IL-1
and prostaglandins
TNF promotes the proliferation of fibroblasts and their production of protease and collagenase. It is thought fragments of
receptors act as binding points in serum
Systemic effects include pyrexia, increased acute phase proteins and disordered metabolism leading to cachexia
TNF is important in the pathogenesis of rheumatoid arthritis - TNF blockers (e.g. infliximab, etanercept) are now licensed
for treatment of severe rheumatoid
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PHARMACOLOGY
Antibiotics: Mechanism of Action
Inhibit cell wall formation

• Penicillins
• Cephalosporins
• Meropenem
• Vancomycin
• Cycloserin
Inhibit protein synthesis

• Aminoglycosides (cause misreading of mRNA) Ototoxicity is a recognised adverse reaction.
• Chloramphenicol
• Macrolides (e.g. Erythromycin)
Macrolides act by inhibiting bacterial protein synthesis. If pushed to give an answer they are bacteriostatic in
nature, but in reality this depends on the dose and type of organism being treated. Erythromycin was the first
macrolide used clinically. Newer examples include clarithromycin and azithromycin.
Adverse effects of erythromycin
• gastrointestinal side-effects are common
• cholestatic jaundice: risk may be reduced if erythromycin stearate is used
• P450 inhibitor
• Tetracyclines (effective against chlamydial pelvic infections)
• Fusidic acid
Inhibit DNA synthesis

• Quinolones (e.g. Ciprofloxacin)
• Metronidazole
• Sulphonamides
• Trimethoprim
Inhibit RNA synthesis

• Rifampicin
● Doxycycline prevents the amino-acyl t-RNA from binding to the A-site of the Ribosome
● Amikacin binds with 30s subunit of bacterial ribosome to inhibit protein synthesis
● Cephalosporins Used for prophylaxis in abdominal surgery
● Grey baby syndrome : Chloramphenicol use
Biological Agents
Agents Target Uses
Adalimumab TNF alpha inhibitor Crohns disease

Infliximab Rheumatoid disease
Etanercept
Bevacizumab Anti VEGF (anti angiogenic) Colorectal cancer

Renal
Glioblastoma
Trastuzumab HER receptor Breast cancer
Imatinib Tyrosine kinase inhibitor Gastrointestinal stromal tumours

Chronic myeloid leukaemia
Basiliximab IL2 binding site Renal transplants
Cetuximab Epidermal growth factor inhibitor EGF positive colorectal cancers
● Anti TNF-α antibody – Infliximab is given as a single infusion for clinical improvement in steroid resistant CD
● Cytarabine is a DNA polymerase inhibitor

● Irinotecan is a topoisomerase II inhibitor
Important Regiman of Chemotherapeutics
Colorectal Ca : 5FU & Folinic Acid

Breast Ca : CMFU - Cyclophosphamide, MTX, 5-FU
Testicular Ca : Etopocide; Bleomycin; Cisplatin (E radicate B all C ancer)
M/A Chemotherapeutics:
Antimetabolites : MFU (Inhibit DNA synthesis, repair, cellular replication)

MTX (Acts on cell cycle S- phase; folic acid antagonist, DHFR inhibitor);
Mercaptopurine;
5-FU(pyrimidine antagonist, thymidylate synthetase inhibitor)
Anti-tumor antibiotics : BMD (Antracycline group)

B leomycin;
M itomycin-C;
D oxyrubicin /Adriamycin( DNA repair prevent করে by acting as tropomerase-I inhibitor)
Alkylating agents : 3cm (Inhibit DNA replication)

C lorambucil;
C yclophosphamide(uses free radicles to damage DNA)
C isplatin;
M elphalan (Acts on cell cycle all phases )
** All V are vinca alkaloids** Vincristin acts on M phase
● A/E Chemotherapeutics:
Cyclophosphamide : Haemorrhagic cystitis

Cisplatin : Marrow, oto & nephro toxicity, peripheral neuropathy, optic neuritis (less common)
Doxorubicin : Cardiotoxicity
Bleomycin : Dose related lung damage
Cytosin arabinoside : Conjunctivitis & cerebelllar toxicity
MTx : Hepatic fibrosis, pneumonitis
Sulfasalazine : Reversible infertility due to oligospermia
● Oxaliplatin is an alkylating agent used to downsize the liver metatases secondary to colorectal Ca.
● 5-FU is the basis of nearly all regimens of adjuvant & palliative Rx of colorectal Ca
Local anaesthetic agents
Lidocaine
• An amide
• Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
• Hepatic metabolism, protein bound, renally excreted
• Toxicity: due to IV or excess administration. Increased risk if liver dysfunction or low protein states. Note
acidosis causes lidocaine to detach from protein binding.
• Drug interactions: Beta blockers, ciprofloxacin, phenytoin
• Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks inhibitory pathways
then blocks both inhibitory and activating pathways. Cardiac arrhythmias.
• Increased doses may be used when combined with adrenaline to limit systemic absorption.
Cocaine
• Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic purposes as a paste.
• It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to the nasal mucosa. It
has a rapid onset of action and has the additional advantage of causing marked vasoconstriction.
• It is lipophillic and will readily cross the blood brain barrier. Its systemic effects also include cardiac arrhythmias
and tachcardia.
• Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical practice.
Bupivicaine
• Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells,
which prevents depolarization.
• It has a much longer duration of action than lignocaine and this is of use in that it may be used for topical wound
infiltration at the conclusion of surgical procedures with long duration analgesic effect.
• It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails.
• The co-administration of adrenaline concentrates it at the site of action and allows the use of higher doses.
Prilocaine
• Similar mechanism of action to other local anaesthetic agents. However, it is far less cardiotoxic and is therefore
the agent of choice for intravenous regional anaesthesia e.g. Biers Block.
All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The dissociation constant
shifts in tissues that are acidic e.g. where an abscess is present and this reduce the efficacy.
Doses of local anaesthetics
Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-morbidities.
Local anaesthetic toxicity
Toxicity results from either accidental intravascular injection (rapid onset of symptoms-usually correct dose), or from
excessive dosage (slower onset). Local anaesthetic agents not only exert a membrane stabilising effect on peripheral
nerves but will also act on excitable membranes within the CNS and Heart. The inhibitory neurones in the CNS are
suppressed before the central ones. As a result the early symptoms will typically be those of circumoral paraesthesia and
tinnitus, followed by falling GCS and eventually coma.
Management of toxicity
• Stop injecting the anaesthetic agent
• High flow 100% oxygen via face mask
• Cardiovascular monitoring
• Administer lipid emulsion (Intralipid 20%) at 1.5ml/Kg over 1 minute as a bolus
• Consider lipid emulsion infusion, at 0.25ml/ Kg/ minute
Safe doses
10ml of lignocaine 1% contains 100mg of drug, this would constitute 70% of the maximum safe dose in a 50 kg patient.
Up to 7mg / kg can be administered if adrenaline is added to the solution.
Doses of local anaesthetics
Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-morbidities.
Anaesthetic agents
Agent Specific features
Propofol • Rapid onset of anaesthesia

• Pain on IV injection
• Rapidly metabolised with little accumulation of metabolites
• Proven anti emetic properties
• Moderate myocardial depression
• Widely used especially for maintaining sedation on ITU, total IV anaesthesia and for daycase
surgery
Sodium • Extremely rapid onset of action making it the agent of choice for rapid sequence of induction
thiopentone • Marked myocardial depression may occur
• Metabolites build up quickly
• Unsuitable for maintenance infusion
• Little analgesic effects
Ketamine • May be used for induction of anaesthesia

• Has moderate to strong analgesic properties
• Produces little myocardial depression making it a suitable agent for anaesthesia in those
who are haemodynamically unstable
• May induce state of dissociative anaesthesia resulting in nightmares
Etomidate • Has favorable cardiac safety profile with very little haemodynamic instability
• No analgesic properties
• Unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal
suppression
• Post operative vomiting is common
Muscle relaxants
Suxamethonium • Depolarising neuromuscular blocker

• Inhibits action of acetylcholine at the neuromuscular junction
• Degraded by plasma cholinesterase and acetylcholinesterase
• Fastest onset and shortest duration of action of all muscle relaxants
• Produces generalised muscular contraction prior to paralysis
• Adverse effects include hyperkalaemia, malignant hyperthermia and lack of
acetylcholinesterase
Atracurium • Non depolarising neuromuscular blocking drug

• Duration of action usually 30-45 minutes
• Generalised histamine release on administration may produce facial flushing, tachycardia
and hypotension
• Not excreted by liver or kidney, broken down in tissues by hydrolysis
• Reversed by neostigmine
Vecuronium • Non depolarising neuromuscular blocking drug

• Duration of action approximately 30 - 40 minutes
• Degraded by liver and kidney and effects prolonged in organ dysfunction
• Effects may be reversed by neostigmine
Pancuronium • Non depolarising neuromuscular blocker

• Onset of action approximately 2-3 minutes
• Duration of action up to 2 hours
• Effects may be partially reversed with drugs such as neostigmine
Opioids
- Combine to specific opiate receptors in the CNS (periaqueductal grey matter, limbic system, substantia gelatinosa)
- Morphine attaches to mu1 receptors
Opioid misuse
Opioids are substances which bind to opioid receptors. This includes both naturally occurring opiates such as
morphine and synthetic opioids such as buprenorphine and methadone.
Features of opioid misuse

• Rhinorrhoea
• Needle track marks
• Pinpoint pupils
• Drowsiness
Complications of intravenous opioid misuse

• Viral infection secondary to sharing needles: HIV, hepatitis B & C
• Bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising
fasciitis, groin abscess
• Pseudoaneurysm
• Venous thromboembolism
• Osteomyelitis
• Overdose may lead to respiratory depression and death
Emergency management of opioid overdose

• IV or IM naloxone: has a rapid onset and relatively short duration of action
Morphine
Strong opiate analgesic. It is a pro- type narcotic drug and its effects mediated via the µ opioid receptor. Its clinical
effects stem from binding to these receptor sites within the CNS and gastrointestinal tract. Unwanted side effects include
nausea, constipation, respiratory depression and, if used long term, addiction. It may be administered orally or
intravenously. It can be reversed with naloxone.
Diuretic agents
The diuretic drugs are divided into three major classes, which are distinguished according to the site at which they impair
sodium reabsorption: loop diuretics in the thick ascending loop of Henle, thiazide type diuretics in the distal tubule and
connecting segment; and potassium sparing diuretics in the aldosterone - sensitive principal cells in the cortical collecting
tubule.
+ +
In the kidney, sodium is reabsorbed through Na / K ATPase pumps located on the basolateral membrane. These pumps
return reabsorbed sodium to the circulation and maintain low intracellular sodium levels. This latter effect ensures a
constant concentration gradient.
Physiological effects of commonly used diuretics
Site of action Diuretic Carrier or channel inhibited Percentage of filtered

sodium excreted
Ascending limb of loop of Henle Frusemide Na+/K+ 2Cl - carrier Upt to 25%
+ -
Distal tubule and connecting segment Thiazides Na Cl carrier Between 3 and 5%
+
Cortical collecting tubule Spironolactone Na channel Between 1 and 2%
Potassium sparing diuretics

Potassium-sparing diuretics may be divided into the epithelial sodium channel blockers (amiloride and triamterene) and
aldosterone antagonists (spironolactone and eplerenone).
{Amiloride} is a weak diuretic which blocks the epithelial sodium channel in the distal convoluted tubule.
Usually given with thiazides or loop diuretics as an alternative to potassium supplementation.
{Spironolactone} is an aldosterone antagonist which acts act in the distal convoluted tubule.
Indications
• ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or
200mg are often used
• heart failure
• nephrotic syndrome
• Conn's syndrome
Gynaecomastia
Gynaecomastia describes an abnormal amount of breast tissue in males and is usually caused by an increased oestrogen:androgen ratio. It is
important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia
Causes of gynaecomastia
• physiological: normal in puberty
• syndromes with androgen deficiency: Kallman's, Klinefelter's
• testicular failure: e.g. Mumps
• liver disease
• testicular cancer e.g. Seminoma secreting hCG
• ectopic tumour secretion
• hyperthyroidism
• haemodialysis
• drugs: see below
Mnemonic for causes of gynaecomastia: METOCLOPRAMIDE

M etoclopramide
E ctopic oestrogen
T rauma skull/tumour breast, testes
O rchitis
C imetidine, Cushings
L iver cirrhosis
O besity
P araplegia
RA
A cromegaly
M ethyldopa
I soniazid
D igoxin
E thionamide
Drug causes of gynaecomastia

• spironolactone (most common drug cause)
• cimetidine
• digoxin
• cannabis
• finasteride
• oestrogens, anabolic steroids
Mnemonic for drugs causing gynaecomastia: DISCO

D igitalis
I soniazid
S pironolactone
C imentidine
O estrogen
Very rare drug causes of gynaecomastia
• tricyclics
• isoniazid
• calcium channel blockers
• heroin
• busulfan
• methyldopa
Carbimazole is not associated with gynaecomastia.
Inotropes and cardiovascular receptors
Inotrope Cardiovascular receptor action
Adrenaline α-1, α-2, β-1, β-2
Noradrenaline α-1,( α-2), (β-1), (β-2)
Dobutamine β-1, (β 2)
Dopamine (α-1), (α-2), (β-1), D-1,D-2
Minor receptor effects in brackets
Effects of receptor binding
α-1, α-2 vasoconstriction
β-1 increased cardiac contractility and HR
β-2 vasodilatation
D-1 renal and spleen vasodilatation
D-2 inhibits release of noradrenaline
Heparin
• Causes the formation of complexes between antithrombin and activated thrombin/factors 7,9,10,11 & 12
Advantages of low molecular weight heparin

• Better bioavailability
• Lower risk of bleeding
• Longer half life
• Little effect on APTT at prophylactic dosages
• Less risk of HIT
Complications
• Bleeding
• Osteoporosis
• Heparin induced thrombocytopenia (HIT): occurs 5-14 days after 1st exposure
• Anaphylaxis
In surgical patients that may need a rapid return to theatre administration of unfractionated heparin is preferred as low
molecular weight heparins have a longer duration of action and are harder to reverse.
Warfarin
Warfarin is an oral anticoagulant which inhibits the reduction of vitamin K to its active hydroquinone form, which in turn
acts as a cofactor in the formation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C
Factors that may potentiate warfarin

• Liver disease
• P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
• Cranberry juice
• Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
• Inhibit platelet function: NSAIDs
Side-effects
• Haemorrhage
• Teratogenic
• Skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary
procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration.
Thrombosis may occur in venules leading to skin necrosis.
Tamoxifen
• Synthetic partial oestrogen agonist, acts primarily by binding to the oestrogen receptor.
• Half life of 7 days, takes 4 weeks for drug to reach plasma steady state.
• Should usually be considered in patients with oestrogen receptor positive tumours (alternative agents may be
preferred in some groups).
• Although antagonistic with respects to breast tissue tamoxifen may serve as an agonist at other sites. Therefore
risk of endometrial cancer is increased, preservation of bone density and decreased cardiovascular risks.
• Climateric side effects are common, 3% stop taking the drug because of these.
• Aromatase inhibitors are an alternative class of drugs, these work by blocking the peripheral aromatization of
androgens (post menopausal women produce oestrogens in this way). They may treat cancers for which
tamoxifen is no longer effective.
Laxatives
Bulk forming laxatives
Bran
Psyllium
Methylcellulose
Osmotic laxatives
Magnesium sulphate
Magnesium citrate
Sodium phosphate
Sodium sulphate
Potassium sodium tatrate
Polyethylene glycol
Stimulant laxatives
Docusates
Bisacodyl
Sodium picosulphate
Senna
Ricinoleic acid
PHYSICAL SIGNS IN DIFFERENT MOTOR DEFICIT
C/F UMNL LMNL EPL Cerebellar Lesion Functional
Power ● Weak;
Upper Limb-extensor weaker ● Weak ● No Weakness No Weakness Give-way
Lower limb – flexor weaker Weakness
● Lesion @
● Lesion @ Pyramidal system Basal ganglia
Wasting None Yes, after interval None None None
Fasciculation None Yes, after interval None None None
Clonus Clonus(+)ve Clonus(-)ve
Tone Spastic increase(after interval) Flaccid from onset Cogwheel Normal / reduced Normal
rigidity
Reflexes Increase, usually deep Reduced / absent Normal Disarthria; Nystagmus; Normal
Intention Tremor
Planter Extensor – Babinski sign (+)ve Flexor Flexor Flexor Normal
Coordination Reduced by weakness Reduced by Normal(but Impaired Normal (may

weakness slow) be laborious)
TYPES OF BLADDER LESION CAUSES PATHOGENESIS CLINICAL FEATURES

Uninhibited ● Midbrain ● CVA, ● Micturition voluntary control
● Superior Frontal ● Head Injuries, is lost
Gyrus ● Brain Tumors ● Hesitancy, precipitancy of
evacuation is present
Reflex Complete transaction ● Transverse myelitis ● Transaction causes urine
of cord above sacral ● Trauma retention during spinal shock.
segments ● Neoplasms ● Leads to retention of residual
● Meningitis urine.
● Disseminated Sclerosis ● During recovery stage, reflex
activity begins & automatic
evacuation results.
Autonomous Sacral segment of ● Congenital : Spina Bifida, ● Loss of bladder sensation
spinal nerve Meningomyelocele ● Inability to initiate micturition
● Trauma: Gunshot, Auto accidents ● Paralysis of pariurethral
● Infective: Arachnoiditis, Radiculitis striated muscles
● Neoplasms of the cord ● Associated ē anesthesia &
● Surgery: combined perineal and absent bulbocavernous
abdominal resection reflex.
Motor Atonic Efferent fibers of the ● Poliomyelitis ● Since the sensory nerves are ● Painful distention& inability
bladder ● Polyradiculopathy intact, if bladder left alone, it to initiate micturition.
● Congenital anomalies distends and decompensates. ● Size, force of steam
● Tumor decreases and interrupted.
● Trauma ● Recurrent episodes UTI.
Sensory Atonic afferent fibers from ● Tabes dorsalis ● Loss of bladder sensation, ● Initially asymptomatic.
the bladder ● Pernicious anemia leads to over distension ● Gradually terminal dribbling
● Diabetes ● Initially normal capacity raises & later overflow incontinence.
● Disseminated sclerosis & residual urine appears.
● Syringomyelia
BIOSTTISTICS
Screening test statistics
It would be unusual for a medical exam not to feature a question based around screening test statistics. The available
data should be used to construct a contingency table as below:
TP = true positive; FP = false positive; TN = true negative; FN = false negative
Disease present Disease absent
Test positive TP FP
Test negative FN TN
The table below lists the main statistical terms used in relation to screening tests:
Sensitivity TP / (TP + FN ) Proportion of patients with the condition who have a positive test
result
Specificity TN / (TN + FP) Proportion of patients without the condition who have a negative
test result
Positive predictive value TP / (TP + FP) The chance that the patient has the condition if the diagnostic
test is positive
Negative predictive value TN / (TN + FN) The chance that the patient does not have the condition if the
diagnostic test is negative
Likelihood ratio for a positive sensitivity / (1 - How much the odds of the disease increase when a test is
test result specificity) positive
Likelihood ratio for a negative (1 - sensitivity) / How much the odds of the disease decrease when a test is
test result specificity negative
Positive and negative predictive values are prevalence dependent. Likelihood ratios are not prevalence dependent
AUDIT
Audit is a tool to show the progress or performance of a clinical area/topic. Complete audit cycle is :
Identify problem
Agree on standards
Collect data
Analyse and identify area for improvement
Implement necessary changes
Re-audit
NORMAL DISTRIBUTION *****
• Family of distributions with the same general shape.

• Symmetrical and bell-shaped
• The distribution is defined by two parameters: the mean (μ) and the standard deviation (σ). If these are known
then one knows essentially as much as if one had access to all the data *
• Mean = median = mode *

• Data are unimodal (have one highest value) *
• Area under the curve = 1
• 68% of the data fall within 1 standard deviation of the mean (34% above and 34% below) *
• 95% of the data fall within 2 (1.96) standard deviations of the mean *
• 99.7% of the data falls within 3 standard deviations (SD)of the mean *
• The standard normal distribution has a mean of 0 and SD of 1 *
TESTS FOR NORMALITY *****

• Visual inspection of the frequency distribution histogram -number of peaks and symmetry
• Use statistical packages for values of
a) Skew (A distribution is skewed if one of its tails is longer than the other) and
b) Kurtosis (degree of peakedness of a distribution). The kurtosis value for a normal

distribution is 0. Negative value -observations cluster more closely to the centre; positive
value - observations cluster less closely to the centre
• Kolmogorov-Smirnov test - principal goodness of fit test for normal and uniform data sets.
• Shapiro-Wilk test - reliable when n<50.
Limitations of normality tests *****

• Small samples almost always pass a normality test.
• With large samples, minor deviations from normality may be statistically significant. However, such small
deviations will not affect the results of most statistical tests
• Decisions on which statistical tests to use should not be based on a normality test of one data set.
PARAMETRIC & NON-PARAMETRIC TESTS *****
Parametric Tests *
Assumption
• Data are interval or ratio

• Normally distributed data (skew and kurtosis are between -1 and +1)
• Variance is equal between groups (variance can be up to 4 times different from each other, but no more than
that). This assumption only applies to independent design
Examples include:
• Independent t-test
• Paired or repeated measures t-test
• ANOVA (with posthoc tests to compare group means)
Non-Parametric Tests *
• Do not require parametric assumptions because interval data are converted to rank-ordered data. All tests
involving ranked data, i.e. data that can be put in order, are non-parametric
• Mann-Whitney U Test - one of the most powerful non-parametric tests for comparing two populations. It is used
to test the null hypothesis that two populations have identical distribution functions against the alternative
hypothesis that the two distribution functions differ only with respect to location (median), if at all
• Kruskal-Wallis Test - non-parametric test used to compare three or more samples
• Wilcoxon Signed Ranks Test - designed to test a hypothesis about the location (median) of a population
distribution. It often involves the use of matched pairs, for example, before and after data, in which case it tests
for a median difference of zero.
• Chi squared test
RISK & ODDS *****
• Attributable risk: Disease rate in exposed persons minus rate in unexposed persons
• Relative risk: ratio of rate of disease in exposed persons to rate in unexposed persons
• Attributable risk = rate of disease in unexposed persons (relative risk - 1)
• Odds *- a ratio of the probability that an event will occur versus the probability that the event will not occur =
probability / (1-probability).
• The probability of pulling a jack of hearts is 1/52 whereas the odds of pulling the jack of hearts is 1/51
• For example, if you draw cards and have 3 spades and 1 diamond, then the odds of drawing a diamond = [(1/4)/
(3/4)] = 1/3 = 0.33.
• This differs from risk (or probability): the risk drawing a diamond =
(No. of diamonds) / (total No. of cards drawn) = 1/4 = 0.25.
• Odds ratio *- the ratio of odds - the ratio of the odds of an event occurring in the exposed group versus the
unexposed group.
• Most RCTs express results as risk ratios. Case-control studies (when data are obtained retrospectively) and
meta-analyses typically report results as odds ratios
• When the primary outcome is rare, relative risk and odds ratio are ~ equal.
• Odds ratio and relative risks are presented with 95% confidence intervals, for instance, relative risk (RR = 2.5;
95% CI 0.6 to 4.4)
• When the 95% CI of the odds ratio or relative risk includes 1 (as above) then the groups are NOT statistically
significantly different (p > 0.05)
TYPES OF DATA *****
• Nominal / categorical - names or categories that do not use / require an order - eye colour, sex, ethnic group.
The values of the scale have no 'numeric' meaning
• Ordinal - numbers, names or categories
• Data are ordered - for instance, pain scores of 1-10
• The magnitude of the difference between the numbers is unimportant - the difference between a score of 1 and
2 is not necessarily the same as that between 4 and 5 - the intervals between adjacent scale values are
indeterminate
• Interval - data are ordered
• Intervals between adjacent scale values are equal with respect the attribute being measured - the difference
between 8 and 9 is the same as the difference between 80 and 81
• Ratio - data are ordered with mathematically meaningful intervals
• The ratio of the numbers is mathematically meaningful
• There is a rational zero point for the scale - zero actually means none
• Example is length / distance in cm
• Nominal and ordinal data cannot be normally distributed and their analysis require non-parametric tests
• Interval / ratio data can be analysed by both parametric and non-paremetric tests
DESCRIPTIVE STATISTICS *****
• Mean - numerical middle / average = sum of all the values divided by the number of values. Data must be
interval or ratio (continuous) *
• Median - middle of the frequency distribution - half of the data entries lie above and half below the median. Data
must be ordinal, interval or ratio *
• Mode - the value that is reported most frequently for a variable - valid for ordinal, interval or ratio data *
• Normal distribution: mean = median = mode *
• Positively skewed data: mean > median > mode *
• Negatively skewed data: mean < median < mode *
• Variance *- measure of how spread out a distribution is. However, all the negative values that are lower than the
mean will cancel out all the positive values that are greater. To avoid this, the average squared deviation of
each number from its mean is calculated. For example, for the numbers 1, 2, and 3, the mean is 2 and the
variance is:
2
σ =[ (1-2) squared + (2-2) squared + (3-2) squared ] divided by 3
• Standard Deviation - square root of the variance. It is the most commonly used measure of spread *
• Sandard error of a sample of sample size n is the sample's standard deviation divided by the square root of n .It
estimates the standard deviation of the sample mean based on the population mean *
• Confidence intervals *
If a series of samples are selected from a population and the mean of each calculated, 95% of the means would be
expected to fall within the range of two standard errors above / below the mean of these means.
This common mean would be expected to lie very close to the population mean.
The standard error of a mean provides a statement of probability about the difference between the mean of the
population and the mean of the sample.
Mean + 2(standard error) and mean - 2(standard error) give the range which has a 95% chance of including the
population mean = 95% confidence interval
Mean +/- 3(standard error) = 99.7% confidence interval
TYPES OF STUDIES *****

• Observational - Sampling the target population and simply observing which risk factors are present in each
subject.
• Can be prospective - samples consists of subjects who possess / do not posses the risk factor and the
occurrence of the primary outcome is observed.
• Can be retrospective - samples consists of subjects who have exhibited the primary outcome (cases) or have
not exhibited the primary outcome (called controls) and the investigator looks backwards to identify the risk
factors in the two groups
• Experimental study - the investigator specifies the exposure for each subject then follows the subjects to detect
the effects of the exposure
• Cohort study - observational study in which outcomes in a group of patients that received an intervention are
compared with outcomes in a similar group of patients that did not receive the intervention. Involves
identification of two groups (cohorts) of patients, one which did receive the exposure of interest, and one which
did not, and following these cohorts forward for the outcome of interest.
• Randomised study *- participants are assigned by chance to separate groups that compare different treatments;
neither the researchers nor the participants can choose which group. Using chance to assign people to groups
means that the groups will be similar and that the treatments they receive can be compared objectively.
• Blind assessment *- The investigator does not know which treatment the subject is receiving. When the subject
knows which treatment they are receiving, this is a single blind study. When neither the subject nor the
investigator know, this is a double blind study
Randomisation *****
 Process of assigning clinical trial participants to treatment groups. Gives each participant a know
chance of being assigned to any of the groups.
 Group assignment cannot be predicted in advance.
 Removes the possibility that any differences observed between the treatment groups are a
consequence of a systematic difference (or bias) between the groups due to factors other than the
intervention.
 Ensures similar levels of all risk factors (known and unknown) in each group
 Successful randomisation does not, however, guarantee perfect balance in risk factors between
groups (due to the play of chance)
 There are a variety of acceptable methods of randomisation including random number generators
and block randomisation depending on the sample size.
 Some methods may result in unequal number of patients in the study groups
 Methods of allocation such as alternate allocation to treatment group, or methods based on patient
characteristics such as date of birth, order of entry into the clinic or day of clinic attendance, are not
reliably random and are therefore not acceptable methods of randomisation
Epidemiological definitions *****
• Prevalence * - The number of people in a given population affected by a particular disease at a given time as a
proportion of the total population at risk of developing the disease - a snapshot of all existing cases at a
specified time
• Incidence *- The number of new disease cases reported in a population over a certain period of time, usually 1
year, as a proportion of the total population at risk of developing the disease
• Centile (percentile) *- any of the 99 numbered points that divide an ordered set of scores into 100 parts each of
which contains one-hundredth of the total. The 50th centile is the median
• Sensitivity *- the ability of a test to detect a disease when it is truly present. Determined as the number of true
positives divided by the sum of true positives + false negatives (True positives / True positives + False
negatives)
• Specificity *- the ability of a test to exclude the presence of a disease when it is truly not present. The proportion
of non-diseased patients for whom there is a correctly negative test. (True negatives / True negatives + False
positives)
• Positive predictive value *- the probability that an individual with a positive test has, or will develop, a particular
disease that the test is designed to detect. True positives / all positives = True positives / True positives + False
positives
• Negative predictive value *- the probability that a subject with a negative test result actually does not have the
disease. True negatives / all negatives = True negatives / True negatives + false negatives
• Numbers needed to treat *- numbers of patients needed to undergo treatment to prevent one bad outcome, as
compared to the alternative treatment arm or placebo. Numerical representation of the effectiveness of an
intervention. For example, the NNT to prevent one stroke with aspirin over two years is 38 - if you treat 38
people with aspirin for two years one stroke will be prevented that would otherwise have occurred
• Metaanalysis *- statistical method of combining the results of a number of studies in an attempt to overcome the
problem of reduced statistical power in studies with small sample sizes. Analysing the results from a group of
studies can allow more accurate estimation of effects
• Correlation *- the degree to which one phenomenon or variable is associated with or can be predicted from
another. The degree to which a linear predictive relationship exists between random variables, as measured by
a correlation coefficient (r). May be positive (but never larger than 1) - both variables increase or decrease
together OR negative (but never smaller than -1) - one variable increases when the other decreases; OR zero -
a change in one variable does not affect the other
• Regression *- technique used to establish the relationship of a dependent variable and one or more
independent variables. Regression analysis attempts to measure the degree of correlation between the
dependent and independent variables, thereby establishing the latter's predictive values. For example,
regression analysis could predict your life expectancy by combining your grandparents' age at death, whether
you smoke...
• Statistical power * - a gauge of the sensitivity of a statistical test - its ability to detect relationships. The
probability of rejecting a null hypothesis when it is false. In general, the statistical power increases with your
sample size. An index of the probability a study has of obtaining a statistically significant effect. A high power of
80 percent, or 0.8, indicates that the study - if conducted repeatedly-would produce a statistically significant
effect 80 percent of the time, if one exists. On the other hand, a power of only 0.1 means there would be a 90
percent chance that the research missed the effect-if one exists at all. Also called "Power"
• Perinatal mortality rate * - The total number of deaths of a fetus or infant between the end of the 20th week
gestation and the end of the 6th day of life in a calendar year per 1,000 total births (live and still) in the same
calendar year.
• Neonatal mortality rate * - the number of children dying under 28 days of age divided by the number of live
births that year.
• Post-neonatal death * - includes deaths after 28 days of life but before one year
• Infant mortality rate - number of live newborns dying under a year of age per one thousand live births
• Maternal mortality rate *- The number of women who die while pregnant or during the first 42 days following
termination of the pregnancy per 100,000 women of reproductive age in a given year for any cause related to or
aggravated by pregnancy, but not from accidental or incidental causes. This is irrespective of the gestation age
th
or site of pregnancy. The 10 revision of the International Classification of Diseases makes provision for
including late maternal deaths occurring between six weeks and one year afterchildbirth
• Maternal deaths are divided into Direct obstetric deaths resulting from obstetric complications of pregnancy,
from interventions, omissions or incorrect treatment; or from a chain of events resulting from any of
these.Indirect obstetric deaths result from previously existing disease or disease that developed during
pregnancy and that was not directly due to obstetric causes but was aggravated by the physiologic effects of
pregnancy
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SURGERY
GENERAL SURGICAL PRINCIPLE
ASA grading
Class I : Normal Healthy

Class II : ē Mild systemic disease
Class III : ē Severe systemic disease that limits activities but not incapacitating
Class IV : ē Incapacitating disease that’s a constant threat of life
Class V : ē Moribund pt. not expected to survive ē / ē out an operation(ē in next 24hrs)
Preparation for surgery
Elective cases Elective and emergency patients require different preparation:

• Consider pre admission clinic to address medical issues.
• Blood tests including FBC, U+E, LFTs, Clotting, Group and Save
• Urine analysis
• Pregnancy test
• Sickle cell test
• ECG/ Chest x-ray
Exact tests to be performed will depend upon the proposed procedure and patient fitness.
Risk factors for development of deep vein thrombosis should be assessed and a plan for thromboprophylaxis formulated.
Diabetes
Diabetic patients have greater risk of complications.
Poorly controlled diabetes carries high risk of wound infections.
Patients with diet or tablet controlled diabetes may be managed using a policy of omitting medication and checking blood
glucose levels regularly. Diabetics who are poorly controlled or who take insulin will require a intravenous sliding scale.
Potassium supplementation should also be given.
Diabetic cases should be operated on first.
Emergency cases
Stabilise and resuscitate where needed.
Consider whether antibiotics are needed and when and how they should be administered.
Inform blood bank if major procedures planned particularly where coagulopathies are present at the outset or anticipated
(e.g. Ruptured AAA repair)
Don't forget to consent and inform relatives.
Special preparation Some procedures require special preparation:

• Thyroid surgery; vocal cord check.
• Parathyroid surgery; consider methylene blue to identify gland.
• Sentinel node biopsy; radioactive marker/ patent blue dye.
• Surgery involving the thoracic duct; consider administration of cream.
• Pheochromocytoma surgery; will need alpha and beta blockade.
• Surgery for carcinoid tumours; will need covering with octreotide.

• Colorectal cases; bowel preparation (especially left sided surgery)
• Thyrotoxicosis; lugols iodine/ medical therapy.
Proactive care of older people undergoing surgery (POPS)

• Comprehensive geriatric assessment
• MDT assessment preoperatively
• Main predictors of complications are co-morbidities cardiac disease and reduced functional capacity -
preoperative assessment is the key to preventing adverse postoperative outcomes
• Patients screened for risk factors (albumin <30, co morbidities)
• Management plan made and disseminated to all involved
• Patients education: pain relief, post op exercises, nutrition
Outcomes:
• Fewer postoperative medical complications
• Reduced length of stay by 4.5 days
Thromboprophylaxis in surgical patients
Deep vein thrombosis may develop insidiously in many surgical patients. Untreated it may progress to result in
pulmonary embolism.
The following surgical patients are at increased risk of deep vein thrombosis:
• Surgery greater than 90 minutes at any site or greater than 60 minutes if the procedure involves the lower limbs
or pelvis
• Acute admissions with inflammatory process involving the abdominal cavity
• Expected significant reduction in mobility
• Age over 60 years
• Known malignancy
• Thrombophilia
• thrombosis
• BMI >30
• Taking hormone replacement therapy or the contraceptive pill
• Varicose veins with phlebitis
Mechanical thromboprophylaxis
• Early ambulation after surgery is cheap and is effective
• Compression stockings (contra -indicated in peripheral arterial disease)
• Intermittent pneumatic compression devices
• Foot impulse devices
Therapeutic agents
Agent Mode of action Uses
Low molecular Binds antithrombin In patients with normal renal function, low doses typically given in those
weight heparin resulting in inhibition of with moderate to high risk of thromboembolic events. It is given as once
factor Xa daily subcutaneous injection
Unfractionated Binds antithrombin III Effective anticoagulation, administered intravenously it has a rapid onset
heparin with affects thrombin and its therapeutic effects decline quickly on stopping and infusion. Its
and factor Xa activity is measured using the APTT. If need be it can be reversed using
protamine sulphate
Dabigatran Orally administered Used prophylaxis in hip and knee surgery. It does not require therapeutic
direct thrombin inhibitor monitoring. It has no known antidote and should not be used in any
patient in whom there is a risk of active bleeding or imminent likelihood of
surgery
Intravenous access
Venous access: A number of routes for establishing venous access are available.
Peripheral venous cannula

Easy to insert with minimal morbidity. Wide lumen cannulae can provide rapid fluid infusions. When properly managed
infections may be promptly identified and the cannula easily re sited. Problems relate to their peripheral sites and they
are unsuitable for the administration of vaso active drugs, such as inotropes and irritant drugs such as TPN (except in the
very short term setting).
Central lines
Insertion is more difficult and most operators and NICE advocate the use of ultra sound. Coagulopathies may lead to
haemorrhage following iatrogenic arterial injury. Femoral lines are easier to insert and iatrogenic injuries easier to
manage in this site however they are prone to high infection rates. Internal jugular route is preferred. They have multiple
lumens allowing for administration of multiple infusions. The lumens are relatively narrow and thus they do not allow
particularly rapid rates of infusion.
Intraosseous access This is typically undertaken at the anteromedial aspect of the proximal tibia and provides access
to the marrow cavity and circulatory system. Although traditionally preferred in paediatric practice they may be used in
adults and a wide range of fluids can be infused using these devices.
Tourniquets
• These may be applied to reduce blood loss during a procedure or to prevent bleeding obscuring vital structures.
• As a rule they should not be used to control traumatic bleeding. Direct pressure is the preferred method.
Side effects/ complications

• Skin friction injuries
• Neuropraxia (greatest risk in upper limb, usually radial nerve)
• Direct injury to underlying muscle
• Cardiovascular changes due to limb exsanguination using Esmarch bandage, usually increased circulating
blood volume-may cause problems in patients with pre-existing vascular disease.
Hypovolaemia and the surgical patient
Hypovolaemia often represents the end point of multiple pathological processes. It may be divided into the following
categories; overt compensated hypovolaemia, covert compensated hypovolaemia and decompensated hypovolaemia. Of
these three categories the covert compensated subtype of hypovolaemia remains the commonest and is accounted for
by the fact that class I shock will often produce no overtly discernible clinical signs. This is due, in most cases, to a
degree of splanchnic autotransfusion. The most useful diagnostic test for detection of covert compensated hypovolaemia
remains urinanalysis. This often shows increased urinary osmolality and decreased sodium concentration.
In overt compensated hypovolaemia the blood pressure is maintained although other haemodynamic parameters may be
affected. This correlates to class II shock. In most cases assessment can be determined clinically. Where underlying
cardopulmonary disease may be present the placement of a CVP line may guide fluid resuscitation. Severe pulmonary
disease may produce discrepancies between right and left atrial filling pressures. This problem was traditionally
overcome through the use of Swann-Ganz catheters.
Untreated, hypovolaemia may ultimately become uncompensated with resultant end organ dysfunction. Microvascular
hypoperfusion may result in acidosis with a subsequent myocardial depressive effect, thereby producing a viscous
circle.
The treatment of hypovolaemia is with intravenous fluids. In the first instance a fluid challenge such as the rapid infusion
of 250ml of crystalloid will often serve as both a diagnostic and resuscitative measure. In the event that this fails to
produce the desired response the patient will need to be re-evaluated clinically. More fluid may be needed. However, its
important not to overlook mechanical ureteric obstruction in the anuric, normotensive pt.
Intra Operative Fluid Management
-1
Composition of commonly used intravenous fluids mmol
Na K Cl Bicarbonate Lactate
Plasma 137-147 4-5.5 95-105 22-25 -
0.9% Saline 153 - 153 - -
Dextrose / saline 30.6 - 30.6 - -
Hartmans 130 4 110 - 28
Recommendations for intra operative fluid management

• Intra operative fluids are recommended to optimise cardiac stroke volume.
• Patients undergoing non elective orthopaedic or abdominal surgery should receive IV fluids for the 1st 8h post
operatively. This may be supplemented by a low dose dopexamine infusion in selected cases.
Pre Operative Fluid Management
Fluid management has been described in the British Consensus guidelines on IV fluid therapy for Adult
Surgical patients (GIFTASUP)
• Use Ringer's lactate or Hartmann's when a crystalloid is needed for resuscitation or replacement of fluids. Avoid
0.9% N. Saline (due to risk of hyperchloraemic acidosis) unless patient vomiting or has gastric drainage.
• Use 0.4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It should not be used in resuscitation or
as replacement fluids.
• Adult maintenance fluid requirements are: Na 50-100 mmol/day and K 40-80 mmol/day in 1.5-2.5L fluid per day.
• Patients for elective surgery should NOT be nil by mouth for >2 hours (unless has disorder of gastric emptying).
• Patients for elective surgery should be given carbohydrate rich drinks 2-3h before. Ideally this should form part
of a normal pre op plan to facilitate recovery.
• Avoid mechanical bowel preparation.
• If bowel prep is used, simultaneous administration of Hartmann's or Ringer's lactate should be considered.
• Excessive fluid losses from vomiting should be treated with a crystalloid with potassium replacement. 0.9% N.
Saline should be given if there is hypochloraemia. Otherwise Hartmann's or Ringer lactate should be given for
diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also be given in sodium losses secondary to diuretics.
• High risk patients should receive fluids and inotropes.
• An attempt should be made to detect pre or operative hypovolaemia using flow based measurements. If this is
not available, then clinical evaluation is needed i.e. JVP, pulse volume etc.
• In Blood loss or infection causing hypovolaemia should be treated with a balanced crystalloid or colloid (or until
blood available in blood loss). A critically ill patient is unable to excrete Na or H20 leading to a 5% risk of
interstitial oedema. Therefore 5% dextrose as well as colloid should be given.
• Give 200mls of colloid in hypovolaemia, repeat until clinical parameters improve.
A summary of the recommendations for post operative fluid management

• Fluids given should be documented clearly and easily available
• Assess the patient's fluid status when they leave theatre
• If a patient is haemodynamically stable and euvolaemic, aim to restart oral fluid intake as soon as possible
• Review patients whose urinary sodium is < 20
• If a patient is oedematous, hypovolaemia if present should be treated first. This should then be followed by a
negative balance of sodium and water, monitored using urine Na excretion levels.
• Solutions such as Dextran 70 should be used in caution in patients with sepsis as there is a risk of developing
acute renal injury.
SURGICAL NUTRITION
Short term
Naso–gastric
Naso–duodenal
Naso–jejunal (Acute severe Pancreatitis)
Long term
Gastrostomy
Jejunostomy
PEG (P/C Esophago–gastrostomy)
PEJ (P/C Esophago–jejunostomy)
Nutrition requirements < 4 wks:

Fine bore NG tube as well as oral diet
(bike accident, head injury, comatose, no basal skull #; slow recovery;)
Nutrition requirements > 4 wks :

PEG (most case)
NCJ (Needle Catheter Jejunostomy);
Use after major GI surgery; Small bowel stoma done
TPN use করা হয় যেসব ক্ষেত্রে

Pre-operative pt. & needs to be optimized prior 2surgery
Low BMI & Low albumin
Projectile vomiting due 2PS occurred due to obstructing tumor(excludes oral /NG route)
Post operative entero-cutaneous fistula (TPN forms part of the ‘SNAP’ of managing a fistula)
Nutrition options in surgical patients
Oral intake • Easiest option

• May be supplemented by calorie rich dietary supplements
• May contra indicated following certain procedures
Naso gastric feeding • Usually administered via fine bore naso gastric feeding tube
• Complications relate to aspiration of feed or misplaced tube
• May be safe to use in patients with impaired swallow
• Often contra indicated following head injury due to risks associated with tube
insertion
Naso jejunal feeding • Avoids problems of feed pooling in stomach (and risk of aspiration)
• Insertion of feeding tube more technically complicated (easiest if done intra
operatively)
• Safe to use following oesophagogastric surgery
Feeding jejunostomy • Surgically sited feeding tube

• May be used for long term feeding
• Low risk of aspiration and thus safe for long term feeding following upper GI
surgery
• Main risks are those of tube displacement and peritubal leakage immediately
following insertion, which carries a risk of peritonitis
Percutaneous endoscopic • Combined endoscopic and percutaneous tube insertion

gastrostomy • May not be technically possible in those patients who cannot undergo
successful endoscopy
• Risks include aspiration and leakage at the insertion site
Total parenteral nutrition • The definitive option in those patients in whom enteral feeding is contra
indicated
• Individualised prescribing and monitoring needed
• Should be administered via a central vein as it is strongly phlebitic
• Long term use is associated with fatty liver and deranged LFT's
Enteral Feeding
• Identify patients as malnourished or at risk (see below)
• Identify unsafe or inadequate oral intake with functional GI tract
• Consider for enteral feeding
• Gastric feeding unless upper GI dysfunction (then for duodenal or jejunal tube)
• Check NG placement using aspiration and pH (check post pyloric tubes with AXR)
• Gastric feeding > 4 weeks consider long-term gastrostomy
• Consider bolus or continuous feeding into the stomach
• ITU patients should have continuous feeding for 16-24h (24h if on insulin)
• Consider motility agent in ITU or acute patients for delayed gastric emptying. If this doesn't work then try post
pyloric feeding or parenteral feeding.
• PEG can be used 4h after insertion, but should not be removed until >2 weeks after insertion.
Surgical patients due to have major abdominal surgery: if malnourished, unsafe swallow/inadequate oral intake and
functional GI tract then consider pre operative enteral feeding.
Patients identified as being malnourished
2
• BMI < 18.5 kg/m
• unintentional weight loss of > 10% over 3-6/12
2
• BMI < 20 kg/m and unintentional weight loss of > 5% over 3-6/12
AT RISK of malnutrition
• Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
• Poor absorptive capacity
• High nutrient losses
• High metabolism
Parenteral feeding-NICE guidelines

Parenteral nutrition: NICE guidelines summary
Identify patients as malnourished or at risk

Patients identified as being malnourished-
• BMI < 18.5 kg/m2
• BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12
AT RISK of malnutrition-
• eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
• poor absorptive capacity
• high nutrient losses
• high metabolism
Identify unsafe/inadequate oral intake OR a non functional GI tract/perforation/inaccessible
Consider parenteral nutrition:

• for feeding < 14 days consider feeding via a peripheral venous catheter
• for feeding > 30 days use a tunneled subclavian line
• continuous administration in severely unwell patients
• if feed needed > 2 weeks consider changing from continuous to cyclical feeding
• don't give > 50% of daily regime to unwell patients in first 24-48h
Surgical patients: if malnourished with unsafe swallow OR a non functional GI tract/perforation/inaccessible then
consider peri operative parenteral feeding.
Total parenteral nutrition

• Commonly used in nutritionally compromised surgical patients
• Bags contain combinations of glucose, lipids and essential electrolytes, the exact composition is determined by
the patients nutritional requirements.
• Although it may be infused peripherally, this may result in thrombophlebitis.
• Longer term infusions should be administered into a central vein (preferably via a PICC line).
• Complications are related to sepsis, re-feeding syndromes and hepatic dysfunction.
Nutrition Monitoring-NICE guidelines

• Weight: daily if fluid balance concerns, otherwise weekly reducing to monthly
• BMI: at start of feeding and then monthly
• If weight cannot be obtained: monthly mid arm circumference or triceps skin fold thickness
• Daily electrolytes until levels stable. Then once or twice a week.
• Weekly glucose, phosphate, magnesium, LFTs, Ca, albumin, FBC, MCV levels if stable
• 2-4 weekly Zn, Folate, B12 and Cu levels if stable
• 3-6 monthly iron and ferritin levels, manganese (if on home parenteral regime)
• 6 monthly vitamin D
• Bone densitometry initially on starting home parenteral nutrition then every 2 years
Nutrition prescriptions
National institute of clinical excellence (NICE) guidelines

For people not severely ill and not at risk of refeeding syndrome aim to give
• 25-35 kcal/kg/day (lower if BMI > 25)
• 0.8-1.5g protein /kg/day
• 30-35 ml fluid/kg/day
• Adequate electrolytes, minerals, vitamins
• Severely ill patients aim to give < 50% of the energy and protein levels over the first 24-48h.
For people at high risk of refeeding syndrome:

• Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
• Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and
supplements
+
• Give K (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
Oral Nutrition
Oral nutrition: a summary of NICE guidelines

• Identify patients who are or at risk of being malnourished (see below for definitions)
• Check for dysphagia
• If safe swallow, provide food and fluid in adequate quantity and quality
• Give a balanced diet
• Offer multivitamins and minerals
Surgical patients:
• If malnourished and safe swallow and post op caesarean, gynaecological or abdominal surgery, aim for oral
intake within 24h
Patients identified as being malnourished:
• BMI < 18.5 kg/m2
• BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12
AT RISK of malnutrition:
• eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
• poor absorptive capacity
• high nutrient losses
• high metabolism
** SNAP method
. S is for control of Sepsis,
N is for Nutrition in the form of TPN
A is for Anatomy, define the anatomy by the use of contrast radiology,
P is for plan, as in form a management plan.
An entero-cutaneous fistula may close spontaneously if managed appropriately
Nutrition - Refeeding syndrome
Refeeding problems
If patient not eaten for > 5 days, aim to refeed at < 50% energy and protein levels
High risk for refeeding problems : If one or more of the following:

• BMI < 16 kg/m2
• Unintentional weight loss >15% over 3-6 months
• Little nutritional intake > 10 days
• Hypokalaemia, Hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
If two or more of the following:
• BMI < 18.5 kg/m2

• unintentional weight loss > 10% over 3-6 months
• Little nutritional intake > 5 days
• PMH alcohol abuse or DH including insulin, chemotherapy, diuretics, antacids
Prescription
• start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
• start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and
supplements
+
• give K (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
● Only Neurogenic Shock HR reduced

● Only Septic Shock CO raised
● Only Anaphylactic & Septic Shock shows warm periphery
SAMPLE QUESTION Theme from April 2012 Exam

Theme: Critical care
A. Hypovolaemia
B. Normal
C. Cardiogenic shock
D. Septic shock
1. A 45 year old man is admitted to the intensive care unit following a laparotomy. He has a central line, pulmonary
artery catheter and arterial lines inserted.
PAOP CO SVR
Low Low High
Hypovolaemia
Cardiac output is lowered in hypovolaemia due to decreased preload.
2. A 75 year old man is admitted to the intensive care unit following a laparotomy. He has a central line, pulmonary artery
catheter and arterial lines inserted.
PAOP CO SVR
High Low High
Cardiogenic shock
In cardiogenic shock pulmonary pressures are often high. This is the basis for the use of venodilators in the treatment of
pulmonary oedema.
3. A 22 year old lady is admitted to the intensive care unit following a laparotomy. She has a central line, pulmonary
artery catheter and arterial lines inserted.
PAOP CO SVR
Low High Low
Septic shock
Decreased SVR is a major feature of sepsis. A hyperdynamic circulation is often present. This is the reason for the use
of vasoconstrictors.
*** PAOP: Pulmonary artery occlusion pressure; CO: Cardiac output; SVR: Systemic vascular resistance***
Pulmonary artery occlusion pressure monitoring
The pulmonary artery occlusion pressure is an indirect measure of left atrial pressure, and thus filling pressure of the left
heart. The low resistance within the pulmonary venous system allows this useful measurement to be made. The most
accurate trace is made by inflating the balloon at the catheter tip and "floating" it so that it occludes the vessel. If it is not
possible to occlude the vessel in this way then the measurement gained will be the pulmonary artery end diastolic
pressure.
Interpretation of PAOP
PAOP mmHg Scenario
Normal 8-12
Low <5 Hypovolaemia
Low with pulmonary oedema <5 ARDS
High >18 Overload
When combined with measurements of systemic vascular resistance and cardiac output it is possible to accurately
classify patients.
Systemic vascular resistance
Derived from aortic pressure, right atrial pressure and cardiac output.
SVR=80(mean aortic pressure-mean right atrial pressure)/cardiac output
Blood products
Whole blood fractions
Fraction Key points
Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large volumes of fluid may result
in cardiovascular compromise. Product obtained by centrifugation of whole blood.
Platelet rich Usually administered to patients who are thrombocytopaenic and are bleeding or require surgery. It is
plasma obtained by low speed centrifugation.
Platelet Prepared by high speed centrifugation and administered to patients with thrombocytopaenia.
concentrate
Fresh frozen • Prepared from single units of blood.

plasma • Contains clotting factors, albumin and immunoglobulin.
• Unit is usually 200 to 250ml.
• Usually used in correcting clotting deficiencies in patients with hepatic synthetic failure who
are due to undergo surgery.

-1
• Usual dose is 12-15ml/Kg .
• It should not be used as first line therapy for hypovolaemia.
Cryoprecipitate • Formed from supernatant of FFP.

• Rich source of Factor VIII and fibrinogen.
• Allows large concentration of factor VIII to be administered in small volume.
SAG-Mannitol Removal of all plasma from a blood unit and substitution with:
Blood • Sodium chloride
• Adenine
• Anhydrous glucose
• Mannitol
Up to 4 units of SAG M Blood may be administered. Thereafter whole blood is preferred. After 8 units,
clotting factors and platelets should be considered.
Cell saver devices
These collect patients own blood lost during surgery and then reinfuse it. There are two main types:
• Those which wash the blood cells prior to reinfusion. These are more expensive to purchase and more
complicated to operate. However, they reduce the risk of reinfusing contaminated blood back into the patient.
• Those which do not wash the blood prior to reinfusion.
Their main advantage is that they avoid the use of infusion of blood from donors into patients and this may reduce risk of
blood borne infection. It may be acceptable to Jehovah's witnesses. It is contraindicated in malignant disease for risk of
facilitating disease dissemination.
Blood products used in warfarin reversal
In some surgical patients the use of warfarin can pose specific problems and may require the use of specialised blood
products
Immediate or urgent surgery in patients taking warfarin(1) (2):

1. Stop warfarin
2. Vitamin K (reversal within 4-24 hours)
-IV takes 4-6h to work (at least 5mg)
-Oral can take 24 hours to be clinically effective
3. Fresh frozen plasma

Used less commonly now as 1st line warfarin reversal
-1
-30ml/kg
-Need to give at least 1L fluid in 70kg person (therefore not appropriate in fluid overload)
-Need blood group
-Only use if human prothrombin complex is not available
4. Human Prothrombin Complex (reversal within 1 hour)
-Bereplex 50 u/kg
Blood transfusion reactions
Immune mediated Non immune mediated
Pyrexia Hypocalcaemia
Alloimmunization CCF
Thrombocytopaenia Infections
Transfusion associated lung injury Hyperkalaemia
Graft vs Host disease
Urticaria
Acute or delayed haemolysis
ABO incompatibility
Rhesus incompatibility
Notes:
GVHD: lymphocyte proliferation causing organ failure
Transfusion associated lung injury: neutrophil mediated allergic pulmonary oedema
ABO and Rhesus incompatibility: causes acute haemolytic transfusion reaction leading to agglutination and haemolysis
Mnemonic for transfusion reactions: Got a bad unit
G raft vs. Host disease

O verload
T hrombocytopaenia
A lloimmunization
B lood pressure unstable

A cute haemolytic reaction
D elayed haemolytic reaction
U rticaria
N eutrophilia
I nfection
T ransfusion associated lung injury
The diagnosis is of an acute haemolytic transfusion reaction, normally due to ABO incompatibility. Haemolysis of the
transfused cells occurs causing the combination of shock, haemoglobinaemia and loin pain. This may subsequently lead
to disseminated intravascular coagulation. A Coomb's test should confirm haemolysis. Other tests for haemolysis
include: unconjugated bilirubin, haptoglobin, serum and urine free haemoglobin.
Note that delayed haemolytic reactions are normally associated with antibodies to the Rh system and occur 5-10 days
after transfusion.
Surgical drains
• Drains are inserted in many surgical procedures and are of many types.
• As a broad rule they can be divided into those using suction and those which do not.
• The diameter of the drain will depend upon the substance being drained, for example smaller lumen drain for
pneumothoraces vs haemothorax.
• Drains can be associated with complications and these begin with insertion when there may be iatrogenic
damage. When in situ they serve as a route for infections. In some specific situations they may cause other
complications, for example suction drains left in contact with bowel for long periods may carry a risk of inducing
fistulation.
• Drains should be inserted for a defined purpose and removed once the need has passed.
A brief overview of types of drain and sites is given below
CNS
• Low suction drain or free drainage systems may be used for situations such as drainage of sub dural
haematomas.
CVS
• Following cardiothoracic procedures of thoracic trauma underwater seal drains are often placed. These should
be carefully secured. When an air leak is present they may be placed on suction whilst the air leak settles
Orthopaedics and trauma

• In this setting drains are usually used to prevent haematoma formation (with associated risk of infection). Some
orthopaedic drains may also be specially adapted to allow the drained blood to be auto transfused.
Gastro-intestinal surgery
• Surgeons often place abdominal drains either to prevent or drain abscesses, or to turn an anticipated
complication into one that can be easily controlled such as a bile leak following cholecystectomy. The type of
drain used will depend upon the indication.
Response to surgery
Sympathetic nervous system

• Noradrenaline from sympathetic nerves and adrenaline from adrenal medulla
• Blood diverted from skin and visceral organs; bronchodilatation, reduced intestinal motility, increased glucagon
and glycogenolysis, insulin reduced
• Heart rate and myocardial contractility are increased
Acute phase response

• TNF-α, IL-1, IL-2, IL-6, interferon and prostaglandins are released
• Excess cytokines may cause SIRS

• Cytokines increase the release of acute phase proteins
Endocrine response
• Hypothalamus, pituitary, adrenal axis
• Increases ACTH and cortisol production:
increases protein breakdown
increases blood glucose levels
• Aldosterone increases sodium reabsorption
• Vasopressin increases water reabsorption and causes vasoconstriction
Vascular endothelium
• Nitric oxide produces vasodilatation
• Platelet activating factor enhances the cytokine response
• Prostaglandins produce vasodilatation and induce platelet aggregation
Pyrexia- post operative

Many surgical patients will develop a pyrexia post operatively. The cause and investigation depends upon the nature of
the infection.
The following scenarios may account for post operative pyrexia:
Cause Features
Anastomotic leak • Swinging pyrexia

• Ileus
• Increasing abdominal pain
• Raised inflammatory markers
Wound infection • Evidence of superficial erythema, discharge of pus or increasing pain

• Usually mild pyrexia (unless major or deep seated wound infection)
• May be accompanied by evidence of wound dehisence
• Inflammatory markers raised
Atelectasis • Usually complicates abdominal surgery

• Most common after midline laparotomies (pain impairs ventilation)
• Pyrexia usually mild and non swinging
• Most patients will have chest signs on examination
Central line sepsis • Patients with complex venous access

• May have marked pyrexia
• Access site may show evidence of erythema
• Diagnosis is by blood culture from line, line removal and subsequent tip culture
• Groin lines and those for TPN have the highest risk
Urinary tract infection • Common in surgical patients

• Usually occur in patients with indwelling urinary catheters
• Diagnosis is by dipstick and CSU and signs of raised inflammatory markers
• Treatment is with antibiotics (to cover hospital acquired organisms)
Malignant hyperthermia
Overview
• Condition often seen following administration of anaesthetic agents
• Characterised by hyperpyrexia and muscle rigidity
• Cause by excessive release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
• Associated with defects in a gene on chromosome 19 encoding the ryanodine receptor, which controls
2+
Ca release from the sarcoplasmic reticulum
• Neuroleptic malignant syndrome may have a similar aetiology
Causative agents
• Halothane
• Suxamethonium
• Other drugs: antipsychotics (neuroleptic malignant syndrome)
Investigations
• CK raised
• Contracture tests with halothane and caffeine
Management
2+
• Dantrolene - prevents Ca release from the sarcoplasmic reticulum
Surgical complications
Complications occur in all branches of surgery and require vigilance in their detection. In many cases anticipating the
likely complications and appropriate avoidance will minimise their occurrence. For the purposes of the MRCS the
important principles to appreciate are:
• The anatomical principles that underpin complications

• The physiological and biochemical derangements that occur
• The most appropriate diagnostic modalities to utilise
• The principles which underpin their management
This is clearly a very broad area and impossible to cover comprehensively. There is considerable overlap with other topic
areas within the website.
Avoiding complications
• World Health Organisation checklist- now mandatory prior to all operations
• Prophylactic antibiotics - right dose, right drug, right time.
• Assess DVT/ PE risk and ensure adequate prophylaxis

• MARK site of surgery
• Use tourniquets with caution and with respect for underlying structures
• Remember the danger of end arteries and in situations where they occur avoid using adrenaline containing
solutions and monopolar diathermy.
• Handle tissues with care- devitalised tissue serves as a nidus for infection
• Be very wary of the potential for coupling injuries when using diathermy during laparoscopic surgery
• The inferior epigastric artery is a favourite target for laparoscopic ports and surgical drains!
Anatomical principles
Understanding the anatomy of a surgical field will allow appreciation of local and systemic complications that may occur.
For example nerve injuries may occur following surgery in specific regions the table below lists some of the more
important nerves to consider and mechanisms of injury
Nerve Mechanism
Accessory Posterior triangle lymph node biopsy
Sciatic Posterior approach to hip
Common peroneal Legs in Lloyd Davies position
Long thoracic Axillary node clearance
Pelvic autonomic nerves Pelvic cancer surgery
Recurrent laryngeal nerves During thyroid surgery
Hypoglossal nerve During carotid endarterectomy
Ulnar and median nerves During upper limb fracture repairs
These are just a few. The detailed functional sequelae are particularly important and will often be tested. In addition to
nerve injuries certain procedures carry risks of visceral or structural injury. Again some particular favourites are given
below:
Structure Mechanism
Thoracic duct During thoracic surgery e.g. Pneumonectomy, oesphagectomy
Parathyroid glands During difficult thyroid surgery
Ureters During colonic resections/ gynaecological surgery
Bowel perforation Use of Verres Needle to establish pneumoperitoneum
Bile duct injury Failure to delineate Calots triangle carefully and careless use of diathermy
Facial nerve Always at risk during Parotidectomy
Tail of pancreas When ligating splenic hilum
Testicular vessels During re-do open hernia surgery
Hepatic veins During liver mobilisation
Physiological derangements
A very common complication is bleeding and this is covered under the section of haemorrhagic shock. Another variant is
infection either superficial or deep seated. The organisms are covered under microbiology and the features of sepsis
covered under shock. Do not forget that immunocompromised and elderly patients may present will atypical physiological
parameters.
Complication Physiological/ Biochemical Problem

+
Arrhythmias following cardiac Susceptibility to hypokalaemia (K <4.0 in cardiac patients)
surgery
Neurosurgical electrolyte SIADH following cranial surgery causing hyponatraemia

disturbance
Ileus following gastrointestinal Fluid sequestration and loss of electrolytes

surgery
Pulmonary oedema following Loss of lung volume makes these patients very sensitive to fluid overload
pneumonectomy
Anastamotic leak Generalised sepsis causing mediastinitis or peritonitis depending on site of leak
Myocardial infarct May follow any type of surgery and in addition to direct cardiac effects the decreased
cardiac output may well compromise grafts etc.
Diagnostic modalities
Depends largely on the suspected complication. In the acutely unwell surgical patient the following baseline
investigations are often helpful:
• Full blood count, urea and electrolytes, C- reactive protein (trend rather than absolute value), serum calcium,
liver function tests, clotting (don't forget to repeat if on-going bleeding)
• Arterial blood gases
• ECG (+cardiac enzymes if MI suspected)
• Chest x-ray to identify collapse/ consolidation
• Urine analysis for UTI
These will often identify the most common complications.

