This document discusses various pathophysiologies related to female reproductive health. It covers precocious and delayed puberty, hypogonadism, defects in ovulatory function including hypothalamic amenorrhea and polycystic ovary syndrome. It also discusses female pseudohermaphroditism, congenital adrenal virilism, Chiari-Frommel syndrome, and the role of hormones like estrogen in breast cancer growth.

1. ♀♀ PATHOPHYSIOLOGYPATHOPHYSIOLOGY
Kashmeera N.A.
II Sem MSc.Zoology
Roll no: 37
Christ college

2. FEMALE PRECOCIOUS PUBERTY
Precocious pseudopuberty True precocious puberty
Early devpt of 2° sexual
characteristics without
gametogenesis
Caused by abnormal
exposure of immature ♀♀ to
estrogen
Due to early secretion of
gonadotropin from pituitary
Due to hypothalamic
damage
– lesions of ventral
hypothalamus near
infundibulum.
-this lesions interrupt neural
pathways that produce
inhibition of GnRH

3. Delayed puberty
• Primary amenorrhea – menstrual bleeding never
occured
• Turner’s syndrome [45 XO] – gonadal
dysgenesis
• Testicular feminization/androgen resistance –
• Patients are genetic ♂♂ [46 XY]
• Lack testosterone receptors – insensitivity to androgen –
wolffian structures primordial
• MIS present – mullerian structures absent
• External genitalia ♀,but vagina ends blindly because there is no
♀ internal genitalia

4. Hypogonadotropic hypogonadism
• Caused by defect in GnRH or LH/FSH
secretion.
• LH & FSH levels are low.
• Gonad is hypofunctional due to decreased
stimulation.

5. DEFECTS IN OVULATORY
FUNCTION
Ovulatory defects can be classified into three
groups based on the World Health Organization
(WHO) definition.
1. Group I: hypogonadotropic hypogonadism:
• These patients have low LH & FSH levels.
• This category includes women with
hypothalamic amenorrhea (HA), stress-related
amenorrhea etc

6. 2. Group II: eugonadotropic hypogonadism:
 Patients are eugonadotropic ,
normoestrogenic, but anovulatory .
• They exhibit normal FSH and estradiol
levels.
• This category includes women with
polycystic ovary syndrome (PCOS)

7. 3. Group III: hypergonadotropic
hypogonadism:
Caused by defective gonads,resulting in
hypogonadism and high gonadotropin
level (as hypothalamus & pituitary fn
normally)
These patients tend to be amenorrheic
and hypoestrogenic,
category includes all variants of premature
ovarian failure(POF)

8. Hypothalamic amenorrhea (HA)
• Functional abnormality in GnRH secretion -LH & FSH levels
are low.
• Result in low gonadotropin level & secondary
amenorrhea.
• Common in young women with increased psychological
stress.

9. • lesions of the hypothalamus or pituitary
gland can lead to hypothalamic
amenorrhea
• Hypothalamic tumors can lead to HA

10. Polycystic Ovary Syndrome

11. Polycystic Ovary Syndrome
• It is a disorder of chronic anovulation
leading to increased estrogen production
& infertility.
In ovaries, androgens are produced through
de novo synthesis from cholesterol.
They can be aromatized to estrogens

12. • Excessive androgen levels may also
directly inhibit follicle development at the
ovarian level,
• Which may result in the accumulation of
multiple small cysts
• within the ovarian cortex, the so-called
polycystic ovary

13. FEMALE PSEUDOHERMAPHRODITISM
A pseudohermaphrodite is an individual with
genetic constitution and gonads of one sex and
genitalia of the other.
After 13th
week, genitalia are fully formed,but
exposure to androgens cause hypertrophy of the
clitoris
Congenital adrenal virilism
By androgens administered to mother.

14. Chiari –Frommel syndrome
• Persistence of lactation(galactorrhea) &
amenorrhea in women who donot nurse
after delivery.
• Associated with some genital atrophy
• Due to persistent prolactin secretion
without secretion of FSH & LH necessary
to produce maturation of new follicles &
ovulation.
• Non pregnant ♀ - pituitary tumour -CFS

15. HORMONES & CANCERHORMONES & CANCER
• About 35% of carcinomas of the breast in
women of childbearing age are estrogen-
dependent.
• Their continued growth depends upon the
presence of estrogen in the circulation.

16. • Women with estrogen dependent tumours
often have a remission when their ovaries
are removed.
• There is also some evidence that growth
hormone & prolactin stimulate the growth
of breast carcinomas.