Genitourinary system

INDEX :
CHAPTER (1) MALE GENITOURINARY SYSTEM
GENERAL ANATOMY OF URINARY TRACT
MALE REPRODUCTIVE SYSTEM ANATOMY
MALE HYPOGONADISM
CHAPTER (2) FEMALE GENITOURINARY SYSTEM
FEMALE REPRODUCTIVE SYSTEM
PHYSIOLOGY OF PREGNANCY
FEMAL HYPOGONADISM

The urinary system's function is to filter blood and create urine as a
waste by-product. The organs of the urinary system include the
kidneys, renal pelvis, ureters, bladder and urethra.
CHAPTER (1)

Kidneys filter about 1700 liters of
blood daily in the average adult.
 Parts of the kidneys
Cortex
-outer protective portion
Medulla
-inner soft portion
Hilum
-a depression located in the middle of the
concave side of the kidney where blood vessels,
nerves, and the ureters enter and exit the kidneys
Cortex
Medulla
Hilum
CHAPTER (1)

Functions of the kidney
Filter nitrogenous wastes to form urine; about
200 quarts of blood are filtered every day to
form 2 quarts of urine
Maintain proper balance of water, electrolytes
(sodium, potassium), and acids
Release hormones:
• Renin: enzymatic hormone important in adjusting
blood pressure
• Erythropoietin (EPO): hormone that stimulates red
blood cell production in the bone marrow
• Calciferol: active form of vitamin D necessary for the
absorption of calcium from the intestine
Degrade and eliminate hormones from the
bloodstream
CHAPTER (1)

CHAPTER (1)
Urine is produced by filtration of:
water
salts
creatine
uric acid
Each kidney contains more than 1 million nephrons which are the
functional units of the kidneys.
Blood Flow through the Kidneys
Blood enters through the renal artery
arterioles
Each arteriole leads to a nephron
renal corpuscle
(which has a group of capillaries called the glomerulus)
sugar
urea

The Nephron
CHAPTER (1)
.
Each nephron has the following
structures:
‟

 Three steps in the formation of urine
 Glomerular filtration
 Tubular reabsorption
 Tubular secretion
CHAPTER (1)
• The renal artery brings blood with
waste products to the kidney to be
cleansed.
• After the blood is cleansed, it returns
to the heart via the renal vein.


CHAPTER (1)
A tube approximately 6 to 7 inches long attached
to each kidney
Made up of three layers of tissue :
 smooth muscle
 fibrous tissue
 mucous layer
Peristalsis, a rhythmic contraction of
the ureter smooth muscle which
helps to move the urine into the
bladder.

CHAPTER (1)
 Hollow, muscular organ that stores urine
 Sphincter muscles hold the urine in place
 Holds 300 to 400 milliliters of urine before emptying
 Walls contain epithelial tissue that stretch to allow the
bladder to hold twice its capacity
 The trigone is a triangular area at the base of the
bladder where the ureters enter and the urethra exits

GENERAL ANATOMY OF
URINARY TRACT
CHAPTER (1)
Female Urethra Male Urethra
Approximately 1.5 inches long
Opens through the meatus
Approximately 8 inches long
 Passes through three
different regions:
prostate gland
membranous portion
penis
Excreting urine is called voiding or micturition

CHAPTER (1)
*Overview
Male mammals have two testicles which are components of both the reproductive and
the endocrine system. Therefore, the two main functions of the testicles are: producing
sperm (approximately 1 million per hour) and male sex hormones (e.g. testosterone) .

CHAPTER (1)
The major components are :
EpididymisDuctus Deferens
Ejaculatory Duct On Each Side The Urethra
Penis In The Midline.
Testis
*Overview

Accessory Glands:
2 Seminal Vesicles :
secrete fructose (sperm use this sugar for energy) and
prostaglandins (induce muscles to contract)
produces 60% of fluid in semen
1 Prostate Gland :
secretes most of the liquid part of semen (sperm +
glandular secretions). May help buffer the low pH (3.5-4.0)
of vaginal fluid.
33% of semen volume
2 Bulbourethral (Cowper’s) Glands :
a mucus-rich lubricant
CHAPTER (1)
*Overview

CHAPTER (1)
Out pouching of skin that contains both testes; can be moved
closer to or farther from body to help maintain temperature
suitable for sperm formation.
The Scrotum contains :
Testes
Epididymis
the lower ends of the spermatic cords.
The wall of the scrotum has the following layers:
Skin
Superficial fascia
Spermatic fasciae
Tunica vaginalis

CHAPTER (1)
Function:
Produce male gametes .
(Spermatogenesis) in seniniferous tubules.
Produce steroid hormones .
(Steroidogensis) in interstitium.
Nourish the produced sperm.
Location : -
 Lowered in Lower abdomen in external pouch called
scortum. (-2/3 ͦ
 descended from abdomen into scrotum around week
28 of pregnancy.
 Smooth muscle fibers, called the dartos muscle, in the subcutaneous tissue
contract to give the scrotum its wrinkled appearance. When these fibers are
relaxed, the scrotum is smooth.
 the cremaster muscle, consists of skeletal muscle fibers and controls the position
of the scrotum and testes. When it is cold or a man is sexually aroused, this
muscle contracts to pull the testes closer to the body for warm .

CHAPTER (1)
*Internal Structure :




Seminiferous tubules




CHAPTER (1)
(1) SERTOLI CELLS :
Nonreplicating physical support cells .
Function : -
 Remove excess cytoplasm from developing spermatid – tubulobulbar
processes.
 Phagocytosis of defective sperm.
 Nourish developing sperms during spermatogenesis.
 Provide the blood testes barrier, which is also called as sertoli cell barrier.
 Secrete fluid to transport sperm in reproductive tract
 - Secrete hormones and other factors :
Secrete mullerian inhibiting substance(MIS) during intra uterine life.
Secrete paracrine agents facilitating leydig cell function.
Adult - inhibin -estrogen - Other factor (not a hormone) – androgen binding
protein (helps transport androgens from interstitial fluid into seminiferous
tubule -promotes spermatogenesis) .

