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| macrolide w/ amphitatic structure. MOA: nonpolar side binds tightly to ergosterol in fungal cell membrane. , polar side= pores for ions to leak out. 2. some resistance in candida and psuedallescheria- instrinsic resistance. Acquired resistance is not clinically significant 3. broad spectrum. Used as initial treatment for lifethreatening systemic, then switchhed to triazoles. 4.iv suspended in deoxycholate, oral admin only for gi infect. Liposomal prep - higher doses w less toxicity, but more expensive 5. renal damage, interaction with nephrotoxic drugs |
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| MOA: taken up by fungal cytosine permease. Conversio to 5-FU, FUTP (inhbit RNA synth), and 5dUMP (DNA synth) 2.resistance: loss of FC to FU conversion, or FU to FUMP conversion, or loss of permease 3.limited to candida and cryptococcus, 44. oral: absorbed rapidly from GI, well distributed (including CNS), synergu w amphoterecin B, itraconazole. Usually given in combo to avoid resistance 5. toxici ty w renal impairment, can also cause bone marrow imparement, GI effects. |
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| imidazole: MOA of all azoles- inhibit p450 enzyme lanosterol demethhylase (ERG11) blocks ergosterol biosynt. Causes disrupt of membrane, as well as accumulation of toxic precursor methylsterol, blocking membrane enzymes. 2. azole drug resistance: pump overexpression, target enzyme altered or overexpressed. Mutation leading to production of less toxic, alternative sterol 3. broad spectrum 4. minor gi distress, rare hepatitis , p450 drug interactions |
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| imidazole: oral and vulvovaginal candisasis, dermatophyte infect 2. topical |
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| imidazole 2. oral and vulvovaginal candisasis, dermatophyte infect 3. topical |
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| triazole 2. most potent azole, favored over kotconzaole- more ffective less toxic. Its metabolite has antifungal activity 3. GI enhanced by GI acid and food., lipid soluble metabolized by . 4. Cp3a4 isoenzyzme metabolzied, gi distress and teratgeenic , cant be given with proton pumps which decrease acidity. |
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| triazole 2. oral, no need fo acidity. Distirubted in CNS. Fewer interactions with other drugs. |
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| newest triazoles with improved bioavailability |
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| newest triazoles with improved bioavailability |
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| MOA: inhibitor of squalene epoxidase blocks ergosterl synth. Toxic accum of sterol squalene 2. synergistic with triazole compounds, prevents anil bed and skin infections, targets tinea 3. minimal side effects- GI distress and headache |
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| topical amphoterecin derivative 2. local supression of candidal |
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| moa: b(1,3)-glucan synthase inhibitor- messes up cell wall 2. resistance via mutation in FKS1 (B 1,3 glucan synthase) 3. candida and aspergillosis resistant to amphtoericin B 4. parenterally |
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