GROUP 11 FINAL 2023.pptx

MULUNGUSHI UNIVERSITY
LIVINGSTONE CAMPUS (SoMHS)
HUMAN ANATOMY PRESENTATIONS.
GROUP NUMBER 11
TO BE PRESENTED: HISTOLOGY OF THE FEMALE AND MALE REPRODUCTIVE SYSTEMS.
COURSE LECTURER: DR ADEMOLA UTHMAN YUSUF
DR VASEEM SHAIKH

GROUP MEMBERS AS REGISTERED BY THE UNIVERSITY
MEMBER’S NAME MEMBER’S ID NUMBER
260. NSOFU NATASHA 202107976
261. NSUNGA GERALD 202103309
262. NTAMBIKO AGATHA 202103203
263. NYANGU JOSEPHINE 202101704
264. NYIRENDA MWANIDA 202101764
265. NYIRONGO JOHN 202107650
266. NYOMBOLA EVANS 202004044
267. NYONI HAZEL DIANA 202107990
268. NYUNDU JOEL 202106800
269. PHIRI HOPE 202108066
270. PHIRI JASMINE BIBIAN 201903929
271. PHIRI NAOMI DALITSO 202105573
272. PHIRI OLIPA 202102430
273. PHIRI PETER 202204962
274. PHIRI SARAH 202106311
275. SABATA KAWANGA 202108466
276. SAILI ROBERT 202107529
277. SAKALA DALITSO 202107885

278. SAMPA MULENGA 202106429
279. SASOKOLOKE RABECCA 202105170
280. SASOKOLOKE KASANGILI 202102424
281. SHAPENGA MANASSEH 202101755
282. SHIKABONE GIVEN 202108111
283. SHIPANGULA OWEN 202103274
284. SHONGA THANDO 202104787
285. SIACHITEMA CYNTHIA 202106497

SEQUENCE OF HISTOLOGICAL CONTENTS TO BE FOLLOWED BY THEIR RESPECTIVE PRESENTERS.
1. HISTOLOGY OF THE MALE REPRODUCTIVE SYSTEM
 SCROTUM
 TESTES
 SEMINIFEROUS TUBES
 INTERSTITIAL TISSUE
 SERTOLI CELLS
 SPERMATOGENIC CELLS
 SPERM CELL
 EPIDIDYMIS
 VAS DEFERENS
 EJACULATORY DUCT
 SPERMATIC CORD
 ACCESSORY GLANDS
 SEMINAL VESICLE
 COWPER’S GLAND/BULBOURETHRAL GLAND
 PROSTATE GLANDS
 PENIS

2. HISTOLOGY OF THE FEMALE REPRODUCTIVE SYSTEM
 OVARIES
 FOLLICLES
 CORPUS LUTEUM
 UTERINE TUBES
 UTERUS
 MENSTRUAL CYCLE
 PLACENTA
 IMPLANTATION
 CERVIX
 VAGINA
 EXTERNAL FEMALE GENITARIAL
 MAMMARY GLANDS

HISTOLOGY OF THE MALE REPRODUCTIVE SYSTEM

SCROTUM
A Scrotum is an external fibromuscular sac located between the Penis and the Anus, it is composed of a skin
and smooth muscles and It is divided by the spermatic septum. It consists of a testis, epididymis, ducts deferens and
spermatic cord. The main function of the scrotum is to protect and provide favourable environment or conditions
for testes and other components found inside the scrotum.
LAYERS OF THE SCROTUM
The scrotum is anatomically made up of six layers namely, skin, dartos muscle, external
spermatic fascia, cremasteric muscle, internal spermatic fascia and tunica vaginalis.
• SKIN
The skin of the scrotum is a brownish layer, containing roots of scattered, crisp hairs that cover the scrotum surface. The
skin contains stratified squamous keratinized epithelium It is very elastic and capable of great distension, and on account of
the looseness and amount of subcutaneous tissue, the scrotum becomes greatly enlarged in cases of edema, to which this
part is especially liable as a result of its dependent position.

• DARTOS MUSCLE
Dartos muscle is a fat-free thin layer of smooth muscular muscle
that act to regulate the temperature of testicles, which promotes
spermatogenesis by expanding or contracting to wrinkle the scrotal
skin. The temperature is regulated at 3-4 degrees Celsius lower
than the internal core temperature.
• EXTERNAL SPERMATIC FASCIA
The external spermatic fascia is a thin membrane layer prolonged
downward around the surface of the spermatic cord and testis. It is
derived from the aponeurosis of the external oblique muscle and
separated from the dartos by loose areolar tissue.
• CREMASTERIC FASCIA
It is a thin layer of skeletal muscle found in the scrotum between
the external and internal layers of spermatic fascia, surrounding the
testis and spermatic cord.
• INTERNAL SPERMATIC FASCIA
It is a thin downward continuation layer of the transversalis fascia,
which loosely invests the spermatic cord.
• TUNICA VAGINALIS
It is a serous membrane covered by a layer of endothelial cells in
the inner surface that invests the testes

CLINICAL CORRELATIONS
Enlargement of the scrotum
The scrotum can swell in response to the enlargement of its contents, some of the causes are
 varicocele ; dilation of the veins draining the testes ,which is sometimes referred to as the bag of worms due to its
appearance.
 inguinal hernia; the contents of the abdominal cavity protrude into the scrotum via the inguinal canal.
 hydrocele; excess serous fluid in the vaginal cavity
 haematocele ; a collection of blood in the tunica vaginalis .

 Haematoma of the scrotum
It may develop as result of scrotal surgery or trauma in the genital region, this results in swelling and discolouration of
the scrotal skin. Sometimes the origin of bleeding may not come from scrotal contents but from the basal part of
urethra.

HISTOLOGY OF THE TESTES
• It is a pair of oval shaped male reproductive organ that sits in the scrotum.
• Functions both as an exocrine and endocrine grand, the exocrine product is
chiefly the sex cells(spermatozoa) and the endocrine product is testosterone.
Hence, the testis may be referred to as the cytogenic grand.
• Each testis is covered on the anterolateral surface by serous membrane called
tunica vaginalis, beneath which is the thick, white capsule composed of the
collagenous connective tissue known as tunica albuginea. Deep to the tunica
albuginea there is tunica vasculosa which is a high vascularised connective tissue.
Measurements
In a normal adult the volume of the testis (25ml) ,length (3-5 cm), width (2.5-3 cm).

Cont.
COVERINGS OF THE TESTIS
Tunica vaginalis
• The uttermost covering( peritoneal covering of the testis and the epididymis).
• They are basically two layers of the tunica vaginalis; the visceral and
the parietal.
• The visceral layer remains adhered to the tunica albuginea while the
parietal layer is adhered to the scrotum.
• A thin fluid cavity separates the two sections of the tunica vaginalis
and reduces friction between the testes and the scrotum.
• An increased quantity of the fluid between the layers can form a
hydrocele( accumulation of fluid).

cont.
Tunica albuginea
• Capsule of the testis
• The tunica albuginea gives connective tissue trabeculae called septula
testis which converge towards the mediastinum testis.
• The mediastinum testis is a connective tissue area containing the channels
of rete testis, large blood and lymph vessels.
• The septula testis divides the testicular parenchyma into 200 -300
testicular lobules. Each lobule contains 1-4 seminiferous tubules.
Tunica vasculosa
• Beneath the tunica albuginea there is a layer of loose areolar connective
tissue containing network of blood vessels. This layer is known as the
tunica vasculosa also lines the septula testis.

Clinical correlations
cryptorchidism; failure of one or both testes to descend from the abdomen to the
scrotum, it occurs in 4% of the male neonates , but in most of these individuals the
testes move to the scrotum during the first year. Bilateral cryptorchidism causes
infertility in not surgically corrected by 2- 3 years of the age.
hydrocele; an excessive accumulation of serous fluid in one or both sides of the
scrotal sac.

HISTOLOGY OF THE SEMINIFEROUS TUBULES

Seminiferous Tubules
 These are coiled tubules found within the testis.
 There are sites where spermatogenesis, sperm production and maturation takes
place.
 Each testis contains approximately 500-750 sperm producing seminiferous tubules
inside each testicle, these tubules may be up 70cm long and approximately
250micrometes in diameter.
 The tubules are lined with specialized stratified epithelium called germinal or
spermatogenic epithelium which consists of a basement membrane. the basement
membrane is covered by fibrous tissue with an innermost layer containing flattened
smooth muscle like myoid cells.
 The cells of the seminiferous tubules have tight junctions that relate between them
this closes all gaps of the structure.

Fig.2 Methylene blue x40 magnification screened specimen
showing overall cross section of seminiferous tubules

germinal epithelium
The thick seminiferous epithelium (germinal epithelium) is composed of two
different epithelial cell types;
1. the sertoli (supporting) cells
2. spermatogenic cells that are in the process of differentiation to form
spermatozoa.
It is surrounded by a basal lamina and a loose vascular connective tissue
called the tunica propria.

fig 2 labelled microscopic slide showing seminiferous tubules
at x40 magnification

Interstitial tissue
 The seminiferous tubules are surrounded by interstitium or interstitial
tissue. This is a loose intertubular connective tissue which contains clumps
of darker eosinophilic cells called the Leydig cells which produce and
release testestoren it also contains fibroblasts, lymphatics and blood vessels
including fenestrated capillaries.
 The fibroblasts and other cellular components adjacent to the to the
seminiferous tubules fuse with the myoid cells to form a continuous
peritubular tissue known as the lamina propria. This fibrous structure
corresponds to the existing lumen of the tubules, providing extra structural
framework

fig 3; x100 magnification showing cross section of interstitial tissue

During puberty, the
interstitial cells or leydig
cells mentioned in the above
diagram develop as large
round or polygonal cells with
a central nuclei and
eosinophilic cytoplasm rich
in small lipid droplets
responsible for androgen
synthesis (most important is
testosterone) with aid from
enzymes in the smooth
endoplasmic reticulum and
mitochondria.

lamina propria
 The fibroblasts and other cellular components adjacent to the to the
seminiferous tubules fuse with the myoid cells to form a continuous
peritubular tissue known as the lamina propria. This fibrous structure
corresponds to the existing lumen of the tubules, providing extra
structural framework.
 The myoid cells have a lot of rough endoplasmic reticulum indicating their
role in collagen synthesis. Rhythmic contraction of myeloid cells make
peristatic waves that help move spermatozoa and testicular fluid through
the seminiferous tubules.

fig 5 general overview of the seminiferous tubules at x100 magnification

Medical Relevance
 Normal spermatogenesis is dependent on the action of luteinizing
hormone(LH) and follicle stimulating hormone (FSH) produced by the
pituitary gland. LH binds to receptors on interstitial cells (of Leydig)
and stimulates them to synthesize the hormone testosterone.
 testosterone is involved in the development of the male secondary
sexual characteristics such as facial hair, pubic hair, increased
muscular build, deep voice etc.

