Toxicology and antidotes: lead and haem synthesis: practice question

A Pharmacology 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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Pharmacology · Toxicology and antidotes: lead and haem synthesis

Sample item

A child with chronic lead exposure has microcytic anaemia with basophilic stippling and raised urinary delta-aminolaevulinic acid. Which pair of haem synthesis enzymes does lead inhibit most?

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

The answer and the reasoning

D. ALA dehydratase and ferrochelatase

Lead inhibits delta-aminolaevulinic acid dehydratase and ferrochelatase, the latter blocking insertion of iron into protoporphyrin. Urinary ALA and erythrocyte protoporphyrin therefore rise, and the anaemia is microcytic with stippling because lead also inhibits pyrimidine 5'-nucleotidase.

Option by option

  • A. Porphobilinogen deaminase and uroporphyrinogen decarboxylase

    Porphobilinogen deaminase deficiency causes acute intermittent porphyria and uroporphyrinogen decarboxylase deficiency causes porphyria cutanea tarda.

  • B. ALA synthase and heme oxygenase

    ALA synthase is derepressed, not inhibited, when haem falls, and heme oxygenase breaks down haem.

  • C. Biliverdin reductase and UDP-glucuronosyltransferase

    Biliverdin reductase and UDP-glucuronosyltransferase act in bilirubin formation and conjugation, after haem breakdown.

  • D. ALA dehydratase and ferrochelatase (correct)

    Correct. Lead blocks ALA dehydratase and ferrochelatase.

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 Pharmacology question

What is the answer to this Pharmacology question?

The best answer is D, ALA dehydratase and ferrochelatase. Lead inhibits delta-aminolaevulinic acid dehydratase and ferrochelatase, the latter blocking insertion of iron into protoporphyrin.

Why is "Porphobilinogen deaminase and uroporphyrinogen decarboxylase" not the answer?

Porphobilinogen deaminase deficiency causes acute intermittent porphyria and uroporphyrinogen decarboxylase deficiency causes porphyria cutanea tarda.

Why is "ALA synthase and heme oxygenase" not the answer?

ALA synthase is derepressed, not inhibited, when haem falls, and heme oxygenase breaks down haem.

Why is "Biliverdin reductase and UDP-glucuronosyltransferase" not the answer?

Biliverdin reductase and UDP-glucuronosyltransferase act in bilirubin formation and conjugation, after haem breakdown.

What concept does this question test?

It tests Toxicology and antidotes: lead and haem synthesis in Pharmacology. Urinary ALA and erythrocyte protoporphyrin therefore rise, and the anaemia is microcytic with stippling because lead also inhibits pyrimidine 5'-nucleotidase.

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 Toxicology and antidotes: lead and haem synthesis?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology 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.