Haemodynamics: warfarin-induced skin necrosis: practice question

A Pathology 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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Pathology · Haemodynamics: warfarin-induced skin necrosis

Sample item

On day 4 of warfarin started without heparin cover, a 55-year-old woman develops painful, well-demarcated areas of skin necrosis on the thighs and breasts. Biopsy shows fibrin thrombi in dermal venules. Which underlying mechanism is most likely?

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

The answer and the reasoning

C. Fall in protein C before other vitamin K-dependent factors, causing a transient procoagulant state

Protein C has the shortest half-life of the vitamin K-dependent factors, so early warfarin lowers it faster than factors II, IX and X. The brief imbalance favours clotting and microvascular thrombosis in fatty areas. It is more likely in protein C deficiency, and it is avoided by overlapping with heparin.

Option by option

  • A. Release of procoagulant substances by an occult pancreatic tumour

    Cancer-related thrombosis is slower, migratory and not tied to warfarin initiation.

  • B. Antibodies against heparin-platelet factor 4 complexes

    Heparin-PF4 antibodies cause HIT, and this patient had no heparin exposure.

  • C. Fall in protein C before other vitamin K-dependent factors, causing a transient procoagulant state (correct)

    Correct. Protein C falls first, leaving a short window of unopposed procoagulant activity.

  • D. Immune complex deposition along the walls of small vessels

    Immune complex vasculitis is leukocytoclastic, with neutrophils and no primary venular fibrin thrombi.

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 Pathology question

What is the answer to this Pathology question?

The best answer is C, Fall in protein C before other vitamin K-dependent factors, causing a transient procoagulant state. Protein C has the shortest half-life of the vitamin K-dependent factors, so early warfarin lowers it faster than factors II, IX and X.

Why is "Release of procoagulant substances by an occult pancreatic tumour" not the answer?

Cancer-related thrombosis is slower, migratory and not tied to warfarin initiation.

Why is "Antibodies against heparin-platelet factor 4 complexes" not the answer?

Heparin-PF4 antibodies cause HIT, and this patient had no heparin exposure.

Why is "Immune complex deposition along the walls of small vessels" not the answer?

Immune complex vasculitis is leukocytoclastic, with neutrophils and no primary venular fibrin thrombi.

What concept does this question test?

It tests Haemodynamics: warfarin-induced skin necrosis in Pathology. The brief imbalance favours clotting and microvascular thrombosis in fatty areas. It is more likely in protein C deficiency, and it is avoided by overlapping with heparin.

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 Haemodynamics: warfarin-induced skin necrosis?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.