Viva in Medical Physiology 2nd (Kenneth) PDF
Viva in Medical Physiology 2nd (Kenneth) PDF
Viva in Medical Physiology 2nd (Kenneth) PDF
Medical Physiology
Viva in
Medical Physiology
Second Edition
AK Basak PhD
Professor and Head
Department of Physiology
Haldia Institute of Dental Sciences and Research,
Haldia, Purba Medinipur, West Bengal, India
Formerly
Associate Professor and Head
Department of Physiology
Institute of Dental Sciences , Bareilly, UP, India
Associate Professor and Head
Department of Physiology
Avadh Institute of Dental Sciences, Lucknow, UP, India
Asst. Professor in Physiology
Universal College of Medical Sciences, Nepal
Asst. Professor in Physiology
Nepalgunj Medical College, Nepal
Branches
• 2/B, Akruti Society, Jodhpur Gam Road Satellite
Ahmedabad 380 015 Phones: +91-79-26926233, Rel: +91-79-32988717
Fax: +91-79-26927094 e-mail: [email protected]
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Bengaluru 560 001 Phones: +91-80-22285971, +91-80-22382956, +91-80-22372664
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Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089
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Hyderabad 500 095 Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929
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Kochi 682 018, Kerala Phones: +91-484-4036109, +91-484-2395739, +91-484-2395740
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Rel: +91-33-32901926 Fax: +91-33-22656075, e-mail: [email protected]
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Lucknow 226 016 Phones: +91-522-3040553, +91-522-3040554
e-mail: [email protected]
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Mumbai 400012 Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896
Fax: +91-22-24160828, e-mail: [email protected]
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To
my dear son
'Sohom’,
my students
and
well wishers
Preface to the Second Edition
AK Basak
Preface to the First Edition
While examining the MBBS and BDS students in their viva voce
examination, I have felt that even the good students hardly answer
the questions very precisely and to the point. Though there are small
number of viva books in Physiology with us, these are not sufficient
to meet the demand of the students so that they can answer A to Z of
viva questions generally asked by the examiners. Moreover, it is never
possible to the students to go through any text book while going to face
viva-voce examinations. These facts led me to write the book Viva in
Medical Physiology . While writing thisbook I have tried my best to
include all types of viva questions dealt with basic, brainstorming,
applied and clinical. Language of the book has also been kept easily
understandable. I hope this book will serve the purpose for not only
the BDS students but equally also the MBBS , MSc and BSc (Medical/
Human Physiology), MD (Physiology) students and also other allied
health subjects like physiotherapy, nursing, etc.
I am highly grateful to my students, colleagues and well wishers
of Avadh Institute of Dental Sciences (Lucknow); Universal College
of Medical Sciences (Nepal) and also Nepalgunj Medical College
(Nepal) for their encouragement and sincere suggestions for writing
up of this book. I am also deeply indebted to Prof. B N Koley and
Dr (Mrs) J Koley (Calcutta University), Prof NK Mishra and Prof SN
Pandeya (Nepalgunj Medical College), Prof V Reghunandanan and
Dr (Mrs) R Reghunandanan (Universal College of Medical Sciences),
Prof VK Negi (Harsaran Dass Institute of Dental Sciences, Gaziabad),
Prof SK Saxena (Sikkim-Manipal Institute of Medical Sciences),
Dr Rajuma Baudha (Avadh Institute of Dental Sciences) who always
thought very good of mine. I am also highly grateful to my family
members who always supported me in my academic pursuit.
I am really obliged to my wife, Mrs Dhriti Basak not only for
editing the language of this book but also for her sacrifice whose time
I usurped during the preparation of this book.
Finally I also express my sincere gratitude to Shri Jitendar P Vij,
Chairman and Managing Director, Tarun Duneja, Director-
x VIVA IN MEDICAL PHYSIOLOGY
Publishing and other Staff of M/s Jaypee Brothers Medical
Publishers (P) Ltd. for publishing this book.
I will be grateful if this book meets the demand of the students. I
will be very happy to receive opinions , comments and valuable
suggestions from all my senior colleagues, fellow teachers and
students so that every aspects of this book can be reviewed in
succeeding editions.
AK Basak
Contents
1.1
Basic Concepts
1. What do you mean by unit membrane?
Not only the cell membrane but also the nucleus,
chloroplast and mitochondria are double membranous,
i.e. they are covered by two wall layers each of which, is
consisting of protein-lipid-lipid-protein. This type of
membrane is known as unit membrane.