Leydig cell hypoplasia
This is a genetic condition characterised by an underdevelopment of
interstitial cells, thereby causing low production of testosterone hormone in
the male genitalia. this in turn leads to numerous disorders such as ambiguous
genitalia and no development of secondary sexual characteristics in men.

x40 magnification of isolated seminiferous tubules surrounded by few or absent
Leydig cells.

Leydig cell hyperplasia
 This is the uncontrolled mitotic division that dictates over production of
testosterone due to the increase in Leydig cells.
 excess testosterone in men leads to low sperm count, shrinking of the testis
and importence.
 other related adverse effects include;
 prostrate cancer
 increased sex drive

hematoxylin stain x100 magnification of abnormal increase in number of Leydig cells

HISTOLOGY OF SERTOLI CELLS
• These are tall columnar epithelial cells that nourish
the spermatogenic cells.
• They divide the seminiferous tubules into two ,
namely
(a)basal compartment-contain primary spermatogenic
cells
(b)adluminal compartment-contain meiotically active
cells
Each sertoli cell supports 30-50 developing germ cells

FUNCTIONS OF SERTOLI CELLS
• Secrete inhibin which suppresses the release of follicle
stimulating hormone.
• Production and release of androgen protein (ABP) which
increases the concentration of testosterone
• Protects seminiferous tubules from circulating immune
components
• Secrete fructose that is necessary for transportation of
sperms
• Release of mature sperm into the lumen of seminiferous
tubules
• Secrete mullerian-inhibiting hormone which suppresses
the development of mullerian ducts and female
reproductive organs in males.

• Forms Blood Testis Barrier
Formed due to the presence of tight junction ,
hence , prevents autoimmune attacks against
spermatogenic cells.
CLINICAL RELEVANCE
Sertoli cells are immune privileged cells ,hence ,
they are used in treatment of disease.
FUNCTION OF SERTOLI CELLS

SPERMATOGENIC CELLS
• Are reproductive cells formed in seminiferous
tubules and stored in the epidydimis
• Have a length of 50 micrometer and
cytoplasm lacks most cytoplasmic organelles .
• However , they contain mitochondria,haploid
nucleus and acrosomal vesicles.
TYPES OF SPERMATOGENIC CELLS
• Type A-are dark and are renewing stem cells
• Type B-have spherical shape and a pale nuclei

THE SPERMATOGENIC PROCESS
• Sperms are formed through a process called
spermatogenesis.
• Spermatogenesis is the process through which
matured sperm cells are formed.
• The spermatogenic sperm (Type B)cells undergo
mitotic divisions producing a new spermatogonia
and a primary spermatocyte.
• Primary spermatocyte undergo meiosis I
producing two haploid secondary spermatocyte.

SPERMATOGENIC PROCESS
• The secondary spermatocyte undergo meiosis
II forming four spermatids.
• The spermatids differentiate and undergo
morphological changes (spermiogenesis) and
eventually become motile, matured cells.
Summary of Differenciation & Morphological
Changes of Spermatids
1. Acrosomal Phase
• Formation of head,acrosmal enzymes and
acrosomal cap

SPERMATOGENIC PROCESS
2.Tail Formation Phase
• Formation of tail from elongation of centrioles
3.Removal of excess cytoplasm

CLINICAL RELEVANCE
1. Azoospermia
• No sperm count in the semen
• Caused by blockage in the ejaculatory ducts and
higher temperatures
2.Asthenospermia
• A condition in which there is reduced sperm
mortility which occurs due to lack of nutrients
3.Decreased Semen Quality
• Is idiopathic, meaning the causes are unknown
and is a major cause of male infertility

The sperm is the male sex cell that is produced in the seminiferous tubules of
the testis and then later stored in the epididymis awaiting ejaculation.
• The length of the sperm cell is approximately 50 micrometers with the head
measuring 5.1 micrometers by 3.1 micrometers ( Head is oval in shape ) and
the tail measuring about 45 micrometers. A Sperm cell is light cream in color.
• A matured sperm cell does not contain most cytoplasmic organelles in its
cytoplasm. It contains mitochondria, haploid nucleus and acrosome vesicle.
• The mitochondria is located in the mid-piece and it is tightly packed into a
sheath where it provide ATP for energy to drive the movement of the
flagellum.
• Haploid nucleus contain tightly packed DNA, while the acrosome vesicle
contains hydrolytic enzymes ( Hyaluronidase and acrosin ) released when
sperm meets egg.

THE SPERMIOGENESIS PROCESS
Spermiogenesis is the process by which the complete structure of the sperm
cell is formed. It takes place after spermatogenesis. Spermiogenesis is a
temperature sensitive process, which basically takes place in four phases. These
phases are
1. Golgi Phase: In this phase, spermatids begin to gain polarity. The head forms
on one end and the Golgi apparatus forms and the enzymes that will
become the acrosome. On the other hand, a thickened mid-piece is formed
where the mitochondria gather and the distal centrioles begin to form an
axoneme.
2. Cap / Acrosome phase: During this phase, the Golgi apparatus surrounds
the condensed nucleus becoming the acrosomal cap. The cap spreads over
about half the condensed nucleus.
• Acrosome is a specialized lysosome containing mainly the enzyme Hyaluronidase and acrosin which
penetrate the corona radiate and zona pellucida of the oocyte ( egg ). Acrosome reaction

3. Tail Formation phase: Head remains embedded in the sertoli cells while the
growing axoneme extends into the lumen of the tubule. Nuclei becomes
condensed and histones replaced by protamine.
• Flagellum growth continues distally in the tail and the mitochondria aggregate around it proximally to
form a middle piece where ATP for flagellum movement is generated.
4.Maturation Phase: During this phase excess cytoplasm known as residues is
removed by phagocytosis by surrounding sertoli cells. Remaining intracellular
bridges are lost.
Fully formed, but not yet functional or mobile sperm are released into the lumen
of the seminiferous tubule.

PARTS AND CONTENTS OF SPERM CELL
Head: Acrosomal cap, Nucleus and Cytoplasm
Neck: Constriction distal to the head. Also called the connecting piece. Has Basal
Body
Body (Mid piece): swollen part behind the neck. Consists of: Cell membrane,
Cytoplasm, Mitochondrial sheath, Axial filament.
Annulus: Distal to the mid piece ,Also called Jenseng’s ring.
Tail or principle piece
 Proximal principle piece; Extends from the annulus to the end piece. it contains;
Axoneme, surrounding fibers which are then encircled by fibrous sheath.
 Distal End piece: Contains; Axoneme, plasma membrane

CLINICAL CORRELATION
Decreased semen quality, which is often idiopathic (arising from unknown causes),
it’s a major cause of male infertility. Common features of poor semen quality are oligospemia
(ejaculate volume > 2ml. Ranging 1.5 to 5.0 ml). Sperm cell density<10-20 million per liter.
Fewer than 15 million sperm per milliliter or less than 39 million sperm total per ejaculation.
Asthenospermia; It is basically the reduced sperm motility less than 40% or 35%. This is
an infertility condition characterized by the inability of the sperm cell to swim through the
female reproductive tract to reach the oocyte for fertilization.
This is due to lack of nutrients that helps in the production of energy such as( fructose, vitamin c, lactic acid
proteins and vitamin 12).
Varicocele; also contributes to the reduced sperm motility due to enlargement of veins in the
scrotum.
Azoospermia; No sperm count in the semen. This is caused by blockage in the ejaculatory
ducts and higher temperature that can result to sperm death. Causes can be due to
inflammation, trauma or infections or development of a cyst.
Globozoospermia; inherent gene Mutation condition characterized by abnormal sperm cell
in which the sperm does not develop an acrosome, no acrosomal enzymes and head
becomes round. This leads to inability of the sperm to penetrate the egg, thus infertility.

ABNORMAL SPERM MORPHOLOGY
1. ABNORMAL HEAD
• No head (Pin headed sperm)
• large head or Bent head
• Double head
• Abnormal midpiece
2. Bad Swimmer ( Asthenospermia )
Can as well be Asthernozoospermia
Asthernozoospermia is a condition in which a
person has zero sperm motility.
Characterized by long tail or double tail such that the
flagellum cant propel the cell normally.
3. PYOSPERMIA ( Leukocytospermia )
• This is a condition in which an unusually high number
of white blood cells are in semen. WBCs come from
the epididymis.
• These white blood cells can damage the genetic
matter in the sperm and weaken the sperm cells.
• Generate reactive oxygen Species (ROS) that can
impair sperm motility (defects in the tail function)
CAUSES
Viral infection, Varicocele, or trauma.
30% of infertile males have Leukocytospermia, although
in 80% of leukocytospermic infertile males, no microbial
infection can be detected in their semen.

TREATMENT
• There is no clear treatment for Leukocytospermia
• However, Antimicrobial therapy can be considered in an infertility setting.
• Antibiotics ( but there is no evidence of increased pregnancy rates after antibiotics treatment ).

4.TERATOZOOSPERMIA
 This is characterized by the presence of spermatozoa with NORMAL SPERMS LESS THAN 4% (abnormal morphology over
85%) in sperm.
 When all the spermatozoa display an abnormality teratozoospermia is said to be monomorphic.
 Two forms of monomorphic teratozoospermia: representing less than 1% of male infertility include;
1. Macrozoospermia (also called macrocephalic sperm head syndrome)
2. Globozoospermia (also called round-headed sperm syndrome)
Majority of the studies found that globozoospermic males had a sperm DNA fragmentation index higher than the
fertile men.
Mutations or deletion in three genes
1. SPATA16 (protein localizes to Golgi apparatus and the proacrosomal granules that are transported into the acrosome
in round and elongated spermatids)
2. PICK1 (localizes to Golgi derived proacrosome granules and is involved in vesicle trafficking from the Golgi to the
acrosome and participates in acrosome biogenesis).
3. DPY19L2 (cell polarity)
have show to be responsible for Globozoospermia.
 These are rare cases observed in less than 0.1% of infertile Males.
 NOTE: for pregnancy; 15 million /ml sperms in 1.5ml semen and 32% motility and 4% normal morphology

TREATMENT FOR GLOBOZOOSPERMIA
Is by using Assisted oocyte activation using 4-Bromo calcium Ionophore
This test allows for the sperm even though it does not have an acrosome to achieve fertilization.
Morphological test should follow Kruger’s strict criteria
IVF test showed that only morphologically normal sperm cells were binding to the oocyte.
HOW TO IMPROVE SPERM MORPHOLOGY
1. Healthy lifestyle
2. Taking walk for 45 to 60 minutes – walking helps improve testosterone production. Hence enhance quality of
sperms.
3. Sleep for 6 to 8hrs helps to improve early morning testosterone production. Hence good sperm quality.
4. Taking folic acid and glycerate for 75 days (1 cycle of sperm production).
AVOID
Smoking, Alcohol, Marijuana and drug abuse.

