Mifepristone used for medical abortion acts as an antiprogestogen. Its additional property that makes it useful combined with misoprostol is:

• A It inhibits HCG production from the trophoblast, causing luteal regression
• B It acts as a glucocorticoid receptor agonist, reducing implantation-supporting inflammation
• C It sensitises the myometrium to prostaglandins by upregulating prostaglandin receptors and oxytocin receptors, and increases intrinsic myometrial contractility ✓
• D It directly inhibits progesterone synthesis in the corpus luteum

Explanation

Mifepristone blocks progesterone receptors in the decidua, leading to decidual breakdown, and simultaneously sensitises the myometrium by upregulating prostaglandin receptors (especially PGE2 receptors) and oxytocin receptors. This priming action makes the uterus much more responsive to misoprostol given 36–48 hours later, producing efficient uterine contractions. Mifepristone does not inhibit HCG or progesterone synthesis directly; it does have antiglucocorticoid activity (which is why it can cause adrenal insufficiency at high doses) but this is not the mechanism for abortion.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.