2. What is fluid mosaic model of cell membrane?
1 As per this model all membranes of different cell
organelles along with the plasma membrane are made
up of double layer of lipid molecules in which proteins
are embedded like the tiles of mosaic floors. This model
is first proposed by Singer and Nicholson.
3. Mention the chemical nature of proteins present
in plasma membrane with special reference to its
functions.
Chemically the proteins present on plasma membrane
are of two types:
i. Lipoproteins—It functions as enzymes and ion
channels.
ii. Glyco-proteins—It functions as receptor for
hormone and neurotransmitters.
4. Classify the proteins as per their location on plasma
membrane and mention each of their functions.
As per their location proteins are of 3 types:
2 VIVA IN MEDICAL PHYSIOLOGY
1.2
Blood
• Hemorrhagic anemia
• Dietary deficiency anemia like folic acid deficiency and
iron deficiency anemia.
• Anemia due to abnormal hemopoiesis, i.e. aplastic
anemia.
• Hemolytic anemia.
44. What are the signs and symptoms of anemia?
• Signs: Paleness of skin and mucous membrane of
mouth cavity, etc. spoon-shaped nails and
hemorrhages in the retina. In severe cases there may
be enlargement of heart and even heart failure.
• Symptoms: Breathlessness, fatigue, palpitation, loss
of appetite and bowel disturbances.
45. What is the commonest form of anemia in the world?
It is iron deficiency anemia.
46. What is the etiology of pernicious anemia?
It is due to deficiency of hematinic principle, i.e. lack of
castle’s intrinsic factor, resulting failure of absorption of
vitamin B12 from diet through ileum.
47. Name the physiological and pathological condition
of anemia?
Physiological—Pregnancy.
Pathological—Thalassemia, spherocytosis, malaria, iron
deficiency, etc.
48. What is polycythemia? What is its difference with
polycythemia vera?
Polycythemia refers to the increase in the number of RBC
above normal level. Polycythemia vera is the condition
characterised by very high RBC count due to gene
abnormalities of hemopoietic cells.
49. Name the physiological and pathological condition
of polycythemia.
Physiological—Muscular exercise, high altitude, high
environmental temperature, etc.
Pathological—Cardiac failure, diarrhoea, etc.
SECTION I : THEORY VIVA BLOOD 19
RBC s are microcytic and RBC s are macrocytic RBC s are macrocytic
hypochromic
Bone marrow shows Bone marrow shows Bone marrow shows
hyperplasia of red cell megaloblastic megaloblastic changes
precursors changes and presence and presence of
of erythroblasts erythroblasts
Nuclear maturation of Nuclear maturation of Nuclear maturation of RBC
RBC is normal RBC is impaired is impaired.
No associated No associated Associated neurological
neurological hazzards neurological hazzards hazzards
95. What do you mean by shift to the left and what is its
significance?
In Arneth count, if N1 + N2 + N3 becomes greater than 80
percent then it is known as shift to left or regenerative
shift. It indicates the hyperactive bone marrow.
96. What is shift to the right? What is its significance?
In Arneth count, if N4 + N5 + N6 is greater then 20 per
cent it is called as shift to right or degenerative shift which
indicates the hypoactive bone marrow.
97. Is trilobed eosinophil possible?
Yes, 15 percent of eosinophils are trilobed.
98. What are the stages of phagocytosis of WBC?
These are as follows:
Diapedesis → chemotaxis → opsonisation and then
phagocytosis → which causes degranulation → then
inflammatory response → finally stops or limits
inflammation.
99. Classify the lymphocytes.
Histologically—two types: Small and large lymphocytes.
Functionally—two types: T-lymphocytes (responsible for
cellular immunity) and B-lymphocytes (responsible for
humoral immunity).
100. Define neutrophilia and neutropenia. Mention each
of their causes.
Increase in the number of neutrophils in differential count
and absolute count (over 10,000 cumm of blood) is called
as neutrophilia.
Causes
Pathological
• Acute pyogenic infection like abscess, tonsilitis,
appendicitis, etc.
• Burn, acute hemorrhage and hemolysis
• Tissue necrosis like myocardial infarction and renal
infarction.
28 VIVA IN MEDICAL PHYSIOLOGY
1.3
Cardiovascular System
left forearm, left shoulder, neck and side of the face. This
clinical condition is known as angina pectoris.
