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REPRODUCTIVE PHYSIOLOGY

TOPICS COVERED HERE - 1. GAMETOGENESIS

2. GYNE NEUROENDOCRINOLOGY

a) HPO AXIS

b) STEROIDOGENESIS

c) OVARIAN CYCLE

3. MENSTURAL CYCLE AND ITS REGULATION

GAMETOGENESIS
● Females have karyotype XX, and males have karyotype XY.
● So, initial germ cells that are formed in females and males are respectively XX and XY.
● These initial germ cells are called as PRIMORDIAL GERM CELLS.
● This means initial germ cells are DIPLOID (2n).
● In the adults, the germ cells are found in gonads, but embryologically the germ cells were not there in the
gonads to begin with.
● Important– Germ cells originate in the embryonic life in the “PRIMITIVE ECTODERM”.
● After that they migrate to developing yolk sac of the embryo and this is the site where they get first
identified.
● So, remember germ cells are 1st identified in the PRIMITIVE YOLK SAC which is ENDODERMAL in origin.
● They are identified in yolk sac by 3rd week of fertilization.
● After that, germ cells travel along the splanchnic mesoderm of the hindgut to reach to the Gonadal Ridge
(area where gonads are developing)
● Germ cells reach the gonadal ridge by 6 weeks of fertilization.
OOGENESIS:

● Begins in the Intra-uterine life (IUL) itself.

● Primordial germ cells are diploid (2n).
● These cells divide by mitosis and form OOGONIA (2n).
● Oogonia further undergo mitosis and form PRIMARY OOCYTE (2n)
● Primary oocyte now undergoes 1st meiosis (meiosis I), but arrested in the DIPLOTENE stage of the PROPHASE
till the puberty.
● At puberty, during ovulation, primary oocyte completes meiosis I (reduction division) and form SECONDARY
OOCYTE which is haploid (n) and 1st polar body is also formed at the time of ovulation.
● Secondary oocyte (n) also gets arrested in the meiosis II in the METAPHASE.
● Meiosis II gets completed during fertilization and we get MATURE OOCYTE (n) and 2 nd polar body is released
during fertilization.

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COUNTS TO BE REMEMBERED:

● Maximum number of oogonia is present at around 20 weeks of IUL. ~ which is around 7 million in number.
● After that cycle of atresia begins, many oogonia and primary oocytes die along the way.
● By birth when a female child born, she is having only 2 million primary oocytes left.
● This process of the atresia doesn’t stop here, this continues in entire childhood and entire reproductive life of
the female also.
● So at the time of puberty, only 4 lacs primary oocytes remain.
● Among these 4 lacs, only 400 primary oocytes will ovulate in the entire reproductive life of the female.
● Remember, for every 1 egg that ovulates, 1000 die or under atresia.

COMPARISON WITH SPERMATOGENESIS:

● Spermatogenesis begins at puberty in the testis.

● Spermatogonia (2n) form PRIMARY SPERMATOCYTE (2n) by mitosis.
● There is no arrest anywhere.
● Primary spermatocyte (2n) undergoes meiosis I (reduction division) and form SECONDARY SPERMATOCYTE
which is haploid (n).
● Then 20 spermatocyte undergoes meiosis II and form SPERMATIDS (immature sperms).
● Then maturation occurs in the epididymis and spermatids converted into MATURE SPERMS. This process of
maturation is called as SPERMIOGENESIS.
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DURATION:

● The process of spermiogenesis takes around 14 days.

● The entire process of spermatogenesis takes around 72 days to complete.

GYNE NEUROENDOCRINOLOGY
{HYPOTHALAMO-PITUITARY-OVARAIN AXIS (HPO AXIS)}:

GnRH:

● In the hypothalamus, neurons in the arcuate neurons secrete a neuro-hormone that is GnRH.
● GnRH is a neuro-hormone because it is released from the neurons.
● GnRH is a DECAPEPTIDE (contains 10 AA), means it is a peptide hormone and having a short structure, so it
gets very easily metabolized.
● i.e. it has VERY SHORT HALF LIFE ~ around 2-4 minutes.
● It is secreted in a PULSATILE MANNER.
● Receptors for GnRH are present on anterior pituitary.
● As long as it secreted in a pulsatile manner, it will lead to stimulation of pituitary.
● But if there is a continual secretion, it will lead to receptor desensitization.
● APPLIED: GnRH analogues produce gonadal suppression.

