A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 31-year-old woman comes to the physician for evaluation of worsening pain, swelling, and erythema in her left leg for the past 4 hours. She returned from a trip to Taiwan to celebrate her sister's wedding 2 days ago. She has no history of serious illness. She is sexually active with one male partner and uses a combined oral contraceptive pill (OCP). She does not smoke, drink, or use illicit drugs. Her only other medication is a multivitamin. Her temperature is 37.2°C (99°F), pulse is 67/min, respirations are 16/min, and blood pressure is 90/60 mm Hg. Examination shows swelling in her left calf and pain behind her left knee when she is asked to dorsiflex her left foot. Laboratory results show elevated D-dimers. Which of the following is the most likely cause of this patient's clinical presentation?
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A
Decreased fibrinogenIncorrect. Fibrinogen is INCREASED by OCPs (it is a positive acute-phase reactant and is upregulated by estrogen) — and decreased fibrinogen would impair clotting, not promote thrombosis.
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B
ADAMTS13 deficiencyIncorrect. ADAMTS13 deficiency causes thrombotic thrombocytopenic purpura (TTP) — a microangiopathic hemolytic anemia with thrombocytopenia and neurologic symptoms, not isolated DVT.
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C
Vitamin K supplementationIncorrect. Vitamin K SUPPLEMENTATION promotes synthesis of factors II, VII, IX, X AND proteins C and S — its net effect is typically procoagulant in deficient states but not a recognized mechanism of OCP-related DVT.
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D
Decreased protein SCorrect. Estrogen-containing OCPs decrease protein S (and antithrombin III), impairing the natural anticoagulant pathway and predisposing to venous thromboembolism, especially with stasis from long travel.
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E
Factor V Leiden mutationIncorrect. Factor V Leiden is a genetic cause of activated protein C resistance and predisposes to DVT, but the temporal trigger here is OCP use plus long-distance travel — making decreased protein S from estrogen the more likely acquired etiology.
↑ Tap an answer to reveal the reasoning
Answer: D. A young woman with unilateral leg swelling, calf pain, positive Homan sign (pain on dorsiflexion), and elevated D-dimer after long-haul travel and oral contraceptive use has a deep venous thrombosis. The most likely underlying mechanism is OCP-INDUCED HYPERCOAGULABILITY.
Estrogens in combined oral contraceptives INCREASE hepatic synthesis of clotting factors (II, VII, VIII, IX, X, fibrinogen) AND DECREASE levels of natural anticoagulants — specifically antithrombin III, PROTEIN S, and protein C activity. Decreased protein S impairs protein C cofactor function, leaving activated factors V and VIII unchecked and shifting the hemostatic balance toward thrombosis. Combined with stasis from prolonged travel, this is the classic Virchow's triad mechanism.
Clinical pearl: women with hereditary thrombophilia (factor V Leiden, prothrombin G20210A, AT III deficiency) are at much higher VTE risk on OCPs — screening is warranted with personal/family history.
**Why each option:**
**A.** Fibrinogen is INCREASED by OCPs (it is a positive acute-phase reactant and is upregulated by estrogen) — and decreased fibrinogen would impair clotting, not promote thrombosis.
**B.** ADAMTS13 deficiency causes thrombotic thrombocytopenic purpura (TTP) — a microangiopathic hemolytic anemia with thrombocytopenia and neurologic symptoms, not isolated DVT.
**C.** Vitamin K SUPPLEMENTATION promotes synthesis of factors II, VII, IX, X AND proteins C and S — its net effect is typically procoagulant in deficient states but not a recognized mechanism of OCP-related DVT.
**D.** Correct. Estrogen-containing OCPs decrease protein S (and antithrombin III), impairing the natural anticoagulant pathway and predisposing to venous thromboembolism, especially with stasis from long travel.