o Reproductive System Physiology, Anatomy

and Pathology
By :Ameer Khamise and Ali Khalid
3rd Year Medical Students- University of Buckingham Medical School
Email address: [email protected]
[email protected]
IMPORTANT NOTICE
These revision slides are high yield content which we believe are
important and they are entirely based on university material.
These slides are free for all medical students who attended the session
and not to be shared or sold.
Table of Contents
• Clinical anatomy of the female reproductive tract.
• Pelvic floor and perineum.
• Anatomy of the male reproductive tract.
• Hormonal control of reproduction.
• Puberty and menopause.
• Coitus and fertilisation.
• Infertility and contraception..
• Placenta development and pregnancy.
• Foetal growth and development.
• Foetal physiology.
• Parturition.
• Breast feeding and human lactation.
• Breast disease and breast cancer.
• Infections of reproductive tract.
• Gynaecological tumours.
• Follicle anatomy: Oogenesis: Spermatogenesis:

Secondary oocyte
arrests at metaphase
of meiosis 2 until
ovulation.
Anatomy of female reproductive tract.
• Key structure: • Ovaries
1- Ovaries Ø Develop within mesonephric ridge in lumbar region of
posterior abdominal wall—> into pelvis.
2- Uterine tubes/fallopian tubes
Ø NOTE!
3- Uterus
Ovaries do nOt pass into inguinal canals
4- Vagina and external genitalia
Testicles pass through inguinal canal.
5- Pelvic bones, ligaments, muscles,
nerves and vessels. Ø Location: posterior and lateral to uterus+inferior to
pelvic inlet.
Ø Note!
Ø Purpose: Produce ova (fertilisation)+ steroid hormones (
Two important anatomical relationships : mainly oestrogen and progesterone).
1- Urinary tract: especially important in Ø Blood supply: ovarian arteries (direct branches of
males. abdominal aorta).
2- GI tract (esp. rectum and lower end of Ø Venous drainage:
tract): important in males and females.
Right ovarian vein—>IVC
Left ovarian vein—>left renal vein—>IVC
 Ø Procedures:
• Uterus • Fallopian Tubes
Ø Development: paramesonephric (mullerian ducts)à connect to urogential sinus sinus caudally and
Ø Location: Open ended tubes that extend from superior 1) Tubal ligation: ligate (clip) the uterine
are open cranially—> persist in the presence of MIH( from testis) —>The ducts fuse in the midline—
> broad transverse fold ( will develop to uterus later). end of uterus body & enclosed within Mesosalpinx part tubes, and it’s the most common
of broad ligament. contraceptive method worldwide.
Ø Location: between bladder and rectum.
Advantages: simple and effective
Ø Anatomy: pear shaped muscular organ, anchored to pelvis by ligaments, contains 4 parts: Ø Functions: method of birth control.
1- Fundus- At the top
2) Body 1) Conduct oocyte released in ovulation into uterine cavity. 2) Salpingo-oophorectomy: Removal of
3) Uterine tube fallopian tubes and ovaries.
4) Cervix- At the bottom and leads to vagina. 2) Site of fertilisation (commonly in Ampulla)
NOTE!! Functionally uterus is divided into muscular body ( upper 2/3rds) and fibrous cervix (lower Indications: cancer risk and
1/3rd). 3) Opening into peritoneum via the ostium of the fallopian reproductive disorders.
tube
ØThere are 2 peritoneal recesses:
1) Vesico-uterine pouch ANTERIORLY
2) Pouch of Douglas (recto-uterine pouch) POSTERIORLY Ø Anatomy: The uterus has 3 parts: • Q:What is clinical significance of
- Culdocentesis: Aspirating peritoneal fluid from pouch of Douglas through posterior fornix to evaluate fallopian tubes?
women with lower abdo pain/ pelvic pain to determine whether intra-abdominal fluid is present. 1) Isthmus: Closest part to uterus.
(Nowadays ultrasound is used instead). • A: 1- Fallopian tubes are open
2) Ampulla: Most common site for fertilisation.
• Q: What’s the clinical significance of pouch of Douglas? And how can it be reached? ended tubes that open into the
• A: LOWEST point in peritoneal cavity—> Fluid in the cavity will collect in this spaceà can be accessed 3) Infundibulum: Farthest from uterus peritoneum, meaning there’s a
through posterior fornix of the vagina. route of infection form external
• NOTE!! In unsafe abortions, peritoneal cavity can be breached through penetrating pouch of Douglasà ** Fimbriae: catches the ova released in ovulation and move environment into peritoneum (
Infections and other complications. it into the tube. vagina—> cervix—> uterus—>
fallopian tubes—> peritoneum).

• 2- Ectopic pregnancy when

fertilised embryo implant in the
tube, however it can’t survive and
can cause complications because:
a) Lining and histology is NOT that of
uterine cavity and can’t support
embryo development.

b) Doesn’t have same blood supply as

uterus.

c) Not big enough.

Uterine and Ovarian ligaments
Ø Function: Anchor ovaries and uterus in the 3) Cardinal/Transverse cervical ligament: from cervix to
pelvis lateral pelvic walls.
Ø 4 major uterine ligaments: - One of the most important ligaments in stabilising
the uterus.
1) Broad ligament: Double fold of peritoneum
which extends laterally to side walls of pelvis. It’s 4) Uterosacral ligament: from cervix to posterior pelvic
the largest ligament and contains 3 parts: walls.
1- Mesovarium: covers ovary. - Important in maintaining anteversion.
2- Mesosalpinx: covers uterine tubes. Remember!! Transverse and uterosacral ligaments
are IMPORTANT in stabilising the uterus.
3- Mesometrium: Covers uterus body.
5) Pubocervical ligament: from cervix to anterior pelvic
** Round ligament, uterine vessels and wall.
ureters pass through the broad ligament. (USEFUL
FOR LABELLING!!) Ø 2 major ligaments for ovaries:
2) Round ligament: develops from caudal part of 1) Ovarian ligaments: connect uterus to ovaries.
gubernaculum.
- develops from cranial part of gubernaculum.
- Uterus—> through inguinal canal—> labia
major 2) Suspensory ligaments of ovaries: carry blood vessels
and nerves from abdomen to pelvis.
• Q: what’s the clinical significance of round
ligament? • Q: What happens if the ligaments fail?
(Rupture/stretch)
• A: Route for various lymphatic vessels—>
the lymphatic drainage can spread cancer from • A: Uterine and/or vaginal prolapse.
reproductive organs to other lymph nodes e.g
inguinal lymph nodes.
Position of uterus Cervix
Ø Inferior part of the uterus.
Ø Cervix epithelium;
1) Endocervix: Simple columnar
Ø Vagina is found behind the uterusà cervix epithelium.
changes direction—> uterine body changes Ø Broad cylinder with narrow central channel.
direction. 2) Ectocervix: Stratified squamous
Ø 5 structures related to cervix:
non keratinised epithelium.
Ø Anteverted: with respect to vagina. 1) Anterior fornix: gutter between cervix and vagina
anteriorly. ** Separated by Squamocolumnar
Ø Anteflexed: with respect to cervix. Junction (SCJ).
2) Posterior fornix: gutter between cervix and vagina
posteriorly. ( Leads to pouch of Douglas)

3) Internal os: the slight constriction the endocervical

canal.

4) External os: the opening into the vagina canal.

5) Endocervical canal.

What can go wrong?

Cercinoma of Cervix
Ø Retroverted uterus: points upwards.
- Strongly associated with HPV ( mainly 16 & 18)—>
Ø Retroflexed uterus: points backwards.
hence it’s usually found in younger women!! (Ask
Note! Think about the cervix to help you about sexual history- 5Ps).
- Majority are Squamous cell carcinoma (few are
orientate yourself.
adenocarcinoma)
NOTE! The cervix lumen is narrow and it helps reduce - Diagnosis: inspection, cell collection, biopsy,
Retroversion Retroversion & Retroflexion
infections entry. imaging.
- Treatment: may be treated with resection of
cervix/uterus.
- Spread: internal and common iliac lymph nodes.
- Cervical screening program: 25-49 (every 3 years),
50-64 (every 5 years).
Blood supply and lymphatic drainage Female external genitalia
Blood supply: 1) Vestibule:

Ø Uterine artery: WATER UNDER THE BRIDGE( ureter - orifices of vagina, urethra and greater &
lesser vestibular glands. (These glands creat the
under artery) secretions in this area).
--> Gives: Vaginal branch+ Vaginal artery. 2) Labia minora: ( stretches around the clitoris)
Ø Ovarian artery: brach of abdominal aorta—> gives - Encloses the vestibule of vagina.
Tubal branches (supply uterine tubes) + Ovarian
branches (supply ovaries). - Bulbs of vestibule.
- Clitoris.
Ø Internal pudendal arteryà perineal artery.
3) Labia majora:
Ø NOTE! Big network of anastomosis,—> can be
useful if one artery got blocked. - Encloses the pudendal cleft.