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● MOA of GnRH analogues: these are synthetic products, so metabolize very slowly and have longer half-life and
they bind to receptors continuously. They attach to receptors present on the pituitary and remain attached
and after sometime drug-receptor complex will move inside the cell and whole complex gets metabolized. So
receptor will be gone. (Receptor desensitization.)
● GnRH analogues are the treatment modalities of all the conditions where we want gonadal suppression.
● There are 2 types of GnRH analogues – GnRH agonists and GnRH antagonists.
● Difference b/w them is agonists will lead to initial positive action k/a initial flare and after then suppress
gonads, whereas antagonists will lead to suppression only with no initial flare reaction.

GONADOTROPINS (LH & FSH):-

● FSH and LH both hormones are glycopeptide in nature. So as compared to peptide hormones they are
metabolized slowly and have comparatively longer half-lives.
● Half-life of FSH is 3-4 HOURS.
● Half-life of LH is 20 MINUTES.
● Both FSH and LH have alpha and beta subunits (almost all hormones of anterior pituitary have these 2
subunits).
● Remember that the alpha subunit of FSH and LH are exactly similar whereas both have specific/distinct beta
subunit.
● Infact alpha unit of these are similar to TSH and HCG. So they can be used sometimes in place of these.
● Action: FSH acts on the ovaries and lead to follicle stimulation (folliculogenesis). LH also acts on the ovaries
on the developing follicles and lead to ovulation.

OVARIAN STEROIDS
STEROIDOGENESIS:
● Begins primarily with parent compound ACETATE
● Acetate forms the CHOLESTEROL.
● The main source of the cholesterol in the ovary is the BLOOD. (blood carries LDL cholesterol and this is used
by ovarian follicles to form steroid hormones)
● Cholesterol then converts into PREGNENOLONE.
● From here pathway divides into two.

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 ACETATE

CHOLESTEROL

PREGNENOLONE

17 ALPHA HYDROXYLASE 3 BETA HSD

17 HYDROXY PREGNENOLONE PROGESTERONE 🡪🡪CORTISOL

17 ALPHA HYDROXYLASE 17 ALPHA HYDROXYLASE

DEHYDROEPIANDROSTERONE 17 HYDROXY PROGESTERONE

3 BETA HSD 17 ALPHA HYDROXYLASE

ANDROSTENEDIONE TESTOSTERONE

AROMATASE 17 BETA HSD AROMATASE

17 BETA HSD

ESTRONE
AfraTafreeh.comESTRADIOL
(E1) (E2)

● The immediate precursor for estrogen is always an androgen.**

● So ovary can produce all the three hormones whether progesterone, androgen, or estrogen.
● ANOTHER ORGAN THAT PRODUCE STEROID IS – ADRENAL GLAND.
● But in adrenal gland estrogen is not formed bcz, the enzyme aromatase is absent is the adrenal gland.
● And progesterone produced in the adrenal gland is used up in synthesis of cortisol and aldosterone.
● The main androgen produced from the ovary is ANDROSTENEDIONE mainly and some amounts of testosterone.
● The main estrogen produced by the ovary is ESTRADIOL (E2). It is the predominant form of estrogen in
reproductive age group. And estradiol is also the most potent form of estrogen.
● In post menopausal age, ovaries are quiet i.e. they are not synthesizing anything but some amounts of
androstenedione is being synthesized by the ovary.
● This androstenedione will get aromatized to ESTRONE (E1) in the peripheral tissues such as fat cells.( aromatase
enzyme is also present in the adipocytes ). Therefore, the predominant form of estrogen in postmenopausal
women is Estrone.
● Also, aromatization is a one sided process i.e. estrogen cannot be converted back to androgen.

● Predominant form of estrogen in reproductive life – ESTRADIOL (E2)

● Predominant form of estrogen in post menopausal women – ESTRONE (E1)

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OVARIAN CYCLE & HORMONES

● Mature ovarian follicle has two types of cells –
● Granulosa cell layer is an avascular layer.
● Whereas theca cell layer is a vascular layer.

● 2 cell – 2 gonadotropins hypothesis:

- 2 cells are - Granulosa cell and theca cell.
- 2 gonadotropins are – FSH and LH
- Granulosa cell has receptor for FSH and Theca cell has receptor for LH.
- Theca cells produce androgens under stimulation from LH
- Granulosa cells produce estrogens under stimulation from FSH

- FSH acts on the granulosa cell 🡪🡪 stimulates the enzyme aromatase 🡪🡪 it converts androgen to estrogen 🡪🡪
estrogen is released by granulosa cells.
- But from where androgen is coming in the granulosa cell ??
- Theca cells are producing androgen bcz of action of LH on theca cells . And remember theca cells are
vascularised, so they take up LDL cholesterol from the blood and synthesize the androgens from it.
- And this androgen produced here diffuses out of the theca cell and enter into the granulose cell to produce
estrogen.

