PCOS

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POLYCYSTIC OVARY SYNDROMESPOTLIGHTS : 

POLYCYSTIC OVARY SYNDROMESPOTLIGHTS Dr. Mohammed AbdallaEgypt, Domiat Hospital

Pathogenesis (etiology?) : 

Pathogenesis (etiology?) Hypersecretion of adrenal androgens? Hypersecretion of ovarian androgens? A genetic disorder with an autosomal dominant mode of inheritance? A multifactorial genetic disorder?

Prevalence : 

Prevalence PCO on ultrasound 20% Oligomenorrhea 4 – 21 % Oligomenorrhea + hyperandrogenemism 3.5 – 9 %

Ultrasound in vs Meglocystic ovaries PCO : 

Ultrasound in vs Meglocystic ovaries PCO Polycystic ovaries Bilateral Multiple cysts Cyst diam <4-6 mm Stroma increased Megalocystic ovaries Bilateral Multiple cysts Cyst diam > 6-10 mm Stroma not increased

Long term risks in PCOS : 

Long term risks in PCOS Definite Type 2 diabetes Dyslipidemia (Hypercholesterolemia with diminished HDL2 and increased LDL) Endometrial cancer (OR 3.1 95% CI 1.1 -7.3)

Long term risks in PCOS : 

Possible Hypertension Cardiovascular disease Gestational diabetes mellitus Pregnancy-induced hypertension Ovarian cancer Unlikely Breast cancer Long term risks in PCOS

Slide 7: 

Cholesterol Pregnenolone Progesterone 17 OH-Pregnenolone 17 OH-Progesterone DHEA Androstenandion 17-20 Lyase 17 hydroxylase Theca cell Estrone estradiol Granulosa cell FSH LH OVARIAN STEROIDOGENESIS T

Slide 8: 

LH FSH follicular maturation Androgen excess Extra glandular aromatization Stim. Of stroma and theca Chronic anovulation Adipose tissue acyclic estrogen Adrenal androgen Cyclic estrogen Ovarian androgen Abnormal hormonal feedback mechanisms

Obesity and insulin resistance : 

Obesity and insulin resistance

Slide 10: 

Obesity Insulin resistance Hyperinsulinemic state Androgens Serum insulin

Slide 11: 

Obesity Insulin Free testosterone SHBG IGF-1 5-alfa reductase activity is stimulated IGF*** insulin like growth factor

PCOS - Pathogenesis : 

PCOS - Pathogenesis Excessive ovarian stimulation caused by the progressively rising insulin and insulin like growth factor - I (IGF-I) levels during puberty induces a PCOS in predisposed girls Nobels and Devailly FertilSteril 1992 5-alfa reductase activity is stimulated by iGF-I. This intensifies the hirsute response in hyperandrogenic patients Speroff 1993

Slide 13: 

“Insulin resistance” is characterized by decreased sensitivity to insulin in peripheral tissues (muscle and adipose tissue), but not in hepatic tissue Franks 1995

Slide 14: 

Wt. increase Insulin receptor disorder Insulin increase Free estradiol increase High LH Low FSH Free testosteron increase Androstenandion increase SHBG decrease atresia Theca (IGF-I) Endometrial cancer Testosteron increase Estrone increase hirsutism IGFBP-I **** decrease IGFBP*** insulin like growth factor binding protein

Slide 15: 

Insulin effects related to ovarian function Directly stimulates steroidogenesis Stimulates 17-hydroxylase Stimulates or inhibits aromatase Up-regulates LH receptors Promotes ovarian growth and cyst formation synergistically with LH/hCG Up-regulates Type I IGF receptors Inhibits IGFBP-1 production Inhibits SHBG production Potentiates the effect of GnRH on LH/FSH Ovary Ovary Ovary and adipose Ovary Ovary Ovary Ovary and liver Ovary Hypothalamus/pituitary

Slide 16: 

PUBERTY LH LH pulses > 25pulses /24h INSULIN resistance ANDROGEN INCREASE HIRSUTISM ACNE ALOPECIA ANOVULATION Ratio of LH/FSH: 2-3/1

Gonadotropin Secretion in PCOS : 

Gonadotropin Secretion in PCOS Increased LH secretion: •Ratio of LH/FSH: 2-3/1 •Prevalence: 30 to 90% !

Treatments for PCOS : 

Treatments for PCOS Oral Contraceptives. Clomiphene. Ovarian diathermy/laser tx. ART. Cyproterone acetate+ EE, Spironolactone. Insulin sensitizing agents. Biguanides (metformin) Thiazolidinediones (troglitazone). Weight loss.

Slide 19: 

thank you

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