Chronic inflammation: TNF and granulomas: 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 · Chronic inflammation: TNF and granulomas

Sample item

A 50-year-old woman with rheumatoid arthritis has been taking infliximab for six months. She now has fever, night sweats, weight loss and a chest radiograph showing miliary shadows. Which mechanism most directly explains her new illness?

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

The answer and the reasoning

C. Loss of TNF-dependent macrophage activation and maintenance of granulomas

Tumour necrosis factor, along with interferon-gamma from Th1 cells, activates macrophages and maintains granuloma architecture around Mycobacterium tuberculosis. Blocking TNF allows latent infection to disseminate, producing miliary tuberculosis. Patients are screened for latent infection before anti-TNF therapy.

Option by option

  • A. Depletion of circulating B lymphocytes and antibodies

    Antibodies are not central to control of mycobacteria, and infliximab does not deplete B cells.

  • B. Selective depletion of CD8 T cells by the drug

    Infliximab neutralises TNF and does not selectively deplete CD8 T cells.

  • C. Loss of TNF-dependent macrophage activation and maintenance of granulomas (correct)

    Correct. TNF blockade breaks down granuloma containment, so latent bacilli reactivate and spread.

  • D. Failure of neutrophil adhesion to endothelium

    Failure of neutrophil adhesion is the defect in leukocyte adhesion deficiency, a congenital disorder.

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.

More Pathology questions

Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is C, Loss of TNF-dependent macrophage activation and maintenance of granulomas. Tumour necrosis factor, along with interferon-gamma from Th1 cells, activates macrophages and maintains granuloma architecture around Mycobacterium tuberculosis.

Why is "Depletion of circulating B lymphocytes and antibodies" not the answer?

Antibodies are not central to control of mycobacteria, and infliximab does not deplete B cells.

Why is "Selective depletion of CD8 T cells by the drug" not the answer?

Infliximab neutralises TNF and does not selectively deplete CD8 T cells.

Why is "Failure of neutrophil adhesion to endothelium" not the answer?

Failure of neutrophil adhesion is the defect in leukocyte adhesion deficiency, a congenital disorder.

What concept does this question test?

It tests Chronic inflammation: TNF and granulomas in Pathology. Blocking TNF allows latent infection to disseminate, producing miliary tuberculosis. Patients are screened for latent infection before anti-TNF therapy.

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 Chronic inflammation: TNF and granulomas?

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.