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Antifungal study

for peds pharm

QuestionAnswer
Amphotericin B formulation IV only
Amphotericin B MOA binds to ergosterol in fungus cell wall causing leakage and death
Amphotericin B Kinetics Poor PO abs. Poor CNS penetration. Highly protein bound. Elimination?? Renal, feces, bile. Do not adjust dose for renal/ liver issues
Amphotericin B Dosing 0.5-1mg/kg/day Dosing dependent of disease being treated. Duration dependent on location of infection. 10-40 days
Amphotericin B coverage candida albicans, candida tropicalis, candida parapsilosis Aspergillus, histoplasmosis, blastomycosis, Cryptoccus neoformans
Amphotericin B infusion related side effects fever, chills, H/A, muscle aches, phlebitis. Premed with tylenol, benedryl, demoral for rigers & fluid bolus with NS to protect kidneys
Amphotericin B non infusion realted side effects Anticipated: hypo K+, hypo Mg+ Observed: anemia, thrombocytopenia, seizures, renal failure
Rx to treat Aspergillus Amphotericin B
Rx to treat histoplasmosis Amphotericin B
Rx to treat candida albicans, candida tropicalis, candida parapsilosis Amphotericin B
Rx to treat Cryptoccus neoformans Amphotericin B
3 names for Lipid amphotericin abelcet, amphotec, ambisome
% pt who experience renal dysfunction from amphotericin B 25-30%
% pt who experience renal dysfunction from lipid amphotericin 10-15%
Infusion time for amphotericin B 4 hrs
Infusion time for amphotericin lipid 2 hrs
Flucytosine MOA anti fungal: interferes with fungal RNA, DNA & protein synthesis
Flucytosine Kinetics Good CNS penetration (75% of serum), elimination renal 75-90%, monitor levels 25-100mcg/ml
Flucytosine uses synergy with amphotericin B
Flucytosine SE bone marrow suppression @ high levels, LFT ^, hypoK+, hypoglycemic.
Fluconazole MOA inhibits ergosterol production = inhibit cell wall formation
Fluconazole CSF penetration good
Fluconazole SE N/V, H/A, rash, diarrhea, ^LFT
Organisms sensitive to fluconazole candida albicans, cryptococcos
Fluconazole formulations IV & PO NB:100% bioavaliablity PO
Ketoconazole formulations PO, Shampoo, creams
Ketoconazole uses cradle cap, tinnea
Ketoconazole MOA inhibits ergosterol production = inhibit cell wall formation
Ketoconazole kinetics absorption pH dependent (needs low pH) if on H1 or PPI won't work Poor CSF penetration, metabolized in liver excreted in bili & feces
Ketoconazole SE liver toxic, N/V, abdominal pain
voriconazole formulations IV, PO
voriconazole MOA inhibits ergosterol production = inhibit cell wall formation
Voriconazole kinetics 96% PO availability, good CSF penetration, metabolized in the liver,p 450, excreted in bili & feces
voriconazole SE vision changes (blurred photophobia), rash, ^LFT, hepatitis, cholestasis, ARF, hypoK+, photosensitivity, Preg cat D, cardiac arrhythmias, QT prolongation
Posaconazole MOA inhibits ergosterol production = inhibit cell wall formation
Posaconazole kinetics food increases absorption, Lare Vd, highly protein bound, metabolized in liver t1/2=35 hrs, excretion =>70% in stool (66% unchanged)
Posaconazole SE edema, HTN, QT prolongation, hypoK+, Hypo Mg+, hypo Ca, ^ glucose, severe diarrhea, vomiting, mucositis, anemia, neutropenia, thromocytopenia, Liver toxic ^LFT, ^bili, Hepatitis, weakness, tremor
Caspofungin MOA inhibits enzume 1,3-beta-Dglucan synthases which forms glucan -polymer of glucose molecules which are necessary for cell wall syntheses
Caspofungin coverage broad spectrum, good 2nd line agent after ampho
Caspofungin kinetics Iv only, hightly protein bound 97%, metabolised in liver, excreted as inactive metabolite 41% urine, 35% stool
caspofugin formulations IV only
caspofungin SE fever (3-26%) vein irritation (15%) N/V, headache, puritis, rash, histamine related infusion reactions, hypoK+ anemia, ^LFT
Caspofungin is incompatible with what carrier fluid dextrose
Griseofulvin MOA inhibits mitosis by disrupting cells mitotic spindle structure
Griseofulvin uses tinea capitis
Griseofulvin administration shake very well falls out of suspension, need fat to absorb, not well absorbed
Created by: JennRN
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