5. Necrozoospermia
This is a condition in which there is low percentage of live sperms and a very high percentage of immotile
spermatozoa in semen.
This is a medical term used to describe the presence of dead sperms in fresh semen sample.
It is a common cause of male infertility.
Can be moderate = 50 – 80% or severe = >80%
CAUSES
• Prolonged period of no ejaculation
• Testicular cancer
• Toxins such as pesticides, mercury or cadmium
• Testicular cause: Abnormal high temperature (40◦ C sperms start to die and 42◦ C ≈ all sperms will be
dead) as in hyperthyroidism, Varicocele and hot tab baths.
• Post testicular: Epididymal Necrozoospermia. Vasectomy reversal, anti-sperm antibodies, seminal
plasma abnormalities and adult polycystic kidney disease.

DIAGNOSIS
Can be diagnosed by a semen analysis done by using Eosin test or Hypo-osmotic flagella coiling test.
TREATMENT
Etiological i.e. directed towards the cause by the avoiding exposure to high temperatures or toxins and
giving antibiotics to treat the infections.
 Medications: like antioxidants or anti inflammatory drugs can be used.
 IVF with ICSI: Fertilization chances are low in Necrozoospermia but in vitro fertilization with ICSI
improves the chances of conception.
 IVF with TESE & ICSI: in conditions caused by post testicular causes,
IVF with ICSI using sperm obtained by TESE is the best treatment possible wherein sperms are
obtained directly from the testis by taking a small incision and removing a small tissue.
 IVF with DONOR SPERMS: Alternative in vitro fertilization with the donor sperms should be considered
if other treatment fails.

General Common causes
i. Abnormally increased testicular temperature
ii. Exposure to toxic chemicals
iii. Reproductive or urinary infections
iv. Genetic Traits
DIAGNOSIS
Examined under a microscope (semen Analysis)
TREATMENT
i. Sperm washing – way of removing low quality sperms and mucus from semen to increase chances of pregnancy
ii. Intrauterine insemination (IUI) – this form of artificial insemination involving the placing of the sperm directly
into the uterus. Boosting the chances of successful pregnancy.
iii. In Vitro Fertilization (IVF) – this involves fertilization of the egg in the lab before transferring the embryo to a
woman so that it can be carried to term.
iv. Intracytoplasmic Sperm Injection (ICSI) – may be used as part of IVF, this involves direct injection of sperm into
the egg
v. Sperm Donation – sometimes it may be ideal to rely on a donor sperm, which is healthy and of good quality.
Sperm donor can be selected via appearance and personality profile to ensure a good match and a greater
chance of treatment success.

The epididymis is a long comma shaped structure that is on the posterior
aspect of each testes.
It is about 4 to 5m in length and consists of three main parts; The head
which is formed by the efferent ductules ,the body and lastly the tail that
continues as the vans deferens.
Apart from the epididymis being the storage medium of spermatozoa, it is
a site for fuctional maturation of the sperm.
The epididymis is lined with psuedostratified columnar epithelium with
stereocilia.
The lumen of the epididymis contains spermatozoa.

LAYERS
 The epididymis is made up three layers.
1. EPITHELIUM
The epithelium is the innermost layer of the epididymis that
forms close contact with the lumen.
2.LAMINA PROPRIA
The lamina propria is a thin layer where the epithelium rests
3.SMOOTH MUSCLE LAYER
The smooth muscle layer comes after the lamina propria and
increase from the tail region to the head region.It contains cells
that undergo peristaltic contractions moving the spermatozoa
towards the middle segment of the duct, which is the site of final
functional maturation of the spermatozoa - now they are motile.
The terminal segment of the ductus epididymidis is the site of
storage of the mature spermatozoa. Smooth muscle fibres of the
terminal part of the ductus epididymidis do not contract
spontaneously. They contract during sexual stimulation
concurrently with the contraction of the musculature of the duct
into which it opens, the vas deferens.

CELLS
 Within the epithelium there are two main cells that are
embedded in the layer.
1.THE PRINCIPAL CELLS
The pricinpal cells are the main cells and are resposible for
the secretion and absorption of fluids for the fuctional
maturation of the sperm.
These cells are pseudostratified epithelial cells with
stereocilia which is thick microvilli that is puhed towards
the lumen of the epididymis.
FUNCTIONS includes
reabsorption of fluids and secretion of sialic
2.BASAL CELLS
These are cuboidal cells that do not reach the lumen of the
epididymis,they are seen close to the basement
membrane.They are precursor cells for the principal cells
and do not have any secretory properties but rather play a
role in renewal and mainteinance of the epididymal
epithelium.

OTHER CELLS
 The other cells that are region based include;
INTRAEPITHELIAL MACROPHAGES
These cells are embedded within the epithelium of the epididymis and are
mainly for phagocytosis of defective spermatozoa
APICAL CELLS
These cells are mostly found in the head redion of the eoididymis and contain
numerous mitochondria.
CLEAR CELLS
These are present on the tail region of the epididymis with few microvilli active
for endocytic reaction.They are specialised in secretion of glycoproteins which
help maintain the proper environment for sperm maturation.

1.Epididymitis
This is the inflammation of the epididymis,it can either be acute (which means it can last for six weeks or less) or chronic
(which means it can last for six weeks or more).It is caused by a bacterial infection such as urinary tract infecions,prostate
infections,tuberculosis and other non-sexually transmitted diseases or sexually transmitted infections such as gonorrhea
and chlamydia and is common in individuals of all ages but common in males aged 14 to 35
years.Ocassionally,complications with severe epididymitis arise which involves the condition spreading from the epididymis
to the testes which now becomes epididymo-orchitis

symptoms includes;
-low-grade fever
-enlargement lymph nodes in the groin
-urgent or frequent urination
-abnormal discharge from the penis
-or blood in the semen
Treatment
Treatment for epididymitis is dependent on the underlying infection.
Treatment for bacteria infection often includes medication such as
antibiotics, pain medication and anti-inflammatory medication.
If no other treatment prove successful, surgery may become an option
(especially in epididymo-orchitis). In these circumstances, all or part of
the epididymis and in rare cases, the testicle may be removed.

2.Epididymal cyst
This is a fluid-filled growth on the testicle (testes).
They are asymptomatic but once one has a small water ballon-like mass is noticed. They rarely
require treatment unless it is painful or when it brings discomfort a surgery is done..

3. CANCER OF THE EPIDIDYMIS
Epididymal tumors are commonly soft tissues or mesothelial neoplasm in
origin.
Tumors of the epididymis, both primary and secondary whether benign or
malignant are very rare, symptoms include tender, swollen or hardened
epididymis.

DUCTUS (VAS)DEFERENS
 Each ductus or(vas) deferens, a long straight
tube with a thick muscular wall and a relatively
small lumen leaves the scrotum and contains
towards the prostate urethra where it empties.
 The vas deferens is a pair of long muscular
tubes of about 0.118 inches thick and 30-
45cm long that extends from the epididymis
into the pelvic cavity, just behind the bladder.

Histologically, the ductus deferens consists of
3 layers, the outer layer, the middle muscular
layer, and the internal mucous layer.
The middle or muscular layer is remarkably
thick in proportion to the luminal diameter and
consists mostly of outer longitudinal smooth
muscle Fibers with inner circular muscle fibers.
Interestingly, at the proximal most segment of
the Ductus deferens, the muscular layer is
divided into 3 sections,
 an outer and inner layer of longitudinal muscle
fibers with a middle layer of circular fibers.

However, as the ductus ascends towards the
inguinal canal, only 2 muscular layers are present
and the inner most longitudinal muscle fibers are no
longer present. This muscular layer is about 1.5mm
thick is palpable in the spermatic cord.
The mucosal layer is protective for the lumen and
consists of pseudostratified columnar epithelial cells
arranged in a longitudinal fashion.
The lamina propria is rich in elastic fibers. The
columnar cells have apical stereocilia that help
project the sperm along the tube. There is also a
layer of basal cells that function primarily to replenish
the columnar cells. The lumen is about 2.5mm in
diameter.

The ampulla (which is the distal portion of the
vas deferens) receives a duct draining from the
seminal vesicle forming the short ejaculatory
duct. These converge to join the urethra as they
pass through the prostate gland. The ejaculatory
duct lacks a thick muscular wall, but it has a
mucosa similar to that of the vas deferens.
The main function of the vas deferens is to carry
sperm from the epididymis to the ejaculatory duct
which in turn empties the sperm into the urethra.
The vas deferens propels the sperm via
peristalsis. The peristaltic contractions are
stimulated by the sympathetic nervous system

Vasectomy
A vasectomy is a common surgical procedure that involves cutting, burning
or otherwise purposely occluding or impairing the function of the vas
deferens as a means to render a man sterile. It is one of the most widely
used forms of male contraception available. This procedure is done by
making a very small incision though the scrotum so as to expose the vas for
cutting, while the patient is under local anesthesia. It is often performed by a
specialized healthcare provider called an urologist although other types of
healthcare providers may be qualified to do the risks of a vasectomy include
a negative reaction to the anesthetic medication used, bleeding, infection at
the site of the incision (or puncture), recanalization, hematoma and sperm
granuloma. It is also possible to develop chronic pain, a condition called
post-vasectomy pain syndrome. It is normal to have some pain for a few
days following a vasectomy and ice packs are recommended to help with
any pain or swelling. Follow your healthcare provider's instructions exactly
following the procedure to minimize your risks for any post-operative
complications.

Natural Variants
In some men, a non-functional anomalyis found associated with
the ductus deferens. The vas aberrans of Haller is a long tube
commencing at the tail end of the epididymis or with the ductus
deferens and extends into the spermatic cord. The tube length
is variable and has been measured anywhere from 2-14inches.
Itterminates abruptly and has no effect on the male
reproductive tract.

 Inflammation
Inflammation of the vas deferens is a rare condition
sometimes referred to as vasitis. It often occurs after a
vasectomy in which case it may cause no symptoms
other than a palpable mass in the vas deferens. This
mass may not necessitate any treatment but may need
to be biopsied to confirm that it is benign. While rarer,
infections can also cause inflammation of the vas
deferens. These rare infections are usually caused by
the same types of bacteria that cause urinary tract
infections and once diagnosed can typically be treated
with antibiotics.

Tests
Semen analysis may be done to check for male fertility and blockages of
the vas deferens. This test will include the volume, number of sperm per
milliliter, percentage of motile sperm, the shape of the sperm, and the
presence of white blood cells. A semen culture may be performed to
check for infection or inflammation. Imaging may be done to look for
conditions affecting the vas deferens, including ultrasound,
computerized tomography (CT), or magnetic resonance imaging (MRI).
In the case of a suspected malignancy, a biopsy may be performed.