Lymphatic drainage: - Come together to form mons pubis.

Clinically applied anatomy of uterus:
Remember: deep lymph vessels follow arteries 1) Bimanual examination: Should be able to
(pulsation drives movement of lymph). feel top of uterus, pouch of Douglas &
the posterior fornix.
Ø Uterus and ovarian lymphatic drainage follows 2) Cervical examination.
blood supply: 3) Ectopic implantation.

1) Fundus + upper body: Para-aortic & superficial

inguinal nodes.
2) Body (lower part) + cervix: External & internal iliac
nodes + sacral nodes.
3) Ovary: lumbar para-aortic nodes.
 Muscle Underlying structures

Bulbospongiosus Bulb of vestibule

Ischiocavernosus Crus of clitoris

Perineal body** ** Vital structure for

(Fibro-muscular structure) muscle various muscles
attachments.

Ø Speculum is used to look inside the

vagina—> the following structures can
be identified:
- Greater vestibular glands ( Bartholin glands): their ducts Muscles

open into the vestibule. ( on either side of vaginal 1) Vaginal orifice.

orifice). 2) Anterior vaginal fornix ( on top) and
- Clitoris has 2 parts: posterior vaginal fornix (at the bottom).
1) Body of clitoris: corpora cavenosa.
2) Crus of clitoris: corpus cavernosum. 3) Cervix:: a swab/ biopsy can be taken, and
that is what is done in the cervix
** glans clitoris is the part we can see. screening program. Underlying
NOTE! Clitoris and penis have the same embryological structures
origin, hence their structure is similar- See later. 4) External cervical os. ( internal os CAN’T
- Bulb of vestibule. be seen).
- Para-urethral openings:
on each side of external
urethral meatus.
- Opening of the duct of
bartholin’s glands: on each
side of vaginal orrifice.
 • Pudendal Nerve:
Innervation • Root: s2-s4 (high yield)
• Route: exits pelvis via greater
Structure Innervation
sciatic foramen—> enters
Vagina superior 4/5ths Visceral from
uterovaginalis perineum via lesser sciatic
Vagina inferior 1/5th Somatic from foramenà through pudendal
pudendal nerve canal.
** Pain afferents depend on PELVIC PAIN LINE: • Branches:
➢Above the line:
- Uterine fundus, body
- Inferior thoracic lumbar spinal ganglia
- Visceral afferent pain fibers
follow sympathetic fibers ( superior—
> sympahetic)
➢Below the line:
- cervix, vagina
- s2-s4 spinal ganglia ( covers the majority of the
lower part of female tract).
- visceral afferent pain fibers
follow parasympathetic fibers.
Pelvic floor
• Overview of the pelvis structure:
False pelvis—> pelvic inlet—> true
- Muscular and fibrous diaphragm pelvis—>pelvic floor—> perineum (
- Fills the lower part of pelvic canal and closes the abdominal cavity external genitalia + openings of GI &
- Defines upper border of perineum genitourinary system).
- supports and lifts pelvic organs Ø Reminder of body cavities:
- pierced by urethra, vagina, rectum—> these holes form weakness
points 1) Thoracic cavity
2) Abdominal cavity: diaphragm—>
True and false pelvis
pelvic inlet
-False/ greater pelvis:
Above pelvic inlet 3) Pelvic cavity: pelvic inlet—> pelvic
Related to upper parts of pelvic bones—> part of the abdomen floor
- True pelvis:
4) Peineum
- Below pelvic inlet
- Anterior(pubic symphysis), sacral promintory(posterior), pelvic
brim( sides)
 Pelvis
• Pelvic Inlet

Pubic symphysis (anterior), pelvic

brim (sides), Sacral promontory
(posterior).

• Pelvic walls Pelvic outlet.

During labour, baby has to

twist through inlet and
outlet.

Pelvic walls made of ligaments and

muscles, sacrum at the back.
• 2 main ligaments: sacrospinous +
sacrotuberous ( posterior border of greater &
lesser sciatic foramen).
 Pelvic floor/Diaphragm
• Separates pelvic cavity from perineum. • Perineum
• Formed by muscle and fascia (tendons, Ø Diamond shape:
ligaments..).
1) Urogenital triangle: faces
• Functions: inferiorly
1) Support and raise pelvic contents/organs. 2) Anal triangle:
2) Childbirth (support foetus during pregnancy *** Perineal body in the middle.
and stretch during childbirth).
Ø Pelvic floor muscles Ø contains and anchors roots of
external genitalia.
1) Levator Ani: Iliococcygeus+ pubococcygeus+
puborectalis
2) Coccygeus: ** has more important roles in
other species.
Urogenital triangle 3) Perineal membrane: thick triangular
1) Superficial fascia of urogenital fascial sheet inferior to pelvic floor and
diaphragm. deep perineal pouch—> fills space
2) Deep perineal pouch: betwween arms of pubic arch:
Anterior border: gap anteriorly ( doesn’t
Female Male
reach pubic symphysis).
Posterior border: free posterior border.
Deep transverse perineal muscle Deep transverse perineal muscle. Laterally: attaches to inferior pubic rami.

Opening for vagina and urethra. Opening for urethra.

No glands. Bulbourethral/ cowper’s glands.

External urethral sphincter. External urethral sphincter.

2 additional muscle:
- Sphincter of urethrovaginalis.
- Compressor urethra.
• 4) Superficial Perineal Pouch: Notice:
- Bulb of vestibule in females is similar Posterior anal triangle
- inferior to perineal membrane. to bulb of penis in males, however in
males it fuses and no vagina.
- contents: - Bulb of penis—> corpus spongiosum Ø Faces posteroinferiorly
- Crus of penis—> corpus cavernosum
Ø Borders:
1- superficial transverse perineal - Ischiocavernosus and bulbosponiosus
muscle. muscles are found in males and 1) Anterior wall: horizontal line between 2 ischial
females. tuberosities.
2-Ischiocavernosus muscle Perineal body: 2) Posterior wall: coccyx
3- crus of penis/ clitoris - Connective tissue structure.
- Central fulcrum for pelvic support. 3) Lateral walls: sacrotuberous ligaments.
4- Bulbospongiosus muscles - Connect the urogenital and anal
triangles. 4) Ceiling: pelvic floor (levator ani muscle).
5- bulb of penis/ vestibular bulbs.
- Muscles of pelvic floor and perineum Ø Anal aperture located centrally in triangle—>
attach here. external anal sphincter.
6- perineal body - Situated midline, along posterior
7- Bartholin’s glands (female) border of perineal membrane.
8- branches of internal pudendal
vessls and perineal nerve. Q: give 4 muscles thhat attach to
perineal body.
A: 1)Deep transverse perineal muscles
2) Superficial transverse perineal
muscles.
3) External anal sphincter
4) Bulbospongiosus muscles
5) Compressor urethra muscle.
• Ischioanal/ ischiorectal fossa:
- lateral to anal canal and inferior to pelvic floor. Anal canal Anorectal junction:
- Pulled forward by PUBORECTALIS (part
- 2 gutters on each side of the anal aperture and normally filled
with fat—> allow movement and cushioning of pelvic • Mainly below pelvic diaphragm.
of levator ani)—> anal canal moves in
diaphragm and expansion of anal canal. posterior position as it passes through
• Pelvic floor and perineal muscles extend/ anchored
towards anal canal and rectum.
pelvic floor.
- Q: what’s the clinical significance?
• Pectinate/ dentate line separate upper 2/3rd and lower
- A: 1)spread of infection between ischioanal fossa and 1/3rd of anal canal:
perineum.
- upper 2/3rds : visceral innervation
2) ischioanal abscess: anal mucosa vulnerable to injury—>
if torn by faeces—> inflammation/ infection spread from anal - lower 1/3rd: somatic innervation
canal to fossa—> fistulas develop—> infection spread to pelvic
Ø Haemorrhoids:
cavity.
1) Internal haemorrhoids:

- Above dentate line.

- Covered by mucous membrane.

- Pain fibers are General Visceral Afferent from

sympathetic nerves.

- More likely to bleed, not particularly painful.

2) External haemorrhoids:

-Below dentate line.

- Covered by skin.

- More painful, don’t particularly bleed as much as

internal haemorrhoids.