Early part of the cycle (follicular phase) ~ 14 days :

● In early part of ovarian cycle , folliculogenesis occur in response of FSH.

● Primordial follicle 🡪 Primary follicle 🡪 Preantral follicle 🡪 Antral follicle 🡪 Preovulatory follicle.
● FSH acts on the follicles and increase the number of granulosa cells and hence increase the amount of
ESTRADIOL (E2) production.
● Also remember that for the production of estrogen, androgens are required and for androgens LH is required.
Means, alone FSH cannot mature the follicles, it also needs LH.

● Remember:
● Initiation of folliculogenesis is done by – FSH.
● Whereas, final maturation of follicle is done by – LH.
● Resumption of the meiosis is done by – LH.
● Ovulation is done by – LH.

Late part of the cycle (luteal phase) ~ 14 days :

● After ovulation, follicle is converted into CORPUS LUTEUM.

● Corpus luteum contains :–
- Theca cells
- Luteinized granulosa cells

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● Luteinized granulosa cells refers to the acquisition LH receptors by the granulosa cells.
● Both theca cells and luteinized granulosa cells produce MAINLY PROGESTERONE and SOME ESTROGEN also.

V.IMP:- In non-pregnant state, corpus luteum is sustained by LH. (another important function of LH even in
luteal phase)

FUNCTIONS OF THE ESTROGEN AND PROGESTRONE:-

SITE ESTROGEN PROGESTRONE

Uterus Proliferation of the endometrium Secretory changes of endometrium

Pregnant uterus Growth of endometrium Decidualisation of endometrium

Cervical mucus ● Causes thinning ● Causes thickening

● SPINBARKEIT: can stretch b/w the ● TACK: cannot stretch b/w fingers , it
fingers breaks apart bcz of thick and
● FERNING: when dried on glass slide, tenacious nature.
ferning appearance occurs. (estrogen
increase the NaCl amount in the cervical
mucus)

Fallopian tube Increase motility Decrease motility

Breast Ductular development Glandular development

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Lipid profile ● Increase HDL (cardio-protective) and TGs ● Decrease in HDL and TGs
● Decrease in LDL ● Increase in LDL

Effect on growth ● Initiation of growth at puberty No role

● Ultimately epiphyseal closure

Coagulation Hypercoagulable state* No role

Bones Causes mineralization No role

*there has to be pharmacologically high levels for this, in normal states not cause this. Ex- Pregnancy, OCPs ,
inherited thrombophilia etc.

MENSTURAL CYCLE
● DEFINITION: Cycle of endometrium growth and regression.
● Main role of endometrium is to support growth and nourishment of early embryo.
● In the absence of pregnancy , the endometrium is shed off , this process is c/a menstruation.
● Superficial 2/3rd part of endometrium is FUNCTIONALIS LAYER – supplied by the spiral arteries.
● Deeper1/3rd part is called as BASALIS LAYER – supplied by the Basal arteries.
● This functionalis layer is being shed off during menstruation.

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Blood supply of the uterus: uterine artery 🡪 arcuate artery (form arc around the uterus) 🡪 radial artery
(perpendicular to arcuate artery , penetrate the myometrium and supplies it) 🡪 basal artery & spiral artery ( supplies
endometrium deeper 1/3 and superficial 2/3 respectively) .

● IMP:- Spiral artery is an end artery. And it is responsive to hormonal changes, whereas basal artery is not an
end artery and not respond to hormones also.
● In response of hormones, spiral artery undergoes vasoconstriction and functionalis layer shed off.
● But basalis layer remain intact with intact blood supply and it is responsible for the regeneration of entire
endometrium.
● Stoppage of menses occurs bcz of
- Vasoconstriction of the spiral artery
- Clotting mechanisms
- Epithelial regeneration of endometrium.