Obstructive Azoospermia
Obstructive azoospermia is a condition where either the vas deferens, the
epididymis, or the ejaculatory ducts are blocked or obstructed preventing sperm
from traveling properly along its normal route to leave the body. Typical causes of
obstruction may include congenital deformities (congenital absence of the vas
deferens is actually a form of obstructive azoospermia), trauma, injuries, or
complications from surgeries including hernia repair or vasectomy. Sometimes these
obstructions can be surgically corrected to restore the proper flow of sperm and
fertility.
Anatomical Variations
While rare, it is possible to be born without vas deferens—a condition which causes
infertility. The congenital absence of the vas deferens can occur alone but is often
associated with another genetic condition called cystic fibrosis. While males who are
born without the vas deferens are typically infertile the condition does not affect
their sex drive or ability to have sex. Some people with congenital absence of the vas
deferens are able to father children with the assistance of reproductive technology

THE EJACULATORY DUCT
• The ejaculatory duct is a straight duct that penetrates through the prostate gland
and is formed by the union of the vas deferens and the duct of the seminal vesicle
.It serves as a route for sperm from the vas deferens and transports into the
urethra.(Opens into the urethra above the seminal colliculus)
• It is two cent meters in length and functions as a route through which the
seminal vesicle empties its secretions.
• It delivers sperm into the urethra , adding secretions and additives from the
prostate necessary for sperm function while providing an interface between the
reproductive and urinary system in men.
• Under a microscope , the ejaculatory ducts consists of three layers that are
extremely thin; the outer muscular layer, the middle layer made up of collagenous
material and an inner mucosal layer consisting of pseudo stratified columnar
epithelium.

• In the proximal region of the ejaculatory duct the epithelium is
simple or pseudostratified columnar epithelium.
• It often appears as transitional epithelium in the distal region.
• The epithelial cells appear to have secretory activity and contain
large numbers of yellow pigment granules.
• The mucosa of the ejaculatory duct is thrown into slender folds that
extend into the lumen but are less elaborate then those of the
ampulla.
• The lamina propria contains abundant elastic fibres .
• There are no muscularis in the wall of the ejaculatory duct . This
portion of the ductus deferens is surrounded by the fibromuscular
tissue of the prostate gland.

• The bovine ejaculatory duct is lined with pseudostratified columnar epithelium
. Two cell types are present; small basal cells and columnar principle cells in
different functional states .The basal cells are able to accumulate lipid material
which is essential for the function and integrity of the spermatozoa
.The principle cells are observed in a less active state and in a state of either
increased endocytocis and fluid uptake or active spermiophagy.
Endotitically active cells are characterise by an apical brush boarder and a
system of microvesicles , microvascular bodies and lysosomal dense bodies.

• EJACULATORY DUCT OBSTRUCTION
• This is an acquired or congenital pathological condition in which one or both
ejaculatory ducts are obstructed . In the case that both of the ducts are obstructed,
this illness presents with symptoms of aspermia and male infertility.
• SURGERY TO CORRECT BENINGN PROSTATIC HYPERPLASIA.(PROSTATE ENLARGEMENT)
• This surgery may destroy the duct leading to retrograde ejaculation.
• Retrograde ejaculation empties the seminal fluid formed in the emission phase into
the bladder of the male instead of expelling it through the urethra and out the tip of
the penis . This results in dry orgasm where the orgasm may be still experienced but
without expulsion of semen from the ejaculatory ducts.
• ANATOMICAL VARIATIONS
• It is possible to be born without a vas deferens, a rare condition that causes infertility . Males
who are born without vas deferens are typically infertile but it does not affect their sex dive or
ability to have sex. The congenital absence of a vas deferens is usually associated with another
genetic condition known as cystic fibrosis. Males with the congenital absence of vas deferens

OBSTRUCTIVE AZOOSPERMIA
OBSTRUCTIVE AZOOSPERMIA
Obstructive azoospermia is defined as the absence of spermatozoa in the
ejaculate despite normal spermatogenesis . It occurs as a result of obstruction
or due to abnormal sperm production. It is a common urologic condition and
accounts for 61 percent and 13 percent of patients presenting for fertility
evaluation.
Obstructive azoospermia accounts for 40 percent of all azoospermia cases.

THE SPERMATIC CORD
Collection of structures that pass to and from the testes.
It extends from the inferior abdominal wall and ends in the scrotum.(is normal diameter is about 11 to 22 mm)
It starts at the deep inguinal ring, lateral to the epigastric vessels and extends through the inguinal canal terminating at
the superficial ring into the scrotum where its contents disperse to supply various structures in the testes and scrotum. it is
also refered to as the testicular cord.
CONTENTS
Testicular artery
Cremasteric artery
Artery to the vas deferens
Pampiniform plexus
Genital branch of the genital femoral nerve
sympathetic and parasympathetic nerve fibres
Vas deferens
Remains of processus vaginalis
Lymph vessels

CONTENTS.
 Blood vessels
 Testicular artery:branch of the aorta that arises just inferiorly to the renal arteries.
 Cremasteric artery and vein: supply the cremasteric fascia and muscle.
 Artery to the vas deferens: branch of the inferior vessicle artery which arises from the internal iliac.
 Pampiniform plexus: network of veins that drains venous blood from the testes into the testicular vein. It wraps around the testicular artery and acts as a heat
exchanger by cooling arterior blood before it reaches the testes. As it travels into the inguinal canal, it condenses into a single testicular vein.
 NERVES
 Genital branch of the genital femoral nerve: supplies the cremasteric muscle.
 Autonomic nerves.
 OTHER STRUCTURES
 Vas deferens: a straight thick muscular tube that transports sperms from the epidydimis to the ampulla and eventually to the ejaculating duct(converges with seminal
vessicle duct). Its wall consists of 3 mainly muscles; 1.inner layer (longitudinal smooth muscle)
2. intermediate layer(circular smooth muscle)
3. outer layer(longitudinal smooth muscle)
 These layers are rich in autonomic innervation which allows fast sperm movement towards ejaculatory duct. Fast sperm movement is also facilitated by inner mucosal
layer of vas deferens which is lined by microvilli.
 Remains of the processus vaginalis: projection of the peritoneum that forms the pathway of descent for the testes during embryonic development. In adults, it is fused
shut.
 Lymph vessels: drain into paraaortic node located in the lumbar region.

COVERING OF THE SPERMATIC CORD
 Internal spermatic fascia: derived from fascia transversalis.
 Cremasteric fascia: a discontinuous layer of striated muscle that is oriented
longitudinally and is derived from the internal oblique transversus abdominis
muscle and its facial coverings. It consists of loosely arranged muscle fasculi
that are united by the loose areola tissue to form a sac like investment for
the spermatic cord and the testis.
 External spermatic fascia: derived from the external oblique muscle.
The three fascial layers are covered by a layer of superficial fascia layer which
lies directly below the scrotal skin.
CLINICAL RELEVANCE
 TESTICULAR TORSION : twisting of the spermatic cord upon itself which can
lead to strangling of the testicular artery resulting in necrosis/ infarct of the
testes.
 - A common cause is a spasm of cremasteric muscle fibres which force the
testicle to spin around its cord. It may be due to anatomical condition(e.g a
loose testicle in a large peritoneal sac). Diagnosis can be confirmed via
ultrasound and colour doppler scanning.
- main clinical feature: severe, sudden pain in the affected testes which usually
lies higher in the scrotum.
- A surgical repair or orchiopexy is usually required as treatment to restore blood
flow to testicles. Annual incidence has been noted to be 4.5 per 100,000 males

CREMASTERIC REFLEX :
superfiscial reflex found in human
males that is elicited when the
superior and medial part of the thigh
is stroked. this produces an
immediate contraction of the
cremaster muscle elevating the testis
on the side being stimulated.
VARICOCELE: A scrotal swelling
caused by swollen veins(pampiniform
plexus) in the spermatic cord. It may
increase testicular cell apoptosis ,
alter sertoli cell function and
decrease leydig cell testosterone
secretion. it may also affect sperm
development as it causes an increase
in temperature of the testicles and
DNA damage in sperms.It is identified
in 15% of health males and 35 % of
men with primary infertility.

 Leiomyosarcoma of the spermatic cord
Is a rare condition it may arise from mesenchymal cells of the spermatic cord and occurs mainly in elderly
people.
This diagnosis is difficult if based on emerging procedures, its reviewed by histological examination post
surgery.
Histological features
The tumor is compressed of spindle cell proliferation forming rough bundles of fascicles.
NOTE: a sarcoma is a malignant tumor, a type of cancer that arises from transformed cells of mesenchymal
origin.

The seminal vesicles
 There are a pair of twisted leaf shaped tubes which are located between the
bladder and the rectum.
 It is about 15cm long
 The wall of the seminal vesicles consists of three main layers namely;
 The endopelvic fascia,the middle smooth muscles layer and the inner mucosal
layer.
 The endopelvic fascia is also called the adventitia or the extra peritoneal
connective tissue.It is the outermost layer.
 The seminal vesicles consists of folds which are lined with simple or pseudo
stratified columnar epithelial cells rich in secretory granules.The lamina propria
consists of elastic fibers and is surrounded by smooth muscles with innner
circular and outer longitudinal layers,which empty the gland during ejaculation.

 The inner mucosal layer is the innermost layer of the seminal vesicle. It has
the outer primary mucosal folds which branch into the secondary mucosal folds.
 •The secondary mucosal folds anastomose and form irregular cavities or
mucosal crypts.
 •The grandular epithelia varies in appearance, usually low pseudostratified and
low columnar or cuboidal.

 •This gland produces a yellowish secretion which makes up 70% of the
ejaculation. This secretion contains:
 •FRUCTOSE- (Inosital, citrate): it is a source of energy for the sperm
 •PROSTAGLANDINS: Which stimulate the activity in the female reproductive
tract (muscle contraction)
 •FIBRINOGEN: which allows semen to coagulate after ejaculation.

Clinical relevances of the seminal
vesicles
 Seminal vesiculitis
 This is the inflammation of the seminal vesicle, it may be due to exposure to
excessive heat or bacterial infection. it may also be caused by the obstruction
of blood to the to the perineal region.

COWPERS GLANDS (BULBOURETHRAL GLANDS)
• They are a pair of small pea shaped exocrine glands
that are located poster-laterally to the membranous
urethra and superiorly to the bulb of the penis. There
about 3 – 5 mm in diameter
• They are described as compound tubulo-alveolar
glands because they are made of tubules and acini.
Each gland is formed of a number of lobules which
are enclosed in the fibrous capsule and lined by the
pseudostratified epithelia
• These glands have ducts which open into the
proximal portion of the spongy urethra.
• Within these lobules we find acini which are lined by
the columnar cells and each acinus is surrounded by
a thin layer of myoepithelial cells.
• During sexual arousal, these glands secrete an
alkaline mucus fluid containing glycoproteins. This
fluid is also called the pre-ejaculate.

Functions Of The Pre-ejaculate fluid;
• It serves as a lubrication for the urethra and
the tip of the penis
• It expels the urine and dead cells that might
have been left in the urethra thus creating a
clean and lubricated pathway
• It creates a suitable environment for the
sperm as it neutralises the residue acidity in
the urethra.