Special tests
• CT scanning for identification of intra-abdominal abscesses, air and if luminal contrast is used an anastamotic
leak
• Gatrograffin enema- for rectal anastamotic leaks
• Doppler USS of leg veins- for identification of DVT
• CTPA for PE
• Sending peritoneal fluid for U+E (if ureteric injury suspected) or amylase (if pancreatic injury suspected)
• Echocardiogram if pericardial effusion suspected post cardiac surgery and no pleural window made.
Management of complications
The guiding principal should be safe and timely intervention. Patients should be stabilised and if an operation needs to
occur in tandem with resuscitation then generally this should be of a damage limitation type procedure rather than
definitive surgery (which can be more safely undertaken in a stable patient the following day).
Remember that recent surgery is a contra indication to thrombolysis and that in some patients IV heparin may be
preferable to a low molecular weight heparin (easier to reverse).
As a general rule laparotomies for bleeding should follow the core principle of quadrant packing and then subsequent
pack removal rather than plunging large clamps into pools of blood. The latter approach invariable worsens the situation
is often accompanied by significant visceral injury particularly when done by the inexperienced. If packing controls a
situation it is entirely acceptable practice to leak packs in situ and return the patient to ITU for pack removal the
subsequent day.
Sterilisation
• Cleaning refers to removal of physical debris.

• Disinfection refers to reduction in numbers of viable organisms.
• Sterilisation is removal of all organisms and spores.
The method chosed depends upon the type of instrument and the procedure for which it will be used.
• Sterilisation of surgical instruments typically takes place in an autoclave which uses pressurised steam at a
temperature of 134 degrees. This method is reproducible and safe.
• However, endoscopy equipment cannot be sterilised by this method as it would damage it. Therefore they are
sterilised using 2% glutaraldehyde solution. Since staff may develop hypersensitivity its use is restricted to
those pieces of equipment that cannot be sterilised by an alternative means.
• In the industrial setting gamma irradiation is used.
Ionizing radiation(γ ray is used) : Sterilizing disposable products & instruments.

DPS & needles
Plastic syringes
Transfusion equipment
Biological materials
UV radiation: Acts as disinfectants

Absorps purine & pyrimidine base of DNA
n
Form of thymine dimmers
–
Addition of OH group to the base
Hot air oven: All glass wares

Swabsticks
Powder, oily substances
Ethylene Oxide: Rubber goods, plastics

Plastic syringes / DPS
Sutures
Complex apparatus
Gluteraldehyde: Endoscopes
Formaldhyde: Rooms
Beddings, Clothings
Tyndalization: Heat labile matters containing sugar, milk, gelatine
Boiling: All bacteria + certain spores

Syringes; rubber goods
Surgical instruments
● All sutures are FBs & therefore irritating 2tissues; synthetic sutures (nylon) less irritating ē monofilament being least
irritating
● Abdominal wall closure – two type answer found 1-PDS and Nylon, so be careful !!!
● Bowel anastomosis --- PDS
urethroplasty ----vicryl
Suture material
Agent Classification Durability Uses Special points
Silk Braided Theoretically Anchoring devices, skin closure Knots easily, poor cosmesis
Biological permanent although
strength not
preserved
Catgut Biological 5-7 days Short term wound Poor cosmesis

Braided approximation Degrades rapidly
Not available in UK
Chromic catgut Braided Up to 12 weeks Apposition of deeply sited Unpredictable degradation

Biological tissues pattern
Not in use in UK
Polydiaxonone Synthetic Up to 3 months Widespread surgical Used in most surgical

(PDS) Monofilament (longer with thicker applications including visceral specialties (avoid dyed form
sutures) anastomoses, dermal closure, in dermal closure)
mass closure of abdominal wall
Polyglycolic acid Braided Up to 6 weeks Most tissues can be apposed It has good handling
(Vicryl, Dexon) Synthetic using polyglycolic acid properties, the dyed form of
this suture should not be
used for skin closure
Polypropylene Synthetic Permanent Widely used, agent of choice for Poor handling properties
(Prolene) Monofilament vascular anastomoses
Polyester Synthetic Permanent Its combination of permanency It is more expensive and

(Ethibond) Braided and braiding makes it useful for has considerable tissue
laparoscopic surgery drag
Absorbable vs Non absorbable

• Time taken to degrade absorbable materials varies
• Usually by macrophages hydrolysing material
• Consider absorbable sutures in situations where long term tissue apposition is not required. In cardiac and vascular
surgery non absorbable sutures are usually used.
Suture size
• The higher the index number the smaller the suture i.e. : 6/0 prolene is finer than 1/0 prolene.
• Finer sutures have less tensile strength. For example 6/0 prolene would not be a suture suitable for abdominal mass
closure but would be ideal for small calibre distal arterial anastomoses.
Braided vs monofilament
Generally speaking braided sutures have better handling characteristics than non braided. However, they are associated with
higher bacterial counts. Braided materials are unsuitable for use in vascular surgery as they are potentially thrombogenic
Suture sizes
USP Suture size and corresponding suture diameter
USP Size Diameter in mm
11-0 0.01
10-0 0.02
6-0 0.07
3-0 0.2
0 0.35
1 0.4
Methods of wound closure
Method of closure Indication
Primary closure • Clean wound, usually surgically created or following minor trauma
• Standard suturing methods will usually suffice
• Wound heals by primary intention
Delayed primary • Similar methods of actual closure to primary closure

closure • May be used in situations where primary closure is either not achievable or not advisable
e.g. infection
Vacuum assisted • Uses negative pressure therapy to facilitate wound closure

closure • Sponge is inserted into wound cavity and then negative pressure applied
• Advantages include removal of exudate and versatility
• Disadvantages include cost and risk of fistulation if used incorrectly on sites such as
bowel
Split thickness skin • Superficial dermis removed with Watson knife or dermatome (commonly from thigh)
grafts • Remaining epithelium regenerates from dermal appendages
• Coverage may be increased by meshing
Full thickness skin • Whole dermal thickness is removed

grafts • Sub dermal fat is then removed and graft placed over donor site
• Better cosmesis and flexibility at recipient site
• Donor site "cost"
Flaps • Viable tissue with a blood supply

• May be pedicled or free
• Pedicled flaps are more reliable, but limited in range
• Free flaps have greater range but carry greater risk of breakdown as they require
vascular anastomosis
Tissue reconstruction
Skin Grafts and Flaps

Skin flaps or grafts may be required where primary wound closure cannot be achieved or would entail either significant
cosmetic defect or considerable functional disturbance as a result of wound contraction.
Reconstructive ladder
Method Types
Direct closure The simplest option where possible
Grafting techniques • Split thickness

• Full thickness
• Skin Substitute
• Composite
Flap technique Local:

• Transposition
• Pivot
• Alphabetplasty (e.g. Z-Y)
Regional:
• Myocutaneous
• Fasciocutaneous
• Neurocutaneous
Distant:
• Free tissue transfer
Prelamination techniques Allows creation of specialised flaps e.g. buccal mucosa
Tissue expansion Involves placement of tissue expanders to increase amount of tissue at donor sites
Skin Grafts Vs. Flaps
Skin Grafts Flaps
No size limit (Split)/ Relative size limit (full thickness) Size limited by territory of blood supply
Rely on wound bed for blood supply Tissue has its own blood supply
Take better on clean well vascularised wound beds Will survive independent of the wound bed
Split skin graft donor site typically heals in 12 days Direct closure of donor site or secondary skin graft
Donor site may be reused Donor site cannot be reused
Split thickness skin grafts

• Available in range of thicknesses.
• Thigh is the commonest donor site
• Size may be increased by meshing the graft. However this comes with compromise on cosmesis.
• Donor sites, especially if thin grafts are taken can be reused following re-epithelialisation
Full thickness grafts

• Most commonly used for facial reconstruction
• Include dermal appendages
• Provide superior cosmetic result
Composite grafts
These are grafts containing more than one tissue type, such as skin and fat. They are usually used to cover small
defects in cosmetically important areas.
Flaps
• Flaps have their own blood supply and may be pedicled or free.
• May have multiple components e.g. skin, skin + fat, skin + fat + muscle.
• They will have the ability to take regardless of the underlying tissue bed.
• The type of intrinsic blood supply is important. For example in breast surgery pedicled latissimus dorsi flaps will
be less prone to failure than microsvascular anastomosed free Diep flaps.
Tissue sampling
Tissue sampling is an important surgical process. Biopsy modalities vary according to site, experience and subsequent
planned therapeutic outcome
The modalities comprise:

- Fine needle aspiration cytology
- Core biopsy
- Excision biopsy
- Tru cut biopsy
- Punch biopsy
- Cytological smears
- Endoscopic or laparoscopic biopsy
When the lesion is superficial the decision needs to be taken as to whether complete excision is desirable or whether
excision biopsy is acceptable. In malignant melanoma for example the need for safe margins will mean that a more
radical surgical approach needs to be adopted after diagnostic confirmation from excision biopsy than would be the case
in basal cell carcinoma. Punch biopsies are useful in gaining histological diagnosis of unclear skin lesions where excision
biopsy is undesirable such as in establishing whether a skin lesion is vasculitic or not.
Fine needle aspiration cytology (FNAC) is an operator dependent procedure that may or may not be image guided and
essentially involves passing a needle through a lesion whilst suction is applied to a syringe. The material thus obtained is
expressed onto a slide and sent for cytological assessment. This test can be limited by operator inexperience and also
by the lack of histological architectural information (e.g. Follicular carcinoma of the thyroid). Where a discharge is present
a sample may be sent for cytology although in some sites (e.g. Nipple discharge ) the information gleaned may be
meaningless.
Tissue samples may be obtained by both core and tru cut biopsy. A core biopsy is obtained by use of a spring loaded
gun with a needle passing quickly through the lesion of interest. A tru cut biopsy achieves the same objective but the
needle moved by hand. When performing these techniques image guidance may be desirable (e.g. In breast lesions).
Consideration needs to be given to any planned surgical resection as it may be necessary to resect the biopsy tract
along with the specimen (e.g. In sarcoma surgery).
Visceral lesions may be accessed percutaneously under image guidance such as ultrasound guided biopsy of liver
metastases. Or under direct vision such as a colonoscopic biopsy.
Anastomoses
• A wide variety of anastomoses are constructed in surgical practice. Essentially the term refers to the restoration
of luminal continuity. As such they are a feature of both abdominal and vascular surgery.
Visceral anastomoses For an anastomosis to heal three criteria need to be fulfilled:

• Adequate blood supply
• Mucosal apposition
• Minimal tension
When these are compromise the anastomosis may dehisce (leak). Even in the best surgical hands some anastomoses
are more prone to dehiscence than others. Oesophageal and rectal anastomoses are more prone to leakage and
reported leak rates following oesophageal and rectal surgery can be as high as 20%. This figure includes radiological
leaks and those with a clinically significant leak will be of a lower order of magnitude. As a rule small bowel anastomoses
heal most reliably.
The decision as to how best to achieve mucosal apposition is one for each surgeon. Some will prefer the use of stapling
devices as they are quicker to use, others will prefer to perform a sutured anastomosis. The attention to surgical
technique is more important than the method chosen and a poorly constructed stapled anastomosis in thickened tissue is
far more prone to leakage than a hand sewn anastomosis in the same circumstances.
If an anastomosis looks unsafe then it may be best not to construct one at all. In colonic surgery this is relatively clear cut
and most surgeons would bring out an end colostomy. In situations such as oesophageal surgery this is far more
problematic and colonic interposition may be required in this situation.
Vascular anastomoses
Most arterial surgery involving bypasses or aneurysm repairs will require construction of an arterial anastomosis.
Technique is important and for small diameter distal arterial surgery the intimal hyperplasia resulting from a badly
constructed anastomosis may render the whole operation futile before the patient leaves hospital. Some key points about
vascular anastomoses:
• Always use non absorbable monofilament suture (e.g. Polypropylene).
• Round bodied needle.
• Correct size for anastamosis ( i.e. 6/0 prolene for bottom end of a femoro-distal bypass).
• Suture should be continuous and from inside to outside of artery to avoid raising an intimal flap.
Gases For Laparoscopic Surgery
Laparoscopic surgery may be performed in a number of body cavities. In some areas irrigation solutions are preferred. In
the abdomen insufflation with CO2 is commonly used. The amount of gas delivered is adjusted to maintain a constant
intra-abdominal pressure of between 12 and 15 mmHg. Pressures < 7mm Hg are not usually compatible with
satisfactory views. Pressures >15mm Hg are usually associated with decreased venous return and hypotension. Too
little insufflation will risk obscuring the surgical view.
Pneumoperitoneum- therapeutic
During a laparoscopic procedure a surgeon will need to create a pneumoperitoneum. This can be achieved by use of a
Verress needle (risk of visceral injury). An alternative is the open "Hassan" style technique. Once access to the
abdominal cavity is secured carbon dioxide gas is insufflated to induce a working space. Higher intra-abdominal
pressures may compromise venous return and reduce cardiac output. If the blood pressure is seen to drop in this way
then release of air, will often improve matters. Should this not be the case then a laparotomy may be necessary to
exclude a more significant internal injury.
Abdominal incisions
Midline incision • Commonest approach to the abdomen

• Structures divided: linea alba, transversalis fascia, extraperitoneal fat, peritoneum
(avoid falciform ligament above the umbilicus)
• Bladder can be accessed via an extraperitoneal approach through the space of
Retzius
Paramedian incision • Parallel to the midline (about 3-4cm)

• Structures divided/retracted: anterior rectus sheath, rectus (retracted), posterior
rectus sheath, transversalis fascia, extraperitoneal fat, peritoneum
• Incision is closed in layers
Battle • Similar location to paramedian but rectus displaced medially (and thus denervated)
• Now seldom used
Kocher's Incision under right subcostal margin e.g. Cholecystectomy (open)
Lanz Incision in right iliac fossa e.g. Appendicectomy
Gridiron Oblique incision centered over McBurneys point- usually appendicectomy (less cosmetically
acceptable than Lanz)
Gable Rooftop incision
Pfannenstiel's Transverse supra pubic, primarily used to access pelvic organs
McEvedy's Groin incision e.g. Emergency repair strangulated femoral hernia
Rutherford Morrison Extraperitoneal approach to left or right lower quadrants. Gives excellent access to iliac vessels
and is the approach of choice for first time renal transplantation.
Nerve Lesions During Surgery
• Anterior resection of rectum and hypogastric autonomic nerves.

• Axillary node clearance: long thoracic nerve, thoracodorsal nerve and intercostobrachial nerve.
• Inguinal hernia surgery and ilioinguinal nerve.
• Varicose vein surgery- sural and saphenous nerves.
Nerve Mechanism
Accessory Posterior triangle lymph node biopsy
Sciatic Posterior approach to hip
Common peroneal Legs in Lloyd Davies position
Long thoracic Axillary node clearance
Pelvic autonomic Pelvic cancer surgery
Recurrent laryngeal During thyroid surgery
Hypoglossal During carotid endarterectomy
Ulnar and median During upper limb fracture repairs
In addition to nerve injuries certain procedures carry risks of visceral or structural injury. Again some particular favourites
are given below:
Structure Mechanism
Thoracic duct During thoracic surgery e.g. Pneumonectomy, oesphagectomy
Parathyroid glands During difficult thyroid surgery
Ureters During colonic resections/ gynaecological surgery
Bowel perforation Use of Verres Needle to establish pneumoperitoneum
Bile duct injury Failure to delineate Calots triangle carefully and careless use of diathermy
Facial nerve Always at risk during Parotidectomy
Tail of pancreas When ligating splenic hilum
Testicular vessels During re-do open hernia surgery
Hepatic veins During liver mobilisation
Again many could be predicted from the anatomy of the procedure.
Physiological derangements
A very common complication is bleeding and this is covered under the section of haemorrhagic shock. Another variant is
infection either superficial or deep seated. The organisms are covered under microbiology and the features of sepsis
covered under shock. Do not forget that immunocompromised and elderly patients may present will atypical physiological
parameters.
Selected physiological and biochemical issues are given below:
Complication Physiological/ Biochemical Problem

+
Arrhythmias following cardiac Susceptibility to hypokalaemia (K <4.0 in cardiac patients)
surgery
Neurosurgical electrolyte SIADH following cranial surgery causing hyponatraemia

disturbance
Ileus following gastrointestinal Fluid sequestration and loss of electrolytes

surgery
Pulmonary oedema following Loss of lung volume makes these patients very sensitive to fluid overload
pneumonectomy
Anastamotic leak Generalised sepsis causing mediastinitis or peritonitis depending on site of leak
Myocardial infarct May follow any type of surgery and in addition to direct cardiac effects the decreased
cardiac output may well compromise grafts etc.
Postoperative cognitive management

Definition
• Deterioration in performance in a battery of neuropsychological tests that would be expected in < 3.5% of
controls Or
• Long term, possibly permanent disabling deterioration in cognitive function following surgery
Early POCD
• Increasing age
• GA rather than regional
• Duration of anaesthesia
• Reoperation
• Postoperative infection
Late POCD
• Increasing age
• Emboli
• Biochemical disturbances
Electrosurgery
Electrosurgery utilises the heat generated by the passage of high frequency alternating electrical current through living
tissues. The application of a voltage across human tissue results in the formation of an electrical circuit between the
voltage source and the tissue. The tissue acts as a resistor and the level of resistance is determined by the water
content of the tissue. It is this resistance that results in the formation of heat.
Most diathermy units operate at a frequency of 200,000 kHZ to 5MHz. This means - tissue such as nerves and muscles
will not depolarise (since this seldom occurs at frequencies above 10,000Hz). The current waveform can be adjusted to
deliver three main therapeutic modalities; cutting, coagulation and blend.
Types of current
Cutting • Sinusoidal and non modulated waveform

• High average power and current density
• Precise cutting without thermal damage
Coagulation • Modulated current with intermittent dampened sine waves of high peak voltage
• Evaporation, rather than vapourisation of intracellular fluid occurs
• Results in formation of coagulum
Desication • Active electrode in direct contact with tissue

• Low current and high voltage system
• Results in loss of cellular water but no protein damage
Fulguration • Electrode probe is held away from tissue

• Produces spray effect with local, superficial tissue destruction
• Low amplitude and high voltage system
Blend • Alternating cutting and coagulation modes

• Total average power is less than with cutting
Diathermy
• Diathermy devices are used by surgeons in all branches of surgery.

• Use electric currents to produce local heat and thereby facilitate haemostasis or surgical dissection.
• Consist of a generator unit that is located outside the patient and can be set to the level of power required by
the surgeon.
• There are two major types of diathermy machine;
Monopolar
• The current flows through the diathermy unit into a handheld device that is controlled by surgeon.
• Electricity can flow from the tip of the device into the patient.
• The earth electrode is located some distance away.

• The relatively narrow tip of the diathermy device produces local heat and this can be used to vaporise and
fulgurate tissues.
• In cutting mode sufficient power is applied to the tissues to vaporise their water content.
• In coagulation mode the power level is reduced so that a coagulum is formed instead.
• In blend mode, the alternate cutting and coagulation functions, these tend to be used during procedures such as
colonoscopic polypectomy.
Bipolar
• The electric current flows from one electrode to another however, both electrodes are usually contained within
the same device e.g. a pair of forceps.
• The result is that heating is localised to the area between the two electrodes and surrounding tissue damage is
minimised.
Ultrasound based devices

• These include CUSA and Harmonic scalpel.
• They generate high frequency oscillations that seal and coagulate tissues.
• They have different energy settings that allow them to dissect and simultaneously seal vessels if required.
• The CUSA device leaves vessels intact that may then be divided.
Ligasure device
• Delivers tailored energy levels to allows simultaneous haemostasis and dissection.
• The device senses the impedance of the tissues and tailors energy levels accordingly.
Hazards of diathermy
• Inadvertent patient burn. This may result of careless handling of the device or in the case of monopolar devices
forgetting to apply a return electrode plate, In this situation patients may develop a contact burn when electricity
flows to earth
• Explosion or fire. This may occur when volatile anaesthetic gases or skin preparation fluid have been used
Sample question Theme: Electrosurgery

A. Cutting current
B. Coagulation current
C. Blended current
D. Fulguration
E. Desiccation
For each of the following electrosurgical applications please select the most likely modality used.
1. In this modality the active electrode is placed in direct contact with the tissue and is characterised by low current and
high voltage over a broad area.
The correct answer is Desiccation
In desiccation the device is placed in direct contact with the tissues (unlike fulguration). Because it is applied over a
broad area it tends not to cause protein damage (unlike coagulation).
2. An electrosurgical mode whereby the electrode is held away from the tissue. The current utilises a low amplitude and
high voltage.
The correct answer is Fulguration
Fulguration typically avoids contact between the electrode and the tissue with the current configured to favor arc
formation.
3. A modality in which a sinusoidal, non modulated waveform is produced and vapourises the tissues.
The correct answer is Cutting current
The high energy levels result in tissue vapourisation and cleavage of tissues.
Bowel Preparation
- CLOSED, STRICTURED/OBSTRUCTED cases: clear fluids for 24hrs prior 2procedure ē low residue
diet;
- FLEXIBLE SIGMOIDOSCOPY:- PO4 Enema prior to procedure, it clears distal bowel well
- COLONOSCOPY:- Na PicoSO4 & clear fluids for 24hours prior 2procedure used to maximize
emptying of bowel & optimizes the views obtained @ colonoscopy
- RECTAL MALIGNANCY:- To do LOW ANTERIOR RESECTION RECTUM, Na PicoSO4 & clear fluids for
24hours prior to procedure usually used
Management of pain
WHO Analgesic Ladder

• Initially peripherally acting drugs such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) are
given.
• If pain control is not achieved, the second part of the ladder is to introduce weak opioid drugs such as codeine
or dextropropoxyphene together with appropriate agents to control and minimise side effects.
• The final rung of the ladder is to introduce strong opioid drugs such as morphine. Analgesia from peripherally
acting drugs may be additive to that from centrally-acting opioids and thus, the two are given together.
The World Federation of Societies of Anaesthesiologists (WFSA) Analgesic Ladder

• For management of acute pain
• Initially, the pain can be expected to be severe and may need controlling with strong analgesics in combination
with local anaesthetic blocks and peripherally acting drugs.
• The second rung on the postoperative pain ladder is the restoration of the use of the oral route to deliver
analgesia. Strong opioids may no longer be required and adequate analgesia can be obtained by using
combinations of peripherally acting agents and weak opioids.
• The final step is when the pain can be controlled by peripherally acting agents alone.
Local anaesthetics
• Infiltration of a wound with a long-acting local anaesthetic such as Bupivacaine
• Analgesia for several hours
• Further pain relief can be obtained with repeat injections or by infusions via a thin catheter
• Blockade of plexuses or peripheral nerves will provide selective analgesia in those parts of the body supplied by
the plexus or nerves
• Can either be used to provide anaesthesia for the surgery or specifically for postoperative pain relief
• Especially useful where a sympathetic block is needed to improve postoperative blood supply or where central
blockade such as spinal or epidural blockade is contraindicated.
Spinal anaesthesia
Provides excellent analgesia for surgery in the lower half of the body and pain relief can last many hours after completion
of the operation if long-acting drugs containing vasoconstrictors are used.
- Side effects of spinal anaesthesia include: hypotension, sensory and motor block, nausea and urinary retention.
Epidural anaesthesia
An indwelling epidural catheter inserted. This can then be used to provide a continuous infusion of analgesic agents. It
can provide excellent analgesia. They are still the preferred option following major open abdominal procedures and help
prevent post operative respiratory compromise resulting from pain.
- Disadvantages of epidurals is that they usually confine patients to bed, especially if a motor block is present. In addition
an indwelling urinary catheter is required. Which may not only impair mobility but also serve as a conduit for infection.
They are contraindicated in coagulopathies.
Transversus Abdominal Plane block (TAP)

In this technique an ultrasound is used to identify the correct muscle plane and local anaesthetic (usually bupivicaine) is
injected. The agent diffuses in the plane and blocks many of the spinal nerves. It is an attractive technique as it provides
a wide field of blockade but does not require the placement of any indwelling devices. There is no post operative motor
impairment. For this reason it is the preferred technique when extensive laparoscopic abdominal procedures are
performed. They will then provide analgesia immediately following surgery but as they do not confine the patient to bed,
the focus on enhanced recovery can begin sooner.
-The main disadvantage is that their duration of action is limited to the half life of the local anaesthetic agent chosen. In
addition some anaesthetists do not have the USS skills required to site the injections.
Patient Controlled Analgesia (PCA)
- Patients administer their own intravenous analgesia and titrate the dose to their own end-point of pain relief using a
small microprocessor - controlled pump. Morphine is the most popular drug used.
Strong Opioids
Severe pain arising from deep or visceral structures requires the use of strong opioids
Morphine
• Short half life and poor bioavailability.
• Metabolised in the liver and clearance is reduced in patients with liver disease, in the elderly and the debilitated
• Side effects include nausea, vomiting, constipation and respiratory depression.
• Tolerance may occur with repeated dosage
Pethidine
• Synthetic opioid which is structurally different from morphine but which has similar actions. Has 10% potency of
morphine.
• Short half life and similar bioavailability and clearance to morphine.
• Short duration of action and may need to be given hourly.
• Pethidine has a toxic metabolite (norpethidine) which is cleared by the kidney, but which accumulates in renal
failure or following frequent and prolonged doses and may lead to muscle twitching and convulsions. Extreme
caution is advised if pethidine is used over a prolonged period or in patients with renal failure.
Weak opioids
Codeine: markedly less active than morphine, has predictable effects when given orally and is effective against mild to
moderate pain.
Non opioid analgesics - Mild to moderate pain.

Paracetamol
• Inhibits prostaglandin synthesis.
• Analgesic and antipyretic properties but little anti-inflammatory effect
• It is well absorbed orally and is metabolised almost entirely in the liver
• Side effects in normal dosage and is widely used for the treatment of minor pain. It causes hepatotoxicity in over
dosage by overloading the normal metabolic pathways with the formation of a toxic metabolite.
NSAIDs
• Analgesic and anti-inflammatory actions
• Inhibition of prostaglandin synthesis by the enzyme Cyclooxygenase which catalyses the conversion of
arachidonic acid to the various prostaglandins that are the chief mediators of inflammation. All NSAIDs work in
the same way and thus there is no point in giving more than one at a time. .
• NSAIDs are, in general, more useful for superficial pain arising from the skin, buccal mucosa, joint surfaces and
bone.
• Relative contraindications: history of peptic ulceration, gastrointestinal bleeding or bleeding diathesis;
operations associated with high blood loss, asthma, moderate to severe renal impairment, dehydration and any
history of hypersensitivity to NSAIDs or aspirin.
Neuropthic pain National Institute of Clinical Excellence (UK) guidelines:

• First line: Amitriptyline (Imipramine if cannot tolerate) or pregabalin
• Second line: Amitriptyline AND pregabalin
• Third line: refer to pain specialist. Give tramadol in the interim (avoid morphine)
• If diabetic neuropathic pain: Duloxetine
Neuropathic pain
Neuropathic pain may be defined as pain which arises following damage or disruption of the nervous system. It is often
difficult to treat and responds poorly to standard analgesia. Examples include:
• diabetic neuropathy
• post-herpetic neuralgia
• trigeminal neuralgia
• prolapsed intervertebral disc
NICE issued guidance in 2010 on the management of neuropathic pain:

• first-line treatment*: oral amitriptyline or pregabalin
• if satisfactory pain reduction is obtained with amitriptyline but the person cannot tolerate the adverse effects,
consider oral imipramine or nortriptyline as an alternative
• second-line treatment: if first-line treatment was with amitriptyline, switch to or combine with pregabalin. If first-
line treatment was with pregabalin, switch to or combine with amitriptyline
• other options: pain management clinic, tramadol (not other strong opioids), topical lidocaine for localised pain if
patients unable to take oral medication
*please note that for some specific conditions the guidance may vary. For example carbamazepine is used first-line for
trigeminal neuralgia, duloxetine for diabetic neuropathy
Pain - neuronal transmission
Somatic pain
• Peripheral nociceptors are innervated by either small myelinated fibres (A-gamma) fibres or by unmyelinated C
fibres.
• The A gamma fibres register high intensity mechanical stimuli. The C fibres usually register high intensity
mechanothermal stimuli.
Surgical site infection

• Surgical site infections may occur following a breach in tissue surfaces and allow normal commensals and other
pathogens to initiate infection. They are a major cause of morbidity and mortality.
• Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at least 5% of
patients undergoing surgery will develop an SSI as a result.
• In many cases the organisms are derived from the patient's own body. Measures that may increase the risk of
SSI include:
• Shaving the wound using a razor (disposable clipper preferred)
• Using a non iodine impregnated incise drape if one is deemed to be necessary
• Tissue hypoxia
• Delayed administration of prophylactic antibiotics in tourniquet surgery
Preoperatively
• Don't remove body hair routinely
• If hair needs removal, use electrical clippers with single use head (razors increase infection risk)
• Antibiotic prophylaxis if:
- placement of prosthesis or valve
- clean-contaminated surgery
- contaminated surgery
• Use local formulary
• Aim to give single dose IV antibiotic on anaesthesia
• If a tourniquet is to be used, give prophylactic antibiotics earlier
Intraoperatively
• Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
• Cover surgical site with dressing
• A recent meta analysis has confirmed that administration of supplementary oxygen does not reduce the risk of
wound infection. In contrast to individual RCT's(1)
Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention
Use of diathermy for skin incisions

In the NICE guidelines the use of diathermy for skin incisions is not advocated(2). Several randomised controlled trials
have been undertaken and demonstrated no increase in risk of SSI when diathermy is used(3).
Wound Contamination
Clean : Non-infected skin with no hollow organ is cut

Clean-contaminated : Cut of hollow organ except COLON (e.g. GB, unruptured Appendix)
Contaminated : Colon incision; open #; animal/ human bites; colon insion ē minimal spillage.
Dirty : Perforation; wounds made in presence of pus; perforated viscus/traumatic wound>4hrs
Abdominal Wound Dehiscence
• Superficial - skin wound alone fails.

• Complete - failure of all layers.
Factors increase the risk are:

• Malnutrition
• Vitamin deficiencies
• Jaundice
• Steroid use
• Major wound contamination (e.g. faecal peritonitis)
• Poor surgical technique (Mass closure technique is the preferred method– Jenkins Rule)
The Jenkins Rule: The required length of the surgical suture material for closure of a wound with interrupted
stitches is four times the length of the wound, as each bite should be 1 cm from the edge, and placed 1 cm from the
previous suture.
When sudden full dehiscence occurs the management is as follows:

• Analgesia
• Intravenous fluids
• Intravenous broad spectrum antibiotics
• Coverage of the wound with saline impregnated gauze (on the ward)
• Arrangements made for a return to theatre
Surgical strategy
• Correct the underlying cause (eg TPN or NG feed if malnourished)
• Determine the most appropriate strategy for managing the wound
Options
Resuturing • When wound edges are healthy and enough tissue for sufficient coverage.
• Deep tension sutures are used for this purpose.
Application of a wound • Its a clear dressing with removable front.

manager • Suitable when some granulation tissue is present over the viscera or where there is a high
output bowel fistula present in the dehisced wound.
Application of 'Bogota • Its a clear plastic bag that is cut and sutured to the wound edges
bag' • Temporary measure to be adopted when the wound cannot be closed
• Necessarily a return to theatre for definitive management.
Application of VAC • These can be used ONLY if the correct layer is interposed between the suction device and
dressing system the bowel.
• Failure to adhere to this absolute rule will almost invariably result in the development of
multiple bowel fistulae and create an extremely difficult management problem.
Surgical jaundice
Jaundice can present in a manner of different surgical situations. As with all types of jaundice a carefully history and
examination will often give clues as the most likely underlying cause. Liver function tests whilst conveying little in the way
of information about liver synthetic function, will often facilitate classification as to whether the jaundice is pre hepatic,
hepatic or post hepatic. The typical LFT patterns are given below:
Location Bilirubin ALT/ AST Alkaline phosphatase
Pre hepatic Normal or high Normal Normal
Hepatic High Elevated (often very high) Elevated but seldom to very high levels
Post hepatic High-very high Moderate elevation High- very high
In post hepatic jaundice the stools are often of pale colour and this feature should be specifically addressed in the
history.
Modes of presentation
Diagnosis Typical features Pathogenesis
Gallstones Typically history of biliary colic Usually small calibre gallstones which can pass through the
or episodes of chlolecystitis. cystic duct. In Mirizzi syndrome the stone may compress the bile
Obstructive type history and duct directly- one of the rare times that cholecystitis may present
test results. with jaundice
Cholangitis Usually obstructive and will Ascending infection of the bile ducts usually by E. coli and by
have Charcots triad of definition occurring in a pool of stagnant bile.
symptoms (pain, fever,
jaundice)
Pancreatic cancer Typically painless jaundice Direct occlusion of distal bile duct or pancreatic duct by tumour.
with palpable gallbladder Sometimes nodal disease at the portal hepatis may be the culprit
(Courvoisier's Law) in which case the bile duct may be of normal calibre.
TPN associated Usually follows long term use Often due to hepatic dysfunction and fatty liver which may occur
jaundice and is usually painless with with long term TPN usage.
non obstructive features
Bile duct injury Depending upon the type of Often due to a difficult cholecystectomy when anatomy in Calots
injury may be of sudden or triangle is not appreciated. In the worst scenario the bile duct is
gradual onset and is usually of excised and jaundice offers rapidly post operatively. More
obstructive type insidious is that of bile duct stenosis which may be caused by
clips or diathermy injury.
Cholangiocarcinoma Gradual onset obstructive Direct occlusion by disease and also extrinsic compression by
pattern nodal disease at the porta hepatis.
Septic surgical Usually hepatic features Combination of impaired biliary excretion and drugs such as
patient ciprofloxacin which may cause cholestasis.
Metastatic disease Mixed hepatic and post Combination of liver synthetic failure (late) and extrinsic
hepatic compression by nodal disease and anatomical compression of
intra hepatic structures (earlier)
Diagnosis
An ultrasound of the liver and biliary tree is the first line test. This will establish bile duct calibre, often ascertain the
presence of gallstones, may visualise pancreatic masses and other lesions. The most important clinical question is
essentially the extent of biliary dilatation and its distribution.
CT scan – Where pancreatic neoplasia is suspected.
MRI/ MRCP – With liver tumours and cholangiocarcinoma . If MRCP fails to give adequate information and ERCP may
be necessary. It is however, invasive and certainly not without risk and highly operator dependent
PET scans may be used to stage a number of malignancies but do not routinely form part of first line testing.
Management
Clearly this will depend to an extent upon the underlying cause but relief of jaundice is important even if surgery forms
part of the planned treatment as patients with unrelieved jaundice have a much higher incidence of septic complications,
bleeding and death.
Screen for and address any clotting irregularities
In patients with malignancy a stent will need to be inserted. These come in two main types; metal and plastic. Plastic
stents are cheap and easy to replace and should be used if any surgical intervention (e.g. Whipples) is planned.
However, they are prone to displacement and blockage. Metal stents are much more expensive and may compromise a
surgical resection. However, they are far less prone to displacement and to a lesser extent blockage than their plastic
counterparts.
If malignancy is in bile duct/ pancreatic head and stenting has been attempted and has failed, then an alternative
strategy is to drain the biliary system percutaneously via a transhepatic route. It may also be possible to insert a stent in
this way. One of the main problems with temporary PTC's is their propensity to displacement which may result in a bile
leak.
In patients who have a bile duct injury surgery will be required to repair the defect. If the bile duct has been inadvertently
excised then a hepatico-jejunostomy will need to be created (difficult!)
If gallstones are the culprit then these may be removed by ERCP and a cholecystectomy performed. Where there is
doubt about the efficacy of the ERCP an operative cholangiogram should be performed and bile duct exploration
undertaken where stones remain. When the bile duct has been formally opened the options are between closure over a
T tube, a choledochoduodenostomy or choledochojejunostomy.
Patients with cholangitis should receive high dose broad spectrum antibiotics via the intravenous route. Biliary
decompression should follow soon afterwards and instrumenting the bile duct of these patients will often provoke a septic
episode (but should be done anyway).
● (+) ve DPL (Diagnostic Peritoneal Lavage):
3
- RBC>100000/mm . - Peritoneal Lavage Fluid (+)ve in catheter or ICD
3
- WBC> 500/mm - Aspiration of GI contents
- Gm staining showing organisms
● SIRS
- HR >90 / min
- Temp >380C or < 360C
- RR > 20 / min
- PaCO2 > 4.3 kPa
- WBC > 12000 or < 4000
DIFFERENCE BETWEEN JEJUNUM AND ILEUM

FEATURE JEJUNUM ILEUM
Wall Thick, vascular Thin, less vascular
Length ↓ ↑
Lumen ↑ ↓
Villi ↑ ↓
Fat ↓ ↑
Window (+) (-)
Vasa Recta / Straight Artery Long and less Short and more
Arterial Arcade 1-2 ↓ 3-6 ↑
Payer’s patches (-) (+)
Solitary Lymph Node ↓ ↑
Circular fold Large and closely set Less
ACCIDENT AND EMERGENCIES; TRAUMA
Glasgow Coma Scale

Responses are taken from each category (marks in descending order) to produce an overall score. Severe brain injuries
SCORE MOTOR TO PAIN VERBAL EYE

6 Normal/ Obeys Command RESPONSE OPENING
5 Localize pain Normal

4 Withdraw Confused Spontaneous
3 Abnormal Flexion/ Decorticate Inappropriate Words To Speech
2 Abnormal Extension/ Incomprehensible Sounds/ To Pain
Decerebrate Mumbles
1 None None None
are generally associated with GCS <8.
Trauma management
Following trauma there is a trimodal death distribution:

Immediately:- Following injury. Typically as result of brain or high spinal injuries, cardiac or great vessel damage.
In early hours:- Deaths due to phenomena(e.g.splenic rupture, sub dural haematoma; haemopneumothoraces)
In the days:- following injury. Usually due to sepsis or multi organ failure.
Aspects of trauma management

• ABCDE approach.
• Tension pneumothoraces will deteriorate with vigorous ventilation attempts, so be careful.
• Patients with head and neck trauma - Must be assumed to have a Cervical Spine Injury until proven otherwise.
• External haemorrhage is managed as part of the primary survey.
o As a rule tourniquets should not be used.
o Blind application of clamps tend to damage surrounding structures - so packing is the preferred
method of haemorrhage control.
• Urinary catheters and NG tubes may need to insert. But never in case of basal skull fracture & urethral injury.
Airway management
Oropharyngeal • Easy to insert and use

airway • No paralysis required
• Ideal for very short procedures
• Most often used as bridge to more definitive airway
Laryngeal mask • Widely used

• Very easy to insert
• Device sits in pharynx and aligns to cover the airway

• Poor control against reflux of gastric contents
• Paralysis not usually required
• Commonly used for wide range of anaesthetic uses, especially in day surgery
• Not suitable for high pressure ventilation (small amount of PEEP often possible)
Tracheostomy • Reduces the work of breathing (and dead space)

• May be useful in slow weaning
• Percutaneous tracheostomy widely used in ITU
• Dries secretions, humidified air usually required
Endotracheal tube • Provides optimal control of the airway once cuff inflated
• May be used for long or short term ventilation
• Errors in insertion may result in oesophageal intubation (therefore end tidal
CO2 usually measured)
• Paralysis often required
• Higher ventilation pressures can be used
Thoracic trauma
Tension pneumothorax • Often laceration to lung parenchyma with flap

• Most common cause: Mechanical ventilation in patient with pleural injury
• Symptoms overlap with cardiac tamponade, hyper-resonant percussion note is more
likely in tension pnemothorax
Pneumothorax • Most common cause: Lung laceration with air leakage
Flail chest • Multiple rib fractures (At least two fractures per rib in at least two ribs)
• Associated with pulmonary contusion
• Abnormal chest motion
Haemothorax • Most common cause: due to laceration of lung, intercostal vessel or internal
mammary artery
• Large Haemothoraces in CXR
Cardiac tamponade • Beck's Triad: (v.v.v. Imp. For scenario in SBA)

o Elevated Venous Pressure
o Reduced Arterial Pressure
o Reduced Heart Heart Sounds.
• Pulsus Paradoxus
• May occur with as little as 100ml blood
Pulmonary contusion • Most common potentially lethal chest injury

• Arterial blood gases and pulse oximetry important
• Early intubation within an hour if significant hypoxia
Blunt cardiac injury • Usually occurs secondary to chest wall injury

• ECG may show features of myocardial infarction
• Sequelae: hypotension, arrhythmias, cardiac wall motion abnormalities
Aorta disruption • Commonest cause of death after RTA or falls.

• Deceleration injuries. Usually incomplete laceration near Ligamentum Arteriosum
• Contained haematoma
• Widened mediastinum-Only 1-2% will have a normal chest x-ray
Diaphragm disruption • Most due to motor vehicle accidents and blunt trauma causing large radial tears
(laceration injuries result in small tears)
• More common on left side
• Insert gastric tube, which will pass into the thoracic cavity
Mediastinal traversing • Exit and entry wounds in separate hemithoraces.

wounds • Mediastinal haematoma or pleural cap suggests great vessel injury
Management of thoracic trauma

• Simple pneumothorax
o insert chest drain.
o Aspiration is risky in trauma as pneumothorax may be from lung laceration and convert to tension
pneumothorax.
o Patients with traumatic pneumothorax should never be mechanically ventilated, if needed - until a
chest drain is inserted
• Mediastinal traversing
o All patients should undergo CT angiogram and Oesophageal Contrast Swallow.
o Indications for thoracotomy are largely related to blood loss.
• Tracheobronchial tree injury

o In blunt trauma most injuries occur within 4cm of the carina.
o Features suggesting this injury include haemoptysis and surgical emphysema.
o These injuries have a very large air leak and may have tension pneumothorax.
• Haemothorax
o A wide bore 36F chest drain.
o Indications for thoracotomy include:
→ loss of more than 1.5L blood initially
→ ongoing losses of >200ml per hour for >2 hours.
• Cardiac contusions Usually cardiac arrhythmias.

o Perform echocardiography to exclude pericardial effusions and temponade.
o Risk of arrhythmias falls after 24 hours.
• Diaphragmatic injury
o Direct surgical repair is performed.
• Traumatic aortic disruption

o Surgical
• Pulmonary contusion
o Early intubation and ventilation
Chest drains
• Large bore chest drains -trauma and haemothorax drainage.

• Smaller diameter chest drains - pneumothorax or pleural effusion drainage.
• Insertion can be performed - either using anatomical guidance or through ultrasound guidance.
In the exam, the anatomical method is usually tested.
It is advised that chest drains are placed in the 'safe triangle'. The triangle is located in the mid axillary line of the
5th ICS. It is bordered by:
Anterior edge of latissimus dorsi,
The lateral border of pectoralis major,
A line superior to the horizontal level of the nipple, and the apex below the axilla.
Another triangle is situated behind the scapula. (also called triangle of auscultation) It is bounded
Above by the trapezius,
Below by the latissimus dorsi,
And laterally by the vertebral border of the scapula;
The floor is partly formed by the rhomboid major.
If the scapula is drawn forward by folding the arms across the chest, and the trunk bent forward, parts of the sixth and
seventh ribs and the interspace between them become subcutaneous and available for auscultation. The space is
therefore known as the triangle of auscultation
.
Management of acute coronary syndrome
All patients should receive

- Aspirin 300mg
- Nitrates or Morphine to relieve chest pain if required
Antithrombin Treatment: LMWH for patients who are not at a high risk of bleeding and who are not having angiography
within the 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 umol/l unfractionated
heparin should be given.
Clopidogrel 300mg- Clopidogrel should be continued for 12 months.
Intravenous Glycoprotein (IIb/IIIa receptor antagonist) (eptifibatide or tirofiban) should be given to patients who
have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who
are scheduled to undergo angiography within 96 hours of hospital admission.
(Coronary angiography) should be considered within 96 hours of first admission to hospital to patients who have a
predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically
unstable.
Aortic dissection
• More common than rupture of the abdominal aorta

• 33% of patients die within the first 24 hours, and 50% die within 48 hours if no treatment received
• Associated with hypertension
• Features of Aortic Dissection:
Tear in the intimal layer,
Followed by formation and propagation of a subintimal hematoma.
Cystic medial necrosis (Marfan's)
• Most common site of dissection: 90% occurring within 10 centimetres of the aortic valve
Stanford Classification
Type Location Treatment
A Ascending aorta/ Surgery- aortic root replacement

aortic root
B Descending Medical therapy with

aorta antihypertensives
DeBakey classification
Type Site affected
I Ascending aorta, aortic arch, descending aorta
II Ascending aorta only
III Descending aorta distal to left subclavian artery
Clinical features
• Tearing, sudden onset chest pain (painless 10%)
• Hypertension or Hypotension
• A blood pressure difference greater than 20 mm Hg
• Neurologic deficits (20%)
• Early Diastolic murmur may be found
• The right coronary artery may become involved in the dissection, causing myocardial infarct in up to 2% cases
(hence ST elevation in the inferior leads)
Investigations
• CXR: widened mediastinum, abnormal aortic knob, ring sign, deviation trachea/oesophagus
• CT (spiral)
• MRI
• Angiography (95% of patients diagnosed)
Management
Beta-blockers: aim HR 60-80 bpm and systolic BP 100-120 mm Hg.
Urgent surgical intervention: type A dissections. This will usually involve aortic root replacement
Abdominal trauma
• Deceleration injuries are common.
• In blunt trauma requiring laparotomy the spleen is most commonly injured (40%)
• In blunt trauma if CT scanning shows a large amount of retroperitoneal air then it is Duodenal injury
• Stab wounds traverse structures most commonly liver (40%)
• Gunshot wounds have variable effects depending upon bullet type. Small bowel is most commonly injured
(50%). The enteric contents will tend to result in a large amount of intra abdominal fluid.
• Patients with stab wounds and no peritoneal signs up to 25% will not enter the peritoneal cavity
• Blood at urethral meatus suggests a urethral tear
• High riding prostate on PR = urethral disruption
Investigations In Abdominal Trauma
Diagnostic Peritoneal Lavage Abdominal CT scan USS
Indication Document bleeding if Document organ injury if Document fluid if hypotensive

hypotensive normotensive
Advantages Early diagnosis and sensitive; Most specific for localizing injury; 92 Early diagnosis, non invasive
98% accurate to 98% accurate and repeatable; 86 to 95%
accurate
Disadvantages Invasive and may miss Location of scanner away from Operator dependent and may
retroperitoneal and facilities, time taken for reporting, miss retroperitoneal injury
diaphragmatic injury need for contrast
Amylase may be normal following pancreatic trauma

Urethrography if suspected urethral injury
Pelvic Fractures
Open Book Fracture

Often the result from a heavy impact to the groin (pubis - forces from anterior-posterior direction usually cause
external rotation of the hemi-pelvis results the injury) - a common motorcycling accident injury.
Left and Right halves of the pelvis are separated at front and rear, the front opening more than the rear, i.e. like an
open book that falls to the ground and splits in the middle.( Pubic Diastasis > 2.5 cm)
Open fractures have increased risk of infection and hemorrhaging from vessel injury, leading to higher mortality.
Inter-relationship between Tile's and Young and Burgess Classification

Rotationally + Vertically Stable : Isolated Iliac Wing Fracture; Isolated Pubic Ramus Fracture
Rotationally Unstable + Vertically Stable : Lateral Compression; Open Book Fracture
Rotationally + Vertically Unstable : Vertical Shear Fracture
Lower Genitourinary Tract Trauma

• Most bladder injuries occur due to blunt trauma
• 85% associated with pelvic fractures
• Easily overlooked during assessment in trauma
• Up to 10% of male pelvic fractures are associated with urethral or bladder injuries
Types of Injury
Urethral Injury • Mainly in males

• Blood at the meatus (50% cases)
• There are 2 types:
i.Bulbar rupture
- Most Common
- Straddle type injury e.g. bicycles
- Triad signs: Urinary Retention, Perineal Haematoma, Blood @ Meatus
ii. Membranous rupture

- Can be extra or intraperitoneal
- Commonly due to pelvic fracture
- Penile or perineal oedema/ hematoma
- DRE: prostate displaced upwards (beware of co-existing retroperitoneal
haematomas)
as they may make examination difficult)
- Investigation: Ascending Urethrogram

- Management: Suprapubic Catheter (surgical placement, not percutaneously)
External genitalia injuries (i.e., • Secondary to injuries caused by penetration, blunt trauma, continence- or
the penis and the scrotum) sexual pleasure-enhancing devices, and mutilation
Bladder injury • Rupture is intra or extra peritoneal

• Presents with haematuria or suprapubic pain
• H/O pelvic fracture +Void inability : Suspect bladder or urethral injury
• Inability to retrieve all fluid used to irrigate the bladder through a Foley
catheter indicates bladder injury
• Investigation- IVU or cystogram
• Management: laparotomy if intraperitoneal, conservative if extraperitoneal
Spinal and Cervical Injuries
Vascular trauma
Assessment
Check for signs of distal perfusion
Doppler signal distally (monophasic/ biphasic or triphasic)
Anatomical location (which vessel is likely to be involved)
Duplex scanning and angiography are "gold standard" tests
Management
Simple lacerations of arteries is directly closed, or a Vein Patch applied if there is a risk of subsequent stenosis.
Transection of the vessel is treated by either end to end anastomosis (often not possible) or an interposition
vein graft.
Use of PTFE in traumatic open injuries (will invariably result in infection)
Shock
The pathophysiology of shock is an important surgical topic and may be divided into the following aetiological groups:
• Septic
• Haemorrhagic
• Neurogenic
• Cardiogenic
• Anaphylactic
SEPTIC SHOCK
Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response Syndrome (SIRS). This is
characterised by:
o o
→ Body temperature outside 36 C - 38 C
→ HR >90 beats/min
→ Respiratory rate >20/min
3 3
→ WBC count >12,000/mm or < 4,000/mm .
Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ
failure have severe sepsis and those with refractory hypotension -septic shock.
During the septic process there is marked activation of the immune system with extensive cytokine release. This may be
coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of Excessive Inflammation, Coagulation and Fibrinolytic
Suppression.
Surviving sepsis - following key areas for attention:

→ Prompt administration of antibiotics
→ Haemodynamic stabilisation: Hypovolaemia needs fluid administration, target CVP 8-12cm H2O, MAP >65mmHg.
→ Modulation of septic response: Glycaemic control, use of activated Protein C and sometimes i/v steroids.
Summary :
Occurs when the peripheral vascular dilatation causes a fall in SVR. Similar response may occur in anaphylactic shock,
neurogenic shock
Reduced SVR
Increased HR
Normal / Increased CO
Decreased BP
HAEMORRHAGIC SHOCK
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will equate to 5 litres. This
changes in children (8-9% body weight) and is slightly lower in the elderly. The table below outlines the 4 major classes
of haemorrhagic shock and their associated physiological sequelae:
Decreasing BP during hemorrhagic shock causes organ hypoperfusion and relative myocardial ishaemia. The cardiac
index gives a numerical value for tissue oxygen delivery and is given by the equation: Cardiac index= 13.4 - [Hb] -
SaO2 + 0.03 X PaO2.
In patients suffering from trauma the most likely cause of shock is haemorrhage. When assessing trauma patients it is
worth remembering that in order to generate a palpable femoral pulse, arterial pressure of >65mmHg is required.
Once bleeding is controlled and circulating volume normalized the levels of transfusion should be to maintain Hb of 7-8 in
those with no risk factors for tissue hypoxia and Hb 10 for those who have such risk factors.
Summary :
Blood vol. depletion: Haemorrhage, Vomiting, Diarrhoea, Dehydration, Third-Space Losses during major operations:
Increased SVR
Increased HR
Decreased CO
Decreased BP
NEUROGENIC SHOCK
Occurs mostly following a spinal cord transaction, usually at a high level.
There is resultant interruption of the autonomic nervous system.
Decreased sympathetic tone or raised parasympathetic tone → Vasodilation → Decreased peripheral vascular
resistance → Decrease preload → Decrease CO (Starlings law) → Decrease peripheral tissue perfusion → SHOCK
In contrast with many other types of shock, Peripheral Vasoconstrictors are used to return vascular tone to normal.
CARDIOGENIC SHOCK
The main medical cause is ischaemic heart disease.
In trauma, direct myocardial trauma or contusion is more likely.
Evidence of ECG changes and overlying sternal fractures or contusions should raise the suspicion of injury.
Treatment is supportive and transthoracic echo used to determine pericardial fluid or direct myocardial injury.
Troponin levels in trauma patients may be undertaken but less useful in delineating the extent of myocardial trauma
than following MI.
When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the
most likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and
will require cardiopulmonary bypass to achieve this. Some may require intra aortic balloon pump as a bridge to
surgery.
Summary : e.g. MI, valve abnormality

Increased SVR (vasoconstriction in response to low BP)
Increased HR (sympathetic response)
Decreased CO
Decreased BP
ANAPHYLACTIC SHOCK
Antigen recognised by IgE molecules on the surface of mast cells.
Rapid degranulation with release of histamine and other inflammatory cytokines.
Treatment:
Adrenaline Hydrocortisone Chlorpheniramine
< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg
6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg
6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg
Adult +child >12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg
Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the
middle third of the thigh.
Common identified causes of anaphylaxis:
o food (e.g. Nuts) - the most common cause in children
o drugs
o venom (e.g. Wasp sting)
Management Summary
- Remove allergen
- ABCD
- Drugs:
Adrenaline 1:1000 0.5ml I/M (not I/V). Repeat after 5 minutes if no response.
Then Chlorpheniramine 10mg IV
Then Hydrocortisone 100-200mg IV
Craniomaxillofacial injuries (Le Fort Fractures)
Le Fort I (Horizontal)
Fracture extends from the nasal septum laterally through the maxilla just above the teeth and thence backwards to the
pterygoid region
Le Fort II (Pyramidal)
Fracture extending from the nasal bridge below the nasofrontal suture through the frontal processes of the maxilla,
inferolaterally through the lacrimal bones and inferior orbital floor and rim through the inferior orbital foramen, and
inferiorly through the anterior wall of the maxillary sinus; it then travels under the zygoma, across the pterygomaxillary
fissure, and through the pterygoid plates. Important Clinical Features are:
Infraorbital Parasthesia
Palatal Mobility
Malocclusion of Teeth
Le Fort III (Transverse)

Fracture is complex injury which is often bilateral and extends right across the fronto ethmoid regions, superior and
lateral orbits to the zygomatic arch laterally and back through the ethmoid to the sphenoid. It is a form of craniofacial
dysjunction. Important Clinical Features are:
Flat Face; Pan/Dish face is the classical feature.
Ocular injuries
Superior Orbital Fissure Syndrome

Severe force to the lateral wall of the orbit resulting in compression of neurovascular structures. Results in :
→ Complete opthalmoplegia and ptosis (Cranial nerves 3, 4, 6 and nerve to Levator Palpebrae Superioris)
→ Relative afferent pupillary defect
→ Dilatation of the pupil and loss of accommodation and corneal reflexes
→ Altered sensation from forehead to vertex (frontal branch of trigeminal nerve)
Orbital Blow Out Fracture

→ When an object of slightly larger diameter than the orbital rim strikes the incompressible eyeball.
→ The bone fragment is displaced downwards into the antral cavity, remaining attached to the orbital periosteum.
→ Priorbital fat may be herniated through the defect, interfering with the Inferior Rectus and Inferior Oblique
muscles which are contained within the same fascial sheath.
→ This prevents upward movement and outward rotation of the eye and the patient experiences diplopia on
upward gaze.
→ Initial bruising and swelling make assessment difficult and patients should be reviewed 5 days later.
→ Residual defects may require orbital floor reconstruction.
Nasal Fractures
→ Control epistaxis
→ CSF rhinorrhoea implies that the cribriform plate has been breached and antibiotics will be required.
→ Usually best to allow bruising and swelling to settle and then review patient clinically.
→ Major persistent deformity requires fracture manipulation, best performed within 10 days of injury.
Retrobulbar haemorrhage
• P ain (usually sharp and within the globe)
• P roptosis
• P upil reactions are lost
• P aralysis (eye movements lost)
• V isual acuity is lost (colour vision is lost first)
Management:
Mannitol 1g/Kg as 20% infusion, Osmotic diuretic, Contra-indicated in CCF and pulmonary oedema
Acetazolamide 500mg IV, Reduces aqueous pressure by inhibition of carbonic anhydrase (used in glaucoma)
Dexamethasone 8mg orally or intravenously
In a traumatic setting an urgent Cantholysis may be needed prior to definitive surgery.
Consider Papaverine 40mg smooth muscle relaxant and Dextran 40 500mls IV improves perfusion
Head Injury
Bleeding in between the Dura Mater and Skull.

