Inflammation and repair: pseudomembranous colitis: 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: pseudomembranous colitis

Sample item

A 70-year-old woman develops profuse watery diarrhoea 8 days after a course of clindamycin. Colonoscopy shows yellow-white plaques, and biopsy shows a volcano-like eruption of necrotic crypts topped by a cap of fibrin, mucin and neutrophils. What is the mechanism of the mucosal injury?

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

The answer and the reasoning

C. Toxins that glucosylate Rho GTPases and disrupt epithelial cytoskeleton

Antibiotic-associated pseudomembranous colitis is caused by toxins A and B of Clostridioides difficile, which glucosylate Rho family GTPases. The result is cytoskeletal collapse, loss of tight junctions and epithelial necrosis with inflammatory exudate forming the pseudomembrane. Overgrowth follows suppression of normal flora by antibiotics.

Option by option

  • A. Direct mucosal invasion with intracellular multiplication in colonocytes

    Mucosal invasion with intracellular growth describes organisms such as Shigella and enteroinvasive E. coli.

  • B. Toxin raising cAMP by ADP-ribosylation of the Gs protein

    Raising cAMP through Gs ADP-ribosylation is the cholera mechanism, causing watery diarrhoea without mucosal necrosis.

  • C. Toxins that glucosylate Rho GTPases and disrupt epithelial cytoskeleton (correct)

    Correct. Glucosylation of Rho GTPases by the clostridial toxins destroys the epithelial cytoskeleton.

  • D. Shiga toxin inhibiting the 60S ribosomal subunit in endothelium

    Shiga toxin acts on ribosomes of endothelium and enterocytes in haemorrhagic colitis and HUS, not antibiotic-associated colitis.

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, Toxins that glucosylate Rho GTPases and disrupt epithelial cytoskeleton. Antibiotic-associated pseudomembranous colitis is caused by toxins A and B of Clostridioides difficile, which glucosylate Rho family GTPases.

Why is "Direct mucosal invasion with intracellular multiplication in colonocy…" not the answer?

Mucosal invasion with intracellular growth describes organisms such as Shigella and enteroinvasive E. coli.

Why is "Toxin raising cAMP by ADP-ribosylation of the Gs protein" not the answer?

Raising cAMP through Gs ADP-ribosylation is the cholera mechanism, causing watery diarrhoea without mucosal necrosis.

Why is "Shiga toxin inhibiting the 60S ribosomal subunit in endothelium" not the answer?

Shiga toxin acts on ribosomes of endothelium and enterocytes in haemorrhagic colitis and HUS, not antibiotic-associated colitis.

What concept does this question test?

It tests Inflammation and repair: pseudomembranous colitis in Pathology. The result is cytoskeletal collapse, loss of tight junctions and epithelial necrosis with inflammatory exudate forming the pseudomembrane. Overgrowth follows suppression of normal flora by antibiotics.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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: pseudomembranous colitis?

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.