 Adenocarcinoma: (cancer) this is due to abnormal
and uncontrollable new growth of the cells
(neoplasm). It can lead to stricture of the urethral
duct which results in the urinary retention.
 Cowperitis: This is the inflammation of the
Cowper’s glands which may result into fever, pain
or malaise (general feeling of discomfort). It is
mainly caused by bacterial infection
 Stones: they form when the minerals crystalize,
these minerals include, salts, sugar and fats. It
may also come about as a result of lacking vitamin
A and B. It may cause severe pain in the perineal
region, malaise and fever.

THE PROSTATE GLAND
• The prostate gland is a fibromusculoglandular organ found in
the male reproductive system.
• It produces fluid that makes up a significant portion of semen
• It surrounds the prostatic part of the urethra.
• It has three zones, ie;
 1. Central
 2. Transitional
 3. Peripheral

HISTOLOGY OF THE
PROSTATE GLAND
• Histologically, the prostate gland is
composed of different types of
tissues including glandular,
fibromuscular and connective
tissue.
• The glandular tissue is composed of
glands that produce a milky fluid
which contributes to semen. These
glands are surrounded by a layer of
smooth muscle called the
myoepithelial layer, which helps to
expel the glandular secretions into
the urethra.
• The fibromuscular tissue is
composed of fibrous and smooth
muscle tissue (stroma), which
helps to support the glands and
regulate the flow of urine and
semen.
• The connective tissue is composed
of collagen and elastic fibers,
which provide additional support
and elasticity to the gland. It also

• The prostate is an
encapsulated accessory
genital gland.
 FIGURE A
• Identification
1. Contains tubuloacinar glands
2. Glands are embedded in the
fibromuscular stroma which
contains fiber tissue like
fibrocytes, fibroblasts and
smooth muscle
3. Smooth muscle contracts at
ejaculation
4. Individual glands may
converge but all of them
open into the prostatic
urethra
5. Prostatic concretions

• Corpora amylaceum
concretion (prostatic
concretion)
 FIGURE B
• The prostate gland is
lined by simple to
pseudustratified to
columnar epithelium;
• Secretory epithelium
surrounded by
1. Lamina propria
2. Thick smooth muscles

lamellar nature of
a corpus
amylaceum
(laminated
concretion)-
formed by
glycoprotein and
keratin sulphate
 FIGURE C
 Simple columnar,
cuboidal or
pseudostratified
columnar
epithelium
 Lamina propria

PROSTATIC SECRETIONS
 These are fluids produced by the glands within the prostate gland making up a
significant portion of semen.
 Fibrinolysin
 Glycoproteins
 Acid phosphatase
 Citric acid
 prostaglandins
 NB: secretion is regulated by dihydrotestosterone

Histology of Prostate
Gland
Clinical Correlations

121
• This is the largest of the
accessory glands, it is
pierced by the urethra and
the ejaculatory ducts.
• It is a slender capsule
shaped like a walnut and is
composed of a richly
vascularized, dense
irregular dense connective
tissue interspersed with
smooth muscle cells.
During ejaculation, the
smooth muscle contracts
and leads to the expulsion
of the glandular content.
• Is made up of 30 to 50
individual compound
tubuloalveolar glands,
• The tubuloalveolar glands
have pseudostratified
columnar epithelium of
varying height.
• The columnar cells contain apical
secretory granules. Basal cells are
found between the columnar cells for
regeneration of the epithelium. The
prostate glands open on both sides of
the Colliculus in the prostatic urethra

122
Section of the central region of the prostate
showing the prostatic urethra and
tubuloalveolar glands surrounded by
connective tissue and smooth muscle.

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• The prostate
gland is lined
by simple to
pseudustratifie
d to columnar
epihelium;
surrounded by
fibromuscular
stroma (made
up of
connective
tissue and
smooth
muscle).
COMPONENTS OF THE PROSTATE GLAND

125
• The glands are arranged in
three major zones around
the urethra:
1. The transition zone
occupies only about 5% of
the prostate volume,
surrounds the superior
portion of the urethra, and
contains the periurethral
mucosal glands.
2. The central zone
comprises 25% of the
gland’s tissue and contains
the periurethral
submucosal glands with
longer ducts.
3. The peripheral zone, with
about 70% of the organ’s
tissue, contains the
prostate’s main glands
with still longer ducts.

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Labeled diagram of the prostate (source; oncology.net)

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Footer Text 127
• Mucosal glands are closest to the urethra and thus are the
shortest of the glands
• Submucosal glands are peripheral to the mucosal glands and
are consequently larger than the mucosal glands.
• Largest and most numerous of the glands are the peripheral
most main glands, which compose the bulk of the prostate.
• Lumina of the tubuloalveolar glands frequently house round
to oval prostatic concretions (corpora amylacea),
composed of calcified glycoproteins, whose numbers
increase with a person’s age.

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FUNCTIONS OF THE PROSTATE
• Prostatic Secretion
The prostatic fluid is thin, slightly acidic (pH 6.4) and forms
about 20% of semen volume. It contains spermine (for the
motility of sperms), spermidine, prostataglandins (for uterus
stimulation), zinc (affects testosterone metabolism of the
prostate), citric acid (buffer), immunoglobulins, phosphatases
and proteases (see liquefaction of the semen).
• Control of Urine or Semen Flow
The prostate acts as a kind of valve, preventing urine flow
during the ejaculation and or permitting urine flow in between.
Micturition is made possible under parasympathetic activity and
low sympathetic activity, this leads to the relaxation of the
bladder neck. Ejaculation is controlled by the sympathetic
nervous system. The activation of prostatic alpha-receptors
leads to the contraction of the smooth muscle stroma of the
bladder neck; this causes the expulsion of the prostate gland
content and closes the bladder neck for an antegrade

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CLINICAL CORRELATIONS OF THE PROSTATE
GLAND
The prostate gland is prone to four common problems:
(1) Chronic Prostatitis
Usually involving bacteria or other infectious agents; It is simply inflammation of
the prostate.
 Treatment
 Intravenous antibiotics for a period of about 4-6weeks
 Pain can be relieved by medication such as acetaminophen or ibuprofen.

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CLINICAL CORRELATIONS OF THE PROSTATE GLAND
The prostate gland is prone to three common problems:
(1) Chronic Prostatitis, usually involving bacteria or other
infectious agents; It is simply inflammation of the prostate.

(2) Nodular hyperplasia or Benign Prostatic Hypertrophy,
occurring mainly in the periurethral mucosal glands. Overgrowth of prostate tissue often leads to compression of
the urethra and problems with urination;
 Treatment
 Urinary retention medication which relax muscle fibres in the prostate making urination easier (Alpha blockers
include: Doxazosin, Tamsulosin and Silodosin.)
 In severe cases Transurethral resection which is the removal of prostate tissue is needed.

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(3) Prostatic Intraepitelial Neoplasia (PIN): This is a condition
defined by neoplasmic growth of epithelial cells within pre
existing benign prostatic acini or ducts. High-Grade PIN (HGPIN)
is widely accepted as a precursor to prostate cancer.
 Treatment
 There is no known routine treatment but some doctors may
recommend surgery or radiation treatment
(4) Glandular Prostate Cancer (adenocarcinoma), the most
common cancer in nonsmoking men, occurring mainly in glands
of the peripheral zone.
 Treatment
 Hormone Associated Therapy, stops or slows production of
hormones.
 Chemotherapy, unwanted reactions to drugs given for the
purpose of killing cancer cells.
 Prostasectomy which involves the removal of part or all of
the prostate gland.

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CLINICAL CORRELATIONS OF THE PROSTATE GLAND
(4) Glandular Prostate Cancer (adenocarcinoma), the most common
cancer in nonsmoking men, occurring mainly in glands of the peripheral
zone

 The penis consists of three cylindrical masses of erectile tissue plus the
penile urethra surrounded by skin.
 The two of the erectile masses the corpora cavernosa are dorsal and
the ventral corpus spongiosum surrounds the urethra.
 At its end the corpus spongiosum expands forming the glans.
 Most of the penile urethra is lined with pseudostratified epithelium.
 In the glans, it becomes stratified squamous epithelium continuous
with that of thin epidermis covering the glans surface .
 Small mucus-secreting urethral glands are found along the length of the
penile urethra
 The corpora carvenosa are each surrounded by a dense fibroelastic
layer , the tunica albuginea
 All three erectile tissues consist of many venous cavernous spaces lined
with endothelium and separated by trabeculae with smooth muscle and
connective tissue continuation with the surrounding tunic.

 Central arteries in the corpora cavernosa branch to form nutritive
arterioles and small coiling helicine arteries, which leads to the
cavernous vascular spaces of erectile tissues.
 Penile erection involves blood filling the cavernous spaces in the three
masses of erectile tissue
 For erection parasympathetic stimulation relaxes the muscles of small
helicene arteries and adjacent tissues , allowing vessels of the cavernous
tissue to fill with blood ; the enlarging corpora compress the venous
drainage , producing further enlargement and turgidity in the three
corpora masses.
 The sympathetic stimulation at ejaculation constricts blood flow
through the helicine arteries, allowing blood to empty from the
cavernous tissues.

HISTOLOGY THE FEMALE REPRODUCTIVE SYSTEM

HISTOLOGY OF THE OVARIES
 The paired ovaries develop within the mesonephric ridge
and descend down the abdomen and stop in the pelvis.
 They are found on the posterior wall of the pelvis
laterally to the uterus. Ovaries are attached to the broad
ligament by peritoneal fold, the mesovarium.
 Ovaries are almond shape approximately 3cm long, 1.5cm
wide and 1 cm thick. The ovaries have mainly four layer;
germinal epithelium, tunica albuginea, outer cortex and
inner medulla.
 Ovaries are responsible for production of female gametes
and also produces hormones estrogen and progesterone
responsible for development of secondary sexual
characteristics and maintenance of uterus wall during
pregnancy respectively.

Germinal Epithelium
The germinal epithelium also known as waldeyer epithelium is made of
simple cuboidal epithelial cells and continues with the mesothelium layer
of the peritoneum. This layer covers the ovary.
The germinal layer does not produce any germ cells despite its name
saying so.
The cells of the layer bear microvilli and numerous mitochondria during
pregnancy.

Tunica Albuginea
The germinal layer rests on the tunica albuginea. The tunica albuginea is
a layer of dense connective tissue capsule it is thinner than that of the
testis.

Outer cortex
The cortex or cortical region is found on the peripheral portion of the ovary surrounding the
medulla. The cortex contains several ovarian follicles developing in different stages
embedded in the connective tissue stroma. Smooth muscles are present in this layer
surrounding the follicles.

