Which mechanism explains the increased risk of endometrial hyperplasia and carcinoma in women with chronic anovulation due to polycystic ovary syndrome?
- A Unopposed oestrogen stimulation of the endometrium due to absence of cyclic progesterone ✓
- B Direct mitogenic effect of elevated LH on endometrial glands
- C Excess androgen conversion to oestrogen within endometrial tissue
- D Impaired apoptosis of endometrial cells caused by hyperinsulinaemia
Correct answer: A. Unopposed oestrogen stimulation of the endometrium due to absence of cyclic progesterone
Explanation
Chronic anovulation means no corpus luteum forms and no luteal-phase progesterone is secreted. Oestrogen from peripheral aromatisation of androgens continues to stimulate the endometrium without the counterbalancing antiproliferative effect of progesterone, producing persistent proliferation, hyperplasia and carcinoma risk. Elevated LH acts on theca cells, not directly on endometrium, and hyperinsulinaemia contributes indirectly through increased androgen production rather than as the primary mechanism.
Reference: Williams Gynecology, 4th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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