- Pain fibers are General Somatic Afferent from inferior

rectal nerves.
Blood supply and venous drainage • Anterior division of internal iliac
artery:
• Rectal venous drainage: the rectum has dual venous
drainage into systemic circulation. 1) Internal pudendal artery ( same
- Superior rectal vein—> superior mesenteric vein—> branches as pudendal N)
portal vein
- inferior rectal artery
- Inferior and middle rectal veins—> internal iliac vein—>
IVC - perineal artery
Q: what’s the clinical significance of the dual venous
drainage? - dorsal artery of penis/ clitoris
A: in liver damage—> blood flow impaired in portal system— 2) Obturator artery
> back pressure of blood—> haemorrhoids and rectal varices.
3) Umbilical artery
- vesical artery
4) uterine and vaginal artery (
females)
Anterior division of internal iliac Summary of routes
Tip for exam: apart from ovaries
and testicles, almost
everything else in the pelvis is
supplies by internal iliac artery
(directly or indirectly).
Blood Supply:

Ovarian and testicuar arteries (directly off Aorta)

- Ovarian—> reaches ovaries via suspensor ligament.

- Testicular—> reaches testicles via inguinal ligament

2) Internal iliac artery (anterior and posterior divisions)

- EVERYTHING ELSE basically! —> pelvic viscera, pelvic

walls and floor, perineum, erectile tissues of clitoris and
penis, gluteal region( upper thigh).
Nerves to the pelvic
• Q: what can cause pelvic floor damage:
• The main nerve to know is Pudendal • A : 5 main reasons:
Nerve (s2,s3,s4):
Exits through greater sciatic foramen 1) Age: gravity
(between piriformis and coccygeus 2) menopause: atrophy of tissues after
muscles)—> crosses ischial spine (close oestrogrn withdrawal
to sacrospinous lig)—> renenters pelvis
intro perineum via lesser sciatic 3) obesity: increases load upon pelvic
foramen ( with internal pudendal masculature
artery)—> enters pudendal canal/
Alcock’s canal—> gives 3 branches: 4) Chronic cough
(see slide 13)
5) childbirth:
- Inferior rectal nerve:
- stretch of pudendal nerve—>
- Perineal nerve neuroparaxia and muscle weakness
- Terminates as dorsal nerve of the - stretch and damage to pelvic floor and
penis perineal muscles—> muscle weakness
- stretch/ rupture of ligaments which
support muscles—> ineffective muscle
action
—à all these can cause PROLAPSE and/or
incontinence (uriine or fecal).
Anatomy of male reproductive tract • Seminiferous Tubules:

• Leydig cells—> outside the lumen between tubules—>

• Overview: Under LH control—> produce Testosterone.

- Scrotum and testes. • Sertoli cells—>somatic cells fixed to BM within the

lumen—> under FSH control—> involved in
- Spermatic cord (contains vas spermatogenesis.
deferens) • Myoid cells—> smooth muscle cells—> contract to
transport spermatozoa through seminiferous tubules.
- Seminal vesicles, prostate gland,
bulbourethral glands • Vascular supply:

- Testicular artery—> from Aorta directly—> into spermatic

- Penis cord( with testes).
Testis: - Right testicular vein—> IVC

- Left testicular vein—> left renal vein—> IVC

** testicular veins form pampiniform plexus which surrounds
testicular artery—> this plexus is what gets swollen in
varicocoele.
 • 3) Vericocoele: “ bag of worm”—> varicose veins within
• Scrotum: scrotum .

• Contain testes. —> Pampiniform plexus gets swollen.

• 2 main layers:: Q: why 95% of varicocele happen on left side?

1- skin A: 2 reasons:

2- Superficial fascia containing dartos muscle. 1- left testicular vein drains perpendicularly into left renal vein—>
more likely to pool. ( the right oblique angle into IVC)
** Dartos muscle regulates temperature of testes by
2- Left testicular vein goes higher up than the right one..
contracting ( in cold) and relaxing (heat)—> testes
need to be maintained at a temp slightly cooler (2-3 ** varicocele on the right is RED FLAG—> could be a tumor
degrees) than the body and that’s essential for causing obstruction.
spermatogenesis—> if testes are warmer than they
should be it leads to infertility/ subfertility. Q : how to differentiate hydrocele and spermatocoele?

Scrotal lumps/ swelliings: A: hydrocele surrounds the whole testes and epididymis,
whereas spermatocoele is more on the epididymis side.
1) Hydrocoele: serous fluid in tunica vaginalis
- Transillumination test: if scrotum transluminates
Cryptorchidism ( Undescended Testes):
then it’s hydrocoele. ( in haematocoele or if there’s a
solid mass, wouldn’t transluminate). Most tete descend by 6 months of age—> if left untreated—>
remain in abdominal area—> elevated temperatures for testes—
> infertility/ testicular cancer.

2) Epididymal cyst/ spermatocoele: fluid filled cyst in

epididymis .

( spermatocoele is epididymal cysts that contains

sperm cells).
• Spermatic cord:

- If processus vaginalis remain patent

can cause:
1- Hydrocoele (fluid only)—> common
in children.
2- Indirect inguinal hernia (abdominal
contents plus fluid).
• Vas/ ductus deferens: • Accessory male sex glands: (3)

• Muscular tube (smooth muscle) capable of 1- Seminal vesicles

peristaltic action via sympathetic innervation. 2- prostate gland

• 3 muscle layers: inner and outer longitudinal 3- bulbourethral gland

muscles and intermediate circular muscle.
• Pseudostratified columnar epithelium with
stercocilia.
Seminal vesicles:

- don’t produce sperm!!

- Develops as outgrowth of ductus deferens, lies between bladder

and rectum

- Duct of seminal vesicles join ductus deferens—> form ejaculatory

duct—> prostatic urethra

- Internal iliac artery ( inferior vesical and middle rectal) and drains
into vesical and prostatic venous plexus

- Lymphatic drainage into internal & external iliac nodes and sacral
nodes.

- Secretions: (70-80% of ejaculate volume)

Alkaline—> neutralises acidity of urethra and vagina

Fructose—> energy source ( sperms fructose and glucose)

• Vasectomy ( male sterilisation): ductus is cut and
ligated just distal to superficial inguinal ring. Prostaglandinds—> suppresses female immune system

Clotting factors—> keeps semen in female reproductive tract post

ejaculation( semen in broken down later by other enzymes such as PSA).

Bulbourethral glands: (Cowper’s)

- Posterolaterally to membranous urethra.

- Secrete pre-ejaculate into spongy urethra—> lubricates urethra

and tip of penis, expels residues of urine and dead cells and
mucous, neutralises acidity in male urethra.

- Pre-ejaculate doesn’t usually contain sperm—> however

sometimes it does and can cause pregnancy ( hence why
withdrawal method can be ineffective method of contraception).
• Prostate gland:
• Prostate gland zones and lobes help localise
- Surrounds urethra and lies between pathologies.
bladder and levator ani.
• Zones: peripheral—> central—> transitional.
- Mainly glandular and contain
fibromuscular part. • Lobes: anterior, posterior, median.

- Internal iliac artery (vesical and rectal

arteries).
- lymph to internal iliac lymph nodes.
- Closely related to rectum—> can be
examined by digital rectal examination.
- Venous drainage into prostatic venous
plexus then to vertebral veins.
Q: what’s the clinical significance of the • Q: why prostatic cancer prognosis is bad?
venous drainage? A: mostly start in peripheral zone—> symptoms
develop when the the tumor reaches the inner zones
A: prostatic cancer easily spreads to so the tumor is asymptomatic initially.
vertebra via the venous plexus ( valveless
veins from the plexus and it runs the Q: in which zone BPH develop?
length of vertebral column). A: transitional lobe—> symptoms appear early and
include problems with voiding: difficulty starting
urinating, poor stream, intermittent stream, dribbling.

• Prostatic secretions:

Around 20% of volume

Acidic fluid

Enzymes: such as PSA breaks down clotting

proteins and enables semen to reliquify in vagina (PSA
is raised in prostate cancer).

Citric acid and acid phosphatase

• Digital rectal examination: • Penis anatomy:
- Walls of anal canal
- walls of inferior rectum
- Sacrum, coccyx and sacral lymph nodes
- Prostate: posterior and median lobes and
median sulcus—> can’t feel the whole gland
hence if there’s cancer on the other side it
can’t be felt—> normal examination doesn’t
exclude prostate cancer!!!

• Root: 3 erectile tissues (2 crus and 1

• Urethral areas: (HIGH YIELD PICTURE)
bulb) + covered by 2 muscles (
ischiocavenosus and
bulbospongiosus).
• Body: 3 erecile tissues ( 2 corpora
cavernosa+ 1 corpus spongiosum).
• Glans: opening of urethra—> corpus
spongiosum.
Blood supply :

• Prostatic urethra: receives ejaculatory duct.

