ID 19 Flashcards
griseofulvin uses
1) oral treatment of superficial infections
2) inhibits growth of dermatophytes (tinea, ringworm)
other griseofulvin AE
metabolizes Warfarin
permethrin MOA
blocks sodium channels (*thus neurotoxic)
malathion mechanism
acetylcholisterase inhibitor
lindane mechanism
blocks GABA channels (*thus neurotoxic)
chloroquine MOA
blocks detoxification of heme into hemozoin –> heme accumulates and is toxic to plasmodia
resistance to chloroquine?
membrane pump that decreases intracellular concentration of drug.
only drug you can’t use chloroquine for?
p falciparum
p falciparum treatment options
1) artemether/lumefantrine
2) atovaquone/proguanil
life-threatening malaria treatment
artesunate
*quinidine in US (quinine elsewhere)
chloroquine AE’s
retinopathy
pruritus (especially in dark-skinned individuals)
drug like oseltamivir…
zanamivir
oseltamivir/zanamivir uses
treatment and prevention of both influenza A and B
Why do acyclovir/valacyclovir have few adverse effects in uninfected cells?
not phosphorylated
acyclovir/valacyclovir usage caveat
no effect on latent forms of HSV and VZV
difference between valacyclovir and acyclovir?
valacyclovir is a prodrug of acyclovir that has better oral bioavailability
acyclovir/valacyclovir MOA of resistance
mutated viral thymidine kinase
acyclovir/valacyclovir AE’s
1) Obstructive crystalline nephropathy
2) ARF
Ganciclovir MOA
5-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinase. Preferentially inhibits viral DNA polymerase.
ganciclovir prodrug
valganciclovir, better oral bioavailability.
ganciclovir MOA of resistance
mutated viral kinase
Foscarnet MOA
Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.
*binds to pyrophosphate-binding site of enzyme (pyrophosphate analog)
foscarnet vs. ganciclovir/acyclovir
foscarnet doesn’t require kinase activation.
foscarnet uses
1) CMV retinitis in immunocompromised patients when ganciclovir fails
2) acyclovir-resistant HSV