A woman taking a combined oral contraceptive pill (OCP) containing ethinyl estradiol and levonorgestrel has a venous thromboembolism. The increased VTE risk is primarily due to which mechanism?
- A Estrogen-stimulated hepatic synthesis of coagulation factors II, VII, VIII, X and decreased protein S ✓
- B Progestin-induced platelet aggregation via thromboxane A2
- C Estrogen-induced endothelial dysfunction causing arterial thrombus formation
- D Progestin-mediated inhibition of fibrinolysis via PAI-1 elevation
Explanation
The estrogenic component of OCPs (ethinyl estradiol) acts on the liver to upregulate synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, X) and fibrinogen while simultaneously decreasing natural anticoagulants (protein S, antithrombin III). This shifts the hemostatic balance toward hypercoagulability and venous thrombosis. The progestin component influences VTE risk modestly — third/fourth generation progestins (desogestrel, gestodene) carry higher VTE risk than levonorgestrel-containing pills.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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