Lipid metabolism: salicylate and Reye syndrome: practice question

A Biochemistry 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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Biochemistry · Lipid metabolism: salicylate and Reye syndrome

Sample item

A 7-year-old recovering from varicella was given aspirin and now has persistent vomiting, confusion, hypoglycaemia and hyperammonaemia. Liver biopsy shows microvesicular fat. Which mechanism best explains the fatty change?

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

The answer and the reasoning

B. Mitochondrial injury that impairs fatty acid beta-oxidation

In Reye syndrome, mitochondrial dysfunction after a viral illness and aspirin exposure impairs fatty acid oxidation and the urea cycle. Fat accumulates as many small droplets in hepatocytes, and hypoglycaemia and hyperammonaemia follow. Aspirin should be avoided in children with viral illness.

Option by option

  • A. Blocked export of triglycerides because apolipoprotein B is absent

    Absent apolipoprotein B is abetalipoproteinaemia, which causes macrovesicular steatosis with fat malabsorption from infancy.

  • B. Mitochondrial injury that impairs fatty acid beta-oxidation (correct)

    Correct. Mitochondrial injury reduces beta-oxidation and ureagenesis, leaving microvesicular fat and hyperammonaemia.

  • C. Lysosomal accumulation of cholesteryl esters from acid lipase deficiency

    Acid lipase deficiency (Wolman) presents in early infancy with adrenal calcification and is not triggered by aspirin.

  • D. Increased lipogenesis driven by chronic alcohol use

    Alcohol-related steatosis results from an altered NADH to NAD ratio and is not relevant in a child with no alcohol exposure.

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 Biochemistry question

What is the answer to this Biochemistry question?

The best answer is B, Mitochondrial injury that impairs fatty acid beta-oxidation. In Reye syndrome, mitochondrial dysfunction after a viral illness and aspirin exposure impairs fatty acid oxidation and the urea cycle.

Why is "Blocked export of triglycerides because apolipoprotein B is absent" not the answer?

Absent apolipoprotein B is abetalipoproteinaemia, which causes macrovesicular steatosis with fat malabsorption from infancy.

Why is "Lysosomal accumulation of cholesteryl esters from acid lipase deficie…" not the answer?

Acid lipase deficiency (Wolman) presents in early infancy with adrenal calcification and is not triggered by aspirin.

Why is "Increased lipogenesis driven by chronic alcohol use" not the answer?

Alcohol-related steatosis results from an altered NADH to NAD ratio and is not relevant in a child with no alcohol exposure.

What concept does this question test?

It tests Lipid metabolism: salicylate and Reye syndrome in Biochemistry. Fat accumulates as many small droplets in hepatocytes, and hypoglycaemia and hyperammonaemia follow. Aspirin should be avoided in children with viral illness.

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 Lipid metabolism: salicylate and Reye syndrome?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry 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.