Warfarin therapy affects certain coagulation factors. Which set of factors is affected?

Warfarin therapy affects certain coagulation factors. Which set of factors is affected?

• A. VIII, IX, and X
• B. I, II, V, and VII
• C. II, VII, IX, and X
• D. II, V, and VII

Answer: (C)

Warfarin works by blocking vitamin K recycling, so the liver can’t gamma-carboxylate certain coagulation factors. Only those factors that require this vitamin K–dependent modification become functionally deficient. The factors that rely on this process are II (prothrombin), VII, IX, and X. Because gamma-carboxylation enables calcium binding and proper interaction with phospholipid surfaces, these factors fail to function when vitamin K is disabled, leading to anticoagulation. Factor VII has the shortest half-life, so changes in the extrinsic pathway (and the PT/INR) appear relatively quickly, while Factor II has a longer half-life, so the full anticoagulant effect develops over several days. Warfarin also lowers proteins C and S (natural anticoagulants), which is why bridging therapy is sometimes used at initiation. The other options mix factors that are not vitamin K–dependent (like V and VIII) or include non–vitamin K–dependent factors (like fibrinogen I), so they don’t reflect warfarin’s mechanism.

Warfarin works by blocking vitamin K recycling, so the liver can’t gamma-carboxylate certain coagulation factors. Only those factors that require this vitamin K–dependent modification become functionally deficient. The factors that rely on this process are II (prothrombin), VII, IX, and X. Because gamma-carboxylation enables calcium binding and proper interaction with phospholipid surfaces, these factors fail to function when vitamin K is disabled, leading to anticoagulation.

Factor VII has the shortest half-life, so changes in the extrinsic pathway (and the PT/INR) appear relatively quickly, while Factor II has a longer half-life, so the full anticoagulant effect develops over several days. Warfarin also lowers proteins C and S (natural anticoagulants), which is why bridging therapy is sometimes used at initiation.

The other options mix factors that are not vitamin K–dependent (like V and VIII) or include non–vitamin K–dependent factors (like fibrinogen I), so they don’t reflect warfarin’s mechanism.