• Membranous urethra: NON DISTENSIBLE
PART
• Penile urethra: receives bulbourethral gland
secretions
• Venous drainage: dorsal veins( deep • Deep perineal pouch in males:
and superficial)—> prostatic venous
plexus—> vertebral plexus.

• Superficial perineal pouch males:

• Innervation of penis: Contains penis, urethra, scrotal contents and

superficial perineal muscles.
Anatomy of erection:
- Flaccid penis: arterio-venous anastamoses allow
blood to bypass corpus cavernosum.
- Erection: 1) smooth muscle in helicine arteries
relax and straightened—> blood flow into corpus
cavernosum. 2) bulbospongiosus and
ischiocavernosus muscles compress venous plexus
to retain blood in penis.
• Bulbospongiosus muscle: helps
urethral emptying—> essential for
ejaculation.
• Ischiocavernosus muscle—> helps in
maintaining erection. • Lymphatic drainage:

Both are somatic muscles supplied by

pudendal nerve.
• Anatomy of ejaculation:
Sympathetic nervous system closes
internal urethral sphincter—> persitalsis ** Testes and ovaries: lumbar para-aortic( think of their origin!!!).
of ductus deferens and seminal vesicles— •Clinical problems of the penis:
> secretion expelled into ejaculatory - Priapism: persistent painful non-stimulated erection lasting more
duct—>prostate smooth muscle
contraction—> ejaculate squeezed into than 4 hours. (Medical emergency).
penile bulb. - Balanitis: inflammation of gland penis and often the foreskin
(common).
• Innervation of erection and ejaculation: -Penile cancer: mostly squamous cell carcinoma (rare).
point—> erection—>parasympathetic (s2- -Male catheterisation: (important)
s4) Why? Difficulties and dangers?

Shoot—> ejaculation—> sympathetic (L1- Urinary retention Navicular fossa

L2)
incapacitated Angle at penile bulb and membranous urethra

Surgery Prostate ( crest/ enlarged lobes)

Sphincters
Hormonal control of reproductive system
• In both sexes:
• Pulsatile GnRH—> Amount & Proportion of FSH and LH.
• FSH and LH secretion depends on signaling molecules that
act at gonadotrophs: 1) gonadal steroids 2) inhibin 3)
activins.
• FSH and LH care controlled independently. (Gonadotrophs
release one at a time).
• Gonadal peptides: inhibin and activin:
- Inhibin—> released from sertoli(males) and
granulosa(females) cells—> selectively inhibits FSH and is
released from developing gametes (the bigger the gamete the
more inhibin the more negative feedback)- See later the clinical
relevance.
- Activins—> from gonads and other tissues—> feedback to
pituitary and selectively activates FSH secretion.
Note!!
Females have intermittent fertility ( cycle)
Males have continuous fertility from puberty.
HPG axis hormones have multiple effects:
Gamete production, fertilisation, pregnancy, labour, neonatal
support.
Male system • LH binds to Leydig cells( outside tubules)—> testosterone production—> promotes
• Testosterone reduces GnRH (-ve feedback on
hypothalamus) and reduces FSH & LH (-ve feedback on spermatogenesis in 3 ways: 1) spermatogonial mitotic steps 2) sertoli cells
pituitary gland). interactions with gametes 3) sperm release.
• Q: which 2 hormones enhance testosterone production? (Not replace LH)
• Male reproductive apparatus must be always ready( • A: inhibin(sertoli cells) & prolactin( lactotrophs).
since females have small fertility window)—> hormone • 2 feedback systems in males:
levels are constant in medium and long term—> 1) LH promotes testosterone—> which inhibits GnRH and LH—> bring testosterone
continuous spermatogenesis—> achieved by negative levels back to normal.
feedback. 2) if spermatogenesis speeds up—>more inhibin secretion—> reduces FSH—>
brings spermatogenesis levels to normal.
• FSH binds to Sertoli cell—> stimulates sermatogenesis( ** That’s how constant levels of and a balance between testosterone and
mainly meiotic steps)—> sertoli cells produce inhibin. spermatogenesis is achieved.
(FSH works similarly in femals but on granulosa cells). • Q: give 5 actions of testosterone in male reproductive system.
A: testosterone functions: (think of if systematically from testes outwards)
• Q: what’s the marker for spermatogenesis rate
1) gamete production
2) Maintains epididymis and vas deferens
A: Inhibin secretion
3) Maintains prostate, seminal vesicles and bulbo-urethral glands (semen production)
4) Development and maintenance of external genitalia and secondary sexual
characteristics
5) sexual dimorphism throughout the body and behaviour

*** shorter term variations in testosterone levels exist in response to environmental

factors: circadian rhythm( higher in the morning), neuronal inputs, stress hormones etc.
Female system- Menstrual cycle
- Ovaries and uterus synchronise activities in each phase via hormones:
GnRH—> hypothalamus
Gonadotrophins(LH and FSH)—> pituitary
Gonadal steroids—> oestrogen and progesterone
Follicular/proliferative phase Ovulation
Luteal/secretory phase - Days 12-17 (normally 14) .
- days 0-12.
- 2nd half of cycle.
- Previous cycle unsuccessful. -Mid cycle.
- Corpus luteum in ovary.
- Follicle grow in ovary and uterus is prepared for -Brief period of fertility
- Changes in uterus in preparation
sperm transport and implantation, and changes to - Formation of corpus
for implantation and pregnancy.
fascilitate sexual interaction. luteum (remnant of
- LH maintains corpus luteum—>
- Menstruation: days 1-7 where uterine lining sheds. follicle)
secretes oestrogen and
- Preovulatory phase: endometrium proliferates
progesterone—> progesterone
(while follicle develops).
makes changes to uterus to be Q: which phase is variable in
- FSH binds to granulosa cells, LH binds to theca
more suitable for implantations and length and which is
internal cells—> stimulate development of follicle.
pregnancy. constant:
- LH surge stimulates ovulation.
- Progesterone is dominant, and A: follicular phase is
- Oestrogen dominates, and aims at achieving
aimed at implantation through: variable ( affected by
fertilisation through:
1) Thickening of endometrium into multiple factors e.g stress
1) Fallopian tube function
secretory form. and follicle quality)
2) Thickening of endometrium
2) Myometrium thickening but
3) Growth and motility of myometrium( to move luteal phase(ovulation to
reduction of motility
sperm) menses) is constant (14
3) Thick acidic cervical mucus.
4) Thin alkaline cervical mucus days) always!!!!
4) Changes in mammary tissue.
5) Vaginal changes
5) Increased body temp.
6) Changes in skin, hair, metabolism, Ca+ metablism.
6) Metabolic and electrolyte changes.
- Progesterone is low in this phase.
Menstruation
Mid follicular Pre-ovulatory phase and Luteal phase
- No corpus luteum
phase ovulation - Corpus luteum forms
- Follicles are only part
- Oestrogen an - High oestrogen spontaneously as a remnant
developed and secrete very
inhibin rise—> levels—> window of the follicle—> secretes
little steroid/ inhibin—>
oestrogen and progesterone selective opportunity of LH progesterone and
inhibition of oestrogen(( mainly
levels low—> little inhibition surge and ovulation.
FSH—> no new progesterone)—> suppress
on hypothalamus& pituitary—
follicles FSH and LH (no positive
> FSH rise which stimulates - Exact time of
develop. feedback)—> corpus luteum
follicle development. ovulation within this
- FSH binds to granulosa cells— - Oestroegn grows (by LH) and secrete
levels reach a window is dependent more steroids: oestrogen
> secrete inhibin—> follicle
threshold and on environement e.g. (granulosa cells) and
grows—> more granulosa
exert positive stress. progesterone (thecal cells) to
cells and FSH receptors—>
feedback on maintain uterine lining.
theca interna develops with
LH receptors—> secrete pituitary and - LH surge—> - Decrease in size after 10 days
hypothalamus— ovulation ( autophagy due to
androgens which is converted
> LH rise (FSH hypoxia/starvation and lack
to oestrogen by granulosa
less due to of HCG).
cells.
inhibin) - CL dies after 14 days!!!!
- Menses+ FSH rise and cycle
starts again.
 • Histology:
• Oestrogen feedback:

Moderate/ low titres of oestrogen—>

negative feedback—> reduce GnRH and
LH& FSH

High titres of oestrogen alone—> positive

Follicle: Stratum functonalis changes
throughout the cycle, stratum basalis

Uterine lining:
remains the same
feedback—> increase GnRH( and LH
&FSH)—> LH surge

• Progesterone effect:

Increases inhibitory effects of moderate

oestrogen

Prevents positive feedback of high

oestrohen–> no LH surge—> no ovulation
in luteal phase

• Progesterone and oestrogen effect on

GnRH:

Oestrogen reduces amount per pulse

Progesterone reduces frequency

• What happens when conception

occurs?