21. Why cardiac muscle cannot be tetanised?
It is because of it's long absolute refractory period and
thus summation of contractile response is not possible
which is essential for tetanisation of heart muscle.
22. What is staircase effect in heart muscle?
When the cardiac muscle begins to contract after a brief
period of rest (e.g. following vagal stimulation) its initial
length of contraction increases before reaching to a
plateau. This phenomenon is called as staircase effect
or treppe response.
23. What is cardiogram?
The record of the mechanical activity of the heart is known
as cardiogram.
24. Mention the maximum and minimum pressure in
heart during systole and diastole?
Chamber Peak pressure in systole Min. pressure in diastole
Left ventricle 120 mm Hg 5-12 mm Hg
Right ventricle 25 mm Hg 2-6 mm Hg
Left atrium 15 mm Hg 5-8 mm Hg
Right atrium 6 mm Hg 1-5 mm Hg
Aorta 120 mm Hg 80 mm Hg
Pulmonary artery 25 mm Hg 5-12 mm Hg
Contd...
Phases of cardiac cycle Duration in sec
131. How does the ECG record changes with time after
MI?
• Within few hours after MI: Elevation of ST segment.
• After some days of MI: Elevation of ST segment along
with inversion of T wave.
• After several weeks of MI: ST segments return to
normal but inversion of T wave is still present along
with appearance of Q wave.
• After months and years of MI: T wave becomes normal
and Q wave becomes deep.
132. What do you mean by mean circulatory filling
pressure and mean systemic filling pressure?
If the heart beat is stopped, the flow of blood every where
in the circulation ceases after few seconds resulting equal
pressure within the whole circulation which is known as
mean circulatory filling pressure.
Whereas the mean systemic filling pressure is the
pressure measured everywhere in the systemic circulation
after blood flow is stopped by the clamping of the large
blood vessels at the heart. Normally the amount of both
are almost equal.
133. Name different types of blood vessels in vascular
system with examples of each.
These are as follows:
a. Distensible (Windkessel) vessels—aorta, pulmonary
artery and their large branches.
b. Resistance vessels—arterioles, meta-arterioles
c. Exchange vessels—capillaries
d. Capacitance vessels—venules and venous
compartments
e. Shunt vessels—AV anastomoses.
134. Blood flow to the different body organs can be so
effectively regulated by only small chages in the
caliber of the arteries. How is it possible?
As resistance to blood flow is inversely proportional to
the 4th power of the radius (r) of arterioles,the small
68 VIVA IN MEDICAL PHYSIOLOGY
1.4
Figs 1.4.2A and B: Sham feeding. (A) represents the opening of the
divided oesophagus and (B) is the body of stomach with fistula
1.5
Respiratory System
• Expiratory muscles:
• Internal intercostal muscles
• Abdominal muscles: These include abdominal recti,
transverse abdominis, internal oblique.
13. Why the 'Wheeze' sound is heard during expiration
but not in inspiration of an asthma patient?
During inspiration the intrapleural and mediastinal
negativity rises and as a result the bronchial diameter
increases. Reverse occurs during expiration. Therefore
resistance to airflow is normally low in inspiration and
high in expiration. This is why in bronchial asthma
inspiration may not be difficult but expiration becomes
difficult. This explains why the "Whezze" in bronchial
asthma is heard during expiration but not in inspiration.
14. Define and give the normal value of TV, IRV, ERV
and EV.
• Tidal volume (TV): It is the amount of air breathed in
or out of lungs during quiet respiration. Normal value
is 500-800 ml.
• Inspiratory reserve volume (IRV): It is the maximum
amount of air that can be inspired from the end
inspiratory position by forceful and maximal activity.
Its normal value is 2000-3200 ml.
• Expiratory reserve volume (ERV): It is the maximum
amount of air that can be expired by maximum forcible
effort from the end of normal expiratory position.
Normally its value is 750-1000 ml.
• Residual volume (RV): It is the volume of air which
remains in lungs even after forceful expiration. Normal
value =1200 ml.
15. Define and give the normal value of IC, FRC and
TLC.
• Inspiratory capacity (IC): It is the maximum amount of
air that can be inspired from the end expiratory
position. Normal value: 2500-3700 ml.
SECTION I : THEORY VIVA RESPIRATORY SYSTEM 95
• Vagal apnoea,
• Anoea vera (due to change in blood pressure),
• Acapnic apnoea (due to complete lack of CO2),
• Deglutition apnoea,
• Sleep apnoea,
• Adrenaline apnoea.
