## Mechanism of Action of Antifungals ### Correct Mechanisms **Key Point:** The first three options describe accurate mechanisms of action for their respective antifungal agents. | Agent | Class | Mechanism | Target | |-------|-------|-----------|--------| | Amphotericin B | Polyene | Binds ergosterol → pore formation → cell lysis | Cell membrane | | Fluconazole | Azole | Inhibits CYP51 (lanosterol 14α-demethylase) | Ergosterol synthesis | | Terbinafine | Allylamine | Inhibits squalene epoxidase | Early ergosterol synthesis | | Caspofungin | Echinocandin | Inhibits β(1,3)-D-glucan synthase | Cell wall | ### Why Caspofungin is Different **High-Yield:** Caspofungin does NOT inhibit DNA topoisomerase II. Instead, it inhibits **β(1,3)-D-glucan synthase**, an enzyme critical for fungal cell wall synthesis. This leads to disruption of the β-glucan layer and cell wall integrity loss. **Clinical Pearl:** DNA topoisomerase inhibitors (like etoposide or doxorubicin) are used in cancer therapy and bacterial infections, NOT fungal infections. Confusing caspofungin's mechanism with topoisomerase inhibition is a classic trap. ### Mnemonic: FACE **F** = Fluconazole → ergosterol synthesis (Fungal sterol) **A** = Amphotericin B → binds ergosterol (membrane pore) **C** = Caspofungin → β-glucan synthase (Cell wall) **E** = Echinocandins → cell wall (β-glucan) **Warning:** Do not confuse antifungal mechanisms with antibacterial or anticancer mechanisms. Topoisomerase inhibition is NOT a fungal target.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.