Cell injury and adaptation: proteolysis in cachexia: 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: proteolysis in cachexia

Sample item

A 58-year-old man with advanced lung cancer has marked wasting of skeletal muscle and a raised TNF level. Which proteolytic system is chiefly responsible for the loss of myofibrillar protein?

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

The answer and the reasoning

B. Ubiquitin-proteasome pathway

Atrophy results from reduced protein synthesis and increased degradation. In cachexia, cytokines such as TNF activate the ubiquitin-proteasome pathway, which tags cytoskeletal and myofibrillar proteins and breaks them down. Autophagy contributes as well.

Option by option

  • A. Caspase-1 pyroptotic pathway

    Caspase-1 acts in inflammasome-driven inflammatory cell death and is not the muscle-wasting route.

  • B. Ubiquitin-proteasome pathway (correct)

    Correct. Ubiquitin tagging directs myofibrillar proteins to the proteasome for degradation.

  • C. Matrix metalloproteinase pathway

    Matrix metalloproteinases remodel extracellular matrix and do not degrade myofibrils.

  • D. Complement-mediated lysis

    Complement lysis damages membranes in immune injury and is not the cause of cachexia.

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 B, Ubiquitin-proteasome pathway. Atrophy results from reduced protein synthesis and increased degradation.

Why is "Caspase-1 pyroptotic pathway" not the answer?

Caspase-1 acts in inflammasome-driven inflammatory cell death and is not the muscle-wasting route.

Why is "Matrix metalloproteinase pathway" not the answer?

Matrix metalloproteinases remodel extracellular matrix and do not degrade myofibrils.

Why is "Complement-mediated lysis" not the answer?

Complement lysis damages membranes in immune injury and is not the cause of cachexia.

What concept does this question test?

It tests Cell injury and adaptation: proteolysis in cachexia in Pathology. In cachexia, cytokines such as TNF activate the ubiquitin-proteasome pathway, which tags cytoskeletal and myofibrillar proteins and breaks them down. Autophagy contributes as well.

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: proteolysis in cachexia?

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.