MONTHLY ENDOMETRIAL CYCLE

Endometrial Changes
• 3 phases of endometrium changes:
– Proliferative phase
– Secretory phase
– Menstrual phase
Endometrium in the late
proliferative phase

Endometrium in the early Uterine glands

proliferative phase

Endometrium in the late

proliferative phase
 Proliferative Phase
• Ovary is in follicular phase, there is proliferation of the
endometrium (intensive mitosis in the glandular epithelium
and in the stroma)
• Estrogens, secreted in follicular phase of ovarian cycle
causes stromal and epithelial cells to proliferate rapidly
• Estrogen stimulate growth of endometrial glands and
stimulate the production of receptors for progesterone
• Rising levels of estrogen cause the vaginal epithelium to
become “Cornified/ keratinization"
– the surface cells become large and flattened, with small
or absent nuclei
 Proliferative Phase
• Spiral arteries develop in the endometrium
• Endometrial thickness is 3-5mm
• Endometrial glands in the cervical region
secrete thin, stringy mucus
–The mucus strings actually align
themselves along the length of the
cervical canal, forming channels that help
guide sperm in the proper direction from
the vagina into the uterus
 Secretory Phase /Progestational Phase

• Ovary is in Luteal phase

• Progesterone and Estrogen are secreted in large
quantities by the corpus luteum
• Estrogens cause additional proliferation in the
endometrium
• Glands and vessels become highly tortous
 Secretory Phase
• Progesterone causes marked swelling and secretory
changes in the endometrium. Progesterone stimulates
development of glands
• At the cellular level in glandular epithelial cells, there is
abundant of endoplasmic reticulum,, Glycogen & lipid rich
vacuoles increase in glands, displacement of nuclei basally
and glycogen apically in late secretory phase.
– Cytoplasm of the stromal cells increases
– Endometrium becomes thick (5-6mm), highly vascular
and spongy
• Cervical mucus thickens and becomes sticky
Early & late secretory changes
 Importance of secretory phase is
to:
• Prepare endometrium for implantation & provide
appropriate conditions for implantation of a fertilized ovum
– Produce secretory endometrium that contains large
amount of stored nutrients
– Uterine secretions (uterine milk) provide nutrition for
the early dividing ovum in the time period after ovulation
& migration of ovum in uterus and before its implantation
– After ovum implants, trophoblastic cells on the surface of
the implanting ovum begin to digest the endometrium
and absorb the stored substances in the endometrium
 Menstrual Phase
• If the ovum is not fertilized, the corpus luteum in
the ovary suddenly involutes
• There is rapid decrease in estrogens and
progesterone especially
• Menstruation follows
– Decreased stimulation of the endometrial cells by
estrogens and progesterone, resulting in rapid
involution of the endometrium itself to about 65 per
cent of its previous thickness
 Vascular mechanisms basic to menstruation
• Reduction in the estrogen and progesterone lead to a
constriction of spiral arteries
Only the functional layer of the endometrium is affected
by these cyclic changes - the basal layer remains intact.
The uterine vessels show selective sensitivity with regard
to the cyclic hormonal alterations.
• The radial and basal arterioles do not react to hormonal
variations, whereas the spiral arteries of the functional
layer are hormone sensitive and constrict. Constriction
of spiral arteries results in the dying out of the functional
layer of the endometrium. Necrotic tissue together with
blood is eliminated.
• Vasoconstrictor Prostaglandins are released
which causes and vasospasm of tortuous blood
vessels
– Vasospasm & decrease in nutrition to the
endometrium & loss of hormonal stimulation causes
necrosis and sloughing of endometrium
– There is also necrosis of blood vessels
– Blood seeps into the vascular layer of the
endometrium, hemorrhagic areas grow rapidly over a
period of 24 to 36 hours
– necrotic outer layers of the endometrium separate
from the uterus at the sites of the hemorrhages
• Superficial layers of the endometrium are
desquamated in 48 hours after the onset of
menstruation
• This mass of desquamated tissue, blood in the
uterine cavity & contractile effects of
prostaglandins initiate uterine contractions
that expel the uterine contents
• Menstrual fluid contains fibrinolysin and
doesn’t clot
 Why uterus is highly resistant to infection during
menstruation even though the endometrial surfaces
are denuded?

