Mifepristone (RU-486) is a 19-norsteroid that acts as a competitive antagonist at progesterone and glucocorticoid receptors. In medical abortion, what is the specific mechanism by which mifepristone sensitises the uterus to subsequent misoprostol?
- A Mifepristone upregulates myometrial oxytocin receptors and increases gap junction density in myometrial cells ✓
- B Mifepristone directly stimulates prostaglandin synthesis in the decidua
- C Mifepristone causes cervical dilation by directly inhibiting collagen cross-linking
- D Mifepristone increases uterine blood flow, making the endometrium more responsive to prostaglandins
Explanation
Mifepristone blocks progesterone receptors in the myometrium and decidua. The consequence of progesterone receptor blockade is: upregulation of myometrial oxytocin receptors (progesterone normally suppresses oxytocin receptor expression), increased gap junction formation between myometrial cells (progesterone normally inhibits gap junctions, keeping the uterus quiescent), and increased endogenous prostaglandin release from the decidua. Together, these changes dramatically increase uterine sensitivity to the prostaglandin E1 analogue misoprostol administered 24–48 hours later, producing effective uterine contractions for expulsion.
Reference: Williams Obstetrics, 26th ed.
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Written and medically reviewed by the StethoPrep medical team.