Adaptation: 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 · Adaptation: hypertrophy

Sample item

A 55-year-old man with long-standing hypertension has a left ventricle that is thick-walled, with increased heart weight. Why does the heart enlarge by hypertrophy rather than by hyperplasia?

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

The answer and the reasoning

A. Adult cardiac myocytes divide minimally, so they enlarge by making more myofilaments

Adult cardiac myocytes are terminally differentiated and have very limited capacity to divide. Mechanical overload, signalled by stretch and growth factors, increases synthesis of structural proteins and the number of sarcomeres in each cell, enlarging the cells. Beyond a limit the vascular supply is inadequate and decompensation follows.

Option by option

  • A. Adult cardiac myocytes divide minimally, so they enlarge by making more myofilaments (correct)

    Correct. Limited mitotic capacity leads to cell enlargement rather than increased cell number.

  • B. The increase in weight is entirely due to proliferation of fibrous tissue

    Increased fibrous tissue accompanies late hypertensive heart disease but does not account for the wall thickness at this stage.

  • C. Cardiac myocytes divide readily but are held back by low blood supply

    Myocytes do not divide readily, and hypoxia is not the reason hyperplasia fails.

  • D. Hyperplasia can be triggered only by hormones and not by mechanical load

    Hyperplasia can also follow growth factor and mechanical stimuli in labile tissues, so the real barrier in the heart is the myocyte's limited division, not the type of stimulus.

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, Adult cardiac myocytes divide minimally, so they enlarge by making more myofilaments. Adult cardiac myocytes are terminally differentiated and have very limited capacity to divide.

Why is "The increase in weight is entirely due to proliferation of fibrous ti…" not the answer?

Increased fibrous tissue accompanies late hypertensive heart disease but does not account for the wall thickness at this stage.

Why is "Cardiac myocytes divide readily but are held back by low blood supply" not the answer?

Myocytes do not divide readily, and hypoxia is not the reason hyperplasia fails.

Why is "Hyperplasia can be triggered only by hormones and not by mechanical l…" not the answer?

Hyperplasia can also follow growth factor and mechanical stimuli in labile tissues, so the real barrier in the heart is the myocyte's limited division, not the type of stimulus.

What concept does this question test?

It tests Adaptation: hypertrophy in Pathology. Mechanical overload, signalled by stretch and growth factors, increases synthesis of structural proteins and the number of sarcomeres in each cell, enlarging the cells. Beyond a limit the vascular supply is inadequate and decompensation follows.

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 Adaptation: 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.