Inflammation and repair: complement and PNH: 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 · Inflammation and repair: complement and PNH

Sample item

A man has episodic haemoglobinuria and venous thrombosis. His red cells lyse excessively through complement because they lack GPI-anchored regulators. Which are the missing proteins?

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

The answer and the reasoning

D. CD55 (DAF) and CD59

In paroxysmal nocturnal haemoglobinuria, a PIGA mutation prevents GPI anchor synthesis, so CD55 (decay-accelerating factor) and CD59 (which blocks membrane attack complex) are missing. Red cells are then susceptible to complement-mediated lysis.

Option by option

  • A. C1 esterase inhibitor and C4 binding protein

    C1 inhibitor deficiency causes hereditary angioedema, not haemolysis.

  • B. CR1 and CR3

    CR1 and CR3 are complement receptors involved in opsonisation.

  • C. Factor B and properdin

    Factor B and properdin promote alternative pathway activation and are not regulatory GPI proteins.

  • D. CD55 (DAF) and CD59 (correct)

    Correct. GPI-anchored CD55 and CD59 protect cells from complement and are lost in PNH.

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 D, CD55 (DAF) and CD59. In paroxysmal nocturnal haemoglobinuria, a PIGA mutation prevents GPI anchor synthesis, so CD55 (decay-accelerating factor) and CD59 (which blocks membrane attack complex) are missing.

Why is "C1 esterase inhibitor and C4 binding protein" not the answer?

C1 inhibitor deficiency causes hereditary angioedema, not haemolysis.

Why is "CR1 and CR3" not the answer?

CR1 and CR3 are complement receptors involved in opsonisation.

Why is "Factor B and properdin" not the answer?

Factor B and properdin promote alternative pathway activation and are not regulatory GPI proteins.

What concept does this question test?

It tests Inflammation and repair: complement and PNH in Pathology. Red cells are then susceptible to complement-mediated lysis.

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 Inflammation and repair: complement and PNH?

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.