Inner Medulla
The medullary region is found at the center of the ovary and contains
loose connective tissue, blood vessels, lymphatic vessels and nerves.
The boundary between medulla and cortex is indistinct.(refer to image
on previous page)
1. Ovarian cysts: are fluid filled masses that may develop within or on
the surface or an ovary. They are commonly caused by hormonal
problems or drugs used to help in ovulation and usually are derived
from the ovarian follicles reaching approximately 2-2.5 cm. large
cysts may require surgical removal if not treated can cause bleeding
and pain in the pelvis.

Ovarian tumors: Ovarian tumors are abnormal growths on the ovaries.
About 85-90% of ovarian cancers arise from the epithelium of the
ovaries. Most germ cell tumors are teratomas.
Polycystic ovaries: Characterized by hormone dysfunction and multiple
ovarian cysts. The condition leads to increase in testosterone levels in
females and leads to infertility

• Ovarian follicle consists of an oocyte surrounded by one or two epithelial cells in
the cortex of an ovary.
• Development of ovarian follicles (folliculogenesis)
• This is a process of growth and maturation of an the ovarian follicles.
Stages of development
• Primordial follicle
• Primary follicle
Unilaminar primary follicle
Multilaminar primary follicle
• Secondary follicle or atria follicle
• Tertiary or graafian follicle
• Corpus luteum
• Corpus albican

• Primordial follicles
Primordial follicles are the smallest and simplest in structure, located at the
periphery of the cortex. Each follicle consists of a primary oocyte (20–25 μm)
surrounded by a single layer of squamous follicular cells.
The oocyte is arrested

Primary follicle
• The primordial follicle changes into primary follicle under the influence of FSH
and shows the following changes:
• Primary oocyte enlarges in size (50–80 μm diameter).
• Flattened squamous follicular cells become cuboidal (unilaminar primary follicle)
and then divide to form stratified cuboidal layer of granulosa cells (multilaminar
primary follicle).
• The oocyte is separated from the surrounding follicular cells by a glycoprotein
layer called zonula pellucida.
• The connective tissue stroma surrounding the follicle begins to condense and
form theca folliculi. Theca folliculi later differentiate into two layers; the theca
interna and theca externa

Secondary (antral) follicle
The primary follicle becomes the secondary follicle after undergoing following
changes
• The oocyte enlarges and reaches its full size (125 μm).
• Irregular fluid filled spaces appear among the follicular cells and join to form a
crescentic space or antrum filled with liquor folliculi.
• The follicle increases in size (2 mm) mainly due to the formation of antrum and
liquor folliculi.
• The theca folliculi differentiates into two layers, an internal cellular layer, theca
interna and an outer fibrous layer, theca externa. Follicular cells and cells of theca
interna secrete oestrogen

• Mature Graafian (tertiary) follicle
• With further development the follicle enlarges in size as fluid accumulates in the
antrum dividing the follicular cells into two sets:
• The outer set of cells that lines the cavity forms the membrana granulosa and
the inner set that surrounds the ovum and attaches it to one pole of the follicle
forms the cumulus oophorus. Now the Graafian follicle measures about 10 mm
or more in diameter and is seen bulging out of cortex on the surface
• At this stage the primary oocyte completes its first meiotic division and becomes
a secondary oocyte (ovum). (It is worth noting that all the primary oocytes enter
into prophase of 1st meiotic division during foetal life but meiosis remains
arrested at that stage till just before ovulation).
• At mid-cycle (about 14th day of a 28-day cycle), under the influence of oestrogen,
there is a sudden increase in the amount of liquor folliculi causing rupture of the
mature follicle and release of the secondary oocyte along with one layer of
loosely adherent granulosa cells (corona radiata) into the peritoneal cavity. This
process is called ovulation. From the peritoneal cavity the ovum is rapidly drawn
into the uterine tube.

HISTOLOGY OF THE CORPUS LUTEUM

THE CORPUS LUTEUM
 The corpus luteum is a dynamic endocrine gland that is formed from
the remains of the dominant follicle after it undergoes ovulation and
plays an important role in the menstrual cycle and early pregnancy.
 After ovulation occurs, the raptured follicle accumulates with blood
from disrupted capillaries and fill in the former antrum. The granulosa
is now invaded with capillaries.
 The walls of the follicle made up of granulosa and theca cells of the
ovulated follicle collapses and becomes enfolded and transforms into
the corpus luteum.
 The cells of the theca interna and granulosa cells increase greatly in
size and are filled with lipochrome pigments(yellowish pigment) to
become lutein cells .
 Granulosa cells become granulosa lutein cells and the theca cells
become theca lutein cells.

CONT
 The theca lutein cells are small cells which are concentrated mainly
along the periphery of the corpus luteum.
 They are derived from the cells of the theca interna. They are found
at the periphery and are along the connective tissue strands that
invade the structure.
 The Theca externa with fibroblasts and smooth muscle merges
gradually with the surrounding stroma and forms a poorly defined
capsule around the developing corpus luteum.
 It invades the granulosa cells along with the blood vessels from the
periphery to occupy the remnant of the follicular cavity in the center.
 These lutein cells contain lipid droplets, abundant smooth
endoplasmic reticulum and mitochondria(these are the characteristic
features of steroid synthesizing cells), these two types of cells are
seen in the corpus luteum.

CONT
 Granulosa lutein cells, that form the predominant cell type of corpus
luteum are derived from the granulosa cells.
 They are large pale-staining cells with vesicular nuclei found at the
deeper part of the corpus luteum.
 These luteal cells synthesize and secrete the hormone progesterone.
 If the liberated ovum is fertilized, the corpus luteum will survive for
4-5 months under the influence of human chorionic
gonadotrophin(HCG). HCG is a glycoprotein hormone produced by
trophoblast cells of the implanted embryo and targets and functions
similar to that of LH.
 HCG maintains and promotes further growth of the corpus luteum,
stimulating secretion of progesterone to maintain to maintain the
uterine mucosa to prevent it from undergoing menstruation because
the embryo would be lost. Hence it is called the corpus luteum of
pregnancy.

CONT
 The corpus luteum is maintained by HCG for 4-5 months, by which
time the placenta itself produces progesterone and estrogen at the
levels adequate to maintain the uterine mucosa. It then degenerates
and is replaced by a large corpus albicans.
 If fertilization does not occur, the corpus luteum functions for only 10-
12 days and is called corpus luteum of menstruation.
 After its functional activity is over, it undergoes regression and is
replaced by fibrous hyalinized scar, called the corpus albicans(white
body).
 This corpus albicans is remnant of the degenerated corpus luteum. It
becomes a small scar on the surface of the ovary.

CLINICAL CORRELATIONS OF THE CORPUS LUTEUM
 Persistent corpus luteum
 A corpus luteum that fails to regress within 14 -16 days after in a non
pregnant woman
 This is caused by chronic uterine infections resulting in destruction of
the endometrium and therefore decreased prostaglandin release.
 Corpus luteum cyst
 This is a type of ovarian cyst which may rupture about the time of
menstruation and take up to 3 months to disappear entirely. It
contains blood and other fluids.
 This cysts rarely occurs in women over the age of 50 because eggs are
no longer being released after menopause.

HISTOLOGY OF THE UTERINE TUBES

 The uterine tubes are also known as oviducts, fallopian tubes or salpinx. They are a pair of ‘J-
shaped’ tubes found in the female reproductive tract. Each uterine tube measures 10 to 12cm in
length and lies from the upper boarder of the broad ligament extending laterally from the uterus
and opens up into the peritoneal cavity near the ovary.
 Each uterine tube is subdivided into four parts. Lateral to medial, these are;
 The infundibulum, which is a funnel shaped opening fringed with finger like extensions called
fimbriae that are used to capture the ovum from the surface of the ovary.
 The ampulla, the longest and most expanded region. This is usually the site of fertilization.
 The isthmus, a short narrow section of the oviducts connecting the ampulla to the uterine
cavity.
 The intramural or uterine part, which is the part that passes through the thick wall of the
uterus and opens up into the uterine cavity

LAYERS OF THE UTERINE WALLS
• The walls of the uterine tubes consist of three main layers; the mucosa, muscularis and
serosa. The figure below shows the transverse section of the uterine tubes, particularly
the ampulla, showing the different layers as seen under a microscope
• Fig 2: Transverse section of ampulla at low magnification. Stain: hematoxylin and
eosin.

• The Mucosa is a layer composed of many branching, longitudinal folds which are most prominent in
the ampulla and resemble a labyrinth when a cross-section of the uterine tubes is viewed under a
microscope. These mucosal folds become smaller in regions near the uterus and are absent in the
intramural part of the oviducts. Along its length, the mucosa is lined by simple columnar epithelium on
a lamina propria of loose connective tissue. This epithelium contains two functionally important cells
spaced across it, these are ciliated cells and secretory peg cells. Ciliated cells aid in wafting fluid
towards the uterus by ciliary movement. They are more predominant in the distal portion of the tube
and develop more cilia in the first half of the menstrual cycle. Secretory peg cells are non-ciliated and
darker staining; they are more predominant in the proximal portion of the tubes. Peg cells secrete
glycoproteins of a nutritive mucus film that covers the epithelium. This secretion has nutritive and
protective functions for both the oocyte and the sperm, including capacitation factors that activate
sperm and make those cells able to fertilize an oocyte. During the follicular growth phase of the ovarian
cycle, oestrogens trigger the elongation of cilia and enlargement of both ciliated and peg cells, these
cells undergo atrophy with loss of cilia during the late luteal phase

• The Musclaris is thick and well defined, it is arranged into two layers made up of an inner interwoven circular
and outer longitudinal layer of smooth muscle. Innervation of these layers results in peristaltic contractions of the
uterine tubes thereby aiding in the movement of the fertilized ovum to the uterus for implantation. Shown in figure
2 above by (4) and (5).
• The Serosa is a layer of tissue coating the outside of the uterus. The serosa is composed of simple squamous
epithelium overlying a thin connective tissue layer seen as (11) in figure 2 above.
CLINICAL RELEVANCE OF THE UTERINE TUBES
 Ectopic/ Tubal pregnancy, an ectopic pregnancy occurs when a fertilized oocyte implants and grows in the
uterine tubes instead of the uterus. If not diagnosed early, the implanted blastocyst can cause rupture and
haemorrhage of the affected tube. The affected fallopian tube may rupture after about 6 to 16 weeks, the fetus
always dies and in severe cases an ectopic pregnancy also leads to the death of the woman due to severe internal
bleeding. Ectopic pregnancies can be treated by methotrexate, a medication that stops the growth of the
pregnancy and dissolves the existing cells, it can also be treated by surgical removal of the embryo usually
together with the affected tube.

 Salpingitis is an inflammation of the uterine tubes usually caused by bacterial
infection. It can cause adhesion of the mucosal folds which may partially or
completely block the lumen of the oviducts and potentially results in infertility or
ectopic pregnancy.
 Ligation of the uterine tubes is a surgical procedure for female sterilization, it
prevents the oocyte from passing into the uterus and getting fertilized by the sperm
and thus prevents pregnancy. The two main methods of tubal ligation are open
abdominal and laparoscopic. Open abdominal is carried out via a suprapubic
incision while a laparoscopic incision is via a fibre optic laparoscope inserted
through a small incision near the umbilicus.

