Cell injury: carbon tetrachloride toxicity: 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.

Try it

Pathology · Cell injury: carbon tetrachloride toxicity

Sample item

A worker in a dry-cleaning unit accidentally inhales a large amount of carbon tetrachloride vapour. Over the next three days he develops centrilobular hepatic necrosis with fatty change. Which sequence best explains the injury?

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

The answer and the reasoning

A. Cytochrome P450 conversion to the CCl3 free radical, causing membrane lipid peroxidation and impaired lipoprotein export from hepatocytes

Carbon tetrachloride is metabolised by the cytochrome P450 system, which is richest in centrilobular hepatocytes, to the highly reactive CCl3 free radical. The radical peroxidises membrane phospholipids, damages the endoplasmic reticulum and stops apoprotein synthesis, so triglycerides cannot leave the cell as lipoprotein. The result is fatty change and zone 3 necrosis.

Option by option

  • A. Cytochrome P450 conversion to the CCl3 free radical, causing membrane lipid peroxidation and impaired lipoprotein export from hepatocytes (correct)

    Correct. Metabolic activation by P450 in zone 3 explains both the site and the fatty change.

  • B. Binding of the solvent to canalicular membranes, causing cholestasis and periportal necrosis

    Cholestatic periportal injury is typical of some drugs and bile duct disease, not of this centrilobular pattern.

  • C. Direct inhibition of mitochondrial cytochrome oxidase, causing ATP depletion throughout the lobule

    Cytochrome oxidase inhibition is the mechanism of cyanide poisoning and would not spare the periportal region selectively.

  • D. Immune complex deposition in hepatic sinusoids, activating complement and recruiting neutrophils

    Immune complex injury is a hypersensitivity mechanism and is not involved in direct solvent toxicity.

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.

More Pathology questions

Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is A, Cytochrome P450 conversion to the CCl3 free radical, causing membrane lipid peroxidation and impaired lipoprotein export from hepatocytes. Carbon tetrachloride is metabolised by the cytochrome P450 system, which is richest in centrilobular hepatocytes, to the highly reactive CCl3 free radical.

Why is "Binding of the solvent to canalicular membranes, causing cholestasis…" not the answer?

Cholestatic periportal injury is typical of some drugs and bile duct disease, not of this centrilobular pattern.

Why is "Direct inhibition of mitochondrial cytochrome oxidase, causing ATP de…" not the answer?

Cytochrome oxidase inhibition is the mechanism of cyanide poisoning and would not spare the periportal region selectively.

Why is "Immune complex deposition in hepatic sinusoids, activating complement…" not the answer?

Immune complex injury is a hypersensitivity mechanism and is not involved in direct solvent toxicity.

What concept does this question test?

It tests Cell injury: carbon tetrachloride toxicity in Pathology. The radical peroxidises membrane phospholipids, damages the endoplasmic reticulum and stops apoprotein synthesis, so triglycerides cannot leave the cell as lipoprotein. The result is fatty change and zone 3 necrosis.

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: carbon tetrachloride toxicity?

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.