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23 Cards in this Set
- Front
- Back
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Mechanism of action of the anti-fungal therapy polyenes.
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Form artificial pores in the cytoplasmic membrane.
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Mechanism of action of the anti-fungal therapies terbinafine and azoles.
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Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.
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Mechanism of action of the anti-fungal therapy flucytosine.
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Inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil.
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Mechanism of action of the anti-fungal therapy griseofulvin.
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Disrupts microtubles. Deposits in keratin-containing tissues.
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Mechanism of action of Amphotericin B.
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Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."
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Clinical uses of Amphotericin B.
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Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.
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Symptoms of Amphotericin B toxicity.
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Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").
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Mechanism of action of Nystatin.
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Binds to ergosterol, disrupting fungal membranes.
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Clinical use of Nystatin.
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Swish and swallow for oral candidiasis (thrush). Topical for diaper rash or vaginal candidiasis.
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Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
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Inhibits fungal steroid (ergosterol) synthesis. Blocks: lanosterol -> ergosterol
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Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.
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Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.
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Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.
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Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.
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Mechanism of action of Flucytosine.
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Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.
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Clinical uses of Flucytosine.
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Used in sytemic fungal infections (e.g. Candida, Cryptococcus).
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Flucytosine toxicity.
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Nausea, vomitting, diarrhea, bone marrow suppression.
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Mechanism of action for Caspofungin.
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Inhibits cell wall synthesis.
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Clinical use of Caspofungin.
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Invasive aepergillosis.
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Symptoms of Caspofungin toxicity.
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GI upset, flushing.
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Mechanism of action of Terbinafine.
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Inhibits the fungal enzyme squalene epoxidase. Inhibits squalene -> lanosterol
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Clinical use of Terbinafine.
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Used to treat dermatophytoses (especially onychomycosis).
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Mechanism of action of Griseofulvin.
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Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).
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Clinical use of Griseofulvin.
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Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).
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Symptoms of Griseofulvin toxicity.
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Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.
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