3 PARTS OF THE UTERUS
1.FUNDUS
2.BODY
3. CERVIX

ENDOMETRIUM (Mucosa)
• Inner mucosa lining of the uterus. It consist of simple columnar
epithelium supported by a lamina propria.
• Its simple columnar epithelial lining has both ciliated and secretory
cells and numerous uterine glands which penetrate the full
thickness of the endometrium.
• Its divided into two layers:
• Deep Stratum basalis: changes little through out the menstrual
cycle and is not shed at menstruation.
• It has a highly cellular lamina propria and contains deep basal ends
of the uterine glands.
• superficial stratum functionalis layer: temporal layer at the
luminal surface. Proliferates in response to oestrogen and becomes
secretory in response to progesterone. It is shade during
menstruation and regenerates from cells in the stratum basalis.

MYOMETRIUM
• Thickest tunic of the uterus composed of three poorly defined
layers of smooth muscle fibres separated by connective tissue
containing venous plexus and lymphatics.
• The inner and outer are longitudinal layers and the middle
layer which is circular and highly vascularised.
• During pregnancy, the myometrium goes through a period of
extensive growth involving both hyperplasia (increasing the
number of smooth muscle cells), cell hypertrophy, and
increased collagen production by the muscle cells, which
strengthens the uterine wall.
• This well-developed uterine myometrium contracts very
forcefully during parturition to expel the infant from the
uterus. After pregnancy, uterine smooth muscle cells shrink
and many undergo apoptosis, with removal of unneeded
collagen, and the uterus returns almost to its prepregnancy
size.

PERIMETRIUM
• Outer layer of the uterus that is composed of simple
squamous epithelium supported by connective tissue
that is rich in blood vessels and elastic fibres.
• The serous layer secretes a lubricating fluid that
helps to reduce friction.
• It is also part of the peritoneum that covers some
organs of the pelvis.
• .

DISORDERS OF THE ENDOMETRIUM
ENDOMETRIOSIS
• Condition in which endometrial tissue grows in wrong places out side the
uterus, most commonly the ovaries and ligaments of the uterus.
• The ectopic tissue is still responsive to oestrogenic stimuli therefore cyclic
proliferation and bleeding occur, often forming a cyst .It is a common cause
of infertility
• Common symptoms are pain and menstrual irregularities.
• It commonly affects women during their reproductive years between the
age of 25 and 35.
• Risk factors
 Early menstruation(before age 11)

Treatment
Medication e.g.
Hormones
Electrosurgery
Laparoscopy

FIBROIDS
• They are benign tumour growths in the uterus . They are
oestrogenic dependent , they enlarge during pregnancy.
• Most fibroids are asymptomatic, but if large enough the uterine
mass can cause symptoms including menorrhagia, pelvic pain and
infertility.
• Causes are not known but genetics and prolonged exposure to
oestrogen may increase the risk of developing fibroids.
Other risk factors are obesity, late entry to menopause and a positive
family history of fibroids
Treatment
 Medication e.g. sex hormone suppression
 Hysterectomy
 uterine myomectomy (removal of fibroids)
 Uterine artery embolization

FIBROIDS ARE NAMED DEPENDING ON LOCATION

ENDOMETRIAL CARCINOMA
• Abnormal growth of cancer cells on the endometrium.
Two types endometrial carcinoma
• Type 1 - tumours look like normal uterine glands
• Type 2-affects women who have endometrial atrophy and low body
weight.
Common causes may include:
• Genetic mutation
• High levels of oestrogen
symptoms
 Pain in the pelvis
 Heavy or irregular menstruation
 Anaemia or fatigue
Some women experience no symptoms.

Treatment
Hysterectomy
Laparotomy
Medication e.g.
Chemotherapy(anti caner drugs)

ABNORMAL POSITIONING OF THE UTERUS
Normal position: Anteflexed and anteverted
Three common dispositions are:
 Excessively anteflexed
 retroverted
 retroflexed
These abnormal arrangements do not inherently cause any medical
problems.
 However, the retroverted uterus is positioned directly above the
vagina. In instances of increased abdominal pressure the uterus is
more likely to prolapse into the vagina.
 A retroverted uterus may create more pressure on the bladder
during the first trimester. This may cause difficulties in urinating.
 It may also be hard to see the uterus via ultrasound until it begins
to enlarge during pregnancy.

Retroverted uterus is a normal finding, but in some cases it may be caused by
endometriosis(pulls the uterus backward), uterine fibroids, pelvic
inflammatory disease, adhesions and history of pelvic surgery.
About 20%of women have these.

HISTOLOGY OF THE MENSTRUAL CYCLE
Objectives:
To
 Define and understand what menstrual cycle is.
 Know and understand how and where menstrual cycle occurs.
 View microscopic structure of a tissue that undergoes
menstrual cycle.
 Know the clinical relevance of menstrual cycle.

INTRODUCTION TO MENSTRUAL CYCLE
Well, the term menstrual cycle refers to a respectively repetitive series of changes in the endometrium
(innermost lining layer of the uterus) of a nonpregnant female that prepares the lining of the uterus to
receive a fertilized ovum. Since the cycle occurs in the uterus, therefore, we can safely say that
menstrual cycle is as well known as uterine cycle. This menstrual cycle occurs when the female reaches
the stage of puberty and there is development of a mature follicle that in turn undergoes ovulation
(release an ovum), thus, involving the ovarian and uterine cycle. The approximate age in females to
experience their first period or menarche (menstruate= shed the active part of the endometrium layer)
is 10 years and above of which it may vary in some females. Even during menopause between ages of 45
and 55. Further, the endometrium is made up of three layers, namely stratum compactum, stratum
spongiosum and stratum basalis. Stratum compactum (stratum= layer, compact=neatly packaging) and
stratum spongiosum (spongio=spongy= perforated holes for blood vessels sum=total=many) are two
functional layers of the endometrium which develop into stratum functionalis during the first half of
menstrual cycle (proliferative phase) and thus, expecting the stratum functionalis to contain more blood
vessels which supplies and drains blood. On the other hand, stratum basalis, a layer adjacent to
myometrium remains intact throughout the menstrual cycle because of its unresponsiveness to hormonal
stimulation and plays a respective and cardinal role in proliferative phase of the menstrual cycle.

Diagrammatic Interpretation of Endometrium Histology

Circular Histological Appearance of Endometrium

The hormonal stimulation begins when the median eminence part of the hypothalamus secretes
Gonadotropin-releasing hormone (GnRH), (Gonad= Ovaries) into the fenestrated capillaries of portal
circulation which stimulates the release of follicle stimulating hormone (FSH) and Luteinizing hormone
(LH) when it reaches the anterior pituitary gland. The follicle stimulating hormone stimulates, follicular
growth and secretion of estrogen by the growing ovarian follicle in the first phase of menstrual cycle.
Luteinizing hormone stimulates further development of follicles and their full secretions of estrogen. At
mid-cycle about 14th day of the total number of menstrual cycle days, which are approximately 28 days,
luteinizing hormone triggers ovulation which is the release of a grown and mature ovum and thus,
promoting the formation of corpus luteum, hence, the name as luteinizing hormone. Corpus luteum
secretes estrogen, progesterone, relaxin and inhibin hormones. Inhibin hormone helps in regulating the
release of FSH by the anterior pituitary gland.
 The normal range of menstrual cycle is 21 to 35 days.
(Did you know that you can make estrogen word from progesterone??? Just rearrange the letters in
progesterone).

Gonadotropin releasing hormone(GnRH) and its effective stimulation hormonal cascade

Menstrual Phases
There are four phases of menstrual cycle namely, the menstrual, preovulatory (pre=before), ovulatory (during
ovulation) and postovulatory (post=after) phase.
Sequence of Menstrual Phases:
Menstruation Preovulatory Ovulation Postovulatory
The Menstrual Phase
Overview
This phase is as well known as menstruation because it involves the shedding or sloughing
Off the layer called stratum functionalis. The spiral (coiled) arterioles that supply blood to the stratum functionalis
undergoes vasoconstriction in a manner such that the coiled shape of this arterioles cuts or deprives the stratum
functionalis of oxygenated blood and stratum functionalis receives no nutrients, oxygen and resulting in ischaemia
(inadequate supply of blood to a tissue or organ), thus, degeneration of the layer. The arteries haemorrhage
(ruptures), resulting in blood flow that dislodge (carry) the necrotic (dead and sloughed off) stratum functionalis.
All these highlighted events occurs under the influence of the declined or decreased levels of estrogen and
progesterone levels because of the degenerated corpus luteum of the previous cycle.
Events in the Ovaries
From the previous discussion, we learnt that the FSH stimulates the growth of follicles. In this case, the FSH
stimulates the primordial follicles to develop into primary follicle and then into secondary follicles. The follicular
fluid secreted by granulosa cells and filtered from blood in capillaries of the theca folliculi, accumulates in the
spaces of the follicles that induces the motility (movement) of the oocyte to be near the edge of the follicle.

Events in the Uterus
Blood discharge from the uterus during menstruation ranges approximately from
50-150 mL. Menstrual flow contains blood, mucus, tissue fluid, and some sloughed
off ciliated simple columnar epithelial cells that forms the endometrial glands
from the endometrium. This results in decline or decrease in estrogen and
progesterone levels that stimulates the release of prostaglandins which causes
uterine spiral arterioles to undergo vasoconstriction, thus, depriving oxygenated
blood to the stratum functionalis and the layer sloughed off completely. During
this time, the endometrium is very thin, about 2-5 mm because only the stratum
basalis remains (may signify the size of stratum basalis). The menstrual flow
passes from the uterine cavity through the cervix and vagina to the exterior. The
menstrual phase roughly lasts for the first 5 days and the first day of menstrual
phase is the start of the new cycle.