CHAPTER (1)
(1) SERTOLI CELLS :

CHAPTER (1)
(2) MESENCHYMAL CELLS :
Each seminiferous tubule is surrounded
by mesenchymal cells, which comprise
the peritubular myoid cells whose
contractile elements generate
peristaltic waves along the tubules, but
do not present a tight diffusion barrier.
(3) Interstitial or Leydig cells :
Leydig cells release a class of
hormones called androgens in
male are :
 Testosterone.
 androstenedione
 dehydroepiandrosterone
(DHEA),
Leydig cells are the most potent
cells in androgen synthesis .

CHAPTER (1)
Functions :
Initiation & Maintenance Of Spermatogenesis.
GNRH From The Hypothalamus
Inhibits LH Secretion Via Anterior Pituitary.
Differentiation & Maintenance Of Male Secondary Sexual
Characteristics : facial Hair & Body Habitus.
Induces Differentiation & Maintains Accessory Reproductive Organs.
Stimulates Protein Anabolism, Bone Growth & It’s Cessation.
Enhances Libido & Aggressive Behavior By Masculinizing The Brain .
Stimulates Secretion Of Erythropoietin From The Kidneys .

CHAPTER (1)
(4) SPERMATOGENIC CELLS :
Stem cells which regularly replicate and differentiate into mature
sperm as they migrate toward the lumen
Function:
spermatogenesis continue the spermatocytes progressively
move from basement membrane to the luminal side of
seminiferous tubule .

CHAPTER (1)
Shape :-
a long, coiled tube. -
Functions :-
1. Maturational changes of spermatozoa
2. Stabilization of condensed chromatin.
3. Changes in surface charge of the
plasma membrane.
4. New sperm surface proteins.
5. Sperm storage.
6. Sperm transport by peristalsis (sperm
epididymal maturation requires
2-12 days).
7. Release of spermatozoa during
ejaculation.
8. Elimination of aged
9. Single highly coiled tube (4-6 m).
Location : -
a curved structure on the
posterior (back) margin of each
testis.

CHAPTER (1)
 Upon ejaculation the epididymis contracts, expelling sperm
into the ductus deferens.
 Can also store sperm several months
 Ampulla of the vas deferens :-
• Terminal portion of the vas deferens enlarges
into an ampulla.
After the ductus deferens exits the deep
inguinal canal, it heads superiorly towards the
urinary bladder.
• Lumen of ampulla larger than vas deferens.
• After crossing the ureters, the ampulla of the
ductus deferens joins the seminal vesicle.

CHAPTER (1)
• Their secretions provides the bulk of semen.

CHAPTER (1)
1. Seminal vesicles (glandulae vesiculosae)
Paired, elongated, saclike structures, and highly folded
tubular gland. - The duct of each joins with the distal end of
the ductus deferens to form an ejaculatory duct. - Empty its
secretions into vas deferens.
Functions:
1. secrets a strongly acidophilic and constitutes 45-80 % of the ejaculate
volume (2-2.5 mL).
2. Its secrets contains several proteins, enzymes, mucus and vitamin C .
3. Rich in Fructose ( major sourse of energy)
Location : -
On posterior wall of urinary bladder.

CHAPTER (1)
2. Prostate
The largest accessory gland consisting of 30-50 branched
tubuloalveolar glands. Empty its secretions in the urethra.
Functions:-
1. Secretions are acidic (pH 6.5).
2. Prostatic fluid contributes 15-30 % or about 0.5 mL to the
volume of the semen.
3. Contains a high citric acid content (maintain the osmotic
equlibirium in semen) , acid phosphatase and zinc.
4. Contains enzymes required for liquefaction of the ejaculate
coagulum.
Location : -
surrounds and opens into the urethra where it leaves the bladder.

CHAPTER (1)
3. Bulbourethral glands (Cowper´s glands)
Functions:
1. Secretions including galactose, sialic acid .
2. has a lubrication function (mucoprotiens) and precedes
emission of semen along the penile urethra.
3. forming a part of the ejaculate (0.1-0,2 mL = 5%) .
Location : -
located in the urogenital diaphragm, close to the bulb of the
penis.
pair of pea-sized structures

CHAPTER (1)
3. Bulbourethral glands (Cowper´s glands)

CHAPTER (1)
Is a short passageway (2 cm) at junction of ampulla and
seminal vesicle duct Penetrates wall of prostate gland
Empties into urethra.

CHAPTER (1)
Passageway for urine and male reproductive fluids Extends
18–20 cm: Extends from urinary bladder to distal end (tip) of
penis.
Is divided into 3 regions:
prostatic
membranous
spongy

CHAPTER (1)
Site of Sperm Formation :
Occur in the seminiferous tubules in
the testis
The Sperm formulation involves three
steps:
 Spermatocytogenesis:
spermtogenic cells form
rounded cells called spermatids
 Spermiogenesis:
spermatids which in the second
step differentiate into specialized
cells known as sperms.
 Spermiation

CHAPTER (1)
Steps of Spermatocytogenesis :
The primitive sex cells appear earliest in 4th week of intra uterine life in the
wall of yolk sac
1
At puberty the germ cells awaken and start the actual process of spermato
genesis
Spermatogonia are the Germ-Line cells. They are diploid (2n). They
undergo mitosis to reproduce themselves.(Increase in No.) About 64-72
days are required to go from a spermatogonium to be a sperm.
One of these spermatogonia undergoes meiosis, and it is called a primary
spermatocyte. It is diploid (2n).
The primary spermatocyte undergoes MEIOSIS I to produce two secondary
spermatocytes. These are now haploid (n) but still contain two chromatids
per
2
3
4
5
6
Each of these secondary spermatocytes undergoes MEIOSIS II to each
produce two spermatids.
1

