A 55-year-old man with chronic alcoholism and jaundice presents with easy bruising and prolonged bleeding after dental extraction. PT is markedly prolonged, aPTT is moderately prolonged, platelet count is 90,000/µL, and fibrinogen is normal. Which mechanism best explains the coagulopathy?
- A Autoantibody against ADAMTS13 causing accumulation of ultra-large von Willebrand factor multimers
- B Uncontrolled activation of the fibrinolytic system with excess plasmin generation
- C IgG-mediated platelet destruction with autoantibodies targeting GPIIb/IIIa
- D Impaired hepatic synthesis of vitamin K-dependent and independent coagulation factors ✓
Explanation
Hepatocellular disease impairs synthesis of all coagulation factors except factor VIII (produced by endothelial cells) and reduces clearance of activated factors. The prolonged PT (reflects extrinsic pathway with factor VII, shortest half-life) with moderately prolonged aPTT, mild thrombocytopenia (hypersplenism), and normal fibrinogen are classic for liver disease. HIT, ITP, and primary fibrinolysis would not produce this pattern with isolated liver pathology.
Reference: Harrison's Principles of Internal Medicine, 20th ed.
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