Mifepristone (RU-486) used for medical termination of pregnancy blocks which receptor, and what is its mechanism in facilitating cervical ripening and uterine contractions?
- A Estrogen receptor antagonism: blocking estrogen removes uterotrophic support for uterine quiescence
- B GnRH receptor antagonism: suppresses LH and progesterone production from the corpus luteum
- C Progesterone receptor antagonism: blocks progesterone's inhibitory effect on uterine contractions, increases prostaglandin synthesis and sensitivity, softens cervix and induces decidual necrosis; followed by misoprostol for complete expulsion ✓
- D Oxytocin receptor agonism: directly stimulates uterine contractions by binding OTRs on myometrium
Explanation
Mifepristone is a competitive antagonist at progesterone receptors (and glucocorticoid receptors at higher doses). By blocking progesterone's pro-quiescent effect on the myometrium and its anti-inflammatory effect on the cervix, mifepristone allows uterine contractility to increase and sensitizes the myometrium to prostaglandins. It also promotes endogenous prostaglandin synthesis and causes decidual necrosis leading to embryo detachment. A prostaglandin analogue (misoprostol, a PGE1 analogue) is administered 36–48 hours later to complete uterine evacuation; together they achieve >95% efficacy in first-trimester termination.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.