94. What are the causes of asphyxia?
These are–CO2 excess, O2 lack and change in blood
pH.
95. What are the various stages of asphyxia?
These are hyperapnoea, respiratory convulsions and
stage of exhaustion.
96. What are the various factors causing respiratory
insufficiency?
These are–alveolar hyperventilation, decrease in
pulmonary diffusion capacity and decrease in O2 transport.
97. What is hypoxia? Enumerate its type.
Hypoxia is the condition characterised by the lack of O2
in the tissue. It is of 4 types—hypoxic, anaemic, stagnant
and histotoxic hypoxia.
98. Define hypoxic hypoxia. What are its causes?
The condition characterised by a low arterial PO2 keeping
O2 carrying capacity of blood and rate of blood flow
normal or elevated is known as hypoxic hypoxia.
Causes:
• Low PO2 in inspiratory air
• Reduced pulmonary ventilation
• Decrease in gaseous exchange through alveolar
capillary membrane.
99. Define anemic hypoxia. What are its causes?
Hypoxia in which arterial PO2 is normal but the amount of Hb
available to carry O2 is reduced, is known as anemic hypoxia.
Causes: Anaemia, hemorrhage, formation of carboxy
hemoglobin or methaemoglobin.
112 VIVA IN MEDICAL PHYSIOLOGY
• Nailbeds
• Tip of the nose.
105. In which type of hypoxia cyanosis cannot take place
and why?
• In anemic and histotoxic anemia, cyanosis is absent.
• In case of anemic hypoxia, the amount of Hb becomes
too low and thus enough reduced Hb to produce blue
colour is lacking.
• In case of histotoxic hypoxia, O2 is not taken up by
the tissues and thereby there is minimum chance to
produce reduced Hb in greater amount to produce
cyanosis.
106. Compare the central and peripheral cyanosis?
1.6
Myelinated Unmyelinated
1. Presence of myelin sheath. Absence of myelin sheath.
2. Location - in all preganglionic Location - in all post-ganglionic
fibers of ANS and somatic fibers and somatic nerve fibers
nerve fibers more than 1µm of <1µm in diameter.
diameter.
3. Conduction rate through it is fast. It is rather slow.
SECTION I : THEORY VIVA NERVE MUSCLE PHYSIOLOGY 119
EPP AP
Pre-load After-load
1. This is the load which acts on This is the load which acts on the
the muscle before it begins to muscle after it begins to contract.
contract.
2. It results isometric contraction. It causes isotonic contraction.
3. In vivo it is the degree to which It is the resistance against which the
the myocardium is stretched ventricles pump the blood.
before it contracts.
1.7
Excretory System
1.8
1.9
Chemical Electrical
EPSP AP
δ and C fibers.
54. Distinguish between Aδ
Aδ fibers C fibers
LMNL UMNL
a. Single individual muscle is Group of muscles are affected.
affected
b. Flaccid type of muscle Spastic type of muscle paralysis
paralysis due to due to hypertonia
hypotonia
c. Disuse atropy of muscle Not severe
takes place
Contd...
SECTION I : THEORY VIVA CENTRAL NERVOUS SYSTEM 167
Contd...
d. All reflexes are absent as Deep reflexes are hyperactive due
motor pathway is damaged. increased γ motor activity and
some superficial reflexes like
abdominal, cremastric reflexes
are lost.
e. Babinski’s sign is negative It is positive.
Features:
• Lead pipe or Cogwheel rigidity—due to increase in
muscle tone.
• Static tremors—Tremor at rest and disappears
during voluntary activity due to oscillatory continuous
discharge of pyramidal system by a closed circuit
through basal ganglia.
• Akinesis—It is difficulty in initiation or starting movement
due to rigidity of the muscles so the automatic associated
movements do not occur resulting:
• Mask like face (no facial expression)
• Statue like posture.
• Festinant Gait—The person walks with short quick
steps with the body bent forwards as if the person is
trying to prevent himself from falling.
95. Differentiate REM and NREM sleep.
Slow wave sleep or orthodox or Non rapid eye movement
(NREM) sleep:
• It occupies 70% of sleep period.
• Lasts for every 70-90 min and interrupted by 10-20
mins of REM sleep.
• Produced by absence of desynchronising activity via RAS.
• EEG shows slow, synchronised theta and delta waves.
