A 16-year-old at 8 weeks gestation requests medical abortion. She is given mifepristone 200 mg orally followed 48 hours later by misoprostol 800 µg vaginally. The mechanism of mifepristone in this protocol is best described as:
- A Prostaglandin E1 analogue causing uterine contractions and cervical softening
- B Competitive progesterone receptor antagonist causing decidual breakdown and cervical ripening ✓
- C Anti-estrogenic action inhibiting implantation of the trophoblast
- D Selective oestrogen receptor modulator (SERM) preventing corpus luteum maintenance
Explanation
Mifepristone (RU-486) is a 19-norsteroid that acts as a competitive antagonist at progesterone receptors (PR-A and PR-B) with approximately 5× higher affinity than progesterone itself. By blocking progesterone action, it causes decidual breakdown (destabilising the endometrium), sensitises the myometrium to prostaglandins (upregulates prostaglandin receptors), and promotes cervical ripening. Misoprostol, a prostaglandin E1 analogue, completes the process by directly causing uterine contractions. The combination achieves > 95% complete abortion efficacy up to 10 weeks. Mifepristone has no anti-estrogenic primary mechanism in this indication.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.