Pathophysiology
1) lack of regular menses with chronic anovulation and presence of acyclic estrogen 2) caused by extraglandular conversion of androstenedione to estrogen 3) originally termed Stein-Leventhal syndrome and was erroneously thought to occur only in setting of enlarged ovaries
Signs and Symptoms
1) obesity 2) hirsuitism 3) amenorrhea or oligomenorrhea 4) menarche occurs at expected age
Characteristic Test Findings
Laboratory – 1) increased LH 2) decreased FSH 3) LH:FSH > 2.0 4) increased androgens (androstenedione) 5) increased testosterone
Histology/Gross Pathology
1) enlarged ovaries (variable) 2) whitish sclerotic smooth capsule around ovary 3) multiple atretic cysts 4) hyperplastic stroma and theca of ovary 5) absent corpora albicans 6) lipid-filled cells in ovarian stroma
Associated Conditions
1) strongly associated with obesity 2) acanthosis nigricans 3) insulin resistance/hyperinsulinemia
Biochemistry
1) adipose tissue converts excess androgens to estrogen 2) eventually the ovary and adrenal begin to secrete excess androgens, causing a positive feedback loop
Inheritance/Epidemiology
affects 5% of women in the USA; usually presents at puberty
Treatment
1) weight reduction (decreases conversion of androgen to estrogen 2) oral contraceptives (decreases ovarian androgen production) 3) wedge resection of ovary (decreases ovarian androgen secretion) 4) clomiphene or human menopausal gonadotropin (increases FSH secretion)
Tips for USMLE
1) the two hallmarks – no menses (or very few and irregular menses) and an increased level of androgens (androstenedione) 2) if LH:FSH > 2.0, think polycystic ovarian syndrome 3) if a 13 year-old girl who is 75 lbs overweight has her first menses at age 13 and then has no menses until she is 16 and then has another menstrual period 6 weeks later, think polycystic ovarian syndrome
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