CHAPTER (1)
Steps of Spermatocytogenesis :1

CHAPTER (1)
Steps of Spermiogensis:2
Spermatids modify to assume specific shape of the sperm . They elongate
and reorganize internal structure to acquire the particular shape.
The changes include ;
o Golgi apparatus forms acrosomal cap-proteolitic enzymes
o Nucleus is condensed
o Centriols: make collar around neck
o Microtubules, forrm flagellum,
o Mitochondria arrange as spiral around neck
o Excess cytoplasm cast off as residual body
o Cytoplasmic bridges break and sperms release from Sertoli cells to
lie free in lumen of seminiferous tubules .

CHAPTER (1)

CHAPTER (1)
Steps of Spermiation :3
mature spermatids are released from Sertoli cells into the
seminiferous tubule lumen prior to their passage to the epididymis.
extensive restructuring and remodeling of the spermatid to produce a
streamlined spermatozoan .
involves several discrete steps including :
 remodeling of the spermatid head and cytoplasm
 removal of specialized adhesion structures.
 the final disengagement of the spermatid from the Sertoli cell.

CHAPTER (1)
• A mature sperm has head, neck and tail From lumen of seminiferous tubules .
• sperms enter duct of epididymis They take 20 days to travel this 4-6 meter long tortuous duct
• If ejaculation does not occur they die and degenerate

CHAPTER (1)
1
32
Gonadotropin
releasing
hormone
Luteinizing
hormone
follicle-stimulating
hormone
Testosterone
Negativefeedback

CHAPTER (1)
GnRH (gonadotropin-releasing hormone) :
Secreted by hypothalamus Stimulates secretion of anterior pituitary
secretion hormones (FSH/LH)
FSH and LH (follicle stimulating hormone and leuteinizing
hormone)
• LH - as Interstitial Cell Stimulating Hormone Secreted by anterior
pituitary Directly stimulate the testes LH - stimulates interstitial cells to
secrete testosterone
• FSH - stimulates formation of ABP (androgen binding protein) by
nurse cells LH - stimulates interstitial cells to secrete testosterone .
Feedback inhibition on the hypothalamus and pituitary results
from:
• Rising levels of testosterone
• Increased inhibin

CHAPTER (1)
 Produced: Seminiferous tubules (Testis).
 Stored: Epididymis
 Transported : through epididymis by rhythmic peristaltic
contractions as they mature
Epididymis Vas Deferens
Ejaculatory duct (ampulla
of vas deferens fuses
with duct of seminal
vesicle “ejaculatory
duct”)
prostate
prostatic urethra (then
passes the
bulbourethral gland)
membranous urethrapenile urethra
Sperm Summary

CHAPTER (1)
Semen Has:
Sperms
Secretions:
 Seminal Vesicles
 Prostate
 Cowper’s Glands
 Bulbo-urethral Glands
Is A Test For Infertility.
 Volume: 2.5 to 3.5 ml Per ejaculate.
 Sperm count: 100 millions/ml. <20% can be abnormal.
If the count is <20 million/ml, it indicates that he is sterile
 Speed Of Sperms: 3mm/min.
 Reach fallopian tube : 30- 40 minutes after coitus.

CHAPTER (1)
Semen Composition :
COLOR: White, Opalescent
SPECIFIC GRAVITY: 1.028
PH : 7.35 – 7.50
Other Constituents:
 Seminal Vesicles: 60% Volume.
 Prostate Gland: 20% Volume
Character of semen :
Is Liquid When Ejaculated
Coagulates Both:
 In Vitro &
 The Vagina
undergoes secondary liquefaction after 15 minutes.

Oligospermia – sperm concentration <15 million/ml
Asthenozoospermia – <40% grade (PR+NP) or < 32 PR%
Teratozoospermia – <4% spermatozoa
OAT =Oligo-astheno-teratozoospermia
Azoospermia – no spermatozoa in semen
Polyzoospermia – ++ high sperm concentration, >200M/ml
Hypospermia – semen volume < 1.5 ml
Hyperspermia – semen volume > 4.5 ml
Aspermia – no semen volume
Pyospermia – leukocytes present in semen, >1M/ml
Hematospermia – red blood cell present in semen
Necrozoospermia – “dead” sperm
CHAPTER (1)

CHAPTER (1)
Lower Reference LimitParameter
1.5Semen volume (ml)
15Sperm concentration (106/ml)
39Total sperm number (106/ejaculate)
23Progressive motility (PR, %)
40Total motility (PR +NP, %)
58Vitality (live sperms, %)
4Sperm morphology (NF, %)
>/=7.2pH*
<1Leucocyte* (106/ml)
<50MAR/Immunobead test* (%)

CHAPTER (1)
inadequate gonadal function, as manifested by deficiencies in
gametogenesis and/or the secretion of gonadal hormones.”
*definition
Types Of Hypogonadism
Primary Hypogonadism
Secondary Hypogonadism
These abnormalities usually result from disease of the testes .
Primary testicular hypogonadism eg- klinefelter syndrome
Hypergonadotrophic hypogonadism
These abnormalities usually result from
disease of the pituitary or
hypothalamus
 Secondary testicular hypogonadism
 Hypogonadotrophic hypogonadism

CHAPTER (1)

CHAPTER (1)
Hypergonadotropic Hypogonadism
(Primary)
Increased FSH level
Increased LH level
Low testosterone level
Impaired production of sperm
Hypogonadotropic Hypogonadism
(Secondary)
Low or low-normal FSH level
Low or low-normal LH level
Low testosterone level
Impaired production of sperm