• Some substance liberated by the endometrial

necrosis causes increase in leukocytes
recruitment
• As a result of these leukocytes and possibly
other factors, the uterus is highly resistant to
infection
 Regulation of the Female Monthly
Rhythm—Interplay Between the
Ovarian and Hypothalamic-Pituitary
Hormones
• Intermittent, Pulsatile Secretion of GnRH by
the Hypothalamus Stimulates Pulsatile
Release of LH from the Anterior Pituitary
Gland.
 Hypothalamic Centers for Release
of GnRH
• Arcuate nuclei in mediobasal hypothalamus
causes pulsatile release of GnRH
• Preoptic area of the anterior hypothalamus also
to some extent secrete GnRH
• Limbic system also transmit signals into the
Arcuate nuclei to modify both the intensity &
frequency of the pulses of GnRH release
• psychic factors (signals from limbic system) modify female
sexual function
• Positive feedback effect
of estrogen to cause LH
surge
• Negative feedback
effects of estrogen and
progesterone to
decrease LH and FSH
secretion
• Inhibin from the Corpus
Luteum Inhibits FSH and
LH Secretion
 ESTROGENS
• β-Estradiol
• Estrone
• Estriol
– Secreted by
–Ovaries
–Adrenal cortices
–Placenta
 Synthesis of female hormones
• synthesized in the ovaries mainly
from cholesterol derived from LDL
in the blood but also to a slight
extent from acetyl coenzyme A
 β-Estradiol

• β-Estradiol is a principal estrogen secreted by

the ovaries
 ESTRONE

• Ovaries produces some amount of Estrone

• Adrenal cortices and ovarian theca cells
secrete androgens which are converted in
peripheral tissues by aromatase activity to
estrone
Synthesis of female hormones
Interaction of follicular theca and granulosa
cells for production of estrogens
• The theca cells, under the control of LH
produce androgens that diffuse into the
granulosa cells
• In mature follicles FSH acts on granulosa cells
to stimulate aromatase activity, which
converts the androgens to estrogens
 ESTRIOL
• Estriol is a weak
estrogen
• It is an oxidative
product derived
from the conversion
of estradiol and
estrone occurring in
the liver
 PROGESTINS
• Progesterone
• 17-α-hydroxyprogesterone
• Estrogens and Progesterone Are Transported in
the Blood Bound to Plasma Proteins
• Estrogen Degradation in Liver:
– liver conjugates the estrogens to form glucuronides
and sulfates, and about one fifth of these conjugated
products is excreted in the bile; most of the
remainder is excreted in the urine. Liver converts
estradiol and estrone into inactive Estriol
– In Liver diseases there is increases the activity of
estrogens in the body - causing hyperestrinism
 Fate of Progesterone
• Within a few minutes after secretion, most of the
progesterone is degraded to other steroids that have no
Progestational effect.
• Metabolic degradation occurs in Liver
• The major end product of progesterone degradation is
pregnanediol.
• Excreted in the urine in this form
• We can estimate the rate of progesterone formation in the
body from the rate of this excretion.
 Actions of Estrogens
• Effect on External Female Sex Organs
• Effect on the Uterus
• Effect on the Fallopian Tubes
• Effect on the Breasts
• Effect on the Skeleton
– Osteoporosis
• Increase Protein Deposition
• Increase Fat Deposition
• Increase Body Metabolism
• Little Effect on Hair Distribution
• Effect on the Skin
• Effect on Electrolyte Balance
Estrogen
+ve
 FUNCTIONS OF PROGESTERONE
• Progesterone Promotes Secretory Changes in
the Uterus
• Decreases the frequency and intensity of
uterine contractions
• Effect on the Fallopian Tubes
• Development of the Breasts
Feedback regulation of ovarian
function
 Menopause
• The period during which the cycle ceases and the
female sex hormones diminish to almost none is
called menopause
– Age 40 to 50 years
– Cessation of ovarian activity
– Ovaries depleted of follicles
– LH and FSH increase
– Estradiol and inhibin withdrawal causes hot flashes,
and atrophy of the vaginal wall
 Abnormalities of Secretion by the Ovaries
• Reduced Secretion by the Ovaries -Hypogonadism
• Less than normal secretion of hormones by the ovaries result from:
– Poorly formed ovaries
– lack of ovaries
– genetically abnormal ovaries that secrete the incorrect
hormones because of missing enzymes in the secretory cells
– Hypothyroidism in which gonads are secreting small quantities
of estrogens
• Hypersecretion by the Ovaries
– Granulosa cell tumor secrete large quantities of estrogens,
which causes hypertrophy of the uterine endometrium and
irregular bleeding
 Indicators of Ovulation
• Rise in the basal body temperature 1 to 2 days
after ovulation
• Presence of Pregnanediol, the end product of
progesterone metabolism in urine, during the
latter half of the sexual cycle
 Female Fertility