Extradural Results from acceleration-deceleration trauma or a blow to the side of the head.
Haematoma Majority occur in the temporal region where fractures cause rupture of Middle Meningeal Artery.
(EDH) Occipital region also can be involved.
Features
• Raised intracranial pressure(ICP)
• Some patients may exhibit a lucid interval
Subdural Blood collects between Dura and Arachnoid - Acute Venous Hemorrhage. Hemorrhage of Cortical
Haematoma Bridging Veins draining cortical blood into Superior Saggital Sinus
(SDH) Commonly occur around the Frontal and Parietal lobes.
May be either acute or chronic. Chronic SDH are most common in the elderly and chronic alcoholics
who have brain atrophy, which increases the space traversed by the bridging veins and renders the
stretched vein susceptible to tearing.
Hematomas may develop within 1 week after injury but present with clinical signs within hours
Clinical Signs: Decreased consciousness level, Ipsilateral Pupillary Dilation, Headache, Contralateral
Hemiparesis
Sub- Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in
arachnoid association with other injuries when a patient has sustained a traumatic brain injury.
Hemorrhage Spontaneous Intracranial Haemorrhage
(SAH) Most commonly SAH which is due to intra cranial aneurysm in 85% cases.
Approximately 10% of cases have normal angiography and the cause will remain unclear.
Patients with inherited connective tissue disorders are at higher risk although most cases are
sporadic.
>95% cases will have headache (often thunderclap)
>15% will have coma
Investigation
CT scan (although as CSF blood clears the sensitivity declines)
Lumbar puncture if CT normal (very unlikely if normal)
CT angiogram to look for aneurysms.
Management
Supportive treatment, optimising BP and ventilation if needed.
Nimodipine reduces cerebral vasospasm and reduces poor outcomes.
Untreated patients most likely to rebleed in first 2 weeks.
Patients developing hydrocephalus will need a V-P shunt
Electrolytes require careful monitoring and hyponatraemia is common.
Treatment of aneurysm
>80% aneuryms arise from the anterior circulation
Craniotomy and clipping of aneurysm
Lesions may be coiled using an endovascular approach. Outcomes are better with coiling than
surgery
Intra- Usually hyperdense lesions on CT scanning.

cerebral Arise in areas of traumatic contusion with fuse to become a haematoma.
haematoma Areas of clot and fresh blood may co-exist on the same CT scan (Swirl sign).
Large haematomas and those associated with mass effect should be evacuated.
Intra- Haemorrhage occurs into the ventricular system

Ventricular Rare in adult and is typically associated with severe head injuries.
Hemorrhage In premature neonates it may occur spontaneously. The blood may clot and occlude CSF flow,
(IVH) hydrocephalus may result.
Majority of IVH occur in the first 72 hours after birth,
Aetiology is not well understood and is suggested to occur as a result of birth trauma combined with
cellular hypoxia
Treatment:
Is supportive, therapies such as intraventricular thrombolysis and prophylactic CSF drainage have not
shown benefit.
Hydrocephalus and rising ICP is an indication for shunting.
Depressed skull fracture

Depressed skull fractures are also referred to as Signature Fractures.
Results from the impact of a moving object on the cranial vault.
High velocity objects disrupt bone, and also drive the fracture fragments into the brain.
Blunt objects at low velocity produce a defect in skull that is of similar dimensions to the object (c.f. signature)
Injuries may affect the outer table alone or extend to involve the inner table.
Open fractures and those associated with intracranial haematomas may require surgery, uncomplicated
fractures without significant cosmetic deformities may be managed conservatively.
CT scanning is the initial imaging modality of choice.
Head injury and haematoma

Risk of haematoma (requiring removal) in adults attending accident and emergency units following head injury.
Injury Conscious level Risk of haematoma requiring removal
Concussion, no skull fracture Orientated 1 in 6000
Concussion, no skull fracture Not orientated 1 in 120
Skull fracture Orientated 1 in 32
Skull fracture Not orientated 1 in 4
Pathophysiology
Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
Diffuse axonal injury :mechanical shearing following deceleration, causing disruption and tearing of axons
Intra-cranial haematomas can be extradural, subdural or intracerebral,
Contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation
exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma
rendering the brain more susceptible to blood flow changes and hypoxia
The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
Management
Where there is life threatening rising ICP such as in extra dural haematoma and whilst theatre is prepared or
transfer arranged use of IV mannitol/ frusemide may be required.
Diffuse cerebral oedema may require decompressive craniotomy
Exploratory Burr Holes have little management in modern practice except where scanning may be unavailable
and to thus facilitate creation of formal craniotomy flap
Depressed skull fractures that are open require formal surgical reduction and debridement, closed injuries may
be managed non operatively if there is minimal displacement.
ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
ICP monitoring is mandatory in those who have GCS 3-8 and Abnormal CT scan.
Hyponatraemia is most likely to be due to syndrome of inappropriate ADH secretion.
Minimum of cerebral perfusion pressure of 70mmHg in adults.
Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.
Head injury management- NICE Guidelines
Summary of guidelines
All patients should be assessed within 15 minutes on arrival to A&E
Document all 3 components of the GCS
If GCS <8 or = to 8, consider stabilising the airway
Treat pain with low dose IV opiates (if safe)
Full spine immobilisation until assessment if: - GCS < 15
- neck pain/tenderness
- paraesthesia extremities
- focal neurological deficit
- suspected c-spine injury
If a c-spine injury is suspected a 3 view c-spine x-ray is indicated. CT c-spine is preferred if:
- Intubated
- GCS <13
- Normal x-ray but continued concerns
- Regarding c-spine injury
Immediate CT head (within 1h) if:

GCS < 13 on admission
GCS < 15 , 2hours after admission
Suspected open or depressed skull fracture

Suspected skull base fracture (panda eyes, Battle's sign, CSF from nose/ear, bleeding ear)
Focal neurology
Vomiting > 1 episode
Post traumatic seizure
Coagulopathy
Contact neurosurgeon if:

Persistent GCS < 8 or = 8
Unexplained confusion > 4h
Reduced GCS after admission
Progressive neurological signs
Incomplete recovery post seizure
Penetrating injury
Cerebrospinal leak
Observations
• 1/2 hourly GCS until 15
Head injury paediatrics
Criteria for immediate request for CT scan of the head (children)
Loss of consciousness lasting more than 5 minutes (witnessed)

Amnesia (antegrade or retrograde) lasting more than 5 minutes
Abnormal drowsiness
Three or more discrete episodes of vomiting
Clinical suspicion of non-accidental injury
Post-traumatic seizure but no history of epilepsy
GCS less than 14, or for a baby under 1 year GCS (paediatric) less than 15, on assessment in A&E
Suspicion of open or depressed skull injury or tense fontanelle
Any sign of basal skull fracture (haemotympanum, ‘panda' eyes, CSF leakage from ear or nose, Battle's sign)
Focal neurological deficit
If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head
Dangerous mechanism of injury (high-speed road traffic accident either as pedestrian, cyclist or vehicle occupant, fall
from a height of > 3 m, high-speed injury from a projectile or an object)
Interpretation of pupillary findings in head injuries
Pupil size Light response Interpretation
Unilaterally dilated Sluggish or fixed 3rd nerve compression secondary to tentorial herniation
Bilaterally dilated Sluggish or fixed Poor CNS perfusion

Bilateral 3rd nerve palsy
Unilaterally dilated or equal Cross reactive (Marcus - Gunn) Optic nerve injury
Bilaterally constricted May be difficult to assess Opiates

Pontine lesions
Metabolic encephalopathy
Unilaterally constricted Preserved Sympathetic pathway disruption
Brain death
Criteria for brain death

Fixed pupils which do not respond to sharp changes in the intensity of incident light
No corneal reflex
Absent oculo-vestibular reflexes - no eye movements following the slow injection of at least 50ml of ice-cold
water into each ear in turn (the caloric test)
No response to supraorbital pressure
No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5
minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in
patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and
diffusion oxygenation during the disconnection (so the brain stem respiratory centre is not challenged by the
ultimate, anoxic, drive stimulus)
The test should be undertaken by two appropriately experienced doctors on two separate occasions.
Burns
Type of burn Skin layers affected Skin appearance Blanching Management
Epidermal/Superficial Epidermis Red, moist Yes
Superficial partial Epidermis and part of papillary Pale, dry Yes Normally heals with no
thickness dermis affected intervention
Deep partial thickness Epidermis, whole papillary Mottled red colour No Needs surgical intervention
dermis affected (depending on site)
Full thickness Whole skin layer and Dry, leathery hard No Burns centre
subcutaneous tissue affected wound
Depth Of Burn Assessment

• Bleeding on needle prick
• Sensation
• Appearance
• Blanching to pressure
Percentage burn estimation

Lund Browder chart: most accurate even in children
Wallace rule of nines
Palmar surface: surface area palm = 0.8% burn
>15% body surface area burns in adults needs urgent burn fluid resuscitation
Transfer to burn centre if:

• Adult > 20% BSA total burns (second or third degree) or > 5% full thickness (third degree) burns
• Injuries to specific body areas, e.g. eyes, ears, face, hands, genitalia, associated inhalation injury
• Significant electrical/chemical burns
• Any child (< 10 years) with partial or full-thickness burns > 10% BSA.
Escharotomies
• Indicated in circumferential full thickness burns to the torso or limbs.
• Careful division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the
torso), or relieve compartment syndrome and oedema (where a limb is involved)
Burns pathology
Extensive burns
Haemolysis due to damage of erythrocytes by heat and microangiopathy

Loss of capillary membrane integrity causing plasma leakage into interstitial space
Extravasation of fluids from the burn site causing hypovolaemic shock (up to 48h after injury)- decreased blood
volume and increased haematocrit
Protein loss
Secondary infection e.g. Staphylococcus aureus
ARDS
Risk of Curlings ulcer (acute peptic stress ulcers)
Danger of full thickness circumferential burns in an extremity as these may develop compartment syndrome
Healing
Superficial burns: keratinocytes migrate to form a new layer over the burn site
Full thickness burns: dermal scarring. Usually need keratinocytes from skin grafts to provide optimal coverage.
Fluid resuscitation burns
Indication: >15% total body area burns in adults (>10% children)

• The main aim of resuscitation is to prevent the burn deepening
• Most fluid is lost 24h after injury
• First 8-12h fluid shifts from intravascular to interstitial fluid compartments
• Therefore circulatory volume can be compromised. However fluid resuscitation causes more fluid into the
interstitial compartment especially colloid (therefore avoided in first 8-24h)
• Protein loss occurs
Fluid Resuscitation Formulas
Parkland formula (Perhaps the simplest and most widely used, also important for exam)
(Crystalloid only e.g. Hartman's solution/Ringers' lactate)
Total fluid requirement in 24 hours = 4 ml X [Total Burn Area (%) X Body Weight (kg)]
• 50% given in first 8 hours
• 50% given in 16 hours
Resuscitation endpoint: Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)
Points to note:
• Starting point of resuscitation is time of injury
• Deduct fluids already given
After 24 hours
• Colloid infusion is begun @ rate: 0.5 ml X [ Total Burn Area (%) X Body Weight (kg) ]
• Maintenance crystalloid (usually dextrose-saline) is continued @ rate: 1.5 ml X (Burn Area) X (Body Weight)
• Colloids used include albumin and FFP
• Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to the inflammatory
cascade in burns
• High tension electrical injuries and inhalation injuries require more fluid
• Monitor: packed cell volume, plasma sodium, base excess, and lactate
● Muir-Barclay Formula (Not important)

[% of surface area of burn X mass(kg)] / 2 = volume of fluid ml
4hrly for 12 hrs then 6hrly for 12 hrs then once in 12 hrs
● American Burn Association Guidelines (Not important)

Formula = 2–4 ml Ringer’s lactate / kg / % BSA partial or full-thickness burn over 24 h;
50% given in the first 8 hours and 50% in the second 16 hours.
● Burn Fluid combination calculation (was set in the previous years' exam several times)
st
1 24 hrs
- Colloid (Plasma; plasma substitutes; dextran) : i/v 0.5ml / kg / % TBSA
- Crytalloid(Ringer’s Lactate): i/v 1.5ml / kg / % TBSA
- H2O (5% DA) : 2000ml i/v
nd
2 24 hrs
- Half of 1st 24 hrs
Lead poisoning
Along with acute intermittent porphyria, lead poisoning should be considered in questions giving a combination of
abdominal pain and neurological signs
Features
• abdominal pain
• peripheral neuropathy (mainly motor)

• fatigue
• constipation
• blue lines on gum margin (only 20% of adult patients, very rare in children)
Investigations
• The blood lead level greater than 10 mcg/dl is significant
• Full blood count: Microcytic Anaemia. Blood film shows red cell abnormalities including Basophilic Stippling and
Clover-Leaf Morphology
• Raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to
differentiate from acute intermittent porphyria
• Urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly
increased)
Management - various chelating agents are currently used:

• Dimercaptosuccinic acid (DMSA)
• D-penicillamine
• EDTA
• Dimercaprol
Oculogyric crisis
An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions
Features
• Restlessness, agitation
• Involuntary upward deviation of the eyes
Causes
• Phenothiazines
• Haloperidol
• Metoclopramide
• Postencephalitic Parkinson's disease
Management: Procyclidine
Management of acute cases- Paediatric
• Children will often insert objects into orifices such as the nose and external auditory meatus
• Assessment includes assessment of airway and haemodynamic status
• Where the airways is not immediately threatened decisions can be made as to whether to manage in the
emergency department or transfer to theatre
• In general children do not tolerate procedures well and it is usually safer to remove objects in theatre and under
general anaesthesia with a secure airway
• A chest x-ray is required to ensure that no object is present in the chest, not all objects are radiolucent.
However, signs such as focal consolidation may indicate small airway obstruction
• In the case of small bore missile injuries the decision relating to surgery depends on the size of the missile and
its location. Airgun pellets are a common culprit, if there is a long time interval between the incident and
presentation and the object has not caused any significant problems then it may be best left alone
• Airgun pellets lodged in the soft tissues (and glass) are usually notoriously difficult to localise and extract, no
matter how superficial. Removal in theatre is usually the best option. If the object is radiolucent then an image
intensifier should be used
Acute dystonic reaction
The anti dopaminergic drugs (such as antipsychotics) may result in extrapyramidal side effects. These may range from
mild parkinsonian symptoms such as resting tremor and bradykinesia. Through to acute dystonic reactions which are
characterised by abnormal and involuntary facial and bodily movements, such as spasmodic torticollis, oculogyric crisis
and oromandibular dystonia.
Chronic cases are generally only encountered in psychiatric units. In surgical practice the administration of the anti
dopaminergic drug metoclopramide may be sufficient to precipitate an attack.
Treatment may be required if symptoms are sufficiently troublesome; benzhexol and procyclidine are two drugs which
may be used.
HERNIA KEY POINTS

Bubonocele ● Hernia limited to Inguinal Canal
Funiculur ● Processus Vaginalis closed above the epididymis
Epiplocele ● Omentum as sac content
Scrotal Hernia ● Complete Hernia
Inguinal Hernia ● Hasselbach’s Triangle
Indirect: Leaves Abd. Cavity lat. to Inf. Epigastric Vessel→Travels entire canal → Enters
scrotum
Direct: Leaves Abd. Cavity med. to Inf. Epigastric Vessel→ Don’t traverse entire canal &
rarely enters scrotum
Spigelian Hernia ● Through the bands of Internal Oblique Muscle @ the level of Line of Douglas or Arcuate
or Linea Semicircularis ● Linea Semilunaris
Epigastric or
Paraumbilical ● Linea Alba
Laugier’s Hernia ● Through the gap of Lacunar Ligament
Gluteal Hernia ● Through the Greater Sciatic Foramen
Sciatic Hernia ● Through the Lesser Sciatic Foramen
Lumber Hernia ● Through the Triangle of Petit
Perineal Hernia ● Through the Pelvic floor; other name is Mery’s hernia
Obturator Hernia ● Through the Obturator canal
● Hernia passes between Pectineus & Adductor Longus
Pudendal Hernia ● Lateral protrution of peritoneum through hiatus of Schwalble between the origins of
Levator Ani from Obturator Internus following the surgical removal of pelvic organ
Litter’s Hernia ● Meckel’s Diverticulum as sac content
● Strangulation of Meckel’s
Richter’s Hernia ● Portion of circumference of Intestine as sac content
● Part of bowel @ antemesenteric margin strangulated
Maydel’s Hernia ● “W” loops of small bowel
● 2 separate loops of bowel as sac content
Pantaloon Hernia ● 2 sacs straddling the Inferior Epigastric Artery on either side; both direct & indirect
hernial sac present but vclinically present as direct
Morgagni Hernia ● Transverse colon enters Thoracic cavity – diaphragmatic hernia
Bochdalek Hernia ● If Morgagni hernia causes displaced apex beat; respiratory problem; scaphoid abdomen
Ventral Hernia ● Presence of a large scar atop a midline hernia
Inflammed Hernia ● Inflammation of sac contents
● Large red, hot trophic ulcer @ dependent aspect of large Umbilical Hernia
Incarcerated Hernia ● Fixation of contents within hernial sac (not assoc. ē any systemic or GIT upset);
irreducible
Narath’s Hernia ● Hernia in CDH due to lateral displacement of Psoas Muscle (Hidden behind femoral
vessels)
Prevesical Hernia ● Prevescical fat + Portion of Bladder protrude though small defect of Conjoint Muscle
Sliding Hernia ● Portion of Bladder forms the posterior wall of hernial sac
Cloquet’s Hernia ● Presence of sac under the fascia covering the Pectineus Muscle
● Only found during laparotomy – Obturator; Gluteal; Sciatic; Pelvic; Pudendal Hernia
● N.B.: if it’s a Hernia (a lump) but not evident, then Herniogram
But there is any confusion, whether it is hernia or not, then USG of the lump
● Hydrocele operation: Tunica Vaginalis is to be divided which is derived from Peritoneum
Note: Green coloured are more important for the Final exam
ABDOMEN (Part - 1)
VESSELS AND RELATED INFORMATION
Epigastric Arteries
Inferior Epigastric Artery arises (← External Iliac Artery) above the Inguinal Ligament → then passes along
the medial margin of the Deep Inguinal Ring → continues superiorly → lie back of the Rectus Abdominis
Muscle in front of the posterior layer of the Rectus Sheath → finally divides into numerous branches, which
anastomose (Above Umbilicus), with the branches of Superior Epigastric Artery (← Internal Thoracic Artery)
Within the Rectus Abdominis Muscle.
For CABG - Internal Thoracic Arteries are used. Then Rectus Abdominis Muscle is backed up by
Inferior Epigastric arteries to maintain blood supply
Superficial Epigastric Artery (Don't confuse with Superior Epigastric Artery) arises from the front of Femoral
Artery (1cm Below the Inguinal Ligament) → passes through Femoral Sheath & Cribriform Fascia → turns
upward In Front of the Inguinal Ligament → Ascends between two layers of Superficial Fascia (Camper's
and Scarpa's) → anastomoses ē Inferior Epigastric branches + its fellow of opposite side.
Distributes the Superficial Subinguinal Lymph Glands, Superficial Fascia, Skin
Abdominal aorta
The aorta enters the abdomen at T12 in the midline running in the Retroperitoneal space in front of the
vertebral column. It gives off (Superior To Inferior):
Ventral: (Unpaired Anterior Branches)

- Celiac trunk (T12 * / Upper part L1) *most sources tells - T12
(Celiac Trunk branches: Left Gastric; Hepatic; Splenic → Left Hand Side)
- SMA (Lower Part L1)
- IMA (L3)
Dorsal: - Lumber (4pairs; Lateral Paired Parietal) (L1-L4)
- Median Sacral (Unpaired, Terminal?) (LAST BRANCH)
Lateral: - Inferior Phrenic (lateral paired Parietal) (FIRST BRANCH) T12
[3 Lateral Paired Visceral branches]

- Middle supra-renal (L1)
- Renal (L1- L2)
- Gonadal Arteries (L2)
It then bifurcates into:
the Common Iliac Arteries ( L4)
** If surgical access is difficult during AAA surgery, then Left Renal Artery is divided to achieve the
access**
Abdominal aortic branches (chart)
Branches Level Paired Type
Inferior phrenic T12 (Upper border) Yes Parietal
Coeliac T12 No Visceral
Superior mesenteric L1 No Visceral
Middle suprarenal L1 Yes Visceral
Renal L1-L2 Yes Visceral
Gonadal L2 Yes Visceral
Lumbar L1-L4 Yes Parietal
Inferior mesenteric L3 No Visceral
Median sacral L4 No Parietal
Common iliac L4 Yes Terminal
Abdominal aortic topography
Origin T12
Termination L4
Posterior relations L1-L4 Vertebral bodies
Anterior relations Lesser omentum

Liver
Left renal vein
Inferior mesenteric vein
Third part of duodenum
Pancreas
Parietal peritoneum
Peritoneal cavity
Right lateral relations Right crus of the diaphragm

Cisterna chyli
Azygos vein
IVC (becomes posterior distally)
Left lateral relations 4th part of duodenum

Duodenal-jejunal flexure
Left sympathetic trunk
Abdominal Aorta Aneurysm (AAA)
• They may occur either true or false aneurysm.

• True has all 3 layers of the arterial wall are involved
• False has only a single layer of fibrous tissue forming the aneurysm wall.
• True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people.
• In UK the Aneurysm Screening Program is done by aortic ultrasound measurement in all men of 65 years.
Pathology
• After the age of 50 years, normal diameter of the Infrarenal Aorta is 1.5cm in females and 1.7cm in males.
Diameters ≥ 3cm = Aneurysmal.
• Result of the failure of elastic proteins within the extracellular matrix with a change in the balance of collagen and
elastic fibres.
• Loss of the intima with loss of elastic fibres from the media.(This process is associated with, and potentiated by,
increased proteolytic activity and lymphocytic infiltration)
Types
Fusiform Aneurysms
Appear as symmetrical bulges around the circumference of the aorta. They are the most common shape of aneurysm.
Saccular Aneurysms
Asymmetrical and appear on one side of the aorta. They are usually caused by trauma or a severe aortic ulcer.
Causes
Major risk factors for the development of aneurysms include smoking and hypertension.
• Atherosclerotic
– The commonest who are hypertensive, have diabetes and have been or are smokers
• Mycotic
– Staph and Salmonella species commonly
– Iatrogenic
– Traumatic
– Self-induced - IV drug Abusers
– Beside Aorta, it can occur at these arteries (SMA, Iliac, Femoral, Brachial,Radial, Ulnar, Carotid)
• Connective Tissues Diseases
– Marfans syndrome (genetically
genetically determined abnormality of a connective tissue protein, fibrillin
fibrillin)
– Ehlers Danlos syndrome (inherited
( collagen disorders, having fragile arteries which tear & bleed
following minimal injury))
• Rare but important causes include Syphilis
Management
• Most AAA are an incidental finding.
• Symptoms most often relate to rupture or impending rupture.
• 20% rupture anteriorly into the peritoneal cavity. Very poor prognosis.
• 80% rupture posteriorly into the retroperitoneal space
This is explained by La Places' law which relates size to transmural pressure. For this reason most vascular surgeons
will subject patients with an aneurysm size of 5cm or greater to CT scanning of the chest, abdomen and pelvis with the
aim of delineating anatomy and planning treatment. Depending upon co-morbidities, surgery is generally offered once
the aneurysm is between 5.5cm and 6cm.
Indications for surgery

• Symptomatic aneurysms (80% annual mortality if untreated)
• Increasing size above 5.5cm if asymptomatic
• Rupture (100% mortality without surgery)
Special groups
Supra renal AAA

These patients will require a supra renal clamp and this carries a far higher risk of complications and risk of renal failure.
Ruptured AAA
• In patients with symptoms of rupture (typical pain, haemodynamic compromise and risk factors),ideally prompt
laparotomy.
• In those with vague symptoms and haemodynamic stable, the ideal test is CT scan.
• Most common rupture site is retroperitoneal 80%. These patients will develop retroperitoneal haematoma. This can
be disrupted if BP is allowed to rise too high - so aim for BP is 100mmHg.
• Surgery should be swift.
Surgical Note: Plunging vascular clamps blindly into a pool of blood at the aneurysm neck carries the risk of injury of
Vena Cava. Occasionally a Supracoeliac Clamp is needed to effect temporary control, although leaving this applied for
more than 20 minutes tends to carry a dismal outcome
EVAR (EndoVascular Aneurysm Repair)

Patients are now being offered endovascular aortic aneurysm repair.
This is done by surgeons and radiologists jointly.
The morphology is important and not all are suitable. Features favoring a suitable aneurysm:
• Long neck
• Straight iliac vessels
• Healthy groin vessels
Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated grafts can allow
supra renal AAA to be treated.
Coeliac Axis
The coeliac axis has three main branches - Left Hand Side (LHS)
• L eft Gastric
• H epatic branches – Rt. Gastric, Gastroduodenal, Rt. Gastroepiploic, Superior Pancreaticoduodenal, Cystic.
• S plenic: branches – Pancreatic, Short Gastric, Left Gastroepiploic
It occasionally gives off one of the Inferior Phrenic Arteries. The coeliac axis branches off the aorta at T12.
Relations
Anteriorly Lesser omentum
Right Right coeliac ganglion and caudate process of liver
Left Left coeliac ganglion and gastric cardia
Inferiorly Upper border of pancreas and renal vein
Gastroduodenal artery
Supplies
Pylorus, proximal part of the duodenum, and indirectly to the pancreatic head (via the anterior and posterior superior
pancreaticoduodenal arteries)
Path
Most commonly arises from the common hepatic artery of the coeliac trunk
Terminates by bifurcating into the right gastroepiploic artery and the superior pancreaticoduodenal artery
Inferior vena cava

Origin
• L5
Path
• Left and right common iliac veins merge to form the IVC and Passes right of midline
• Paired segmental lumbar veins drain into the IVC throughout its length
• The Right Gonadal Vein empties directly into IVC and Left Gonadal Vein usually empties into Left Renal Vein.
• The next major veins are the Renal Veins and the Hepatic Veins
• Pierces the central tendon of diaphragm at T8 and enters Right atrium
Relations with Aorta

Proximally IVC lies to the right and anterior to the Aorta.
Distally the vena cava is on the right but posterior to the Aorta.
This means that the Right Renal Artery passes behind the IVC, whilst the Right Common Iliac Artery passes in
front of the Common Iliac Veins.
Other Relations
Anteriorly Small bowel, first and third part of duodenum, head of pancreas,
liver and bile duct, right common iliac artery, right gonadal artery
Posteriorly Right renal artery, right psoas, right sympathetic chain, coeliac
ganglion
Levels
Level Vein
T8 Hepatic vein, inferior phrenic vein, pierces diaphragm
L1 Suprarenal veins, renal vein
L2 Gonadal vein
L1-5 Lumbar veins
L5 Common iliac vein, formation of IVC
● IVC Tributaries: I Like To Rise So High; [Think, IVC wanting to rise high up to heart- NO VALVE.] (N-247,314)
I lilacs (common illiac)
L umbar (3rd & 4th)
T esticular (right) or ovarian
R enal
S uprarenal (right) (It can be injured during the right adrenalectomy)
H epatic vein
● A patient presents with superior vena caval obstruction. How many collateral circulations exist as alternative
pathways of venous return?
Ans: There are 4 collateral venous systems:
Azygos venous system
Internal mammary venous pathway
Long thoracic venous system with connections to the femoral and vertebral veins (2 pathways)
Despite this, venous hypertension still occurs.
Superior Mesenteric Artery Discussion (SMA)

• Branches off aorta at L1
• Supplies small bowel from duodenum (distal to ampulla of vater) through to mid transverse colon
• Takes more oblique angle from aorta and thus more likely to receive emboli than coeliac axis
Relations of SMA
Superiorly Neck of pancreas
Postero-inferiorly Third part of duodenum

Uncinate process
Posteriorly Left renal vein
Right Superior mesenteric vein
● SMA BRANCHES: MIIRJi

M iddle colic
I liocolic (Appendicular artery is the branch of iliocolic artery)
I nferior pancreaticoduodenal
R ight colic
J ejunal+ i leal (12-15 branches)
n
● Occlus of IMA is seldom asymptomatic as it gets supply also by Middle Colic Artery; usually between middle & left
colic.
● All veins in the body usually run a course parallel to the artery of the same name except Inferior Mesenteric Vein
● During development midgut bends around Superior Mesenteris Artery to form the Midgut Loop.
Inferior Mesenteric Artery Discussion (IMA)
Mesenteric vessel disease
● Primarily caused by arterial embolism resulting in infarction of the colon.

● More likely to occur in areas( such as the splenic flexure) that are located at the borders of the territory supplied by
SMA and IMA.
Acute mesenteric • Sudden onset abdominal pain followed by profuse diarrhoea.

embolus (commonest • May be associated with vomiting.
50%)
• Rapid clinical deterioration.
• Serological tests: WCC, lactate, amylase may all be abnormal particularly in
established disease. These can be normal in the early phases.
Acute on chronic • Usually longer history.

mesenteric ischaemia • Post prandial abdominal discomfort and weight loss.
• Patients will usually present with an acute on chronic event, but mostly not present
until mesenteric flow is reduced by >80%.
• When acute thrombosis occurs presentation may be as above. In the chronic
setting the symptoms will often be those of Ischaemic Colitis (mucosa is the
most sensitive area to this insult).
Mesenteric vein • Usually a history over weeks.

thrombosis • Abdominal signs and symptoms not occur until venous thrombosis
compromise arterial inflow.
• Thrombophilia accounts for 60% of cases.
Low flow mesenteric • Occurs when mesenteric perfusion is compromised by overuse of inotropes
infarction or background cardiovascular compromise.
• The bowel is not adequately perfused and infarcts occur from the mucosa outwards.
Diagnosis
• Serological tests: WCC, lactate, CRP, Amylase (can be normal in early disease).
• CT Angiography - Diagnosis of choise for arterial AND venous mesenteric disease. Arterial phase with thin
slices (<5mm) is done. Venous phase contrast is not helpful.
• SMA duplex USS - To evaluate the proximal SMA disease in patients with Chronic Mesenteric Ischaemia.
• MRI - Limited usefulness due to gut peristalsis and movement artefact.
Management
• Signs of peritonism: Laparotomy
o Limited resection of frankly necrotic bowel done. Relook laparotomy at 24-48h.
o In between urgent bowel revascularisation via endovascular (preferred) or surgery
• Mesenteric vein thrombosis: If no peritonism, Medical management with IV heparin
Prognosis
Overall poor.
Best outlook is from an acute ischaemia from an embolic event where surgery occurs within 12h.
Survival may be 50%. This falls to 30% with treatment delay. The other conditions carry worse survival figures.
Internal Iliac Artery
● Internal Iliac Artery Branches: I Love Going Places In My Very Own Underwear: (N-369, 373)
I leolumbar
L ateral sacral
G luteal (superior)
[From Posterior Division]
P udendal (internal)
I nferior vesicle (uterine in females)
M iddle rectal
V aginal
O bturator
U mbilical
[From Anterior Division]
Arteries Encountered In Colorectal Surgery
Hemicolectomy (Right) : RC; IC; (+ MC, if extended)

Hemicolectomy (Left) : LC; S; (+ MC, if extended) (ureter can be injured, as its under Psoas Major)
Sigmoid-colectomy : LC; S
n
Abdominoperineal Resec : S; SR
Anterior resecn : SR (+ left Ureter)
**RC= Rt. Colic; LC= Lt. Colic; MC= Middle Colic; IC= Iliocolic; S = Sigmoid; SR= Superior Rectal**
**Posteriorly Gonadal vessels also can be injured**
NERVE AND RELATED INFORMATION
● PUDENDAL N. BRANCHES(N-382)
Inf. Rectal N. : EAS; Skin around anus; Anal canal below pectinate line
Perineal N : Med & lat. Post scrotal; Muscular br.urogenital muscle
Dorsal N. Penis : Skin of body & glans of penis
Vagus supplies Para sympathetic to abdominal organs, which receive blood from Coeliac Trunk/SMA -
means,up to last part of Transverse Colon. End of Transverse Colon & all GIT structures distal to that point
receive Para sympathetic innervation from pelvic splanchnic & blood from IMA.
Cremesteric reflex – Genitofemoral Nerve
GENERAL DISCUSSION
Levels & Planes
Transpyloric plain of Addison. It Is the halfway point between Suprasternal Notch and Pubic Symphysis.
From posterior to anterior, the significant structures crossed by transpyloric plane in midline are:
The conus or termination of the spinal cord

L1 vertebra
Aorta
Superior mesenteric artery
Neck of the pancreas
Superior mesenteric vein
The pylorus of the stomach
More laterally at this level:

Kidney hila
Renal vein
Hilum of the spleen
Second part of duodenum
Origin of the portal vein
Duodenojejunal flexure
Fundus of the gall bladder
9th costal cartilage
Root of the transverse mesocolon
Mnemonic
Flat # GB
Renal villa (hila)
Duodenojejunal junction
9th (rib) Pyloric street
Pancreatic Neck circus Road (root of Transverse mesocolon)
Dhaka.
Subcostal plane : Lowest margin of 10th costal cartilage

Intercristal plane : Level of body L4 (highest point of iliac crest)
Intertubercular plane : Level of body L5
Common level landmarks
Inferior mesenteric artery L3
Bifurcation of aorta into common iliac arteries L4
Formation of IVC L5 (union of common iliac veins)
Diaphragm apertures • Vena cava T8

• Oesophagus T10
• Aortic hiatus T12
Abdominal wall
2 main muscles of abdominal wall are the Rectus Abdominis (anterior) and the Quadratus Lumborum (posterior).
The remaining abdominal wall consists of 3 muscular layers. Each muscle passes from the lateral aspect of the
quadratus lumborum posteriorly to the lateral margin of the rectus sheath anteriorly. Each layer is muscular
posterolaterally and aponeurotic anteriorly.
Muscles of Abdominal Wall
Surgical Notes
→ During abdominal surgery it is usually necessary to divide either the muscles or their aponeuroses.
→ During a midline laparotomy aponeurosis is divided.
→ Rectus Sheath is intact above the arcuate line and the muscles intact below it.
→ Straying off the midline will often lead to damage to the rectus muscles, particularly below the arcuate line
where they may often be in close proximity to each other.
Rectus Sheath
Formation
Landmark Anterior wall Posterior Wall
th th th
Above Costal Margin • EO Aponeurosis • 5 ; 6 ;7 costal cartilages
From Costal Margin to • EO Aponeurosis • IO Aponeurosis (Posterior Lamina)
Arcuate Line • IO Aponeurosis(Anterior Lamina) • TA Aponeurosis
Below Arcuate Line • All 3 Aponeuroses • Fascia Transversalis
Contents
2 Muscles
• Rectus Abdominis
• Pyramidalis
4 vessels
• Superior Epigastric Artery and Vein
• Inferior Epigastric Artery and Vein
6 Nerves
• Lower five intercostal nerve (T7-T11)

• Subcostal nerve (T12)
The arcuate line or Linea Semicircularis or Fold of Douglas

→ Midway between the umbilicus and pubic symphysis.
→ Posterior wall of Rectus Sheath ends in arcuate line.
→ The line is concave downwards
→ Is the point at which the Inferior Epigastric Vessels enter the Rectus Sheath.
Arterial Supply of Anterior Abdominal Wall (see Figure on Page 1)
Lateral side (Deep Branches)

• 10th and 11th Posterior Intercostal Arteries (← Descending Aorta)
• Subcostal Artery (← Descending Aorta)
• Lumbar Arteries(all 4) (← Descending Aorta)
Anteriorly From Above Downwards(Deep Branches)

• Musculophrenic Artery (← Internal Mammary Artery)
• Superior Epigastric Artery (← Internal Mammary Artery)
Anteriorly From Below Upwards (Deep Branches)

• Inferior Epigastric Artery (← External Iliac Artery)
• Deep Circumflex Iliac Artery (← External Iliac Artery)
Superficial Arteries
• Superficial Circumflex Iliac Artery (← Femoral Artery)
• Superficial Epigastric Artery (← Femoral Artery)
Thoracoepigastric veins
• These are Longitudinal venous connections between Lateral Thoracic Vein (→ Cephalic Vein) and Superficial
Epigastric Vein (→ GSV).
• Provide a collateral route for venous return if a caval or portal obstruction occurs.
Lymphatic Drainage of the Anterior Abdominal Wall

Region Above The Umbilicus : Drain into the Axillary Lymph Nodes.
Region Below The Umbilicus : Drain into the Inguinal Lymph Nodes.
The Neuro-vascular plane of Anterior Abdominal wall Lies between IO and TA muscles.
There 3 Umbilical Folds (If seen from inside of the abdominal wall) - Two of them covering two Ligaments and
Rest one covering Inferior Epigastric Vesels.
→ One Median Umbilical Fold - On the Median Umbilical Ligament (Oblietered Urachus)
→ Medial Umbilical Fold - On the Occluded Umbilical Artery
→ Lateral Umbilical Fold - On the Inferior Epigastric Vessels
MIFs = Medial Inguinal Folds; LIFs = Lateral Inguinal Folds
Hesselbach's Triangle
Superolaterally Epigastric vessels
Medially Rectus Muscle Lateral edge
Inferiorly Inguinal ligament
Surgical Importance: Direct hernias pass through this triangle.
Ischiorectal Fossa
Base : Skin
Apex : Meeting point of Ob. Fascia + inf. Fascia pelvic diaphragm

Anterior : Perineal membrane (post. border)
Posterior : G. max.
Sacrotuberous ligament
Lateral : Ischial tuberosity

O.I. muscle ē fascia
Pudendal canal with its contents
Medial : Levator ani ē anal fascia

Ext. Anal sphincter
Contents
 Pad of fat
 Inferior Rectal Nerve & Vessels
 Pudendal canal ē its contents (Internal pudendal vessels & Pudendal Nerve, Perineal Nerve)
 Post. Scrotal Nerves & Vessels
 S4 perineal branch
 S2,3 Cutaneous branch
Peritoneum
Parrietal Layer: Derived from Lateral Plate Mesoderm (Somatopleural Layer)

Viscerall Layer: Derived from Lateral Plate Mesoderm (Splanchnopleura Layer)
Retroperitoneal Structures List: Sad Pucker: (N– 257)

– Suprarenal glands – Aorta & IVC – Duodenum (except 1st part)
– Pancreas
– Ureters
– Colon (ascending & descending)
– Kidneys
– Esophagus (anterior & left covered)
– Rectum
**Spleen is the only organ which is completely covered with visceral peritoneum**
Pseudomyxoma Peritonei
• Rare mucinous tumour
• Most commonly arising from the appendix (other abdominal viscera are also recognised as primary sites)
• Incidence of 1– 2/1,000,000 per year
• The disease is characterised by the accumulation of large amounts of mucinous/jelly like material in the
abdominal cavity
Treatment
Is usually surgical and consists of cytoreductive surgery (and often peritonectomy c.f Sugarbaker procedure) combined
with intra peritoneal chemotherapy with mitomycin C.
Survival is related to the quality of primary treatment and in Sugarbakers own centre 5 year survival rates of 75% have
been quoted. Patients with disseminated intraperitoneal malignancy from another source fare far worse.
In selected patients a second look laparotomy is advocated and some practice this routinely.
Epiploic Foramen of Winslow
It is the communication between greater and lesser sacs of peritoneal cavity.

The lesser sac is a site for potential internal herniation of the bowel.
Boundary
• Anteriorly : Free border Lesser Omentum / Hepatoduodenal Ligament, (contains CBD, HA, PV)
• Posteriorly : IVC; Diaphragm; Rt. Suprarenal gland; T12 vertebra body
• Superiorly : Caudate lobe
st
• Inferiorly : Duodenum 1 part; HA.; (BD & PV may be)
• Left lateral : Gastrosplenic and Splenorenal Ligament
Pringle's Manoeuver used to stop bleeding from the liver during laparotomy or liver surgery. It involves placing a
vascular clamp across the anterior aspect of the epiploic foramen i.e. compression of Hepatic Artery where it lies in
the free edge of the lesser omentum. Structures occludes:
Common Bile Duct
Hepatic Artery
Portal Vein
Common Sites For Intra-Abdominal Collections To Form :

The most dependent place for fluid to collect in the abdomen, when supine, is the Hepatorenal Pouch of
Rutherford-Morrison (Right Subhepatic Space). Other common sites are:
In the pelvis (Recto-uterine, Rcetovesical)
Between loops of bowel
Left subphrenic spaces
Right and left paracolic gutters
Abdominal signs
• Rovsings sign – appendicitis; palpation of the left iliac fossa causes pain in the right iliac fossa
• Psoas stretch sign – Acute retrocaecal appendicitis is indicated when right thigh is passively extended with
patient lying on their side with their knees extended
• Boas Sign – cholecystitis. Hyperesthesia beneath the right scapula
• Murphys Sign – cholecystitis – pain/catch of breath, on palpation of right hypochondrium during inspiration
• Cullens Sign – pancreatitis (other intra– abdominal haemorrhage); Peri–umbilical bruising
• Grey– Turners Sign – pancreatitis (or other retroperitoneal haemorrhage); Bruising in the flanks.
Abdominal Radiology
Plain abdominal x– rays are often used as a first line investigation in patients with acute abdominal pain.
Features which are usually abnormal

Large amounts of free air (colonic perforation), smaller volumes seen with more proximal perforations.
A positive Riglers Sign (gas on both sides of the bowel wall).

Caecal Diameter of >8cm
Fluid levels in the colon
Ground Glass Appearance to film (usually due to large amounts of free fluid).
Sentinel loop in patients with inflammation of other organs (e.g. pancreatitis).
Features which should be expected/ or occur without pathology

• In Chiladitis syndrome, a loop of bowel may be interposed between the liver and diaphragm, giving the
mistaken impression that free air is present.
• Following ERCP (and Sphincterotomy) air may be identified in the biliary tree.
• Free intra abdominal air following laparoscopy / laparotomy, although usually dissipates after 48– 72 hours.
Derivatives of Dorsal Mesogastrium

Spleen
Pancreas
G. omentum (gastrosplenic, gastrophrenic, gastrocolic)
Splenorenal ligament (pancreas tail is here…)
ABDOMEN (Part – 2)
Oesophagus
• 25cm long
• Starts at C6 vertebra, pierces diaphragm at T10 and ends at T11
• Squamous epithelium
Constrictions
Surgical Importance: Site of Foreign body impaction
Structure Distance from incisors
Cricoid cartilage 15cm – C6
Arch of the Aorta 22.5cm – T4
Left principal bronchus 27cm – T6
Diaphragmatic hiatus 40cm – T10
Relations
Anteriorly • Trachea to T4
• Recurrent laryngeal nerve
• Left bronchus, Left atrium
• Diaphragm
Posteriorly • Thoracic duct to left at T5

• Hemiazygos to the left T8
• Descending aorta
• First 2 intercostal branches of aorta
Left • Thoracic duct

• Left subclavian artery
Right • Azygos vein
Arterial, venous and lymphatic drainage of the oesophagus
Part Artery Vein Lymphatics Muscularis Externa
Upper third Inferior thyroid Brahiocephalic Deep cervical Striated muscle
Mid third Aortic branches Azygos Veins Posterior Smooth & striated muscle
Mediastinal
Lower third Left gastric Left Gastric → Portal Vein Left Gastric Smooth muscle
Nerve supply
• Upper half is supplied by Recurrent Laryngeal Nerve
• Lower half by oesophageal plexus (vagus)
Histology
• Mucosa :Nonkeratinized Stratified Squamous Epithelium
• Submucosa: glandular tissue
• Muscularis externa (muscularis)
• Adventitia
Oesophageal disease
Disorder Features
Mallory– Weiss Tear ● H/O antecedent vomiting. Followed by the vomiting of a small amount of blood.
● There is usually little in the way of systemic disturbance or prior symptoms.
● 90% cases spontaneously stopped, others usually responds to endoscopic
adrenaline(1:10000) injection. Usually 3% cases need surgery (Gastrotomy & underrunning)
Hiatus hernia of gastric ● Long H/O dyspepsia

cardia ● Patients are often overweight.
● Complicated cases associated with dysphagia or haematemesis.
Squamous cell ● H/O progressive dysphagia.

carcinoma ● Weight loss.
● Usually little or no history of previous GORD symptoms.
Adenocarcinoma ● Progressive dysphagia.

● May have previous symptoms of GORD or Barretts oesophagus.
Peptic stricture ● Longer H/O dysphagia, not progressive in maximum cases.

● Usually symptoms of GORD.
● Often lack systemic features seen with malignancy
Dysmotility disorder ● Episodic, non progressive Dysphagia.

● Retrosternal pain may accompany the episodes.
Diagnosis
● Upper GI endoscopy (usually most patients).
● Where this fails to demonstrate a mechanical stricture, – pH and manometry studies together with Radiological
Contrast Swallows are used.
Dysphagia
Causes
Extrinsic • Mediastinal masses

• Cervical spondylosis
Oesophageal • Achalasia
wall • Diffuse oesophageal spasm
• Hypertensive lower oesophageal sphincter
Intrinsic • Tumours
• Strictures
• Oesophageal web
• Schatzki rings
Neurological • CVA
• Parkinson's disease
• Multiple Sclerosis
• Brainstem pathology
• Myasthenia Gravis
Investigation
• Upper GI endoscopy.
• Fluoroscopic swallowing studies – (Motility disorders)
• Full blood count.
• Ambulatory Oesophageal pH and manometry studies – Achalasia; GORD (when considered for Fundoplication)
Gastro Oesphageal Reflux Disease (GORD)
• Weak lower oesophageal sphincter

H
• p < 4 for >4% for 24hr monitoring
• C/F
o Angina type pain
o Odynophagia while swallowing hot drinks
o Food reflux(not vomit) specially on bending
o Globus (lump in throat)
• Dx
o pH monitoring (gold standard)
o Endoscopy (Invx of choice)
o Biopsy (80% dxtic)
o Esophageal manometry
o Ba– swallow(not definite)
• Complication
o Stricture
o Barrett’s oesophagus
o Bleeding
• Rx
o Antacid
o H2 blocker
o PPI
o Metochlopromide
• Surgery
0
o Floppy Nissen 360 fundoplication(Post. Partial & Ant. Partial)
o Hill repair
o Angel chick prosthesis
o Belsey Mark iv : transthoracic fundoplication
o Roux– en Y (in case of recurrence)
● Endoscopic placement of Self– Expanding Metal Stents (SEMS)

o Now placed most frequently in patients presenting with Malignant Dysphagia.
o Early Complications
→ Malposition,
→ Oesophageal perforation
→ Bleeding
→ Stent migration.
o Late Complications
→ Related to eating (food bolus blocking a stent) – Initial management is to consume a fizzy drink, which
helps to break up the food bolus, otherwise endoscopy is required to dislodge the food bolus
→ Tumour overgrowth.
Barrett's Oesophagus
• Intestinal metaplasia
• Squamous epithelium replaced by columnar epithelium in the lower oesophagus
• 3 types of columnar epithelium:
1. Junctional
2. Atrophic fundal
3. Specialised
• Presence of goblet cells important in identification
• Premalignant change (progress to dysplasia)
• Risk of adenocarcinoma
• Risk factors: middle age, men, smoker, Caucasian, gastro– oesophageal reflux, obesity
Treatment
• Long term proton pump inhibitor.
• Consider pH and manometry studies.
• Regular endoscopic monitoring (more frequently if moderate dysplasia). With quadrantic biopsies every 2– 3
cm.
• If severe dysplasia be very wary of small foci of cancer.
Kh
Achalasia; Pseudoachalasia; Diffuse Oesophageal Spasm
FEATURES ACHALASIA PSEUDO DOS

ACHALASIA
Age 30– 60 yrs >50
Predispose to SCC
Pain Retrosternal chest pain Ca @ LOS, Angina type chest pain ē radiatn
extrinsic tumor to jaw, Interscapular region –
CAG normal
Clammy & pale
Food Problem Solid + liquid
Dysphagia + recurrent pneumonia Dysphagia+Odynophagia both
Dysphagia exacerbate with stress
Regurgitation Present Absent
Manometry Absent peristalsis Nut– cracker / Corkscrew
High lower oesophageal sphincter Oesophagus
pressure ē failure to relax during Segmental spasm

swallowing Pseudodiverticulosis
Endoscopy To exclude stricture / Ca Can’t pass thru’
Ba swallow Bird’s beak
Mega– Esophagus
No gastric air bubble
Food residue may present
Double right heart border
n
Rx Esophageal Bouginage/ballon dilat Nifedipine
st
(1 line)
Heller’s cardiomyotomy(2nd line)
Inj. Botulinum toxin ē endoluminal
US guide
● C orkscrew esophagus – D iffuse oesophageal spasm

B ird’s Beak oesophagus – A chalasia Cardia ... A – B & C – D
● Oesophageal varices patient, band ligation done, bleeding unstoppable; RX– Balloon temponade (Sengstaken–
Blakemore / Minnesota tube)
Oesophageal cancer
→ SCC (Upper 2/3 associated with Achalasia, PUD, Celiac disease, Webs, Stricture,Vit. A & C deficiency)
→ Adenocarcinoma (Lower 1/3 associated with GORD and Barrett's)
→ Oat Cell Carcinoma (very rare and poor Prognosis)
→ Commonest benign tumor of oesophagus is Leiomyoma
• Barretts oesophagus is a major risk factor for most cases.
• In Western world most number of cases is Adenocarcinoma – in the UK adenocarcinomas account for 65% of
cases. In other regions of the world SCC is more common
• Associated with smoking, alcohol intake, diets rich in nitrosamines.
Oesophageal Ca Diagnosis
• UGI Endoscopy – Best 1st line Investigation for anyone ē dysphagia
• Contrast swallow – Benefitial in benign motility disorders but has no place in the assessment of tumours
• CT scan – To see lung & liver metastasis & distant lymphadenopathy.
• Endoscopic US – If CT does not show metastasis, then best method for preoperative local staging.
• Staging Laparoscopy – Detect occult peritoneal disease.
• PET CT – Performed, If laparoscopy is negative.
rd
• Thoracoscopy is not routinely performed. Bronchoscopy can be done in prox & middle 3 tumor adjacent
tracheobroncheal tree.
Stages
→ 1A : T1 N0 M0
→ 1B : T2 N0 M0
→ 2A : T3 N0 M0
→ 2B : T1/2 N0 M0
→ 3A : T4a N0 M0
T3 N1 M0
T1/2 N2 M0
→ 3B : T3 N2 M0
→ 3C : T4a N1/2 M0
T4b N0– 3 M0
T1– 4 N3 M0
→ 4 : T1– 4 N1– 3 M1
Source: Baily and Love's: 26th

Treatment
Surgical resection–
o Neoadjuvent chemotherapy is given in most cases prior to surgery
o In general resections are not offered to those patients with distant metastasis, not to those with N2
disease.
In situ disease – Endoscopic Mucosal Resection
In more proximal lesion – Total Oesphagectomy (McKeown Type) with anastomosis to cervical Oesophagus
In lower third disease – Ivor– Lewis type procedure.
In very distal tumors – Transhiatal Procedure. (its an attractive option – because in Ivor– Lewis procedure two
visceral cavities penetration is require; which ultimately increases the morbidity)
In unresectable disease – Local Ablative Procedures, Palliative Chemotherapy or Stent Insertion.
● 2 Stages Ivor Lewis (also called Lewis– Tanner) Method –

– Initial laparotomy and construction of a gastric tube(A Rooftop Incision is made)
– Right thoracotomy to excise tumor and create an esophagogastric anastomosis. (Incision through
5th ICS performed 10cm above the tumour)
– Preferred for middle & lower third tumor
– Azygos Vein is divided to allow mobilization of oesophagus
● 3 Stages McKeown Method –

– Ivor Lewis (also called Lewis– Tanner) approach + Neck Incision
n
– Third incision in the neck is made to complete anastomosis betw stomach & cervical esophagus.
● Transhiatal Resection–
– Laparotomy & incision in the neck.
– Esophagus is mobilized by blunt dissection from above & below.
– Stomach used as conduit & brought up to the neck & cervical anastomosis carried out as in the 3
phase procedure
– Indication
• Elderly patient ē lower tumor
• Thoracotomy not suitable
• Severe dysplasia
• Barrett’s
● Ivor– Lewis Post operative complication

*Atelectasis– due to the effects of thoracotomy and lung collapse
*Anastomotic leakage – High risk because of a relatively devascularised stomach as the only blood supply is
from Gastroepiploic Artery and others have been divided. If a leak occurs, manage conservatively with prolonged
NG tube drainage and TPN. Up to 50% patients developing anastomotic leak will not survive.
* Delayed gastric emptying – (may be avoided by performing a pyloroplasty).
Oesophageal candidiasis
– Characterised by white spots in the oropharynx with extension into the oesophagus.
– Associated with broad spectrum antibiotic usage, immunosupression and immunological disorders.
– Patients may present with oropharyngeal symptoms, odynophagia and dysphagia.
– Treatment is directed both at the underlying cause and with oral antifungal agents.
Sample Theme
Oesophageal disease Rx
A. Oesophagectomy
B. Endoscopic sub mucosal dissection
C. Photodynamic therapy
D. Insertion of oesophageal stent
E. Chemotherapy
F. Radiotherapy
● A 52 year old man with long standing Barretts oesophagus is diagnosed with high grade dysplasia on recent
endoscopy. The lesions are multifocal and mainly distally sited.
The answer is Oesophagectomy
Some may argue for local therapy. However, Look at the age – in young patients who are otherwise fit, multifocal
disease such as this should probably be resected.
● A 72 year old man presents with dysphagia. He is investigated and found to have an adenocarcinoma of the distal
oesophagus. His staging investigations have revealed a solitary metastatic lesion in the right lobe of his liver.
The answer is Insertion of oesophageal stent
Although he may be palliated with chemotherap, a stent will produce the quickest clinical response(here dysphagia).
Metastatic disease is usually a contra– indication to oesophageal resection.
● An 83 year old lady with long standing Barretts oesophagus is diagnosed with a 1cm focus of high grade dysplasia
3cm from the gastrooesophageal junction.
The answer is Endoscopic Sub Mucosal Dissection
As she is elderly and the disease localised EMR is an appropriate first line step.
The technique involves raising the mucosa containing the lesion and then using an endoscopic snare to remove it. This
technique is therefore minimally invasive. However, it is only suitable for early superficial lesions. Deeper invasion would
carry a high risk of recurrence.
Stomach
n
Stomach Bed Form (N– 256)
– Diaphragm
– Lt. suprarenal gland
– Lt. Kidney
– Left colic flexure
– Splenic artery
– Transverse mesocolon
– Ant. Surface pancreas (body & tail)
– Spleen
Peristalsis
Circular Smooth Muscle contracts behind the food bolus
Longitudinal Smooth Muscle propels the food through the oesophagus.
Primary Peristalsis moves the food from the oesophagus into the stomach (9 seconds)
Secondary Peristalsis occurs when food, which doesn't enter the stomach, stimulates stretch receptors to
cause peristalsis
In the small intestine each peristalsis waves slows to a few seconds and causes mixture of chyme
In the colon three main types of peristaltic activities are recognised (see below)
Colonic peristalsis
Segmentation Contractions • Localised contractions

• Bolus is subjected to local forces
• Maximise mucosal absorption
Antiperistaltic contractions • Localised reverse peristaltic waves

towards ileum • Slow entry into colon
• Maximise absorption
Mass movements • Migratory peristaltic waves along the entire colon

• Empty the organ prior to the ingestion of food bolus
Omentum
• Omentum is divided into two parts - Greater and Lesser Omentum.
• Greater Omentum - attached to the inferolateral border of Stomach and houses the Gastro– Epiploic Arteries.
• Omentum protects against visceral perforation (e.g. Appendicitis).
• Inferiorly between the omentum and transverse colon is one potential entry point into the lesser sac.
• Among Several malignant processes involving the omentum, ovarian cancer is the most notable.
Ulcers Cause (N– 282)

Post. Gastric : Splenic artery (← Celiac Trunk)
Lesser curvature : Left. Gastric Artery (← Celiac Trunk)
Greater curvature : Gastro– Epiploic vessels (← GDA ← CHA ← Celiac Trunk)
Post. Duodenal : Gastro– Duodenal Artery (← CHA)
Various Types of Cells

Chief / zymogenic cell : Pepsinogen (Fundus)
Parietal / oxyntic cell : HCl; IF; Na; Ca; Mg (Body) (pH)
–
Mucous neck cell : Mucous, HCO3 (Pylorus)
G cell : Gastrin, (Pylorus)
Pancreatic acinar cell : Chymotrypsinogen; Collipase; Amylase; Phospholypase
Enterochromaffin cell : Serotonin; Bradykinin, Histamin
Gastrointestinal secretions
• Up to 7 litres of secretions enter the lumen of the GI tract in 24 hour.

• Formed stool is created, it will contain, on average 200ml water.
The common secretions together with their approximate volumes (not so important !!!)
+ + –
Origin ml/24 hrs Na mmol/L K mmol/L Cl mol/L HCO3
Salivary glands 1500 10 26 10 30
Stomach 1500 60 10 130
Duodenum 100– 2000 140 80 80
Pancreas 800 140 5 70 115
Bile 50– 800 145 100 100 35

Jejunum/ileum 3000 140 104 104 30
Colon 100 60 30 40
→ In extensive intestinal resection High output, proximally sited stoma is created.

→ Administration of hypotonic rather than isotonic solutions will result in worsening of electrolyte
disturbances as electrolyte rich secretions will enter the jejunum.
→ Colectomy or similar procedure results in formation of an End or Loop ileostomy.

→ Ileostomies typically lose between 500 - 1000ml / 24 hour
→ High output ileostomies can rapidly become dehydrated. Ileostomy runoff typically contains
126mmol/L of sodium and 22mmol/L of potassium.
Gastric secretions
Gastric acid
• Is produced by the Parietal Cells in the stomach. pH of gastric acid is around 2.
• Acidity maintained by H+/K+ ATP-ase pump
Phases of gastric acid secretion – 3phases
1. Cephalic phase (smell / taste of food)

• 30% acid produced
• Vagal cholinergic stimulation causes secretion of HCl and Gastrin release from G cells
2. Gastric phase (distension of stomach)

• Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)

• High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via enterogastrones
(CCK, secretin) and neural reflexes.
Regulation of gastric acid production
1. Factors increasing production: Very Good History

• V agus stimulation
• G astrin
• H istamine [(indirectly following gastrin release) from enterchromaffin like cells]
2. Factors decreasing production: S econdary S chool C ertificate

• S omatostatin (inhibits histamine release)
• S ecretin
• C holecystokinin
Major hormones involved in food digestion:
Source Stimulus Actions
Gastrin G cell - Stomach • Stomach Distension • Increase HCl

n
Antrum • Extrinsic Nerve Inhibit • Pepsinogen and IF secretion
by - Low Antral pH, • Increases Gastric Motility
- Somatostatin • Trophic Effect on Gastric Mucosa
CCK I cell - Upper Small • Partially digested • Enzyme– rich fluid secretion from
Intestine proteins pancreas
• Triglyceride • GB contraction
• Sphincter of Oddi relaxation
• Decreases gastric emptying
• Trophic effect on Pancreatic acinar cell
• Induces satiety
Secretin S cell - Upper Small Acidic chyme, fatty acids • HCO3– rich fluid secretion from
Intestine pancreas and hepatic duct cells
• Decreases Gastric Acid secretion
• Trophic effect on Pancreatic acinar cell
VIP Small Intestine Neural • Stimulates secretion by Pancreas and

Pancreas Intestines
• Inhibits acid and Pepsinogen secretion
Somatostatin Fat, Bile Salts and • Decreases Acid and Pepsin secretion
D cell - Pancreas Glucose in the Intestinal • Decreases Gastrin secretion
All secretion Enterochromaffin cell Lumen • Inhibits Trophic Effects of Gastrin
Inhibitor - Gut • Delays Gastric Emptying
except • Decreases Pancreatic Exocrine
Gastric mucous Brain tissue Secretion (may be used therapeutically
secretion to treat pancreatic fistulae)
• Decreases Insulin Glucagon secretion
• Inhibits GH (released by hypothalamus
causing negative feedback response
on GH)
• Stimulates Gastric Mucous Production
● Intestinal Motility is Increased by: CCK, Gastrin, Insulin, Motilin

● Only Gastrin secretion is stimulated by protein, but rests secretions are by fat or fatty acid.
Gastric emptying
Delay emptying Increase emptying
Gastric inhibitory peptide Gastrin
Cholecystokinin
Enteroglucagon
Iatrogenic Impacts delay/hamper Gastric Emptying

Gastric surgery.
Any procedure disrupting the vagus.
Distal Gastrectomy
Gastro– enterostomy: Posterior-Retrocolic Gastroenterostomy will empty better than an anterior one.
Malignancies
Distal Gastric Cancer bstruct the pylorus and delay emptying.
Malignancies of the pancreas cause extrinsic compression of the duodenum and delay emptying.
o Treatment: Gastric decompression by a wide bore nasogastric tube and insertion of stent
o Surgical gastroenterostomy (Gastroenterostomies are placed at anterior wall of stomach) (though the fact is,
they empty less well).
Congenital Hypertrophic Pyloric Stenosis

Most babies present around 6 weeks of age with projectile non bile stained vomiting.
More common in males.
Diagnosis:
o History and examination: A mass may be palpable in the epigastrium (often cited seldom felt!).
o Ultrasound: Hypertrophied pylorus.
o Blood tests: Hypochloraemic Metabolic Alkalosis - long standing vomiting.
Treatment: Pyloromyotomy is performed (usually laparoscopically).
Gastroperesis
– Occurs due to Vagal neuropathy, (difference with Pyloric Stenosis is – No obstruction or stricture found
in gastroperesis, otherwise rest are same features)
Diabetic Gastroparesis
Due to Vagal neuropathy.
The Stomach empties poorly and patients may have episodes of repeated and protracted vomiting.
Diagnosis
o UGI Endoscopy and contrast studies,
o A Radio Nucleotide Scan is needed to demonstrate the abnormality more clearly.
Conservative Management:
More frequent, smaller meals -Soft and liquid foods; chew food well before swallowing
Non-fizzy liquids with each meal

Domperidone; Erythromycin; (Metoclopramide is less effective as they effect via the vagus nerve).
Invesive Managemet:
Gastroelectrical Stimulation
Botulinum toxin
Nasojejunal Tube or Jejunostomy or TPN
Gastroenterostomy or Gastrojejunostomy
(Source: http://www.nhs.uk/conditions/gastroparesis/Pages/Introduction.aspx)
Upper gastrointestinal bleeding
Patients may present with:

• Haematemesis and/ or malaena
• Epigastric discomfort
• Sudden collapse
Mortality is higher in patients presenting with haematemesis than malaena alone.
Oesophageal Bleeding
Cause Presenting Features
Oesophagitis • Small volume of fresh blood, often streaking vomit.

• Malaena rare.
• Often ceases spontaneously.
• Usually H/O antecedent GORD type symptoms.
Cancer • Usually small volume of blood, except as pre terminal event with erosion of major vessels.
• Symptoms of dysphagia and weight loss.
• May be recurrent until malignancy managed.
Mallory Weiss Tear • Typically brisk small to moderate vol. of bright red blood following bout of repeated vomiting.
• Malaena rare.
• Usually ceases spontaneously.
Varices • Usually large volume of fresh blood.

• Swallowed blood may cause malaena.
• Often associated with haemodynamic compromise.
• May stop spontaneously but re– bleeds are common until appropriately managed.
Gastric Bleeding
Cause Presenting features
Gastric cancer • May be frank haematemesis or altered blood mixed with vomit.
• Usually features of dyspepsia.
• Erosion of major vessels may produce considerable haemorrhage.
Dilafeuoy Lesion • Usually located in the gastric fundus, within 6 cm of the gastroesophageal junction.
• No features prior to haematemesis and malaena,
• Produce considerable haemorrhage and may be difficult to detect endoscopically
Diffuse erosive • Usually haematemesis and epigastric discomfort.

gastritis • Usually underlying cause (NSAID usage).
• Haemorrhage may occur with considerable haemodynamic compromise.
Gastric ulcer • Small low volume bleeds

• Coffee ground vomitus
• May present as Iron deficiency anaemia.
• Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.
• Eating may sometimes relieve the pain
Duodenal Bleeding
Major haemorrhage cause is Posterior Ulcer. Though any ulcers may present with haematemesis, malaena and
epigastric discomfort.
Pain is slightly different to that of Gastric Ulcer - occurs several hours after eating.
Peri ampullary tumours may bleed but these are rare.
Previous AAA surgery aorto– enteric fistulation is rare cause associated with high mortality.
● Epigastric pain relieved by eating; increased ē stress & anxiety; associated ē presence of nocturnal dyspepsia – What
is the Dx? Duodenal Ulcer answer(April-2011)
Summary of Acute Upper GI bleeding recommendations

All patients should have a pre– endoscopic Rockall score (see later)
Consider admission if: – Aged over 60 years
– Witnessed haematemesis
– Systolic BP < 100mmHg or HR > 100 bpm
– Liver disease/known varices
Resuscitation: – In shock, Give fluid

– Transfuse if 30% circulating volume is lost
– Administration of PPIs prior to endoscopy may reduce evidence of haemorrhage
Give IV PPI e.g. 80mg Omeprazole bolus then 8mg/h over 72h, if bleeding ulcer identified
If post endoscopy Rockall score < 3 consider discharge and follow– up
● Episode of Haematemesis and collapse – Duodenal Ulcer is the answer → Gastro-duodenal Artery culprit vessel
Rockall Scoring System
Points
Variable
0 1 2 3
Age(yr) <60 60-79 >80 -
Pulse rate <100 >100 - -
Systolic BP Normal >100 <100 -
Comorbidity None - IHD Renal failure

Cardiac failure Hepatic failure
Metastatic ca
Diagnosis Mallory Weiss All other Malignant -

tear or no lesion diagnosis lesions
observed
Endoscopic No stigmata or - Blood in UGIT -

stigmata dark spot in Visible vessel
ulcer base etc.
Risk category: High (> 5); Intermediate (3–5); Low (0–2)
Total Mortality Rebleeding

Score (%) (%)
0 0 4.9
1 0 3.4
2 0.2 5.3
3 2.9 11.2
4 5.3 14.1
5 10.8 24.1
6 17.3 32.9
7 27.0 43.8
≥8 41.1 41.8
Gastric Ulcer Surgical Rx
– Bilroth-I Partial Gastrectomy

o Benign distal ulcer; Gastric curvature ulcer
rd
o Distal 3 stomach removed & anastomosis ē duodenum
Fig: Billroth I – pylorus is removed and distal stomach is anastomosed directly to the duodenum
– Bilroth-II Gastrectomy
o Used for more proximal ulcer
o Removal of distal 2/3rd stomach & gastro– jejunostomy.
o Duodenal stump is closed, and the stump of the stomach is connected to a loop of jejunum.
o Such a gastrojejunostomy can be constructed in front of the transverse colon (Antecolic Bilroth-II
Polya) or in retrocolic fashion (Retrocolic Bilroth-II Hofmeister Finsterer).
o In the Bilroth-II-Polya procedure, afferent loopshoould be free from colon, and a side-to-side
anastomosis of afferent and efferent loops is created.
– Vagotomy, Pyloroplasty & Excision of Ulcer

o Used as alternative of Bilroth– I when contraindicated
o If Surgery is not possible then excision of the ulcer.
– Vagotomy. Antrectomy & Roux– en– Y

nd
o Reserved as 2 operation for bilious vomiting
Figure: A, Total gastrectomy; B, Roux– en– Y esophagojejunostomy
Figure: A, High subtotal gastrectomy; B, with Roux– en– Y gastrojejunostomy.
** Lesser Omentum needs to be divided to gain access to celiac axis **
Post Gastrectomy Complications (Only red marked headigs are Important for the exam, details not needed)
- May vary depending upon whether a total or partial gastrectomy is performed.