Primary Hypogonadism
Congenital :
 Chromosomal defect eg- klinefelter syndrome
 Congenital anorchia
 Undescended testicles (cryptorchidism).
 Androgen receptor / enzyme defect
Acquired :
 Testicular trauma or injury
 Surgical removal
 Chemotherapy / irradiation
 Infection e.g: mumps orchities
Complication of illness e.g : diabetes . Renal failure .cirrhosis
CHAPTER (1)

Primary Hypogonadism ( Congenital )
CHAPTER (1)
 klinefelter syndrome -KS or 47, XXY
Male is born with an extra copy of the X chromosome
Symptoms :
Babies -
 Weak muscles
 Slow motor development — taking longer than average to sit up, crawl
and walk
 Delay in speaking
 Problems at birth, such as testicles that haven't descended into the
scrotum

CHAPTER (1)
Symptoms :
Teenagers -
 Taller than average stature
 Longer legs, shorter torso and broader hips compared with other
boys
 Absent, delayed or incomplete puberty
 After puberty, less muscle and less facial and body hair compared
with other teens
 Small, firm testicles
 Small penis
 Enlarged breast tissue (gynecomastia)
 Weak bones
 Low energy levels
 Tendency to be shy and sensitive
 Difficulty expressing thoughts and feelings or socializing
 Problems with reading, writing, spelling or math

CHAPTER (1)
Symptoms :
Adult -
 Low sperm count or no sperm
 Small testicles and penis
 Low sex drive
 Taller than average height
 Weak bones
 Decreased facial and body hair
 Less muscular compared with other men
 Enlarged breast tissue
 Increased belly fat

CHAPTER (1)

CHAPTER (1)
 Congenital anorchia
is a disorder of sex development in which a person with XY
karyotype, rare condition in which one or both testes are
absent in a phenotypically and genotypically normal male
born without testes. the testes fail to develop within eight
weeks in the intrauterine fetal life .
 Undescended testicles (cryptorchidism).
It's estimated about 1 in every 25 boys
are born with undescended testicles
In most cases no treatment is necessary,
as the testicles will usually move down
into the scrotum naturally during the
first 3 to 6 months of life after the if
descending not occur the testecals get
necrosis and become non functional
become cancer

CHAPTER (2)
Internal Anatomy Female Reproductive System
 The Female Reproductive organs comprise:
 The Gonads- in the form of two ovaries
 The accessory sex organs consisting of:
 The Fallopian Tube
 Uterus
 Cervix
 Upper end of Vagina

Function of the female reproductive system
Produces, sustains , and allows oocytes to be fertilized by sperm
Supports the development of an offspring (gestation)
Gives birth to a new individual (parturition) .
CHAPTER (2)

 Located : between the bladder and rectum.
 The Function of the uterus is to support the growing fetus
during pregnancy.
There is dramatic growth of the uterus during pregnancy, occurring by a
process of both muscle cell hyperplasia and production of new muscle cells
from the resident stem cells.
The uterus is a pear-shaped muscular organ within the
pelvis
CHAPTER (2)

Anatomical Structure
The uterus is a thick-walled muscular organ capable of expansion to
accommodate a growing fetus. It is connected distally to the vagina, and
laterally to the uterine tubes.
The Uterus Has Three Parts;
Fundus – top of the uterus, above the entry point of the uterine
tubes.
Body – usual site for implantation of the blastocyst.
Cervix – lower part of uterus linking it with the vagina. This part is
structurally and functionally different to the rest of the uterus. See
here for more information about the cervix
CHAPTER (2)

Tissue layers of Uterus :
Peritoneum or Perimetrium (fibrous connective tissue)
Myometrium (smooth muscle)
Endometrium (epithelial and connective tissues) .
Endometrium:
 Inner mucous membrane lining the uterus. It can be further
subdivided into 2 parts:
• Deep stratum basalis: Changes little throughout the menstrual
cycle and is not shed at menstruation.
• Superficial stratum functionalis: Proliferates in response to
oestrogens, and becomes secretory in response to
progesterone. It is shed during menstruation and regenerates
from cells in the stratum basalis layer.
CHAPTER (2)

Myometrium:
 under the stimulation of oxytocin, contracts during labor to expel the
fetus into the vagina .
 The base of uterus is closed by a narrow passageway called cervix to
prevent the entry of foreign substances .
Peritoneum :
 a double layered membrane, continuous with the abdominal
peritoneum. Also known as the perimetrium.
CHAPTER (2)

Ligaments :
Broad Ligament: This is a double layer of peritoneum attaching the
sides of the uterus to the pelvis
Round Ligament: A remnant of the gubernaculum extending from the
uterine horns to the labia majora via the inguinal canal. It functions to
maintain the anteverted position of the uterus.
Ovarian Ligament: Joins the ovaries to the uterus.
Cardinal Ligament: Located at the base of the broad ligament, the
cardinal ligament extends from the cervix to the lateral pelvic walls. It
contains the uterine artery and vein in addition to providing support to
the uterus.
Uterosacral Ligament: Extends from the cervix to the sacrum. It
provides support to the uterus.
CHAPTER (2)

Vascular Supply and Lymphatic's :
The blood supply :
is via the uterine artery.
Venous drainage:
is via a plexus in the broad ligament that drains into the
uterine veins.
Lymphatic drainage :
via the iliac, sacral, aortic and inguinal lymph nodes.
Innervation :
 Sympathetic nerve fibres of the uterus arise from the uterovaginal
plexus.
 Parasympathetic fibres of the uterus are derived from the pelvic
splanchnic nerves (S2-S4)
CHAPTER (2)