Embryo (then placenta)) secrete HCG—>

preserves corpus luteum—> progesterone
and oestrogen—> maintain uterine lining
for implantation—> cycle does NOT start
again.
 Puberty • GnRH control:
• Puberty: development of reproductive maturity.
Released under the control of several signals
• GnRH pulsatile secretion stimulates puberty.
Kiss 1 neuron which release kisspeptin neuropeptide is a
• It’s release is pulsatile (once an hour)—> frequency of pulses and key player.
amount of GnRH per pulse can change.
Environmental effects and body weight influence kiss 1
• General note!! Most hormones from hypothalamus are releasing neuron or GnRH directly
hormones (terminate with –RH).
Also feedback from gonadal steroids affect GnRH
• Puberty follows specific order- Taner staging ( 5 stages).

• Gitls puberty:

- Onset: 8-13 years • Factors affect puberty:

- Breast bud—> pubic hair start—> growth spurt—> menarche—> adult - Weight: leptin from adipose tissue stimulate GnRH via
breast and pubic hair. kisspeptin
- Breast development: no glandular tissue—> breast bud under areola( 1st - Melatonin from pineal gland: less melatonin—> less
pubertal sign in females)—> breast tissue outside areola—> areola
elevated above contour of breast and double scoop appearance—> GnRH
nipple protrusion and pigmentation.
- Timing: maturation of signal mechanisms—>
- Boys puberty glutamate, GABA down regulation, kisspeptin
neuropeptide.
- Onset:9-14 years

- Genital development begins(testes then penis)—> pubic hair growth—>

growth spurt—> spermatogenesis begins—> genitalia and pubic hair of
an adult. - Clinical conditions:

- Growth spurt: precocious puberty(early): GnRH secretion activated early—

> d/t weight, central (pineal tumour, meningitis),
Growth spurt starts later in males, longer and higher growth rate. uncontrolled gonadotrophins or steroids secretion
(hormone secreting tumour of gonads/ pituitary).
Proliferation of chondrocytes and terminates by fusions of epiphyseal plate
Delayed puberty: no breast by 13/ no menarche b 15 ad no
Under oestrogen control in both sexes. testicular growth by 14 in boysà treat with pulsatile GnRH
infusions.
 Menopause symptoms can be
relieved by Hormone Replacement
• Pre menopause: Therapy—> oestrogen given orally/
- Typically from age 40. patches/ topically/ gel.
- Follicular phase —> early/no ovulation

- Oestrogen Post menopause—> 12 months

- LH & FSH due to reduced feedback with no period.
- Fertility

- Hormone levels used as marker

• Menopause:

Oestrogen —> LH & FSH à occurs at age 49-50 years

vascular changes Hot flushes

uterus Regression and shrinkage of

myometrium and thinning of
cervix
Breast Involution some breast
tissue
Skin and bladder

Bone Reduces density

(osteoporoses) d/t increased
osteoclast activity
• Phases of coitus in male:
1) Excitement (erection)
Coitus
2) Plateau phase
3) Orgasm (emission and ejaculation)
• Uterine tube histology:
4) Resolution
Isthmus
Excitement:
Pscychogenic and tactile factors—> parasympathetic
(s2-s4)—> decrease Ca+ in SM.
Erecile dysfunction: 1) corpora cavernosa tear 2)
psychological issues 3) drugs.
-Ampula looks
like a maze—>
Sildenafil : phosphodiesterase 5 ectopic
inhibitor pregnancies!!

- Ciliated
columnar ep.

Ejaculation:
- Contraction of gland and ducts Capacitation: further maturation of sperm in the female system.

- Bladder internal sphincter contracts ( prevent

backflow)
- Muscle contraction
Semen inside the vagina:
- oxytocin—> uterine contraction
- Oestrogen—> thin alkaline mucous to allow
sperm passing
- Progesterone: thick acidic mucous prevents
infections.
• Fertilisation: (ampula)

1) Acrosome reaction Sperm head binds to zp3–> 2 enzymes released:

1) hyaluronidase: breaks between corona radiata cells
2) Acosin: breaks down ZP proteins.
2) Gamete fusion Sperm travels through zp—> reach oocyte—> sperm nucleus enters egg
cytoplasm.
3) Oocyte activation Fusion of gamete membranes triggers Ca+ release from SER—> cortical
granules release thir content to change membrane structure (prevent
polyspermy)

• Extopic pregnancy: implantation in uterine tube/ovary/abdomen—> embryo dies—> severe risk of maternal heamorrhage.

• Contraception:
Method Mechanism of action
Vasectomy Cut vas deferens bilaterally bilaterally (ensure ejaculate free of sperm)

diaphragm Hold sperm in acidic environment—> reduce survival

Cap Across cervix, 8 hours before and 48 hours after
Sterilisation Occlude fallopian tube (clips, rings, ligation)
Progesterone pill/ implant Thick mucousà prevent sperm from passing and may inhibit
ovulation
Combined oral contraception pill( oestrogen+ progesterone) -ve feedback to hypothalamus/ pituitary—> prevent follicular
development + loss of positive feedback of oestrogen mid cycle—> no
LH surge—> no ovulation
Intrauterine contraceptive device (IUD)- copper Interferes with endometrial enzymes + interferes with sperm
transport in tubes.
Emergency hormonal contraception High dose of oestrogen and progesterone, up to 72/120 hours after
intercourse—> disturb ovulation.
 Infertility

PCOS( polycystic ovarian syndorme):

• Definition: failure to Male Female
- Multiple small ovarian cysts—> raised LH &
conceive within one
Abnormal production d/t Anovulation (pituitary LH/FSH ratio—> oestrogen normal/ slightly
testicular disease tumours, weight loss, diete)+
raised.
year.
PCOS can cause anovulation
Obstruction of ducts d/t Tube defects ( e.g adhesion
infection/vasectomy d/t infection such as in PID)

• Primary: no previous Hypothalamic/pituitary Antisperm antibodies Induced ovulation:

pregnancy dysfunction (hormonal) - Depends upon on what levels the problem is!
- FSH administration: pituitary problem
Hormonal abnormalities

• Secondary: previous Endometrium abnormalities

- GnRH agonist: increase ovulation (pulsatile
administration)
pregnancy - Anti-oestrogen: decrease negative feedback—
> increase GnRH and FSH
• Causes of infertility:
(Important!!! Be
specific, and think of
the repro systems
systematically when
answering)
 Development of placenta and pregnancy
• The week of 2

2 cellular layers:

1) Trophectoderm: syncytiotrohpblast + cytotrophoblast—> extraembryonic structures: Yolk sac(provide

nutrients), amnion( membrane surrounding amniotic fluid), allantois( becomes umbilical cord),
chorion( becomes placenta).
2) Embryoblast/ inner cell mass: epiblast + hypoblsat —> embryonic structures

Day 6: syncytiotrophoblast invades uterine epithlium

Day 9: syncytiotrophoblast ingests meternal content to provide ATP

End of week 2: conceptus implanted, amniotic cavity and yolk sac suspended by connecting stalk

Aims of implantation:

1) Establish basic unit of exchange

2) Establish maternal blood supply within placenta

3) Anchor placenta
3 types of villi:

Primary villi: projections of trophoblasts—> outer:

syncytiotrophoblasts, inner: cytotrophoblast.

Secondary villi: invasion of mesenchyme into core—> outer:

sync.+cyto., centre: extraembryonic mesoderm

Tertiary villi: invasion of foetal vessels

• Decidualisation: changes to endometrium to promote Placenta anatomy:
implantation of embryo, induced by progesterone:

1) Endometrial stromal cells: secrete growth factors &

signaling molecules.

2) Uterine natural killer cells: regulate immune response

against non-self embryo

3) Remodeling of spiral arteries →low Resistance vascular

bed—> maintain high flow to meet fetal demands.

