Cell injury and adaptation: molecular basis of cardiac hypertrophy: 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: molecular basis of cardiac hypertrophy

Sample item

A 62-year-old man with long-standing severe aortic stenosis has a concentrically thickened left ventricle. Which molecular change in his cardiac myocytes contributes to this adaptation?

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

The answer and the reasoning

D. Re-expression of fetal genes such as beta-myosin heavy chain and ANP

Pressure overload triggers signalling pathways that increase protein synthesis and revive a fetal gene programme, including beta-myosin heavy chain and atrial natriuretic peptide. Adult cardiac myocytes cannot divide, so the wall thickens by increasing cell size, not cell number. The adaptation eventually fails and the ventricle dilates.

Option by option

  • A. Switch from beta-myosin to alpha-myosin heavy chain isoform

    The change in overload runs the other way, towards beta-myosin heavy chain.

  • B. Replacement of myocytes by proliferating fibroblasts

    Fibrosis may follow in decompensation, but it is not the adaptive hypertrophic change.

  • C. Mitotic division of adult myocytes to increase cell number

    Adult cardiac myocytes are terminally differentiated and enlarge without dividing.

  • D. Re-expression of fetal genes such as beta-myosin heavy chain and ANP (correct)

    Correct. Fetal gene re-expression accompanies myocyte enlargement under pressure load.

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, Re-expression of fetal genes such as beta-myosin heavy chain and ANP. Pressure overload triggers signalling pathways that increase protein synthesis and revive a fetal gene programme, including beta-myosin heavy chain and atrial natriuretic peptide.

Why is "Switch from beta-myosin to alpha-myosin heavy chain isoform" not the answer?

The change in overload runs the other way, towards beta-myosin heavy chain.

Why is "Replacement of myocytes by proliferating fibroblasts" not the answer?

Fibrosis may follow in decompensation, but it is not the adaptive hypertrophic change.

Why is "Mitotic division of adult myocytes to increase cell number" not the answer?

Adult cardiac myocytes are terminally differentiated and enlarge without dividing.

What concept does this question test?

It tests Cell injury and adaptation: molecular basis of cardiac hypertrophy in Pathology. Adult cardiac myocytes cannot divide, so the wall thickens by increasing cell size, not cell number. The adaptation eventually fails and the ventricle dilates.

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: molecular basis of cardiac hypertrophy?

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.