Microscopic structure of the menstrual phase
Uterus events

Preovulatory or Proliferative Phase
After menstruation has occurred, the endometrium of the uterus has to be proliferated or regenerated or regrown
via stratum functionalis because at any time during nearly days of ovulation, in the event of fertilization, the
fertilized ovum can be supported by the full functioning of the endometrium and this makes it possible for
preparation of the uterus to receive a fertilized ovum and thus, repeating the cycle. The following two respective
events occur in this cycle.
Events in the Ovaries
Some of the immature secondary follicles in the ovaries begin to secrete estrogen and inhibin and approximately
by 6th day, only a single secondary follicle in one of the two ovaries outgrows all the follicles and becomes a
dominant and mature (graafian) follicle which secretes more inhibin and estrogen that causes a reduction in follicle
stimulate hormone (FSH), thus, depriving the less well developed follicles from follicular hormonal stimulation and
in the end, the follicles forms polar bodies and degenerates. The mature follicle forms a blister-like bulge due to
the continuous follicular fluid accumulation in the follicle, thus, resulting in the swelling antrum (nearly closed
cavity) on the surface of the ovary and in final maturation process, the mature follicle continues to increase
estrogen production.
 Inhibin hormone inhibits FSH by negative feedback mechanism or end product inhibition.
Note:
proliferation = life

Events in the uterus
Estrogen secreted into blood stimulates the repair (proliferation) of the
endometrium, cells of the stratum basalis undergo mitosis because the stratum
basalis is not affected as it is continuously supplied by straight and dilated
arterioles and produces a new stratum functionalis. As the endometrium thickens,
the short, straight endometrial glands develops, arterioles recoil, straighten and
lengths as they penetrate the stratum functionalis and the thickens of the
endometrium almost doubles to about 4-10mm.

Microscopic structure of the preovulatory or proliferative phase
Uterus events
Small portion of
secreted substance

Microscopic structure of the preovulatory or proliferative phase
Ovarian events

Ovulation phase
This phase occurs due to rupture of the mature follicle and overlying germinal
epithelium of the ovary and the release of secondary oocyte into the peritoneal
cavity, of which usually, occurs on a 14th day in a 28 day cycle. A secondary oocyte
remains surrounded by its two protective layers called zona pellucida and corona
radiate and is contained in the cumulus oophorus. Development of a secondary
follicle into a fully mature follicle generally take a total of about 20 days, that is
calculated as spanning of the last 6 days of the previous cycle and the first 14 days
of the current cycle.
During this phase, the primary oocyte completes meiosis I and develop into a
secondary oocyte which begins meiosis II but get arrested or halt in metaphase
until it is fertilized. From time to time, a secondary oocyte is ovulated into the
peritoneal cavity where it later disintegrates. A small surge of blood that
sometimes leaks into peritoneal cavity from the ruptured mature follicle can cause
pain known as Mittelschmerz, a German word pronounced as ‘mitelschmere’’
which means pain in the middle (mittel=middle, schmarz=pain)at the time of
ovulation. And the most fertile days to get pregnant are the three days leading up
to and including ovulation, after ovulation, the ovum only lives for 12 to 24 hours,
after this day, the chances of getting pregnant are either zero or minimal.

Microscopic structure of the ovulation phase

Continuation of microscopic structure on ovulation phase

Mittelschmerz diagrammatic representation

Postovulatory phase
This phase of the female reproductive cycle is the time between ovulation and onset of the next menses and is
broadly divided into luteal and secretory phase with respect in which event they occur. It lasts for 14 days in a 28
day cycle, 15 to 28 days.
Events in the ovaries
After ovulation, the mature follicle collapses and the basement membrane between granulosa cells and theca
internal breaks down, becomes yellow due to deposition of lipids and lutein pigment. Once a blood clot forms form
minor bleeding of the ruptured mature follicle, the follicle becomes the corpus hemorrhagicum (corpus=part of the
body, hemo=blood, rrhagicum=bursting forth). Theca internal cells, formed by stromal cells, mix with granulosa
cells as they all become transformed into corpus luteum under the influence of luteinizing hormone. Stimulated by
the luteinizing hormone, the corpus luteum secretes progesterone, estrogen, relaxin and inhibin hormones. Luteal
cells of the corpus luteum absorbs clots of blood. The corpus luteum have a life span of only two weeks and at the
end of this period, its secretory activity declines and then it degenerates into a corpus albican, a fibrous scar. As the
level of progesterone, estrogen and inhibin declines, the release of GnRH, FSH and LH rises due to loss negative
feedback to supress the ovarian hormone stimulation from the hypothalamus and anterior pituitary gland. Because
of this activity, the postovulatory phase is as well known as the luteal phase of the ovarian cycle.
 You may be familiar with the term corpuscles (red or white), these are just cells that supplies, supports the
corpus, which is the part of an organ or body.

Events in the uterus
Progesterone and estrogen produced by the corpus luteum promotes growth and
coiling of the endometrial glands, vascularization of the superficial endometrium
which leads to thickening of the endometrium to 12-18mm and production of thick
acidic mucus to prevent polysperm. The endometrial glands begins to secrete
glycogen, thus, this period is as well referred to as secretory phase of the uterine
cycle. These preparatory changes peak about one week after ovulation at a time a
blastocyst might arrive in the uterus in case of fertilization as the human chorionic
gonadotropin hormone is released by trophoblast to prevent luteolysis and corpus
luteum functions until placenta takes over the hormone production. If fertilization
does not occur, there is withdraw of progesterone and estrogen hormones, causing
menstruation (menses).
 Vascularization is a medical term which means development of blood vessels in
an organ or tissue to improve oxygen and nutrient supply.
 Remember that blastocyst is formed after fertilization has taken place before
implantation.
 Glycogen is secreted because glucose if the main source of energy in
developing embryo or fetus.

Histology of the postovulatory phase
secretory phase in uterine cycle

Histology of the postovulatory phase continued
luteal phase in ovarian cycle
Luteal cells

Summary events of the menstrual cycle

Diagrammatic summary of the menstrual cycle.

APPLIED ANATOMY OF THE MENSTRUAL CYCLE
QUESTION: HOW DO MORNING AFTER PILLS WORK???
 Well, morning after pills are of two types, namely, Levonelle and ellaOne which both contains estrogen hormone
that is as well found in females.
 These pills delays or inhibits the ovulation phase from 14 days to 21 days as maximum, which is one week.
 Delaying the ovulation phase occur due to reshuffling timeline of the LH Surge which causes ovulation and thus,
quick shedding or sloughing of the stratum functionalis of the uterus endometrium.
 Hence, it is advised to take the morning after pills within 72 hours (58%) or best immediately after having an
unprotected sexual intercourse (95%) and that should be done prior to the ovulation phase, that is, less than 14
days.
 If taken after ovulation phase, there are high chances that the female will becomes pregnant because
progesterone hormone will increase in levels which triggers the secretory phase, supporting the developing
embryo with nutrients it needs.
 And if you have taken the pills before or after ovulation and you haven’t experienced your menses within three
to four weeks, kindly don’t hesitate to take a pregnancy test.
 Note
 Do not take barbiturates such as amobarbital (used in treatment of insomnia) together with morning after pills
as barbiturates decreases the effectiveness of the pills.
 Do not confuse abortive pills with morning after pills as morning after pills do not end implanted embryo

COUNTED AS SAFE DAYS DURING THE MENSTRUAL CYCLE
QUESTION: WHAT ARE SAFE DAYS???
 Well, safe days are said to occur after the ovulation phase in the postovulatory phase.
 Two people, male and female can have sexual intercourse after 3 days in the postovulatory phase as such days
are of low probability or chance of getting pregnancy.
 However, studies show that there is a failure rate of about 25 percent using safe days because no one really and
exactly knows when and which day is ovulation going to take place as there is sometimes a pathophysiological in
hormonal levels in the body and it is always under the autonomic nervous system.
 Therefore, there are no solidifying safe days in the menstrual cycle because at any time, a female can get
pregnant.

 CLINICAL RELEVANCE
 Amenorrhoea
 A=without, men=month, rhea=a flow
 Definition, is the absence of menstruation
 Can be of two types namely, primary and secondary amenorrhoea.
 in primary amenorrhoea, there is an absence of menses due to genetic problems
 Secondary amenorrhoea, absence of three or more menses by a woman who had menses in the past.
 Common causes of secondary amenorrhoea are pregnancy and menopause, of which aren’t caused by underlying
diseases. Other cause are intrauterine devices (IUDs), chemotherapy and radiation therapy for cancer and
previous uterine surgery.
 In female athletes, amenorrhoea is caused by the reduction in gonadotropin-releasing hormone (GnRH), which
causes the reduction in FSH and LH thus, ovarian follicles fails to develop, ovulation does not occur, synthesis of
progesterone and estrogen wanes, and monthly menstrual bleeding ceases. Experiences secondary amenorrhoea
 Mostly occurs in women with low adipose tissues since the adipocytes will secretes low levels of leptin hormone.

CLINICAL RELEVANCE CONTINUED
 Primary Dysmenorrhoea
 Dysmenorrhoea which are painful periods, is the most common gynaecological symptom.
 Occurs at <20 years of age
 Occurs only in ovulatory cycles
 No pelvic pathology
 Patients may describe it as a ‘’crampy’’ lower abdominal pain which starts with menstruation, in the absence
of demonstrable disease, of which pain may be associated sometimes with other symptoms such as malaise
(general feeling of discomfortness), nausea, vomiting, diarrhoea and dizziness.
 Cause is excessive secretion of prostaglandins, results in myometrium contraction, vasospasm and ischaemia.
Management and treatment
 Stopping smoking
 Analgesic
 Hormonal contraception
 Non-pharmacological measures such as heat pads

 Secondary Dysmenorrhoea
 Secondary dysmenorrhoea is recurrent, lower abdominal pain associated with menstruation that occurs in non-
pregnant women with a pelvic pathology that could account for the symptoms.
 Starts 1-2 weeks before menstruation and increases with onset of menstruation
 Occurs several years after menarche >20 years of age
 Associated with heaviness in pelvic and backache
Causes
 Endometriosis
 Adenomyosis
 Cervical stenosis
 Ovarian mass
Treatment
 Use of nonsteroidal anti-inflammatory drugs (NSAIDs) for specific causes.

 Menstrual migraine
 Defined as hormonal headaches that hits just before or during menses
 Can be triggered by reduction in estrogen levels and it is referred to as estrogen-associated migraine.
 Are of two types namely, pure menstrual and menstrual related migraine.
 Pure menstrual migraine refers to attacks of migraine of perimenstrually 2 days before to 3 day after
menstruation.
 Menstrual related migraine refers to attack of migraine of perimenstrually and other times.
Treatment
 Combined oral contraceptive pills such as calcium channel blockers, progestin, beta blockers, antidepressants.
 Abortive therapy (example is Triptan as the first line abortive analgesic against migraines)

Self Health Care Tips At Times of Menstruation
 Take a warm shower or bath
 Putting on a well recommended and verified sanitary pad, tampon, menstrual cup and period
underwear specifically for your age
 Count the menstrual calendar days as this may help you to prepare for the next menses in advance
 Drink plenty of water
 Eat a balanced diet meal especially the one containing iron
 Wear clean and dry comfy or loose clothes
 Get fresh air
 Take a painkiller if only necessary and advised by the medical personnel
 Change sanitary pads every 4-6 hours to prevent bad odors with vaginal yeast infection and accidental
leaks
 Proper discard of used sanitary pads properly

• The placenta is the site of exchange for
nutrients, wastes, O2, and CO2 between
the mother and the fetus.
• It contains tissues from both individuals.
The embryonic part is the chorion,
derived from the trophoblast and the
maternal part is from the decidua basalis.

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