• Fertile Period of Each Sexual Cycle is 4-5 days

– Ovum remains viable for 72 hours after it is expelled
from the ovary (fertilizable for <24hrs)
– Sperm can remain fertile in the female reproductive
tract for up to 5 days
– Time for sperm to fertilize is between 4 and 5 days
before ovulation up to few hours after ovulation
 Rhythm Method of Contraception
• Interval from ovulation to the onset of next menstruation is almost
always between 13 and 15 days that is 14th day before next cycle
• In 28 days cycle ovulation usually occurs within 1 day of the 14th day
of the cycle
• If the cycle is of 40 days, ovulation usually occurs within 1 day of the
26th day of the cycle
• If the cycle is of 21 days ovulation usually occurs within 1 day of the
7th day of the cycle
• Hence unsafe days are 4 days before the calculated day of ovulation
and 3 days afterwards ( in 28 d cycle- 10,11,12, 13,14th,15, 16, 17)
– Such a method of contraception can be used only when the cycle
is regular
– Failure rate of this method is 20-25% per year
 Hormonal Suppression of Fertility
• Use of Oral Contraceptive Pills
• Estrogen or progesterone, given
during the first half of the cycle,
inhibit ovulation
• These hormones prevent
preovulatory surge of LH
• Before LH surge occurs, a sudden
decrease of estrogen secretion
occurs, which might be the
necessary signal that causes
feedback effect on the anterior
pituitary that leads to the LH surge
– Estrogens or progesterone when given prevent the
initial hormonal depression that might be the initiating
signal for ovulation
– Pills used for the control of fertility consist of
combination of synthetic estrogens and progestins
– synthetic estrogens are Ethinyl Estradiol & Mestranol
– synthetic progestins are Norethindrone,
Norethynodrel, Ethynodiol & Norgestrel
– Pills are given in early stages of the monthly cycle and
continued beyond the time that ovulation would
normally occur. Then the drug is stopped, allowing
menstruation to occur and a new cycle to begin.
– Failure rate is 8 to 9 percent per year.
 FSH &LH
• They are glycoproteins
• Loss-of-function mutations in the FSH receptor cause
hypogonadism
• Gain-of-function mutations cause ovarian
hyperstimulation syndrome
– condition in which many follicles are stimulated and cytokines
are released from the ovary, causing increased vascular
permeability and shock
 Prolactin
• Prolactin contains 199 amino acids &three
disulfide bridges
• Structure similar to growth hormone and
human chorionic somatomammotropin (hCS)
• The half-life of prolactin, like that of growth
hormone, is 20 min
• Structurally similar prolactins are secreted by
the endometrium and by the placenta
 Prolactin
• Secretion is tonically inhibited by the
hypothalamus (PIH- dopamine)
• Bromocryptin stimulate dopamine receptors
• L- dopa binds dopamine receptors- increase
• Chlorpromazine (Largectil) blocks dopamine
receptors-increase prolactin
• Maxalon antagonize the release of Dopamine
in CNS
Factors affecting the secretion of Prolactin
 Fertilization
• Ejaculation 300 million
sperm, 100 reach
(uterine) fallopian tube.
• Fertilization occurs in the
uterine tubes
• Acrosomal reaction:
– Acrosome of sperm
contains hyaluronidase, an
enzyme that digests and
forms channel through
zona pellucida.
• Sperm fuses with ovum
cell membrane.
 Fertilization

