Ulipristal acetate (UPA) 30 mg is a selective progesterone receptor modulator used for emergency contraception. A woman takes UPA 90 hours after unprotected intercourse. Which mechanism explains its continued efficacy at this time point compared to levonorgestrel?

• A UPA has a post-fertilization anti-implantation mechanism that levonorgestrel lacks
• B UPA is metabolized more slowly than levonorgestrel, maintaining active serum levels for 5 days
• C UPA inhibits ovulation effectively even at the late follicular phase (LH surge already initiated), unlike levonorgestrel ✓
• D UPA inhibits sperm capacitation for longer than levonorgestrel

Explanation

Both levonorgestrel and ulipristal acetate act primarily by inhibiting or delaying ovulation. The critical mechanistic advantage of UPA is that it can delay follicular rupture even when the LH surge has already begun (late follicular phase) — it inhibits follicular rupture by opposing progesterone receptor activation needed for the ovulatory cascade. Levonorgestrel is ineffective once the LH surge is underway. This explains UPA's superior efficacy (both in the 72-hour window and extending to 120 hours) especially when ovulation is imminent. There is no confirmed post-fertilization (anti-implantation) mechanism for either agent under current evidence.

Reference: Shaw's Textbook of Gynaecology, 17th ed.

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