Anti-fungals Flashcards
(21 cards)
3 mechanisms of antifungals
- alteration in cell membrane function
- mitotic spindle inhibition
- antimetabolite
aspergillosis DOC (drug of choice)
voriconazole IV
blastomycosis (mild) DOC
itraconazole PO
blastomycosis (severe) DOC
amphitericin B IV
itraconazole PO
candidiasis DOC
fluconazole PO
coccidioidomycosis DOC
fluconazole PO/IV
itraconazole PO
cryptococcus DOC
amphitericin B IV + flucytosine PO
then
fluconazole PO
histoplasmosis DOC
amphotericin B IV + itraconazole PO
mucormytosis DOC
amphotericin B IV
sporotrichosis DOC
amphotericin B IV and/or
itraconazole PO
terbinafine MOA
blocks conversion of squalene to squalene epoxide via inhibition of squalene epoxidase (interrupts cell membrane ergosterol and also causes build up or squalene which is toxic intermediate)
azole group MOA (drugs that end in azole)
blocks conversion of lanosterol to ergosterol-mediate by P450 enzymes (within the fungus) (can cause drug-drug interactions through inhibition of CYP3A4)
-produce GI side effects
amphotericin B MOA
form pores in the fungal cell membrane by binding to ergosterol, IV administration only
nystatin MOA
identical to amphotericin B but topical only
echocandins MOA (drugs that end in fungi)
beta 1,3 glucan synthesis inhibition leading to loss of cell wall
Azole with renal excretion and able to penetrate CSF
fluconazole
Azoles with hepatic excretion and unable to penetrate CSF
ketoconazole, itraconazole, vorionazole, posaconazole
Only azole to cause adrenal insufficiency
ketoconazole, leads to reduction in aldosterone, cortisol, and testosterone, also effects hepatic function
flucytosine MOA
enters fungus via cytosine permease
converted to 5-flurouracil which causes interruption in DNA and RNA synthesis.
mammalian cells don’t conduct first conversion step to 5FU but intestinal microflora do so typical side effects of cell cycle inhibition expected
griseofulvin MOA
mitotic spindle inhibitor
infusion reactions
amphoteracin B
caspofungin
