Cell injury and adaptation: Werner syndrome: 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: Werner syndrome

Sample item

A 32-year-old man has premature greying, bilateral cataracts, thin tight skin over the limbs, type 2 diabetes and has just been treated for a sarcoma. Growth was normal until puberty. Which mechanism underlies this premature ageing?

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

The answer and the reasoning

A. Defective DNA helicase causing genomic instability

Werner syndrome is an adult-onset progeroid disorder caused by mutation of the WRN gene, a RecQ DNA helicase needed for DNA repair and replication. Genomic instability accelerates ageing and predisposes to cancers, particularly sarcomas. Growth failure in childhood with lamin A abnormality characterises Hutchinson-Gilford progeria instead.

Option by option

  • A. Defective DNA helicase causing genomic instability (correct)

    Correct. A helicase defect leads to DNA damage and early ageing with cancer risk.

  • B. Mutation of lamin A causing abnormal nuclear envelope

    Lamin A mutation causes Hutchinson-Gilford progeria, which presents in early childhood.

  • C. Failure of collagen cross-linking from lysyl oxidase loss

    Lysyl oxidase loss weakens connective tissue and does not cause a progeroid syndrome.

  • D. Excess telomerase activity with cell immortalisation

    Telomerase is in fact insufficient in ageing syndromes, not excessive.

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 A, Defective DNA helicase causing genomic instability. Werner syndrome is an adult-onset progeroid disorder caused by mutation of the WRN gene, a RecQ DNA helicase needed for DNA repair and replication.

Why is "Mutation of lamin A causing abnormal nuclear envelope" not the answer?

Lamin A mutation causes Hutchinson-Gilford progeria, which presents in early childhood.

Why is "Failure of collagen cross-linking from lysyl oxidase loss" not the answer?

Lysyl oxidase loss weakens connective tissue and does not cause a progeroid syndrome.

Why is "Excess telomerase activity with cell immortalisation" not the answer?

Telomerase is in fact insufficient in ageing syndromes, not excessive.

What concept does this question test?

It tests Cell injury and adaptation: Werner syndrome in Pathology. Genomic instability accelerates ageing and predisposes to cancers, particularly sarcomas. Growth failure in childhood with lamin A abnormality characterises Hutchinson-Gilford progeria instead.

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 Cell injury and adaptation: Werner syndrome?

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.