CHARACTERISTICS OF THE NORMAL MENSTRUAL CYCLE:

● Length of the cycle = 21-35 days (average 28 days)
● Duration of bleeding = 2-8 days (average 4-5 days)
● Average amount of blood loss = 35-50 ml
IMPORTANT TERMINOLOGY:
● Cycle length < 21 days = POLYMENORRHEA (short cycles)
● Cycle length > 35 days = OLIGOMENORRHEA (Delayed cycles)
● Bleeding duration < 2 days or < 20ml in amount = HYPOMENNORHEA
● Bleeding duration > 8 days or > 80ml in amount = MENORRHAGIA
● Irregular cycles = METRORRHAGIA

1ST HALF OF THE CYCLE (Proliferative phase):-

● D1 is the day when bleeding starts.

● During 1st half , folliculogenesis is going on in the ovary. These follicles release estrogen (E2).
● This estrogen causes proliferation of the endometrium.
✔ Means , follicular phase of the ovary corresponds with the proliferative phase of the endometrium.
● Histology
- Glands are narrow and tubular.
- Stroma is loose and syncytial.
- Endometrial lining is CILIATED COLUMNAR.
● D-14 is the day of ovulation.

2ND HALF OF THE CYCLE(secretory phase):-

● During 2nd half, corpus luteum is present in the ovary which secretes large amount of progesterone.
● This progesterone causes secretory changes in the endometrium.
✔ Means luteal phase of the ovary corresponds with the secretory phase of the endometrium.
● Histology
- Glands become convoluted and cork-screw shaped.

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 - Vacuolization of the epithelium occurs.
st
● 1 change seen in secretory phase = Basal/Subnuclear vacuolization(seen on D 17-18)
nd
● 2 change seen = vacuole moves to the apical location.
● Late secretory changes
- Cork screw glands
- Leucocytic infiltration of the stroma
- Stroma becomes edematous.
● Peak secretory changes occur on Day 7-8 after ovulation (progesterone is maximum at this time).

ENDOMETRIAL THICKNESS (ET):-

● Post menstrually = thickness is only 0.5mm.
● Periovulatory period (around day 14) = 5-6 mm.
● Secretory phase = 5 - 6 mm
CONCEPTS:
✔ During proliferation, ET also increases. But during secretory phase there is no further increase in the ET.
✔ Progesterone leads to stabilization and secretory changes of an endometrium that has already undergone
proliferation under the effect of estrogen.
✔ Means progesterone can act only on the endometrium that is primed by estrogen.
✔ Bcz estrogen upregulates the progesterone receptors on the endometrium.

LUTEOLYSIS:- AfraTafreeh.com
● If there is no pregnancy, corpus luteum spontaneously dies k/a luteolysis.
● Life span of corpus luteum in non-pregnant state = 10 -12 days
● After death of corpus luteum, there is sudden decrease in progestrone k/a progesterone withdrawl.
● It leads to release of cytokines, prostaglandins (PGF2 alpha), MMPs(matrix metallo-proteinases).
● These above products will lead to enzymatic auto-digestion of the endometrium.
● This will lead to menses.

PROSTAGLANDINS IN MENSTRUAL CYCLE:-

● During ovulation in the ovary = PGE2 🡪 it digests the surface of follicle and helps in coming out of the oocyte i.e.
ovulation.
● This PGE2 is also responsible for mid-cycle pain in some females K/a MITTLESCHERMZ.
● During menses = PGF2 alpha (this is responsible for painful periods k/a dysmenorrhea).
● PGF2 alpha came bcz of progesterone withdrawl 🡪 occurs due to luteolysis 🡪 means corpus luteum is formed in cycle
🡪 means ovulation has occurred in the cycle.
● So, ovulatory cycles are painful, whereas anovulatory cycles are painless.

⮚ Length of the follicular phase changes with the cycle length.

⮚ But length of the luteal phase always become constant = 14 days
⮚ Example – in a 32 days cycle , ovulation will occur around D18.

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REGUALTION OF MENSTRUAL CYCLE

FEEDBACK REGULATION:-

● Feedback signals / mechanisms of the HPO axis.

AUTOCRINE AND PARACRINE INFLUENCES IN THE OVARY:-

● In this Granulosa cells in the ovary secrete some substances which modulate/fine tune the signals coming from
the above i.e. HPO axis.

● These substances are

- INHIBIN:- Inhibits FSH action as well as its secretion.
- ACTIVIN:- Augments FSH action as well as its secretion.
- FOLLISTATIN:- Binds and deactivates Activin.(i.e., act like inhibin)

Ques - Time taken for complete folliculogenesis? OR

Time taken for primordial follicle to become preovulatory follicle?