The ovaries are the female pelvic reproductive organs that house the
ova and are also responsible for the production of sex hormones.
They are paired organs located on either side of the uterus within the
broad ligament below the uterine (fallopian) tubes.
The ovary is within the ovarian fossa, a space that is bound by the
external iliac vessels, obliterated umbilical artery, and the ureter.
The ovaries are responsible for housing and releasing ova, or eggs,
necessary for reproduction.
At birth, a female has approximately 1-2 million eggs, but only 300 of
these eggs will ever become mature and be released for the purpose
of fertilization.
CHAPTER (2)

Components of the Ovary :
Surface – formed by simple cuboidal epithelium (known as germinal
epithelium). Underlying this layer is a dense connective tissue capsule.
Cortex – comprised of a connective tissue stroma and numerous
ovarian follicles. Each follicle contains an oocyte, surrounded by a
single layer of follicular cells.
Medulla – formed by loose connective tissue and a rich neurovascular
network, which enters via the hilum of the ovary.
CHAPTER (2)

Ligaments Two peritoneal ligaments attach to the ovary:
Suspensory ligament of ovary –
fold of peritoneum extending from the mesovarium to the pelvic wall.
Contains neurovascular structures.
Ligament of ovary –
extends from the ovary to the fundus of the uterus. It then continues from
the uterus to the connective tissue of the labium majus, as the round
ligament of uterus.
CHAPTER (2)

Neurovascular Supply :
arterial supply –
The main arterial supply to the ovary is via the paired ovarian arteries. These
arise directly from the abdominal aorta (inferior the renal arteries). There is
also a contribution from the uterine arteries.
Venous drainage –
Venous drainage is achieved by paired ovarian veins. The left ovarian vein
drains into the left renal vein, and the right ovarian vein drains directly into
the inferior vena cava.
Innervation –
The ovaries receive sympathetic and parasympathetic innervation from the
ovarian and uterine (pelvic) plexuses, respectively
Lymphatic Supply –
Lymph from the ovaries drains into the para-aortic nodes.
CHAPTER (2)

Produces :
 Oocytes in a process called oogenesis
 Female sex hormones: estrogens and progesterone
Developed:
 Near the kidneys during fetal development
 Toward the end of pregnancy descend into the pelvic cavity
CHAPTER (2)

also known as uterine tubes or salpinges (singular salpinx), are
tubes that stretch from the uterus to the ovaries
Functions :
The main function of the uterine tubes is to assist in the transfer and
transport of the ovum from the ovary, to the uterus.
 The ultra-structure of the uterine tubes facilitates the movement of the
female gamete:
 The inner mucosa is lined with ciliated columnar epithelial cells
and peg cells (non-ciliated secretory cells). They waft the ovum
towards the uterus and supply it with nutrients.
 Smooth muscle layer contracts to assist with transportation of
the ova and sperm. Muscle is sensitive to sex steroids, and thus
peristalsis is greatest when oestrogen levels are high.
CHAPTER (2)

Anatomical Structure
Fimbriae – finger-like, ciliated projections which
capture the ovum from the surface of the ovary.
Infundibulum – funnel-shaped opening near the
ovary to which fimbriae are attached.
Ampulla – widest section of the uterine tubes.
Fertilization usually occurs here.
Isthmus – narrow section of the uterine tubes
connecting the ampulla to the uterine cavity.
CHAPTER (2)

The arterial supply to the uterine tubes :
is via the uterine and ovarian arteries.
Venous drainage:
is via the uterine and ovarian veins.
Lymphatic drainage:
is via the iliac, sacral and aortic lymph nodes.
CHAPTER (2)

:
The vagina is a fibromuscular tube with anterior and posterior walls
Function :
"birth canal" during parturition
copulatoryreceptacle, where it receives the penis during sexual
intercourse
secretion :
acids secretion from cervix
uterine secretions (i.e. menstrual flow).
The arterial supply to the vagina is via the uterine and vaginal arteries
Venous return is by the vaginal venous plexus
Lymphatic drainage is divided into three sections:
 Superior – drains to external iliac nodes
 Middle – drains to internal iliac nodes
 Inferior – drains to superficial inguinal lymph nodes.
CHAPTER (2)

Hormones involved in ovulation include:
• Gonadotropin-releasing hormone (GnRH) is a tropic peptide
hormone made and secreted by the hypothalamus. It is a
releasing hormone that stimulates the release of FSH and LH
from the anterior pituitary gland
• Follicle-Stimulating Hormone (FSH) is a gonadotropin
synthesized and secreted from the anterior pituitary gland FSH
stimulates the growth and maturation of immature oocytes
into mature (Graafian) secondary follicles before ovulation
• Estrogen is a steroid hormone that is responsible for the
growth and regulation of the female reproductive system and
secondary sex characteristics. Estrogen is produced by the
granulosa cells of the developing follicle and exerts negative
feedback on LH production in the early part of the menstrual
cycle.
However, once estrogen levels reach a critical level as oocytes
mature within the ovary in preparation for ovulation, estrogen
begins to exert positive feedback on LH production,
CHAPTER (2)

hypothalamus
Gonadotropin-releasing hormone (GnRH)
anterior
pituitary gland
Follicle-Stimulating Hormone (FSH)
immature oocytes
1
2
mature (Graafian)
secondary follicles
Luteinizing Hormone (LH)
Estrogen
++++++
Estrogen ++
high-frequency GnRH
slow-frequency pulsatile GnRH
 theca cells
 luteinized granulosa cells
inducingovulation
Production of Progesterone
 preparing the endometrium for
the uterine implantation of the
fertilized egg .
corpus luteum
secretes progesterone
in early pregnancy until
the placenta develops
fertilizationoccurNofertilization
If
Menses occur
CHAPTER (2)

