Blood: warfarin and protein C: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · Blood: warfarin and protein C

Sample item

On day 4 of warfarin started without heparin cover, a patient develops painful, well-demarcated skin necrosis over the thighs. What is the underlying mechanism?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

C. Protein C, with a short half-life, falls before factors II and X, giving a transient hypercoagulable state

Warfarin inhibits vitamin K epoxide reductase, reducing carboxylation of factors II, VII, IX, X and also proteins C and S. Protein C has a half-life of only a few hours, so it falls before prothrombin (about 60 hours), leaving a brief prothrombotic window with microvascular thrombosis and skin necrosis. Heparin bridging protects against this.

Option by option

  • A. Platelet aggregation is stimulated by vitamin K deficiency

    Vitamin K deficiency does not stimulate platelets; it impairs clotting factor synthesis.

  • B. Antithrombin is directly inactivated by warfarin

    Antithrombin is a heparin-dependent inhibitor and is not directly altered by warfarin.

  • C. Protein C, with a short half-life, falls before factors II and X, giving a transient hypercoagulable state (correct)

    Correct. Early loss of anticoagulant protein C leaves procoagulant factors temporarily unopposed.

  • D. Factor VIII levels rise because warfarin inhibits its clearance

    Factor VIII is not vitamin K dependent and is not affected by warfarin.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is C, Protein C, with a short half-life, falls before factors II and X, giving a transient hypercoagulable state. Warfarin inhibits vitamin K epoxide reductase, reducing carboxylation of factors II, VII, IX, X and also proteins C and S.

Why is "Platelet aggregation is stimulated by vitamin K deficiency" not the answer?

Vitamin K deficiency does not stimulate platelets; it impairs clotting factor synthesis.

Why is "Antithrombin is directly inactivated by warfarin" not the answer?

Antithrombin is a heparin-dependent inhibitor and is not directly altered by warfarin.

Why is "Factor VIII levels rise because warfarin inhibits its clearance" not the answer?

Factor VIII is not vitamin K dependent and is not affected by warfarin.

What concept does this question test?

It tests Blood: warfarin and protein C in Physiology. Protein C has a half-life of only a few hours, so it falls before prothrombin (about 60 hours), leaving a brief prothrombotic window with microvascular thrombosis and skin necrosis. Heparin bridging protects against this.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Blood: warfarin and protein C?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.