Development of placenta:
1st trimester: placenta estabished—> thick placental
barrier and multiple layers of cytotrophoblast
Term: thin barrier, cytotrophoblast lost—>
haemomonochorial!!! (1 layer of syncytiotrophoblats)
Functions of placenta:
** placenta takes over hormonal production by 11th
1) Metabolism—> storage point for glycogen( to release glucose),
week. cholesterol(precursor for oestrogen and progesterone), FA.
2) Endocrine: 2 steroid and 4 protein hormones:
Umbilical cord: - oestrogen
- Link placenta blood to foetus (week3). -progesterone
- Contains 2 umbilical arteries( deoxygenated blood - Human chorionic gonadotrophin
from foetus to placenta) - Human placental lactogen: important for maternal
- 1 umbilical vein—> oxygenated blood from metabolism to provide glucose for foetus.
placenta to foetus -Human chorionic thyrotrophin
- Human chorionic corticotrophin( similar to ACTH)
**Relaxin: by placenta & ovaries—> increase flexibility of
pubic symphysis and relax ligaments+ suppress oxytocin to
prevent premature labour.
3) Transport: 3) Trophoblast disease: (HCG raised not from pregnancy)
- Hydatidiform mole: trophectoderm is present but ICM
- Simple diffusion: water, electrolytes, urea & uric acid, gases.
is not.
- Facilitated diffusion: glucose - Choriocarcinoma: gestational disease—> trophoblast
cells which aren’t associated with embryo prolifrate—>
- Active: transporter on syncytiotrophoblasts (amino acids, iron, can also happen after pregnancy if trophoblasts remain in
vitamin) the uterus.
- immunity: only IgG antibodies
4) Drugs crossing placenta: mainly teratogenic drugs—>
Q: what hormone is detected in pregnancy? thalidomide (limb defects revise MSK), alcohol, vit A,
retinoids, therapeutic drugs, smoking, recreational drugs.
A: HCG—> produce by SYNCYTIOTROPHOBLASTS during 1st 2
months of pregnancy—> detected in urine.
5) Infectious agents:
Dysfunctions: -CMV
- Rubella—> cataracts and PDA
1) Implantation defects. - varicella zoster
- Zika virus—> damage placenta itself—> microcephaly
- SARS-CoV2–> crosses placenta and damages it.

6) Haemolytic disease of the newborn

- Rhesus blood group incompatibility between mother
and foetus—> Mother is rhesus negaive and foetus is
rhesus positive
- mother’s immune system will produce antibodies
attacking foetal RBC causing haemolysis
2) Pre-eclampsia: incomplete invasion of trophoblasts (T) to reach - Prophylactic treatment: Anti D antibodies.
maternal vessels (V)—> result in maternal hypertension (d/t
placenta contraction and vessels constrictions)
 Physiological changes in pregnancy
System Changes
Cardiovascular - Inreased blood volume, stroke volume, HR and cardiac output
- BP NEVER increases in normal conditions: T1 &T2 progesterone
decreases SVR(BP decrease), T3 aortocaval compression by gravid
uterus (BP normal)
- SVR decreases: vasodilation (more blood flow)+ increase leakage
through endothelium.

Renal - Increase: GFR, renal plasma flow, creatinine clearance, protein

exrtetion
-Decrease: urea & uric acid, bicarbonate, creatinine
Functional renal reserve decreases as GFR increases
Respiratory Increase: O2 consumption, tidal volume, PaO2.
Decrease: PaCO2, functional residual capacity( diaphragm moves
up)
Subcostal angle, anterior posterior diameter, and transverse
diameter increase
Carbohydrate metabolism - Placenta transport of glucose and store glycogen (GLUT1)
- Increase maternal peripheral insulin resistance—> switches to
gluconeogenesis and other fuels
- Achieved by Human placental Lactogen, prolactin,
oestrogen/progesterone, cortisol

Lipid metabolism - Increase lipolysis from T2 (before mother increases fat storage
to be broken down later).
- Increase in fasting plasma FA—> provide substrate for maternal
metabolism—> leave glucose for foetus
- Decrease fasting maternal plasma glucose
GI - SM relaxation by progesterone
- GI: delayed emptying (progesterone causes constipation)
- Biliary tract: stasis+ increased risk of pancreatitis
• Haematological changes:
• Dubovits score and Ballard: assessment of
Prothrombotic state—> fibrin deposition at implantation site—> increased
clotting factors and decreased fibrinolysis+ stais &venodilation—> DVT/PE gestational age of foetuses with no antenatal care.

• Physiological anaemia: Plasma volume increases while red cell mass • 3 stages of foetal development:
doesn’t increase as much.
1) germinal/pre-embryonic: 0-2 weeks
• Immune system:
2) Embryonic: 3-8 weeks
Placenta (foetal origin) produced antibodies to target maternal IgGs
against paternal antigens—> if antibodies are transferred: 1) Haemolytic 3) Foetal: 9 weeks- birth
disease (Rhesus incompatibility) 2) graves disease and Hashimotos
thyroiditis

Q: what are the risks associated with gestationtal diabetes in babies: • Pre-embryonic phase:

A: 1) macrosomia 2) stillbirth 3) congenital defects 4) hypoglycaemia in - Fertilisation (0): formation of zygote

newborn (d/t high insulin) 5) shoulder dystocia
- Cleavage(30h): 2 blastomeres of equal size
Q: in which trimester miscarriage and major developmental errors most
likely to happen? - Morula: compaction (cells held via tight junctions,
communicate via gap junctions)
A: First trimester—> since most organs and systems develop in this
period—> errors at this stage are significant. - Hatching: zona pellucida detatch d/t increased pressure.

Foetal Growth and Development - Blastocyst (day 6): outer (trophoblast), inner (embryoblast),
blastocyst cavity.
- Estimated day of delivery: add 280 days (40 weeks) to first day
of LMP.
- Gestational age: from the first day of LMP.
- Foetal age: from day of conception. - Implantation(day 6-10): formation of bilaminar disc, amniotic
cavity.
• Twins:
- Dizygotic: fertilisation of 2 oocytes
- Monozygotic: fertilisation of 1 oocyte—>
embryo split after 1st cleavage( 2placentas) or
inner cell mass duplicates( share placenta).
- Embryonic phase:
-Amniotic cavity, yolk sac, amnion, chorion,
allanotois. • Foetal well being:
- All body systems form in this stage. - pre-conception: folic acid, vit D, exercise, stop
smoking/alcohol/drugs.
Advice: know the origin of each organ and example
of organ that develops from each layer.
Material condition

Smoking Poor growth of placenta and

baby
Alcohol Foetal alcohol syndrome

Drugs Neonatal abstinence

• Foetal phase: syndrome

embryo called foetus—> increase protein mass then

adipose mass. - Symphysis- fundal height: estimated
age/growth of foetus.
12-14W: uterus fundus above pubic bone.
20-22: uterus top around belly button
36-40: uterus fundus under ribs
• Tests and scans:
• 4) Combined test
Q: Give 3 scans, when they’re done, and what are the findings.
Done between week 10 &14
A:
Combines: nuchal translucency+ beta HCG+ pregnancy associated
1) Dating scan: Crown-rump length plasma protein A.
Done between 7 &13 weeks. Findings: screen for Down’s syndrome

Findings: date pregnancy and estimate EDD+ rule out ectopic • 5) Quadruple test: (if not possible to measure NT)
pregnancy + number of foetuses.
Done between 14-20 weeks

Alpha-fetoprotein+ total HCG+ unconjugated oestriol+ inhibin-A

Findings: detect pregnancies at high risk of developing chromosomal

abnormalities ( Down’s, edward’s, Patau’s)

If result <1/150–> down’s syndrome—> amniocentesis or chorion

villous sampling( 0.5-1% risk of miscarriage).
2) Ultrasound- Anomaly scan:

Done at around 20 weeks

6) At birth: physical examination (72hrs), new born blood spot (1
Assess foetal growth and foetal abnormalities+ determine sex. week), newborn hearing screening.

3) Nuchal translucency test

Done in 1st trimester (11-13 weeks) Monitoring of foetal growth:

Sonographic appearance of fluid under the skin behind foetal neck—> - Biparietal diameter: distance between the parietal bones of the
detect chromosomal abnormalities. foetal skull

Used in combination with abdominal circumference and femur length

to assess growth in T2 &3.
• Problems with growth:
-Respiratory system doesn’t carry out physioogical function until birth. Resp
tract, diaphragm and lungs form early in embronic development.
- Small for age: (causes)
- Threshold of viability: viability is only a possibility once the lungs have
1) Premature entered terminal sac stage of development. (Before 24 weeks lungs
aren’t viable).
2) Constitutionally small
3) Urinary system: (week 10)
3) Growth restriction d/t pathology in mother/ placenta/baby.
-Foetal urine is a major contributor to amniotic fluid volume.
4) Infections (rubella, CMV, toxoplasmin)
-Development of urinary system is closely related to development of
- Macrosomia: reproductive system, mainly in early stages.

Can be caused by foetal hyperinsulinism (e.g mother with - NOTE!! Renal system in pregnancy is not necessary for homeostasis for
diabetes) the foetus—> however essential for amniotic fluid.