- Roux-n-Y reconstruction generally gives the best functional outcomes.
- Gstrojejunostomy is performed as reconstruction following a distal gastrectomy the gastric emptying is generally better
if the jejunal limbs are tunneled in the retrocolic plane. The following may occur following gastrectomy:
Small capacity (early satiety)

Recurrent Ulceration
Dumping Syndrome
→ Most common complications of gastrojejunostomy. Having hyperosmolar food (usually simple
carbohydrates) → rapidly enters the jejunum → sudden shift in fluid → fall in plasma volume.
→ Bloating, diarrhoea,weakness,dizziness, sweating, pallor, and tachycardia

→ Initial hyperglycemia but later rebound hypoglycemia and hypokalemia occurs.
→ Treatment: Dietary management - elimination of simple-carbohydrate foods and fluid. Consuming high
fibre foods; patients are advised to consume smaller meals - best to increase protein and fat contents.
→ Somatostatin Therapy: Slows emptying → Delays the glucose onset and insulin release.
→ Conversion to Roux-en-Y: if long-term Somatostatin treatment if needed
Gastroperesis
→ Associated with truncal vagotomy or basic motility disturbance, as occurs in diabetes.
→ Symptoms: Nausea; Inability to eat; Vomiting
Postvagotomy Diarrhoea
→ Anti-dirrhoeal agent.
→ Somatostatin Therapy: If severe symptoms
Afferent Loop Syndrome

→ Occurs only in gastrojejunostomy.
→ Loop from the duodenum running to the gastrojejunostomy become obstructed
→ Symptoms: Epigastric fullness; Upper abdominal pain-relieved only by bilious vomiting. Features of
obstruction caused by scarring or adhesions or twisting of the intestinal loop.
→ Diagnosis: Radiography; Endoscopy
→ Treatment: surgery, with conversion of the gastrojejunostomy to either a Billroth I or a Roux-en-Y.
Bile Reflux Gastritis

→ Bile reflux from the gastrojejunostomy into gastric stump, → inflammation of gastric lining.
→ Symptoms: Pain or occasional vomiting.
→ Treatment: Therapy with coating agents, such as sucralfate; Prokinetic agents
Gastric Adenocarcinoma
Anaemia (B12 deficiency)
Metabolic bone disease
DUODENAL ULCER SURGICAL TREATMENT
• Truncal Vagotomy & Pyloroplasty

o Both vagal trunks are cut @ abdominal oesophagus level
o As stomach is denervated, stasis occurs
o Gastrojejunostomy / pyloroplasty done
• Selective Vaotomy & Pyloroplasty

o Denervation of stomach with preservation of intact pylorus’ nerve supply
o Preserve celiac & hepatic branches of vagus
• Highly Selective / Parietal Cell/ Proximal Vagotomy

o Only branches of body & fundus are cut
o Doesn’t interrupt celiac , hepatic & pyloric branches

o No diversion procedure needed
o High recurrence rate
Gastric cancer
Type 1 • True oesophageal cancers

• Associated with Barrett's oesophagus.
Type 2 • Carcinoma of cardia, arising from cardiac type epithelium

• With intestinal metaplasia at the oesophagogastric junction.
Type 3 • Sub cardial cancers that spread across the junction

• Involve similar nodal stations to Gastric cancer.
Close Endoscopic Monitoring Group

• Intestinal metaplasia (columnar type)
• Atrophic gastritis
• Dysplasia (Low to medium grade)
• H/O Benign PUD resections (except highly selective vagotomy).
Referral To Endoscopy
Any age ē Dyspepsia + Without Dyspepsia Worsening Dyspepsia

any of the following
Dysphagia Dysphagia Barretts oesophagus
Upper abd. mass Upper abd. mass Intestinal metaplasia
Weight loss Weight loss / Unexplained abd. pain Dysplasia
Fe def.Anaemia Vomiting Atrophic gastritis
Chronic GIT bleeding Jaundice >55 years + unexplained or persistent dyspepsia
"UGI endoscopy performed for dyspepsia. Addition of dye spraying may facilitate identification of smaller tumours"
Staging
• CT scanning of the chest abdomen and pelvis - First line staging investigation
• Laparoscopy- to identify occult peritoneal disease
• PET CT - For junctional tumours
Treatment
• Type 2 Junctional Tumours (extending into oesophagus) – Oesophagogastrectomy
• <5cm from OG junction – Total gastrectomy
• Proximally sited disease greater than 5– 10cm from the OG junction – Subtotal Gastrectomy
• Mid– sector tumors – Total Gastrectomy
th
• Distal tumor – Partial or sub– total (4/5 removed)– entire pylorus also removed
• Confined to mucosa & perhaps sub mucosa (debated!) – Endoscopic Submucosal Resection (Snare)
• Lymphadenectomy should be performed: D2 lymphadenectomy is widely advocated by the Japanese.
However, the overall recommendation is that a D2 nodal dissection be undertaken.
o LN, surrounding tissue : D1 opn (stomach part ē lesion removal & atleast 5cm clearance + N1 nodes)
st n nd
o LN, 1 11LN stations: D2 op (2 rank LN removal ē LGA, CHA & Splenic A.)
st n
o LN, 1 16LN stations: D3 op
• Most patients will receive chemotherapy either pre or post operatively.
Figure A, Total gastrectomy; B, subtotal gastrectomy.
Figure. Surgical lymphadenectomy; D1 and D2 indicate the extent of lymph node removal.
(Please be informed that these information is to clear conception, not for exam)
--------------------------------------------------------------------------------------------------------------------------------------------------------------
Japanese Research Society for study of gastric cancer recognized 16 different LN stations that surround the stomach.
- 16 nodal stations are grouped according to the location and extension of the primary tumor (N0-N4)
- Extent of lymphadenectomy is classified according the level of LND (Lymph node dissection) ( D1-D4).
D1 Dissection:
Only the perigastric nodes directly attached along the lesser curvature and greater curvatures of the stomach are
removed (stations 1-6, N1 level):
1. Right cardia Lymph Nodes

2. Left cardia Lymph Nodes
3. Lymph Nodes along the Lesser Curvature
4. Lymph Nodes along the Greater Curvature
4sa: Lymph Nodes along the Short Gastric Vessels
4sb: Lymph Nodes along the Left Gastroepiploic Vessels
4d: Lymph Nodes along the Right Gastroepiploic Vessels
5. Suprapyloric Lymph nodes

6. Infrapyloric Lymph Nodes
An incomplete N1 dissection is labelled a D0 lymphadenectomy.
D2 dissections (N2 level):
7. Lymph Nodes along the Left Gastric Artery

8. Lymph Nodes along the common hepatic artery (station 8)
9. Celiac Trunk Lymph Nodes (station 9)
10. Splenic Hilus Lymph Nodes
11. Splenic Artery Lymph Nodes
D3 Dissections
Dissection of lymph nodes at stations 12 through 14
Along the hepatoduodenal ligament
Root of the mesentery (N3 level):
12. Lymph Nodes in the Hepatoduodenal Ligament

13. Lymph Nodes on the posterior surface of the head of the pancreas
14. Lymph Nodes at the root of the mesentery

14A. Lymph Nodes along the superior mesenteric artery
14V. Lymph Nodes along the superior mesenteric vein
D4 Dissections
stations 15 and 16 in the para-aortic and the paracolic region (N4 level) (Ref: Standardization of the extent of
lymphadenectomy for gastric cancer: impact on survival. Advances in Surgery, volume 35 2001, 203-223)
--------------------------------------------------------------------------------------------------------------------------------------------------------------
Prognosis UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%
Caecum
Location • Proximal right colon below the ileocaecal valve

• Intraperitoneal
Posterior relations • Psoas

• Iliacus
• Femoral nerve
• Genitofemoral nerve
• Gonadal vessels
Anterior relations Greater omentum
Arterial supply Ileocolic artery
Lymphatic drainage Mesenteric nodes accompany the venous drainage
Clinical Note: The caecum is the most distensible part of the colon and in complete large bowel obstruction with a
competent ileocaecal valve the most likely site of eventual perforation.
Appendix
• Location: Base of caecum. mid gut structure
• Up to 10cm long.
• Mainly lymphoid tissue (Hence Mesenteric Adenitis may mimic Appendicitis)..
• Appendicular orifice is guarded "Valve of Gerlacti"
• Arterial supply: Appendicular Artery (←
← Ileocolic artery ← SMA).
• It is intra peritoneal.
Clinical Note: Caecal taenia coli converge at base of appendix and form a longitudinal muscle cover over the appendix.
This convergence should facilitate its identification at surgery if it is retrocaecal and difficult to find
McBurney's point
• 1/3 of the way along a line drawn from the Anterior Superior Iliac Spine to the Umbilicus
6 Positions:
• Retrocaecal 74%
• Subcaecal 3.5%
• Pelvic 21%
• Preileal 1%
• Postileal 0.5%
• Paracolic
Appendicitis
History
• Peri umbilical pain radiating to the RIF (due to localised parietal peritoneal inflammation).
• Vomit once or twice (but marked and persistent vomiting is unusual)
• Diarrhoea is rare. (pelvic appendicitis may cause rectal irritation to cause loose stool. Pelvic abscess may also
cause diarrhoea)
o
• Mild pyrexia is common – temperature is usually 37.5 – 38 C. Higher temperatures are more typical of
conditions like mesenteric adenitis.
• Anorexia is very common.
Examination
• Generalised peritonitis if perforation.
• Retrocaecal appendicitis may have relatively few signs.
• DRE may reveal boggy sensation if pelvic abscess or even tenderness with a pelvic appendix.
Diagnosis
• Raised inflammatory markers
• Positive history and examination findings.
• Urine analysis may show mild leucocytosis but no nitrites.
• Ultrasound: If Pelvic organ pathology is suspected. Appendix is not possible to visualise. Presence of free fluid
(always pathological in males) raise suspicion. Ultrasound examination may show evidence of lumenal
obstruction and thickening of the appendiceal wall.
Treatment
Appendicectomy which can be performed via either an open or laparoscopic approach.
Metronidazole reduces wound infection.
Perforated appendicitis require copious abdominal lavage.
Appendix mass without peritonitis: Should receive broad spectrum antibiotics and later appendicectomy.
Be wary in older patients who may have an underlying caecal malignancy or perforated sigmoid diverticular
disease.
Emergency appendicectomy – iliohypogastric nerve (L1) injury, results numbness of pubic region
Colon Anatomy
The colon is about 1.5m long although this can vary considerably.
Arterial supply
Ascending colon: Ileocolic; Right Colic Artery ← SMA
Transverse colon: Middle Colic Artery ← SMA
Descending and sigmoid colon: IMA
Venous Drainage
From regional veins (that accompany arteries) to SMV and IMV
Lymphatic Drainage
To para– aortic nodes.
Embryology
Midgut– Second part of duodenum to 2/3 transverse colon
Hindgut– Distal 1/3 transverse colon to anus
Peritoneal location(very important)

The right and left colon are part intraperitoneal and part extraperitoneal.
The sigmoid and transverse colon are generally wholly intraperitoneal.
Right colon
Posterior aspect is extra peritoneal and the Anterior aspect intraperitoneal
Ileocaecal valve
• Entry point of the terminal ileum to the caecum
• Important colonoscopic landmark
• The valve is not always competent and this may allow partial decompression of an obstructed colon
Relations
• Posterior
Iliacus, Iliolumbar ligament, Quadratus lumborum, Transverse abdominis, Diaphragm at the tip of the last rib;
Lateral cutaneous, ilioinguinal, and iliohypogastric nerves; the iliac branches of the iliolumbar vessels, the fourth
lumbar artery, gonadal vessels, ureter and the right kidney.
• Superior
Right kidney which is embedded in the perinephric fat
• Medial
Mesentery which contains the ileocolic artery that supplies the right colon and terminal ileum. A further branch ,
the right colic artery, also contributes to supply the hepatic flexure and proximal transverse colon. Medially these
pass through the mesentery to join the SMA. This occurs near to the head of the pancreas and care has to be
taken when ligating the ileocolic artery near to its origin in cancer cases for fear of impinging on the SMA.
• Anterior
Coils of small intestine, the right edge of the greater omentum, and the anterior abdominal wall.
Nerve Supply
• Parasympathetic fibres of the 10th nerve
Arterial Supply
• Ileocolic Artery + Right Colic Artery ← SMA.
• Iileocolic Artery is almost always present, the right colic can be absent in 5– 15% of individuals.
Left Colon
Position
• Its posterior aspect is extraperitoneal, and the ureter and gonadal vessels are at posterior relations.
• At L3– L4 level (variable) it becomes the sigmoid colon and wholly intraperitoneal.
• The sigmoid colon is highly mobile structure and may even lie of the right side of the abdomen
• It passes towards the midline, the taenia blend and this marks the transition between sigmoid colon and upper
rectum.
Blood supply
• IMA
• Marginal Artery (from the right colon) contributes and this contribution becomes clinically significant when the
IMA is divided surgically (e.g. During AAA repair)
Transverse Colon
• Intraperitoneal.
Relations
Superior Liver and GB, Greater curvature stomach, and the lower end of the spleen
Inferior Small intestine
Anterior Greater omentum
Posterior From right to left with the descending portion of the duodenum, the head of
pancreas, convolutions of the jejunum and ileum, spleen
Colonic pseudo– obstruction
Characterised by the progressive and painless dilation of the colon.

Abdomen may become grossly distended and tympanic.

Usually little pain, Unless a impending bowel necrosis or perforation.
Diagnosis: Plain Film And Contrast Enema(May be Therapeutic) to Exclude mechanical bowel obstruction.
Management: Cause is usually electrolyte imbalance and condition will resolve with correction of this. Who do not
respond to supportive measures should be treated with colonoscopic decompression and/ or the drug neostigmine.
In rare cases, surgery may be required.
Colonic obstruction
Cause Features Treatment
• Usually insidious onset • Laparotomy and resection,
• History of progressive constipation stenting, defunctioning

Cancer colostomy or bypass
• Systemic features (e.g. anaemia)
• Abdominal distension
• Absence of bowel gas distal to site of obstruction
• Usually history of acute diverticulitis • Usually surgical resection

Diverticular • Long history of altered bowel habit • Colonic stenting should not be
Stricture performed for benign disease
• Imaging or endoscopy
• Twisting of bowel around its mesentery • Initially untwist the loop, a
• Sigmoid colon affected in 76% cases flexible sigmoidoscopy is
• Patients usually present with abdominal pain, needed
bloating and constipation • Ischaemia: surgery

Volvulus • Recurrent volvulus: Resection
• Examination usually shows asymmetrical distension
• Plain X– rays usually show massively dilated
sigmoid colon, loss of haustra and "U" shape are
typical, the loop may contain fluid levels
Intussceception affecting the colon (most often due to tumours in the adult population) remains a rare but recognised
cause.
Large Bowel Obstruction Imaging modalities

Gastrograffin enema is the method of determining whether a structural lesion is indeed present.
In UK the use Gastrograffin enema has declined and in most units the CT scan is the first line investigation by the
majority of radiologists (and is advocated by ACPGBI - Association of Coloproctology of Great Britain and Ireland).
CT scan this will provide sufficient detail to allow operative planning, and since malignancy accounts for most
presentations may also stage the disease.
When radiologist cannot provide a clear statement of lesion site, the surgeons request a contrast enema.
Surgical Options
Unstable patients require resuscitation prior to surgery and admission to a critical care unit for invasive monitoring and
potential inotropic support may be needed. Who are otherwise stable the decision then rests on the radiological and
clinical findings.
Clinical Note: Caecal diameter ≥ 12cm in the presence of complete obstruction with a competent ileocaecal valve and
caecal tenderness is a sign of impending perforation and a relative indication for prompt surgery.
Colonic lesions – DALM

• The term DALM lesion refers to a Dysplasia Associated Lesion or Mass.
• They may complicate dysplasia occurring in patients with longstanding ulcerative colitis.
• They have a high incidence of invasive foci.
• When they complicate longstanding ulcerative colitis, they should be treated by panproctocolectomy.
Colonic Polyps
The risk of malignancy in association with adenomas is related to size and is the order of 10% in a 1cm adenoma.
Isolated adenomas seldom give risk of symptoms (unless large and distal).
Distally sited villous lesions may produce mucous and if very large electrolyte disturbances may occur.
Inflammatory polyps have no malignant potential
FAP must show Family H/O colorectal ca
Juvenile polyp shows painless bleeding, mixed with stool without family history
Colonic tumours associated ē hereditary Non-Polyposis Colorectal Cancer (HNPCC) occur on average 20yrs
before the peak incidence of sporadic tumours & are frequently synchronous & metachronous ē predilection for the
proximal colon. Mucinous, poorly differentiated and “signet-ring” in appearance.
Follow Up of Colonic Polyps

Low risk : 1 or 2 adenomas <1cm. No follow up or re– colonoscopy at 5 years.
Moderate risk: 3 or 4 small adenomas or 1 adenoma >1cm. Re– scope at 3 years.
High risk: >5 small adenomas or >3 with 1 of them >1cm. Re scope at 1 year.
Segmental resection or complete colectomy should be considered when:

1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
FAP's Extra intestinal Menifestation (EIM)

– Desmoid tumor
– Hamartomatous polyp stomach
– Adenoma duodenum
– Dental Cyst
– Supernumerary teeth
– Epidermoid Cyst
– Osteoma Jaw
– Retinal Pigmentation
** FAP with the presence of EIM is called Gardener’s Syndrome.
Colorectal cancer screening and diagnosis
Overview
Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been shown to reduce
mortality by 16%
The NHS national screening programme offering screening every 2 years to all aged 60 to 69 years. Patients
aged over 70 years may request screening
Eligible patients are sent faecal occult blood (FOB) tests through the post
Patients with abnormal results are offered a colonoscopy
At colonoscopy, approximately:
5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer
Diagnosis
Essentially the following patients need referral:
– Altered bowel habit for > 6 weeks
– New onset of rectal bleeding
– Symptoms of tenesmus
Colonoscopy: Gold standard. Complete and good mucosal visualisation is achieved.
Double Contrast Barium Enema
CT Colonography.
Maximum center use CT scan in ≥ 80yrs group with Primary Colorectal Carcioma.
Suspected, acutely obstructing Large Bowel Carcinoma. Suitable investigation – Gastrografin enema
Rectal ca. Tissue invasion within the pelvis is best assessed with MRI
Staging
Patients with diagnosed colonic cancer will be staged using chest / abdomen and pelvic CT.
Patients with rectal cancer will also undergo evaluation of the mesorectum with pelvic MRI scanning.
Examination purposes the Dukes and TNM systems are preferred.
● DUKES CLASSIFICATION (Very imp)

Dukes' A : Confined to bowel wall
Dukes' B : Through the bowel wall ; Not involving LN
Dukes' C : LN Involved; no other metastasis
Dukes' C2 : Highest nodes involved
Dukes' D : Distant metastasis; long term survival rare without liver resection
Tumour markers
Carcinoembryonic antigen (CEA).
Not all tumours secrete this, and may be raised in conditions such as IBD.
Colorectal Cancer Treatment
Surgical. many centres now utilise enhanced recovery programmes which encourage prompt recovery by:
Early mobilisation
Judicious administration of fluid
Carbohydrate loading drinks on day of surgery
Early resumption of normal diet
Avoidance of mechanical bowel preparation
In many elective cases mechanical bowel preparation can be avoided; this is universally true for right sided colonic
surgery. Controversy exists as to whether it is needed for left sided surgery.
Which operation is best? (Very Important)
Site of cancer Type of resection Anastomosis Risk of leak
Right colon Right hemicolectomy Ileo– colic Low <5%
Transverse Extended right hemicolectomy Ileo– colic Low <5%
Splenic flexure Extended right hemicolectomy Ileo– colic Low <5%
Splenic flexure Left hemicolectomy Colo– colon 2– 5%
Left colon Left hemicolectomy Colo– colon 2– 5%
Sigmoid colon High anterior resection Colo– rectal 5%
Upper rectum Anterior resection (TME) Colo– rectal 5%
Low rectum Anterior resection (Low TME) Colo– rectal 10%

(±Defunctioning stoma)
Anal verge Abdomino– perineal excision None n/a

of colon and rectum
During emergency, where bowel has perforated,- the risk of an anastomosis is much greater,( particularly when it is
colon– colon) In this situation End Colostomy is safer and can be reversed later.
When Sigmoid Colon resection is done and an end colostomy is created: Hartmans procedure.
Left sided resections are more risky, ileo– colic anastomoses are relatively safe even in the emergency setting
and do not need to be defunctioned.
Basics :
Right Colon carcinoma – – – commonly shows
Pain @ RIF
Mass rt side, per abd. Exam
Anaemia ± wt. loss
Left Colon + Trnsverse Colon carcinoma – – – commonly shows

Bowel habit change
Abd. Distensn
Abdominal Pain (relieved with flatus…)
Tenesmus
Early morning diarrhoea
Mass in DRE
Blood mixed stool ± wt. loss থাকে
Lower Gastrointestinal bleeding
Colonic Bleeding
Typically presents as bright red or dark red blood per rectum.

Rarely presents as malaena type stool, this is because blood in the colon has a powerful laxative effect and is rarely
retained long enough for transformation to occur and because the digestive enzymes present in the small bowel are
not present in the colon.
Right sided bleeds present with darker coloured blood than left sided bleeds.
Haemorrhoidal bleeding presents as bright red rectal bleeding that occurs post defecation either on toilet paper or
into the toilet pan.
Causes
Cause Presenting features
Colitis • Bleeding may be brisk in advanced cases.

• Diarrhoea is commonly present.
• Abdominal x– ray may show featureless colon.
Diverticular • Acute diverticulitis is not usually complicated by major bleeding and often occur sporadically.
disease • 75% will cease spontaneously within 24– 48 hours.
• Bleeding is dark.
Cancer • Colonic cancers often bleed and this may be the first sign of the disease.
• Major bleeding from early lesions is uncommon
Haemorrhoids • Typically bright red bleeding occurring post defecation.
Angiodysplasia • Bleeding, may be massive.

• Right colon is more affected.
Management
• Prompt correction of any haemodynamic compromise.
• When haemorrhoidal bleeding - proctosigmoidoscopy is reasonable. Colonoscopy are usually time consuming
and often futile.
• In unstable patient: Angiogram (either CT or percutaneous), when these are performed during a period of
haemodynamic instability these show bleeding point and may be the only way of identifying a patch of
angiodysplasia.
• In stable patient: Colonoscopy is the standard. In patients undergoing angiography attempts can be made to
coiling the lesion. Otherwise surgery will be necessary.
• Ulcerative colitis with haemorrhage: Standard approach is Sub-total Colectomy, if medical management has
already been tried and is not effective.
Indications For Surgery
• Patients > 60 years

• Continued bleeding despite endoscopic intervention
• Recurrent bleeding
• Known cardiovascular disease with poor response to hypotension
Surgery
• Selective mesenteric embolisation if life threatening bleeding - most hellpful if conducted during a period of
relative haemodynamic instability. If all haemodynamic parameters are normal then the bleeding is most likely to
have stopped and any angiography normal in appearance.
• If source of bleeding unclear, do laparotomy, on table colonic lavage and following this attempt a resection.
Summary of Acute Lower GI bleeding recommendations Consider admission if:

* Over 60 years
* Haemodynamically unstable/profuse PR bleeding
* On aspirin or NSAID
* Significant co morbidity
Irritable Bowel Syndrome
The diagnosis of IBS is made according to the ROME III diagnostic criteria:
Recurrent abdominal pain or discomfort at 3 days per month for the past 3 months associated with two or more
of the following:
• Improvement with defecation.
• Onset associated with a change in the frequency of the stool.
• Onset associated with a change in the form of the stool.
Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis
Red Flag features:

• Rectal bleeding
• Unexplained/unintentional weight loss
• Family history of bowel or ovarian cancer
• Onset after 60 years of age
Suggested investigations:
• Full blood count
• ESR/CRP
• Coeliac disease screen (tissue transglutaminase antibodies)
• Colonoscopy (if worrying symptoms, positive family history)
• Thyroid function tests
• Glucose (ensure not diabetic)
Treatment
• Usually reduce fibre intake.
• Laxatives or Loperamide according to clinical picture.
• Dietary modification (caffeine avoidance, less carbonated drinks).
• Consider low dose Tricyclic Antidepressants if pain is a dominant symptom.
• Biofeedback may help.
Ulcerative Colitis
Inflammation always starts at Rectum, never spreads beyond ileocaecal valve and is continuous.
The peak incidence among aged 15– 25 years and in those aged 55– 65 years.
Less common in smokers.
The initial presentation is usually following insidious and intermittent symptoms. Features include:
• Bloody Diarrhoea
• Urgency
• Tenesmus
• Left Lower Quadrant abdominal pain
• Extra– Intestinal Features (See later)
Crohns disease
UC & CD Difference
FEATURES CD UC
Sex Females are more sufferer Equal
Site Mouth to anus, anywhere • Only Large Bowel
• Occasional “Backwash Ileitis”
Lesion type Skip Lesion No skip lesion; continuous
Histology • Deep Ulcer- Rose Thorn Ulcer • Small & shallow ulcer
• Whole thickness affected– "Hose Pipe • Limited to mucosa– not affecting muscularis
Thickening", Luminal Narrowing; Fibrosis. propria (unless fulminant disease)
• MUCOSA: Cobblestone • MUCOSA: Atrophic– inflammatory pseudopolyps
• SEROSA: Fatty Encroachment • SEROSA: unaffected until Toxic Megacolon
Granuloma Non– caseating Caseating

C/F • Tenesmas absent Tenesmas + incontinence present
• Pain is relieved by bowel movement
Ba enema Kantor’s String Sign found • Loss of haustrations
Blood picture Platelet raised None

Unique • Fistula(enterovesical); Fissure • Pseudopolyp;
Features • Mass • Crypt Abscess & distortion (neutrophils migrate
• Infection through the walls of glands to form it)
• Stricture • Goblet cell mucous depletion
• Skin tags • Hemorrhage
• Toxic megacolon (but Large bowel obstruction is
not a feature of UC)
Spread Trans mural Confined to Lamina propria
Malignancy Less Chance More chance for Metaplasia, Dysplasia
Lymphoid Found. And lymphocyte infiltrate of Lamina Not found
follicle Propria present
Surgical RX Less Beneficial Beneficial as Diseased segment is removed
● Anti TNF– α antibody – Infliximab is given as a single infusion for clinical improvement in steroid resistant CD
Extra– Intestinal Menifestations (EIM)
Common in both CD and UC Important Points
Related to disease activity Arthritis: asymmetric Arthritis is the most common EIM in both CD and UC
Erythema nodosum Episcleritis is more common in CD
Episcleritis
Osteoporosis
Unrelated to disease activity Arthritis: polyarticular, symmetric Primary Sclerosing Cholangitis more common in UC
Uveitis Uveitis is more common in UC
Pyoderma gangrenosum
Clubbing
Primary sclerosing cholangitis
MUST REMEMBER:(Very Imp.)

EIMs for UC + CD are same.But occur more in UC;
If both are given in options then answer the UC. (But anything in orally and anus then answer will be CD).
Fistula(specially enterovesical); Fissure; Mass; Infection; Stricture → CD’s Unique features
Pseudopolyp; Crypt Abscess; Crypt distortion; Malignancy → UC’s Unique features
Perforation can occur in both cases; but bleeding in UC > bleeding in CD
GB stone & Kidney stone → CD
Surgery for inflammatory bowel disease
Ulcerative Colitis
• Emergency: Sub total Colectomy+ end ileostomy ± mucous fistula.( Rectum either stapled off and left in situ,
or, if the bowel is very oedematous, may be brought to the surface as a mucous fistula.)
• Electively: Pan-proctocolectomy ± ileoanal pouch (Ileoanal pouch - can only be performed whilst the rectum is
in situ and cannot usually be undertaken as a delayed procedure following proctectomy)
• Dysplasia with mass: Proctocolectomy.

• Ileoanal pouch complications
o Anastomotic Dehiscence
o Pouchitis
o Poor physiological function with seepage and soiling.
• Patients with IBD have a high incidence of DVT and appropriate thromboprophylaxis is mandatory.
Crohns Disease
• Indications for surgery include complications: Fistulae, Abscess formation and strictures.
• Crohn's patients need minimal resections as it doesn't cure, but produce symptomatic improvement.
• Management of ano-rectal sepsis: Simply drain sepsis and use setons to facilitate drainage.
• Complex Perianal Fistula: Long term draining seton sutures, (Definitive fistula surgery should be avoided e.g.
advancement flaps, may be complicated to non healing and fistula recurrence)
• Localised Stricturoplasty: To preserve the intestinal length.
• Severe perianal and / or rectal Crohns: may require Proctectomy.
• Ileoanal pouch:Carries a high risk of fistula formation and pouch failure and not recommended.
• Terminal ileal Crohns: commonest site and treated with Limited Ileocaecal Resections. This Chron's affect
enterohepatic bile salt recycling and increase the risk of gallstones.
• Extensive small bowel resections may result in short bowel syndrome
Principles of Surgery Inflammatory Bowel Disease
Proctocolectomy ē ileostomy : Traditional, Common procedure for UC

Procedure of choice among Middle aged and Elderly
Leaves the pt. ē permanent colostomy
Proctocolectomy ē ileal / ileo– anal pouch
n
(Sphincter preserving) : Best opr for UC
Procedure of choice among young
n
Rectum excised, Anal canal reserved ē intact sphincter act
Pouch is anastomosed @ dentate line
Colectomy ē ileo– rectal anastomosis : Used in Both UC + CD

Used when rectum isn’t or mildly affected
Used rarely bcz– (recurrent disease, risk of ca, good result
in pouch surgery)
Proctectomy is used, in failed cases.
Sub– total colectomy ē end ileostomy : Perforation

± mucous fistula Severe hemorrhage
Toxic Megacolon
Fistulation leading to sepsis
Severe acute colitis resistant to medical management
Obstruction due to stricture
Large bowel obstruction resulting from carcinoma should be resected, stented or defunctioned. Colonic resections with
an anastomosis below the peritoneal reflection may have an anastomotic leak rate (both clinical and radiological) of up to
15%. End ileostomy & End colostomy typically apply to tumours above the peritoneal reflection. Lower tumours should
be defunctioned with a loop colostomy and then formal staging undertaken prior to definitive surgery.
Fig: Rx of UC Fig: Restorative proctocolectomy (ileoanal pouch procedure)
Fig: Ileal pouch anal anastomosis (mucosal lining left intact) Fig: ileal pouch anastomosis with distal rectal mucosal stripping
Fig: low ant– resection– j– pouch
Fig: low ant– resection
Fig: APR
Fig: Total proctocolectomy with Brooke ileostomy
Fig: colectomy vs total proctocolectomy
Fig: Colectomy with ileorectal anastomosis
Fig: ex– rt– hemicolectomy
Abdominal Stomas
Name of stoma Use Common sites
Gastrostomy • Gastric decompression or fixation Epigastrium
• Feeding
Loop jejunostomy • Seldom used as very high output Any location according to
• May be used following emergency laparotomy with need

planned early closure
Percutaneous • Usually performed for feeding purposes and site in Usually Left Upper
jejunostomy the proximal bowel Quadrant
Loop ileostomy • Defunctioning of colon e.g. following rectal cancer Usually Right Iliac Fossa
surgery
• Does not decompress colon (if ileocaecal valve
competent)
End ilestomy • Usually following complete excision of colon or Usually Right Iliac Fossa
where ileo– colic anastomosis is not planned
• May be used to defunction colon, but reversal is
more difficult
End colostomy Where a colon is diverted or resected and anastomosis is Either Left or Right Iliac
not primarily achievable or desirable Fossa
Loop colostomy • To defunction a distal segment of colon May be located in any
• Since both lumens are present the distal lumen region of the abdomen,
acts as a vent depending upon colonic

segment used
Caecostomy Stoma of last resort where loop colostomy is not possible Right iliac fossa
Mucous fistula • To decompress a distal segment of bowel following May be located in any
colonic division or resection region of the abdomen
• Where closure of a distal resection margin is not according to clinical need
safe or achievable
** End ileostomy + End Colostomy usually applied for tumors above peritoneal reflection.
Lower tumors should be defunctioned with a Loop Colostomy**
● Fulminant UC = Total Colectomy + End Ileostomy is performed usually in the Right iliac fossa.(RIF)
● In Crohn’s disease, Proximal small bowel strictures can be treated with segmental resection if only isolated areas
are affected, otherwise Stricturoplasty done if multiple segments involved.
● Pt. having large tumours not immediately resectable (peritoneal seeding, fixed to lateral pelvic wall ) may be
suitable for pre– operative radiotherapy to downsize the lesion. These cases require Loop Colostomy to divert the
faecal stream – commonly performed @ transverse or sigmoid colon
rd n
● Abd. Perineal resection – Middle & lower 3 of rectal ca – Its use when adequate distal resect margin not
achievable. If MRI shows resectable lesion present, then Total Mesorectal Excision (TME) done.(Waldeyer’s Fascia
is cut to mobilize)
● Below 5 cm of anal verge there will be not enough bowel left for an anastomosis, so APR is performed with a
permanent LIF end colostomy
● High Anterior Resection – Left Ureter is in high risk (of injury)
● Young person, bright red rectal bleed without other symptoms. Investigation of choice – Flexible Sigmoidoscopy
● Young person, maroon rectal bleed without other symptoms, both UGI endoscopy & Colonoscopy normal.
Investigation of choice – Technetium – 99m scanning
● Young person, maroon rectal bleed without other symptoms, both UGI endoscopy & Colonoscopy normal.
Diagnosis is Meckel’s Diverticulam
● Aged person, bright red rectal bleed without other symptoms, Fresh blood on rectal exam gloves – – – commonest
nd
cause? Ans:– Diverticular disease, 2 option Angiodysplasia
● Aged person, bright red rectal bleed without other symptoms; Gastroscopy & Colonoscopy normal i.e. don’t think about
Diverticular disease; ans will be Angiodysplasia. Mesenteric Angiography Or Radionucleotide Scan may be used. But
maximum cases cant be identified. In case of continued bleeding, with negative invx – RX – Total Colectomy
Angiodysplasia
– Small, submucosal vascular swelling of unknown etiology

– Associated with Aortic Stenosis
– Common sites are – Ascending Colon; Caecum
– PR bleed may present as Anemia; (+)ve FOBT; Recurrent small bleed or torrential acute bleed
– Association ē hereditary telangiectasia skin & mouth in Osler– Weber– Rendu disease.
st nd
– Investigation : 1 choice Colonoscopy; 2 choice Meseteric Angiography – if all fails,
Technetium– 99m labeled RBC can localize source of haemorrage.
Colonoscopy shows spider naevi like lesion
Diverticular disease
Herniation of colonic mucosa through the muscular wall of the colon.

Usual site is between the taenia coli which vessels pierce the muscle to supply the mucosa.
Symptoms
• Altered bowel habit
• Bleeding
• Abdominal pain
Complications
• Diverticulitis
• Haemorrhage
• Development of fistula
• Perforation and faecal peritonitis
• Perforation and development of abscess
• Development of diverticular phlegmon
Diagnosis
• Colonoscopy
• Barium enema
Difficult to confidently exclude cancer with these two, particularly in Diverticular Strictures.
• Plain abdominal films and Erect chest x– ray: Identify perforation.
• Abdominal CT scan with oral and intravenous contrast: Identify whether acute inflammation is
present or not . Also the presence of local complications (abscess)
Suspected Diverticular Mass suitable investigation USG

Diverticular Abscess suitable investigation CT abdomen & pelvis
Diverticular disease suitable investigation Enema
Fig: Severity Classification
Treatment
• Increase dietary fibre intake. Mild attacks of diverticulitis is managed conservatively with antibiotics.
• Peri colonic abscess: Drained either surgically or radiologically.
• Recurrent episodes of acute diverticulitis: Segmental Resection.
• Hinchey IV perforations (generalised faecal peritonitis) : Resection and usually a stoma.
• Less severe perforation: Laparoscopic washout and drain insertion.
Example Themes
Aged person, Constipation, requires perineal massage to defaecate; female paitent complains vagina bulging during
defaecation (rectocele). Diagnosis? – Outlet Obstruction Constipation
Aged person, psychogenic, Constipation & abdominal distension. Which investigation to do? – Supine Abdominal
nd
Xray. But if this option is not given, Colonoscopy will be the 2 option.
● Suspected colovesical fistula suitable investigation double contrast Ba enema

● Suspected Psoas abscess suitable investigation CT abdomen.
Coeliac disease typical histological features
Villous atrophy (‘gold standard’)

Crypt hyperplasia / hypertrophy,
Inflammatory infiltrate of the lamina propria
Intra– epithelial lymphocytes
Anti TTG (Tissue Trans Glutaminase) antibody present in >90% cases.

(However, detection of TTG ab has high specificity and sensitivity and is widely used as a screening test)
Fistulas
A fistula is defined as an abnormal connection between two epithelial surfaces.
4 TYPES FISTULAE
Enterocutaneous
Link the intestine to the skin.
May be high (>1L) or low output (<1L).
Result from spontaneous rupture of abscess cavity onto the skin (such as following perianal abscess drainage) or
may occur as a result of iatrogenic input
In some cases it may be surgically desirable e.g. Mucous Fistula following Sub Total Colectomy for Colitis. Suspect if
there is excess fluid in the drain.
Duodenal /Jejunal Fistulae (High Output):

Produce high volume, electrolyte rich secretions
Severe excoriation of the skin.
Colo– Cutaneous Fistulae:
Leak faeculent material.
Enteroenteric or Enterocolic
Involves the large or small intestine.
May originate in a similar manner to enterocutaneous fistulae.
A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes. This
may be particularly serious in IBD
Enterovaginal
Aetiology as above.
Enterovesicular
This fistula goes to the Bladder.
Result in frequent UTIs, or passage of gas(or air bubbles) from the urethra during urination.
Management
They will heal (if no underlying IBDs and no distal obstruction) so conservative measures is the best option.
If skin involves: protect skin, often using stoma bag.
High Output Fistula: Easily managed by Octreotide (reduce the pancreatic secretions volume)
Nutritional complications are common with High Output Fistula ( High Jejunal or Duodenal) - which necessitate
the use of TPN to provide nutritional support together with the use of Octreotide to reduce vol.and protect skin.
Perianal Fistulae: Avoid probing the fistula where acute inflammation is present, this always worsens outcomes.
Use Goodsall's Rule (explained later) in relation to internal and external openings.
Perianal Fistulae occuring secondary to Crohn's disease, the best management option is: Drain acute sepsis and
maintain that drainage through the use of setons; at the same time as medical management is implemented.
Always attempt to delineate the fistula anatomy.

Abscesses and Fistulae that have an intra abdominal source, Barium and CT studies show a track.
Rectum
Approximately 12 cm long. It is a capacitance organ.

Has both intra and extraperitoneal components.
The transition between Sigmoid Colon is marked by the disappearance of the Tenia Coli.
The extra peritoneal rectum is surrounded by mesorectal fat that also contains lymph nodes.
This mesorectal fatty layer is removed surgically during rectal cancer surgery (Total Mesorectal Excision).
The fascial layers that surround the rectum are important clinical landmarks, anteriorly lies the fascia of Denonvilliers.
Posteriorly lies Waldeyers fascia.
Extra Peritoneal Rectum

• Posterior upper third
• Posterior and lateral middle third
• Whole lower third
Support
• Pelvic floor
• Waldeyer’s fascia with sacrum
• Rectovesical fascia of Denonvilier’s
• Laeral ligament of rectum
• Pelvic peritoneum
Relations
Anteriorly (Males) Rectovesical pouch

Bladder
Prostate
Seminal vesicles
Anteriorly (Females) Recto– uterine pouch (Douglas)

Cervix
Vaginal wall
Posteriorly Sacrum
Coccyx
Middle sacral artery
Laterally Levator ani

Coccygeus
Arterial Supply
Superior rectal artery ← IMA
Middle rectal artery ← IIA (ant. division)
Median sacral artery ← AA
Venous Drainage
Superior rectal vein → IMV
Middle rectal vein → IIV
Lymphatic Drainage
• Mesorectal lymph nodes (superior to dentate line)
• Internal iliac and then para– aortic nodes
• Inguinal nodes (inferior to dentate line)
Nerve supply (thru’ inf. Hypogastric + Inf. Mesenteric / sup. Rectal plexus)
Sympathetic(L1,2):– Vasoconstrictor; Rectal muscle (–); IAS(+); Pain
P. Sympathetic(S2,3,4):– Rectal muscle(+); IAS (–); Rectal distension sense; Pain
Rectal bleeding
Type of Features in history Examination findings

Cause bleeding
Fissure in ano Bright red Painful small volume bleeding Muco– epithelial defect usually
Occurs post defecation in the midline posteriorly
Antecedent feature of constipation Anterior fissures more likely to
be due to underlying disease
Haemorroids Bright red Post defecation bleeding Normal colon and rectum.
Found both on toilet paper and drips into pan. Proctoscopy- internal
Altered bowel habit + H/O straining. haemorrhoids.
No blood mixed with stool. Internal haemorrhoids are
No local pain. impalpable.
Crohns Bright red or Bleeding is accompanied by altered bowel Perineal inspection show
Disease mixed habit, malaise, H/O Fissures (especially fissures or fistulae.
anterior) and abscess Proctoscopy- Indurated
mucosa and possibly
strictures.
Colonoscopy-Skip lesions.
Ulcerative Bright red mixed Diarrhoea, weight loss Proctitis is the most marked
Colitis with stool Nocturnal incontinence, finding.
Passage of mucous PR. Peri anal disease is usually
absent.
Colonoscopy show continuous
mucosal lesion.
Rectal Cancer Bright red blood Altered bowel habit. Mucosal abnormality.
mixed volumes Tenesmus may be present. Lesion may be fixed or mobile
Symptoms of metastasis. Surrounding mucosa often
normal - polyps may be
present.
Investigation
DRE and Procto– Sigmoidoscopy: Baseline. Haemorrhoids are typically impalpable
Sigmoidoscopy:
Young patient with no other features - If demonstrates clear haemorrhoids that may be sufficient.
If clear views cannot be obtained - bowel preparation with an enema and Flexible Sigmoidscopy.
Colonoscopy: Best test for patients with H/O altered bowel habit or suspicion of IBD.
Examination under GA or LA: Patients with excessive pain and suspected fissure.
young patients with external stigmata of fissure and a history - he/she should undergo medical treatment and
defer internal examination until the fissure is healed.
If the fissure fails to heal, then internal examination becomes necessary to exclude internal disease.
Special tests
MRI - For staging, to identify circumferential resection margin; to identify mesorectal nodal disease.
CT scan - Chest, Abdomen and Pelvis is necessary to stage for more distant disease.
Endo Rectal Ultrasound - Some centres stage the mesorectum with this but less common.
Ano Rectal Manometry With Endo Anal Ultrasound - Fissure in ano waiting for surgical sphincterotomy and
Females who have an obstetric history. (not mandatory but in the absence of such information there are
continence issues that may arise following sphincterotomy)
Management
Disease Management
Fissure in ano GTN ointment 0.2% or diltiazem cream applied topically is the usual first line treatment. Botulinum
toxin for those who fail to respond. Internal sphincterotomy for those who fail with botox, can be
considered at the botox stage in males.
Haemorroids Lifestyle advice, for small internal haemorrhoids can consider injection sclerotherapy or rubber band
ligation. For external haemorrhoids consider haemorrhoidectomy. Modern options include HALO
procedure and stapled haemorrhoidectomy.
Inflammatory Medical management– although surgery may be needed for fistulating Crohns (setons).
bowel disease
Rectal cancer Anterior resection or abdomino– perineal excision of the colon and rectum. Total mesorectal excision
is now standard of care. Most resections below the peritoneal reflection will require defunctioning
ileostomy. Most patients will require preoperative radiotherapy.
Anal Canal (Figures available with Rectum above)

3.8 cm long
Upper 1.5 cm; middle 1.5cm; lower 0.8cm
Arterial supply
Above pectinate line : Superior rectal artery ← IMA
Below pectinate line : Inferior rectal artery ← IPA ← IIA (ant. division)
Venous drainage
– Internal rectal venous plexus (haemorrhoidal; lies @ submucosa) → SRV → IMV
(It can freely connect ē External plexus thus ē Middle & Inf. Rectal vein – important site for porto– systemic anastomosis)
– External rectal venous plexus (outside muscular coat) – Inf. Rectal vein → IPV
– Mid. Rectal vein → IIV
Nerve supply (thru’ inf. Hypogastric + Inf. Mesenteric / sup. Rectal plexus)
Above pectinate line : Inf. Hypogastric plexus(Sympathetic L1,2) – Pain
Pelvic splanchnic (S2,3,4) – Pain
Below pectinate line : Inferior rectal S2,3,4 (Somatic)
Lymphatic drainage
Above pectinate line: IIN
Below pectinate line: Superficial IN
Anal sphincter
• Internal anal sphincter composed of Smooth Muscle continuous with the circular muscle of the rectum. It
surrounds the upper two– thirds of the anal canal and is supplied by sympathetic nerves.
• External anal sphincter is composed of Striated Muscle which surrounds the internal sphincter but extends
more distally.
• The nerve supply of the external anal sphincter is from the inferior rectal branch of Pudendal Nerve (S2 and
S3) and the perineal branch of the S4 nerve roots.
Ano rectal disease
Location: 3, 7, 11 o'clock position

Haemorrhoids Internal or external
Treatment: Conservative, Rubber band ligation, Haemorrhoidectomy
Fissure in ano Location: midline 6 (posterior midline 90%) & 12 o'clock position. Distal to the
dentate line
Chronic fissure > 6/52: triad: Ulcer, sentinel pile, enlarged anal papillae
Proctitis Causes: Crohn's, Ulcerative Colitis, Clostridium difficile
Ano rectal abscess E.coli, staph aureus

Positions: Perianal, Ischiorectal, Pelvirectal, Intersphincteric
Anal fistula Usually due to previous ano– rectal abscess

Intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric.
Goodsalls rule determines location
Rectal prolapse Associated with childbirth and rectal intussceception. May be internal or external
Pruritus ani Systemic and local causes
Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum
Solitary rectal ulcer Associated with chronic straining and constipation. Histology shows mucosal
thickening, lamina propria replaced with collagen and smooth muscle
(fibromuscular obliteration)
Pruritus ani
• Extremely common.
• Check not secondary to altered bowel habits (e.g. Diarrhoea)

• Associated with underlying diseases such as haemorrhoids.
• Examine to look for causes such as worms.
• Proctosigmoidoscopy to identify associated haemorrhoids and exclude cancer.
• Treatment is largely supportive and patients should avoid using perfumed products around the area.
Pruritis Ani is associated with:

Systemic (DM, Hyperbilirubinaemia, aplastic anaemia)
Mechanical (diarrhoea, constipation, anal fissure)
Infections (STDs)
Dermatological
Drugs (quinidine, colchicine)
Topical agents
Haemorrhoids Rx
10 (confined anal canal) : Bulking agents; tropical anaesthesia > if unresponsive, inj. Sclerotherapy
0 n
2 (prolapse on defaecat &
n
spontaneous/digital reduct ): Rubber band ligation
30 (permanent prolapse) : Haemorrhoidectomy
Fistula
● Goodsall’s Rule
The external opening situated behind the transverse anal line will open into the anal canal in the midline
posteriorly. An anterior opening is usually associated with a radial tract.
In more direct terms, it means that anterior– opening fistulas tend to follow a simple direct course while
posterior– opening fistulas may follow a devious, curving path being horseshoe– shaped before opening in the
posterior midline
Intersphincteric : Fistulotomy
Dentate line + its above : Seton suture
Rest : Fistulectomy
● Complex anal fistula is best assessed with MRI
● Sphincters destruction - suitable investigation Endo-anal USG . Other investigations Anorectal Manometry.
Anal Fissure
Most fissures are idiopathic

Mostly present as mucocutaneous defect in the posterior midline (90% cases).
Fissures are more likely to be anteriorly located in females, particularly if multiparous.
Multiple fissures and those which are located at other sites are more likely to be due to underlying causes:
Sexually transmitted diseases (syphilis, HIV)
Inflammatory bowel disease (Crohn's up to 50%)
Leukaemia (25% of patients)
Tuberculosis
Previous anal surgery
Treatment:
st
1 line : GTN ointment 8hourly X 8wks
2nd line : If Headache with GTN, then Diltiazem ointment, 2nd option
Chronic : Botulinum toxin is an effective treatment (73% efficacy)** if it fails –
Lateral internal sphincterotomy (male – but associated ē flatus incontinence in 10%)
Advancement flaps (Female).
Rectal prolapse
Common especially in multiparous women.
May be internal or external.
Patients with internal prolapse
o May present insidiously,
o Have internal intussceception of the rectum
o Present with constipation, obstructed defecation and occasionally faecal incontinence
Patients with external rectal prolapse
o Have a full thickness external protrusion of the rectum.
o Can ulcerate and in long term impair continence
Diagnostic work up includes
o Colonoscopy,
o Defecating proctogram,
o Ano rectal manometry studies
o If doubt exists and examination under anaesthesia.
o Sinister pathology should be excluded with endoscopy
Treatment
In the acute setting reduce it (covering it with sugar may reduce swelling)
Delormes operation
o Perineal approaches
o may be used for external prolapse
o Excises mucosa and plicates the rectum – this avoids resection and is relatively safe.
o Associated with high recurrence rates.
Altmeirs procedure
o Resection of colon via the perineal route
o Has lower recurrence rates

o but carries the risk of anastamotic leak
Rectopexy
o Abdominal procedure.
o The rectum is mobilized, elevated and fixed onto the sacral promotary.
o Post operative constipation may be reduced by limiting the dissection to the anterior plane
(laparoscopic ventral mesh rectopexy).
o The recurrence rates are low and the procedure is well tolerated (particularly if performed
laparoscopically).
Thirsch tape– this is a largely historical procedure and involves encircling the rectum with tape or wire. It may
be of use in a palliative setting.
Solitary rectal ulcer syndrome treatment – – – – Biofeedback

Perianal hematoma treatment– – – – – 4% Formalin (topical)
Levator ani (pubococcygeus+puborectalis+iliococcygeus) and Coccygeus muscles form Pelvic

Diaphragm(N– 363)
Levator ani arises from Back of Pubis Body; Ischial spineand the tendinous arch of Obturator internus
fascia.
Thrombosed piles can be treated conservatively or by incision and drainage to evacuate clot under LA
Laparoscopic repair is indicated in bilateral inguinal hernia unless there is any contraindicated.
Sigmoid colon most likely to be involved in left– sided indirect inguinal hernia as it is mobile due2 sigmoid
mesocolon.
Fallopian tube lies between the layers of the mesosalpinx
● OSLER WEBER RENDU SYNDROME : TEACH (after OCP use)

T elengiectasia
E pistaxis
A V malformation
C erebral abscess
H aemorrhages– pulmonary,GIT
Acute abdominal pain– diagnoses
Condition Features Investigations Management
• H/O migratory pain. • Differential WBC count Appendicectomy

• Fever & Anorexia. • Pregnancy test
Appendicitis • RIF tenderness. • C– Reactive protein
• Mild pyrexia. • Amylase
• Urine dipstick testing
• Recent Upper RTI • Full blood count - slightly • Manage conservatively

• High fever. raised WBC count. • appendicectomy if diagnostic
Mesenteric Adenitis • Generalised abdominal • Urine dipstick often doubt
discomfort– true localised normal.
pain and signs are rare. • Abd.USG – no free fluid
• Only in Females. • Full blood count– normal • Manage conservatively

• Mid cycle pain. • Urine dipstick– normal • Laparoscopy -if doubt/
• Occurs two weeks after • USG – show a trace symptoms fail to settle.
Mittelschmerz LMP. pelvic free fluid.
• Supra– pubic area Pain
• Subsides within 24-48 hours.
• Usually in Females • Abd. USG– free fluid. Usually medically managed–

• Disseminated infection with • High vaginal swabs – doxycycline or azithromycin
Fitz– Hugh Curtis Chlamydia. . show evidence of STDs
Syndrome • PID with peri – hepatic
inflammation & adhesion
formation.
• Older adults Haemodynamically stable • Urgent Surgery- Unstable pt.

• Sudden onset of pain patients should have a CT • Immediate Surgery- contained
radiating to back following scan leak in CT
Abdominal Aortic collapse. • Increasing aneurysmal size -
Aneurysm • Moribund on arrival in surgery (can wait until the next
(Ruptured) casualty - more stable if working day)
contained haematoma.
• May reveal pulsatile mass.
• Sudden onset of pain • Erect CXR - may show • Laparotomy (laparoscopy for
(usually epigastric). free air. perforated peptic ulcers is safe
• Often preceding H/O upper • CT scan - where there is and feasible)
Perforated Peptic abdominal pain. diagnostic doubt
Ulcer • Soon develop generalised
abd.pain.
• May have peritonitis.
• Colicky abdominal pain • Plain abdominal X-ray • Laparotomy

• Vomiting • CT scan - where there is
Intestinal • Abdominal distension and diagnostic doubt
Obstruction constipation
• Peritonism may occur where
local necrosis of bowel loops
is occurring.
• Sudden pain and forceful • Arterial pH and lactate • Laparotomy and resection of
evacuation. • Arterial phase CT - most affected segments,
• Acute on chronic events sensitive. • In acute embolic events SMA
Mesenteric have a long history and embolectomy may be needed.

Infarction previous weight loss.
• On examination- pain is
typically greater than the
physical signs
Gynaecological causes of abdominal pain
Diagnosis Features Investigation Treatment
• Only in Females. • Full blood count– normal • Manage conservatively

• Mid cycle pain. • Urine dipstick– normal • Laparoscopy -if doubt/
Mittelschmerz • Occurs two weeks after LMP. • Abdominal and pelvic USG symptoms fail to settle.
• Supra– pubic area Pain – may show a trace pelvic
• Subsides within 24-48 hours.. free fluid.
• 25% asymptomatic, 25% ē pelvic organ • USG– free fluid • Conservative

pathology. Rest 50% have cycle • Laparoscopy- show Management.
irregularity, infertility, pain and lesions. • Complex disease -
dyspareurina. surgery
• Complex disease results in pelvic • Colonic and Rectal
Endometriosis adhesion with intermittent small bowel resections if these
obstruction. involved
• Intra– abdominal bleeding may produce
localised peritoneal inflammation.
• Recurrent episodes common.
• Sudden onset of colicky abd.pain. • USG- free fluid Laparoscopy

Ovarian Torsion • Vomiting and distress. • Laparoscopy is both
• Vaginal exam- adnexial tenderness. diagnostic; therapeutic
• Symptoms of pregnancy without • USG - No intra uterine • Laparoscopy or

evidence of intra uterine gestation. pregnancy - May show laparotomy.
• Present as emergency with evidence of intra abdominal free fluid • Salphingectomy is
Ectopic rupture or impending rupture. • Beta HCG - elevated usually performed.
Gestation • Open tubular ruptures -sudden onset
abd.pain and circulatory collapse.
• Small vaginal discharge is common.
• Usually adnexial tenderness.
• Bilateral lower abd. pain associated • CBC – Leucocytosis Usually medical

with vaginal discharge. • Pregnancy- negative. management
• Dysuria • Amylase–normal or slightly
Pelvic • Peri– hepatic inflammation secondary raised
Inflammatory to Chlamydia (Fitz Hugh Curtis • High vaginal and urethral
Disease Syndrome) may produce right upper swabs

quadrant discomfort.
o
• Fever >38
Sample theme
A 19 year old lady is admitted with lower abdominal pain. On examination she is diffusely tender. A laparoscopy is
performed and at operation multiple fine adhesions are noted between the liver and abdominal wall. Her appendix is
normal.
Answer: Pelvic inflammatory disease
This is Fitz Hugh Curtis syndrome in which pelvic inflammatory disease (usually Chlamydia) causes the formation of
fine peri hepatic adhesions.
Right iliac fossa pain
Differential diagnosis
• Pain radiating to right iliac fossa

• Anorexia
Appendicitis
• Typically short history
• Diarrhoea and profuse vomiting rare
• Often long history

Crohn's Disease • Signs of malnutrition
• Change in bowel habit, especially diarrhoea
• Mainly affects children

• Causes include Adenoviruses, Epstein Barr Virus, beta–
haemolyticStreptococcus, Staphylococcus spp., Escherichia
Mesenteric Adenitis coli, Streptococcusviridans and Yersinia spp.
• Patients have a higher temperature than those with appendicitis
• If laparotomy is performed, enlarged mesenteric lymph nodes will be present
Diverticulitis • Both left and right sided disease may present with right iliac fossa pain
• Clinical history may be similar, although some change in bowel habit is usual
• When suspected a CT scan may help in refining the diagnosis
Meckel's diverticulitis • A Meckel's diverticulum is a congenital abnormality that is present in about 2% of

the population
• Typically 2 feet proximal to the ileocaecal valve
• May be lined by ectopic gastric mucosal tissue and produce bleeding
Perforated peptic ulcer • This usually produces upper quadrant pain but pain may be lower
• Perforations typically have a sharp sudden onset of pain in the history
Incarcerated right • Usually only right iliac fossa pain if right sided or bowel obstruction.
inguinal or femoral hernia
Bowel perforation • Seldom localised to right iliac fossa, although complete large bowel obstruction
secondary to caecal or with caecal distension may cause pain prior to perforation.
colon carcinoma
Gynaecological causes • Pelvic inflammatory disease/salpingitis/pelvic abscess/Ectopic pregnancy/Ovarian

torsion/Threatened or complete abortion/Mittelschmerz
Urological causes • Ureteric colic/UTI/Testicular torsion
Other causes • TB/Typhoid/Herpes Zoster/AAA/Situs inversus
Abdominal compartment syndrome
It is defined as sustained intra abdominal pressure >20mmHg along with new organ dysfunction / failure.
Intra– abdominal pressure is the steady state pressure concealed within the abdominal cavity.
• In critically ill adults the normal intra abdominal pressure = 5– 7mmHg
• Intra abdominal hypertension has pressures of 12– 25mmHg
• Changes >15mmHg are associated with microvascular hypoperfusion
• It may occur either - Primarily, without previous surgical intervention e.g. Following intestinal ischaemia or
Secondarily, following a surgical procedure
• Diagnosis: Made by Transvesical Pressure Measurements coupled with clinical suspicion.
Management
Non operative Treatment. Including:
• Gastric decompression
• Improve abdominal wall compliance e.g. muscle relaxants/ sedation
• Drain abdominal fluid collections.
• Consider fluid restriction/ diuretics if clinically indicated.
Surgical treatment:
• If non operative treatment is failing;
• Treatment is Laparotomy and Laparostomy.
→ Options for laparostomy are many. Bogota bag or VAC techniques are mostly practised.
• Re– look laparotomy and attempts at delayed closure are next steps
Gastro Intestinal Parasitic Infections
Enterobiasis • Due to organism Enterobius vermicularis

• Common cause of pruritus ani
• Diagnosis: place scotch tape at anus -this traps eggs, can be viewed microscopically.
• Treatment: Mebendazole.
Ancylostoma • Hookworms that anchor in proximal small bowel.

duodenale • Most infections are asymptomatic although may cause Iron Deficiency Anaemia
• Larvae may be found in stools left at ambient temperature, otherwise infection is difficult
to diagnose.
• *Infection: Cutaneous penetration, migrates to lungs, coughed up and then swallowed.
• Treatment is with Mebendazole.
Ascariasis • Due to infection with roundworm Ascaris lumbricoides

• Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to
lungs, coughed up and swallowed, cycle begins again.
• Diagnosis is made by identification of worm or eggs within faeces.
• Treatment is with Mebendazole
Strongyloidiasis • Due to infection with Strongyloides stercoralis

• Rare in west
• Organism is a Nematode living in duodenum of host
• *Infection is via skin penetration → migrate to lungs → coughed up and swallowed→
mature in small bowel→excreted and cycle begins again. An auto infective cycle is also
recognised where larvae will penetrate colonic wall.
• May be asymptomatic, although they may also have respiratory disease and skin lesions.
• Diagnosis is usually made by stool microscopy
• In the UK mebendazole is used for treatment.
Cryptosporidium • Protozoal infection

• Organisms produce cysts which are excreted and thereby cause new infections
• Symptoms: Diarrhoea; Cramping abdominal pain- worse in immunosuppressed people
• Cysts identified in stools.
• Treatment is with metronidazole
Giardiasis • Diarrhoeal infection caused by Giardia lamblia (protozoan)

• Infections occur as a result of ingestion of cysts
• Symptoms: abdominal pain, bloating and passage of soft or loose stools.
• Diagnosis is by serology or stool microscopy
• First line treatment is with Metronidazole
Lymphatic drainage of the uterus and cervix

• The uterine fundus has a lymphatic drainage that runs with the ovarian vessels and may thus drain to the para–
aortic nodes. Some drainage may also pass along the round ligament to the inguinal nodes.
• The body of the uterus drains through lymphatics contained within the broad ligament to the iliac lymph nodes.
• The cervix drains into three potential nodal stations; laterally through the broad ligament to the external iliac
nodes, along the lymphatics of the uterosacral fold to the presacral nodes and posterolaterally along lymphatics
lying alongside the uterine vessels to the internal iliac nodes.
Obesity: physiology
Leptin
Leptin is thought to play a key role in the regulation of body weight.
Produced by adipose tissue and acts on satiety centres in the hypothalamus and decreases appetite.
More adipose tissue (e.g. in obesity) results in high leptin levels.
Leptin stimulates the release of melanocyte– stimulating hormone (MSH) and corticotrophin– releasing hormone
(CRH). Low levels of leptin stimulates the release of neuropeptide Y (NPY)
Ghrelin
Where as leptin induces satiety, ghrelin stimulates hunger.
It is produced mainly by the fundus of the stomach and the pancreas.
Ghrelin levels increase before meals and decrease after meals
BARIATRIC SURGERY
– Wt. reducing surgery.

