Cell injury and apoptosis: 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 apoptosis

Sample item

Which event is the key trigger of the intrinsic (mitochondrial) pathway of apoptosis?

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

The answer and the reasoning

D. Leakage of cytochrome c from mitochondria into the cytosol

In the intrinsic pathway, loss of BCL2 protection allows BAX and BAK to permeabilise the mitochondrial membrane. Cytochrome c then escapes, binds Apaf-1 and activates caspase-9, which in turn activates the executioner caspases.

Option by option

  • A. Binding of Fas ligand to the Fas receptor

    Fas-FasL binding starts the extrinsic death receptor pathway, not the mitochondrial one.

  • B. Binding of TNF to its type 1 receptor

    TNF acting on TNFR1 is also a death receptor signal, belonging to the extrinsic pathway.

  • C. Entry of granzyme B from a cytotoxic T cell

    Granzyme B delivered by cytotoxic T cells activates caspases directly and is the killing mechanism of the effector cell, not the mitochondrial trigger.

  • D. Leakage of cytochrome c from mitochondria into the cytosol (correct)

    Correct. Cytochrome c release forms the apoptosome with Apaf-1 and activates caspase-9.

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, Leakage of cytochrome c from mitochondria into the cytosol. In the intrinsic pathway, loss of BCL2 protection allows BAX and BAK to permeabilise the mitochondrial membrane.

Why is "Binding of Fas ligand to the Fas receptor" not the answer?

Fas-FasL binding starts the extrinsic death receptor pathway, not the mitochondrial one.

Why is "Binding of TNF to its type 1 receptor" not the answer?

TNF acting on TNFR1 is also a death receptor signal, belonging to the extrinsic pathway.

Why is "Entry of granzyme B from a cytotoxic T cell" not the answer?

Granzyme B delivered by cytotoxic T cells activates caspases directly and is the killing mechanism of the effector cell, not the mitochondrial trigger.

What concept does this question test?

It tests Cell injury and apoptosis in Pathology. Cytochrome c then escapes, binds Apaf-1 and activates caspase-9, which in turn activates the executioner caspases.

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 apoptosis?

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.