A patient with cholestatic liver disease shows prolonged prothrombin time (PT), bruising, and low plasma phylloquinone (K1). What mechanism best explains these findings, and what is the appropriate immediate management?

• A. Cholestasis reduces bile acid secretion impairing micelle-mediated absorption of vitamin K; treat with parenteral vitamin K and correct underlying bile flow issues while monitoring PT until absorption is restored.
• B. The findings are diagnostic of vitamin E toxicity causing impaired vitamin K action; immediate high-dose vitamin E antagonists should be administered.
• C. Low phylloquinone reflects renal loss of vitamin K in urine; start aggressive oral vitamin K because renal excretion will not affect parenteral therapy.
• D. Liver disease causes overproduction of vitamin K–dependent clotting factors leading to hypercoagulability; immediate anticoagulation is required to prevent thrombosis.

Answer: (A)