– Body Mass Index(BMI) exceeding 40, or BMI > 35 with serious co– morbidities (eg sleep apnoea, type 2 DM).
– Post– operative mortality ranges from 0.1 – 2 %.
– Vomiting is associated with bariatric surgery, as is dumping syndrome and nutritional deficiencies.
NICE Guidelines
Consider surgery for people with severe obesity if:
2 2
• BMI >/= 40 kg/m or between 35– 40 kg/m and other significant disease (for example, type 2 diabetes,
hypertension) that could be improved with weight loss.
• All non– surgical measures have failed to achieve or maintain adequate clinically beneficial weight loss for at
least 6 months.
• Will receive intensive specialist management
• They are generally fit for anaesthesia and surgery
• They commit to the need for long– term follow– up
2
• First– line option for adults with a BMI > 50 kg/m in whom surgical intervention is considered appropriate;
consider Orlistat if there is a long waiting list.
Notes
• After bariatric surgery patents are found to have partial or complete resolution of co morbidities associated with
obesity.
• Bariatric surgery is the only intervention to demonstrate long– term weight loss in randomised controlled trials.
Surgical options
Adjustable gastric • Laparoscopic placement of adjustable band around proximal stomach.

band • Contains an adjustable filling port
• Effective method for lifestyle control
• Reversible
• Takes longer to achieve target weight
• Complications such as band erosion (rare), slippage or loss of efficacy may require re–
intervention
Gastric bypass • Combines changes to reservoir size with malabsorptive procedure for more enduring
weight loss.
• Technically more challenging
• Risks related to anastomoses (2% leak rate)
• Irreversible
• Up to 50% may become B12 deficient
Sleeve gastrectomy • Resection of stomach using stapling devices

• Body and fundus resected to leave a small section of stomach
• Less popular now as initial promising results not sustained
Biliopancreatic diversion +/– Duodenal Switch: bypass the small bowel. Greatest weight loss but a very complex
procedure associated with malnutrition and diarrhoea.
Vertical Banded Gastroplasty (stomach stapling): rarely performed due to longterm failure rate
Vomiting
Reflex oral expulsion of gastric (and sometimes intestinal) contents – reverse peristalsis and abdominal contraction
The vomiting centre is in part of the medulla oblongata and is triggered by receptors in several locations:
• Labyrinthine receptors of ear (motion sickness)
• Overdistention receptors of duodenum and stomach
• Trigger zone of CNS – many drugs (e.g., opiates) act here
• Touch receptors in throat
• Sensory innervation rich, both extrinsic and intrinsic
HEPATOPANCREATIC AND SPLENIC SYSTEM
● NORMAL VALUES
AST : 10 - 45 i.u./ l
ALT : 10 - 50 i.u./ l
Alk.PO4 : 40 - 125 i.u./ l
Amylase : <100 i.u./ l
Liver
Structure of The Liver
Right lobe Supplied by right hepatic artery

Contains Couinard segments V to VIII (-/+Sg I)
Left lobe Supplied by the left hepatic artery

Contains Couinard segments II to IV (+/- Sg1)
Quadrate lobe Part of the right lobe anatomically, functionally is part of the left
Couinard segment IV
Porta hepatis lies behind
On the right lies the gallbladder fossa
On the left lies the fossa for the umbilical vein
Caudate lobe • Supplied by both right and left hepatic arteries

• Couinard segment I
• Lies behind the plane of the porta hepatis
• Anterior and lateral to the inferior vena cava
• Bile from the caudate lobe drains into both right and left hepatic ducts
• Between the liver lobules are portal canals which contain the portal triad: Hepatic Artery, Portal Vein, tributary of
Bile Duct.
Relations of the liver
Anterior Postero inferiorly
Diaphragm Oesophagus
Xiphoid process Stomach
Duodenum
Hepatic flexure of colon
Right kidney
Gallbladder
Inferior vena cava
Bare areas
- GB Fossa
- Groove for IVC
- Bare area of liver
Porta hepatis
Location Postero inferior surface, it joins nearly at right angles with the left sagittal fossa, and separates the caudate
lobe behind from the quadrate lobe in front
Transmits • Common hepatic duct

• Hepatic artery
• Portal vein
• Sympathetic and parasympathetic nerve fibres
• Lymphatic drainage of the liver (and nodes)
Ligaments
Falciform ligament • 2 layer fold peritoneum from the umbilicus to anterior liver surface
• Contains ligamentum teres (remnant umbilical vein)
• On superior liver surface it splits into the coronary and left triangular ligaments
Ligamentum teres Joins the left branch of the portal vein in the porta hepatis
Ligamentum venosum Remnant of ductus venosus
False Ligament : Formed by Peritoneum

- Right and Left Triangular ligament
- Falciform ligament
- Coronary ligament
True Ligament :Formed by Facsia, capsule and embryological remnant

- Round ligament
- Ligamentum venosum
Arterial Supply: Hepatic artery
Venous : Hepatic veins Portal vein
Nervous supply: Sympathetic and parasympathetic trunks of coeliac plexus
HEPATIC SEGMENTS
Caudate : Segment I
Left : Segment II & III
Quadrate : Segment IV
[ Upto this, they are functionally the part of the left lobe.]
Right : Segment V- VIII
Benign Liver Lesions
Haemangioma • Most common benign tumours of mesenchymal origin

• Incidence in autopsy series is 8%
• Cavernous haemangiomas may be enormous
• Clinically they are reddish purple hypervascular lesions
• Lesions are normally separated from normal liver by ring of fibrous tissue
• On ultrasound they are typically hyperechoic
Liver cell adenoma • 90% develop in women in their third to fifth decade
• Linked to use of oral contraceptive pill
• Lesions are usually solitary
• They are usually sharply demarcated from normal liver although they usually lack a
fibrous capsule
• On ultrasound the appearances are of mixed echoity and heterogeneous texture. On CT
most lesions are hypodense when imaged prior to administration of IV contrast agents
• In patients with haemorrhage or symptoms removal of the adenoma may be required
Mesenchymal Congential and benign, usually present in infants. May compress normal liver
hamartomas
Liver abscess • Biliary sepsis is a major predisposing factor

• Structures drained by the portal venous system form the second largest source
• Common symptoms include fever, RUQ pain. Jaundice may be seen in 50%
• Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in
chronic abscesses
Amoebic abscess • Liver abscess is the most common extra intestinal manifestation of amoebiasis
• Between 75 and 90% lesions occur in the right lobe
• Presenting complaints typically include fever and right upper quadrant pain
• Ultrasonography will usually show a fluid filled structure with poorly defined boundaries
• Aspiration yield sterile odorless fluid which has an anchovy paste consistency
• Treatment is with Metronidazole
Hyatid cysts • Seen in cases of Echinococcus infection

• Typically an intense fibrotic reaction occurs around sites of infection
• The cyst has no epithelial lining
• Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick and
has an external laminated hilar membrane and an internal enucleated germinal layer
• Typically presents with malaise and right upper quadrant pain. Secondary bacterial
infection occurs in 10%.
• Liver function tests are usually abnormal and eosinophilia is present in 33% cases
• Ultrasound may show septa and hyatid sand or daughter cysts.
• Percutaneous aspiration is contra indicated
• Treatment is by Sterilisation of the cyst with Mebendazole and may be followed by
surgical resection. Hypertonic swabs are packed around the cysts during surgery
Polycystic Liver • Usually occurs in association with Polycystic Kidney Disease

Disease • Autosomal dominant disorder
• Symptoms may occur as a result of capsular stretch
Cystadenoma • Rare lesions with malignant potential

• Usually solitary multiloculated lesions
• Liver function tests usually normal
• Ultrasonography typically shows a large anechoic, fluid filled area with irregular margins.
Internal echos may result from septa
• Surgical resection is indicated in all cases
Liver tumours
Primary Liver Tumours

The most common primary tumours are cholangiocarcinoma and hepatocellular carcinoma. Overall metastatic disease
accounts for 95% of all liver malignancies making the primary liver tumours comparatively rare.
Primary liver tumours include:
• Cholangiocarcinoma
• Hepatocellular carcinoma
• Hepatoblastoma
• Sarcomas (Rare)
• Lymphomas
• Carcinoids (most often secondary although primary may occur)
Hepatocellular Carcinoma
• These account for the bulk of primary liver tumours (75% cases).
Diagnosis
• CT/ MRI: (usually both) are the imaging modalities of choice
• α-fetoprotein: Elevated
• Biopsy should be avoided as it seeds tumors cells through a resection plane.
• Diagnostic Doubt: Serial CT and AFP measurements are the preferred strategy.
Treatment
• Staging: liver MRI and chest, abdomen and pelvic CT scan.
• Testis should be examined in males (testicular tumours may cause raised AFP).
• PET CT: Used to identify occult nodal disease.
• Surgical resection: Mainstay of treatment in operable cases.
Patients with small primary tumor + cirrhotic liver + primary disease process is controlled = Primary
whole liver resection and transplantation.
But most cases occur in an already diseased liver the operative risks and post-operative hepatic
dysfunction are far greater than is seen following metastectomy.
• Tumors are not particularly chemo or radiosensitive however, both may be used in a palliative setting - Tumor
ablation is a more popular strategy.
Survival
Poor, overall survival is 15% at 5 years.
Cholangiocarcinoma
Second most common type of primary liver malignancy.

Tumours arise in the Bile Ducts. Up to 80% of tumors arise in the Extra Hepatic Biliary Tree.
Most present with jaundice but by this time of presentation majority will have unresectable disease.
Primary Scelerosing Cholangitis is the main risk factor.
In deprived countries Typhoid and Liver Flukes are also major risk factors.
Diagnosis
• Typically obstructive picture on liver function tests.
• CA 19-9, CEA and CA 125 are often elevated
• CT/ MRI and MRCP are the imaging methods of choice.
Treatment
• Surgical resection: the best chance of cure.
Local invasion of peri hilar tumours + Lobar atrophy = contra indicate surgical resection.
• Metallic stents should be avoided in those considered for resection.
Survival
Is poor, approximately 15% 5 year survival.
● In Obstructive Jaundice → Stool Stercobilinogen Reduced = Pale stool

Beside this, Hampered fat digestion = Stool has no fat = Stool get pasted in commode, cannot be removed by flash. --
-----------------------------Very Important Scenario for the exam
● Jaundice + GB palpable = Don’t think GB stone / Cholelithiasis first → (+)ve Courvoisier’s Sign
● if CBD stone causes obstruction = GB is fibrotic, never distended

● if CBD shows increase in diameter = before operation ERCP to be done to see any duct calculi present or not
st
(Choledocholithiasis). If in scenario, it is said that, duct calculi is present; then 1 step is - try to clear the duct by
ERCP,sphincterotomy. Then later date operation.
● Multiple liver metastasis: Palpable Liver can be found not palpable GB
● Primary Biliary Cirrhosis -

S. Bilirubin, Alk.PO4, γ-GT; IgM raise but ALT, AST normal
AMA may be present
Associated CREST syndrome may present
● Autoimmune hepatitis: ANA; SMA; Anti-Liver

Anti Kidney Microsome type I antibody
● If any scenario indicate Ulcerative Colitis

olitis - then give answer: "Primary Sclerosing Cholangitis
holangitis" ---These types
of scenarios may sometimes mention: Raised IgM, SMA
● Aged + operation risky + Empyema GB then answer will be --- Percutaneous Radiology
adiology guided drainage.
● Pyogenic Liver Abscess

Are polymicrobial,
Gm(-)ve
)ve species (E.coli mainly, others are Streptococci; Bacteroids).
Percutaneous aspiration ē pig-tail
tail catheter, combined ē i/v antibiotic, is effective.
● Alcoholic Hepatitis ---- liver biopsy shows Mallory bodies

● Child-pugh’s system: Liver disease severity indicator
No need for the exam
HEPATIC HAEMANGIOMA
Most common primary tumor.
Usually asymptomatic, < 5 cm, incidental findings – should monitored ē further imaging.
(In rare type Kasbach–Merritt
Merritt syndrome, large haemangiomas present with thrombocytopenia and DIC)
Kasabach–Merritt Syndrome
yndrome (KMS), also known as Hemangioma with thrombocytopenia is a rare disease, usually of
infants, in which a vascular tumor leads to decreased platelet counts and sometimes other bleeding problems,
problems which can
be life-threatening.It
It is also known as hemangioma thrombocytopenia syndrome.
Gallbladder
• Fibromuscular sac with capacity of 50ml
• Columnar epithelium
Relations of the gallbladder
Anterior Liver
Posterior • Covered by peritoneum

• Transverse colon
• 1st part of the duodenum
Laterally Right lobe of liver
Medially Quadrate lobe of liver
Arterial supply : Cystic artery (branch of Right hepatic artery)
Venous drainage: Cystic vein
Nerve supply : Sympathetic- mid thoracic spinal cord,

Parasympathetic- anterior vagal trunk
Common bile duct
Origin Confluence of cystic and common hepatic ducts
Relations at origin • Medially - Hepatic artery

• Posteriorly- Portal vein
Relations distally • Duodenum - anteriorly

• Pancreas - medially and laterally
• Right renal vein - posteriorly
Arterial supply Branches of hepatic artery and retroduodenal branches of gastroduodenal artery
Calot's triangle
Medially Common hepatic duct
Inferiorly Cystic duct
Superiorly Inferior edge of liver
Contents Cystic artery
GALL STONES COMPOSITION

Mixed (75%) : multiple; increased cholesterol
Cholesterole (20%) : solitary/ pairs/ rarely multiple mulberry; strawberry GB; Cholestasis of GB
Bile pigment (5%) : small; black; irregular; multiple; gritty; fragile; occurs in hemolytic anaemia
Bile
Produced at a rate of between 500ml and 1500mL per day.

Composed of bile salts, bicarbonate, cholesterol, steroids and water.
3 main factors regulating bile flow: Hepatic Secretion; Gall Bladder Contraction; Sphincter Of Oddi Resistance.
Bile salts are absorbed in the terminal ileum (and recycled to the liver).
>90% of bile salts are recycled in this way -Total pool of bile salts is recycled up to six times a day.
Primary Bile Salts

Cholate
Chenodeoxycholate.
Secondary Bile Salts

Formed by bacterial action on primary bile salts.
Deoxycholate and Lithocholate.
Of these Deoxycholate is reabsorbed, and Lithocholate is insoluble and excreted.
Pathophysiology of Gallstones
Bile salts have a detergent action.
Aggregate to form micelles and these have a lipid centre in which fats may be transported.
Excessive cholesterol cannot be transported in this way and will precipitate, results = cholesterol rich gallstones
Aschoff-Rokitansky Sinuses
Chronic Cholecystitis assoc.ē fibrotic thick walled GB.
Within thickened wall Aschoff-Rokitansky Sinuses are present,
They form as a result of increased pressure in the GB and recurrent damage to the wall.
Histologically:
→ These are outpouchings of GB mucosa into the GB muscle layer and subserosal tissue
→ Result of hyperplasia and herniation of epithelial cells through the fibromuscular layer of the GB wall.
→ They are usually referred to as Adenomyomatosis
Aschoff-Rokitansky Sinus
CHOLEDOCHAL CYST
- Congenital segmental cystic dilatation of biliary tree.
- In type I cysts (dilatation of the extrahepatic bile duct),
- RX : - Roux-en-Y hepaticojejunostomy.
- Choledochal cysts are premalignant & Biliary Ca can arise from incomplete resection.
● Acute Cholecystitis + no evidence of CBD stones = immediate surgery indicated, because interval surgery plan
creates chance of further attack / complication
● Absolute Contraindication of Lapchole

– VwB disease
– Abdominal sepsis
– Late pregnancy
● Relative Contraindication of Lapchole

– H/O previous abdominal surgery
– Acute Gall stone at pancreas
– Unilateral bile duct stone
– Intraabdominal malignancy
Biliary disease
Diagnosis Typical features Pathogenesis
Gallstones Typical H/O biliary colic or Usually small calibre gallstones which can pass through the
episodes of chlolecystitis. cystic duct.
Obstructive type history and test In Mirizzi syndrome the stone may compress the bile duct
results. directly- one of the rare times that cholecystitis may present
with jaundice
Cholangitis Usually obstructive Ascending infection of the bile ducts usually by E. coli and by
Will have Charcot's triad of definition occurring in a pool of stagnant bile.
symptoms (pain, fever, jaundice)
Pancreatic Painless jaundice + palpable GB Direct occlusion of distal bile duct or pancreatic duct by tumour.
cancer (Courvoisier's Law) Sometimes nodal disease at the portal hepatitis may be the
culprit in which case the bile duct may be of normal calibre.
TPN Usually follows long term use Often due to hepatic dysfunction and fatty liver which may occur
associated Usually painless + non with long term TPN usage.
jaundice obstructive features
Bile duct Depends on the type of injury Often due to a difficult laparoscopic cholecystectomy when
injury May be sudden or gradual onset anatomy in Calots triangle is not appreciated.
Usually of obstructive type In the worst scenario the bile duct is excised and jaundice
offers rapidly post operatively.
More insidious is that of bile duct stenosis which may be
caused by clips or diathermy injury.
Cholangio Ca Gradual onset obstructive pattern Direct occlusion by disease and also extrinsic compression by
nodal disease at the porta hepatis.
Septic Usually hepatic features Combination of impaired biliary excretion and drugs such as
surgical ciprofloxacin which may cause cholestasis.
patient
Metastatic Mixed hepatic and post hepatic Combination of liver synthetic failure (late) and extrinsic
disease compression by nodal disease and anatomical compression of
intra hepatic structures (earlier)
Cholangitis
• Combination of bacterial infection and biliary obstruction
• Most common organisms are: (most frequent at top of list)
Escherichia coli
Klebsiella species
Enterococcus species
Streptococcus species
Clinical Features
1. Charcot's Triad: 2. Reynolds Pentad: Charcot's triad plus
Fever (90% cases) Confusion
Right upper quadrant pain Hypotension
Jaundice
Investigations
USS: 1st line
CT scan
ERCP: may be 1st line if high clinical suspicion and suitable for treatment
Treatment
ERCP -usually after 72 hours of antibiotics
Percutaneous Transhepatic Cholangiogram and Biliary Drain
Biliary atresia
• Biliary tree lumen is obliterated by an inflammatory cholangiopathy causing progressive liver damage
Clinical features
• Infant well in 1st few weeks of life
• No family history of liver disease
• Jaundice in infants > 14 days in term infants (>21 days in pre term infants)
• Pale stool, yellow urine (colourless in babies)
• Associated with cardiac malformations, polysplenia, situs inversus
Investigation
• Conjugated bilirubin (prolonged physiological jaundice or breast milk jaundice will cause a rise in unconjugated
bilirubin, whereas those with obstructive liver disease will have a rise in conjugated bilirubin)
• USG of the liver (excludes extrahepatic causes, in biliary atresia infant may have tiny or invisible gallbladder)
• Hepato-iminodiacetic acid radionuclide scan (gooduptake but no excretion usually seen)
Management
• Early recognition is important to prevent liver transplantation.
• Nutritional support.
• Roux-en-Y portojejunostomy (Kasai procedure)
• If Kasai procedure fails or late recognition, a liver transplant becomes the only option.
Pancreas
Retroperitoneal organ and lies posterior to the stomach.

Accessed surgically by dividing the peritoneal reflection that connects the greater omentum to the transverse colon.
The pancreatic head sits in the curvature of the duodenum.
It's tail lies close to the hilum of the spleen, a site of potential injury during splenectomy
Relations
Posterior to the pancreas
Pancreatic head Inferior vena cava

Common bile duct
Right and left renal veins
Superior mesenteric vein and artery
Pancreatic neck Superior mesenteric vein, portal vein
Pancreatic body- Left renal vein

Crus of diaphragm
Psoas muscle
Adrenal gland
Kidney
Aorta
Pancreatic tail Left kidney
Anterior to the pancreas
Pancreatic head 1st part of the duodenum

Pylorus
Gastroduodenal artery
SMA and SMV(uncinate process)
Pancreatic body Stomach

Duodenojejunal flexure
Pancreatic tail Splenic hilum
Superior to the pancreas

Coeliac trunk and its branches common hepatic artery and splenic artery
Grooves of the head of the pancreas

2nd and 3rd part of the duodenum
Arterial supply
• Head: pancreaticoduodenal artery
• Rest: splenic artery
Venous drainage
• Head: superior mesenteric vein
• Body and tail: splenic vein
Ampulla of Vater
• Merge of pancreatic duct and common bile duct
• Is an important landmark, halfway along the second part of the duodenum, that marks the anatomical transition
from foregut to midgut (also the site of transition between regions supplied by Coeliac Trunk and SMA).
Management of Pancreatitis
Management of Acute Pancreatitis in the UK

Diagnosis
• Traditionally hyperamylasaemia has been utlilised with amylase being elevated three times the normal range.
• However, amylase may give both false positive and negative results.
• Serum lipase is both more sensitive and specific than serum amylase. It also has a longer half life.
• Serum amylase levels do not correlate with disease severity.
Differential causes of hyperamylasaemia
Acute pancreatitis
Pancreatic pseudocyst
Mesenteric infarct
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis
Assessment of severity
• Glasgow, Ranson scoring systems and APACHE II
• Biochemical scoring e.g. using CRP
16
● GLASGOW SCORING SYSTEM (PANCREAAS)
- P aO2 <60mmHg
- A ge >55yrs
9
- N eutrophilic leukocytosis >15X10
++
-Ca <2mmol/ l
- R aised urea >16mmol/ l
- E nz. LDH >600i.u./ l
- A lbumin <32gm/ l
- A ST/ALT >100i.u./ l
- S ugar >10 mmol / l
● RANSON’S CRITERIA (initially) – BAWLA

- B lood sugar >11 mmol / l
- A ge >55yrs
9
- W CC >16X10
- L DH >350 i.u./ l
- A ST >250i.u./ l
● RANSON’S CRITERIA (48hrs) ABCDEF

- A ir (PaO2) <60mmHg
- B ase deficit >4mmol/ l
- C a++ <2mmol / l
- D ecreased HCT > 10%
- E levated BUN >1.8 mmol/ l
- F luid sequestration > 6 liter
17
Source: Baily & Love 26th
● Acute Pancreatitis 2 signs

Grey Turner's sign : Flank bruising
Cullen's sign : Around Umbilicus bruising (cool belly button!!!)
● Acute Pancreatitis avg. mortality 20%
● Ischaemic retinopathy, which causes retinal oedema and micro infarcts(Ophthalmoscopy shows cotton wool
spots), causes acute visual loss - complication of Acute Pancreatitis. CT Abd. will be useful in diagnosis and
evaluation.
● SIRS
- HR >90 / min
0 0
- Temp >38 C or < 36 C
- RR > 20 / min
- PaCO2 > 4.3 kPa
- WBC > 12000 or < 4000
● ↑ S. amylase Could indicate perforated viscus; DKA; Ect.preg.; Mes. Ischaemia & Infarct, Acute cholecystitits,
Usually peaks within first 12-48 hours. May return to normal value after 72 hours. So, if there is late
presentation then S. Lipase and Urinary amylase conc. will be in value.
Features that may predict a severe attack within 48 hours of admission to hospital
Initial assessment • Clinical impression of severity

• Body mass index >30
• Pleural effusion
• APACHE score >8
24 hours after admission • Clinical impression of severity

• APACHE II >8
• Glasgow score of 3 or more
• Persisting multiple organ failure
• CRP>150
48 hours after admission • Glasgow Score of >3

• CRP >150
• Persisting or progressive organ failure
Pancreatitis: sequelae
Peripancreatic fluid collections

• Occur in 25% cases
• Located in or near the pancreas and lack a wall of granulation or fibrous tissue
• May resolve or develop into pseudocysts or abscesses
• Since most resolve aspiration and drainage is best avoided as it may precipitate infection
Pseudocysts
• In acute pancreatitis result from organisation of peripancreatic fluid collection. They may or may not
communicate with the ductal system.
• The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after an attack of
acute pancreatitis
• Most are retrogastric
• 75% are associated with persistent mild elevation of amylase
• Investigation is with CT, ERCP and MRI or Endoscopic USS
• Symptomatic cases may be observed for 12 weeks as up to 50% resolve
• Treatment is either with endoscopic or surgical cystogastrostomy or aspiration
Pancreatic necrosis
• Pancreatic necrosis may involve both the pancreatic parenchyma and surrounding fat
• Complications are directly linked to extent of parenchymal necrosis and extent of necrosis overall
• Early necrosectomy is associated with a high mortality rate (and should be avoided unless compelling
indications for surgery exist)
• Sterile necrosis should be managed conservatively (at least initially)
• Some centres will perform fine needle aspiration sampling of necrotic tissue if infection is suspected. False
negatives may occur and the extent of sepsis and organ dysfunction may be a better guide to surgery
Pancreatic abscess
• Intra abdominal collection of pus associated with pancreas but in the absence of necrosis
• Typically occur as a result of infected pseudocyst
• Transgastric drainage is one method of treatment, endoscopic drainage is an alternative
Haemorrhage
• Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de novo or as a
result of surgical necrosectomy.
• When retroperitoneal haemorrhage occurs Grey Turners sign may be identified
Management
Nutrition
• There is reasonable evidence to suggest that the use of enteral nutrition does not worsen the outcome in
pancreatitis
• Most trials to date were underpowered to demonstrate a conclusive benefit.
• The rationale behind feeding is that it helps to prevent bacterial translocation from the gut, thereby contributing
to the development of infected pancreatic necrosis.
Use of antibiotic therapy
• Many UK surgeons administer antibiotics to patients with acute pancreatitis.
• A recent Cochrane review highlights the potential benefits of administering Imipenem to patients with
established pancreatic necrosis in the hope of averting the progression to infection.
• There are concerns that the administration of antibiotics in mild attacks of pancreatitis will not affect outcome
and may contribute to antibiotic resistance and increase the risks of antibiotic associated diarrhoea.
Surgery
• Acute pancreatitis due to gallstones = Early cholecystectomy.
• Obstructed biliary system due to stones = Early ERCP.
• Fail to settle with necrosis + have worsening organ dysfunction = debridement ± FNA
• Infected necrosis = Radiological drainage or surgical necrosectomy.
The choice of procedure depends upon local expertise
● H/O Alcohol intake + leaning forward reduces the pain +Amylase raised ± wt. loss = Chronic Pancreatitis.
Beside these, decreased B12 absorption; Pancreatic Calcification in USG or plain X-Ray can be found. Remember
Amylase may not always raised.
Pancreatic Ca
• Adenocarcinoma
• Risk factors: Smoking, diabetes, Adenoma, Familial adenomatous polyposis
• Mainly occur in the head of the pancreas (70%)
• Spread locally and metastasizes to the liver
• Ca pancreas should be differentiated from other periampullary tumours with better prognosis
Clinical Features
• Weight loss
• Painless jaundice
• Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature)
• Pancreatitis
• Trousseau's sign: Migratory Superficial Thrombophlebitis
Don't confuse with Trousseau sign of latent tetany - which is a sign observed in patients with low calcium. This
sign may be positive before other manifestations of hypocalcemia such as hyperreflexia and tetany.To elicit the sign,
a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure
and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's
hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm.
The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct.
Investigations
• USS: May miss small lesions
• CT Scanning (pancreatic protocol): If unresectable on CT then no further staging needed.
• PET/CT: For those with operable disease on CT alone
• ERCP/ MRI: for bile duct assessment.
• Laparoscopy: to exclude peritoneal disease.
Management
• Head: Whipple's resection (SE dumping and ulcers). Newer techniques:pylorus preservation and SMA/ SMV
resection.
• Body and tail: poor prognosis, distal pancreatectomy if operable.
• Resectable Disease: Adjuvent chemotherapy
• ERCP and stent for jaundice and palliation. Plastic stent is the best option for biliary decompression in
resectable disease. Metallic stents are contraindicated in resectable biliary disease. Surgical bypasses have no
place in the management of operable malignancy as a bridge to definitive surgery.
• Surgical bypass may be needed for duodenal obstruction.
Pancreatic stents
Both benign and malignant biliary obstruction may be treated by placement of stents.
These may be either plastic tubes or self expanding metallic stents.

They can be placed either percutaneously, at ERCP, or, less commonly now, open surgery.
Complications include blockage, displacement and those related to the method of insertion.
Metallic Vs Plastic stents
Metallic stents Plastic stents
Expensive Cheap
Embed in surrounding tissues Do not usually embed
Displacement rare Displacement common
Blockage rare Blockage common
Contraindicated in resectable malignant disease May be used as a bridge to resectional surgery
● Pancreatitis & Ca head of Pancreas - pain type same, difference is →

Pancreatitis pain relieved by leaning forward but
Ca head shows constant pain + Classical feature of palpable GB
● Ca head of Pancreas --- preferred Investigation is CT abdomen
Pancreatic Neuroendocrine Tumors - NET (Islet Cell Tumors)
Insulinoma
o Most common functional NETs. Almost
o 60% occur in middle-aged women. Insulinomas can be sporadic or familial,
o Component of MEN-1 syndrome. Approximately 10% of patients with insulinoma have the MEN-1 syndrome.
o Most of the tumors are solitary, relatively benign< 2.5 cm in diameter, and evenly distributed throughout the
pancreas.
o Shows Whipple’s triad
- Hypoglycaemia symptoms during fasting
- ↓ FBS
- Symptoms relieved by i/v Dextrose
● VIPoma shows WaDHA

Wa : Watery
D Diarrhoea (Octreotide therapy gives prompt relief from diarrhea.)
H : Hypokalamia
A : Achlorhydria
- Tumor enucleation and partial pancreatectomy are surgical options
Gastrinoma / Zollinger Ellison Syndrome

• The most common Neuro Endocrine Tumor found in MEN-1 patients.
• Composed of the triad:

1. Non beta islet cell tumours of the pancreas
2. Hypergastrinaemia
3. Severe ulcer disease
• Most commonly found in the duodenum. Other ectopic areas include Stomach, Spleen, Gallbladder.
• Pancreatic gastrinomas are normally solitary and highly malignant.
• > 4/5 numbers of gastrinomas are found within the triangle bounded by:
Cystic and common bile duct (Top)
2nd & 3rd part of the duodenum (Bottom)
Neck and body of pancreas (Medial)
• Diagnosis is based on 3 criteria:

1. Fasting hypergastrinaemia
2. Increased basal acid output
3. Secretin stimulation test poitive
Management
• Effective control of gastric hypersecretion is possible with a proton pump inhibitor.
• Octreotide: is effective in suppressing gastrin release.
• Most gastrinomas in the pancreas can be removed by enucleation, and large tumors can be removed by
resective procedures.
Spleen
• The spleen is the Largest Lymphoid Organ.

• Intraperitoneal organ
• Blood supply: Splenic Artery (← Coeliac axis) and to the Splenic Vein (+ IMV =>SMV).
• Embryology: derived from MESENCHYMAL TISSUE (Most of the gut derived Endodermally except Spleen)
• Shape: Clenched fist
• Position: Below 9th-12th ribs
• Weight: 75-150g
1,3,5,7,9,11 (odd numbers up to 11)

The spleen is: 1 inch thick, 3 inches wide, 5 inches long, weighs 7oz (200g), lies between the 9th and 11th ribs
Relations
• Superiorly- Diaphragm
• Anteriorly- Gastric impression
• Posteriorly- Kidney
• Inferiorly- Colon
• Hilum: Pancreas tail & Splenic vessels (Splenic Artery divides here, pass to the White Pulp transporting plasma)
• Forms apex of lesser sac (containing short gastric vessels)
Contents
- White pulp
o Immune function.
o Contains central trabecular artery.
o The germinal centres are supplied by arterioles called penicilliary radicles.
- Red pulp
o Filters abnormal red blood cells
Disorders of the spleen - Massive splenomegaly

• Myelofibrosis
• Chronic Myeloid Leukaemia
• Visceral leishmaniasis (kala-azar)
• Malaria
• Gaucher's syndrome
Other causes (as above plus)

• Portal hypertension e.g. secondary to cirrhosis
• Lymphoproliferative disease e.g. CLL, Hodgkin's
• Haemolytic anaemia
• Infection: hepatitis, glandular fever
• Infective endocarditis
• Sickle-cell*, thalassaemia
• Rheumatoid arthritis (Felty's syndrome)
Accessory spleens
- 10% population
- 1 cm size
- Locations:
o Hilum of the spleen
o Tail of the pancreas
o Along the splenic vessels
o In the gastrosplenic ligament
o Splenorenal ligament
o Walls of the stomach or intestines
o Greater omentum
o Mesentery
o Gonads
*The majority of adults patients with sickle-cell will have an atrophied spleen due to repeated infarction
Functions
The functions of the spleen can be remembered by the mnemonic 'FISH':
F iltration of encapsulated organisms and blood cells

I mmunological function
S torage of platelets
H aematopoiesis in the foetus
Further Details of Function

• Filtration of abnormal blood cells and foreign bodies such as bacteria.
• Immunity: IgM. Production of properdin, and tuftsin which help target fungi and bacteria for phagocytosis.
• Haematopoiesis: up to 5th month gestation or in haematological disorders.
• Pooling: storage of 40% platelets.
• Iron reutilisation
• Storage red blood cells-animals, not humans.
• Storage monocytes
Management of splenic trauma
Conservative Small subcapsular haematoma

Minimal intra abdominal blood
No hilar disruption
Laparotomy Increased amounts of intraabdominal blood

with Moderate haemodynamic compromise
conservation Tears or lacerations affecting <50%
Resection Hilar injuries

Major haemorrhage
Major associated injuries
Splenectomy
Indications
• Trauma: 1/4 are iatrogenic
• Spontaneous rupture: EBV
• Hypersplenism: Hereditary Spherocytosis or Elliptocytosis etc
• Malignancy: Lymphoma or Leukaemia
• Splenic Cysts, Hydatid Cysts, Splenic Abscess
Organs May Be Damaged During A Splenectomy

Tail of the pancreas (in relation to the hilum of the spleen)
Diaphragm above
Stomach
Left kidney
Splenic flexure of the colon
The spleen is attached to the greater curvature of the stomach by the Gastrosplenic Ligament, in which the
Short Gastric and Left Gastro-Epiploic Vessels lie. The Lienorenal Ligament attaches it to the left kidney
(containing the Splenic Vessels and tail of the pancreas).
Post Splenectomy Blood Film Changes

• PLATELETS WILL RISE FIRST (during Splenectomy for ITP treatment, platelet is transfused*** after the
Splenic Artery is clamped) and may be persistent, oral antiplatelets may be needed.
• Immediately - Agranulocytosis (mainly Neutrophils), which is replaced by a Lymphocytosis &

Monocytosis over the following weeks.
• In First Few Days - Target Cells, Siderocytes & Reticulocytes will appear.
• over Following Weeks - Cytoplasmic Inclusions seen e.g., Howell Jolly Bodies.
• Other changes include Target Cells and Pappenheimer bodies
• Splenectomy results in the inability to readily remove immature or abnormal RBCs from the circulation. The
RBC count does not alter significantly.
Clinical Note:
***Platelet, which are necessary to maintain hemostasis during surgery, should not be given (started) while blood is
perfusing the spleen. So Platelet transfusions should be started as soon as the splenic vessels are ligated.
Blood film in Hyposplenism: Howell-Jolly bodies (over following weeks)

Pappenheimer bodies
Poikilocytes (Target cells)
Erythrocyte containing siderotic granules (Irregular contracted erythrocytes)
Heinz bodies
Complications
• Haemorrhage (may be early and either from Short Gastric or Splenic hilar vessels)
• Pancreatic fistula (from iatrogenic damage to pancreatic tail)
• Thrombocytosis: Prophylactic aspirin
• Encapsulated bacterial infection e.g. Strep. pneumoniae, Haemophilus influenzae and Neisseria meningitides
Post Splenectomy Sepsis Details:

• Typically occurs with encapsulated organisms
• Opsonisation occurs but then not recognized
• Young children are at the highest risk, especially in the first 2 years following surgery.
• Surgery for trauma is associated with lower risk, than, splenectomy for haematological disorders.
• Infection with Encapsulated Organisms is the greatest risk.
Prophylactic vaccinations are usually administered to reduce the risk of Pneumococcal Septicaemia. Since the vaccine
only covers up to 80% of pneumococcal infections, patients will usually receive long term, low dose penicillin prophylaxis
in addition to vaccination.
Organisms Causing Post Splenectomy Sepsis:
Streptococcus pneumoniae
Haemophilus influenzae
Meningococci
Clinical Note:The effects of sepsis following splenectomy are variable - may be due to the result of small isolated
fragments of splenic tissue that retain some function following splenectomy. These may implant spontaneously following
splenic rupture (in trauma) or be surgically implanted at the time of splenectomy.
Splenic vein thrombosis
Thrombosis of the splenic vein may complicate pancreatitis, pancreatic carcinoma, iatrogenic trauma & hypercoagulable
diseases. The condition may predispose to the development of gastric varices, oesophageal varices are uncommon in
splenic vein thrombosis alone. Diagnosis is made by CT angiography. Treatment is with splenectomy.
● Gastrosplenic ligament – injury can cause Short Gastric Artery Injury
● Pancreas lies splenorenal ligament

● Left. radical nephrectomy via a trans-abdominal route, traction on Splenorenal and Splenocolic may produce
significant injury to spleen
BREAST BASICS
The breast itself lies on a layer of pectoral fascia and the following muscles: 1. Pectoralis major
2. Serratus anterior
3. External oblique
Breast anatomy
Nerve supply Branches of intercostal nerves from T4-T6.
Arterial supply • Internal mammary (thoracic) artery

• External mammary artery (laterally)
• Anterior intercostal arteries
• Thoraco-acromial artery
Venous drainage Superficial venous plexus to sub clavian, axillary and intercostal veins.
Lymphatic • 70% Axillary nodes

drainage • Internal mammary chain
• Other lymphatic sites such as deep cervical and supraclavicular fossa (later in disease)
Benign Breast lesions
Lesion Features Treatment
Sclerosing adenosis, (radial scars and • Usually presents as a breast lump or breast Lesions should be
complex sclerosing lesions) pain biopsied, excision is not
• Causes mammographic changes which may mandatory

mimic carcinoma
• Cause distortion of the distal lobular unit,
without hyperplasia (complex lesions will
show hyperplasia)
• Considered a disorder of involution, no
increase in malignancy risk
Fat necrosis • Up to 40% cases usually have a traumatic Imaging and core biopsy
aetiology
• Physical features usually mimic carcinoma
• Mass may increase in size initially
(See chart for remainig notes)
Non malignant breast disease
Intraductal Papilloma
• Growth of papilloma in a single duct
• Usually presents with clear or blood stained discharge originating from a single duct
• No increase in risk of malignancy
Breast Abscess
• Lactational mastitis is common
• Infection is usually with Staphylococcus aureus
• On examination there is usually a tender fluctuant mass
• Treatment is with antibiotics and ultrasound guided aspiration
• Overlying skin necrosis is an indication for surgical debridement, which may be complicated by the development
of a subsequent mammary duct fistula.
Tuberculosis
• Rare in western countries, usually secondary TB
• Affects women later in child bearing period
• Chronic breast or axillary sinus is present in up to 50% cases
• Diagnosis is by biopsy culture and histology
Benign cyclical mastalgia

- Common cause of breast pain in younger females.
- It varies in intensity according to the phase of the menstrual cycle.
- It is not associated with point tenderness of the chest wall (more likely to be Tietze's syndrome).
- The underlying cause is difficult to pinpoint, examination should focus on identifying focal lesions (such as cysts)
that may be treated to provide symptomatic benefit.
- Women should be advised to wear a supportive bra.
- Conservative treatments include flax seed oil and evening primrose oil.
- Hormonal agents such as bromocriptine and danazol may be more effective. However, many women discontinue
these therapies due to adverse effects.
- Tamoxifen can be used

(See chart for remainig notes)…
Nipple discharge
Causes of nipple discharge
Physiological During breast feeding
Galactorrhoea Commonest cause may be response to emotional events, drugs such as

histamine receptor anatagonists are also implicated
Hyperprolactinaemia • Commonest type of pituitary tumour

• Microadenomas <1cm in diameter
• Macroadenomas >1cm in diameter
• Pressure on optic chiasm may cause bitemporal hemianopia
MAMMARY DUCT ECTASIA • Dilatation breast ducts.

• Most common in enopausal women
• Discharge typically thick and green in colour
• Most common in smokers
Carcinoma • Often blood stained

• May be underlying mass or axillary lymphadenopathy
Intraductal Papilloma • Commoner in younger patients

• May cause blood stained discharge
• There is usually no palpable lump
Assessment of patients
• Examine breast and determine whether there is mass lesion present
• All mass lesions should undergo Triple assessment.
Reporting of investigations
Where a mass lesion is suspected or investigations are requested these are prefixed using a system that denotes the
investigation type e.g. M for mammography, followed by a numerical code as shown below:
1 No abnormality
2 Abnormality with benign features
3 Indeterminate probably benign
4 Indeterminate probably malignant
5 Malignant
Source: Netter Clinical
Management of non malignant nipple discharge

• Exclude endocrine disease
• Nipple cytology unhelpful
• Smoking cessation advice for duct ectasia
• For duct ectasia with severe symptoms, total duct excision may be warrented
● Green, cheesy or grumous Discharge: Duct ectasia , But Breast cyst also shows green discharge
● Yellow discharge : Abscess, Cyst, Periductal mastitis
● Haemo-Stix is an easy bedside test used to test for the presence of blood in discharge.
● Benign Mammary Dysplasia

- Young patient mobile breast lump appears during menstruation which disappears after cycle is over.
● Mondors Disease
- Localised thrombophlebitis of a breast vein. Later it forms cord like structure.
● Paget’s Disease
- Unilateral; No pruritis; starts @ nipple, spreads to areola.
- Underlying breast disease(e.g. inv. Ca or DCIS) may present
- Nipple Biopsy shows large cells in dermal –epidermal junction- that sustained positively for mucin
DISEASE GROSS PATHOLOGY CLINICAL FEATURES INVESTIGATIONS TREATMENT COMPLICATIONS

● Develops from ● Well defined capsule ● Smooth; Fram; Mobile; Round mass ● UGS <35yrs ● Reassurance Usually no complication
single lobule ● Fibroblastic stroma ● USG + Mammo >35yrs ● Surgery: Large; Diagnostic but if so, then, Lobular
FIBRO surrounds glandular / difficulties; Patient's choice Carcinoma in situ may
cystic tissue occur
ADENOMA
● OCP user ● Smooth; Tense; Mobile lump; Skin Free; ● USG ● Aspiration: Green, Yellow,
●↑ among ● Sudden onset; ● Mammo Brown or Blood stained
perimenausal women ● Single bt may be bilateral , multiple (often) ● Aspiration (malignancy suspected)
● Excision biopsy: if ● Surgical excision: if
BREAST CYST
- Persists after aspiration - Persists after aspiration
- Blood stained - Blood stained
- Recurrence - Recurrence
● 40-50yrs ● Both epith. + fibrous ● Painless >3cm; Mobile ● Wide local excision ē rim of normal
CYSTOSARCOMA stromal elements ● Massive size ē uneven bosselated surface tissue;
PHYLLODE / ● Stroma shows ● Recent & rapid ↑size <5cm : 2cm margin
PHYLLODE hypercellularity; atypia; ● Overlying skin free; reddened; may >5cm: 5cm margin
TUMOR mitosis ulcerate(due to pressure not infiltrate)
● 50-60yrs ● FNAC shows benign ● Nipple retraction; Tenderness(+) ● Mammo: Coarse ● Fluclox + Metronidazole Mammary duct fistula
● Multiductal cell ● Mass under areola ± erythema retroalveolar calcifcn ● Surgery; Hadfield’s
DUCT ● Subareolar duct ● Cheesy Green discharge; can be Brown (duct is disconnected from back of
dilation ē out marked ● Grumous, blood stained ● FNAC : Benign cell nipple) or microdochectomy (if young)
ACTASIA
Inflammation
PERI DUCTAL ● Smoker ● Purulent discharge ē tenderness ● Co-amoxyclav ; Metronidazole Mammary duct fistula
MASTITIS ● younger ● Peri or subareolar infectn , may be recurrent In chr. case Total duct excision
● Smoker ● Mammo ● Surgery; total duct excisn - It is itself is a P.Ductal
MAMMARY Hadfield’s (occasnally) mastitis & Abscess
DUCT ● Stop smoking drainage complican
FISTULA
● Common ● Polyp of epithelial lined ● Farm mass under areola ● USG : papilloma ē in duct ● Surgery: If atypia presents then
DUCT blood stained breast duct ● Blood stained serous discharge rarely >1cm total duct excisn - Hadfield’s B. Ca occurs
PAPILLOMA discharge without ● Single but may be multiple; asymptomatic; ● Mammo: >35yrs ● Microdochectomy
any cause occasionally palpable
● Among Multipara ● Multiductal white discharge ● No blood on dipstick
PROLACTINOMA ● Cyclical mastalgia
● Nodularity; Visual disturbance
● Wt.gain; irregular period, H/O Headache
DISEASE GROSS PATHOLOGY CLINICAL FEATURES INVESTIGATIONS TREATMENT

● 2 types ● Malignant epithelial cell confined Multifocal ● Mammography: ● Big tumor : Mastectomy
DUCTAL - Comedo type(atypical cell, to duct system doesn’t invade Branching, coarse, ● Small tumor : Wire guided
CARCINOMA IN SITU Luminal necrosis, Linear coarse basement membrane linear, microcalcification wide excisn± Radio
branching calcification) granule Only Comedo type has the
/ EPITHELIAL
- Non-comedo type chance of recurrence after
HYPERPLASIA
surgery
INVASIVE / ● Covers most of all invasive ● Large irregular surface ē hard ● Mammo: ● <5cm : Mastectomy
INFILTRATING carcinoma (75% / 65%) consistency White necrotic area ● >5cm : Wire guided WLE
DUCTAL ● Diagnosis by exclusion ● Single lesion Branching micro follwed by Radio
● Intermediate / high grade - calcificaation ** Poor Prognosis
CARCINOMA
Stellate lesion(+)
(NON SPECIAL
TYPE)
● 5 sub-types: Classic, Solid, ●''Indian File” ● Bilateral, Multiple, Diffuse infiltrative MRI scan, if breast
INVASIVE LOBULAR Alveolar, Mixed, Pleomorphic “Bull’s Eye” pattern ● Poorly circumscribed conserving surgery is
CARCINOMA (worst prognosis) (classic lob. ca) ● Distortion of breast occurs planned
●"Targetoid pattern” **Only Bilateral Carcinoma **
INVASIVE Histologically similar to tubular ● Cribriform / Sieve pattern ● Farm mass ● Good Prognosis
CRIBRIFORM Carcinoma stromal invasion ● Well differentiated
CARCINOMA
● Prominent Lymphocyte + ● Soft, uniform consistency; smooth ● Less associated ē LN
Young women Plasma cell infiltration contour metastasis → associated ē
● Lymphoid stroma ē little fibrosis ● Distinctive smooth & pushing border better Prognosis
surrounding sheets of large ● Well circumscribed
MEDULLARY
vesicular cells ē frequent ● Distortion of breast occurs
CARCINOMA
mitosis
Note: Green coloured diseases are important for the final exam
BREAST CARCINOMA TREATMENT
Breast Cancer Pathology
The invasive component is usually comprised of ductal cells (unless it is an invasive lobular cancer). In situ lesions may
co-exist (such as DCIS).
Typical changes seen in conjunction with invasive breast cancer include:

1. Nuclear pleomorphism
2. Coarse chromatin
3. Angiogenesis
4. Invasion of the basement membrane
5. Dystrophic calcification (may be seen on mammography)
6. Abnormal mitoses
7. Vascular invasion
8. Lymph node metastasis
Immunohistochemistry for oestrogen receptor and herceptin status is routinely performed.
Breast Cancer Staging( Grade, Lymph Node and size are combined to provide Nottingham Prognostic Index)
TNM definitions
Primary tumor (T):
Tis : CIS; Intraductal ca, Lobular ca in situ or Paget's dis. ē no associated tumor.
T1 : ≤ 2 cm
T2 : 2 -5 cm
T3 : > 5 cm
T4 : Any size involving chest wall or skin
Lymph nodes (N):

NX : Regional lymph nodes cannot be assessed (e.g., previously removed)
N0 : No lymph node metastasis
N1 : Palpable, mobile involved ipsilateral axillary lymph node(s) (usually 1-3 nodes)
N2 : Fixed involved ipsilateral axillary lymph node(s) (usually 4-9 nodes)
N3 : Ipsilateral internal mammary lymph node(s) (usually >10 nodes)
Distant metastasis (M):

MX : Presence of distant metastasis cannot be assessed
M0 : No distant metastasis
M1 : Distant metastasis present (includes supraclavicular LN)
AJCC stage groupings

0 : Tis, N0, M0
I : T1, N0, M0
II : T1/2 , N0/1 , M0
III : T4 , N0-3 , M0
IV : Any T, Any N, M1
Nottingham Prognostic Index (NPI)

NPI can be used to give an indication of survival.
In this system the tumour size is weighted less heavily than other major prognostic parameters.
Calculation of NPI : Tumour Size X 0.2 + Lymph node score(From table below)+Grade score(From table below).
Score Lymph nodes involved Grade
1 0 1
2 1-3 2
3 >3 3
Prognosis
Score Percentage 5 year survival
2.0 to 2.4 93%
2.5 to 3.4 85%
3.5 to 5.4 70%
>5.4 50%
● BRCA-1; long arm chromosome-17 : cancers of breast, ovary, prostate, colon

BRCA-2; long arm chromosome-13 : cancers of breast (male, female), ovary
● Triple Assessment should be done in all lumps of breast:

Clinical examination
Imaging (USS or Mammogram)
Cytology/ histology (FNAC, Core / True-cut / Open Biopsy)
st
● USG is the 1 line imaging of breast <35 yrs
st
Mammo is the 1 line imaging of breast >35 yrs, (USG is also done )
● FNAC provides cells for cytology, not tissue for histology.

● If FNAC inconclusive or If features shows (e.g. hard mass, skin tethering present) carcinoma; in these cases, the
only appropriate Investigation is Core / True-cut Biopsy.
● Core / True-cut Biopsy provides tissue for histology. A Positive core biopsy is mandatory before surgery.
● OPEN BIOPSY: done when diagnosis was not possible in Triple Assessment (no more than 20gm tissue is removed.)
● STEREOTYPE CONE BIOPSY is used where there’s no abnormality in palpation but mammography is
suspicious (e.g.diffuse calcification)
● Surgery is performed in most patients suffering from breast cancer. Chemotherapy used to downstage tumours &
allow breast conserving surgery. Hormone therapy may be used for the same purposes.
● Radiotherapy is given to all patients who have undergone Breast Conserving Surgery.
● Patients who have undergone Mastectomy may be offered a reconstructive procedure either in conjunction with their
primary resection or as a staged procedure at a later date.
● Surgical options: Mastectomy v/s Wide local excision
Mastectomy Wide Local Excision
Multifocal tumor Solitary lesion
Central tumor Peripheral tumour
Large lesion in small breast Small lesion in large breast
DCIS >4cm DCIS <4cm
Patient Choice Patient Choice
Central lesions may be managed using Breast Conserving Surgery, where an acceptable cosmetic result may be
obtained, this is rarely the case in small breasts
Axillary Disease
• All patients with Invasive Breast Cancer should have their Axilla staged.
• Patients having not obvious evidence of Axillary nodal involvement, this can be done using Sentinel Lymph
Node Biopsy.
• Patients with positive Sentinel Lymph Node Biopsy or who have imaging and cytological or histological
evidence of Axillary Nodal Metastasis should undergo Axillary Node Clearance.
• Axillary Node Clearance is associated with the development of lymphoedema, increased risk of cellulitis and
frozen shoulder.
(The sentinel lymph node is the hypothetical first lymph node or group of nodes draining a cancer. In case of established
cancerous dissemination it is postulated that the sentinel lymph node/s is/are the target organs primarily reached by
metastasizing cancer cells from the tumor. Thus, sentinel lymph nodes can be totally void of cancer because they were
detected prior to dissemination: Source:Wikipedia)
st
● Surgery is 1 line RX for breast carcinoma, although, breast conserving surgery- WLE (Wide Local Excision) is done
where it's possible.
● INDICATION OF WLE
• stage I or II disease
• single primary lesion
• < 4 cm (poor cosmetic results in> 4cm; however >4 cm may be treated ē WLE if big breast)
● If vascular invasion, an axillary clearance is needed. First surgery, then chemotherapy. Note: the practice of
sentinel node biopsy is alternative & recommended in every woman with breast Ca (RCS guidelines). Using a dye
technique, if the sentinel node is found to be cancer-free, women can be spared axillary surgery.
● Treatment with radiotherapy is mandatory in the case of a young woman who has undergone breast conservation
surgery - WLE
● Usually all patients undergoing breast-conserving surgery, is advised to get a course of ipsilateral chest wall radio to
prevent local recurrence. Beside this, radiotherapy can also be used to treat the chest wall, (post mastectomy) for those
patient with high risk of local recurrence:
- Grade III multifocal or near to skin or muscle
- ≥ 4cm
- Presence of lymphovascular invasion
- >3 LN(+)ve in axilla
● Breast Conserving Surgery, WLE (Wide Local Excision) is usually in UK : high rate of recurrence
● MASTECTOMY is usually required if ca is : >4cm; multi focal; centrally situated.

Simple (Total) : Breast tissue + some skin + nipple ± Sentinel LN
Subcutaneous(Nipple Sparing) : Only breast tissue removed. Skin + nipple intact
Radical(Halsted) : Breast tissue + some skin + nipple + Pectoralis both + axillary contents
Radical (Modified) : Radical mainly (but pectoralis not removed)
Radical (Patey modified) : Modified Radical mainly (Here pectoralis minor division not done)
Extended Radical : Radical mastectomy + intrapleural en bloc resection of internal mammary
lymph node by sternal splitting
● H/O WLE, now presenting with hard mass just below previous scar; mammo & USG inconclusive,-These types cases
requires MRI to differentiate scar from recurrent ca --- please consider, recurrence as answer.
Complications of Breast Surgery

• Long thoracic nerve injury: Occurs during the Axillary dissection and result in winging of the scapula.
• Intercostobrachial nerve injury: These nerves traverse the axilla. When they are divided (which they often
are) the patient will notice an area of parasthesia in the armpit.
• Injury to the thoracodorsal trunk: This nerve and vessels supply Latissimus Dorsi. If they are damaged the
functional effects are not too serious, the greatest setback is that a latissimus dorsi flap cannot be used for
reconstruction purposes.
• Infections: Cellulitis of the chest wall and arm may be a major problem if axillary nodal clearance is
undertaken. Infections may run a protracted course and require polytherapy for treatment.
• Lymphoedema: Usually complicates axillary node clearance or irradiation. Treatment is with manual lymphatic
drainage and compression sleeves.
• Seroma: This is an accumulation of fluid at the site of surgery. The fluid is usually straw coloured and may re-
accumulate despite drainage. Most will resolve with time.
● Axillary LN Clearance
Level 1 : LN upto lat.border of P.Minor (removes nodes around Ax.V. superficial to PM & Ax tail)
Level 2 : All LN upto med.border of P.minor (nodes deep to PM)
Level 3 : All LN of axilla (requires division of P.minor) (upto apex of axilla)
● Axillary LN Stations
Level 1 : Inferior to P.minor
Level 2 : Behind the P.minor
Level 3 : Above the P.minor
Hormonal Thearapy
is Used:
- To ↓ risk of local, regional & distal recurrence
- To ↓ risk of development of contralateral breast Ca.
● Usually ER & PR (+)ve patient cases :- hormonal therapy used
● Hormonal Therapy – 3 types drug used- SERM(Selective Estrogen Receptor Modulator) , Aromatase inhibitor,
LHRH agonist
- Tamoxifen – SERM . It binds with estrogen receptor and blocks estrogen action
TM
- Anastrozole(Arimidex ); Letrozole; Aminoglutethemide; Exemestane:- Aromatase inhibitor. They
block peripheral convertion of androgen to estrogen and also block intra-tumoral synthesis of estrogen
- Goserelin(ZoladexTM): - LHRH agonist. Used incase of pre-menopausal ER(+) ve women
● Elderly & unsuitable for GA ē ER (+)ve ca:– usually Tamoxifen/ Arimidex used to control disease Progression.
Arimidex – most popular
● One of the main problem of Tamoxifen: Can't be used with the H/O thrombosis.
● Post menopausal ē ER(+)ve invasive ca + can't use Tamoxifen = Suggested to take Anastrozole.
● ER(-)ve suggests poor response to hormonal therapy ē tamoxifen. In these cases (+)ve C-erb B2 (HER2/neu)
suggests TRASTUZUMAB (Herceptin) may be effective
● Chemotherapy used usually - FEC (5-FU,Epirubicin, Cyclophosphamide) or CMF(Cyclophosphamide , MTx,5-FU)

- Young / pre-menopausal
- LN (+)ve & lymphoreticular invasion
- ER (-)ve
- Grade III pt.
- Large tumor
● NEO-ADJUVANT CHEMO
- Young pt. with high grade ca specially if >3cm
- To down-stage the tumors with an aim to provide breast conserving surgery
● Treatment Locally Advanced Ca (ulcerating; hard, fixed to skin/muscle of chest, back, neck; nipple retraction;
orange; edematous; large palpable LN; Ca en cuirasse)
- Toilet mastectomy(non-curative attempt)
- Radiotherapy(↓bleeding from ulecerated tumor)
- Hormone therapy if ER(+)ve
- Chemotherapy
● INFLAMMATORY CA : warm, oedematous, erythematous breast, may be get confused with cellulites. Jaundice may
present. Often occurs during pregnancy and lactation. It is classified in Stage – III, straight-forward. Treatment is:
- Primary chemotherapy
- Then mastectomy and axillary clearance
● Metastatic ca Treatment : hormonal & chemo therapy

● Cause of Periductal Mastitis in smoker postmenopausal women is anaerobic bacteria. Rx would be metronidazole.
● ANDI (Aberration of Normal Development & Involution) group

- Cyclical mastalgia
- Cyst
- Sclerosing adenitis
- Duct actasia
- Fibroadenoma
- Pappiloma
THYROID BASICS
Thyroid gland
• Right and left lobes connected by isthmus
• Surrounded by sheath from pretracheal layer of deep fascia
• Apex: Lamina of thyroid cartilage
• Base: 4th-5th tracheal ring
• Pyramidal lobe: from isthmus
• May be attached to foramen caecum at the base of the tongue
Blood Supply
Arterial Superior thyroid artery (1st branch of ECA)

Inferior thyroid artery (from Thyrocervical Trunk)
Thyroidea ima (in 10% of population -from brachiocephalic artery or aorta)
Venous Superior and middle thyroid veins - into the IJV

Inferior thyroid vein - into the brachiocephalic veins
Relations
Anteromedially Sternothyroid
Superior belly of omohyoid
Sternohyoid
Anterior aspect of sternocleidomastoid
Posterolaterally Carotid sheath
Medially Larynx
Trachea
Pharynx
Oesophagus
Cricothyroid muscle
External laryngeal nerve (near superior thyroid artery)
Recurrent laryngeal nerve (near inferior thyroid artery)
Posterior Parathyroid glands

Anastomosis of superior and inferior thyroid arteries
Isthmus Anteriorly: Sternothyroids, sternohyoids, anterior jugular veins

Posteriorly: 2nd, 3rd, 4th tracheal rings (attached via Ligament of Berry)
Thyroid hormones
Triiodothyronine T3 Major hormone active in target cells
Thyroxine T4 Most prevalent form in plasma, less biologically active than T3
Calcitonin Lowers plasma calcium
● NORMAL VALUES (ref. Pastest)

S. Thyroxine T4 : 3 - 9 pmol / l or 70-140 nmol / l
S. Triiodothyronine T3 : 12 - 28 pmol / l
S. Thyrotropin TSH : 0.4 - 4.2 mU / l
++
U. Ca (24 hr) : 2.5 - 7.5 mmol / l
Synthesis and secretion of thyroid hormones

• Thyroid actively concentrates iodide( to 25 times the plasma conc.)
• Iodide is oxidised to atomic iodine by peroxidase( in the follicular cells)
• Atomic iodine then iodinates tyrosine residues (contained in thyroglobulin).
• Iodinated tyrosine residues undergo coupling to either T3 or T4.
• Process is stimulated by TSH, which stimulates secretion of thyroid hormones.
• The normal thyroid has approximately 3 month reserves of thyroid hormones.
● BLOOD TESTING IN THYROID DISEASE
Assay Usage
TPO -Thyroid PerOxidase (microsomal) In autoimmune disease

Antibodies (Hashimotos 100%) and Graves (70%)
TSH - receptor Antibody Graves (95%)
Thyroglobulin Antibody Not useful for clinical distinguishing disease,

Used as a part of F/U
Calcitonin Released from the Parafollicular Cells

Usually found in patient with Medullary ca
Hyperthyroidism
Causes of hyperthyroidism include:

• Diffuse toxic goitre (Graves Disease)
• Toxic nodular goitre
• Toxic nodule
• Rare causes
Toxic nodular goitre

In this disorder the goitre is present for a long period of time prior to the development of clinical symptoms. In most
goitres the nodules are inactive and in some cases it is the internodular tissue that is responsible for the goitre.
Toxic nodule
Overactive, autonomously functioning nodule.