Ovarian cycle has 2 phases :
FOLLICULAR PHASE –
consists of the development of a primordial follicle into a
mature or Graafian follicle
LUTEAL PHASE –
consists of the formation of the corpus luteum, a major
secreting gland
• At the middle of the ovarian cycle the
OVULATION takes place
CHAPTER (2)

Follicular Phase
Preovulatory Phase or the proliferative phase
consists of the development of a primordial follicle into a
mature or Graafian follicle
Hypothalamus ------- secret GNRH to stimulate the Anterior
pituitary
Anterior pituitary------- secrets LH and FSH
1. LH stimulate the theca cells to produce cholesterol then
by enzyme called desmolase convert the cholesterol into
androstenodione .The androstenodione goes to
granulosa cell .
2. FSH stimulate the granulosa cell to :
 Produce inhibn as negative feed back to both
Hypothalamus Anterior pituitary glands .
 convert the androstenodione to estrogen by
aromatase enzyme .
 High estrogen levels lead to negative feed back to
both Hypothalamus Anterior pituitary glands .
From day 0 to day 14
CHAPTER (2)

LUTEAL PHASE
At the middle of the ovarian cycle the
OVULATION takes place
( ovaries release an egg )
OVULATION
 Once it releases its egg, the empty follicle develops into a new
structure called the corpus luteum.
 The corpus luteum makes the hormone progesterone, which
prepares the uterus for a fertilized egg to implant.
 Ifa man's sperm has fertilized the egg, the fertilized egg will travel
through the fallopian tube to implant in the uterus.
 Ifthe egg is not fertilized, it passes through the uterus. The lining of
the uterus breaks down and sheds, and the next menstrual period
begins
Day 15
From day 16 to day 21
CHAPTER (2)

Three phases of the menstrual cycle :
PROLIFERATIVE PHASE (days 4 – 14 of cycle)
SECRETORY PHASE (days 14 – 28 of cycle)
MENSTRUAL PHASE (days 1 – 4 of cycle)
under control of estradiol (follicular phase of ovarian cycle)
glands in s. basalis under go mitosis
stroma, glands, spiral arteries grow toward lumen
PROLIFERATIVE PHASE (days 4 – 14 of cycle)
CHAPTER (2)

SECRETORY PHASE (days 14 – 28 of cycle)
under control of progesterone (luteal phase of ovarian cycle )
uterine glands coiled, larger lumens
secrete glycogen, mucin
MENSTRUAL PHASE (days 1 – 4 of cycle)
the involution of the corpus luteum results from a decrease in blood
levels of steroid hormones, leading to an ischemic phase.
a reduction in the normal blood supply-causing intermittent
ischemia-and the consequent hypoxia determine the necrosis of the
functional layer of the endometrium, which sloughs off during the
menstrual phase.
CHAPTER (2)

 OBJECTIVES.
Fertilization & Implantation
Physiological Changes During Pregnancy.
Physiology Of Parurition.
Placenta & Pregnancy Tests
Pregnancy also known as gestation is the term used to
describe the period in which a fetus develops inside a
woman's womb or uterus
Definition
CHAPTER (2)

 Fertilization & Implantation
Transportation of ovum
Transportation of sperm in female genital tract.
Sperm capacitation
Fusion of gametes.
Activation of ovum.
CHAPTER (2)

Fertilization & Implantation
Transportation of ovum
 Fertilization – fusion of male & female gametes.
 Site – Middle segment (Ampulla) of fallopian tube.
 Transport of ovum – from peritoneal cavity after expulsion
enters fallopian tube through fimbria of infundibulum
 Helped by – smooth muscles of tube & ciliated epithelium.
Ovum
 Mature ovum – consists of Oocyte (23unpaired chromosomes)
surrounded by Zona pellucida & Granulosa cells in multilayer
called Corona Radiata.
Fate of ovum.
 Held at ampulla isthmic junction for 2-3 days
 After ovulation ovum viable for 6-24 hrs.
 If fuses with sperm fertilization occurs if not dies and
degenerate.
CHAPTER (2)

Transportation of sperm in female genital tract.
 Each ejaculate contains 200 million cells.
 Out of these only 50-100 manage to reach ovum
 Only 1 penetrate.
Motility of sperms.
 pH of fluid medium
 Cervical mucus secretions
 Fluid currents
 Temperature.
 Hormones.
CHAPTER (2)

Motility of sperms.
 pH of fluid medium :
• Neutralize & alkaline – enhances activity.
• But vaginal fluid is acidic so immediately after ejaculation
sperms become inactive
• Then alkaline semen neutralizes vaginal fluid – sperms
becomes active again for next 24 to 40 hrs.
 Cervical mucus secretions :
• Acts like a mechanical barrier.
• Depend on hormonal levels
• Proliferative phase & near ovulation – more oestrogen –
secretions more thin – allow entry of sperms.
CHAPTER (2)

Motility of sperms.
 Fluid currents :
• Vaginal & uterine cavity currents are setup by ciliary
movements.
• Direction – opposite towards externally.
• Opposes movements.
 Temperature :
• With increase temperature activity increases but life span
decreases.
• Can be stored at -100 0 c for many years.
CHAPTER (2)

Motility of sperms.
 Hormones.
 Oxytocin – release during coitus causes propulsive movements
of uterus which aspirate fluid from vagina into fallopian tube.
 Oestrogen – make cervical secretions thin and watery so
favors transport of sperms.
 Prostaglandins- in semen increases female genital tract
movements.
 Progesterone- in follicular fluid affects sperms motility.
CHAPTER (2)

Sperm capacitation
is the set of natural physical changes that a spermatozoon undergoes in
order to be able to fertilized the ovum. This occurs in vivo following
ejaculation when the spermatozoa come into contact with the different
fluids in the female genital tract .
 Process which makes sperms capable to fertilize ovum
 Takes 1-10 hrs
 Cholesterol content of acrosomal
membrane decreases –leads to easy
release of enzymes from head.
CHAPTER (2)