• As fertilization occurs,
secondary oocyte
completes 2nd meiotic
division.
• Sperm enters ovum
cytoplasm.
• Ovum nuclear membrane
disappears, zygote formed.
Fertilization of the ovum
 A: Ovulation, fertilization of the ovum in the fallopian tube & implantation of the
Blastocyst in the uterus B: Action of trophoblast cells in implantation of the Blastocyst
in the endometrium
 Transport of the Fertilized Ovum
in the Fallopian Tube
• Transport is effected by:
– Feeble movement of fluid from epithelial cell secretions
– Action of the ciliated epithelium
– Weak contractions of fallopian tube
• 3 to 5 days are required for transport of the fertilized ovum
through the fallopian tube into the cavity of the uterus
• The fallopian tubes are lined with a rugged, cryptoid surface
that obstruct passage of the ovum and Isthmus of the fallopian
tube remains spastically contracted for first 3 days after
ovulation.
• Progesterone secreted by corpus luteum increases
progesterone receptors on the smooth muscle in the fallopian
tube & progesterone cases relaxation of fallopian tubes
 Blastocyct Formation
• Cleavage:
30-36 hrs after fertilization
the zygote divides by
mitosis.
• Blastocyst develops:
• Inner cell mass forms fetus
• Cells forming the outer layer of
blastocyst are Trophoblasts,
which provide nutrients to the
embryo and forms extra
embryonic structures-
chorionic membrane ( fetal
part of placenta).
 Implantation of the Blastocyst
in the Uterus
• 6th day after fertilization, Blastocyst
attaches to uterine wall.
• Blastocyst secretes proteolytic
enzymes that allow blastocyst to
burrow into endometrium.
• Once implantation has taken place
the trophoblast cells and other
adjacent cells from the blastocyst
and the uterine endometrium
proliferate rapidly, and forms
placenta and various membranes of
pregnancy.
• Trophoblast cells secrete hCG
 hCG
• Human chorionic
gonadotropin.
• Trophoblast cells secrete
hCG.
• Signals corpus luteum not
to degenerate until
placenta secretes
adequate [hormone].
• Effects similar to LH.
• Basis of pregnancy test.
 Early Nutrition of the Embryo
• Progesterone secreted by the corpus luteum during the
latter half of each cycle converts endometrial stromal
cells into large swollen cells containing extra quantities
of glycogen, proteins, lipids, and minerals necessary for
development of the conceptus (blastocyst)
• After conceptus implants in the endometrium, the
continuous secretion of progesterone causes the
endometrial cells to swell further and to store even more
nutrients. These cells are now called decidual cells, and
the total mass of cells is called the decidua
• Trophoblast cells invade the decidua, digest it , the
stored nutrients in the decidua are used by the
embryo for growth and development.
• First week after implantation, this is the only means
by which the embryo can obtain nutrients
• Continues to provide nutrition in this way for up to 8
weeks
• After one week Placenta also begins to provide some
of the nutrition (16th day beyond fertilization)
Placenta
 Physiologic
Anatomy of the Placenta
• When the Trophoblastic cords from the blastocyst are
attaching to the uterus, capillaries grow into the cords from
the vascular system of the embryo
• By the 16th day after fertilization, blood also begins to be
pumped by the heart of the embryo
• Blood sinuses supplied with blood from the mother
develop around the trophoblastic cords
• Trophoblast cells send out projections, which become
placental villi into which fetal capillaries grow
• Thus, the villi, carrying fetal blood, are surrounded by
sinuses that contain maternal blood.
Relation of the fetal blood in the villus capillaries to
the mother’s blood in the intervillous spaces
 Organization of the Mature Placenta
• Fetal blood flows through
two umbilical arteries, then
into the capillaries of the villi
and finally back through a
single umbilical vein into the
fetus
• Mother’s blood flows from
uterine arteries into large
maternal sinuses that
surround the villi and then
back into the uterine veins of
the mother
 Placental Function
• Exchange of Gas
– 02 and C02
• Exchange of Nutrients