It may occur as part of generalised nodularity or be a true toxic adenoma.
Small swelling @midline/near midline; hot intolerance recently
TSH levels are usually low as the autonomously functioning thyroid tissue will exert a negative feedback.
Treatment : Surgery <45 yrs and Radioiodine >45yrs and family completed persons
Signs and symptoms of hyperthyroidism
Symptoms Signs
Lethargy Tachycardia
Emotionally labile Agitation
Heat intolerance Hot, moist palms
Weight loss Exopthalmos
Excessive appetite Thyroid goitre and bruit
Palpitations Lid lag/retraction
Diagnosis
- The most sensitive test for diagnosing hyperthyroidism is plasma T3 (which is raised).
- Note: in Hypothyroidism the plasma T4 and TSH are the most sensitive tests.
- A TSH level of <0.5U/L suggests hyperthyroidism.
- TSH receptor antibodies may be tested for in the diagnosis of Graves.
n
● Mx plan: only observat & repeat FNAC. If Mechanical prob, then total / subtotal
● IMPORTANT QUESTION FOR READING

A 41-year-old woman presents with a history of weight loss and anxiety. She has 3 year history of thyrotoxicosis for
which she has been treated with previous courses of carbimazole but has failed to attend scheduled outpatient
appointments for over one year. Following the course of Carbimazole which was stopped approximately two years ago
she felt much better but was still aware of a goitre. Most recently she has become aware of a more prominent swelling of
the right side of the neck and her symptoms of anxiety with a 3 kg weight loss. Currently she takes no medication but is a
smoker of 10 cigarettes daily. On examination she has, a pulse of 96 beats per minute, a fine tremor of the outstretched
hands, lid lag and some periorbital puffiness. There is a moderately enlarged and diffuse goitre with a more prominent,
3cm nodule on the left of the gland which is non-tender. Over the goitre is a bruit and no lymphadenoapthy is palpable.
No other abnormalities are noted. Investigations reveal:
Free T4 37.3 pmol/L (10-22)
TSH 0.05 mU/L (0.4-5)
Thyroid peroxidase antibodies 1:2400 U/L
131
I uptake scan Diffuse uptake with no uptake in left nodule
What is the likely diagnosis?

DeQuervains thyroiditis
Graves' disease
Medullary carcinoma of the thyroid
Papillary carcinoma of the thyroid T
Toxic multinodular goitre
This young woman has hyperthyroidism but the prominent nodule which is 'cold' on uptake scanning is highly suggestive
of thyroid carcinoma and the mostly likely diagnosis is Graves disease (periorbital puffiness and thyroid bruit) associated
with Papillary thyroid carcinoma. However, as you are given one choice the most important issue here is not to miss
thyroid cancer. Although she has Graves thyrotoxicosis, you must not miss the associated papillary thyroid cancer as this
may be fatal. Thyroid cancer associated with Graves disease is not uncommon and usually due to papillary
carcinoma and must be considered in suspicious/expanding nodules rather than attributing purely to Graves
disease.Thyroid peroxidase antibodies are found in > 70% of cases of Grave's Disease.
Hypothyroidism
Primary: Hashimoto’s thyroiditis; Radioiodine therapy for hyperthyroidism. Historically iodine deficiency is common
cause of hypothyroidism world-wide.
Secondary: Occurs if pituitary gland does not create enough TSH to induce the thyroid gland to create sufficient
quantity of thyroxine- usually due to pituitary damage by tumor; radiation or surgery.
Tertiary: Also called Hypothalamic – Pituitary Axis Hypothyroidism. Results when hypothalamus fails to instruct
the pituitary to produce sufficient TSH
PENDRED’S SYNDROME: Bilateral sensorineural hearing loss + Goitre + Hypothyroidism
Woltman's sign of hypothyroidism/ Hung reflexes – slow recovery phase of elicited deep reflex. Mostly
observed @ Achilles, patellar or biceps tendon.
Radio-iodine worsen opthalmopathy, contraindicated in pregnancy & those wishing to conceive ē in 6months
● Radioiodine vs. Surgery
Surgery Radioiodine
Symptomatic improvement within 10 days Symptomatic improvement takes up to 2 months
No effect on opthalmopathy Eye signs may worsen
Risk of damage to adjacent anatomical structures No risk of anatomical damage
No restrictions on contact No contact with children for 4 weeks
Parathyroid glands- anatomy

• Four parathyroid glands
• Located posterior to the thyroid gland
• They lie within the pretracheal fascia
Embryology
Superior parathyroids derived from the fourth pharyngeal pouch
Inferior parathyroids derived from the third pharyngeal
Blood supply
The blood supply to the parathyroid glands is derived from the inferior and superior thyroid arteries[1]. There is a rich
anastomosis between the two vessels. Venous drainage is into the thyroid veins.
Relations
Laterally Common carotid
Medially Recurrent laryngeal nerve, trachea
Anterior Thyroid
Posterior Pretracheal fascia
Parathyroid hormone (1- 6.5 pmol /l )

- Polypeptide, containing 84 amino acids
- Secreted by the chief cells of the parathyroid glands. It acts to increase serum calcium concentration by
stimulation of the PTH receptors in the kidney and bone. PTH has a plasma half life of 4 minutes.
Effects of PTH
Bone Binds to osteoblasts → signal to osteoclasts → cause resorption of bone → release Ca
Kidney Active re-absorption of Ca and Mg from DCT.

Decreases re-absorption of phosphate.
Intestine via kidney Raises intestinal Ca absorption by increasing activated vit- D (1,25-Dihydroxycholecalciferol)
Few Basics:
Primary Hyperparathyroidism : Excessive PTH production due to parathyroid gland’s personal problem !!!
(adenoma 80%, hyperplasia 15%, multiple adenoma 4%, ca.1%); Here
PTH may be normal
High Ca++ + Normal / high PTH → Primary Hyperparathyroidism. Alk.PO4 may be raised, PO4 may be reduced
++
Secondary Hyperparathyroidism : Excessive PTH production, due to low Ca , (After adjustment, Ca may be
normal) - Osteitis Fibrosa Cystica may be found
Normal / low Ca++ + Very high PTH → Secondary Hyperparathyroidism. High PO4 level may be present. Beside
++ ++
this if scenario shows both corrected Ca + urine Ca raised; ans. same
++
Tertiary Hyperparathyroidism : Secondary Hyperparathyroidism found but after normalization of Ca , PTH
over production is going on
Persistant Hyper : Within the 6 months of Parathyroidectomy if hypercalcaemia found, (due to missed
adenoma, supernumery hyperplastic gland etc.)
Recurrent Hyper : Postparathyroidectomy- 6months normocalcaemia, then again hypercalcaemia
Ectopic Hyper : A tumor producing PTH like substance
● IMPORTANT QUESTION FOR READING

Brown tumours of bone are associated with which of the following?
A. Hyperthyroidism
B. Hypothyroidism
C. Hyperparathyroidism <ans.
D. Hypoparathyroidism
E. Osteopetrosis
Brown tumors are tumors of bone that arise in settings of excess osteoclast activity, such as hyperparathyroidism, and
consist of fibrous tissue, woven bone and supporting vasculature, but no matrix. They are radiolucent on x-ray. The
osteoclasts consume the trabecular bone that osteoblasts lay down and this front of reparative bone deposition followed
by additional resorption can expand beyond the usual shape of the bone, involving the periosteum thus causing bone
pain. They appear brown because haemosiderin is deposited at the site.
Treatment
Primary hyperparathyroidism: Indications for surgery

• Elevated serum Calcium > 1mg/dL above normal
• Hypercalciuria > 400mg/day
• Creatinine clearance < 30% compared with normal

• Episode of life threatening hypercalcaemia
• Nephrolithiasis
• Age < 50 years
• Neuromuscular symptoms
• Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard
deviations below peak bone mass (T score lower than -2.5)
Secondary hyperparathyroidism Usually managed with medical therapy. Indications for surgery in secondary (renal)
hyperparathyroidism:
• Bone pain
• Persistent pruritus
• Soft tissue calcifications
Tertiary hyperparathyroidism Usually treatment is surgical

The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be identified
then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.
PARATHYROIDECTOMY should be preceded by a THALLIUM TECHNETIUM SCAN

As 80% of Primary Hyper para-thyroidism cases are due to a single adenoma, 10-15% have hyperplasia, 2% have have
2 adenomas. So all 4 parathyroids should be located since they can occur in a variety of positions from hyoid bone to the
mediastinum.
ELECTROLYTES
Calcium homeostasis
Calcium ions are linked to a wide range of physiological processes. The largest store of bodily calcium is contained
within the skeleton. Calcium levels are primarily controlled by parathyroid hormone, vitamin D and calcitonin.
Hormonal regulation of calcium
Hormone Actions
Parathyroid hormone (PTH) Increase calcium levels and decrease phosphate levels
Increases bone resorption
2+
Immediate action on osteoblasts to increase Ca in ECF
Osteoblasts produce a protein signaling molecule that activate
osteoclasts which cause bone resorption
Increases renal tubular reabsorption of calcium
Increases synthesis of 1,25(OH)2D (active form of vitamin D) in the
kidney which increases bowel absorption of Ca2+
Decreases renal phosphate reabsorption
1,25-dihydroxycholecalciferol (the active Increases plasma calcium and plasma phosphate

form of vitamin D) Increases renal tubular reabsorption and gut absorption of calcium
Increases osteoclastic activity
Increases renal phosphate reabsorption
Calcitonin Secreted by C cells of thyroid

Inhibits intestinal calcium absorption
Inhibits osteoclast activity
Inhibits renal tubular absorption of calcium
Both growth hormone and thyroxine also play a small role in calcium metabolism.
Hypercalcaemia
Main causes
• Malignancy
• Primary hyperparathyroidism
Mnemonic for the causes of hypercalcaemia: CHIMPANZEES

C alcium supplementation
H yperparathyroidism
I atrogentic (Drugs: Thiazides)
M ilk Alkali syndrome
P aget disease of the bone
A cromegaly and Addison's Disease
N eoplasia
Z olinger-Ellison Syndrome (MEN Type I)
E xcessive Vitamin D
E xcessive Vitamin A
S arcoidosis
Clinical features
“Stones, bones, abdominal moans, and psychic groans”
Management of hypercalcaemia
• Free Ca is affected by pH (increased in acidosis) and plasma albumin concentration

• ECG changes: Short QT interval
• Urgent management is indicated if:
Calcium > 3.5 mmol/l
Reduced consciousness
Severe abdominal pain
Pre renal failure
Management
• Airway Breathing Circulation
• Intravenous fluid resuscitation with 3-6L of 0.9% Normal saline in 24h
• After hydration, give frusemide (to encourage excretion of Ca)
• Medical therapy (usually if Corrected calcium >3.0mmol/l)
Bisphosphonates
• Analogues of pryrophosphate
• Prevent osteoclast attachment to bone matrix and interfere with osteoclast activity.
• Inhibit bone resorption.
Agents
Drug Side effects Notes
IV Pamidronate pyrexia, leucopaenia Most potent agent
IV Zoledronate response lasts 30 days Used for malignancy associated

hypercalcaemia
Calcitonin
• Quickest onset of action however short duration (tachyphylaxis) therefore only given with a second agent.
Prednisolone
• May be given in hypercalcaemia related to sarcoidosis, myeloma or vitamin D intoxication
Hypocalcaemia: causes and management
The clinical history combined with parathyroid hormone levels will reveal the cause of hypocalcaemia in the majority of
cases
Causes
• Vitamin D deficiency (osteomalacia)

• Acute pancreatitis
• Chronic renal failure
• Hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
• Pseudohypoparathyroidism (target cells insensitive to PTH)
• Rhabdomyolysis (initial stages)
• Magnesium deficiency (due to end organ PTH resistance)
C/F
• Parasthesia in lips (circumoral numbness) & fingers
• Carpopedal spasm; Tetany; Convulsion(grand mal or petit mal); Cramps; Dystonia
• Psychosis
• Chvosteck’s sign (Twitching of facial muscle when facial nerve is tapped)
• Trousseau’s sign (spasm of fingers and wrist when the sphyg cuff is tightened around arm for 3 minutes @
10-20 mm Hg higher than systolic BP
• Prolong QT in ECG
Management
• Acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with
intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
• Intravenous calcium chloride is more likely to cause local irritation
• ECG monitoring is recommended ( Long QT )
• Further management depends on the underlying cause
Hypomagnasaemia
Cause of low magnesium

• Diuretics
• Total parenteral nutrition
• Diarrhoea
• Alcohol
• Hypokalaemia, hypocalcaemia
Features
• Paraesthesia
• Tetany
• Seizures
• Arrhythmias
• Decreased PTH secretion --> hypocalcaemia
• ECG features similar to those of hypokalaemia
• Exacerbates digoxin toxicity
Combined deficiency of magnesium and calcium
• Mg is required for both PTH secretion and its action on target tissues.
• Hypomagnesaemia cause both hypocalcaemia and make patients unresponsive to treatment with calcium and
vitamin D supplementation.
• Mg is the fourth most abundant cation in the body.
• The body contains 1000mmol, - half contained in bone and the remainder in muscle, soft tissues and ECF
• There is no one specific hormonal control of Mg and various hormones including PTH and aldosterone affect the
renal handling of Mg.
• Mg and Ca interact at a cellular level also and as a result decreased Mg will tend to affect the permeability of
cellular membranes to Ca resulting in hyperexcitability.
CORRECTED Ca++ LEVEL ( 2.2 - 2.6 mmol/l )
++
Corrected Calcium is defined as a make up for the change in total Ca
++
due to the change in albumin-bound Ca ,
and gives an estimate of what the Ca++ level would be if the albumin were within normal ranges.
++
Corrected Ca (mg/dL) = Total Ca (mg/dL) + 0.8 (4.0 - serum albumin gm/dL),
where 4.0 represents the average albumin level in g/dL.
In other words, each 1 g/dL decrease of albumin will decrease 0.8 mg/dL in measured serum Ca and thus 0.8
must be added to the measured Calcium to get a corrected Calcium value.
Or: Corrected Ca++ (mmol/L) = Total Ca (mmol/L) + 0.02 (40 - serum albumin g/L),
where 40 represents the average albumin level in g/L
In other words, each 1 g/L decrease of albumin, will decrease 0.02 mmol/L in measured serum Ca and thus 0.02
++
must be added to the measured value to take this into account and get a corrected Ca .
++ ++
So during hypoalbuminemia, corrected Ca level > total Ca must...
Hypokalaemia
Potassium and hydrogen can be thought of as competitors.
Hypokalaemia with alkalosis

• Vomiting
• Diuretics
• Cushing's syndrome
• Conn's syndrome (primary hyperaldosteronism)
Hypokalaemia with acidosis

• Diarrhoea
• Renal tubular acidosis
• Acetazolamide
• Partially treated DKA
ECG features in hypokalemia

• U waves
• Small or absent T waves (occasionally inversion)
• Prolonged PR interval
• ST depression
• Long QT interval
Suggests the following rhyme!

• In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!
Hyperkalaemia
• Plasma potassium levels are regulated by- aldosterone, acid-base balance and insulin levels.
• Hyperkalaemia associated with acidosis - as potassium rise fewer hydrogen ions can enter the cells
• Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other
for exchange with sodium ions across cell membranes and in the distal tubule.
• ECG features in hyperkalaemia
Peaking of T waves (occurs first)
Loss of P waves
Broad QRS complexes
Ventricullar fibrillation
More Pot more T, no P, but broad QRS
Causes of hyperkalaemia
• Acute renal failure
• Drugs: Potassium Sparing Diuretics, ACE inhibitors, Angiotensin 2 receptor blockers, ciclosporin, heparin**
• Metabolic acidosis
• Addison's
• Tissue necrosis/rhabdomylosis: burns, trauma
• Massive blood transfusion
Foods that are high in potassium

• Salt substitutes (i.e. Contain potassium rather than sodium)
• Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
Clinical Note: beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in
renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by
inhibition of aldosterone secretion
Management of hyperkalaemia
Untreated hyperkalaemia may cause life-threatening arrhythmias. Precipitating factors should be addressed (e.g. acute
renal failure) and aggravating drugs stopped (e.g. ACE inhibitors). Management may be categorised by the aims of
treatment
Stabilisation of the cardiac membrane

• Intravenous calcium gluconate (1st line of Managemeny to think in exam paper!!!)
+
Short-term shift in K from ECF to ICF compartment
• Combined insulin/dextrose infusion
• Nebulised salbutamol
Removal of potassium from the body

• Calcium resonium (orally or enema)
• Loop diuretics
• Dialysis
Potassium secretion -GI tract
Salivary glands Up to 60mmol/L
Stomach 10 mmol/L
Bile 5 mmol/L
Pancreas 4-5 mmol/L
Small bowel 10 mmol/L
Rectum 30 mmol/L
A key point to remember for the exam is that – gastric potassium secretions are low. Hypokalaemia may occur in
vomiting, usually as a result of renal wasting of potassium, not because of potassium loss in vomit.
Hyponatraemia
The most common cause in surgery is the over administration of 5% dextrose.

Hyponatraemia may be caused by water excess or sodium depletion.
Causes of Pseudohyponatraemia
Include hyperlipidaemia (increase in serum volume)
Multiple myeloma
Taking blood from a drip arm.
Urinary sodium and osmolarity levels aid making a diagnosis.
Classification
Urinary sodium > 20 mmol/l Sodium depletion, renal loss Mnemonic: Syndrome of
Patient often hypovolaemic INAPPropriate Anti-Diuretic
Diuretics (thiazides) Hormone:
Addison's I n creased
Diuretic stage of renal failure Na (sodium)
SIADH (serum osmolality low, urine PP (urine)
osmolality high, urine Na high)
Patient often euvolaemic
Urinary sodium < 20 mmol/l Sodium depletion, extra-renal loss

Diarrhoea, vomiting, sweating
Burns, adenoma of rectum (if villous
lesion and large)
Water excess (patient often Secondary hyperaldosteronism: CCF,

hypervolaemic and oedematous) cirrhosis
Reduced GFR: renal failure
IV dextrose, psychogenic polydipsia
Management
Symptomatic Hyponatremia :
Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis, may occur from overly rapid
correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1 mEq/h. Normal saline with frusemide is an
alternative method.
The sodium requirement can be calculated as follows : (125 - serum sodium) x 0.6 x body weight = required mEq of
sodium
PAPILLARY/OCCULT/ADENO FOLLICULAR MEDULLARY ANAPLASTIC LYMPHOMA

High Iodine area; Most common Low Iodine area; endemic area ● Autosomal dominant & affect family members Endemic area MOST RADIO SENSITIVE
● 70%, Solid; Smooth; Good Prognosis; 20%, Good Prognosis; 5%; [10 yr survival 90% in confined case,70% ē ● <5%; ● H/O Hashimoto’s
5years Survival 90% overall mortality rate is 24%. Cervical LN, 20% ē distal spread] ● Hard Fixed; Poor Prognosis ● Good Prognosis
● H/O exposure to ionizing radition @childhood
● Young People<40; Older people
● Non Capsulated / Seldom capsulated ● Capsulated. Vascular invasion ● Multifocal (with MEN, Medullary ca. are always ● Capsulated (±) ● Rapidly enlarging;
● Papillary tumor multinodular or Multifocal predominates ē out this finding, lesion is a bilateral and multicentric) ● Rapidly enlarging; ● Obstructive symptoms
follicular adenoma ● Diarrhoea may occur due to 5HT/PG produced ● Overlying skin red blue tinge;
● A solitary nodule or Unifocal tendency ē by tumor cell ● Hoarseness (+)
signs of blood spread indicates follicular ● Episodic flushing
tumour
TSH dependent * due to TSH (+)
Spread through Cervical LN; Blood mets rare Only through blood ( to Lung, Bone, Brain) Through LN (and also blood rarely) Through LN & direct local invasion is
common
● Contain mix of papillary & colloidal filled follicle ● Resected specimen can show– ● Tumor of Parafollicular C-cells which secrets ● Aggressive undifferentiated Tumor ● Only dense lymphatic type
● Orphan Annie Nuclei / Papillary projection & - Mixed papillary – follicular Picture Calcitonin. (C cell is derived from neural crest, Thyroid Nodule shows Malignant cells and tissue is usually present.
pale empty nuclei - Mass ē prominent oxyphil cells & scanty not thyroid tissue) the characteristic vesicular appearance of ● Mainly B-cell i.e.
● Psammoma body (clusters of micro calcificatn) thyroid colloid ● Other polypeptide CEA may b found nuclei Non Hodgkin's B cell lymphoma
● Malignant cell ē vesicular appearance of nuclei ● Differentiation tough between Benign & ● Part of MEN syndrome – Associated
Malignant Phaeochromocytoma present
Dx ● FNAC:- Difficul to differentiate between Recurrance Chance(+) - this is the only one ● Biopsy [Core; Needle; Open] to exclude ● Biopsy [Core; Open]: to Dx &
● Radioisotope Scan : COLD Benign & Malignant and thus all follicular which has the recurrence chance Lymphoma exclude Anaplastic
● TFT :↓
↓T3, TSH(↓
↓ ⁄ N) (pt. may be Euthyroid) FNA's will require at least hemi ● Radioisotope Scan :- COLD ● CT: for staging
thyroidectomy ● TFT : ↓T3, TSH(↓↓ ⁄ N)
Rx: <1cm: ● Lobectomy SAME AS PAPILLARY ● Total ē routine neck dissection. ● Debulking surgery; palliation by ● Radio ± chemo
● Thyroxine whole life * Lobectomy done ē per-operative frozen ● Thyroxine replaced bt TSH need not 2b isthmusectomy ● Surgery(localized /persistant)
● Yearly Thyroglobulin F/U section suppressed ● 90% die ē in a year
>1cm: ● Total Yearly Thyroglobulin F/U to be done ● Yearly F/U Calcitonin as ↑calcitonin indicates ● Total+Radio: only if tumor is confined ē MOST RADIO SENSITIVE
● Radioiodine ablation ** HURTHLE CELL Ca metastasis. in capsule & no evident metastasis Ia, IIa – Radio
● Suppressive thyroxine life long A rare type Follicular ca in which oxyphil ● Family F/U & affected MEN children should go IIa – IVa – Chemo
● Yearly Thyroglobulin F/U cells predominate. They have poorer prox. prophylactic thyroidectomy B4 school Chemotherapy is ineffective.
* Whole body F/U ē I131 may b spread to node + may not uptake I131 ● Not responsive to I131 (As these tumors are not
derived primarily from thyroid cells- C cell is
derived from neural crest)
ACUTE SUB-ACUTE THYROIDITIS CHR. HASHIMOTO’S REIDEL’S

THYROIDITIS (De Quervein’s) AMA (+)ve
Bacterial infection (Streptococci) H/O Viral Infection(EBV; MMR) Immunological disorder in which lymphocytes
become sensitised to thyroidal antigens
Granulomatous Autoimmune Fibrosing (Idiopathic)
Euthyroid Typically presents with hyperthyroidism Hypothyroidism (and associated symptoms) Hypothyroid (± Hypoparathyroid)
Hyper > Hypo > Eu - finally may remain hypo
Pain(+) Pain(++)
Tenderness+ Erythema over gland Hyperplasia +Fibrosis Fibrosis
● Fever; ● H/O infection must(+); ● TPO -Thyroid PerOxidase Antibody(+)ve ● TFT(N)
● ↑ESR; ↑WCC; ● ↑ESR; ↑WCC; Lymphocyte(+)ve (in 100% cases) ● Antibody (N)
● TFT(N) ● TFT ( ↑ T4 ; ↓TSH) ● Thyroglobulin Antibody (+)ve ● Stony hard + * It also can be 3
● Smooth + Soft+ Tender Thyromegaly ● TSH - receptor Antibody (+)ve times large but hardness differs from
(Whole Gland Involved > Bilateral ● Anti Mitochondrial Antibody- AMA (+)ve De-Quervein’s
Enlargement) - *At least 3 times larger [All antibodies are positive]
● Firm Hard + Whole Gland involved(big)
(In Blood – mainly TPO level is checked
because, During early phase Thyroglobulin
Ab markedly raised & then declines)
Dx: USS; FNA Scintiscan Or Technetium Scan: Low Malignant Lymphoma can present FNAC± Core/open biopsy
thyroid uptake globally ● Resection shows intense lymphocytic
infiltrate ē acinar destructn & fibrosis
Rx: ● Antibiotic ● Self-limiting - mostly don't require Rx ● Thyroxine Palliative Surgery( If Compression)
● Analgesia ● Pain may respond aspirin or NSAIDs ● Surgery (If Pressure syndrome / to
● In severe cases Steroids used, particularly confirm Diagnosis)
if hypothyroidism develops
Important Tips: All hard lesions are Hypothyroid: Chronic Hashimoto's; Reidel's
TOXIC MULTINODULAR GRAVE’S THYROID ADENOMA FOLLICULAR

OR PLUMMER’S (TOXIC)
Autonomous hyperfunctioning nodule in ● Immunological Disorders(20-40yrs) Benign
a multinodular goitre(>40yrs) ● Develops IgG Ab to TSH receptors on thyroid gland
C/F: ● Hyperthyroid; irregularly irregular pulse ● Discrete Lesion
● Mild hyper ē no eye sign ● Irritability and altered bowel habit ● Encapsulated
n
● Long history ē recent h/o palpitat ● Smooth enlargement; Diffuse involvement ● Solid
● Hypertrophy and Hyperplasia of the gland. ● Hyperfunction + Hyperthyroid
● Bruit present due to raised vascularity of gland
● Eye Sign, Preorbital Myxoedema
● Clubbing ±
Dx: ● TFT ( ↑T3 T4 ; ↓TSH) ● USG (Solid nature)
● ↕T3 ; ↑ T4 ; ↓TSH ● TSH - receptor Antibody (+) (in 95% cases) ● Isotope Scan (HOT)
● Thyroid peroxidase Antibody (+) (in 70% cases) ● FNA / Core Biopsy
● Anti mitochondrial antibody - AMA (–)ve All fail to Dx because above features are also as
● Isotope Scan (HOT) Follicular Ca. So Dx is made after Excision
Rx: ● Medical Rx Thyroid Lobectomy
st
Surgery 1 line – Carbimazole
(S/E: Leukaemia, Agranulocytosis – if occurs, then Propylthiouracil used)
nd
2 line – Propylthiouracil
N.B. If pregnancy, then Propylthiouracil used, as It is safe.
131
Mx ē I : In small, moerate goitre ē no eye sign
● Surgery (Total/Subtotal) :
Large goiter; Multinoduler; Eye sign; Relapse
case; Plan for Pregnancy
(must be euthyroid & do vocal cord exam before surgery )
Most of toxic goiters are multinodular. Grave’s disease is toxic goiter, so it can be multinodular, bt not always.
Thyroid Carcinoma associated ē Grave’s disease is usually Papillary - If there is associated expanding + suspected mass is mentioned along ē Grave’s.
The hyperthyroidism can be differentiated from Graves’ disease by the low uptake on scintiscanning
GRAVE'S: G = IgG Ab to TSH; R = R aised Thyroxin, Loss of pulse Regularity; A = Altered Bowel Habit & Irritability; E = E ye Sign + Periorbital mexoedema; S = S mooth diffuse
Enlargement
● PARATHYROID GLANDS AND DISORDERS OF CALCIUM METABOLISM
Disease type Hormone profile Clinical features Cause
Primary • PTH (Elevated / Normals)  May be asymptomatic if mild Most cases due to solitary adenoma (80%),
hyperparathyroidism • 2+
Serum Ca (Elevated)  Recurrent abdominal pain (pancreatitis, renal colic) multifocal disease occurs in 10-15% and
2+  Changes to emotional or cognitive state parathyroid carcinoma in 1% or less
• Urine Ca (Elevated)
• PO4 (Low)
• Alk PO4 (Elevated)
• Serum Calcium : Creatinine
clearance ratio > 0.01
Secondary • PTH (Elevated)  May have few symptoms Parathyroid gland hyperplasia occurs as a
hyperparathyroidism • Serum Ca2+ (Low or normal)  Eventually may develop bone disease, osteitis result of low calcium, almost always in a
2+ fibrosa cystica and soft tissue calcifications setting of chronic renal failure
• Urine Ca (Elevated)
• PO4 (Elevated)
• Vitamin D levels (Low)
2+
Tertiary • Serum Ca (Normal or high)  Metastatic calcification Occurs as a result of ongoing hyperplasia
hyperparathyroidism • PTH (Elevated)  Bone pain and / or fracture of the parathyroid glands after correction of
 Nephrolithiasis underlying renal disorder, hyperplasia of all
• PO4 (Low /Normal)
 Pancreatitis 4 glands is usually the cause
• Vitamin D (Low /Normal)
2+
Vitamin D Excess • Serum Ca ( high) Pt is otherwise asymptomatic; but often
• PTH (Low) complaints arthritis
• PO4 (Elevated)
++
DISEASE T3 T4 TSH S. PTH PO4 Alk.PO4 U. Ca OTHERS
++
12-28 3-9 0.4-4.2 Ca 2.5-7.5
Pituitary hyperthyroid All raised MRI of pituitary invx of choice
Primary hyperthyroid High High Low
Thyrotoxicosis (e.g. Grave’s) High High Low Develops IgG Ab to TSH

receptors on the thyroid gland
Over Rx ē thyroxin High High Low
Poor compliance ē thyroxin High / High

Normal
Steroid Therapy Normal Low
Sick euthyroid All reduced Common in hospital inpatients
but in some cases TSH is
normal
Primary hypothyroid Low Low High
Secondary hypothyroid All reduced Replacement steroid therapy is

required prior to thyroxine
Thyroid adenoma, Follicular High High
Toxic nod. / Plummer’s dis. Normal High Low
T4 rises
Acute + Reidel’s + Anaplastic All Normal
Sub-acute (De Quervein’s) Hyper

Hashimoto’s Hypo 3 Antibodies present
Medullary Ca. ↑CALCITONIN
ORTHOPAEDICS AND BONE PATHOLOGY
Osteomalacia
Basics
• Normal bony tissue but decreased mineral content
• Rickets if in growing stage and Osteomalacia if after epiphysis fusion
Causes
• Vitamin D deficiency e.g. malabsorption, lack of sunlight, diet
• Renal failure
• Drug induced e.g. anticonvulsants
• Vitamin D resistant; inherited
• Liver disease, e.g. cirrhosis
Features
• Rickets: knock-knee, bow leg, features of hypocalcaemia
• Osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy
Investigation
• Low calcium, phosphate, 25(OH) vitamin D
• Raised alkaline phosphatase
• X-ray: children - cupped, ragged metaphyseal surfaces; adults - translucent bands (Looser's zones or
pseudofractures)
Treatment
• Calcium with vitamin D tablets
Pseudogout
Pseudogout is a form of microcrystal synovitis caused by the deposition of CPPD - Calcium PyroPhosphate Dihydrate in
the synovium
Risk factors
• Hyperparathyroidism
• Hypothyroidism
• haemochromatosis
• Acromegaly
• Low magnesium, low phosphate
• Wilson's disease
Features
• knee, wrist and shoulders most commonly affected
• joint aspiration: weakly-positively birefringent rhomboid shaped crystals
• x-ray: chondrocalcinosis
Management
• aspiration of joint fluid, to exclude septic arthritis
• NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
● GOUT : Strongly (-) ve bi-fringent

bi Urate crystals found.
● PEUDOGOUT : Weakly (+) ve bi-fringent CPPD crytals found.
Osteomyelitis
Causes
• S aureus and occasionally Enterobacter or Streptococcus species
• In sickle cell: Salmonella species
Clinical features
• Erythema; Pain; Fever
Investigation
• X-ray: lytic centre with a ring of sclerosis

• Bone biopsy and culture
Treatment
• Prolonged antibiotics
• Sequestra may need surgical removal
Osteopetrosis
• aka marble bone disease
• rare disorder of defective osteoclast function resulting in failure of normal bone resorption
• stem cell transplant and interferon-gamma have been used for treatment
Osteoporosis
Risk factors
• Family history
• Female sex
• Increasing age
• Deficient diet
• Sedentary lifestyle
• Smoking
• Premature menopause
• Low body weight
• Caucasians and Asians
Diseases which predispose

• Endocrine: glucocorticoid excess (e.g. Cushing's, steroid therapy), hyperthyroidism, hypogonadism (e.g.
Turner's, testosterone deficiency), growth hormone deficiency, hyperparathyroidism, diabetes mellitus
• Multiple myeloma, lymphoma
• Gastrointestinal problems: inflammatory bowel disease, malabsorption (e.g. Coeliacs), gastrectomy, liver
disease
• Rheumatoid arthritis
• Long term heparin therapy
• Chronic renal failure

• Osteogenesis imperfecta, homocystinuria
Osteoporosis: secondary prevention

NICE guidelines were updated in 2008 on the secondary prevention of osteoporotic fractures in postmenopausal women.
Key points include

• Treatment is indicated following osteoporotic fragility fractures in postmenopausal women who are confirmed to
have osteoporosis (a T-score of - 2.5 SD or below).
• In women aged 75 years or older, a DEXA scan may not be required 'if the responsible clinician considers it to
be clinically inappropriate or unfeasible'
• Vitamin D and calcium supplementation should be offered to all women unless the clinician is confident they
have adequate calcium intake and are vitamin D replete
• Alendronate is first-line
• Around 25% of patients cannot tolerate alendronate, usually due to upper gastrointestinal problems. These
patients should be offered risedronate or etidronate (see treatment criteria below)
• Strontium ranelate and raloxifene are recommended if patients cannot tolerate bisphosphonates (see treatment
criteria below)
Supplementary notes on treatment

Bisphosphonates
• Alendronate, risedronate and etidronate are all licensed for the prevention and treatment of post-menopausal
and glucocorticoid-induced osteoporosis
• All three have been shown to reduce the risk of both vertebral and non-vertebral fractures although alendronate,
risedronate may be superior to etidronate in preventing hip fractures
• Ibandronate is a once-monthly oral bisphosphonate
Vitamin D and calcium

• Poor evidence base to suggest reduced fracture rates in the general population at risk of osteoporotic fractures
- may reduce rates in frail, housebound patients
Raloxifene - selective oestrogen receptor modulator (SERM)

• Has been shown to prevent bone loss and to reduce the risk of vertebral fractures, but has not yet been shown
to reduce the risk of non-vertebral fractures
• Has been shown to increase bone density in the spine and proximal femur
• May worsen menopausal symptoms
• Increased risk of thromboembolic events
• May decrease risk of breast cancer
Strontium ranelate
• 'Dual action bone agent' - increases deposition of new bone by osteoblasts and reduces the resorption of bone
by osteoclasts
• Strong evidence base, may be second-line treatment in near future
• Increased risk of thromboembolic events
Vulgas Deformity Varus Deformity
Compartment syndrome
• This is a particular complication that may occur following fractures (or following ischaemia reperfusion injury in
vascular patients). It is characterised by raised pressure within a closed anatomical space.
• The raised pressure within the compartment will eventually compromise tissue perfusion resulting in necrosis.
The two main fractures carrying this complication include supracondylar fractures and tibial shaft injuries.
Symptoms and signs

• Pain, especially on movement (even passive)
• Parasthesiae
• Pallor may be present
• Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
• Paralysis of the muscle group may occur
Diagnosis
• Is made by measurement of intracompartmental pressure measurements. Pressures in excess of 20mmHg are
abnormal and >40mmHg is diagnostic.
Treatment
• This is essentially prompt and extensive fasciotomies
• In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when
smaller incisions are performed
• Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients
require aggressive IV fluids
• Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to
be considered
• Death of muscle groups may occur within 4-6 hours
Fracture management
• Bony injury resulting in a fracture may arise from trauma (excessive forces applied to bone), stress related
(repetitive low velocity injury) or pathological (abnormal bone which fractures during normal use of following
minimal trauma)
• Diagnosis involves not just evaluating the fracture ; such as site and type of injury but also other associated
injuries and distal neurovascular deficits. This may entail not just clinical examination but radiographs of
proximal and distal joints.
• When assessing x-rays it is important to assess for changes in length of the bone, the angulation of the distal
bone, rotational effects, presence of material such as glass.
Fracture type Description Mechanism

Oblique fracture Fracture lies obliquely to long axis Usually due to sharp edged blow
of bone
Comminuted fracture >2 fragments Due to severe force,e.g. Car
Accident
Segmental fracture More than one fracture along a
bone
Transverse fracture Perpendicular to long axis of bone Long bone Osteopporosis;
Sharp/direct blow/ stress fracture
caused by prolonged running
Spiral fracture Severe oblique fracture with
rotation along long axis of bone
At vertebra Usualy due to Osteoporosis
Open Vs Closed
It is also important to distinguish open from closed injuries. The most common classification system for open fractures is
the Gustilo and Anderson classification system (given below):
Grade Injury
1 Low energy wound <1cm
2 Greater than 1cm wound with moderate soft tissue damage
3 High energy wound > 1cm with extensive soft tissue damage
3 A (sub group of 3) Adequate soft tissue coverage
3 B (sub group of 3) Inadequate soft tissue coverage
3 C (sub group of 3) Associated arterial injury
Key points in management of fractures

• Immobilise the fracture including the proximal and distal joints
• Carefully monitor and document neurovascular status, particularly following reduction and immobilisation
• Manage infection including tetanus prophylaxis
• IV broad spectrum antibiotics for open injuries
• As a general principle all open fractures should be thoroughly debrided ( and internal fixation devices avoided or
used with extreme caution)
• Open fractures constitute an emergency and should be debrided and lavaged within 6 hours of injury
Pathological fractures
• A pathological fracture occurs in abnormal bone due to insignificant injury
Causes
Metastatic tumours • Breast

• Lung
• Thyroid
• Renal
• Prostate
Bone disease • Osteogenesis imperfecta

• Osteoporosis
• Metabolic bone disease
• Paget's disease
Local benign conditions • Chronic osteomyelitis

• Solitary bone cyst
Primary malignant tumours • Chondrosarcoma

• Osteosarcoma
• Ewing's tumour
Upper limb fractures
Colles' Fracture (Extra-articular)

• Fall onto extended outstretched hands - Extension fracture
• Described as a dinner fork type deformity
• Classical Colles' fractures have the following 3 features: Features of the injury
1. Transverse fracture of the radius
2. 1 inch (2.5 cm) proximal to the radio-carpal joint
3. Dorsal displacement and angulation
Smith's Fracture (Reverse Colles' fracture) (Extra-articular)

• Volar angulation of Distal Radius Fragment (Garden spade deformity)
• Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed
Bennett's Fracture
• Intra-articular + Non-comminuted fracture of the first carpometacarpal joint
• Impact on flexed metacarpal, caused by fist fights
• X-ray: triangular fragment at ulnar base of metacarpal
Rolando Fracture
• Intra-articular + Comminuted fracture at the base of the first Metacarpal joint
Monteggia's Fracture
• Dislocation of the proximal radioulnar joint in association with an proximal 1/3 ulna fracture
• Fall on outstretched hand with forced pronation
• Needs prompt diagnosis to avoid disability
Galeazzi Fracture
• Radial shaft fracture with associated dislocation of the distal radioulnar joint
• Occur after a fall on the hand with a rotational force superimposed on it.
• On examination, there is bruising, swelling and tenderness over the lower end of the forearm.
• X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation of the inferior
radio-ulnar joint.
Barton's Fracture
• Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation
• Fall onto extended and pronated wrist
Scaphoid fractures
• Scaphoid fractures are the commonest carpal fractures. Scaphoid fractures:
80% of all carpal fractures
80% occur in men
80% occur at the waist of the scaphoid. of scaphoid is covered by articular cartilage with small
area available for blood vessels (fracture risks blood supply)
• Forms floor of anatomical snuffbox
• Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal third)
• The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on wrist movements
and on longitudinal compression of the thumb.
• Ulnar deviation AP needed for visualization of scaphoid
• Immobilization of scaphoid fracture is difficult
Management (Ref: Netter Orthopaedic Anatomy 2nd Ed.)
Non-displaced fractures - Casts or splints(short or long arm)for 10-12 weeks

- Percutaneous screw
Displaced fracture ORIF, usually with a screw ± Bone graft

Open fracture and should be debrided prior to attempted fixation
Non-union ORIF with tricortical bone graft or vascularized bone graft
Complications
• Non union of scaphoid
• Avascular necrosis of the scaphoid
• Scapholunate disruption and wrist collapse
• Degenerative changes of the adjacent joint
Radial Head Fracture

• Fracture of the radial head is common in young adults.
• It is usually caused by a fall on the outstretched hand.
• On examination, there is marked local tenderness over the head of the radius, impaired movements at the
elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination).
Avascular necrosis
• Cellular death of bone components due to interruption of the blood supply, causing bone destruction
• Main joints affected are hip, scaphoid, lunate and the talus.
• It is not the same as non union. The fracture has usually united.
• Radiological evidence is slow to appear.
• Vascular ingrowth into the affected bone may occur. However, many joints will develop secondary osteoarthritis.
Causes
P ancreatitis
L upus
A lcohol
S teroids
T rauma
I diopathic, infection
C aisson disease, collagen vascular disease
R adiation, rheumatoid arthritis
A myloid
G aucher disease
S ickle cell disease
Presentation
Usually pain. Often despite apparent fracture union.
Investigation
MRI scanning will show changes earlier than plain films.
Treatment
In fractures at high risk sites anticipation is key. Early prompt and accurate reduction is essential.
Non weight bearing may help to facilitate vascular regeneration.
Joint replacement may be necessary, or even the preferred option (e.g. Hip in the elderly).
Septic arthritis
Overview
• Most common organism overall is Staphylococcus aureus
• In young adults who are sexually active Neisseria gonorrhoeae should also be considered
Management
• Synovial fluid should be obtained before starting treatment
• Intravenous antibiotics which cover Gram-positive cocci are indicated. The BNF currently recommends
flucloxacillin or clindamycin if penicillin allergic
• Antibiotic treatment is normally be given for several weeks (BNF states 6-12 weeks)
• Needle aspiration should be used to decompress the joint
• Arthroscopic lavage may be required
Septic arthritis- Paediatric

• Staph aureus commonest organism
• Urgent washout and antibiotics otherwise high risk of joint destruction
Diagnosis
• Plain x-rays
• Consider aspiration
Kocher criteria:
1. Non weight bearing on affected side
2. ESR > 40 mm/hr
3. Fever
3
4. WBC count of >12,000 mm
- when 4/4 criteria are met, there is a 99% chance that the child has septic arthritis
The Kocher criteria do not consider blood culture results
Amputations
Amputations are indicated when the affected limb is one of the following:
• Dead non viable
• Deadly where it is posing a major threat to life
• Dead useless where it is viable but a prosthesis would be preferable
Orthopaedic surgery
• Amputation is often undertaken as an option of last resort e.g. Limb salvage has failed and the limb is so non
functional that mobility needs would be best met with prosthesis.
• Chronic fracture non union or significant limb shortening following trauma would fit into this category.
• Occasionally following major trauma a primary amputation is preferable. This would be the case in an open
fracture with major distal neurovascular compromise and other more life threatening injuries are present.
Vascular Surgery
• Diabetic foot sepsis is often a major cause
• It can spread rapidly in the presence of established peripheral vascular disease.
• As a general rule the main issue in vascular surgery is to optimise vascular inflow prior to surgery. The more
distal the planned amputation is to be, the more important this rule becomes.
• In other situations, embolic event, that has not been revascularised in time. In this case the limb shows fixed
mottling and an amputation will be needed.
Types of amputations
• Pelvic disarticulation (hindquarter)
• Above Knee Amputation
• Gritti Stokes (through knee amputation)
• Below Knee Amputation (using either Skew or Burgess flaps)
• Syme's amputation (through ankle)
• Amputations of mid foot and digits
Choosing a level of amputation depends on:

• The disease process being treated
• Desired functional outcome
• Co-morbidities of the patient
Above Knee Amputations

• Quick to perform
• Heal reliably
• Patients regain their general health quickly
• For this benefit, a functional price has to be paid and many patients over the age of 70 will never walk on an
above knee prosthesis.
• Above knee amputations use equal anterior-posterior flaps
Below Knee Amputations

• Technically more challenging to perform
• Heal less reliably than their above knee counterparts.
• However, many more patients are able to walk using a below knee prosthesis.
• In below knee amputations the two main flaps are Skew flaps or the Burgess Long posterior flap. There is some
evidence that Skew flaps are better vascularised than the long posterior flap and some vascular surgeons
prefer them for this reason.
• It is worth remembering that whilst it may be technically feasible to offer a below knee amputation there may be
circumstances where an above knee option is preferable. For example, in fixed flexion deformities of the lower
limb, little functional benefit would be gained from below knee amputation surgery.
Paediatric orthopaedics
PATHOLOGICAL # AMONG CHILDREN: BuTON

B = Bone Cyst
T = Tumor
O = Osteogenesis Imperfecta
N = N A I (Non Accidental Injury)
Transient tenosynovitis (Irritable Hip)

• 3-8 yrs of age
• URTI or similar infection (viral) history may be present
• Fever and pain present
• Effusion and synovitis
• Blood test and radiologically normal
• Rx
o Analgesics
o Rest
DDH
• Mild dysplasia acetabulum to irreducible dislocation
Clinical Features
• Congenital abnormality(+)ve; More common in extended breech babies
• Left hip more affected but May be bilateral.
• Leg length inequality
• Slight external rotation possible
• As disease progresses child may limp and then early onset arthritis
• Trendelenberg test (+)ve
Diagnosis
• X-rays:
o Initially no obvious change on plain films but small femoral head may be present
o On plain films Shentons line should form a smooth arc
o USS gives best resolution until 3 months of age.
Clinical Examination (Tests)
Barlow's: The maneuver is performed by adducting the hip while applying light pressure on the knee, directing the force
posteriorly. If the hip is dislocatable, the test is considered positive. The Ortolani maneuver is then used, to confirm that
the positive finding (i.e., that the hip actually dislocated).
Ortholoni's:It is performed by gently abducting the infant's leg using the examiner's thumb while placing anterior
pressure on the greater trochanter using the examiner's index and forefinger. A positive sign is a distinctive 'clunk' which
can be heard and felt as the femoral head relocates anteriorly into the acetabulum.
Now here's how to remember the two tests:

Barlow's test - you feel the Dislocation - so Barlow's test is Bad test as you are Dislocating from joint.
ORTHOlani - you try to feel the Reduction - like ORTHOpedicians reducing all fractures and dislocations
Treatment
• Splints and harnesses or traction. In later years osteotomy and hip realignment procedures may be needed. In
arthritis a joint replacement may be needed. However, this is best deferred if possible as it will almost certainly
require revision
o 0 - 6m : Pelvic harness; Surgery is needed in case of dislocated & irreducible cases
o 6m - 18m : Close reduction ± adductor tenotomy; if fail then Arthrogram + open reduction ē hip
0 0
spica cast 60 Abduction and 90 flexion
o 18m - 3yrs : OR ± Femoral varus derotation osteotomy
o 3yrs - 8yrs : OR + Femoral varus derotation osteotomy + pelvic osteotomy
o >8yrs : THR when system justify surgical intervention
Follow-up
• At least until walking normally; WHO recommend upto 5yrs
Perthes Disease
• Idiopathic avascular necrosis of the femoral epiphysis of the femoral head

• Impaired blood supply to femoral head, causing bone infarction. New vessels develop and ossification occurs.
The bone either heals or a subchondral fracture occurs.
Clinical Features
• Males 4x's greater than females; Bilateral in 20%
• Age: 3-12yrs. Rare <4yrs; Common in avg. 5-7yrs;
• Symptoms >2weeks.
• Limp; Hip pain
• Decreased Abduction& internal Rotation → PAbi
• Sometimes limitation of active / passive movement of hip joint in all direction
• Osteonecrosis of proximal femoral epiphysis resulting flattening & fragmentation of epiphysis
• AVN → Deformatn → Subsequent Revascularization (2-4yrs cycle)
Diagnosis
• Earliest avascular change is found in Technitium-99 scan. Xray findings is found more later
• X-rays:
o Flattened femoral head. In untreated case femoral head will fragment
o Sub-chondral crecent shaped radiolucent line
o Calcification lateral to epiphysis
o Metaphyseal rarefaction
o Lateral extrusion of head
o Abnormal physeal growth

o Gage’s sign
o Increased joint spacce
Catterall staging
Stage Features
Stage 1 Clinical and histological features only
Stage 2 Sclerosis with or without cystic changes and preservation of the articular surface
Stage 3 Loss of structural integrity of the femoral head
Stage 4 Loss of acetabular integrity
Management
• To keep the femoral head within the acetabulum: cast, braces
• If < 6 years: observation and symptomatic Rx
• 6-8 yrs: Brace or surgical management with moderate results
• > 8yrs: Surgical containment: (femoral / pelvic )osteotomy
Prognosis
• Most cases will resolve with conservative management. Early diagnosis improves outcomes
Slipped Capital Femoral Epiphysis (SCFE / SUFE)
• Displaced upper femoral epiphysis (head) from neck
Clinical features
• Obese ( remember, only this clue can guide you to the answer !!!)
• Associated with ↑GH; ↓Sex hormone; Hypothyroid
H
• Pain @ thigh and knee; Mild shortening of limb
• Increased Adduction and External
ernal Rotation → AddExt → SAdExt
• Decreased Abduction and Internal Rotation
• Chance of AVN (+)ve
Diagnosis
• X-rays:
o May be normal
o Epiphysis slips back - and falling inferolaterally (like a melting ice cream cone)
o The Southwick angle gives indication of disease severity
Treatment
• Bed rest and non-weight bearing – Aim to avoid avascular necrosis
• Minor to moderate cases : Cannulated Hip Screw
• If severe slippage or risk of it occurring then percutaneous pinning of the hip may be required
• Delayed cases : Femoral neck osteotomy
Talipes Equinovarus (Club Foot)
Features:
• Equinus of the hindfoot.
• Adduction and varus of the midfoot.
• High arch.
Most cases in developing countries. Incidence in UK is 1 per 1000 live births. It is more common in males and is bilateral
in 50% cases. There is a strong familial link(1). It may also be associated with other developmental disorders such as
Down's syndrome.
Key anatomical deformities (2):

• Adducted and inverted calcaneus
• Wedge shaped distal calcaneal articular surface
• Severe Tibio-talar plantar flexion.
• Medial Talar neck inclination
• Displacement of the navicular bone (medially)
• Wedge shaped head of talus
• Displacement of the cuboid (medially)
Management
Conservative first, the Ponseti method is best described and gives comparable results to surgery. It consists of serial
casting to mold the foot into correct shape. Following casting around 90% will require a Achilles tenotomy. This is then
followed by a phase of walking braces to maintain the correction.
Surgical correction is reserved for those cases that fail to respond to conservative measures. The procedures involve
multiple tenotomies and lengthening procedures. In patients who fail to respond surgically an Ilizarov frame
reconstruction may be attempted and gives good results.
Paediatric fractures
Type Injury pattern
Complete fracture Both sides of cortex are breached
Toddlers fracture
Oblique tibial fracture in infants
Plastic deformity Stress on bone resulting in deformity without cortical disruption
Greenstick fracture
Unilateral cortical breach only
Buckle fracture
Incomplete cortical disruption resulting in periosteal haematoma only
Growth Plate Fractures / Epiphyseal Fractures
Salter Harris Classification
Type Description
Type 1 Transverse fracture through the growth plate / physis only
Type 2 Fracture through the physis to the metaphysis (commonest type)
Type 3 Fracture through the physis and epiphyisis to include the joint (with metaphysis spared)
Type 4 Fracture involving the physis, metaphysis and epiphysis
Type 5 Compression fracture of the physis (worst outcome, x-ray may resemble type I, and appear normal)
Management
As a general rule it is safer to assume that growth plate tenderness is indicative of an underlying fracture even if the
x-ray appears normal.
Non displaced Type I injuries can generally be managed conservatively.
Injuries of Types III, IV and V will usually require surgery. Type V injuries are often associated with disruption to
growth.
Non accidental injury

• Delayed presentation
• Delay in attaining milestones
• Lack of concordance between proposed and actual mechanism of injury
• Multiple injuries
• Injuries at sites not commonly exposed to trauma
• Children on the at risk register
Pathological fractures
Genetic conditions, such as osteogenesis imperfecta, may cause pathological fractures.
Osteogenesis imperfecta
• Defective osteoid formation due to congenital inability to produce adequate intercellular substances like osteoid,
collagen and dentine.
• Failure of maturation of collagen in all the connective tissues.
• Radiology may show translucent bones, multiple fractures, particularly of the long bones, wormian bones
(irregular patches of ossification) and a trefoil pelvis.
Subtypes
• Type I The collagen is normal quality but insufficient quantity.
• Type II- Poor collagen quantity and quality.
• Type III- Collagen poorly formed. Normal quantity.
• Type IV- Sufficient collagen quantity but poor quality.
Osteopetrosis
• Bones become harder and more dense.
• Autosomal recessive condition.
• It is commonest in young adults.
• Radiology reveals a lack of differentiation between the cortex and the medulla described as marble bone.
Osgood-Schlatter Disease / Runner’s knee
• Autosomal recessive condition

• Involves traction apophysis of tibial tubercle – due to repeated microtrauma to tibial apophysis
• 10-15 yrs of age range; Male are more sufferer than Female
• Clinical Features
o Very specific point of tenderness over the tibial tubercle – tender palpable lump over proximal tibia .
o Pain knee after activity . No H/O trauma
• Xray : shows fragmentation of apophysis

• Rx
o Rest
o Plaster cast for 6-8 weeks
● FEW SIGNS AND TESTS IN ORTHOPAEDICS

• LudlOFF sign : Avulsion of lesser trochanter ( Lesser trochanter has come OFF )
• ADson's test is for cervical rib / thoracic outlet syndrome ( Remember ADDed rib )
• ALLI's test is for CDH ( Remember ALLICe )
Pott's fracture
• Bimalleolar ankle fracture
• Forced foot eversion
UROLOGY
Renal anatomy
Each kidney is about 11cm long, 5cm wide and 3cm thick. They are located in a deep gutter alongside the projecting
verterbral bodies, on the anterior surface of psoas major. In most cases the left kidney lies approximately 1.5cm higher
than the right. The upper pole of both kidneys approximates with the 11th rib (beware pneumothorax during
nephrectomy). On the left hand side the hilum is located at the L1 vertebral level and the right kidney at level L1-2. The
lower border of the kidneys is usually alongside L3.
● Kidney Relation Anterior (Right)

- S upra renal gland (Rt.)
- L iver
nd
- D uodenum (2 part)
- C olonic flexure(hepatic)
- J ejunum
● Kidney Relation Anterior (Left)

- S upra renal gland (Lt.)
- S pleen
- G astric (Stomach)
- P ancreas (Only organ which is in direct contact)
- J ejunum
- C olonic flexure (splenic)
- V essels (splenic)
● Kidney Relation Posterior (both)

-S ub costal N
- I lioinguinal N.
- I liohypogastric N.
- Q uadratus Lumborum* (Lower Intermediate side)
- T ransversus Abdominis* (Lower Lateral side)
- P soas major* (Lower medial side)
- D iaphragm* (Superiorly)
- A rcuate Lig. (med. + lat.)
* These are the 4 muscles lies back of kidney
th th th
● Beside these, 12 rib lies behind the Right kidney and 11 & 12 rib both lies behind the Left kidney
FASCIAL COVERING
Each kidney and suprarenal gland is enclosed within an bi-layer investing Gerotas Fascia - derived from Transversalis
Fascia. Its posterior layer is also named Zuckerkandl's fascia. Its attachments are:
Anteriorly : Passes anterior to kidney, renal vessels, AA & IVC and fuses ē ant. fascial layer of opposite kidney.
Posteriorly : Fuses with Psoas Fascia and side of the body of vertebrae.
Superiorly : Anterior and Posterior layers fuse at upper pole and then split to enclose adrenals. At the upper part
of adrenal gland they again fuse to form Suspensory Ligament & fuse ē Diaphragmatic Fascia.
Inferiorly : The layers don't fuse. Posterior layer descends downwards and fuses with the Iliac Fascia. Anterior
layer blends with the connective tissue of the Iliac Fossa.
Posterior Approach or Subcostal Flank approach needs the division of Costovertebral Ligament to increase the
th
upward mobility of 12 rib
RENAL STRUCTURE
Kidneys are surrounded by an Outer Cortex and an Inner Medulla which usually contains between 6 and 10 pyramidal
structures. The papilla marks the innermost apex of these. They terminate at the renal pelvis, into the ureter.
Lying in a hollow within the kidney is the renal sinus. This contains:
1. Branches of the renal artery
2. Tributaries of the renal vein
3. Major and minor calyces's
4. Fat
STRUCTURES AT THE RENAL HILUM VAU

The renal Vein lies most anteriorly, then renal Artery (it is an end artery) and the Ureter lies most posterior.
Renal arteries
• The right renal artery is longer than the left renal artery
• The renal vein/artery/pelvis enter the kidney at the hilum
Relations
• Right:
Anterior- IVC, right renal vein, the head of the pancreas, and the descending part of the duodenum.
• Left:
Anterior- left renal vein, the tail of the pancreas.
Branches
• The renal arteries are direct branches off the aorta (upper border of L2)
• In 30% there may be accessory arteries (mainly left side). Instead of entering the kidney at the hilum, they
usually pierce the upper or lower part of the organ.
• Before reaching the hilum of the kidney, each artery divides into four or five segmental branches (renal vein
anterior and ureter posterior); which then divide within the sinus into lobar arteries supplying each pyramid and
cortex.
• Each vessel gives off some small inferior suprarenal branches to the suprarenal gland, the ureter, and the
surrounding cellular tissue and muscles.
Renal Physiology
• Each nephron is supplied with blood from an afferent arteriole that opens onto the glomerular capillary bed.
• Blood then flows to an efferent arteriole, supplying the peritubular capillaries and medullary vasa recta.
• The kidney receives up to 25% of resting cardiac output.
Control of blood flow

• The kidney is able to autoregulate its blood flow between systolic pressures of 80- 180mmHg so there is little
variation in renal blood flow.
• This is achieved by myogenic control of arteriolar tone, both sympathetic input and hormonal signals (e.g. renin)
are responsible.
Glomerular structure and function

• Blood inside the glomerulus has considerable hydrostatic pressure.
• The basement membrane has pores that will allow free diffusion of smaller solutes, larger negatively charged
molecules such as albumin are unable to cross.
• The glomerular filtration rate (GFR) is equal to the concentration of a solute in the urine, times the volume of
urine produced per minute, divided by the plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
• In clinical practice creatinine is used because it is subjected to very little proximal tubular secretion.
• Although subject to variability, the typical GFR is 125ml per minute.
• Glomerular filtration rate = Total volume of plasma per unit time leaving the capillaries and entering the
bowman's capsule
• Renal clearance = volume plasma from which a substance is removed per minute by the kidneys
• Substances used to measure GFR have the following features:
1. Inert
2. Free filtration from the plasma at the glomerulus (not protein bound)
3. Not absorbed or secreted at the tubules
4. Plasma concentration constant during urine collection
Examples: inulin, creatinine
GFR = urine concentration (mmol/l) x urine volume (ml/min)

--------------------------------------------------------------------------
plasma concentration (mmol/l)
• The clearance of a substance is dependent not only on its diffusivity across the basement membrane but also
subsequent tubular secretion and / or reabsorption.
• So glucose which is freely filtered across the basement membrane is usually reabsorbed from tubules giving a
clearance of zero.
● FORMULA :
GFR = Inulin conc.of Urine / plasma X urine flow mn-1 (Filtration test)
-1
RPF = PAH conc.of Urine / plasma X urine flow mn (Secretion test)
RBF = RPF / (1- Hematocrit)
Tubular function
• Reabsorption and secretion of substances occurs in the tubules.
• In the proximal tubule substrates such as glucose, amino acids and phosphate are co-transported with sodium
across the semi permeable membrane.
• Up to two thirds of filtered water is reabsorbed in the proximal tubules.
• This will lead to increase in urea concentration in the distal tubule allowing for its increased diffusion.
• Substances to be secreted into the tubules are taken up from the peritubular blood by tubular cells.
• Solutes such as paraaminohippuric acid are cleared with a single passage through the kidneys and this is why it
is used to measure renal plasma flow. Ions such as calcium and phosphate will have a tubular reabsorption that
is influenced by plasma PTH levels.
• Potassium may be both secreted and re-absorbed and is co-exchanged with sodium.
Loop of Henle
• Approximately 60 litres of water containing 9000mmol sodium enters the descending limb of the loop of Henle in
24 hours.
• Loops from the juxtamedullary nephrons run deep into the medulla.
• The osmolarity of fluid changes and is greatest at the tip of the papilla.
• The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions.
• This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with
adjacent interstitial fluid.
• In the thick ascending limb the reabsorption of sodium and chloride ions occurs by both facilitated and passive
diffusion pathways.
• The loops of Henle are co-located with vasa recta, these will have similar solute compositions to the
surrounding extracellular fluid so preventing the diffusion and subsequent removal of this hypertonic fluid.
• The energy dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this
osmotic gradient.
Reabsorption and Secretions Mnemonics
Reabsorption
P – Glucose + Uric Acid
PD – HCO3
PDLC – rest of all
Secretions
+ +
PDLC – K , H
PDC – NH3
L – Urea
Sites of Drug Action in the Kidney
P CT : MA nnitol MAP
ALL H : F rusemide FALL
D CT : A miloride, T hiazides; A ldosterone DATA
C D: : S pironolactone, A DH SAC
Reabsorption and Secretions Mnemonics
Reabsorption (P = Prox.Con.T.; D = Dist.Con.T.; L = Loop of H.; C = Coll. Duct)