Can lead to : birth complications, post natal hypoglycaemia, - Amniotic fluid early in pregnancy is formed from maternal blood and
surfactant deficiency. foetal. Extracellular fluid .—> Later fluid is produced from renal tract and
urine mainly ( the foetus swallows amniotic fluid then).
Symmetrical vs asymmetrical growth restriction:
Q: what is the result of impaired foeal kidney function (unilateral/bilateral
renal agenesis)?
Symmetrical: biparietal diameter and abdo circumference are
lower than 10th centile expected. Oligohydramnios (little amniotic fluid)—> severe limb deformities+ small
chest+ pulmonary hypoplasia.
Asymmetrical: d/t to nutrition problem (usually placenta
dysfunction)—> preferentially supplies head and neck and brain—
> normal size head circumference, low birth weight, low
abdominal circumference

• Overview of systems: Unilateral renal

agenesis (exam
1) cardiovscular: question).
Middle mesoderm (day 18-19)

Beating and pumping (21-22D)

2) Respiratory : Q: what results from foetus inability to swallow e.g in oesophageal atresia?

-Derived from primitive gut tube A: Polyhydramnios (too much).

 • Foetal Physiology:
• Amniotic fluid:
Placenta:
-Functions: mechanical protection+ movement and growth of
baby. Eternal: uterine wall

- Contains cells from foetus and amnion and variety of Internal: amniotic cavity
proteins—> diagnostically useful in Amniocentesis.
Decidua (pregnancy)= endometrium (non-pregnancy)

These should be NO direct contact between maternal and foetal

blood—> if blood passes( foettomaternal transfusion)—> can cause
thyrotoxicosis in baby (if mother has it) and complete heart block (SLE).

Functions: nutrition+ gas exchange+ waste removal+ endocrine+

source of haematopoietic stem cells.

Q: what are the boundaries of placenta?

Nervous system: A: chorionic plate—> foetal boudary

- First to start developing Decidual plate—> maternal boundary

- Develops from neuroectoderm which forms neural plate Between them intervillous spaces.
along dorsal surface of the embryo.( week 3)
(Contain lakes of maternal blood into
- Corticospinal tracts required for coordinated voluntary
movement begin to form in 4th month. which Fetal villi grow into, surface area increased by brush border)—>
although close proximity there should be no direct contact.
- Myelination by schwan cells and oligodendrocytes begin at
4h month and is NOT complete at birth—> at birth most - The maternal side is divided into 15-20 cotyledones divided by
neonate’s movements are spinal reflexes —> when sulci—> each divided into smaller sections.
myelination of corticospinal tracts happen the higher
centres override these reflexes and voluntary movements
develop at 1st year of life—> damage to these tracts leads
to persistence of the spinal reflexes (features of cerebral
palsy and stroke).
Umbilical Cord Surfactants:
2 umbilical arteries—> deoxygenated blood to mother Produced at week 24–> increased production at
1 umbilical vein—> oxygenated blood to foetus
week 34–> they reduce surface tension on alveoli
surface allowing alveoli to open easily and stopping
** These vessels are longer than the cord—> twist and spiral to add
strength and protect against entanglement, compression, tension. them from collapising—-> breathing work is
reduced.
** delayed separation of the cord can occur in neutrophil dysfunction.
Administration of steroids to a mother with
Factors to allow oxygen exchange across placenta: threatened premature delivery can increase foetal
1) Gradient of partial pressures for passive diffusion (foetal umbilical surfactant production.
PO2<maternal PO2)

2) Large surface area (villi+ brush border)

3) Thin barrier (simple epithelium)

Respiratory and circulatory changes at birth:
4) Foetal Hb has higher affinity for O2 than maternal Hb. (Foetal
dissociation curve to the left) - Physcial, thermal and chemical stimuli occur during and
prior to birth—> baby breaths in—> lungs inflate—>
5) Foetal HIGHER foetal Hb concentration emptied of fluid—> decrease in pulmonary vascular
resistance—> more pulmonary blood flow and
6) Foetal Hb has lower affinity to 2,3 DPG—> higher O2 affinity oxygenation—> increase O2 tension—> increase
pulmonary venous return—> increased left atrial
7) CO2 passively diffuse from foetal to maternal side—> local pressure ( >than RA)—> FORAMEN OVALE CLOSES(
acidosis—> reduces maternal Hb affinity—> O2 is more easily functionally not anatomically at this point).
released—> Bohr effect. - Ductus arteriosus closes soon after birth in response to
increased O2 tension and reduced prostaglandins
Saturation of O2 in foetal blood is 70%! Howwever the high (metabolised by pulmonary circulation.
concentration of Hb allows for O2 delivery. - umbilical cord is cut—> arteries go into spasm and blood
flow in the umbilical vein stops—> ductus venosus
Foetal Circulation: closes.
HIGH yield!!
Q: what structure
remains open after
birth and causes
neonatal murmurs?
A: ductus arteriosus
STIs

Chlamydia life cycle:

Elementary body: rigid walls—> can initiate
new infection.
Reticulate body: larger and don’t initiate new
infection.
Endogenous: Bacterial vaginalis+ candida Q: Label the following picture.
Exogenous: Rest of them.

