Polycystic ovary syndrome is a complex endocrine disorder diagnosed using the Rotterdam criteria (2 of 3: oligo/anovulation, clinical or biochemical hyperandrogenism, polycystic ovarian morphology on ultrasound with exclusion of other etiologies). The molecular pathogenesis centers on a self-amplifying insulin-androgen feedback loop. Insulin resistance (present in 50-70% of PCOS patients regardless of BMI) leads to compensatory hyperinsulinemia. Elevated insulin acts synergistically with LH on ovarian theca cells to upregulate steroidogenic enzymes - specifically CYP17A1 (17α-hydroxylase/17,20-lyase) - increasing androstenedione and testosterone production. Insulin simultaneously suppresses hepatic production of sex hormone-binding globulin (SHBG), increasing free (bioavailable) testosterone levels. Insulin also stimulates adrenal androgen production and enhances IGF-1 bioactivity by suppressing IGF-binding proteins (IGFBPs). At the ovarian level, excess androgens disrupt folliculogenesis. Granulosa cells in developing follicles are unable to aromatize sufficient androgens to estrogens (impaired CYP19A1/aromatase activity), leading to follicular arrest at 2-9 mm. Multiple arrested antral follicles give the classic polycystic ovarian morphology (≥12 follicles per ovary or ovarian volume >10 mL). Chronic anovulation leads to absence of corpus luteum formation, resulting in progesterone deficiency and unopposed estrogen exposure on the endometrium...