Rapid eye movement (REM) or paradoxical or fast wave
or dream sleep:
• Rapid to and fro movement of eye ball occurs.
• HR and respiratory rate becomes irregular.
• Occasional muscle twitch can take place.
• Difficult to wake an individual if he is in this phase of
sleep.
• Dreams are more vivid.
• Shows fast desynchronised waves.
96. Enumerate the site of memory storage.
It is randomly stored in the brain. However important sites
SECTION I : THEORY VIVA CENTRAL NERVOUS SYSTEM 175
1.10
Special Senses
1.11
Endocrinal System
• High BMR.
• Rapid pulse and heart rate.
• Increase in cardiac output.
• Nervous irritability.
• Involuntary tremors of hand muscles.
• Creatinuria and glucosuria.
37. What do you mean by autoregulation of thyroid?
Iodine content in diet regulates the thyroid hormone
production in the body, i.e. excessive ingestion of iodine
decreases I2 transport to follicular cells whereas I2
deficiency leads to the enlargement of thyroid glands.
Thus normal thyroid hormone secretion is maintained
within the physiological limit without altering the TSH
secretion. This intrinsic control system of thyroid hormone
secretion is known as autoregulation.
38. What is myxoedema, idiot child and myxoedema
madness?
• In hypothyroidism because of decreased catabolism,
there is deposition of mucopolysaccharides like
hyaluronic acid and chondroitin sulphate under the
skin and subcutaneous tissue which then exert osmotic
pressure that causes retention of water and NaCl. This
ultimately leads to dry, coarse and puffy appearance
of skin (non-pitting oedema) called myxoedema.
• Deficiency of T4 after birth upto 2 years in child results
under development of brain producing mental
retardation of child. This is known as idiot child.
• The same cause, i.e. T4 deficiency during adulthood
results loss of all intellectual function, memory and
also slow speech and mental and physical lethergy.
These lead to madness or psychosis known as
myxoedema madness.
39. What are the common clinical conditions of
hyperthyroidism?
Exophthalmic goitre and nodular goitre.
SECTION I : THEORY VIVA ENDOCRINAL SYSTEM 197
• On GIT:
• Inhibits Ca++ absorption through intestine.
• Increases intestinal secretion of water and
electrolytes.
49. Are the parathyroid glands essential for life? Justify
your answer.
Yes, as their removal will cause the decrease of plasma
Ca++ level in a greater extent thereby there will be spasm
of laryngeal muscles, thoracic muscles and diaphragm
resulting asphyxia and ultimately death.
50. What are the main signs and symptoms of
hypoparathyroidism?
Hypocalcaemia, hyperphosphataemia, increase in blood
pH, neuromuscular hyperirritability causing tetany.
51. What are the common signs present in tetany?
Explain each of them.
• Trousseau’s sign or carpopedal spasm—It is
manifested in the upper limb as flexion at the wrist
and thumb with hyper-extension of remaining fingers
called obsteric hand/accoucheur’s hand or carpopedal
spasm. If this is demonstrated by occluding the blood
supply to a limb through sphygmomanometer cuff, it
is known as Trousseau’s sign.
• Chvostek’s sign—If skin in front of the ear is tapped,
there is contraction or spasm of facial muscle.
• Erb’s sign—It is depicted by the enhanced motor
excitibility of galvanic current.
52. What is laryngeal stridor?
Due to hypoparathyroidism sometimes the laryngeal
muscle becomes spasmatic resulting airways obstruction
and thereby asphyxia and can also result death. This is
known as laryngeal stridor.
53. What are the main characteristics of hyper-
thyroidism?
These are as follows:
• Weakness, loss of muscle tone, thirst, polyuria,
nousea, vomiting, constipation, etc.
200 VIVA IN MEDICAL PHYSIOLOGY
• Causes
- Postmenopausal women (due to low oestrogen
level resulted from increase in sensitivity of PTH
to bone)
- Hyperparathyroidism
- Hyperthyroidism
- Calcium deficiency
Osteosclerosis: Increased calcified bone in patient with
metastatic tumour, lead poisoning and hypothyroidism.
56. Name the layers of adrenal cortex and the hormones
secreting from them.
• Zona glomerulosa—Secretes mineralocorticoids
(Aldosterone).
• Zona fasciculata—Secretes glucocorticoids.
• Zona reticularis—Secretes androgen.
However in human zona fasciculata and zona reticularis
act as a single functional unit synthesising mainly cortisol
(glucocorticoids) and androgens.