A: 1)Bacteria enter non ciliated

epithelium 2) Phagocytosis by macrphages
3)Neutrophils phagocytose bacteria.
Q: What is the most common organism
that causes bacterial vaginalis? What’s the
mechanism?
A: Gardrenella vaginalis
Replacement of the normal H2o2
producing lactobacillus spp in vagina by
high concentrations of anaerobic bacteria
Q: A woman presented with UTI
symptoms, then an STI was detected.
What is the most likely diagnosis?
A: clamydia
 Ovarian tumours
Gynaecological Tumours Uterine tumour
- 80% benign: young women (20-45)
Cervical cancer 1) benign(fibroid of Myometrium) - 45-65 y.o: malignant
- Squamous cell carcinoma and adenocarcinoma - Oestrogen dependent - Some tymours produce oestrogen +
- Asymptomatic androgens
- HPV16/18 induce morphological changes—> screening
- Heavy/painful periods - Poorer prognosis than other
(koilocytosis)
- Urinary frequency(compress bladder)
- Screening: 25-50 (every 3 years), 50-65( every 5 years) gynaecological tumours d/t difficulty to
- Postpartum haemorrhage
- Infertility (increased frequency of diagnose early.
abortions) - May present late and symptoms can be
confused with IBS
2) Adenocarcinoma of endometrium - Mass effect
- Causes: 1) HPV 16/18( E6&E7) 2) multiple partners 3) Causes: - Hormonal effects: menstrual disturbances,
early pregnancy 4) smoking 5) immunosuppression. - Unopposed oestrogen
inappropriate sex hormones
- Symptoms: early it’s asymptomatic—> then: 1) vaginal - Early menarche
- Late menopause - Late symptoms: ascites, obstruction,
bleeding 2) post coital bleeding 3)pain in sacral region
- Obesity perforation and death.
(invasion of pelvis)
- HRT - Aetiology: Genetic (BRACA 1), smoking,
- Spread: around uterus—> 1) rectum(fistula) 2)
Clinical presentation: obesity, HRT
bladder(fistula+obstruction
- Peak incidence 55-65 years (people live - OCP and pregnancy are protective (d/t
longer)
decreased ovulation and repeated trauma
- Postmenopausal bleeding
- Uterine enlargement (advanced stages) to surface epithelium
** prognosis depends on: 1) grade 2) Stage( - No screening program.
TNM classification)
Q: where endometrial cancer spread?
A: outer 2/3rds—> myometrium
Fallopian tubes metsatasis
Cervical stroma
Bladder/rectum and beyond pelvis
- Gardasil vaccine—> HPV 8,11,16,18 +
- Obturator lymph nodes—> external iliac
vulval/penile/head & neck tumours. nodes—> para-aortic
- External iliac nodes—> para-aortic nodes
3) Malignant Mesenchymal tumours:
- Leiomyosarcoma (highly malignant, poor
prognosis)
- endometrial stromal sarcomas
 -Extra-embryonic tymours Vulval tumours- similar in concepts to cervix cancer
All malignant - Pre invasive: VIN (vulval interepithelial neoplasia)- VIN 1,2,3.
Yolk sac - Squamous cell carcinoma
Choriocarcinoma - Adenocarcinoma
Endodermal sinus tumour- AFP+ B-HCG markers - Basal cell carcinoma
- Malignant melanoma
3) Sex cord stromal tumours - Same aetiology as cervical cancer
- Produce steroid hormones
- Benign or malignant Paget’s disease
- Granulosa cells tumours( malignant), - Presents as pruritic red area on labia majora.
1) Epithelial tumours: serous(spread) + mucinous( thecoma(benign), leydig cell( verilisation) - Mucin containing adenocarcinoma in epidermis
don’t usually spread) + endometrioid (resemble - Chronic condition
endometrial carcinoma) Big pale cells
- All can be benign, malignant, borderline
- associated with peritoneal disease(implants).
2) Ovarian germ cell neoplasms (B-HCG and AFP
can be used to monitor disease) Gestational trophoblastic disease
1) Hydatiform Mole (partial/ complete mole)
- Presentation: larger for date pregnant uterus/ bleeding in early
pregnancy + edematous grape like chorionic villi.
-Mature cystic teratoma: ** Leydig cell tumour can cause verilisation - Complete(risk of neoplasm): sperm fertilises empty ovum—>
Benign
Foreign tissue found ovaries ( skin, hair, teeth, bone, duplicate chromosomes OR dispermy where 2 sperms fertilise empty
thyroid…) ovum.
- Immature teratoma - Partial: 2 sperms fertilise ovum
Malignant - Monitor HCG levels (serum and urine)—> if rise—> chemotherapy.
neuroepithelium - Adviced not to get pregnant due to reactive tumour cells.
- Dysgerminoma
Malignant 2) Choriocarcinoma
Germ cells like seminoma 4) Secondary ovary tumours- metastasis - rare, malignant, high mortality
Radiosensitive - Genital: endometrial carcinoma - Usually after hydatiform mole or miscarriage.
-Monodermal - Extragenital: colonic, gastric( Krukenberg - No villi
Struma oavarii- specialised teratoma tumours), breast - Malignant tumour of trophoblast (syncytio and cytotrophoblasts)
Benign- thyroid like
- High propensity for systemic metastasis (genital tract, lungs,brain)
- Highly treatable with chemotherapy
 Prostate cancer
Males tumours - Peripheral zone
Prostate histology: - RFx: age, black race, family history
Inner cells—> pale—> secretory—> PSA
Outer cells—> basal - Symptoms: initially asymptomatic —> then
Corpora amylacea—> the red part—> normal becomes symptomatic: 1) poor stream 2) difficulty
starting/stopping urinating 3) frequent urination
4)blood in urine/semen
- Bone pain= metastasis
- Routes: seminal vesicles and bladder base (direct
invasion), blood, lymphatics, bone/vertebra(
through venous drainage).
- Diagnosis: palpable on digital rectal examination+
1) BHP biopsy
- Grading: gleason pattern score
- Staging: TNM
- Transitional zone—> compress prostatic urethra—> early signs! - Management: 1) prostatectomy 2) radiotherapy 3)
- Family history+ black race hormonal therapy (castration to remove androgen
- consequences: increased pressure in bladder feeds back into production), oestrogens, CYP17 inhibitors which
ureter—> ureter dilate and transmit pressure into renal calyx—> prevemt androgen production
hydronephrosis—> destroy cortex and medulla. - Prognosis: if detected early—> good prognosis
- Advanced: Thick bladder walls to squeeze urine out. Q: why PSA screening is not used?
- Treatment: 1) open operation(removal of gland) 2) TURP (go A: low sensitivity and specificity ( no normal level of
through urethra and remove the hyperplastic tissue. PSA and not all cancer patient have raised PSA)
Q: why prostate cancer has low prognosis?
A: late symptoms, cancer has already spread
Penis squamous cell carcinoma
- infections: syphilis, gonorrhea, herpes The Breast
Penile condyloma
benign viral wart- HPV 6,11
Koilocytosis: dark nuclei in pale cytoplasm
Squamous papilloma (benign)
Bowen’s disease
HPV 16
Carcinoma in situ (no spread)
Biopsy to determine infection or tumour
Histology: 1) cellular atypia 2) large cells 3) bizarre nuclei 4) prominent
nucleoli
Invasive squamous cell 1)Mammogenesis
HPV 16,18, HIV, not circumcised, smoking - Stimulated by oestrogen and progesterone
surgery
- 4th week of gestation—> born with few ducts and develop with
each ovulation
Testicular cancer
In testis malignant tumours> benign, in ovaries benign> malignant 2) Lactogenesis 1
RFx: chryptorchidism (heat), genetic - 1st phase: ductal-lobular-alveolar system hypertrophy
Germ cell tumours: seminoma+ teratoma - 2nd phase: 16 weeks of pregnancy—> alveoli accumulate
colostrum ( few water and glucose, citrate + rich in protein and
- Seminoma: minerals- good for immature kidneys)
Soft white fleshy mass in testis - Breast, areola, nipples increase in size
Same histology as dysgerminoma 3) Lactogenesis 2
Management: orchiectomy - Stimulated by drop in progesterone
- Teratoma - Day 3-8 postpartum
Mature/benign before puberty, immature/ malignant after puberty - Copious milk production
- Endocrine to autocrine
Sex cord tumours: leydig/sertolià leydig: small tumours with endocrine - Delayed in PCOS, hypothyroidism, obese
secretions (androgen/oestrogen)—> gynaecomastia
4) Galactopoiesis
- day9–> involution
- Maintain secretion
- Autocrine control
- Theoretically if suckling continues, this step can
last for years.

5) Involution
- Decrease in milk secretion
- Apoptosis (replaced by adipose tissues)
- Inhibiting polypeptides—> increase Na levels
- Prolactin inhibiting factor (dopamine agonist i.e
reduce prolactin)—> a component in the milk—>
when baby feeds this substances is excreted from Positive feedback for both
breast. hormones by suckling and smell.
-Prolactin—> from anterior
pituitary—> increase milk
Synthesis of milk: production in lactocytes.
Early colostrum—> late colostrum ** low cortisol helps in water
Early transitional—> late tranisitional transport, TSH promote
Mature milk mammary growth
-oxytocin—> from posterior
In alveolar cells: fat in SER, protein in golgi, sugar pituitary—> milk ejection
reflex—> myoepithelial cells
Q: give 4 benefits of breast feeding contract
A: rich in vitamins ,hydration, growth immunity—> **oxytocin inhibited by high
cortisol. What’s clinical
hence: 1) fewer infections in babies 2) brain growth significance??
3) responsive parenting 4) comfort 5) pain relief ** reduces BP and stimulates
thirst
Breast cancer ( revise the other breast breast conditions from slides)

Invasive ductal carcinoma (majority)

Ductal carcinoma in situ (can progress to invasive)
Invasive lobular carcinoma

RFx:
- Increasing age
- Reproductive history( age at menarche, age at first
birth…)- all related to oestrogen. Oncotype DX test: genomic test for early stage HER2- & ER+
- OCP (increase breast cancer and protective in Prognostic: how likely the cancer will come back
Predictive: likelihood benefit from chemo/radiatiton
uterus)
- HRT Familial breast cancer: BRACA1 and BRACA 2–> tumour suppressor genes
- Family history encode for BRACA1 & 2 protein—> the protein repair dsDNA from damage
caused by ionising radiation.
- Obesity BRACA 1 & 2 associated with ovarian and prostate caner.
- Alcohol and smoking
Diagnosis: Screening:
1) Mammogram 2) MRI 50-70 every 3 years—> mammography (chest xray)
Self examination is vital to identify any lumps!
Treatment: Tamoxifen
1) Surgery
- lumpectomy: preserve breast and remove tumour.
- Mastectomy
- Radical mastectom: removal of breast tissue and axillary lymph nodes.
2) Hormonal therapy
- Block ovarian function: oophorectomy/radiation
- Block oestrogen synthesis: Aromatase inhibitor (aromatase is an enzyme required to convert androgens into
oestrogen)us
- Block oestrogen effect: Tamoxifen—> block oestrogen receptor and reduce recurrence in women with ER+
cancer.
Q: describe the mechanism of action of tamoxifen, and what adverse effect can it have in the body?
A: oestrogen receptor works as a transcription factor—> when tamoxifen binds to ER—> prevents it from
binding to the coactivator protein—> inhibit proliferation of cancer cells. (Tamoxifen works only in oestrogen
receptor positive cancers).
Tamoxifen works as an agonist for ER in endometrium—> promote proliferation and can increase risk of Herceptin
endometrial cancer.
Q: why CYP2D6 is important clinically when tamoxifen is used?
A: tamoxifen is metabolised by CYP2D6 into endoxifen which block the ER—> genetic variations in CYP2D6
means that some people can’t metabolise tamoxifen hence treatment is ineffective.
** aromatase inhibitors are better than tamoxifen at preventing recurrence in menopause.

3) Targeted therapy
- Herceptin: monoclonal antibodies against HER2 receptor.—> bind to HER2 receptor: 1) receptor
internalisation 2) attract effector immune cells and kill cancer cells 3) bind to receptor and block the
cascade
- Pembrolizumab: checkpoint inhibitor—> Prevents PDL1 ligand on cancer cells from binding to PD-1 receptor
on cytotoxic T cells—> induce CTL attack on cancer cells.—> used in PD-L1 positive triple negative cancers
- PARP inhibitors: PARP( poly ADP ribose polymerase inhibitors repair ssDNA hence increase cancer cell
survival—> inhibiting it helps killing cancer cells.—> used in mutated BRCA HER2 negative cancer.