• Exchange of waste products
• Synthesis of proteins and enzymes
 PLACENTAL PERMEABILITY AND
MEMBRANE DIFFUSION CONDUCTANCE
• The major function of the placenta is to allow
diffusion of foodstuffs and oxygen from the
mother’s blood into the fetus’s blood and
diffusion of excretory products from the fetus
back into the mother
• The permeability increases because of thinning
of the membrane
• surface area expands many times and it results
in tremendous increase in placental diffusion
 Diffusion of Oxygen Through the Placental
Membrane
• Dissolved O2 in the blood of maternal sinuses passes into
the fetal blood by simple diffusion as result of gradient
of PO2 from the mother’s blood to the fetus’s blood
• Mean PO2 of the mother’s blood in the placental sinuses
is about 50 mm Hg, and mean PO2 in the fetal blood
after it becomes oxygenated in the placenta is 30 mm
Hg
• Mean pressure gradient for diffusion of O2 through the
placental membrane is about 20 mm Hg
How fetus obtain sufficient O2 when the fetal blood
leaving the placenta has a PO2 of only 30 mm Hg?
• Fetal Hemoglobin
– 2 alpha and 2 gamma chains
– curve for fetal Hb is shifted to the left of that for
maternal Hb
– It means that at low PO2 in fetal blood, the fetal Hb
can carry 20-50 % more oxygen than can maternal Hb
• Hemoglobin Concentration
– Fetal Hb concentration is 50 % greater than that of mother
• Double Bohr Effect
– Enhance the transport of oxygen from mother to fetus
 Effects of 2,3-BPG on Fetal Blood
• 2 alpha and 2 gamma chains in Fetal Hb
(hemoglobin F)
• The affinity of Fetal Hb for O2 is greater than that
for adult hemoglobin
– The cause of this greater affinity is the poor binding of
2,3-BPG with the γ chains in fetal hemoglobin
• This facilitates the movement of O2 from the
mother to the fetus
Oxygen-hemoglobin dissociation curves for maternal
and fetal blood
• More binding of Hb with O2 at a low PCO2
• The fetal blood entering the placenta carries large
amounts of CO2which diffuses from the fetal blood into
the maternal blood
• Loss of the CO2 makes the fetal blood more alkaline,
whereas the increased CO2 in the maternal blood makes
it more acidic
• Alkalinity and decrease of PCO2 in fetal blood increase
binding of Hb with O2
• Whereas acidity and increase in PCO2 in maternal blood
causes more dissociation of O2 from Hb.
Effect of change in pH
Oxygen-hemoglobin dissociation curves for maternal
and fetal blood
 DOUBLE BOHR EFFECT
• Hence there is more association of O2 with Hb
in fetal blood and more dissociation of O2 from
Hb in maternal blood
• Bohr shift operates in one direction (right) in the
maternal blood and in the other direction (left)
in the fetal blood
• These two effects make the Bohr shift twice as
important as it is for oxygen exchange in the
lungs therefore, it is called the double Bohr
effect
• By these three factors i.e. Fetal Hb, Hb
concentration & double Bohr Effect:
– Fetus is capable of receiving adequate O2
through the placental membrane, despite the
fact that fetal blood leaving the placenta has a
PO2 of only 30 mm Hg
– The diffusing capacity of placenta for oxygen is
1.2 ml/min/mm Hg oxygen pressure difference
across the membrane
 Diffusion of Carbon Dioxide Through the
Placental Membrane
• CO2 is excreted from the fetus through the placenta into
the mother’s blood
• The PCO2 of the fetal blood is 2 to 3 mm Hg higher than
that of the maternal blood
• This small pressure gradient across the membrane is
sufficient to allow diffusion of CO2
– because of the extreme solubility of CO2 in the
placental membrane allows it to diffuse 20 times as
rapidly as oxygen
 Diffusion of Foodstuffs Through the Placental
Membrane
• Metabolic substrates needed by the fetus diffuse into
the fetal blood
• In the later stages of pregnancy utilization of glucose by
fetus is as much as is used by the entire body of the
mother
– There is facilitated diffusion of glucose through the
carrier molecules in the trophoblast cells lining the
placental villi
• Glucose level in fetal blood is 20-30 % lower than that in
maternal blood
Transport of Nutrients
 Diffusion of Foodstuffs Through the Placental
Membrane

