In medical management of incomplete abortion at 10 weeks with 3 cm retained products on ultrasound, oral misoprostol is prescribed. The primary mechanism by which misoprostol promotes uterine evacuation is:

• A Inhibiting progesterone synthesis from the corpus luteum, removing the uterine quiescence
• B Stimulating oxytocin receptors directly, bypassing prostaglandin pathways
• C Blocking decidualization through anti-glucocorticoid effects on endometrial stromal cells
• D PGE1 analogue binding to EP3 receptors on myometrium causing cervical ripening and uterine contractions ✓

Explanation

Misoprostol is a synthetic PGE1 analogue that binds prostaglandin E receptors (EP2 and EP3) on myometrial smooth muscle cells and cervical stroma. EP3 receptor activation mediates uterotonic (contraction) effects, while EP2 mediates cervical softening and ripening. This combination of cervical ripening and myometrial contractions causes expulsion of retained products. Mifepristone (not misoprostol) blocks progesterone receptors, acting as a progesterone antagonist. Misoprostol does not directly stimulate oxytocin receptors.

Reference: Williams Obstetrics, 26th ed.

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Written and medically reviewed by the StethoPrep medical team.