57. Are the adrenal cortex essential for life? Justify
your answer.
Yes, as adrenal cortical hormones are essential to
maintain normal metabolic process of cells and also to
control the water and electrolyte balance which are very
much necessary for normal functioning of cells.
58. Which of the layer of adrenal cortex is/are
unaffected by absence of ACTH?
Zona glomerulosa.
59. What are the steroids produced in the body?
• Glucocorticoids—Cortisol, corticosterone, cortisone,
etc.
• Mineralocorticoids—Aldosterone and deoxycortisone.
• Sex steroids—Androgen, estrogen and progesterone.
202 VIVA IN MEDICAL PHYSIOLOGY
1.12
Reproductive System
Part A
Hematology
Human Experiments
b. In isotonic exercise:
• Quick rise in heart rate and stroke volume due to
generalized sympathetic stimulation.
• Increase in cardiac output and systolic pressure.
• Net fall in total peripheral resistance.
• Diastolic pressure may remain same or may fall
or even increase a little.
24. Name some other cardiac efficiency test?
It is Treadmill test (TMT).
25. What do you mean by cardiac pulsation and apex
beat?
Any pulsation in the precordium which is normally due to
the forward systolic thrust of the apex of the left ventricle
is called as cardiac impulse or cardiac pulsation. Whereas
the apex beat is the lowest and outermost point of definite
cardiac pulsation which is usually located in the 5th
intercostal space 8-10 cm (about 3.5-4 inches) from the
mid-sternal line.
26. Is the apex beat visible always in normal person?
No, the apex beat may not be always visible in some
normal persons because:
• It may be located behind the rib.
• Thick chest wall due to fat or muscle.
• The breast may be pendulous
• The emphysematous lung may cover part of the heart.
27. Palpate the apex beat. What is the significance of
palpating apex beat?
Apex beat is palpated by placing the flat part of the hand
over the heart keeping the base of the palm over the
base of the heart and the fingers pointing towards the
apex. Once the cardiac pulsation is felt the ulnar border
of the hand and then the tip of the index finger is used to
locate and confirm the point of the apex beat.
Significance of the apex beat: The change of the normal
position, the force and the nature of the apex beat can
give the idea about the status of the heart, e.g.:
246 VIVA IN MEDICAL PHYSIOLOGY
I. Blood
1. Hemoglobin
• At birth: 22-24 gm% (Avg-22 gm%)
• In adults
- Male: 13.5-18 gm% (Avg-15.5 gm%)
- Female: 11-16 gm% (Avg-14 gm%)
2. RBC count
• At birth: 6-7 million/cumm of blood
• In adults
- Male : 5-6 million/cumm of blood
- Female : 4.5-5.5 million/cumm of blood
3. WBC count (Total)
• At birth : 20000/cumm of blood
• In adults: 4000-11000/cumm of blood
4. WBC count (Differential)
• Neutrophil : 50-70%
• Eosinophil : 1-4%
• Basophil : < 1%
• Lymphocyte : 20-40%
• Monocyte : 2-8%
5. WBC count (Absolute)
• Neutrophil : 3000-6000/cumm of blood
• Eosinophil : 150-300/cumm of blood
• Basophil : 10-100/cumm of blood
• Lymphocyte : 1500-2700/cumm of blood
• Monocyte : 300-600/cumm of blood
6. Reticulocyte count: 24000-84000/cumm of blood
7. Platelet count : 2-5 lacs/cumm of blood
SECTION III : APPENDIX IMPORTANT VALUES TO REMEMBER 253
8. ESR
• Westergren
- Male : 3- 5 mm in 1st hour
- Female : 5-7 mm in 1st hour
• Wintrobe’s
- Male : 0-10 mm in 1st hour
