Aub Mechanisms

Abnormal uterine bleeding (AUB) results from disruption of the normal hormonal regulation of the endometrial cycle or from structural abnormalities of the uterus. In the normal menstrual cycle, the hypothalamic-pituitary-ovarian (HPO) axis coordinates follicular development, ovulation, and endometrial growth and shedding through cyclical estrogen and progesterone production. The proliferative phase is estrogen-driven, stimulating endometrial glandular and stromal growth with neoangiogenesis. After ovulation, the corpus luteum produces progesterone, which transforms the proliferative endometrium into secretory endometrium with coiled spiral arteries and glycogen-rich stroma. If implantation does not occur, progesterone withdrawal triggers prostaglandin release (PGF2-alpha), spiral artery vasoconstriction, tissue ischemia, and controlled endometrial shedding (menstruation). Anovulatory AUB (the most common mechanism in reproductive-age women) occurs when chronic unopposed estrogen stimulates continued endometrial proliferation without the stabilizing effect of progesterone. The endometrium becomes thickened, fragile, and vascularly unstable, leading to irregular, prolonged, or heavy bleeding from random breakdown. Ovulatory AUB may result from luteal phase deficiency (insufficient progesterone duration or amount), endometrial hemostatic dysfunction (excess PGE2 relative to PGF2-alpha causing impaired vasoconstriction), or coagulation disorders (von Willebrand disease affects up to 13% of...