Ans – 85 days

Concept – bcz complete folliculogenesis include

1. Time taken for follicles to grow and mature without action of LH, FSH k/a gonadotropin independent
phase = 70 days
2. Time taken for follicles to grow and mature with action of LH, FSH k/a gonadotropin dependent phase
also k/a follicular phase of the menstrual cycle = 14-15 days.

● Cycle begins with recruitment of 70 days old primordial follicle to develop into the preovulatory follicle.
● This recruitment is done by FSH.
● FSH acts on these follicles and these starts growing further 🡪🡪🡪preovulatory follicle.
● So, there is increase in FSH levels in the early part of the cycle.
● These follicles starting synthesizing -
- ESTRADIOL (E2) [ in low amounts]
(low amounts hereby means that it is in rising phase, it doesn’t means E2 is deficient)
- INHIBIN B.
● Estradiol in low amounts and Inhibin B cause feed back inhibition of the pituitary leading to decrease in FSH
levels.
● When FSH levels start declining, support for growth of follicles is gone, so the smaller follicles begin to die.
● But among the recruited follicles, only one follicle keeps growing that has maximum FSH receptors , that is k/a
DOMINANT FOLLICLE.
● This dominant follicle starts secreting ESTRADIOL in HIGH amounts 🡪 ESTRADIOL PEAK. (E2 in high amounts
stimulate the pituitary)
● For stimulation of the pituitary, estradiol levels should beat least > 200 pg/ml for > 50 hours.
● Stimulation of pituitary releases LH k/a LH SURGE.
● LH surge leads to LH PEAK.
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● LH peak causes ovulation.
● After ovulation – the Corpus luteum secretes – progesterone (HIGH AMOUNTS), Estrogen and INHIBIN-A.
● High levels of progesterone and inhibin A inhibit the pituitary.
● FSH & LH levels both subside in the luteal phase
● Peak progesterone level is around 8 days after ovulation (DAY 22 of cycle)
● After luteolysis 🡪 progesterone and inhibin A levels decrease 🡪 feedback inhibition of the pituitary is lifted off
🡪 automatically stimulation of the pituitary occurs 🡪 release of the FSH and LH by the pituitary 🡪 cycle again
continues.

Q/A -
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✔ Maximum activity of the corpus luteum = 8 days after ovulation
✔ Peak progesterone secretion by corpus luteum = 8 days after ovulation
✔ Peak secretory changes in the endometrium = 8 days after ovulation
✔ Peak progesterone levels seen in luteal phase = 15 ng/ml.

TIMING OF THE SURGES –

✔ Estradiol peak = 24-36 hrs prior to ovulation.

✔ LH surge = 34-36 hrs prior to ovuation.
✔ LH peak = 10-12 hrs prior to ovuation.

LH SURGE IS MAINTAINED BY – ESTROGEN AND PROGESTERONE BOTH.

✔ Estrogen peak (high amounts) which is due to secretion by dominant follicle.

✔ Rising levels of the progesterone (low amounts) in late part of the follicular phase which is secreted by some
luteinised granulosa cells.
✔ Remember, estrogen in high amounts stimulate pituitary.
✔ And progesterone in low amounts stimulate pituitary.
✔ Estrogen in low amounts and progesterone in high amounts inhibit the pituitary.
✔ Progesterone secretion increases in the luteal phase but progesterone secretion starts in the late part of
the follicular phase itself.

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HOW PITUITARY GET TO KNOW WHICH IS TO BE SECRETED (LH OR FSH):

● Feedback signals from the ovarian hormones.

● GnRH pulses*- varying with the menstrual cycle phases.
- whenever there are high frequency, high amplitude pulses = LH is released
- whenever there are low frequency, low amplitude pulses = FSH is released
- So, during early part of follicular phase, pulses are low frequency.
- And during the time of ovulation = GnRH pulses become high frequency.

PHYSIOLOGY OF PUBERTY

● HPO axis in females is functional in IUL.

● But in childhood, it remains DORMANT, means GnRH pulses in the childhood are very irregular and of very -
very low frequency.

● Why HPO axis is dormant in childhood?

- CNS inhibition to the hypothalamus.
- In childhood, hypothalamus is very highly sensitive to negative feedback by peripheral hormones.