• Fatty acids because of the high solubility of FA

in cell membranes also diffuse from the
maternal blood into the fetal blood but slowly
than glucose
• Ketone bodies, potassium, sodium, and
chloride ions diffuse relatively easily from the
maternal blood into the fetal blood
 Excretion of Waste Products Through the
Placental Membrane
• CO2, urea, uric acid, Creatinine diffuse from the fetal
blood into the maternal blood and then they are excreted
along with the excretory products of the mother
– Urea diffuses through the placental membrane with
great ease hence level of urea in fetal blood is only
slightly greater than that in maternal blood
– Creatinine does not diffuse easily, hence fetal blood
concentration is considerably higher than that in the
mother’s blood
• Excretion from the fetus depends on:
–Diffusion gradients across the placental
membrane
–Permeability of membrane
HORMONES PRODUCED FROM PLACENTA
• Human chorionic Gonadotropin
• Estrogens
• Progesterone
• Human Chorionic Somatomammotropin
• Relaxin
• CRH
• POMC
• β- endorphin
• α-MSH
• GnRH
• Inhibin
• Prolactin
• Leptin
 Human Chorionic Gonadotropin
(hCG)
• hCG is produced by the syncytial trophoblast
• It is a glycoprotein in nature and contains
galactose and hexosamine
• It is made up of α and β subunits
• hCG-α is identical to the α subunit of LH, FSH, and
TSH
• hCG is primarily luteinizing and luteotropic in
nature and has little FSH, TSH activity also
• It appears to act on the same receptor as LH
 Detection of hCG
• hCG can be measured by RIA and detected in the
blood as early as 8 to 9 days after ovulation
shortly after the blastocyst implants in the
endometrium and 6 days after conception
• Presence of hCG in urine is the basis of pregnancy
test, and it can sometimes be detected in the
urine as early as 14 days after conception.
• As late as 1 week after missing a period.
Rates of secretion of estrogens and progesterone and concentration of
hCG at different stages of pregnancy
 hCG
• Secretion of hCG rises rapidly to reach a
maximum at 10-12th weeks of pregnancy
• Decreases back to a lower value by 16 to 20
weeks
• It continues at this level for the remainder of the
pregnancy
 Functions of hCG
• hCG prevents involution of the corpus luteum
• It causes the corpus luteum to secrete progesterone and
estrogens for next few months
• progesterone and estrogens prevent menstruation and
cause continuous growth of endometrium-decidual cell
form and store large amounts of nutrients by the time
that the blastocyst implants
• hCG stimulates the male fetal testes to produce
testosterone
• Releases relaxin
• hCG is not absolutely specific for pregnancy
• Small amounts are secreted by a variety of
gastrointestinal and other tumors in both
sexes
• hCG has been measured in individuals with
suspected tumor as a “tumor marker”
• Fetal liver and kidney also produces small
amounts of hCG
 Estrogens
• Estrogens secreted by the syncytial trophoblast cells of
the placenta
• Estrogens are formed almost entirely from androgen
which are formed both in the mother’s & fetal adrenal
glands
– Dehydroepiandrosterone
– 16-hydroxydehydroepiandrosterone
• These androgens are transported by the blood to the
placenta and converted by the trophoblast cells into
Estradiol, Estrone, and Estriol
 Fetoplacental Unit
Interactions between the placenta and the
fetal adrenal cortex in the production of steroids
 Human Chorionic
Somatomammotropin (hCS)
• Human Chorionic Somatomammotropin secreted by the
syncytiotrophoblast about the 5th week of pregnancy
• hCS is lactogenic and also has a small amount of growth-
stimulating activity hence it is also called chorionic growth
hormone-prolactin (CGP) and human placental lactogen (hPL)
• The structure of hCS is similar to that of human growth hormone
and it appears that these two hormones and prolactin evolved
from a common progenitor hormone.
• Large quantities of hCS are found in maternal blood, but very little
reaches the fetus.
• Secretion of GH from the maternal pituitary is not increased
during pregnancy and actually decreased by hCS
 Human Chorionic Somatomammotropin (hCS)
• hCS has most of the actions of growth hormone and
functions as a “maternal growth hormone of pregnancy”
• It causes
– Development of breast & lactation (hPL)
– Formation of protein in tissue (GH)
– Lipolysis provides FA to be used by mother for energy
– Decreased insulin sensitivity and cause insulin resistance
which decreases utilization of glucose in the mother,
thereby making large quantities of glucose available to
the fetus
– Nitrogen, K & Ca retention
 SECRETION OF PROGESTERONE BY THE PLACENTA
• Progesterone:
• Causes decidual cells to develop in the endometrium
which provide nutrition to the early embryo
• Suppresses uterine contractions
• Develops conceptus even before implantation by
increasing the secretions of fallopian tubes and uterus to
provide nutrition to the morula and blastocyst
• Suppresses LH and FSH
• Stimulate development of alveolar tissue of the
mammary gland & prepares it for lactation
Secretion of Relaxin by the Ovaries & Placenta

