14 topics with concise breakdowns: definitions, key facts, and class questions.
This section is dedicated to the clinical pharmacology of antifungal agents (antimycotics). Here we analyze drugs for the treatment of systemic and superficial mycoses, their effects on the fungal cell, pharmacokinetics, and adverse reaction profile. Curiously, the topic of "Viruses" has also found its way into our list — we will briefly touch upon them in the context of differential diagnosis and co-infections against the background of immunosuppression.
The material is strictly structured according to chemical structure and mechanism of action. You will study polyene antibiotics (natamycin), azoles (clotrimazole, ketoconazole, miconazole, modern triazoles), echinocandins, and squalene epoxidase inhibitors. The pharmacology "veterans" — griseofulvin and flucytosine — are discussed separately, along with synthetic topical antifungals.
In classes and exams, you are guaranteed to be asked about the sites of action of antimycotics: who destroys the cell wall, who disrupts membrane permeability (ergosterol), and who targets nucleic acids. A frequent exam question is the toxicity profile of systemic drugs (e.g., ketoconazole-induced hepatotoxicity) and the difference between fungicidal and fungistatic effects.
What groups are mycoses divided into in clinical practice?
There are three main groups that determine the choice of therapy: systemic (deep) mycoses, dermatomycoses (superficial), and candidiasis.
Why are polyene antibiotics relatively safe for human cells?
Mammalian cell membranes contain cholesterol, whereas polyenes have a 500-fold greater affinity for ergosterol, which is the specific sterol of fungal membranes.
To which pharmacological group does natamycin belong?
The drug belongs to the group of tetraene polyene antibiotics. It is important to remember that it is neither a macrolide, nor an azole, nor an allylamine.
Why is griseofulvin not prescribed for candidiasis?
The drug has a very narrow spectrum of activity. It is effective exclusively in dermatomycoses (infections of the skin, hair, and nails) and is completely inactive against the causative agents of candidiasis and systemic mycoses.
Why is flucytosine toxic to humans if we lack the enzyme for its activation?
Intestinal microflora possesses the necessary enzymes and converts part of the drug into toxic 5-fluorouracil, which is absorbed into the bloodstream and acts as a systemic cytostatic agent.
How does the mechanism of action of azoles differ from allylamines (e.g., terbinafine)?
Allylamines work at an earlier stage of the cascade—they inhibit the squalene epoxidase enzyme, causing ergosterol deficiency and the accumulation of toxic squalene. Azoles act later, blocking 14-demethylase and disrupting the conversion of lanosterol.
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