Antimicrobials: griseofulvin: 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 · Antimicrobials: griseofulvin

Sample item

A 7-year-old with tinea capitis is treated with oral griseofulvin for several weeks. Which statement about the drug is correct?

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

The answer and the reasoning

D. Tubulin binding in dermatophytes, with hepatic enzyme induction

Griseofulvin is deposited in keratin precursor cells and binds tubulin, disrupting fungal mitosis, so new keratin is resistant to infection. It induces hepatic CYP enzymes, which can reduce the effect of oral contraceptives and warfarin. Treatment must continue until the infected keratin has grown out.

Option by option

  • A. Ergosterol binding with membrane pore formation

    Ergosterol binding with pore formation is the action of amphotericin B and nystatin.

  • B. Glucan synthase inhibition in the fungal cell wall

    Glucan synthase inhibition is the action of echinocandins.

  • C. Squalene epoxidase inhibition, blocking ergosterol synthesis

    Squalene epoxidase inhibition is the action of terbinafine.

  • D. Tubulin binding in dermatophytes, with hepatic enzyme induction (correct)

    Correct. Tubulin binding disrupts dermatophyte mitosis, and enzyme induction affects other drugs.

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, Tubulin binding in dermatophytes, with hepatic enzyme induction. Griseofulvin is deposited in keratin precursor cells and binds tubulin, disrupting fungal mitosis, so new keratin is resistant to infection.

Why is "Ergosterol binding with membrane pore formation" not the answer?

Ergosterol binding with pore formation is the action of amphotericin B and nystatin.

Why is "Glucan synthase inhibition in the fungal cell wall" not the answer?

Glucan synthase inhibition is the action of echinocandins.

Why is "Squalene epoxidase inhibition, blocking ergosterol synthesis" not the answer?

Squalene epoxidase inhibition is the action of terbinafine.

What concept does this question test?

It tests Antimicrobials: griseofulvin in Pharmacology. It induces hepatic CYP enzymes, which can reduce the effect of oral contraceptives and warfarin. Treatment must continue until the infected keratin has grown out.

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 Antimicrobials: griseofulvin?

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.