Sperm capacitation
 Calcium ions permeability of sperms membrane increases.
 Influx of Ca causes-
• Flagellar movements strong & whipish
• Triggers release of enzymes from acrosome.
CHAPTER (2)

Fusion of gametes.
 Chemo-attraction : By substances produced by ovum.
 Penetration of sperm through ovum coverings.
 Fusion of sperm with oocyte.
CHAPTER (2)

Fusion of gametes.
 Penetration of sperm through ovum coverings Through 2
layers :
 Corona radiata –
• Acrosome of sperm head releases Hyaluronidase enzyme
& other proteolytic enzyme.
• Hyaluronidase enzyme – polymerizes Hyaluronic acid
• Proteolytic enzyme – digest proteins of structural tissue.
 Zona pellucida –
• When reach zone pellucida acts on receptor – Zona
pellucida glycoprotein Triggers Acrosomal reaction.
CHAPTER (2)

Fusion of gametes.
ovum 2 layers :
CHAPTER (2)

Fusion of gametes.
ACROSOMAL REACTION.
 Acrosome releases acrosin.
 Opens penetrating pathway for sperms into perivitteline space
 For effective penetration this reaction takes place at zona
pellucida.
 Also important for actual fusion of sperm cell with oocyte
membrane.
Fusion of sperm with oocyte.
 Site of contact – equatorial region of Acrosome.
 Fertilin on activated sperms contact with protein on vitelline membrane
 With 30 min membrane fuses-genetic material enters & embryo develops.
CHAPTER (2)

Fusion of gametes.
CHAPTER (2)

Activation of ovum.
1. Membrane potential of ovum decreases – Zona pellucida--
structural changes
2. Release of Ca
3. Vitelline block to polyspermy
4. Zona blockade to polyspermy – by glucosidase & protease.
CHAPTER (2)

IMPLANTATION.
is the stage of pregnancy at which the embryo adheres to the wall of
the uterus
 Formation of blastocyst
 Transportation of blastocyst in uterine cavity.
 Implantation of blastocyst in the endometrium.
 Decidual reaction.
CHAPTER (2)

IMPLANTATION.
CHAPTER (2)

• Respiratory, excretory, nutritive, endocrine, barrier function,
immunological function.
• Supplying oxygen and output of co2 is done via simple
diffusion (respiratory) and nutrients to the fetus via the
umbilical cord (nutritive).
• Clearing out waste products, such as urea, creatinine, uric acid
from the fetus (excretory).
• Metabolizing and releasing food substances and required
products into the maternal and fetal blood circulations.
• Protecting the fetus from xenobiotics (compounds including
food additives, drugs, and environmental pollutants).
• Producing steroid and peptide hormones that help in the
growth and development of the baby (endocrine).
• Protecting the fetus from infections (bacterial) and maternal
diseases.
• Fetal membrane protects the transfer of noxious substances
less than 500 dalton except antibody and antigen (barrier).
• Produces different enzymes such as diamine oxidase and
oxytocinase (enzymatic).
Functions Of The Placenta During Pregnancy
CHAPTER (2)

Physiological Changes In
Mother During Pregnancy
Changes in genital organ
Weight gain Hematological Changes
CVS changes RS changes
Urinary system changes GIT ChangesMetabolic changes
Endocrine changes
Changes in skin Psychological Changes
CHAPTER (2)

 Uterus
 Size – increases Due to Hypertrophy & hyperplasia of
myometrium.
 Weight – changes from 30-50 to 1000-1200 gms
 Length – 7.5 to 35 cm
 Thickness - from 1.25 cm to 5 mm
 Volume – few ml to 5-7 lit
 Shape – Pyriform to globular.
CHAPTER (2)

 Ovaries
 First 12- 16 weeks corpus leuteum enlarges
 Then as HCG levels decreases it degenerate
 Its function taken over by placenta.
 Cervix
 Endocervix – hypertrophied
 Cervical gland secretions increases form a plug which
closes cervix
 Tough cervix becomes soft.
CHAPTER (2)

 Fallopian tubes
 Due to enlargement of uterus – pushed upwards
 Blood supply increases Then as HCG levels decreases it
degenerate
 Causes hyperplasia of epithelial cells.
CHAPTER (2)

 Total weight gain – 10-12 kg.
 Fetus – 3kg Placenta & amniotic fluid – 1.5 kg
 Uterus & breast enlargement – 1.5 kg
 Blood volume & interstitai fluid 1.5 kg
 Fat deposition- 3-4 kg.
Weight gain
CHAPTER (2)

 Blood volume – increase 30%
 Blood indices – decrease
 Plasma proteins decrease
 Leucocytes increase
 Platelets decrease
 Coagulation factors increase (VII,VIII,IX & X)
Hematological Changes
CHAPTER (2)

 Position of heart – more laterally & upward & LAD
 Heart rate – Tachycardia (Hyperdynamic circulation)
 Cardiac output. - due to blood volume
 Blood pressure – both decreases mainly due to vasodilation.
 Venous pressure – due to gravid uterus rises causes oedema of
feet, varicose veins, piles & peripheral thrombosis.
 Blood flow - to uterus, kidney & skin.
CVS changes
CHAPTER (2)

 Anatomical changes – Diaphargm elevation
 Hyperventilation – progesterone increases sensitivity to CO2 –
 Ventilatory functions - increase TV & IC and decrease RV & FRC
 Gas exchange increase due to increase pulmonary blood flow
 Oxygen consumption increase by 15%.
RS changes
CHAPTER (2)

 Renal blood flow
 Effective renal plasma flow
 GFR
 Renal tubular absorptive capacity
 Clearance rate
 Glycosuria
 Proteinuria
 Water balance
 Acid base balance Hyperventilation causes respiratory
alkalosis
All increased
Urinary system changes
CHAPTER (2)