- Female : 0-20 mm in 1st hour
9. RBC indices
• PCV (Hct):
- Male : 40-50%
- Female : 36-47%
• MCV : 78-94 µm3
• MCH : 27-32 pg
• MCHC : 30-38%
• CI : 0.85-1.15
10. Fragility of red cells
• Hemolysis begins : 0.5% NaCl
• Hemolysis completes : 0.36% NaCl
11. Bleeding time
• Duke’s method : 2-5 min
• Ivy’s method : 3-9 min
12. Coagulation time
• Capillary blood (Capillary glass tube method): 3-8 min
• Venous blood (Lee and White method) : 5-15 min
13. Prothrombin time : 14-18 sec
14. Total blood volume : 5-6 L
15. Specific gravity
• Of blood : 1.048-1.066
• Of RBC : 1.092-1.095
• Of plasma : 1.026-1.035
16. Frequency distribution of blood group in INDIA
• A blood group : 21%
• B blood group : 39%
• AB blood group : 9%
• O blood group : 31%
• Rh positive : 95%
• Rh negative : 5%
254 VIVA IN MEDICAL PHYSIOLOGY
II. Plasma/Serum
1. Plasma volume
• Male: 39 ml/ kgbw
• Female: 40 ml/kgbw
2. Osmolality:
• Plasma: 285-295 mosm/kg of serum water
• ECF: 3000 mosm/L
• ICF : 300 mosm/L
3. NPN Substances: 20-30 mg/dl
4. Proteins (Total): 5.5-8 gm/dl
• Albumin: 3.5-5 gm/dl
• Globulin: 2-3.5 gm/dl
• Fibrinogen: 0.2-0.5 gm/dl
5. Amino acids: 6-8 gm/dl
6. Total lipid: 450-1000 mg/dl
7. Cholesterol:120-220 mg/dl
8. Fatty acids: 160-270 mg/dl
9. Triglycerides: 25-150 mg/dl
10. Glucose
• Fasting: 80-110 mg/dl
• Post-prandial
- Normal: 140 mg/dl
- Diabetic :> 200 mg/dl
11. Sodium: 135-145 mEq/L
12. Potassium: 3.5-5 mEq/L
13. Chloride: 95-108 mEq/L
14. Bicarbonate: 26-28 mmol/L
15. Calcium : 2.12- 2.62 mEq/l
: 8.5-10.5 mg/dl
16. Magnesium: 2-3 mg/dl
: 1.5-2.0 mEq/L
17. Phosphate : 2.5-4.5 mg/dl
18. Amylase : 13-53 nmol/L
: 60-180 Somogyi unit/dl
19. SGOT: 100-300 μmol/L
20. SGPT: 50-430 μmol/L
21. Alkaline phosphatase: 0.4-1.5 μmol/L
SECTION III : APPENDIX IMPORTANT VALUES TO REMEMBER 255
22. Bilirubin
• Total (Indirect): Up to 1 mg/dl
• Conjugated (direct): Up to 0.4 mg/dl
23. Creatinin: 0.6-1.5 mg/dl
24. Urea: 20-40 mg/dl
25. Uric acid
• Male: 3.6-8.5 mg/dl
• Female: 2.3-6.6 mg/dl
26. Protein bound iodide: 3.5-8 μg/dl
27. Thyroid binding globulin: 7-17 mg/L
28. Thyroxin: 70-140 nmol/L
29. Tri-iodothyronine: 1.2-3.0 nmol/L
9. O2 diffusion capacity
In male : 27-42 ml/min/mmHg
In female : 28-30 ml/min/mmHg
10. Tidal volume: 500-800 ml
11. Inspiratory reserve volume: 2000-3300 ml
12. Expiratory reserve volume: 1100 ml
13. Residual volume: 1200 ml
14. Inspiratory capacity: 3500 ml
15. Expiratory capacity: 1600 ml
16. Functional residual capacity: 2200 ml
17. Vital capacity
In male : 4500-5500 ml
In female : 3500-4500 ml
18. Total lung capacity: 5700 ml
19. Pulmonary ventilation (RMV): 6-7 lit/min
20. Alveolar ventilation: 4.9 lit/min
21. Maximum voluntary ventilation:
• In male : 150-170 lit/min
• In female : 80-100 lit/min
22. FEV1: 75-85%
23. Doesponic index: 60-70 %
24. Respiratory dead space volume: 150 ml
25. Lung compliance:
• Lungs alone : 220 ml/cm of water
• Lungs and Thorax : 130 ml/cm of water
26. O2 transported through plasma: 0.3 ml/100 ml of blood/
100 mmHg PO2
27. O2 carrying capacity of blood: 20 ml of O2
28. CO2 transport
Through plasma: 0.3 ml/100 ml of blood (7%)
• Through bicarbonate: 3 ml/100 ml of blood (70%)
• Through carbamino compound: 0.7 ml/100 ml of blood
(0.7%)
V. Excretory System
1. No. of nephron/Kidney: 1 million
2. GFR : 125 ml/min (180 L/day)
258 VIVA IN MEDICAL PHYSIOLOGY