In the pathophysiology of PCOS, the primary site of excess androgen production leading to LH-driven testosterone synthesis involves which specific cell type?
- A Ovarian granulosa cells under excess FSH stimulation
- B Ovarian theca cells under excess LH stimulation ✓
- C Adrenal zona fasciculata producing DHEAS
- D Pituitary gonadotropes producing excess LH
Explanation
In PCOS, excess LH (from the characteristic high LH/FSH ratio due to increased GnRH pulse frequency) stimulates ovarian theca cells to produce excess androgens, particularly androstenedione and testosterone. Elevated insulin (insulin resistance) further augments theca cell androgen production by acting synergistically with LH. Granulosa cells, which express aromatase, convert androgens to estrogens, but in PCOS this conversion is impaired by relative FSH deficiency. The high androgen environment prevents follicle maturation and triggers atresia. Elevated insulin also reduces hepatic SHBG production, increasing free androgen levels—a key mechanism of clinical hyperandrogenism in PCOS.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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