P – Glucose + Uric Acid
PD – HCO3
PDLC – rest of all
Secretions
+ +
PDLC – K , H
PDC – NH3
L – Urea
Reabsorption Glucose (F. Diffusion) + Na+ = PCT(97% Amino Acid also reabsorbed here);
+
K = DCT;
H2O (counter-current) = PCT (2/3rd of Filtered H2O, >80%);
= DLLH (Hyperosmolar fluid) + CD (both do 14% reabsorption)
● Potassium doesn't work in PCT
● Hormones acting on kidney for reabsorption are: ADH, Aldosterone, Parathormone
Physiological Effects Of Commonly Used Diuretics
Site of Diuretic Carrier or channel % of filtered Na

action inhibited excreted
ALLH Frusemide Na+/K+ 2Cl -carrier Up to 25%
DCT Thiazides Na+Cl- carrier 3-5%
CD Spironolactone Na+ channel 1- 2%
● NEPHROTIC SYNDROME = plasma albumin level reduced, proteinuria+ oedema, (cz decreased colloidal osmotic
pressure.) ECF volume expansion is most likely to be seen.
n
● Anuria or decrease urine out put after major op – cause mainly
Fluid / blood loss
Response of adrenal cortex to stress: ↑Aldosterone (Na, H2O retention) & ADH release (synthesize in
hypothalamic neurons)
Renal Replacement Therapy
n
Continuous Venous Haemodiafiltr : Used in ARF/ATN in unstable critically ill pt (e.g. sepsis from
perforated appendicitis; AAA repair). In these cases haemodialysis not used. Cz in 20-30% pt.it develops
hypotension with huge associated osmotic shifts-disequilibrium syndrome which in case of Many of ICU pt, is
intolerable. Moreover hypotension worsens pre-existing renal injury by ischaemic insult.
Intermittent Haemodialysis : - Most efficient method in stable pt.; polycystic kidney ē end-stage CRF
waiting4replacement
- Large amount of fluid can be removed
- Electrolytes abnormalities can be rapidly corrected
- H/O abd.surg.
Chronic Ambulatory Peritoneal dialysis(PD) :CRF waiting replacement with

Bleedding diathesis;
Needle phobia;
n n
Poor cardiac funct unlikely2 tolerate hypotens czed by
haemodialysis
Travelling job
Angiomyolipoma of kidney
- 4 times more common in female
- Unilateral
- F/H of Tuberous sclerosi
- CT scan shows large mass of low attenuation with some bleeding into it.
- Haematoma containing vasculature, smooth muscle and some fat into it
Urine R/E findings

- Atypical epithelial cells: TCC of renal pelvis
- Semiquantitative sulphosalicylic acid (+): Multiple myeloma
- Hyperplastic arteriosclerosis: Scleroderma
- Oval Fat Bodies: Minimal change disease

Acute renal failure: Pre renal failure vs. acute tubular necrosis
Prerenal uraemia - kidneys retain sodium to preserve volume
Pre-renal uraemia Acute tubular necrosis
Urine sodium < 20 mmol/L > 30 mmol/L
Fractional sodium excretion* < 1% > 1%
Fractional urea excretion** < 35% >35%
Urine:plasma osmolality > 1.5 < 1.1
Urine:plasma urea > 10:1 < 8:1
Specific gravity > 1020 < 1010
Urine 'bland' sediment brown granular casts
Response to fluid challenge Yes No
*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100
**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100
Acute Renal Failure

• Final pathway is tubular cell death.
• Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular hypoxia.
• Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
• Estimates of GFR are best indices of level of renal function. Useful clinical estimates can be obtained by
considering serum creatinine, age, race, gender and body size. eGFR calculations such as the Cockcroft and
Gault equation are less reliable in populations with high GFR's.
• Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce apoptosis. Myoglobinuria
and haemolysis result in necrosis. Overlap exists and proinflammatory cytokines play and important role in
potentiating ongoing damage.
• Post-operative renal failure is more likely to occur in patients who are elderly, have peripheral vascular disease,
high BMI, have COPD, receive vasopressors, are on nephrotoxic medication or undergo emergency surgery.
• Avoiding hypotension will reduce risk of renal tubular damage.
• There is no evidence that administration of ACE inhibitors or dopamine reduces the incidence of post-operative
renal failure.
Renal stones
Type of Features Percentage of all

stones calculi
Calcium Hypercalciuria is a major risk factor (various causes) 85%

oxalate Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with calcium
making it more soluble
Stones are radio-opaque (though less than calcium phosphate stones)
Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine transport leading to 1%

decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense because they contain sulphur
Uric acid Uric acid is a product of purine metabolism 5-10%

May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
Radiolucent
Calcium May occur in renal tubular acidosis, high urinary pH increases supersaturation of 10%
phosphate urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and
4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate 2-20%

Occur as a result of urease producing bacteria (and are thus associated with
chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque
Effect of urinary pH on stone formation

Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine metabolism will produce uric
acid. Then the urine becomes more alkaline (alkaline tide). When the stone is not available for analysis the pH of urine
may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5
Renal stones: imaging
Type Frequency Radiograph appearance
Calcium oxalate 40% Opaque
Mixed calcium oxalate/phosphate stones 25% Opaque
Triple phosphate stones* 10% Opaque
Calcium phosphate 10% Opaque(Most radiodense)
Urate stones 5-10% Radio-lucent
Cystine stones 1% Semi-opaque, 'ground-glass' appearance
Xanthine stones <1% Radio-lucent
*stag-horn calculi involve the renal pelvis and extend into at least 2 calyces. They develop in alkaline urine and are
composed of struvite (ammonium magnesium phosphate, triple phosphate). Ureaplasma urealyticum and Proteus
infections predispose to their formation
Renal lesions
Lesion Disease specific features Treatment
Renal cell • Most present with haematuria (50%) Usually radical or partial nephrectomy
carcinoma • Common renal tumour (85% cases)
Renal mass ; Vericocele
• Paraneoplastic features include hypertension
CT shows – Mass with small cystic center
and polycythaemia
• Most commonly has haematogenous
metastasis – Canon ball matastases lung
Nephroblastoma • Rare childhood tumour Surgical resection combined with
• It accounts for 80% of all genitourinary chemotherapy (usually vincristine,
malignancies in those under the age of 15 actinomycin D and doxorubicin
years
• Up to 90% will have a mass
• 50% will be hypertensive
• Diagnostic work up includes ultrasound and
CT scanning
Neuroblastoma • Most common extracranial tumour of Surgical resection, radiotherapy and

childhood chemotherapy
• 80% occur in those under 4 years of age
• Tumour of neural crest origin (up to 50% occur

in the adrenal gland)
• The tumour is usually calcified and may be
diagnosed using MIBG(Meta Iodo Benzyl
Guanidine) scanning
• Staging is with CT
Transitional cell • Accounts for 90% of upper urinary tracttumour, Radical nephroureterectomy
carcinoma but only 10% of renal tumours
• Males affected 3x more than females
• Occupational exposure to industrial dyes and
rubber chemicals may increase risk
• Up to 80% present with painless haematuria
• Diagnosis and staging is with CT IVU
Angiomyolipoma • 80% of these hamartoma type lesions occur 50% of patients with lesions >4cm will
sporadically, the remainder are seen in those have symptoms and will require surgical
with tuberous sclerosis resection
• Tumour is composed of blood vessels, smooth

muscle and fat
• Massive bleeding may occur in 10% of cases
Renal tumours
Renal cell carcinoma

Renal cell carcinoma is an adenocarcinoma of the renal cortex and is believed to arise from the proximal convoluted
tubule. They are usually solid lesions, up to 20% may be multifocal, 20% may be calcified and 20% may have either a
cystic component or be wholly cystic. They are often circumscribed by a pseudocapsule of compressed normal renal
tissue. Spread may occur either by direct extension into the adrenal gland, renal vein or surrounding fascia. More distant
disease usually occurs via the haematogenous route to lung, bone or brain.
Renal cell carcinoma comprise up to 85% of all renal malignancies. Males are more commonly affected than females and
sporadic tumours typically affect patients in their sixth decade.
Patients may present with a variety of symptoms including; haematuria (50%), loin pain (40%), mass (30%) and up to
25% may have symptoms of metastasis.Less than 10% have the classic triad of haematuria, pain and mass.
Investigation
Many cases will present as haematuria and be discovered during diagnostic work up. Benign renal tumours are rare, so
renal masses should be investigated with multislice CT scanning. Some units will add and arterial and venous phase to
the scan to demonstrate vascularity and evidence of caval ingrowth.
CT scanning of the chest and abdomen to detect distant disease should also be undertaken.
Routine bone scanning is not indicated in the absence of symptoms.
Biopsy should not be performed when a nephrectomy is planned but is mandatory before any ablative therapies are
undertaken.
Assessment of the functioning of the contra lateral kidney.
Management
T1 lesions may be managed by partial nephrectomy and this gives equivalent oncological results to total radical
nephrectomy. Partial nephrectomy may also be performed when there is inadequate reserve in the remaining kidney.
For T2 lesions and above a radical nephrectomy is standard practice and this may be performed via a laparoscopic or
open approach. Preoperative embolisation is not indicated nor is resection of uninvolved adrenal glands. During surgery
early venous control is mandatory to avoid shedding of tumour cells into the circulation.
Patients with completely resected disease do not benefit from adjuvant therapy with either chemotherapy or
biological agents. These should not be administered outside the setting of clinical trials.
Patients with transitional cell cancer will require a nephroureterectomy with disconnection of the ureter at the bladder.
Functional renal imaging
DMSA scan
Dimercaptosuccinic acid (DMSA) scintigraphy
DMSA localises to the renal cortex with little accumulation in the renal papilla and medulla. It is useful for the
identification of cortical defects and ectopic or abhorrent kidneys. It does not provide useful information on the ureter of
collecting system.
Diethylene-triamine-penta-acetic acid (DTPA)

This is primarily a glomerular filtration agent. It is most useful for the assessment of renal function. Because it is filtered
at the level of the glomerulus it provides useful information about the GFR. Image quality may be degraded in patients
with chronic renal impairment and derangement of GFR.
MAG 3 renogram (Invex of choice in Graft failure )

Mercaptoacetyle triglycine is an is extensively protein bound and is primarily secreted by tubular cells rather than filtered
at the glomerulus. This makes it the agent of choice for imaging the kidneys of patients with existing renal impairment
(where GFR is impaired).
Micturating cystourethrogram (MCUG scan)

This scan provides information relating to bladder reflux and is obtained by filling the bladder with contrast media (via a
catheter) and asking the child to void. Images are taken during this phase and the degree of reflux can be calculated
Intra venous urography

This examination is conducted by the administration of intravenous iodinated contrast media. The agent is filtered by the
kidneys and excreted and may provide evidence of renal stones or other structural lesions. A rough approximation of
renal function may be obtained using the technique. But it is not primarily a technique to be used for this purpose. With
the advent of widespread non contrast CT scan protocols for the detection of urinary tract calculi it is now rarely used.
PET/CT
This may be used to evaluate structurally indeterminate lesions in the staging of malignancy.
Complications following renal transplant
Renal transplantation is widely practised. The commonest technical related complications are related to the ureteric
anastomosis. The warm ischaemic time is also of considerable importance and graft survival is directly related to this.
Long warm ischaemic times increase the risk of acute tubular necrosis which may occur in all types of renal
transplanation and provided other insults are minimised, will usually recover. Organ rejection may occur at any phase
following the transplantation process.
Types of organ rejection

• Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO incompatibility).
• Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular
lesions.
• Chronic. Occurs after the first 6 months. Vascular changes predominate.
Renal transplant:HLA typing and graft failure
The human leucocyte antigen (HLA) system is the name given to the major histocompatibility complex (MHC) in humans.
It is coded for on chromosome 6.
Some basic points on the HLA system

• Class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
• When HLA matching for renal transplant the relative importance of the HLA antigens are as follows DR > B > A
Graft survival
• 1 year = 90%, 10 years = 60% for cadaveric transplants
• 1 year = 95%, 10 years = 70% for living-donor transplants
Post-op problems
• ATN of graft
• Vascular thrombosis
• Urine leakage
• UTI
Hyperacute acute rejection
Renal transplants are most susceptible to this process. Risk factors include major HLA mismatch and ABO
incompatibility. The rejection occurs almost immediately and the macroscopic features may become manifest following
completion of the vascular anastomosis and removal of clamps. The kidney becomes mottled, dusky and the vessels will
thrombose. The only treatment is removal of the graft, if left in situ it will result in abscess formation
• Due to antibodies against donor HLA type 1 antigens
• Rarely seen due to HLA matching
Acute graft failure (< 6 months)
All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of transplanted organ are
susceptible and it may occur in up to 50% cases. Most cases can be managed medically
• Usually due to mismatched HLA
• Other causes include cytomegalovirus infection
• Management: give steroids, if resistant use monoclonal antibodies
Causes of chronic graft failure (> 6 months)
Again all transplants with HLA mismatch may suffer this fate. acute rejections and other immunosensitising events all
increase the risk. Vascular changes are most prominent with myointimal proliferation leading to organ ischaemia. Organ
specific changes are also seen such as loss of acinar cells in pancreas transplants and rapidly progressive coronary
artery disease in cardiac transplants
• Chronic allograft nephropathy
• Ureteric obstruction
• Recurrence of original renal disease (MCGN > IgA > FSGS)
● Transitional Cell Ca of renal pelvis treatment : Nephro-ureterectomy.
Ureter
• 25-35 cm long
• Muscular tube lined by Transitional Epithelium
• Surrounded by thick muscular coat. Becomes 3 muscular layers as it crosses the bony pelvis.
• Retroperitoneal structure overlying the L2-L5 Transverse Processes
• Lies anterior to Bifurcation of iliac vessels
• Lies beneath the Uterine Artery
• Not related to Round Ligament of Uterus but Related to Broad Ligament
• It is within 1.5 cm of Supra-vaginal part of cervix
Both ureters are crossed by the gonadal artery and vein. In addition the right ureter is crossed by the right colic and
ileocolic vessels, whilst the left ureter is crossed by the left colic vessels
PARTS OF THE URETER

1) ABDOMINAL PART: 12.5 cm
Course and Relation Right Ureter Left Ureter
− Same course in both Male and Female behind the peritoneum.

− On the Psoas Major Downwards & slightly medially
Course
− Opposite the tips of transverse processes of lower 4 lumbar vertebrae
− Enters pelvis by crossing in front of Common Iliac Artery termination/
bifarcation (at Sacroiliac Joint)
Renal Pelvis
− Branches of renal vessels lie both in front and behind it.
Posterior − Medial border of Psoas Major

− Genito-Femoral Nerve
− Transverse processe tips of lower 4 Lumbar Vertebrae
rd
● Duodenum 3 part ● Peritoneum
● Peritoneum
3 Arteries: ● Left Gonadal (←

← Aorta)
● Right Gonadal (←
← Aorta) ● Left Colic (←
← IMA)
Anterior ● Right Colic (←
← SMA)
● ileo-Colic (←
← SMA)
3 structures related to Mesentry: ● Passes behind Intersigmoid

● Root of Mesentery Fossa
● Superior Mesentric Vessels ● Sigmoid mesocolon
● Terminal Part of ileum ● Sigmoid Colon
● Inferior Mesenteric Vein
Medial IVC
● Left Gonadal Vein
In the lesser or true pelvis the ureter at first runs downwards, and slightly backwards and laterally, following the anterior
margin of the greater sciatic notch. Opposite the ischial spine it turns forwards and medially to reach the base of the
urinary bladder. The ureter enters the bladder wall obliquely to open into it at the lateral angle of its trigone
2) PELVIC PART: 12.5 cm
− Enters pelvis by crossing in front of Common Iliac Artery termination / bifarcation (at Sacroiliac Joint)
− Runs Downwards, Backwards and Laterally - follows the anterior margin of Greater Sciatic Notch till it reaches
Ischial Spine.
− Then runs Forwards and Medially (or Antero-medially) crosses over the Levator Ani (at the level of Ischial Spine).
In its DOWNWARDS COURSE, following relations are found:

Anteriorly :
• Peritoneum (it is retro-peritoneal).
Posteriorly :
• Internal Iliac Artery
• Internal Iliac Artery anterior part commencement
• Internal Iliac Vein
• Lumbosacral Trunk
• Sacroiliac Joint
Laterally :
• Obturator Internus Fascia
• Superior Vesical Artery (← Internal Iliac Artery)
• Obturator Nerve
• Obturator Artery (← Internal Iliac Artery)
• Obturator Vein
• Inferior Vesical Vein
• Middle Rectal Artery
• Forms the posterior boundary of the Ovarian Fossa (in female
IDENTIFICATION OF URETER DURING OPERATION

− Anatomical site:
o Lies on Psoas Major & seen crossing
o The bifurcation of Common Iliac Artery
o The Ischial Spine.
− Not an artery: since the pulsations are not continuous but Peristalsis.
− Not Psoas Minor:
o Psoas Minor: Flat shining tendon.
o Ureter: white cord-like (tubular).
− Not a part of Colon:
o Colon: Blood vessels run Circular.
o Ureter: Blood vessels run Longitudinally.
− Abdominal Ureter should be mobilized Medially.

− Pelvic Ureter should be mobilized Laterally (receives its blood supply from lateral side).
− The stone is the best quide for the Ureter, if present

− The Ureter remains attached to the undersurface of Peritoneum when the it is reflected at surgery.
Anatomy of the Bladder
AN EMPTY BLADDER IS TETRAHEDRAL IN SHAPE.AND HAS

Four Angles; One Base; Three Surfaces
● FOUR ANGLES
Apex
− Points forwards towards the Symphysis Pubis.
− Continuous with Median Umbilical Ligament, (remnant of Urachus). If remains patent, it may cause:
• Urachal sinus, fistula, cyst.
• Congenital diverticulum.
Neck
− The lowest and most fixed part.
− It is anchored into position by Pubovesical Ligament (Female) and Puboprostatic Ligament (Male)
− Lies anterior to the Rectum (Male) or Vagina (Female).
− Lies over Prostate (Male) or Pelvic Fascia (Female).
Two Posterosuperior Angles

− Receiving the 2 Ureters
● ONE BASE
− Is covered by Peritoneum at upper part (In Male)
− Like an inverted triangle and faces Posteroinferiorly
− Ureters enter the bladder at each of the upper corners of the base
− Urethra drains inferiorly from the lower corner of the base
− Inside, the mucosal lining on the base of the bladder is smooth and firmly attached to the underlying smooth
muscle coat of the wall is known as the Trigone.
Trigone
o The least mobile part inside and forms the site of Ureteric Orifices and Internal Urethral Orifice.
o In Empty Bladder, Ureteric Orifices are approx. 2−3 cm apart & in Distended, up to 5cm apart.
o No Rugae
o Pink in colour (rich blood supply) = (if stone ) hematuria
o No submucosa → No Bilharziasis(Schistosomiasis) → No Egyptian cancer
o Richly nerve supply → more sensitive to pain (innervated by sympathetic nerves).
● THREE SURFACES
− Two INFEROLATERAL SURFACES is Retroperitoneal.
− One SUPERIOR SURFACE is covered by Peritoneum.
Clinical Note:
When the bladder distends, it tends to separate the Peritoneum from Fascia Tansversalis.That's why a Suprapubic
Catheter spares the entry into Peritoneal Cavity during acute bladder retention catheterization.
Identification during operation:
• Brownish network of muscles .
• Fill it with saline- Balloons.
• Bluish network of venous plexus
• Stone
FULL BLADDER IS OVOID IN SHAPE AND HAS
• Apex, directed upwards towards the umbilicus;

• Neck, directed downwards,
• Two surfaces, Anterior and Posterior.
In Male, Bladder lies between

Symphysis Pubis Anteriorly
Seminal Vesicle, Ductus Deferens, Rectovesical Pouch Posteriorly. Behind this Pouch
Rectum lies.
Superior Surface
Completely covered by Peritoneum,
Is in contact with the Sigmoid Colon and coils of the Terminal Ileum
In Females, Bladder lies between

Symphysis Pubis Anteriorly
Vesicouterine Pouch Posteriorly, Behind this Pouch →
Uterus+ Vagina − Behind the Uterus →
Rectouterine Pouch (of Douglas) − Behind this Pouch →
Rectum lies.
Superior Surface
Peritoneum covers whole, except a small area near post.border, related to supravaginal part of cervix.
The peritoneum from superior surface is reflected to form Vesicouterine Pouch
Inferolateral Surfaces
- Devoid of peritoneum
- In male, each surface is related to
o Pubis
o Puboprostatic ligaments,
o Retropubic fat,
o Levator ani and Obturator Internus
o In the Female the relations are same, difference is Puboprostatic Ligaments are replaced by Pubovesical
Ligaments.
LIGAMENTS OF URINARY BLADDER

True Ligaments
o Lateral True Ligament of Bladder (Attaches with the Arcus Tendineus of Pelvic Fascia)
o Lateral Puboprostatic Ligament (Attaches the ant. end of A.Tend. ē Prostatic Sheath's upper part)
o Posterior Ligament of Bladder (Attaches the base of the bladder with Pelvic wall)
o Median Umbilical Ligament (The remnant of the Urachus)
o Medial Puboprostatic Ligament (The ligaments of two sides form the floor of Retropubic Space. In
females, bands similar to these ligaments are known as Pubovesical Ligaments. They end around the
neck of the bladder)
False Ligaments
o Median umbilical fold
o Medial umbilical fold
o Lateral false ligament, (Formed by the peritoneum of the Paravesical fossa)
o Posterior false ligament (Formed by the peritoneum of the Sacrogenital folds)
Arterial Supply
The Superior Vesical Artery ( ← Umbilical Artery patent part ← Internal Iliac Artery Anterior Part)
The Inferior Vesical Artery (←
← Umbilical Artery patent part ← Internal Iliac Artery Anterior Part)
Venous Drainage
In males, the bladder is drained by the Vesico−Prostatic Venous Plexus.
In females, the bladder is drained by the Vesico−Uterine Venous Plexus.
In both sexes, this Venous Plexuses will ultimately drain to Internal Iliac Veins.
Lymphatic drainage
Lymphatic drainage is predominantly to the External Iliac Nodes. Beside this Internal Iliac, Para-aortic and Obturator
Nodes also form sites of bladder lymphatic drainage.
Nerve Supply
In simple terms Parasympathetic flow Causes micturition
Sympathetic flow Prevents micturition
Micturition Facilitatory areas

● Pons
● Posterior Hypothalamus
Micturition Inhibitory areas

● Cerebral cortex
● Midbrain
ACTION ON
SYSTEM SOURCE NERVE ROOT DETRUSOR INTERNAL EXTERNAL FUNCTION
WALL SPHINCTER SPHINCTER
Parasympathetic − Pelvic Splanchnic S2,3,4 Contraction Relaxation Not supplied Emptying Bladder
Nervi Erigentes − Inf. Hypogastric Plexus (Motor) (Inhibitory)
Sympathetic − Hypogastric plexuses T11,12 Relaxation Contraction Not supplied Filling Bladder
L1,2 (Inhibitory) (Motor)
Somatic − Pudendal S2,3,4 Not supplied Not supplied Contraction Voluntary control
(Motor) of micturition
● Remember, Parasympathetic is responsible for Pee

● Pain sensation carried by Parasympathetic Nerves and partly by Sympathetic Nerves
Bladder Cancer
Staging
Ta : Non invasive / invasive papillary
Tis : CIS / non invasive flat
T1 : Invades subepithelial connective tissue (thru’ lamina propria)
[Treatment – TURBT + Chemo]
[N.B. Wide spread CIS – Intravesical BCG Instillation is done i.e. medical management.If no response, then
Cystectomy + Urethrectomy + Ileal Conduit (to divert urine) is the treatment of choice.]
T2 : Invades muscle layer (is not palpable bimanually, after resection)

• T2a : Into inner half (superficial muscle)
• T2b : Into outer half (deep muscle)
T3 : Invades through the wall of the bladder and into the pre-vesical / fatty tissue that surrounds it.
• T3a : Microscopically
• T3b : Macroscopically
T4 : Nearby organs or structures.
• T4a : Prostate, Uterus, and/or Vagina
[ Treatment – Radical Cystectomy + M-VAC chemo]
• T4b : Pelvic wall or Abdominal wall

[ Treatment – Inoperable Palliation ]
[In case of Treatment, please remember, if LN is involved, think for only Palliative Treatment, nothing else ]
N categories
NX : Cannot be assessed
N0 : No regional lymph node spread
N1 : A single lymph node < 2cm
N2 : Single lymph node 2-5 cm or multiple nodes, no one is >5cm
N3 : > 5cm; metastasis to lymph nodes that lie along the common iliac artery
M categories
MX : Cannot be assessed
M0 : No signs of distant spread
M1 : The cancer has spread to distant lymph nodes, organs, or tissues (like the Bones, Lungs, or Liver)
Cell differentiation
G1 : Well differentiated
G2 : Moderately differentiated
G3 : Poorly differentiated
Stages of bladder cancer

Stage 0a : Ta, N0, M0
Stage 0is : Tis, N0, M0
Stage I : T1, N0, M0
Stage II : T2, N0, M0
Stage III : T3 or T4a, N0, M0
Stage IV : any of the following:
T4b, N0, M0 OR Any T, N1-3, M0 OR Any T, Any N, M1
Urinary incontinence
It is a disturbance of urine storage that comprises two major components: Overactivity Of The Detrusor Muscle or
Weakness of Urethral Sphincter Function, resulting in failure to store urine. Most cases are female (80%).
Commonest variants include:
• Stress urinary incontinence
• Urge incontinence
• Overflow incontinence
Males
→ Much rarer condition in men.
→ Males have 2 powerful sphincters; one at bladder neck and other in the urethra.
→ Damage to the bladder neck mechanism is a factor in causing retrograde ejaculation following prostatectomy
→ The short segment of urethra passing through the Urogenital Diaphragm consists of striated muscle fibres
and smooth muscle (External Sphincter) capable of more sustained contraction. It is the latter mechanism that
maintains continence following prostatectomy.
Females
→ The sphincter complex at the level of bladder neck is poorly developed in females.
→ As a result the external sphincter complex is functionally more important, its composition being similar to
that of males.
→ Innervation is via Pudendal Nerve and Neuropathy during Obstetric Events may compromise this nerve and
lead to Stress Urinary Incontinence.
STRESS URINARY INCONTINENCE

• 50% of cases, especially in females.
• Damage (often obstetric) to the supporting structures surrounding the bladder may lead to urethral
hypermobility.
• Other cases due to sphincter dysfunction, usually from neurological disorders (e.g. Pudendal neuropathy,
multiple sclerosis).
Mechanism:
→ Urethral mobility: Pressure not transmitted appropriately to the urethra resulting in involuntary passage of
urine during episodes of raised intra-abdominal pressure.
→ Sphincter dysfunction: Sphincter fails to adapt to compress urethra resulting in involuntary passage of urine.
When the sphincter completely fails there is often to continuous passage of urine.
URGE INCONTINENCE
→ There is sense of urgency followed by incontinence.
→ Detrusor Muscle is unstable
→ Urodynamic investigation will demonstrate Overactive Detrusor Muscle at inappropriate times (e.g. Bladder
filling).
→ Urgency may be seen in patients with overt neurological disorders and those without.
→ The pathophysiology is not well understood but poor central and peripheral co-ordination of the events
surrounding bladder filling are the main processes.
OVERFLOW INCONTINENCE
→ Overflow incontinence occurs in both sexes.Symptoms are often relatively few.
→ Patients tend to dribble urine. Men often have a full and palpable bladder. Women often have abnormal
anatomy or a vesicovaginal fistula
Assessment
→ History and examination - including vaginal examination for cystocele.
→ Bladder Diary - for at least 3 days.
→ Exclusion of other organic disease (e.g. Stones, UTI, Cancer)
o Mid stream urine specimen
o Renal function
o PSA in men
o Renal ultrasound
o Flexible cystoscopy
→ Urodynamic Assessment evaluates the function of the bladder and results should be interpreted with the
clinical presentation. Assessment can involve:
o Pad test
o Flow rates
o Residual volume by ultrasound
o Conventional Flow Cystometry (if unclear symptomps or surgery considered and diagnosis is unclear)
o Videocysturethrography – filling and voiding
Management
→ Conservative Measures First
o Stress Incontinence or Mixed symptoms: 3 months of pelvic floor exercise.
o Overactive Bladder - 6 weeks of bladder retraining.
→ Drug Therapy
o Overactive Bladder - Oxybutynin (if conservative measures fail).
→ Operative Therapy
o Sacral Neuromodulation* - In Detrusor Instability who fail non operative therapy. Is considered, with
conversion to permanent implant if good response.
o Augmentation Cystoplasty - is an alternative but involves long term intermittent self catheterisation.
o Urethral Sling - In Stress Incontinence this procedure may be done.
o Where Cystocele is present with incontinence it should be repaired particularly if it lies at the Introitus.
N.B. *Sacral Neuromodulation: Done via implantable system, which sends electrical pulses to an area near the Sacral
Nerve to modulate the neural activity that influences the behavior of the pelvic floor, lower urinary tract, urinary and anal
sphincters, and colon
NICE GUIDELINES
• Initial Assessment urinary incontinence should be classified as stress/urge/mixed.
• At least 3/7 Bladder Diary if unable to classify easily.
• Start Conservative Treatment before urodynamic studies if a diagnosis is obvious from the history
• Urodynamic Studies, if plans for surgery.
• Stress Incontinence: Pelvic floor exercises 3/12, if fails consider surgery.
• Urge Incontinence: Bladder training >6/52, if fails for oxybutynin (antimuscarinic drugs) then sacral nerve
stimulation.
• Pelvic Floor Exercises offered to all women in their 1st pregnancy.
Schistosomiasis
Schistosomiasis, or bilharziasis, is a parasitic flatworm infection. The following types of schistosomiasis are recognised:
• Schistosoma mansoni and Schistosoma Intercalatum: Intestinal Schistosomiasis
• Schistosoma haematobium: Urinary Schistosomiasis
Schistosoma Haematobium
• Typically presents as a 'swimmer's itch' in patients who have recently returned from Africa.
• Schistosoma haematobium is a risk factor for squamous cell cancer of badder.
• Features
o Frequency
o Haematuria
o Bladder calcification
• Management
o Single oral dose of Praziquantel
Prostate gland
The prostate gland is approximately the shape and size of a walnut and is located inferior to the bladder.
It is separated from the rectum by Denonvilliers fascia
Its blood supply is derived from the internal iliac vessels.
The internal sphincter lies at the apex of the gland and may be damaged during prostatic surgery, affected individuals
may complain of retrograde ejaculation.
Arterial supply Inferior vesical artery (from internal iliac)
Venous drainage Prostatic venous plexus (to paravertebral veins)
Lymphatic Internal iliac nodes

drainage
Innervation Inferior hypogastric plexus
Dimensions • Transverse diameter (4cm); AP (2cm); Height (3cm)
Lobes • Posterior lobe: posterior to urethra

• Median lobe: posterior to urethra, in between ejaculatory ducts
• Lateral lobes x 2
• Isthmus
Zones • Peripheral zone: subcapsular portion of posterior prostate. Most prostate cancers are
here
• Central zone
• Transition zone
• Stroma
Relations
Anterior Pubic symphysis

Prostatic venous plexus
Posterior Denonvilliers fascia

Rectum
Ejaculatory ducts
Lateral Venous plexus (lies on prostate)

Levator ani (immediately below the puboprostatic ligaments
Benign Prostatic Hyperplasia
• Prostatic enlargement occurs in many elderly men

• >90% of men aged over 80 will have at least microscopic evidence of benign prostatic hyperplasia
Pathology
As part of the hyperplastic process increase in both stromal and glandular components are seen. The changes are most
notable in the central and periurethral region of the gland.
Presentation
The vast majority of men will present with lower urinary tract symptoms. These will typically be:
• Poor flow
• Nocturia
• Hesitancy
• Incomplete and double voiding
• Terminal dribbling
• Urgency
• Incontinence
Investigation
• Digital rectal examination to assess prostatic size and morphology.
• Urine dipstick for infections and haematuria.
• Uroflowmetry (a flow rate of >15ml/second helps to exclude BOO)
• Bladder pressure studies may help identify detrusor failure and whilst may not form part of first line
investigations should be included in those with atypical symptoms and prior to redo surgery.
• Bladder scanning to demonstrate residual volumes. USS if high pressure chronic retention.
● BEP –তে যদি pt. wants to have baby তাহলে Prazosin দিতে হবে prostatectomy করা যাবেনা (পোলা
পোলা চাইলে prazosin!!)
● If there is only urge incontinence then Anticholinergic is the Rx of choice
● Treatment :
Initially α-blocker. But if hypotension cz professional problem(e.g. Pilot) then give 5-α-reductase
inhibitor -- but remind that it’ll take time to get the outcome.
Prostate Cancer
Prostate Cancer
Usually peripheral part is involved.
Diagnosis
Early prostate cancers have few symptoms.
Metastatic disease may present as bone pain.
Locally advanced disease may present as pelvic pain or with urinary symptoms.
Prostate specific antigen measurement
Digital rectal examination
Trans rectal USS (+/- biopsy)
MRI/ CT and bone scan for staging.
PSA Test
The normal upper limit for PSA is 4ng/ml. However, in this group will lie patients with benign disease and some with
localised prostate cancer. False positives may be due to prostatitis, UTI, BPH, vigorous DRE.
The percentage of free: total PSA may help to distinguish benign disease from cancer. Values of <20% are
suggestive of cancer and biopsy is advised.
Pathology
• 95% adenocarcinoma
• In situ malignancy is sometimes found in areas adjacent to cancer. Multiple biopsies needed to call true in situ
disease.
• Often multifocal- 70% lie in the peripheral zone.
• Graded using the Gleason grading system, two grades awarded 1 for most dominant grade (on scale of 1-5)
and 2 for second most dominant grade (scale 1-5). The two added together give the Gleason score. Where 2 is
best prognosis and 10 the worst.
• Lymphatic spread occurs first to the obturator nodes and local extra prostatic spread to the seminal vesicles is
associated with distant disease.
Treatment
• Watch and wait- Elderly, multiple co-morbidities, low Gleason score
• Radiotherapy (External)- Both potentially curative and palliative therapy possible. Similar survival figures to
surgery. However, radiation proctitis and rectal malignancy are late problems. Brachytherapy is a modification
allowing internal radiotherapy.
• Surgery- Radical prostatectomy. Surgical removal of the prostate is the standard treatment for localised
disease. The robot is being used increasingly for this procedure. As well as the prostate the obturator nodes are
also removed to complement the staging process. Erectile dysfunction is a common side effect.
• Hormonal therapy- Testosterone stimulates prostate tissue and prostatic cancers usually show some degree of
testosterone dependence. 95% of testosterone is derived from the testis and bilateral orchidectomy may be
used for this reason. Pharmacological alternatives include LHRH analogues and anti androgens (which may be
given in combination)
Stage I : Intra Capsular; microscopic; not felt DRE; not seen on imaging; surrounded by normal prostate
Stage II : Confined but deforming gland
[Treatment –Radical Prostatectomy or Ext. Beam Radio ± Hormone]
Stage III : Beyond capsule ē late sulci &/or seminal vesical invasion
[Treatment – Radio / Hormone / both; Watch & wait if preferred]
Stage IV :Fixed & invading surrounding structure;spreads to LN,bones, liver, lungs etc.
[Treatment – Hormone ± Radio; Watch & wait if no symptoms]
** Metastatic CA ē out bone Metastasis : Hormone therapy ; Metastatic CA ē bone Metastasis :

Radio (to reduce pain) **
● Now a days in case of Hormone escaped prostate Ca ē bone metastasis, Zoledronic acid (LHRH agonist) is used
PSA testing
Prostate specific antigen (PSA) is a serine protease enzyme produced by normal and malignant prostate epithelial cells.
It has become an important tumour marker but much controversy still exists regarding its usefulness as a screening tool.
The NHS Prostate Cancer Risk Management Programme (PCRMP) has published updated guidelines in 2009 on how to
handle requests for PSA testing in asymptomatic men. A recent European trial (ERSPC) showed a statistically significant
reduction in the rate of death prostate cancer by 20% in men aged 55 to 69 years but this was associated with a high risk
of over-diagnosis and over-treatment. Having reviewed this and other data the National Screening Committee have
decided not to introduce a prostate cancer screening programme yet but rather allow men to make an informed choice.
Age-adjusted upper limits for PSA were recommended by the PCRMP*:
{Age} {PSA level (ng/ml)}
50-59 years 3.0
60-69 years 4.0
> 70 years 5.0
PSA levels may also be raised by**:

• benign prostatic hyperplasia (BPH)
• prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after
treatment)
• ejaculation (ideally not in the 48 hours)
• vigorous exercise (ideally not in the 48 hours)
• urinary retention
• instrumentation of the urinary tract
Poor specificity and sensitivity

• around 33% of men with a PSA of 4-10 ng/ml will be found to have prostate cancer. With a PSA of 10-20 ng/ml
this rises to 60% of men
• around 20% with prostate cancer have a normal PSA
• various methods are used to try and add greater meaning to a PSA level including age-adjusted upper limits
and monitoring change in PSA level with time (PSA velocity or PSA doubling time)
*aide memoire for upper PSA limit: (age - 20) / 10
**whether digital rectal examination actually causes a rise in PSA levels is a matter of debate
Management
• Lifestyle changes such as stopping smoking and altering fluid intake may help those with mild symptoms.
• Medical therapy includes alpha blockers and 5 alpha reductase inhibitors. The former work quickly on receptor
zones located at the bladder neck. Cardiovascular side effects are well documented. The latter work on
testosterone metabolising enzymes. Although they have a slower onset of action, the 5 alpha reductase
inhibitors may prevent acute urinary retention.
• Surgical therapy includes transurethral resection of the prostate and is the treatment of choice in those with
severe symptoms and those who fail to respond to medical therapy. More tailored bladder neck incision
procedures may be considered in those with small prostates. Retrograde ejaculation may occur following
surgery. The change in the type of irrigation solutions used has helped to minimise the TURP syndrome of
electrolyte disturbances.
Post prostatectomy syndromes
Transurethral prostatectomy is a common and popular treatment for benign prostatic hyperplasia. The procedure
involves insertion of a resectoscope via the penile urethra. The bladder and prostate are irrigated and strips of prostatic
tissue removed using diathermy.
Complications include haemorrhage, urosepsis, retrograde ejaculation and electrolyte disturbances from the irrigation
fluids used during surgery.
Complications of Transurethral Resection: TURP
T ur syndrome
U rethral stricture/UTI
R etrograde ejaculation
P erforation of the prostate
TUR syndrome occurs when irrigation fluid enters the systemic circulation. The triad of features are:
1. Hyponatraemia: dilutional
2. Fluid overload
3. Glycine toxicity
Management involves fluid restriction and the treatment of the complications associated with the hyponatraemia.
● U-trerine artery is the only artery to ross over the U-reter - 2U; Water under the Bridge
– Crossing occurs 2cm (approax.) superior to Ischial spine
– Left ureter is very vulnerable as it lies very close to lateral aspect of cervix
Urogenital triangle (N-357)
The urogenital triangle is formed by the:
• Ischiopubic inferior rami

• Ischial tuberosities
A fascial sheet is attached to the sides, forming the inferior fascia of the urogenital diaphragm.
It transmits the urethra in males and both the urethra and vagina in females. The membranous urethra lies deep this
structure and is surrounded by the external urethral sphincter.
Superficial to the urogenital diaphragm lies the superficial perineal pouch. In males this contains:
• Bulb of penis
• Crura of the penis
• Superficial transverse perineal muscle
• Posterior scrotal arteries
• Posterior scrotal nerves
In females the internal pudendal artery branches to become the posterior labial arteries in the superficial perineal pouch.
Penis
● Innervation of Penis
• Parasympathetic puts it up; sympathetic spurts it out
• "S2, 3, 4 keep the penis off the floor"
o Innervation of the penis by branches of the pudental nerve, derived from spinal cord levels S2-4
Physiology of erection
Autonomic • Sympathetic nerves originate from T11-L2 and parasympathetic nerves from S2-4 join to form
pelvic plexus.
• Parasympathetic discharge causes erection, sympathetic discharge causes ejaculation and
detumescence.
Somatic Supplied by dorsal penile and pudendal nerves. Efferent signals are relayed from Onufs nucleus (S2-4)
nerves to innervate ischiocavernosus and bulbocavernosus muscles.
Autonomic discharge to the penis will trigger the veno-occlusive mechanism which triggers the flow of arterial blood into
the penile sinusoidal spaces. As the inflow increases the increased volume in this space will secondarily lead to
compression of the subtunical venous plexus with reduced venous return. During the detumesence phase the arteriolar
constriction will reduce arterial inflow and thereby allow venous return to normalise.
Priapism
Prolonged unwanted erection, in the absence of sexual desire, lasting more than 4 hours.
Classification of priaprism
Low flow priaprism Due to veno-occlusion (high intracavernosal pressures).

• Most common type
• Often painful
• Often low cavernosal flow
• If present for >4 hours requires emergency treatment
High flow priaprism Due to unregulated arterial blood flow.

• Usually presents as semi rigid painless erection
Recurrent priaprism Typically seen in sickle cell disease, most commonly of high flow type.
Causes
• Intracavernosal drug therapies (e.g. for erectile dysfunction>
• Blood disorders such as leukaemia and sickle cell disease
• Neurogenic disorders such as spinal cord transection
• Trauma to penis resulting in arterio-venous malformations
Tests
• Exclude sickle cell/ leukaemia
• Consider blood sampling from cavernosa to determine whether high or low flow (low flow is often hypoxic)
Management
• Ice packs/ cold showers
• If due to low flow then blood may be aspirated from copora or try intracavernosal alpha adrenergic agonists.
• Delayed therapy of low flow priaprism may result in erectile dysfunction
● The whole urethra is lined by transitional epithelium except for the navicular fossa & external meatus
st
● Membranous urethra is the narrowest part – So during catheterization it’s the 1 site of resistance to be encountered
● Perineum injury + Butterfly hematoma = penile urethra, Buck’s fascia injury
● Perineum injury + swelling of scrotum during micturition= spongy urethra injury
● Perineum injury +urine is not coming+ perineal haematoma +bleeding from External Urethral Meatus = bulbar
urethral injury (bleeding from urethral meatus bulbar). Urine is collected at connective tissue of scrotum.
● Pelvic injury + DRE / PR shows High riding prostate = membranous urethra injury (Perineal or Penile edema)
Penile fracture
Penile fractures are a rare type of urological trauma that may be encountered. The injury is usually in the proximal part of
the penile shaft and may involve the ureter. A classically history of a snapping sensation followed by immediate pain is
usually given by the patient (usually during vigourous intercourse). On examination there is usually a tense haematoma
and blood may be seen at the meatus if the urethra is injured.
When there is a a strong suspiscion of the diagnosis the correct management is surgical and a circumferential incision
made immediately inferior to the glans. The skin and superficial tissues are stripped back and the penile shaft inspected.
Injuries are usually sutured and the urethra repaired over a catheter
● Testicular torsion & Inguinoscrotal hernia confirm. then no need of any invx – surgery is the RX .
st
● Testicular tumor suspected. USG of testicular contents is the 1 Invx of choice. CXR is done to see pul.mets
Urethral anatomy
Female urethra
The female urethra is shorter and more acutely angulated than the male urethra. It is an extra-peritoneal structure and
embedded in the endopelvic fascia. The neck of the bladder is subjected to transmitted intra-abdominal pressure and
therefore deficiency in this area may result in stress urinary incontinence. Between the layers of the urogenital diaphragm
the female urethra is surrounded by the external urethral sphincter, this is innervated by the pudendal nerve. It ultimately
lies anterior to the vaginal orifice.
Male urethra
Pre-prostatic Extremely short and lies between the bladder and prostate gland.It has a stellate lumen and is between
urethra 1 and 1.5cm long.Innervated by sympathetic noradrenergic fibres, as this region is composed of
striated muscles bundles they may contract and prevent retrograde ejaculation.
Prostatic This segment is wider than the membranous urethra and contains several openings for the
urethra transmission of semen (at the midpoint of the urethral crest).
Membranous Narrowest part of the urethra and surrounded by external sphincter. It traverses the perineal membrane
urethra 2.5cm postero-inferior to the symphysis pubis.
Penile urethra Travels through the corpus songiosum on the underside of the penis. It is the longest urethral
segment.It is dilated at its origin as the infrabulbar fossa and again in the gland penis as the navicular
fossa. The bulbo-urethral glands open into the spongiose section of the urethra 2.5cm below the
perineal membrane.
The urothelium is transitional in nature near to the bladder and becomes squamous more distally
Narrowest parts : Bladder neck, Membranous urethra, just proximal to navicular fossa at External
urethral orifice. Among all membranous is the least dilatable part
Widest & most dilatable : Prostatic urethra. Beside this, dilatation found in bulbar region and also before
external origin
Scrotal and testicular anatomy
Spermatic cord : Formed by the vas deferens and is covered by the following structures:
Layer Origin
Internal spermatic fascia Transversalis fascia
Cremasteric fascia From the fascial coverings of internal oblique
External spermatic fascia External oblique aponeurosis
Contents of the cord
Vas deferens Transmits sperm and accessory gland secretions
Testicular artery Branch of abdominal aorta supplies testis and epididymis
Artery of vas deferens Arises from inferior vesical artery
Cremasteric artery Arises from inferior epigastic artery
Pampiniform plexus Venous plexus, drains into right or left testicular vein
Sympathetic nerve fibres Lie on arteries, the parasympathetic fibres lie on the vas
Genital branch of the genitofemoral nerve Supplies cremaster
Lymphatic vessels Drain to lumbar and para-aortic nodes
Scrotum
• Composed of skin and closely attached dartos fascia.
• Arterial supply from the anterior and posterior scrotal arteries
• Lymphatic drainage to the inguinal lymph nodes
• Parietal layer of the tunica vaginalis is the innermost layer
Testes
• The testes are surrounded by the tunica vaginalis (closed peritoneal sac). The parietal layer of the tunica
vaginalis adjacent to the internal spermatic fascia.
• The testicular arteries arise from the aorta immediately inferiorly to the renal arteries.
• The pampiniform plexus drains into the testicular veins, the left drains into the left renal vein and the right into
the inferior vena cava.
• Lymphatic drainage is to the para-aortic nodes
Testicular embryology
Until the end of foetal life the testicles are located within the abdominal cavity. They are initially located on the posterior
abdominal wall on a level with the upper lumbar vertebrae (L2). Attached to the inferior aspect of the testis is the
gubernaculum testis which extends caudally to the inguinal region, through the canal and down to the superficial skin.
Both the testis and the gubernaculum are extra-peritoneal.

As the foetus grows the gubernaculum becomes progressively shorter. It carries the peritoneum of the anterior
abdominal wall (the processus vaginalis). As the processus vaginalis descends the testis is guided by the gubernaculum
down the posterior abdominal wall and the back of the processus vaginalis into the scrotum.
By the third month of foetal life the testes are located in the iliac fossae, by the seventh they lie at the level of the deep
inguinal ring.
The processus vaginalis usually closes after birth, but may persist and be the site of indirect hernias. Part closure may
result in development of cysts on the cord.
Scrotal swelling
Inguinal hernia If inguinoscrotal swelling; cannot "get above it" on examination

Cough impulse may be present
May be reducible
Testicular tumours Often discrete testicular nodule (may have associated hydrocele)
Symptoms of metastatic disease may be present
USS scrotum and serum AFP and β HCG required
Acute epididymo- Often history of dysuria and urethral discharge

orchitis Swelling may be tender and eased by elevating testis
Most cases due to Chlamydia
Infections with other gram negative organisms may be associated with underlying structural
abnormality
Epidiymal cysts Single or multiple cysts

May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Painless
Lie above and behind testis
It is usually possible to "get above the lump" on examination
Hydrocele Non painful, soft fluctuant swelling

Often possible to "get above it" on examination
Usually contain clear fluid
Will often transilluminate
May be presenting feature of testicular cancer in young men
Testicular torsion Severe, sudden onset testicular pain

Risk factors include abnormal testicular lie
Typically affects adolescents and young males
On examination testis is tender and pain not eased by elevation
Urgent surgery is indicated, the contra lateral testis should also be fixed
Varicocele Varicosities of the pampiniform plexus

Typically occur on left (bacause testicular vein drains into renal vein)
May be presenting feature of renal cell carcinoma
Affected testis may be smaller and bilateral varicoceles may affect fertility
Scrotal sensation
The scrotum is innervated by the ilioinguinal nerve and the pudendal nerve. The ilioinguinal nerve arises from L1 and
pierces the internal oblique muscle. It eventually passes through the superficial inguinal ring to innervate the anterior skin
of the scrotum.
The pudendal nerve is the principal nerve of the perineum. It arises in the pelvis from 3 nerve roots. It passes through
both greater and lesser sciatic foramina to enter the perineal region. The perineal branches pass anteromedially and
divide into posterior scrotal branches. The posterior scrotal branches pass superficially to supply the skin and fascia of
the perineum. It cross communicates with the inferior rectal nerve.
Testicular cancer
Testicular cancer is the most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer
are germ-cell tumours. Germ cell tumours may essentially be divided into:
Tumour type Key features Tumour markers Pathology
Seminoma • Commonest subtype  AFP usually normal Sheet like lobular patterns
(50%)  HCG elevated in of cells with substantial
• Average age at 10% seminomas fibrous component.
diagnosis = 40  Lactate Fibrous septa contain

dehydrogenase; lymphocytic inclusions and
• Even advanced
elevated in 10-20% granulomas may be seen.
disease associated with
seminomas (but also in
5 year survival of 73%
many other conditions)
Non seminomatous germ cell  Younger age at presentation  AFP elevated in up Heterogenous texture with
tumours (42%) =20-30 years to 70% of cases occasional ectopic tissue
• Teratoma  Advanced disease carries  HCG elevated in up such as hair
• Yolk sac tumour worse prognosis (48% at 5 to 40% of cases

years)  Other markers rarely
• Choriocarcinoma
 Retroperitoneal lymph node helpful
• Mixed germ cell
dissection may be needed for
tumours (10%)
residual disease after
chemotherapy
Risk factors for testicular cancer

• Cryptorchidism
• Infertility
• Family history
• Klinefelter's syndrome
• Mumps orchitis
Features
• A painless lump is the most common presenting symptom
• Pain may also be present in a minority of men

• Other possible features include hydrocele, gynaecomastia
Diagnosis
• Ultrasound is first-line
• CT scanning of the chest/ abdomen and pelvis is used for staging
• Tumour markers (see above) should be measured
Management
• Orchidectomy (Inguinal approach)
• Chemotherapy and radiotherapy may be given depending on staging
• Abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node dissection.
Prognosis is generally excellent !!!

• 5 year survival for seminomas is around 95% if Stage I
• 5 year survival for teratomas is around 85% if Stage I
Benign disease
Epididymo-orchitis
Acute epididymitis is an acute inflammation of the epididymis, often involving the testis and usually caused by
bacterial infection.
• Infection spreads from the urethra or bladder. In men <35 years, gonorrhoea or chlamydia are the usual
infections.
• Amiodarone is a recognised non infective cause of epididymitis, which resolves on stopping the drug.
• Tenderness is usually confined to the epididymis, which may facilitate differentiating it from torsion where pain
usually affects the entire testis.
Testicular torsion
• Twist of the spermatic cord resulting in testicular ischaemia and necrosis.
• Most common in males aged between 10 and 30 (peak incidence 13-15 years)
• Pain is usually severe and of sudden onset.
• Cremasteric reflex is lost and elevation of the testis does not ease the pain.
• Treatment is with surgical exploration. If a torted testis is identified then both testis should be fixed as the
condition of bell clapper testis is often bilateral.
Teratoma and Seminoma difference
FEATURES TERATOMA SEMINOMA

Age 20-30; Can be cystic swelling 30-40; contains sheets of clear cells; Solid
swelling
% of tumor 40% 60%
Tumor α – fetoprotein Only β- HCG(in 5-10% pure cases); LDH
Markers(TM) β- HCG both can be present Everything can be normal also.
Cut surface Variegated Homogenous

Spread Lymphatic
In both cases initial Rx – Radical inguinal orchidectomy

Confined cases
Rx Close monitoring ē TM & CT scan Radio
In high risk cases: 2cycle chemo indicated monitoring ē TM & CT scan
Metastasis cases
Chemo Radio
& then if residual mass(+)ve -- RPLND Large LN involved --- Chemo(Etopocide;
Bleomycin; Cisplatin (Eradicate Ball Ca.)
● Testicular ca. involved testis removed by orchidectomy, remaining testis undescended but healthy--- biopsy must.
● CAUSE OF STERILE PYURIA : PATCH: Pyuria, - A Tough Condition To Hide…

P- Pregnancy,Prostatitis
A- Acute febrile illness, AGN
T- TB,Trauma,Transplant rejection,Treated UTI, sTone,
C- Corticosteroid use ,cyclophosphamide
H- H.influenza; Health exercise + BALANITIS
Haematuria
Causes of haematuria
Trauma • Injury to renal tract

• Renal trauma commonly due to blunt injury (others penetrating injuries)
• Ureter trauma rare: iatrogenic
• Bladder trauma: due to RTA or pelvic fractures
Infection • Remember TB
Malignancy • Renal cell carcinoma (remember paraneoplastic syndromes): painful or painless

• Urothelial malignancies: 90% are transitional cell carcinoma, can occur anywhere
along the urinary tract. Painless haematuria.
• Squamous cell carcinoma and adenocarcinoma: rare bladder tumours
• Prostate cancer
• Penile cancers: SCC
Renal disease • Glomerulonephritis
Stones • Microscopic haematuria common
Structural • Benign prostatic hyperplasia (BPH) causes haematuria due to hypervascularity of the
abnormalities prostate gland
• Cystic renal lesions e.g. polycystic kidney disease
• Vascular malformations
• Renal vein thrombosis due to renal cell carcinoma
Coagulopathy • Causes bleeding of underlying lesions
Drugs • Cause tubular necrosis or interstitial nephritis: aminoglycosides, chemotherapy

• Interstitial nephritis: penicillin, sulphonamides, and NSAIDs
• Anticoagulants
Benign • Exercise
Gynaecological • Endometriosis: flank pain, dysuria, and haematuria that is cyclical
Iatrogenic • Catheterisation
• Radiotherapy; cystitis, severe haemorrhage, bladder necrosis
Pseudohaematuria
● IVU is gold standard first IX for investigating painless macroscopic haematuria, 2nd Invx Cystourethroscopy
● UTI – deep stick test is (+) ve for nitrates
● UTI in children is commonly associated ē vesicoureteric reflux
● If uncomplicated & the pt. is systematically well, then UTI – most common cz is E.coli and this can be treated ē oral
Ciprofloxacin or Trimethoprim
● Ligation of middle rectal artery is most likely to affect the blood supply to the seminal vesicles
● Abdominal Mass
Nephroblastoma – if midline not crossed
Neuroblastoma – if midline crossed
● Polycystic changes are always bilateral and present from early childhood to old-age
RENAL STONES
Type Features % of
calculi
Calcium oxalate Hypercalciuria is a major risk factor (various causes) 85%

Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with
calcium making it more soluble
Stones are radio-opaque (though less than calcium phosphate
stones)
Hyperuricosuria may cause uric acid stones to which calcium
oxalate binds
Cystine Inherited recessive disorder of transmembrane cystine transport 1%

leading to decreased absorption of cystine from intestine and renal
tubule
Multiple stones may form

Relatively radiodense because they contain sulphur
Uric acid Uric acid is a product of purine metabolism 5-10%

May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown
e.g. malignancy
More common in children with inborn errors of metabolism
Radiolucent
Calcium phosphate May occur in renal tubular acidosis, high urinary pH increases 10%
supersaturation of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone
formation (types 2 and 4 do not)
Most Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate 2-20%

Occur as a result of urease producing bacteria (and are thus
associated with chronic infections)
Under the alkaline conditions produced, the crystals can precipitate
Slightly radio-opaque
Effect of urinary pH on stone formation

Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine metabolism will produce uric
acid. Then the urine becomes more alkaline (alkaline tide). When the stone is not available for analysis the pH of urine
may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5
Management of renal colic
Urolithiasis will affect up to 15% of the worldwide population. The development of sudden onset loin to groin pain which
is colicky in nature is a classic feature in the history. It is nearly always associated with haematuria that is either micro or
macroscopic.
Where the diagnosis is suspected the most sensitive and specific diagnostic test is helical, non contrast, computerised
tomographic (CT) scanning.
Shock wave lithotripsy

A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone
fragmentation. The passage of shock waves can result in the development of solid organ injury. Fragmentation of larger
stones may result in the development of ureteric obstruction. The procedure is uncomfortable for patients and analgesia
is required during the procedure and afterwards.
Ureteroscopy
A ureteroscope is passed retrograde through the ureter and into the renal pelvis. It is indicated in individuals (e.g.
pregnant females) where lithotripsy is contraindicated and in complex stone disease. In most cases a stent is left in situ
for 4 weeks after the procedure.
Percutaneous nephrolithotomy
In this procedure access is gained to the renal collecting system. Once access is achieved, intra corporeal lithotripsy or
stone fragmentation is performed and stone fragments removed.
Therapeutic selection
Disease Option
Stone burden of less than 2cm in aggregate Lithotripsy
Stone burden of less than 2cm in pregnant females Ureteroscopy
Complex renal calculi and staghorn calculi Percutaneous nephrolithotomy
Ureteric calculi less than 5mm Manage expectantly
Management (Basic words)

Most renal stones measuring less than 5mm in maximum diameter will typically pass within 4 weeks of symptom onset.
More intensive and urgent treatment is indicated in the presence of ureteric obstruction, renal developmental abnormality
such as horseshoe kidney and renal transplant. Ureteric obstruction due to stones together with infection is a surgical
emergency and the system must be decompressed. Options include nephrostomy tube placement, insertion of ureteric
catheters and ureteric stent placement.
In the non emergency setting the preferred options for treatment of stone disease include extra corporeal shock wave
lithotripsy, percutaneous nephrolithotomy, ureteroscopy, open surgery remains an option for selected cases. However,
minimally invasive options are the most popular first line treatment.
< 5mm size : 90% cases pass thru’ urine. Conservative Rx- 2wks
> 5mm size : if Obstruction features (RF/ Sepsis/ Solitary Kidney/ Continuing obstruction) present then
n
Nephrostomy. If no Nephrostomy option in answer key, then give Ureteric stent opt .
n n
[Gm(-)ve sepsis is common complicat of instrument renal tract. Organisms –E.coli & bacteroides. Prophylaxis
ē gentamicin recommended b4 surgery/ instrumentn ]
> 5mm size : NO Obstruction. Then find for the site of stone :-
st
Renal Pelvis : ESWL 1 line Rx . If Stag horn or Large stone, >2cm then PCNL
Upper pole calyx : ESWL ≤ 2cm
Lower pole calyx : PCNL, if >1cm, otherwise ESWL
Upper 1/3 ureter : “Push-Bang” or ESWL in situ
st
Middle 1/3 ureter : “Push-Bang”1 line Rx or USG, LASER, Lithoclast, Lithotripsy(if not consider surg.)
Lower 1/3 ureter : Dormia Basket or JJ stent.- (ureteroscopic removal, if mild obstruction)
● <2 cm size : ESWL (appropriate renal anatomy required)
● Stag horn or Large stone : PCNL(large stone); Upper UTI, Obstructed by stone,(size doesn’t matter)
● Small stone @ Collecting system : Flexible Uretero-Renoscopy + LASER Lithotripsy but Never ESWL
● ESWL contraindicated : Pregnancy; Impending AAA rupture; Urosepsis; Uncorected coagulopathy
● Bladder stone : Lithoclast Fragmentation but required surgery if > 5cm
● Cystine Calculi : Dissolves by alkaline diuresis
● Uric Acid Calculi : Formed by Thiazide diuetics & in primary polycythemia
● Nephrectomy is preferred if affected kidney has differential function <15%
● H/O urgency, frequency, nocturia + uroflowmetry flow rate >15ml = Bladder Instability is the most likely Dx.- such
case can be treated with antimuscarinic drug like Tolterodine.
nd
● NSAIDS either i/m or by suppository is 1st line Rx for renal colic. Strong opiates are regarded as appropriate 2 line.
● Diabetic nephropathy can be detected early by microalbuminuria. Histology shows diffuse and nodular
glomerulosclerosis
Hydronephrosis
Causes of hydronephrosis
Unilateral: PACT
• Pelvic-ureteric obstruction (congenital or acquired)
• Aberrant renal vessels
• Calculi
• Tumours of renal pelvis
Bilateral: SUPER
• Stenosis of the urethra
• Urethral valve
• Prostatic enlargement
• Extensive bladder tumour
• Retro-peritoneal fibrosis
Investigation
• USS- identifies presence of hydronephrosis and can assess the kidneys
• IVU- assess the position of the obstruction
• Antegrade or retrograde pyelography- allows treatment
• if suspect renal colic: CT scan (majority of stones are detected this way)
Management
• Remove the obstruction and drainage of urine
• Acute upper urinary tract obstruction: Nephrostomy tube
• Chronic upper urinary tract obstruction: Ureteric stent or a pyeloplasty
Hyperuricaemia
• Increased levels of uric acid may be seen secondary to either increased cell turnover or reduced renal excretion
of uric acid. Hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout
• Hyperuricaemia may be associated with hyperlipidaemia and hypertension. It may also be seen in conjunction
with the metabolic syndrome
Increased synthesis
• Lesch-Nyhan disease
• Myeloproliferative disorders
• Diet rich in purines
• Exercise
• Psoriasis
• Cytotoxics
Decreased excretion
• Drugs: low-dose aspirin, diuretics, pyrazinamide
• Pre-eclampsia
• Alcohol
• Renal failure
• Lead
● Renal Artery stenosis ---- ACE-inhibitor contraindicated.
● CONTRAINDICATION OF IVU :
Metformin therapy; Allergy to sea-food & iodine
Previous allergic reaction to IV contrast medium Pregnancy
● Focal segmental glomerulosclerosis is recognised complicn of renal transplantatn. Higher incidence in intravenous
drug abuser & HIV infection or AIDS. The condition presents with proteinuria, hypoalbuminaemia, edema &
hypercholesterolaemia. Biopsy reveals focal glomerular deposits of IgM
● Urine Plasma (U/P) Osmolarity Ratio
Pre-renal failure : Urine Na low & U/P ratio high.

