Covers the main antifungal drug classes: azoles, allylamines, polyenes and flucytosine, with their mechanisms against ergosterol synthesis and fungal membranes. It then goes through pharmacokinetics in a comparison table, side effects, drug interactions, therapeutic uses from superficial to systemic infections, and pregnancy and lactation. A short set of recap questions closes the note.
Topic 79 of 93 in the MU Sofia syllabus for Pharmacology (Dental Medicine, Year 3). The free AceMed note covers it in 9 sections, about 395 words (4 min of reading), with 10 flashcards.
Azoles (e.g. fluconazole, ketoconazole): Inhibit lanosterol 14α-demethylase, a cytochrome P450 enzyme needed for the synthesis of ergosterol, an essential fungal cell membrane component. Depletion of ergosterol disrupts membrane integrity, leading to fungal cell death.
Allylamines (e.g. terbinafine): Inhibit squalene epoxidase, another enzyme in the ergosterol synthesis pathway. This leads to accumulation of toxic squalene and ergosterol deficiency, damaging the fungal membrane and causing cell death.
Polyenes (e.g. amphotericin B, nystatin): Bind directly to ergosterol in the fungal membrane and create pores, leading to leakage of essential intracellular components like potassium and causing fungal lysis. Amphotericin B is systemic; nystatin is for topical/oral use.
Flucytosine: Enters fungal cells via cytosine permease and is converted into 5-fluorouracil, which inhibits thymidylate synthase (DNA synthesis) and incorporates into RNA, disrupting both DNA and RNA synthesis, causing cell death.
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