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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 . PCO on ultrasound 20%Oligomenorrhea 4
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1. POLYCYSTIC OVARY SYNDROMESPOTLIGHTS Dr. Mohammed AbdallaEgypt, Domiat general Hospital
2. Pathogenesis (etiology?) Hypersecretion of adrenal androgens?
Hypersecretion of ovarian androgens?
A genetic disorder with an autosomal dominant mode of inheritance?
A multifactorial genetic disorder?
3. Prevalence PCO on ultrasound 20%
Oligomenorrhea 4 – 21 %
4. Ultrasound in vs. Megalocystic ovaries PCO Polycystic ovaries
Bilateral
Multiple cysts
Cyst diam <4-6 mm
Stroma increased
5. Long term risks in PCOS
Definite risk
Type 2 diabetes
Dyslipidemia (Hypercholesterolemia with diminished HDL2 and increased LDL)
Endometrial cancer (OR 3.1 95% CI 1.1 -7.3)
6. Possible risk
Hypertension
Cardiovascular disease
Gestational diabetes mellitus
Pregnancy-induced hypertension
Ovarian cancer
Unlikely
Breast cancer
Long term risks in PCOS
9. Obesity and insulin resistance
12. 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
13. “Insulin resistance” is characterized by decreased sensitivity to insulin in peripheral tissues (muscle and adipose tissue), but not in hepatic tissue Franks 1995
17. Gonadotropin Secretion in PCOS Increased LH secretion:
•Ratio of LH/FSH: 2-3/1
•Prevalence: 30 to 90% !
18. Treatments for PCOS Weight loss
Oral Contraceptives.
Clomiphene.
Ovarian diathermy/laser tx.
ART.
Cyproterone acetate+ EE, Spironolactone.
Insulin sensitizing agents. Biguanides (metformin)
Thiazolidinediones (troglitazone).