Renal failure (due 2intrinsic dis./damage) : Urine Na high (failure of absorption) & U/P ratio low
Post-renal failure : CCR low & U/P ratio normal
● PUJ obstruction cause Dietl’s crisis - intermittent hydronephrosis characterized by a swelling in the loin after an
attack of acute renal pain, which disappears with the passage of urine.
VASCULAR
● Primary hypercoagulable states include
Factor V Leiden;
Hyperhomocysteinemia
Deficiencies of antithrombin;
Deficiencies of protein C& S.
these may b responsible for the so –called idiopathic DVT in which no apparent can be found. And rest of all
nd
are 2 ary hypercoagulable state.
n
● Primary hypercoagulable states / idiopathic DVT RX anticoagulation & further evaluat to find cause of
hypercoagulable state.
Claudication
Claudication is a condition in which patients develop pain in a limb during periods of exercise. The underlying disorder is
usually that of arterial insufficiency. Atheroma develops in the arterial wall and once this occludes >50-75% of the
lumenal diameter the supply to metabolising tissues distally may become compromised. The typical claudicant complains
of calf pain that is worse on exercise and relieved by rest. This typical description assumes that the SFA is the site of
disease, more proximal disease may present with other symptoms such as buttock claudication and impotence.
The history is usually a progressive one, patients presenting as an emergency with severe pain, diminished sensation,
pallor and absent pulses have critical limb ischaemia. This may complicate claudication and usually indicates a plaque
related complication, such as thrombosis.
Risk factors
Risk factors for claudication include smoking, diabetes and hyperlipidaemia.
Diagnosis
Diagnostic work -up includes measurement of ankle- brachial pressure indices, duplex scanning and formal
angiography.
Treatment
Those with long claudication distances, no ulceration or gangrene may be managed conservatively. Patients with rest
pain, ulceration or gangrene will almost always require intervention. All patients should receive an antiplatelet agent and
a statin unless there are compelling contra-indications.
Chronic venous insufficiency and Varicose veins
Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability. It is commoner in
women than men and is worse during pregnancy.
• Defined as saccular dilatation of veins (WHO)
The veins of the lower limb consist of an interconnected network of superficial and deep venous systems. Varices occur
because of localised weakness in the vein wall resulting in dilatation and reflux of blood due to non union of valve cusps.
• Histology: fibrous scar tissue dividing smooth muscle within media in the vessel wall
Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage resulting in localised
tissue damage coupled with impaired lymphatic flow.
• Affected veins: normally long and short saphenous veins
Diagnosis Typical symptoms of varicose veins include:

• Cosmetic appearance
• Aching
• Ankle swelling that worsens as the day progresses
• Episodic thrombophlebitis
• Bleeding
• Itching
Symptoms of chronic venous insufficiency include:

• Dependant leg pain
• Prominent leg swelling
• Oedema extending beyond the ankle
• Venous stasis ulcers
The typical venous stasis ulcer is:

• Located above the medial malleolus
• Indolent appearance with basal granulation tissue
• Variable degree of scarring
• Non ischaemic edges
• Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).
Differential diagnosis
• Lower limb arterial disease
• Marjolins ulcer
• Claudication
• Spinal stenosis
• Swelling due to medical causes e.g. CCF.
Exclusion of these differentials is by means of physical examination and ankle brachial pressure index measurement.
Examination
• Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix medial to the femoral
artery
• Brodie-Trendelenburg test: to assess level of incompetence
• Perthes' walking test: assess if deep venous system competent
Investigation
• Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
• Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)
All patients should have a Doppler assessment to assess for venous reflux and should be classified as having
uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency. In the history establishing a
thrombotic event (DVT/ lower limb fracture) is important and patients with such a history and all who have evidence of
chronic venous insufficiency should have a duplex scan performed.
Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan performed and the site
marked by scan on the day of surgery.
Treatment Indications for surgery:
• Cosmetic: majority
• Lipodermatosclerosis causing venous ulceration
• Recurrent superficial thrombophlebitis
• Bleeding from ruptured varix
Condition Therapy
Minor varicose veins - no Reassure/ cosmetic therapy

complications
Symptomatic uncomplicated In those without deep venous insufficiency options include foam sclerotherapy,
varicose veins saphenofemoral / popliteal disconnection, stripping and avulsions, compression stockings
Varicose veins with skin Therapy as above (if compression minimum is formal class I stockings)
changes
Chronic venous Class 2-3 compression stockings (ensure no arterial disease).

insufficiency or ulcers
• Application of formal compression stockings (usually class II/III)
In patients who have suffered ulceration, compression stockings should be worn long term. Where ulceration is present
and established saphenofemoral reflux exists this should be addressed surgically for durable relief of symptoms, either at
the outset or following ulcer healing.
• Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though transient blindness has
been reported. Endo venous laser therapy is another minimally invasive option
• Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV stripping and multiple phlebectomies
Trendelenburg procedure (sapheno-femoral junction ligation)

• Head tilt 15 degrees and legs abducted
• Oblique incision 1cm medial from artery
• Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein, Superficial and deep
external pudendal vein)
• SF junction double ligated
• Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous neuralgia if stripped more
distally
Venous thromboembolism: risk factors
ommon predisposing factors include malignancy, pregnancy and the period following an operation. The comprehensive
list below is partly based on the 2010 SIGN venous thromboembolism (VTE) guidelines:
General
• increased risk with advancing age
• obesity
• family history of VTE
• pregnancy (especially puerperium)
• immobility
• hospitalisation
• anaesthesia
• central venous catheter: femoral >> subclavian
Underlying conditions
• malignancy
• thrombophilia: e.g. Activated protein C resistance, protein C and S deficiency
• heart failure
• antiphospholipid syndrome
• Behcet's
• polycythaemia
• nephrotic syndrome
• sickle cell disease
• paroxysmal nocturnal haemoglobinuria
• hyperviscosity syndrome
• homocystinuria
Medication
• combined oral contraceptive pill: 3rd generation more than 2nd generation
• hormone replacement therapy
• raloxifene and tamoxifen
• antipsychotics (especially olanzapine) have recently been shown to be a risk factor
SIGN also state that the following are risk factors for recurrent VTE:
• unprovoked VTE
• male sex
• obesity
• thrombophilias
● Clinical Features:
Ulcer over ankle,
Developed over long period.
H/O DVT previously long before ulceration occured.
O/E
A superficial slough-based ulcer over medial malleolus ē no evidence of cellulites –1st invx of choice ABPI, 2nd
choice arteriogram.
RX
control of oedema,
treating any infectn & compresn.
n
… However, compressive dressings or devices should not be applied if the arterial circulat is impaired
● Contraindication Thrombolysis
- Possible hge in CT
- Systolic BP >185
- Head trauma in past 3months
- GIT or GUT bleed in past 3months
- Isolated, mild neurological deficits
- Rapidly improving deficit
● AAA <4cm ----1yr interval – USG follow up will do.

If ≥ 4cm ---- 6month interval follow up required
● Surgery indicated when an AAA ≥5.5 cm in diameter, although this subject to patient’s health and fitness for surgery.
● AAA elective intra-luminal repair can be done --- its position should be 2cm below the Renal arteries.
● Small femoral pseudoaneurysms (<6cm diameter) are best treated by Ultrasound Guided Compression (UGC).
● LERICHE’S SYNDROME
Atherosclerotic occlusive disease of AA & / or both Iliac Arteries czing buttock claudication, impotency etc.
● DVT- plasma expander ---Dextran70 used
● ATLS guidelines- recommended initial resuscitatn fluid is Ringer’s / Hartmann’s / Compound sodium lactate sol.
● Critical Ischaemia
- Rest-pain of at least 2 weeks’
- Requires regular adequate analgesia
- Ulceration or gangrene of the foot or toes
- Ankle pressure of < 50 mmHg or a toe pressure of < 30 mmHg.
● Indication of preoperative angiography in extremity vascular trauma

- Distal Ischaemia
- Diminished pulses
- Pulsatile or expanding Haematoma
- Penetrating injury in proximity to neurovascular structures
● Patency Rate 5YR

Aorto bifemoral : 90%
Femoro-femoral : 80%
Femoro-popliteal : 70%
Axillo-femoral : 60%
PTFE : 35%
● Venous conduit is recommended below knee. If suitable vein is not found then, prosthetic graft should be combined
ē vein collar or distal AV fistula to enhance patency rates
● An intermediate cause of graft failure (30 days to 2yrs) ---- Neointimal hyperplasia(NIH), occurs at proximal & distal
point. distal is more vulnerable. If occurs after 2yrs then atherosclerotic cause – main cause
● TIA; Bruit; Amaurosis Fugax ----- Carotid Duplex best diagnostic option
Lower leg ulcers
Venous
• Most due to venous hypertension, secondary to chronic venous insufficiency (other causes include calf pump
dysfunction or neuromuscular disorders)
• Ulcers form due to capillary fibrin cuff or leucocyte sequestration
• Features of venous insufficiency include oedema, brown pigmentation, lipodermatosclerosis, eczema
• Location above the ankle, painless
• Deep venous insufficiency is related to DVT and superficial venous insufficiency is associated with varicose
veins
• Doppler ultrasound looks for presence of reflux and duplex ultrasound looks at the anatomy/ flow of the vein
• Management: 4 layer compression banding after exclusion of arterial disease or surgery
2
• If fail to heal after 12 weeks or >10cm skin grafting may be needed
Marjolin's
• Squamous cell carcinoma
• Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
• Mainly occur on the lower limb
Arterial
• Occur on the toes and heel
• Painful
• There may be areas of gangrene
• Cold with no palpable pulses
• Low ABPI measurements
Neuropathic
• Commonly over plantar surface of metatarsal head and plantar surface of hallux
• The plantar neuropathic ulcer is the condition that most commonly leads to amputation in diabetic patients
• Due to pressure
• Management includes cushioned shoes to reduce callous formation
Pyoderma gangrenosum
• Associated with inflammatory bowel disease/RA
• Can occur at stoma sites
• Erythematous nodules or pustules which ulcerate
ULCERS
Arterial : DM patients; Very painful; Located over pressure areas; Classic “punched out” appearance
Venous : Above Medial malleolus, surrounding lipodermatosclerosis, eczema, pigmentation presents
n
Postphlebitic : H/O intermittently healing, shallow ulcer above medial malleolus; surrounding skin brown discolorat ;
h/o RTA, sustained pelvic #, treated with traction and bedrest.
n
Marjolin’s : Raised & rolled edges ē increase in granulat tissue; Chronic, bleeds readily >SCC/Marjolin’s
Curlings : Severe burn develops stress ulcer of these type
nd
Cushing’s : Stress ulcer 2 ary to head injury
n n n
Meleney’s : Underminig skin & s/c tissue ulcer, usually following a op czed by synergistic interact bet
non-hemolytic streptococci & aerobic hemolytic staphylococci
● NEUROPATHIC ULCERATION CZES
Peripheral nerve lesions : Diabetes, nerve injuries, leprosy,

Spinal cord lesions : Spina bifida, tabes dorsalis and syringomyelia
N
● LEVEL OF OCCLUS IN ARTERIAL DISEASE
Aorto-iliac : Impotence, Buttock claudication

Aorto-iliac and SFA : Rest pain and foot ulcers
External iliac/common femoral : Thigh claudication
SFA occlusion : Calf claudication
● Phlegmasia Caerula Doelns: 4Ps

P ainful
P urple
P urely congested & oedematous
P acked(congested) ileofemoral DVT
Rx – Limb elevation and i/v Heparin –

If unresponsive within 24hrs then thrombectomy or thrombolysis done
Ankle-Brachial Pressure Index (ABPI)

• Measurement of ankle- brachial pressure index (ABPI) is a commonly performed vascular investigation.
• Calculated by dividing lower limb pressure by the highest upper limb pressure.
Results of ABPI
1.2 or greater Usually due to vessel calcification, DM
1.0- 1.2 Normal
0.8-1.0 Minor stenotic lesion

Initiate risk factor management
0.50-0.8 Moderate stenotic lesion

Consider duplex
Risk factor management
If mixed ulcers present then avoid tight compression bandages
0.5- 0.3 Likely significant stenosis

Duplex scanning to delineate lesions needed
Compression bandaging contra indicated
Less than 0.3 Indicative of critical ischaemia

Urgent detailed imaging required
From pastest:
Normal: >0.90
Claudication: 0.50 -0.90
Rest pain: 0.21-0.49
Tissue loss: <0.20
>1.25: commonly seen in DM patients
Peripheral vascular disease
Indications for surgery to revascularise the lower limb

• Intermittent claudication
• Critical ischaemia
• Ulceration
• Gangrene
Intermittent claudication that is not disabling may provide a relative indication, whilst the other complaints are often
absolute indications depending upon the frailty of the patient.
Assessment
• Clinical examination
• Ankle brachial pressure index measurement
• Duplex arterial ultrasound
• Angiography (standard, CT or MRI): usually performed only if intervention being considered.
Angioplasty
In order for angioplasty to be undertaken successfully the artery has to be accessible. The lesion relatively short and
reasonable distal vessel runoff. Longer lesions may be amenable to sub-intimal angioplasty.
Surgery
Surgery will be undertaken where attempts at angioplasty have either failed or are unsuitable. Bypass essentially
involves bypassing the affected arterial segment by utilising a graft to run from above the disease to below the disease.
As with angioplasty good runoff improves the outcome.
Some key concepts with bypass surgery
Superficial femoral artery occlusion to the above knee

• Angioplasty may be attempted but otherwise these patients will require a femoro-popliteal bypass graft.
• Patency rates for Polytetrafluoroethylene (PTFE) and vein are similar, so PTFE preferred unless co-existing
infection makes use of prosthetic material undesirable.
Procedure
• Artery dissected out, IV heparin 3,000 units given and then the vessels are cross clamped
• Longitudinal arteriotomy
• Graft cut to size and tunneled to arteriotomy sites
• Anastomosis to femoral artery usually with 5/0 'double ended' Prolene suture
• Distal anastomosis usually using 6/0 'double ended' Prolene
Distal disease
• Femoro-distal bypass surgery takes longer to perform, is more technically challenging and has higher failure
rates.
• In elderly diabetic patients with poor runoff a primary amputation may well be a safer and more effective option.
There is no point in embarking on this type of surgery in patients who are wheelchair bound.
• In femorodistal bypasses vein gives superior outcomes to PTFE.
Rules
• Vein mapping 1st to see whether there is suitable vein (the preferred conduit). Sub intimal hyperplasia occurs
early when PTFE is used for the distal anastomosis and will lead to early graft occlusion and failure.
• Essential operative procedure as for above knee fem-pop.
• If there is insufficient vein for the entire conduit then vein can be attached to the end of the PTFE graft and then
used for the distal anastomosis. This type of 'vein boot' is technically referred to as a Miller Cuff and is
associated with better patency rates than PTFE alone.
• Remember the more distal the arterial anastomosis the lower the success rate.
Vascular disease
Aortic dissection • Chest pain (anterior chest pain- ascending aorta, back pain - descending aorta)
• Widening of aorta on chest x-ray
• Diagnosis made by CT scanning
• Treatment is either medical (Type B disease) or surgical (Type A disease)
Cervical rib • Supernumery fibrous band arising from seventh cervical vertebra
• Incidence of 1 in 500
• May cause thoracic outlet syndrome

• Treatment involves surgical division of rib
Subclavian steal • Due to proximal stenotic lesion of the subclavian artery

syndrome • Results in retrograte flow through vertebral or internal thoracic arteries
• The result is that decrease in cerebral blood flow may occur and produce syncopal
symptoms
• A duplex scan and/ or angiogram will delineate the lesion and allow treatment to be
planned
Takayasu's arteritis • Large vessel granulomatous vasculitis

• Results in intimal narrowing
• Most commonly affects young asian females
• Patients present with features of mild systemic illness, followed by pulseless phase
with symptoms of vascular insufficiency
• Treatment is with systemic steroids
Patent ductus • Ductus arteriosus is a normal foetal vessel that closes spontaneously after birth
arteriosus • Results in high pressure, oxygenated blood entering the pulmonary circuit
• Untreated patients develop symptoms of congestive cardiac failure
Coarctation of the • Aortic stenosis at the site of the ductus arteriosus insertion
aorta • Most common in boys and girls with Turners syndrome
• Patients may present with symptoms of arterial insufficiency, such as syncope and
claudication
• Blood pressure mismatch may be seen, as may mismatch of pulse pressure in the
upper and lower limbs
• Treatment is either with angioplasty or surgical resection (the former is the most
common)
Vasculitis
The vasculitides are a group of conditions characterised by inflammation of the blood vessel walls. This may, in turn,
compromise vessel integrity. Constitutional symptoms may be present. Whilst certain disease subtypes are reported to
affect specific vessels, there is often a degree of overlap clinically.
Vessel diameter and vasculitis classification
Aorta and branches • Takayasu's arteritis

• Buergers disease
• Giant cell arteritis
Large and medium sized arteries • Buergers disease

• Giant cell arteritis
• Polyarteritis nodosa
Medium sized muscular arteries • Polyarteritis nodosa
• Wegeners granulomatosis
Small muscular arteries • Wegeners granulomatosis

• Rheumatoid vasculitis
Specific conditions
Takyasu's arteritis • Inflammatory, obliterative arteritis affecting aorta and branches

• Females> Males; Asian
• Symptoms may include upper limb claudication
• Sometimes associated with renal artery stenosis
• Clinical findings include diminished or pulseless periphery
• ESR often affected during the acute phase
• Management: steroids
Buergers disease • Segmental thrombotic occlusions of the small and medium sized lower limb
vessels
• Commonest in young male smokers
• Proximal pulses usually present, but pedal pulses are lost
• An acuter hypercellular occlusive thrombus is often present
• Tortuous corkscrew shaped collateral vessels may be seen on angiography
Giant cell arteritis • Systemic granulomatous arteritis that usually affects large and medium sized
vessels
• Females > Males
• Temporal arteritis is commonest type
• Granulomatous lesions may be seen on biopsy (although up to 50% are normal)
Polyarteritis nodosa • Systemic necrotising vasculitis affecting small and medium sized muscular arteries
• Most common in populations with high prevalence of hepatitis B
• Renal disease is seen in 70% cases
• Angiography may show saccular or fusiform aneurysms and arterial stenoses
Wegeners • Predominantly affects small and medium sized arteries

granulomatosis • Systemic necrotising granulomatous vasculitis
• Cutaneous vascular lesions may be seen (ulceration, nodules and purpura)
• Sinus imaging may show mucosal thickening and air fluid levels
Treatment
Conditions such as Buergers disease are markedly helped by smoking cessation. Immunosupression is the main
treatment for vasculitides.
Vascular investigations
Venous disease
Venous Doppler
The simplest investigation for assessment of venous junctional incompetence is a Doppler assessment. This involves the
patient standing and manual compression of the limb distal to the junction of interest. Flow should normally occur in one
direction only. Where junctional incompetence is present reverse flow will occur and is relatively easy to identify.
Venograms and duplex scans

Structural venous information is historically obtained using a venogram. This is an invasive test and rarely required in
modern clinical practice. The most helpful test is a venous duplex scan which will provide information relating to flow and
vessel characteristics. Duplex is also useful in providing vein maps for bypass surgery.
Arterial disease
Ankle-brachial pressure
The ankle brachial pressure index measurement is an important investigation as it will allow classification of the severity
of the flow compromise present. False readings may occur in those with calcified vessels such as diabetics and results in
such settings should be interpreted with caution. When auscultating the vessel note should be made of the character of
the signal. Monophasic signals are associated with a proximal stenosis and reduction in flow. Triphasic signals provide
reassurance of a healthy vessel.
Arterial Duplex
As with the vein the duplex scan can provide a substantial amount of information about arterial patency and flow
patterns. In skilled hands they can provide insight as to the state of proximal vessels that are anatomically inaccessible to
duplex (e.g. Iliacs). Through assessment of distal flow patterns. It is an operator dependent test.
Conventional angiogram
Vessel puncture and catheter angiography is the gold standard method of assessing arteries. High quality information
can usually be obtained. Limitations of the technique include the risk of contrast toxicity and risks of vessel damage.
Severely calcified vessels may be difficult to puncture and in this situation a remote access site (e.g. brachial) may be
used. This technique is particularly useful in providing a distal arterial roadmap prior to femoro-distal bypass.
CT angiography
These tests provide a considerable amount of structural and flow information. They require contrast and thus carry the
risks associated with this. They are particularly useful in the setting of GI bleeding as they are rapidly available and can
be performed by a non vascular radiologist. However, they lack the facility for endovascular intervention. In general they
do not provide high enough resolution for distal arterial surgery.
Magnetic resonance angiography

This has the advantage of being non-invasive and not using nephrotoxic contrast. Movement artifact remains a problem
in some sites and distal arterial resolution is imperfect
HYPERLIPIDAEMIA
Remnant hyperlipidaemia (Type III hyperlipidaemia)

- ↑ Fasting cholesterol (usually >7.8mmol/l)
- ↑ Triglyceride levels (usually >5.0mmol/l)
- Palmar xanthomata
- Early onset cardiovascular disease (CAD, PVD, CVD).
Hypo alpha lipoproteinaemia

- Rare, familial condition
- Associated with ↓ HDL.
Chylomicronaemia
- ↑ Triglyceride and not with large ↑ in cholesterol.
Familial hyperlipidaemia
- LDL-receptor deficiency, & not associated with ↑ triglyceride levels
● Nicoladoni’s sign (+) ve means bradycardia after compression of AV fistula.
● SAMPLE QUESTION
A 68 year old man with critical limb ischaemia is undergoing a femoro-distal bypass graft. During mobilisation of the
proximal part of the posterior tibial artery which of the following is at greatest risk of injury?
A. Tibial nerve
B. Sciatic nerve
C. Saphenous nerve
D. Common peroneal nerve
E. Medial superior genicular artery
The tibial nerve is closely related to the posterior tibial artery. The tibial nerve crosses the vessel posteriorly
approximately 2.5cm distal to its origin. At its origin the nerve lies medial and then lateral after it crosses the vessel as
described.
Vascular disorders of the upper limb
Upper limb arterial disease is less common than lesions causing symptoms in the lower limb. The upper limb circulation
may be affected by embolic events, stenotic lesions (both internal and extrinsic), inflammatory disorders and venous
diseases.
The anatomy of the collateral circulation of the arterial inflow may impact on the history and nature of disease
presentation. In the region of the subclavian and axillary arteries the collateral vessels passing around the shoulder joint
may provide pathways for flow if the main vessels are stenotic or occluded. During periods of increased metabolic
demand the collateral flow is not sufficient and the vertebral arteries may have diminished flow. This may result in
diminished flow to the brain with neurological sequelae such as syncope.
Vascular disease of the upper limb
Condition Features
Axillary/ brachial • 50% of upper limb emboli will lodge in the brachial artery
embolus • 30% of upper limb emboli will lodge in the axillary artery
• Sudden onset of symptoms; pain, pallor, paresis, pulselessness, paraesthesia
• Sources are left atrium with cardiac arrhythmia (mainly AF), mural thrombus
• Cardiac arrhythmias may cause result in impaired consciousness in addition to the embolus
Arterial • Those resulting from atheroma are the most common, trauma may result in vascular changes
occlusions and long term occlusion but this is rare
• Features may include claudication, ulceration and gangrene. Proximally sited lesions may
result in subclavian steal syndrome
• The progressive nature of the disease allows development of collaterals, acute ischaemia
may occur as a result of acute thrombosis
Raynaud's • Idiopathic condition affecting young females

disease • Usually affects hands > feet
• Digits become: white -->blue -->red
• Treatment is with calcium antagonists
Upper limb • Gradual onset of upper limb swelling and discomfort.

venous • Sensation and motor function are normal
thrombosis
• Condition may complicate pre-existing malignancy (especially breast cancer) or arise as a
result of repetitive use of the limb in a task such as painting a ceiling
• The condition is diagnosed with duplex ultrasound and treatment is with anticoagulation
Cervical rib • 0.2-0.4% incidence

• Consist of an anomalous fibrous band that often originates from C7 and may arc towards, but
rarely reaches the sternum
• Congenital cases may present around the third decade, some cases occur following trauma
• Bilateral in up to 70%
• Compression of the subclavian artery may produce absent radial pulse on clinical
examination and in particular may result in a positive Adsons test (lateral flexion of the neck
away from symptomatic side and traction of the symptomatic arm- leads to obliteration of
radial pulse)
• Treatment is most commonly undertaken when there is evidence of neurovascular
compromise. A transaxillary approach is the traditional operative method for excision
Klippel-Trenaunay syndrome
Klippel-Trenaunay-Weber syndrome generally affects a single extremity, although cases of multiple affected limbs have
been reported. The leg is the most common site followed by the arms, the trunk, and rarely the head and the neck
Signs and symptoms

• One or more distinctive port-wine stains with sharp borders
• Varicose veins
• Limb lengthening
• Hypertrophy of bony and soft tissues, that may lead to local gigantism or shrinking.
• An improperly developed lymph system
• History since childhood
• Absence of thrill or bruit
In some cases, port-wine stains (capillary port wine type) may be absent. Such cases are very rare and may be classified
as "atypical Klippel-Trenaunay syndrome".
KTS can either affect blood vessels, lymph vessels, or both. The condition most commonly presents with a mixture of the
two. Those with venous involvement experience increased pain and complications
Leriche syndrome
Atheromatous disease involving the abdominal aorta and/or both of the iliac arteries. Blood flow to the pelvic viscera is
compromised. Patients may present with buttock claudication and impotence (in this particular syndrome). Diagnostic
work up will include angiography, where feasible iliac occlusions are usually treated with endovascular angioplasty and
stent insertion.
Management involves correcting underlying risk factors such as hypercholesterolaemia and stopping smoking.
Classically, it is described in male patients as a triad of symptoms:
1. Claudication of the buttocks and thighs

2. Atrophy of the musculature of the legs
3. Impotence (due to paralysis of the L1 nerve)
Cardiopulmonary bypass
Indications for surgery

• Left main stem stenosis or equivalent (proximal LAD and proximal circumflex)
• Triple vessel disease
• Diffuse disease unsuitable for PCI
The guidelines state that CABG is the preferred treatment in high-risk patients with severe ventricular dysfunction or
diabetes mellitus.
Technique
General anaesthesia
Central and arterial lines
Midline sternotomy or left sub mammary incision
Aortic root and pericardium dissected
Heart inspected
Bypass grafting may be performed using a cardiopulmonary bypass circuit with cardiac arrest or using a number of novel
'off pump' techniques.
Procedure cardiopulmonary bypass

• Aortic root cannulated
• Right atrial cannula
• Circuit primed and patient fully heparinised (30,000 Units unfractionated heparin) as the circuit is highly
thrombogenic
• Flow established through circuit
• Aortic cross clamp applied
• Cardioplegia solution instilled into the aortic root below cross clamp
• Heart now asystolic and ready for surgery
Off pump techniques are evolving on a constant basis and details are beyond the scope of the MRCS.
Conduits for bypass

> Internal mammary artery is best. Use of both is associated with increased risk of sternal wound dehiscence. However,
many surgeons will use both especially for redo surgery.
> Radial artery harvested from forearm. Ensure ulnar collateral working first!
> Reversed long saphenous vein grafts
Typically anastamosed using 7/0-8/0 prolene sutures (distally) and 6/0 prolene for top end.
Once flow established

Anticoagulation reversed using protamine
Patient is taken off bypass
Inotropes given if needed
Sternum closed using sternal closure device or stainless steel wire
Complications
• Post perfusion syndrome: transient cognitive impairment
• Non union of the sternum; due to loss of the internal thoracic artery
• Myocardial infarction
• Late graft stenosis
• Acute renal failure
• Stroke
• Gastrointestinal
Perioperative risk is quantified using the Parsonnet and Euroscores and unit outcomes are audited using this data.
DIS. ASSOCIATION PATHOLOGY CLINICAL FEATURE INVESTIGATIONS TREATMENT COMPLICATION *POINTS*

Down’s ● Ganglion Cell migratn ● Fail 2pass Meconium. ● Rectal Biopsy 3stage Surgery Enterocolitis
failure @ Hindgut ● Abd. Distention ± umbilicus Rect. Suctn -Neonat ● Defunctning Colostomy Abd. Dist; Bloody
HD ● Unco-ordinated displaced downwards Rect. Strip- older child ● Pull Thru’ Dirr.; Circulatory
Neonate peristalsis ● Bile Vomit., Chr. Constipn. ● Ba Enema: Conical look ● Colostomy Closure Collapse;Septicemia
● IO @Transitnl Zone ● Thrive failure ● AXR-fuid level must due to Cl. Diff.
80% TZ @ Rectum/ Sigmoid ●Flared costal margin.
(Short Seg. Dis.) 20% TZ
@whole colon (Long Seg.)
●Down’s ●Bile Vomit @ birth * persistant AXR Side to side Duodenoduodenostomy Passage of Meconium
DA ●Annular Pancreas ● Scaphoid Abd. Double Bubble sign Differs from HD
● Lead Point +ve ● Ileocolic common. ● Rectal Bleeding sp. ● USG(identifies target lesion) ● Pneumatic reductn(if no sign ● Perforation
(Ileal enlarged payer’s ● Ileoileal rare. Redcurrant jelly stool ● AXR(shows IO) peritonitis) ● Peritonitis
patch). Pathological LP is ● Sausage mass- tip ● Laparotomy & reduction
● IO(Small) ● Ba Enema(coiled spring,claw sign)
polyp/ Meckel’s
IT palpable thru’ PR ē blood followed by limited resctn if
●H/O Nephrectomy stained mucous@finger needed(Meckel’s / polyp)
5-9 M
● Bile Vomit; Right abd. mass
● Screaming, drawing up leg,
sleeping betn episode.
● Dehydratn ± peritonitis sign
Cystic fibrosis Intraluminal IO (due2 ● Abd. Dist., Bile Vomit; AXR ● Gastrograffin Enema ● Sweat test Na & Cl
Caucasian; Polyhydramnios viscous meconium due2 ● No meconium, empty rectum ● Mottled ground glass, soap bubble (Act As Detergent To Loose Meconium) >60 mmol/l- 1of the main
MCI points of MCI
pancreatic enz. Lack) ● No stool passed since birth ● Distended bowel coils ● Laparotomy, if perforation
● Fluid level ±
Premature baby Bacteria overwhelm the ● Abd. Dist.+ tenderness AXR ● Surgery ●Perforatn
● Bowel Necrosis immature intestine ● Feeding intolerance ● Bowel dilatatn ē multiple fluid level. ● Nasogastric decomprn ●Peritonitis
● Bloody Diarrhoea ●Gas in bowel wall & Portal V. indicates
● SIRS czing local infectn & ● Fuid, TPN, Antibiotic ●Shock
wall necrosis
SIRS ● Haematochaezia
NEC ● Abd.Wall erythema (adv.)
● Shock(septic), Lathergy
● Cholestasis +Jaundice(rare)
● Non-bileous Vomit projectile ● USG ● NPO

● ↓Cl +↓K = MAL ● Ba meal ● Ramstedt’s pyloromytomy
PS ● Dehydratn
3-6 wks ● Olive shaped pyloric mass
● Visible peristalsis + Jaundice(rare)
URTI ē H/O Prodromal ● Cervical Lymphadenopathy Cervical L. ;
Viral Illness ● Shifting Tenderness Lymphocytosis; Shifting
MA
tenderness differs from
5-10yr ● Temp >380C; ● Headache Appendicitis
●Circumoral pallor
● Mild abd. Pain
SIA 10% atresia multiple ●Abd. Dist. AXR(Multiple fluid level) Laparotomy + end to end
●Bile Vomit ansatomosis
HD:Hirschsprung’s; DA:Duodenal Atresia; IT:Intussp; MCI:Meconium ileus; NEC: Necrotizing enterocolitis; PS:pyloric stenosis; MA: Mes. Adenitis; SIA: Small Int.Atresia; MAL: Metaboloc Alkalosis
PAEDIATRIC SURGERY
Bronchogenic cysts
Overview
Bronchogenic cysts most commonly arise as a result of anomalous development of the ventral foregut. They are most
commonly single, although multiple cysts are described.
They often lie near the midline and most frequently occur in the region of the carina. They may be attached to the
tracheobronchial tree, although they are seldom in direct connection with it.
Cases may be asymptomatic or present with respiratory symptoms early in the neonatal period.
They are the second most common type of foregut cysts (after enterogenous cysts) in the middle mediastinum. Up to
50% of cases are diagnosed prior to 15 years of age.
Investigation
Many cases are diagnosed on antenatal ultrasound. Others may be detected on conventional chest radiography as a
midline spherical mass or cystic structure. Once the diagnosis is suspected a CT scan should be performed.
Treatment
Thorascopic resection is the ideal treatment. Very young babies can be operated on once they reach six weeks of age.
Biliary atresia
• 1 in 17000 affected
• Biliary tree lumen is obliterated by an inflammatory cholangiopathy causing progressive liver damage
Clinical features
• Infant well in 1st few weeks of life
• No family history of liver disease
• Jaundice in infants > 14 days in term infants (>21 days in pre term infants)
• Pale stool, yellow urine (colourless in babies)
• Associated with cardiac malformations, polysplenia, situs inversus
Investigation
• Conjugated bilirubin (prolonged physiological jaundice or breast milk jaundice will cause a rise in unconjugated
bilirubin, whereas those with obstructive liver disease will have a rise in conjugated bilirubin)
• Ultrasound of the liver (excludes extrahepatic causes, in biliary atresia infant may have tiny or invisible
gallbladder)
• Hepato-iminodiacetic acid radionuclide scan (gooduptake but no excretion usually seen)
Management
• Early recognition is important to prevent liver transplantation.

• Nutritional support.
• Roux-en-Y portojejunostomy (Kasai procedure)
• If Kasai procedure fails or late recognition, a liver transplant becomes the only option.
Alagille syndrome autosomal dominant disorder characterised by presence of paucity of bile ducts and cardiac defects.
Only the embryonic form of biliary atresia is associated with cardiac and other embryological defects.
Bilious vomiting in neonates
Causes of intestinal obstruction with bilious vomiting in neonates
Disorder Incidence and Age at presentation Diagnosis Treatment

causation
Duodenal 1 in 5000 (higher in Few hours after birth AXR shows "double Duodenoduodenostomy
atresia Downs syndrome) bubble sign, contrast
study may confirm
Malrotation Usually cause by Usually 3-7 days after Upper GI contrast Ladd's procedure
with volvulus incomplete rotation birth, volvulus with study may show DJ
during compromised circulation flexure is more
embryogenesis may result in peritoneal medially placed, USS
signs and may show abnormal
haemodynamic orientation of SMA
instability and SMV
Jejunal/ ileal Usually caused by Usually within 24 hours AXR will show air- Laparotomy with primary
atresia vascular of birth fluid levels resection and anastomosis
insufficiency in utero,
usually 1 in 3000
Meconium Occurs in between Typically in first 24-48 Air - fluid levels on Surgical decompression, serosal
ileus 15 and20% of those hours of life with AXR, sweat test to damage may require segmental
babies with cystic abdominal distension confirm cystic fibrosis resection
fibrosis, otherwise 1 and bilious vomiting
in 5000
Necrotising Up to 2.4 per 1000 Usually second week of Dilated bowel loops Conservative and supportive for
enterocolitis births, risks life on AXR, pneumatosis non perforated cases,
increased in and portal venous air laparotomy and resection in
prematurity and cases of perforation of ongoing
inter-current illness clinical deterioration
Nephroblastoma (Wilms tumours)
• Usually present in first 4 years of life

• May often present as a mass associated with haematuria (pyrexia may occur in 50%)
• Often metastasise early (usually to lung)
• Treated by nephrectomy
• Younger children have better prognosis (<1 year of age =80% overall 5 year survival)
Paediatric Gastrointestinal disorders
Pyloric stenosis • M>F

• 5-10% Family history in parents
• Projectile non bile stained vomiting at 4-6 weeks of life
• USS diagnosis
• Treatment: Ramstedt pyloromyotomy
Acute appendicitis • Uncommon under 3 years

• When occurs may present atypically
Mesenteric adenitis • Central abdominal pain and URTI

• Conservative management
Malrotation • High caecum at the midline

• Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
Hirschsprung's disease • Absence of ganglion cells from myenteric and submucosal plexuses
• Occurs in 1/5000 births
• Full thickness rectal biopsy for diagnosis
• Delayed passage of meconium and abdominal distension
Oesophageal atresia • Associated with tracheo-oesophageal fistula and polyhydramnios

• PC choking and cyanotic episodes
• VACTERL
Meconium ileus • Majority have cystic fibrosis

• X-Rays will not show a fluid level as the meconium is viscid
Biliary atresia • Jaundice > 14 days

• Increased conjugated bilirubin
• Urgent Kasai procedure
Necrotising • Prematurity is the main risk factor

enterocolitis • Early features include abdominal distension and passage of bloody stools
• X-Rays may show pneumatosis intestinalis and evidence of free air
• Increased risk when empirical antibiotics are given to infants beyond 5 days
Paediatric inguinal hernia
Inguinal hernias are a common disorder in children. They are commoner in males as the testis migrates from its location
on the posterior abdominal wall, down through the inguinal canal. A patent processus vaginalis may persist and be the
site of subsequent hernia development.
Children presenting in the first few months of life are at the highest risk of strangulation and the hernia should be repaired
urgently. Children over 1 year of age are at lower risk and surgery may be performed electively. For paediatric hernias a
herniotomy without implantation of mesh is sufficient. Most cases are performed as day cases.
Paediatric proctology
Children may present with altered bowel habit and/ or rectal bleeding. Classical haemorroidal disease is relatively rare in
children. Painful bright red rectal bleeding is much more common since constipation is a relatively common childhood
disorder. The hard stool causes a tear of the ano-rectal mucosa with subsequent fissure. The pain from the fissure must
be addressed promptly or the child will delay defecation and this fissure will worsen.
Inflammatory bowel disease may present in a similar pattern in paediatric practice with altered bowel habit (usually
diarrhoea) and bleeding. Systemic features may be present and investigation with an endoscopy may be required.
Children with intussceception usually present at a relatively young age and the history is usually one of colicky abdominal
pain, together with a mass on clinical examination.The often cited red current jelly type stool is a rare but classical
feature.
Juvenile polyps may occur as part of the familial polyposis coli syndromes. The lesions, which are hamartomas, are often
cherry red if they protrude externally.
Testicular disorders-paediatric
Cryptorchidism
• The embryological descent of the testicle from within the abdominal cavity may be subject to a number of
variations. Distinctions need to be made clinically from a non descended testis and a testis that is retractile.
• Testis that lie outside the normal path of embryological descent are termed ectopic testis. Undescended testis
occurs in 1% of male infants. Where the testis does not lie in an intra scrotal location, its location should be
ascertained. Where both testes are absent the infant may be intersex.
• MRI scanning may reveal intra-abdominal testes; however a GA is often needed to perform this investigation in
this age group.
• Testes that are undescended should be placed in the scrotum after 1 year of age as the testosterone surge that
may facilitate descent occurs at 6 months of age.
• Where the testes lie distally e.g. Superficial inguinal pouch an open orchidopexy is the procedure of choice.
• With abdominal testes a laparoscopy should be performed. The risk of seminoma is increased in individuals
with a non descended testes and this risk is not reduced by orchidopexy.
Testicular torsion
• Typically the patient has severe sudden onset of scrotal pain. The difficulty in paediatric practice is the lack of
clear history.
• On examination the testis is tender and enlarged.
• Management is by surgical exploration.
• Delay beyond 6 hours is associated with low salvage rates.
• A torted hyatid produces pain that is far more localised and the testis itself should feel normal. However,
diagnostic doubt often exists and in such cases surgical exploration is warranted.
Paediatric umbilical disorders
Embryology
During development the umbilicus has two umbilical arteries and one umbilical vein. The arteries are continuous with the
internal iliac arteries and the vein is continuous with the falciform ligament (ductus venosus). After birth the cord
dessicates and separates and the umbilical ring closes.
Umbilical hernia
Up to 20% of neonates may have an umbilical hernia, it is more common in premature infants. The majority of these
hernias will close spontaneously (may take between 12 months and three years). Strangulation is rare.
Paraumbilical hernia
These are due to defects in the linea alba that are in close proximity to the umbilicus. The edges of a paraumbilical
hernia are more clearly defined than those of an umbilical hernia. They are less likely to resolve spontaneously than a
paraumbilical hernia.
Omphalitis
This condition consists of infection of the umbilicus. Infection with Staphylococcus aureus is the commonest cause. The
condition is potentially serious as infection may spread rapidly through the umbilical vessels in neonates with a risk of
portal pyaemia, and portal vein thrombosis. Treatment is usually with a combination of topical and systemic antibiotics.
Umbilical granuloma
These consist of cherry red lesions surrounding the umbilicus, they may bleed on contact and be a site of seropurulent
discharge. Infection is unusual and they will often respond favorably to chemical cautery with topically applied silver
nitrate.
Persistent uranchus
This is characterised by urinary discharge from the umbilicus. It is caused by persistence of the uranchus which attaches
to the bladder. They are associated with other urogenital abnormalities.
Persistent vitello-intestinal duct

This will typically present as an umbilical discharge that discharges small bowel content. Complete persistence of the
duct is a rare condition. Much more common is the persistence of part of the duct (Meckels diverticulum). Persistent
vitello-intestinal ducts are best imaged using a contrast study to delineate the anatomy and are managed by laparotomy
and surgical closure.
Urethral valves
Posterior urethral valves are the commonest cause of infravesical outflow obstruction in males. They may be diagnosed
on ante natal ultrasonography. Because the bladder has to develop high emptying pressures in utero the child may
develop renal parenchymal damage. This translates to renal impairment noted in 70% of boys at presentation. Treatment
is with bladder catheterisation. Endoscopic valvotomy is the definitive treatment of choice with cystoscopic and renal
follow up.
Cryptorchidism
A congenital undescended testis is one that has failed to reach the bottom of the scrotum by 3 months of age. At birth up
to 5% of boys will have an undescended testis, post natal descent occurs in most and by 3 months the incidence of
cryptorchidism falls to 1-2%. In the vast majority of cases the cause of the maldescent is unknown. A proportion may be
associated with other congenital defects including:
Patent processus vaginalis

Abnormal epididymis
Cerebral palsy
Mental retardation
Wilms tumour
Abdominal wall defects (e.g. gastroschisis, prune belly syndrome)
Reasons for correction of cryptorchidism

• Reduce risk of infertility
• Allows the testes to be examined for testicular cancer
• Avoid testicular torsion
• Cosmetic appearance
Males with undescended testis are 40 times as likely to develop testicular cancer (seminoma) as males without
undescended testis
The location of the undescended testis affects the relative risk of testicular cancer (50% intra-abdominal testes)
Treatment
• Orchidopexy at 6- 18 months of age. The operation usually consists of inguinal exploration, mobilisation of the
testis and implantation into a dartos pouch.
• Intra-abdominal testis should be evaluated laparoscopically and mobilised. Whether this is a single stage or two
stage procedure depends upon the exact location.
• After the age of 2 years in untreated individuals the Sertoli cells will degrade and those presenting late in
teenage years may be better served by orchidectomy than to try and salvage a non functioning testis with an
increased risk of malignancy.
Hypospadias
The urethral meatus opens on the ventral surface of the penis. There is also a ventral deficiency of the foreskin. The
uretral meatus may open more proximally in the more severe variants. However, 75% of the openings are distally
located. The incidence is 1 in 300 male births.
Features include:
• Absent frenular artery
• Ventrally opened glans
• Skin tethering to hypoplastic urethra
• Splayed columns of spongiosum tissue distal to the meatus
• Deficiency of the foreskin ventrally
Management:
• No routine cultural circumcisions
• Urethroplasty
• Penile reconstruction
The foreskin is often utilised in the reconstructive process. In boys with very distal disease no treatment may be needed.
SKIN LESIONS
Port Wine Stain Or Deep Capillary Neavus
- Never cross mid-line

- Associated intracranial vascular malformation resulting in convulsions and delayed development, known as Sturge–
Weber syndrome
- Congenital glaucoma if lesion occurs in ophthalmic division of trigeminal nerve
- Hypertrophy of underlying tissues, eg the limb, causing abnormal growth known as haemangiectatic hypertrophy.
Benign skin diseases
Seborrhoeic keratosis
• Most commonly arise in patients over the age of 50 years, often idiopathic
• Equal sex incidence and prevalence
• Usually multiple lesions over face and trunk
• Flat, raised, filiform and pedunculated subtypes are recognised
• Variable colours and surface may have greasy scale overlying it
• Treatment options consist of leaving alone or simple shave excision
Melanocytic naevi
Congenital melanocytic • Typically appear at, or soon after, birth

naevi • Usually greater than 1cm diameter
• Increased risk of malignant transformation (increased risk greatest for large
lesions)
Junctional melanocytic • Circular macules

naevi • May have heterogeneous colour even within same lesion
• Most naevi of the palms, soles and mucous membranes are of this type
Compound naevi • Domed pigmented nodules up to 1cm in diameter

• Arise from junctional naevi, usually have uniform colour and are smooth
Spitz naevus • Usually develop over a few months in children

• May be pink or red in colour, most common on face and legs
• May grow up to 1cm and growth can be rapid, this usually results in excision
Atypical naevus • Atypical melanocytic naevi that may be autosomally dominantly inherited
syndrome • Some individuals are at increased risk of melanoma (usually have mutations of
CDKN2A gene
- Many people with atypical naevus syndrome AND a parent sibling with melanoma will
develop melanoma
Epidermoid cysts
• Common and affect face and trunk
• They have a central punctum, they may contain small quantities of sebum
• The cyst lining is either normal epidermis (epidermoid cyst) or outer root sheath of hair follicle (pilar cyst)
Dermoid cysts
They are most common in the midline of the neck, external angle of the eye and posterior to the pinna of the ear.
They may develop at other sites such as the ovary and in these sites are synonymous with teratomas.
They typically have multiple inclusions such as hair follicles that bud out from its walls.
Desmoid Tumor
A desmoid tumour may be classified either as low grade fibrosarcomas or non aggressive fibrous tumours.
They commonly present as large infiltrative masses. They may be divided into abdominal, extra abdominal and intra
abdominal. All types share the same biological features.
Extra abdominal desmoids have an equal sex distribution and primarily arise in the musculature of the shoulder,
chest wall, back and thigh.
Abdominal desmoids usually arise in the musculoaponeurotic structures of the abdominal wall.
Intra abdominal desmoids tend to occur in the mesentery or pelvic side walls and occur most frequently in patients
with familial adenomatous polyposis coli syndrome.
Dermatofibroma
• Solitary dermal nodules
• Benign lesion.
• Usually history of trauma.
• Usually affect extremities of young adults
• Lesions feel larger than they appear visually
• Histologically they consist of proliferating fibroblasts, histiocytes, blood vessels and fibrotic changes merging
with sparsely cellular dermal tissues
Painful skin lesions

• Eccrine spiradenoma
• Neuroma
• Glomus tumour
• Leimyoma
• Angiolipoma
• Neurofibroma (rarely painful) and dermatofibroma (rarely painful)
Dermatitis Herpetiformis
• Chronic itchy clusters of blisters.
• Linked to underlying gluten enteropathy (coeliac disease).
Pyogenic granuloma
• Overgrowth of blood vessels- Red nodules,
• Usually follow trauma.
• May mimic amelanotic melanoma.
Acanthosis Nigricans
• Brown to black, poorly defined, velvety hyperpigmentation of the skin.
• Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin, umbilicus,
forehead, and other areas.
• The most common cause of Acanthosis Nigricans is insulin resistance, which leads to increased circulating
insulin levels. Insulin spillover into the skin results in its abnormal increase in growth (hyperplasia of the skin).
In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then commonly
referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare and suggests a coexisting
malignant condition
Sebaceous cysts
• Originate from sebaceous glands and contain sebum.

• Location: anywhere but most common scalp, ears, back, face, and upper arm (not palms of the hands and soles
of the feet).
• They will typically contain a punctum.
• Excision of the cyst wall needs to be complete to prevent recurrence.
• A Cock's 'Peculiar' Tumour is a suppurating and ulcerated sebaceous cyst. It may resemble a squamous cell
carcinoma- hence its name.
Keratoacanthoma
• Generally benign lesions although some do view them as precursors of malignancy
• Dome shaped erythematous lesions that develop over a period of days
• Grow rapidly. They often contain a central pit of keratin.
• Begin to necrose and slough off.
• May be treated by curettage and cautery. If there is diagnostic doubt (they can mimic malignancy) then formal
excision biopsy is warranted.
Koebner phenomenon
The Koebner phenomenon describes skin lesions which appear at the site of injury. It is seen in:
• Psoriasis
• Vitiligo
• Warts
• Lichen planus
• Lichen sclerosus
• Molluscum contagiosum
Malignant Skin Diseases

Skin malignancies include Basal Cell Carcinoma, Squamous Cell Carcinoma and Malignant Melanoma.
Basal Cell Carcinoma (Rodent Ulcer)

• Most common form of skin cancer - occur on sun exposed sites apart from the ear.
• It originates from cells in the stratum germinativum of hair-bearing skin
• Typically slow growing with low metastatic potential.
• As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is
planned.
Risk Factors
Clinical Features
Nodular BCC Commonest variant (60%) - Usually affect the face

Raised translucent papular Lesion
Rolled edges with Pearly sheen
Central depression or ulceration
Superficial Telangiectasia
Large nodular BCC's are locally destructive
Cystic BCC Often have clear or blue - grey appearance

Cystic degeneration may not clinically evident and tumour may resemble nodular BCC
Superficial BCC Usually appears as Superficial Erthematous Macule affecting the Trunk
Younger age at presentation
May show areas of spontaneous regression
Horizontal growth pattern
High recurrence rate (due to sub clinical lateral spread)
Morpheaform BCC Flat, slightly atrophic lesion or plaque without well defined borders
Tumour has sub clinical lateral spread which increases recurrence rates
Basosquamous carcinoma Atypical BCC

Basaloid histological BCC features with eosinophillic squamoid features of SCC
Biologically more aggressive and are more locally destructive

Rare lesion accounts for 1% of all non melanoma skin cancers
Metastatic disease may occur in 9-10% of cases and resemble an SCC
Fig:9.1
Treatment
Surgery
Curettage and electrodesiccation
Common treatment for small BCC.

Might need to be repeated to make sure that all of the cancer has been removed.
Excision:
Used to remove BCCs, along with a margin of normal skin.
Mohs Surgery
Has the best cure rate for BCC.

It’s used in treating
- Large tumors,
- Tumors where the edges are not well-defined,
- Tumors in certain locations (on or near the nose, eyes, ears, forehead, scalp, fingers, and genital area)
- Those that have come back after other treatments.
Radiation therapy
This is ideal for tumors which are hard to manage surgically.
Good option for treating who are not able to tolerate surgery - Elderly patients or others in poor health.
Cure rates are around 90 percent. Radiotherapy is as effective as standard surgery
Not used in sensitive sites such as the periocular area.
Involve long-term cosmetic problems and radiation risks
It’s also sometimes used after surgery if it’s not clear that all of the cancer has been removed.
Immune response modifiers, photodynamic therapy, or topical chemotherapy

Used for treating very superficial tumors.
Follow-up is needed because these treatments do not destroy any cancer cells that are deep under the surface.
Cryosurgery
Used for some small BCC but is not usually recommended for larger tumors - ( can be used to treat large tumors in
one treatment session to relieve symptoms from the cancer)
Done on certain parts of the nose, ears, eyelids, scalp, or legs.
The site of treatment often takes a month or two to heal.
Topical Medication(Just remember the black heeading, not so important)

Imiquimod: Only for superficial BCCs, with cure rates generally between 80 and 90 percent. The cream is rubbed
gently into the tumor five times a week for up to six weeks or longer. The first in a new class of drugs that work
by stimulating the immune system, it causes the body to produce interferon, a chemical that attacks cancer.
5-Fluorouracil (5-FU): For superficial BCCs, with similar cure rates to imiquimod. The liquid or cream is gently
rubbed into the tumor twice a day for three to six weeks. Side effects are variable, and some patients do not
experience any discomfort, but redness, irritation, and inflammation usually occur.
Targeted therapy for advanced BCC
Used in rare cases where basal cell cancers spread to other parts of the body or can’t be cured with surgery or
radiation therapy.
Oral Vismodegib (Erivedge) taken daily - often shrink or slow their growth..
Squamous Cell Carcinoma

• Related to sun exposure; Commonest in fair skinned individuals
• Second most common skin malignancy; Derived from epidermal keratinocytes
• May arise in pre - existing solar keratoses.
• May metastasise if left - has a low but significant potential for metastasis to lymph nodes
• May occur in perianal and genital skin especially in association with HPV 16 and 18 infections.
• Wide local excision is the treatment of choice and where a diagnostic excision biopsy has demonstrated SCC,
repeat surgery to gain adequate margins may be required.
Groups At High Risk
Renal transplant and on immunosuppression
Individuals with HIV
Those who have received psoralen UVA therapy
Chronic wounds (Marjolins ulcer)
Xeroderma pigmentosum
Oculocutaneous albinism
Pre-malignant Lesion of SCC
Actinic keratosis and SCC

• The primary lesion is a rough eryhtematous papule with a white to yellow scale.
• Lesions are typically clustered at sites of chronic sun exposure.
Bowen's Disease / SCC in situ

• It is also called intra-epidermal squamous or in situ SCC.
• Erythematous scaling patch or elevated plaque arising on sun exposed skin in an elderly patient.
• Lesions may arise de novo or from pre-existing actinic keratosis.
• Pathologically there is full thickness atypia of dermal keratinocytes over a broad zone. Nuclear
pleomorphism,
apoptosis and abnormal mitoses are all seen.
Staging of SCC
Treatment
Prognosis
Good Prognosis Poor prognosis
Well differentiated tumours Poorly differentiated tumours
<20mm diameter >20mm in diameter
<2mm deep >4mm deep
No associated diseases Immunosupression for whatever reason
Definitions
Lentigo : Normal position – Increased amount Melanocyte, Normal amount Melanin produced
Freckle : Normal position – Normal amount Melanocyte, Increased amount Melanin produced
Mole / : Cluster position – Increased amount Melanocyte, Increased amount Melanin produced
pigmented neavus
Malignant Melanoma
Risk Factors
NAME AGE SITE PATHx C/F

Most Any part but mainly - Palpable; Rapidly growing
common - Legs+ arms in - Thin but irregular edges
(64%) women - Variegated color;
SUPERFICIAL - Trunk region in - Itchy, give discomfort, or
SPREADING men. bleed
- Single flat black-brown area
< 0.76 mm have a ē irregular margin surrounded
Good prognosis by multiple smaller brown
lesions
Young - Affect Females; - Thick protruding ē smooth

patient - Mostly lower leg surface
NODULAR 27% involved - Regular convex outline;
- Most malignant - Itchy
- have a pronounced - May become ulcerated &
vertical growth phase bleeds
- Poor prognosis
7% - @ face - Arising in Hutchinson’s - Malignant area is thicker

- Older person Melanotic Freckle - Darker area but seldom
LENTIGO - Least Malignant - Malignant melanoma cell @ ulcerate
MALIGNA - < 0.76 mm have a dermis
Good prognosis - Atrophy of epidermis
1% - Thick Epidermis - Irregular expanding area of
ACRAL Rare type - Palm, sole,Beneath brown or black pigmentation
LENTIGINOUS the nail - Present as chronic
- Afro-Caribbean paronychia or subangual
people Hematoma
1% - Poor prognosis - Classically, pink or red,
AMELANOTIC Least - May occur in any appearing as erythematous - Presents ē LN involvement
common of above 4 variants Papules or nodules. - Occasionally appear light
- No melanin brown or tan with grey edges
- Irregular Edges/Margins
● Most melanoma stains S-100 (+)ve in immunohistochemical stains
AJCC CLASSIFICATION (American Joint Committee on Cancer)
Stage
• 0 – Tis, N0, M0
• I – T1a–T2a, N0, M0
• II – T2b–T4b, N0, M0
• III – Any T, N1–3, M0
• IV – Any T, any N, M1a–c
The main diagnostic features (major criteria): Secondary features (minor criteria)
• Change in size • Diameter >6mm
• Change in shape • Inflammation
• Change in colour • Oozing or bleeding
• Altered sensation
For patients of stage I/II, no further investigation is required before management of the primary lesion.
Stage III patients should have a CT scan of the head (controversial), chest, abdomen and pelvis, before node
dissection.
Stage IV patients should have whole-body CT and measurement of Serum LDH , plus PET
Treatment
• Suspicious lesions should undergo excision biopsy(2mm margin). The lesion should be removed in completely
as incision biopsy can make subsequent histopathological assessment difficult.
• Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-
exicision of margins is required
Margins of Excision (Breslow Thickness)
Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph
node groups should be selectively applied.
From pastest online resource
<0.75 mm thickness: 2mm margin;
0.75 – 1.5 mm thickness : upto 20mm marjin;
1.5 – 3 mm or >3 mm thickness: 50 mm margin
Kaposi Sarcoma
• Tumour of vascular and lymphatic endothelium.
• Purple cutaneous nodules.
• Associated with immunosupression.
• Classical form affects elderly males and is slow growing.
• Immunosupression form is much more aggressive and tends to affect those with HIV related disease.
Merkel cell tumours of the skin
• Rare but aggressive tumour.

• Develops from intra epidermal Merkel cells.
• Usually presents on elderly, sun damaged skin. The periorbital area is the commonest site.
• Histologically these tumours appear within the dermis and subcutis. The lesions consist of sheets and nodules
of small hyperchromatic epithelial cells with high rates of mitosis and apoptosis. Lymphovascular invasion is
commonly seen.
• Pre-existing infection with Merkel Cell Polyomavirus is seen in 80% cases.
Treatment
Surgical excision is first line. Margins of 1cm are required. Lesions >10mm in diameter should undergo sentinel lymph
node biopsy. Adjuvant radiotherapy is often given to reduce the risk of local recurrence.
Prognosis
• With lymph node metastasis 5 year survival is 50% or less.
• Small lesions without nodal spread are usually associated with a 5 year survival of 80%.
Treatment Of Suspicious Skin Lesions

Skin lesions may be referred to surgeons for treatment or discovered incidentally. Table below outlines various
therapeutic options:
Method Indication
Tru-cut Most often used for percutaneous sampling of deep seated lesions or used intra operatively for
biopsy visceral lesions
5mm Diagnostic confirmation of lesions suspected to be benign or where the definitive management is
punch unlikely to be surgical.
biopsy Limited usefulness in pigmented lesions where they do not include sufficient tissue for accurate
diagnosis.
May be used in non melanoma type skin disease to establish diagnosis prior to more extensive
resection.
Wide Where the complete excision of the lesion (with healthy margins) is the main objective. In
excision cosmetically sensitive sites, or where the defect is large, this may need to be complemented with
plastic surgical techniques
Incisional Used mainly for deep seated or extensive lesions where there is diagnostic doubt (usually
biopsy following core or tru-cut biopsy). Used rarely for skin lesions.
Diagnostic Primarily used for lesions that are suspicious for melanoma, the lesion is excised with a rim of
excision normal tissue. Excision of margins may be required subsequently.
Suspicious naevi should NOT be partially sampled as histological interpretation is severely compromised. Complete
excision is mandatory where lesions fulfil diagnostic criteria. However, wide excision for margins may be deferred until
definitive histology is available.
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Nasa Khan MRCS A Notes 2018 PDF

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What are the important muscle attachments and related information about the superior extremity?

What are the important muscle attachments and related information about the superior extremity?

What are the functions and innervations of the Brachioradialis muscle?

What are the functions and innervations of the Brachioradialis muscle?

MRCS NoTes

IMPORTANT MUSCLE ATTACHMENT AND RELATED INFORMATION

● 7 muscles attach the Scapula to the chest wall: PORTaLS

● MUSCLES OF F.ARM: (Med. to Lat.) (N-416)

● COMMON FLEXOR ORIGIN (N-416) : PT; PL; FCU; FCR; FDS

● SERRATUS ANTERIOR: INNERVATION AND ACTION: SALT- 567

● Deltoid: Proximal attachments CLASs:

Important Nerve and related infos

● MOVEMENT SEGMENTAL INNERVATION

Wrist flexion/extension C6/C7 extension C6

Brachial Plexus (Also see the Chart Note)

Divisions located at Axilla

Features of Erbs Palsy

During Child birth Lower trunk (C7,8, T1 ) injured.

Radial nerve C5-8 + T1(N-446-47)

Continuation of posterior cord of the brachial plexus (root values C5 to T1)

● RADIAL NERVE: MUSCLES SUPPLIED (SIMPLIFIED)

● RADIAL NERVE PATH

At the Spiral Groove

- Loss of Thumb Extension - Thumb drop

After Piercing the Supinator (Posterior Interosseus Nerve)

Ulnar nerve C7- 8 + T1 (N-445)

Damage at the elbow • Radial deviation of the wrist

ULNAR NERVE PALSY TESTS

• Egawa test (to check dorsal interossei of middle finger)

Median nerve (C5-8 + T1)

Damage at wrist ( e.g. Carpal tunnel syndrome)

Damage at elbow, as above plus:

Anterior interosseous nerve (Motor branch of Median Nerve)

● Named tests for Median nerve:

● MEDIAN AND ULNAR NERVES: COMMON FEATURES

Musculocutaneous nerve C5-7

● if damaged then elbow flexion will be impaired due to defect of Biceps

IMPORTANT VESSELS AND RELATED INFORMATION

AX.A. BRANCH: “Some Times Life Seems A Pain”

Brachial artery (fig with Median nerve page)

● Brachial artery begins at the lower border of Teres Major.

Ulnar artery (fig with Median nerve page)

• Lastly divides into the superficial and deep volar arches.

Radial artery (fig with Median nerve page)

● Radial artery passes under Brachioradialis

Axillary Vein Thrombosis

• 1-2% of all deep venous thrombosis

• Shallow synovial ball and socket type of joint.

Important Anatomical Relations

Anteriorly Brachial plexus

Axillary artery and vein

Posterior Suprascapular nerve

Inferior Axillary nerve

Structures @ risk during Anterior approach of the shoulder joint are:

Boundaries of the axilla (N-399)

Laterally Humeral head mainly.

Anteriorly Pectoralis major;

Fascia Clavipectoral fascia

Thoracodorsal nerve C6-8 Innervate and vascularise Latissimus orsi. (LAT)