• hCG stimulates the secretion of Relaxin

• Relaxin causes:
– Relaxation of the ligaments of the pubis symphysis
– It softens the cervix at the time of delivery
– Act as a vasodilator increases blood flow in various
tissues, including the kidneys
– Increases venous return and cardiac output in
pregnancy
 Other Placental Hormones
• Human placental fragments produce:
• Corticotropin Releasing Hormone
• POMC which produces:
– β- endorphin
– α-MSH
• GnRH and inhibin
– GnRH and inhibin produced locally may act in a paracrine fashion to regulate
hCG
– GnRH stimulates and inhibin inhibits hCG secretion
• Trophoblast cells and amnion cells also secrete Leptin which enter the maternal
circulation & amniotic fluid
• Placenta also secretes Prolactin
• Cytotrophoblast of the chorion contains Prorenin
– A large amount of prorenin is also present in amniotic fluid, but its function
is unknown.
POMC derivatives
 Other Hormonal Factors in Pregnancy
• Pituitary Secretion
• Corticotropin, thyrotropin, and prolactin
• Increased Corticosteroid Secretion
• Glucocorticoids
• Aldosterone
• Increased thyroxin Secretion Caused by:
– thyrotropic effect of hCG
– TSH from ant pituitary
– human chorionic thyrotropin by placenta
• Increased Parathyroid Gland Secretion
• Secretion of Relaxin by the Ovaries and Placenta
Fetoplacental Unit
Fetoplacental Unit
 Fetoplacental Unit
• The adrenals of fetus and the placenta interact with
each other in the formation of steroid hormones
• Pregnenolone and progesterone are synthesized by
Placenta from cholesterol
• Some of the progesterone enters the fetal circulation
and forms cortisol & corticosterone in the adrenal
glands
• pregnenolone from placenta and pregnenolone
synthesized in the fetal liver enter fetal adrenals and
forms DHEAS & 16-OHDHEAS
• DHEAS and 16-OHDHEAS are transported back to the
placenta where forms estrogens:
– DHEAS forms Estradiol
– 16-OHDHEAS forms Estriol
– Urinary Estriol excretion of the mother can be
monitored as an index of the state of the fetus.