The pathogenesis of adenomyosis involves ectopic endometrial glands and stroma within the myometrium. The mechanism by which adenomyosis causes heavy menstrual bleeding (HMB) is best explained by:
- A Direct disruption of junctional zone myocytes impairs the mechanical hemostatic contractions of the uterus
- B Overexpression of aromatase in adenomyotic tissue causes local estrogen excess stimulating endometrial growth
- C Both A and B contribute through impaired myometrial contractility AND enhanced endometrial proliferation ✓
- D Adenomyosis expands uterine cavity surface area, increasing total volume of endometrium shed per cycle
Explanation
Adenomyosis causes HMB through two complementary mechanisms: (1) Disruption of the junctional zone (inner myometrium) by ectopic glands and stroma impairs the myometrial contraction wave responsible for mechanical hemostasis during menstruation — this is the primary mechanical mechanism; (2) Adenomyotic tissue overexpresses aromatase (CYP19A1), converting androgens to estrogens locally, which increases prostaglandin E2 production (via COX-2 upregulation) and promotes endometrial proliferation and angiogenesis. Both mechanisms synergize to produce menorrhagia. Expanded cavity is a consequence, not the primary mechanism of increased bleeding.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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Written and medically reviewed by the StethoPrep medical team.