● At puberty there occur many changes –

✔ CNS inhibition lifted off. (GABA and Neuropeptide Y decreases)
✔ Excitatory neurotransmitters increased in the brain. (Glutamate and kisspeptin increases.)
✔ Hypothalamus is kick started.
✔ Leptin also increases during puberty (permissive role).
✔ Leptin levels are more in the obese people and it is seen that OBESE GIRLS HAVE PUBERTY EARLIER
THAN THIN GIRLS.
✔ Any chronic illness / malnutrition , if present , increases the Neuropeptide Y in the brain , so indirectly
delay the puberty
✔ Initially GnRH pulses are very slow at start, then these pulses increases in frequency gradually.
✔ At first, night time pulses are increased.
✔ And LH pulses increases more than the FSH pulses.
✔ So, initial some cycles of menstruation are ANOVULATORY bcz –
- HPO axis is initially immature and
- Feedback mechanisms are not fully developed at puberty.

SEQUENCE OF THE PUBERTAL EVENTS:-

● 2 independent events occur

1. ADRENARCHE – Adrenal gland start secreting adrenal androgens. This occurs at around 6 yrs of age in
both males and females.
- Adrenarche 🡪 responsible for pubic hair growth k/a PUBARCHE.
2. GONADARCHE – Ovaries start secreting estrogen. It lead to further 2 events.
- THELARCHE = Breast budding.
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 - Initiation of Growth Spurt.
✔ Growth is also maintained by GH and IGF-1.
✔ And estrogen ultimately leads to closure of epiphyses.
● CONCEPT => GIRLS WITH EARLIER PUBERTY 🡪 FINALLY HAVING SHORTER HEIGHTS
● Growth spurt cannot be measured as such.
● But thelarche and pubarche are visible and can be measured and graded.
● These are graded on the pictorial charts k/a TANNER STAGING.

SEQUENCE IN FEMALES -

✔ Ist change – growth spurt

✔ Ist visible sign – Thelarche
✔ After that – Pubarche
✔ After that – Peak height velocity
✔ After 6 months – Menarche
✔ These whole events takes around 4.5 yrs (1-6yrs).

SEQUENCE IN MALES –

✔ Testicular growth
✔ Penile growth
✔ Pubarche
✔ Peak height velocity
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TIMINGS OF THE PUBERTY:-

● Females = 10.5 yrs (average)

● Males = 11.5 yrs (average)

PRECOCIOUS PUBERTY

● Pubertal changes occur earlier than normal.

● In females = Pubertal changes < 8 yrs of age
● In males = Pubertal changes < 9 yrs of age
● MC overall cause = IDIOPATHIC (no cause yet identified , GnRH pulse generator gets activated earlier.)

TYPES OF PRECOCIOUS PUBERTY:-

1. CENTRAL / TRUE / GONADOTROPIN DEPENDENT = HPO axis gets activated early. Gonadotropin levels are
increased.
2. PERIPHERAL / PSEUDO / GONADOTROPIN INDEPENDENT = means estrogen that is responsible for the
pubertal changes is coming directly from the gonads, without HPO axis activity. Gonadotropin levels are low.

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CAUSES OF CENTRAL / TRUE TYPE:-

a. IDIOPATHIC (described earlier)

b. Anything that activates GnRH generator – tumors , CNS infection, CNS trauma
c. GnRH secreting tumor = HAMARTOMAS
d. Severe primary hypothyroidism
- Leads to increase TRH 🡪 increase GnRH gene transcription
- Leads to increase TSH 🡪 have FSH & LH like activity also.
❖ In TRUE type = MENSES ARE USUALLY PRESENT.
❖ Treatment 🡪 DOC = GnRH analogues ( cause pituitary receptor desensitization )

CAUSES OF PERIPHERAL / PSEUDO TYPE:-

a. MC CAUSE –> AUTONOMOUS FUNCTIONAL OVARIAN CYSTS.

b. TUMORS
- Estrogen secreting ovarian tumor.
- Beta HCG secreting ovarian tumo. (beta HCG can act like LH)
- Androgens secreting ovarian tumor.
- Androgens secreting adrenal tumor.
❖ Remember in case of estrogen secreting tumor, there will be isosexual puberty.
❖ Whereas in case of androgen secreting tumor, there will be heterosexual puberty.
c. Congenital adrenal hyperplasia (non classical type) – androgens increases
d. Mc CUNE ALBRIGHT Syndrome = also causes isosexual pseudoprecocious puberty.
- CAFÉ-AU-LAIT spots are seen in this syndrome.
❖ In PSEUDO type = MENSES CAN BE ABSENT

❖ Treatment – T/t of the cause

*Notes -

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