A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 57-year-old florist presents to his family physician with nodular lesions on his right hand and forearm. He explains that he got pricked by a rose thorn on his right "pointer finger" where the first lesions appeared, and the other lesions then began to appear in an ascending manner. The physician prescribed a medication and warned him of gynecomastia as a side effect if taken for long periods of time. Which of the following is the mechanism of action of the medication?
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A
Inhibits ergosterol synthesisCorrect. Azoles (including ketoconazole) inhibit fungal ergosterol synthesis; ketoconazole also inhibits human steroidogenesis, causing gynecomastia with prolonged use.
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B
Binds to ergosterol, forming destructive pores in cell membraneIncorrect. Binding ergosterol to form pores describes amphotericin B and nystatin (polyenes), which cause nephrotoxicity and infusion reactions — not gynecomastia.
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C
Inhibits formation of beta glucanIncorrect. Inhibition of β-glucan synthesis describes echinocandins (caspofungin, micafungin) — not associated with gynecomastia.
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D
Disrupts microtubule functionIncorrect. Microtubule disruption is the mechanism of griseofulvin, used for dermatophyte infections — not for sporotrichosis or associated with gynecomastia.
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E
Inhibits squalene epoxidaseIncorrect. Squalene epoxidase inhibition describes terbinafine, used for dermatophyte onychomycosis; it has no significant antiandrogenic effect and is not first-line for sporotrichosis (treated with itraconazole, an azole).
↑ Tap an answer to reveal the reasoning
Answer: A. A florist with nodular skin lesions ascending up the arm after a rose thorn injury is the classic vignette for sporotrichosis ('rose gardener's disease'), caused by the dimorphic fungus Sporothrix schenckii. The infection spreads via cutaneous lymphangitic channels, producing a chain of subcutaneous nodules and ulcerations extending proximally from the inoculation site. Treatment is itraconazole for several months, or potassium iodide as an older alternative.
The question asks the mechanism of a drug warned to cause gynecomastia — this points to ketoconazole (an older azole). Ketoconazole inhibits fungal cytochrome P450 enzymes responsible for ergosterol synthesis, destabilizing the fungal cell membrane. It also inhibits human steroidogenesis (cytochrome P450 in adrenal and gonadal tissue), leading to decreased androgen synthesis and gynecomastia with long-term use — its most distinctive side effect. Itraconazole is now preferred for sporotrichosis because it has fewer endocrine side effects, but the classic teaching pairs the gynecomastia warning with the ergosterol-synthesis inhibitor mechanism.
Key pearl: azoles inhibit ergosterol synthesis (fungal sterol); polyenes (amphotericin, nystatin) bind ergosterol; echinocandins inhibit β-glucan synthesis; griseofulvin disrupts microtubules.
**Why each option:**
**A.** Correct. Azoles (including ketoconazole) inhibit fungal ergosterol synthesis; ketoconazole also inhibits human steroidogenesis, causing gynecomastia with prolonged use.
**B.** Binding ergosterol to form pores describes amphotericin B and nystatin (polyenes), which cause nephrotoxicity and infusion reactions — not gynecomastia.
**C.** Inhibition of β-glucan synthesis describes echinocandins (caspofungin, micafungin) — not associated with gynecomastia.
**D.** Microtubule disruption is the mechanism of griseofulvin, used for dermatophyte infections — not for sporotrichosis or associated with gynecomastia.