Urinary system changes
CHAPTER (2)

 GIT secretion & motility decrease
 Gall bladder function increase
 Liver function – fibrinogen increase albumin decrease
 Morning sickness – anorexia, nausia & vomiting.
 GTT – Diabetic type
GIT Changes
CHAPTER (2)

 BMR – basal metabolic rate increase
 Protein metabolism – nitrogen retention & positive
nitrogen balance
 Carbohydrate - increase BSL, glycosuria, decrease hepatic
glycogen.
 fat - increase in cholesterol, TG, PL
 Mineral - increase Ca & P retention, iron metabolism.
Metabolic changes
CHAPTER (2)

 Pituitary - increase prolactin, ACTH, TSH & decrease GnRH
 Thyroid - increase thyroid binding globulin.
 Parathyroid - increase active form of Vit D3
 Adrenal cortex - increase all
 Pancreas - increase Insulin.
Endocrine changes
CHAPTER (2)

 Hyperpigmentation – cloasma, linea alba
 Stria gravidarum – linear scar on lower abdomen
Changes in skin
CHAPTER (2)

Psychological Changes
 Craving for particular food
 Alterartion in behaviour, emotion & mood
 In some cases true Psychosis.
CHAPTER (2)

Hypogonadism in females is due to disruption of any section of the
hypothalamic–pituitary–ovarian axis pathway
 In a correctly functioning hypothalamic–pituitary–ovarian
axis pathway:
 The hypothalamus produces gonadotrophin-releasing
hormone (GnRH) at the onset of puberty
 GnRH then acts on the pituitary gland, which produce
follicle-stimulating hormone (FSH) and luteinising hormone
(LH)
 FSH and LH then act on the ovaries to stimulate the
production of oestrogen and progesterone
*Overview
CHAPTER (2)

*clinical features
The clinical features of hypogonadism depend on the age at
presentation
 Estrogen deficiency pre-puberty :
Symptoms of low estrogen levels are rarely present in
hypogonadism pre-puberty.
• The presenting features are absent pubertal development
reduced growth and absence of pubic hair
• primary amenorrhoea (absence of menarche).
 Oestrogen deficiency after completion of puberty :
After the completion of puberty, the features of hypogonadism
include:
• Secondary amenorrhoea (cessation of regular menses for 3
months or the cessation of irregular menses for 6 months)
• Symptoms of the climacteric (peri-menopause): palpitations, heat
intolerance, flushing, night sweats, irritability, anxiety, depression,
sleep disturbance, loss of libido, coarse hair, vaginal dryness, and
fatigue
• Infertility .
CHAPTER (2)

*clinical features
 the complications of oestrogen deficiency :
The long-term risks of oestrogen deficiency include an
increased risk of osteoporosis and cardiovascular disease. The
risk is greater with a younger age of onset. In contrast, the risk
of breast cancer may be slightly reduced.
 skin changes may be due to hypogonadism in females :
• Dry, thin skin
• Potentially increased wrinkles
• Delayed wound healing
• Loss of elasticity, thickness, and moisture of vulval skin, resulting
in genitourinary discomfort.
CHAPTER (2)

*Diagnosis
 hypogonadism diagnosed :
 Human chorionic gonadotropin (hCG) exclude pregnancy
 FSH and LH
 Oestradiol
 Thyroid-stimulating hormone (TSH) — thyroid disorders
can present with amenorrhoea
 Serum prolactin
 Pelvic ultrasound scan — pre-puberty
CHAPTER (2)

Types of female hypogonadism .
Congenital primary ovarian
insufficiency
Acquired primary ovarian
insufficiency
Congenital secondary
hypogonadism
Acquired secondary
hypogonadism
CHAPTER (2)

Congenital primary ovarian
insufficiency
 Chromosomal abnormalities, such as
 Turner syndrome (45,X karyotype),
 fragile X syndrome,
 galactosaemia (inability to process the sugar galactose)
 Ovarian dysgenesis (abnormal organ development) and agenesis
(inability of the organ to develop during embryonic development)
 Congenital adrenal hyperplasia (17α-hydroxylase deficiency).
CHAPTER (2)

 The causes of acquired primary ovarian insufficiency include:
 Medications
• such as chlorambucil, cyclophosphamide, and alkylating
agents
 Radiotherapy .
 Autoimmune diseases including autoimmune polyglandular
syndrome type 1
 Viral infections , including mumps oophoritis, tuberculosis (TB),
malaria, varicella,
 Bacterial infections, such as Shigella
 Iatrogenic disease, such as problems post-oophorectomy (surgical
removal of the ovaries
Acquired primary ovarian
insufficiency
CHAPTER (2)

Congenital secondary
hypogonadism
Congenital secondary hypogonadism is gonadotropin deficiency
due to a genetic mutation, such as in Kallmann syndrome.
CHAPTER (2)

Acquired secondary
hypogonadism
Acquired secondary hypogonadism can be due to damage to the
pituitary/hypothalamus. Causes of acquired secondary hypogonadism
can include:
• Intracranial space-occupying lesions (eg, tumours and cysts)
• Infiltrative disease (eg, sarcoidosis and haemochromatosis)
• Infection (eg, meningitis and TB)
• Pituitary apoplexy (bleeding into pituitary gland)
• Trauma.
CHAPTER (2)

 Gonadotropins can be suppressed by:
• Chronic disease (eg, diabetes, anorexia, obesity, and renal disease)
• Excessive exercise
• Critical illness
• Chronic opiate, glucocorticoid, or anabolic steroid use
• Hyperprolactinaemia (an excess of the milk-inducing hormone
prolactin).
Acquired secondary
hypogonadism
CHAPTER (2)

Genitourinary system

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