Pathophysiology kashmeera

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PATHOPHYSIOLOGY PATHOPHYSIOLOGY Kashmeera N.A. II Sem MSc.Zoology Roll no: 37 Christ college

Transcript of Pathophysiology kashmeera

Page 1: Pathophysiology   kashmeera

♀♀ PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Kashmeera N.A.

II Sem MSc.Zoology

Roll no: 37

Christ college

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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

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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

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Hypogonadotropic hypogonadism

• Caused by defect in GnRH or LH/FSH secretion.

• LH & FSH levels are low.

• Gonad is hypofunctional due to decreased stimulation.

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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

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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)

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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)

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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.

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• lesions of the hypothalamus or pituitary gland can lead to hypothalamic amenorrhea

• Hypothalamic tumors can lead to HA

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Polycystic Ovary Syndrome

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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

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• 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

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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 virilismBy androgens administered to mother.

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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

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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.

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• 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.

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