A 29-year-old woman is started on etonogestrel implant (Nexplanon) for contraception. She reports irregular bleeding at 3 months — light but daily spotting. The mechanism by which the etonogestrel implant primarily achieves contraception is:

• A Inhibition of GnRH secretion from the hypothalamus, suppressing FSH and LH release
• B Continuous low-dose progestogen suppresses the LH surge, preventing ovulation in most cycles with cervical mucus thickening as secondary mechanism ✓
• C Endometrial atrophy leading to implantation failure is the primary mechanism
• D Fallopian tube motility inhibition preventing sperm-egg transport

Explanation

The etonogestrel implant (68 mg released over 3 years) primarily prevents ovulation by suppressing the mid-cycle LH surge through continuous progestogen exposure. In the first 2 years, ovulation suppression is nearly complete; in year 3 some ovulation may occur but cervical mucus thickening provides a reliable backup mechanism. The progestogen's pituitary effect is predominantly at the LH surge level rather than total GnRH suppression. Endometrial atrophy occurs as a tertiary effect and explains irregular bleeding, but is not the primary contraceptive mechanism. The implant has a Pearl index < 0.1 per 100 woman-years, making it one of the most effective reversible contraceptives.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.