Cell injury and adaptation: inflammasome in gout: 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 · Cell injury and adaptation: inflammasome in gout

Sample item

A 55-year-old man has an acutely painful, red first metatarsophalangeal joint, and polarised microscopy of the aspirate shows needle-shaped crystals. Which cytosolic complex in macrophages senses the crystals and drives production of mature IL-1 beta?

AApoptosomeBDeath-inducing signalling complexCNLRP3 inflammasomeD26S proteasome

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

The answer and the reasoning

C. NLRP3 inflammasome

Monosodium urate crystals are engulfed by macrophages and activate the NLRP3 inflammasome, which activates caspase-1 to cleave pro-IL-1 beta. IL-1 then recruits neutrophils and produces the acute attack. This is why IL-1 blockade is effective in gout.

Option by option

A. Apoptosome
The apoptosome is formed by cytochrome c, Apaf-1 and caspase-9 during apoptosis.
B. Death-inducing signalling complex
The death-inducing signalling complex forms at Fas or TNF receptors and activates caspase-8.
C. NLRP3 inflammasome (correct)
Correct. The NLRP3 inflammasome converts pro-IL-1 beta into its active form.
D. 26S proteasome
The proteasome degrades ubiquitinated proteins and does not sense crystals.

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.

Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is C, NLRP3 inflammasome. Monosodium urate crystals are engulfed by macrophages and activate the NLRP3 inflammasome, which activates caspase-1 to cleave pro-IL-1 beta.

Why is "Apoptosome" not the answer?

The apoptosome is formed by cytochrome c, Apaf-1 and caspase-9 during apoptosis.

Why is "Death-inducing signalling complex" not the answer?

The death-inducing signalling complex forms at Fas or TNF receptors and activates caspase-8.

Why is "26S proteasome" not the answer?

The proteasome degrades ubiquitinated proteins and does not sense crystals.

What concept does this question test?

It tests Cell injury and adaptation: inflammasome in gout in Pathology. IL-1 then recruits neutrophils and produces the acute attack. This is why IL-1 blockade is effective in gout.

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 Cell injury and adaptation: inflammasome in gout?

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.