Which contraceptive method requires daily temperature monitoring?

Emergency contraception works by interfering with ovulation, fertilization, or implantationdepending on the type and timing of administration. The most common forms include levonorgestrel and ulipristal acetate. Levonorgestrel inhibits LH surge, preventing ovulation, while ulipristal delays follicular rupture. Normal serum LH levels range from 5–25 IU/L during the mid-cycle surge. These agents do not affect an already implanted embryo and are ineffective once pregnancy is established. Side effects include nausea, headache, and menstrual irregularities. Contraindications include known pregnancy and hypersensitivity to components.

Rationale for correct answers

2.Emergency contraception prevents ovulation or fertilization. Levonorgestrel inhibits the luteinizing hormone surge, blocking ovulation if taken before the peak. Ulipristal acetate delays follicular rupture. These mechanisms act before fertilization, making this the correct explanation.

Rationale for incorrect answers

1.Emergency contraception does not terminate an established pregnancy. It is ineffective once implantation has occurred. Agents like mifepristone are used for termination, not levonorgestrel or ulipristal. Emergency contraception is not abortifacient.

3.Endometrial shedding is not the primary mechanism. While some thinning of the endometrium may occur, it is not reliable or consistent enough to prevent implantation. The dominant action is inhibition of ovulation.

4.Emergency contraception does not immobilize sperm permanently. Sperm motility is unaffected by these agents. Barrier methods or spermicides are used to impair sperm movement, not hormonal emergency contraception.

Take home points

• Emergency contraception prevents ovulation or fertilization, not implantation.
• It is ineffective once pregnancy is established.
• It does not cause permanent sperm immobilization.
• It must be differentiated from abortifacients like mifepristone.

Combined hormonal contraceptives (CHCs) contain estrogenand progestin, and are widely used for pregnancy prevention, cycle regulation, and acne management. In women over 35 who smoke, CHCs are contraindicated due to a synergistic increase in cardiovascular risk. Estrogenpromotes hepatic synthesis of clotting factors, increasing the risk of venous thromboembolism (VTE). Smoking accelerates atherogenesis, raising the risk of myocardial infarctionand stroke. The baseline VTE risk in reproductive-age women is approximately 1–5 per 10,000 annually; CHCs increase this to 9–10 per 10,000, and smoking compounds it further. Blood pressure should be <140/90 mmHg before initiating CHCs.

Rationale for correct answers

3.Women over 35 who smoke have a significantly elevated risk of thrombotic events when using CHCs. Estrogen increases clotting factor production, and smoking promotes endothelial damage and platelet aggregation. Together, they markedly increase the risk of VTE, myocardial infarction, and stroke.

Rationale for incorrect answers

1.Smoking does not reduce the effectiveness of CHCs. The contraceptive efficacy remains high (>99% with perfect use), and metabolism of hormones is not significantly altered to reduce effectiveness.

2.Bone mineral density loss is associated with long-term use of depot medroxyprogesterone acetate (DMPA), not CHCs. Estrogen in CHCs actually helps maintain bone density.

4.Irregular bleeding and spotting are more common with progestin-only methods or during initial CHC use, but not a primary contraindication in smokers over 35. The cardiovascular risk is the dominant concern.

Take home points

• CHCs are contraindicated in women >35 who smoke due to elevated cardiovascular risk.
• Estrogen increases clotting factors; smoking promotes vascular injury.
• CHCs do not reduce bone density; DMPA does.
• CHCs remain highly effective regardless of smoking status.