Haematology: lead poisoning: 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 · Haematology: lead poisoning

Sample item

A 30-year-old man who recycles old batteries has abdominal colic, constipation and anaemia. He has a bluish line on the gums, and the smear shows coarse basophilic stippling. Which pair of enzymes in haem synthesis is inhibited by his toxin?

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

The answer and the reasoning

C. Delta-aminolevulinic acid dehydratase and ferrochelatase

Lead inhibits ALA dehydratase and ferrochelatase, so aminolevulinic acid and protoporphyrin accumulate and haem synthesis falls. It also inhibits pyrimidine 5-prime nucleotidase, which leaves ribosomal RNA in red cells and produces basophilic stippling. Diagnosis is by blood lead level, and chelators such as succimer or EDTA are used.

Option by option

  • A. ALA synthase and uroporphyrinogen decarboxylase

    ALA synthase and uroporphyrinogen decarboxylase are not the main targets; the latter is deficient in porphyria cutanea tarda.

  • B. Heme oxygenase and biliverdin reductase

    Haem oxygenase and biliverdin reductase are involved in haem breakdown, not synthesis.

  • C. Delta-aminolevulinic acid dehydratase and ferrochelatase (correct)

    Correct. Blocking these two enzymes explains the anaemia and basophilic stippling in lead toxicity.

  • D. Porphobilinogen deaminase and uroporphyrinogen III synthase

    Porphobilinogen deaminase is deficient in acute intermittent porphyria, and uroporphyrinogen III synthase in congenital erythropoietic porphyria.

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 C, Delta-aminolevulinic acid dehydratase and ferrochelatase. Lead inhibits ALA dehydratase and ferrochelatase, so aminolevulinic acid and protoporphyrin accumulate and haem synthesis falls.

Why is "ALA synthase and uroporphyrinogen decarboxylase" not the answer?

ALA synthase and uroporphyrinogen decarboxylase are not the main targets; the latter is deficient in porphyria cutanea tarda.

Why is "Heme oxygenase and biliverdin reductase" not the answer?

Haem oxygenase and biliverdin reductase are involved in haem breakdown, not synthesis.

Why is "Porphobilinogen deaminase and uroporphyrinogen III synthase" not the answer?

Porphobilinogen deaminase is deficient in acute intermittent porphyria, and uroporphyrinogen III synthase in congenital erythropoietic porphyria.

What concept does this question test?

It tests Haematology: lead poisoning in Pathology. It also inhibits pyrimidine 5-prime nucleotidase, which leaves ribosomal RNA in red cells and produces basophilic stippling. Diagnosis is by blood lead level, and chelators such as succimer or EDTA are used.

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 Haematology: lead poisoning?

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.