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47 Cards in this Set

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Properties of base analogs
(typical antiviral agents)
activated in cell by phosphorylation
widely distributed
eliminated by kidney
usually non-specific & non-toxic
2 drugs for Influenza A
Amantidine & Rimantidine
Amantidine & Rimantidine MOA
Inhibition of uncoating
amines inhibit viral proton translocator
Used with L dopa in Parkinsons
2 drugs for Influenza A & B
Zanamivir & Oseltamivir
Zanamivir & Oseltamivir MOA
Neuraminidase inhibitor
Prevent viral release & spread
Idoxuirdine MOA
causes DNA breakage- historical drug (or topical) only
very toxic
Acycloguanosine Use
HSV, EBV, Shingles
Acycloguanosine MOA
interferes with DNA replication
(chain terminator)
relys on thymidine kinase
Ganciclovir MOA
competitive inhibitor of dGTP- chain terminator
lacks specificity of Acyclovir
Treatment for CMV
Ganciclovir
Ribavirin MOA
labilizes viral mRNA by reducing 5' cap formation
Ribavirin Toxicities
BM depression, GI, CNS, Teratogenic, mutagenic, carcinogenic
Treatment for RSV, Hep C or Hanta
Ribavirin
Hep C use ribavirin + IFN a
5 (or 6) first line drugs for TB
Isoniazid, Rifampicin, Pyrazinamide, Ethambutol, Streptomycin (ciprofloxacin)
Isoniazid MOA
Bacteriacidal: inhibition of mycolic acid synthesis-
forms inhibitory complex w/MB acyl carrier protein
Isoniazid SEs
Slow acetylators- Neuorpathy b/c loss of pyridoxine- (tx w/pyroxidine NOT benzos or barbits)

Fast acetylators- hepatotoxicity

Lupus like syndrome (like hydralazine & procainamide- gives positive ANA)
Rifampicin MOA
Blocks RNA synthesis
(inhibits DNA dependend RNA polymerase)
RRRRRifampicin
Rifampicin SEs
Drug Interactions!!
oral contraceptives, hormones, coumadin (& theophyline- like Cipro & Zileutin), others
(colors body fluids orange/red)
Ethambutol MOA
inhibits mycolic acid synthesis
Ethambutol SEs
inability to perceive green
optic neuritis
relatively non-toxic
Pyrazinamide MOA
inhibits mycolic acid synthesis- inhibits fatty acid synthetase I (FASI)
Pryazinamide SEs
flushing, arthralgia, hepatotoxicity (monitor enzymes)
synergistic w/isoniazide
Classes of treatment for HIV
NRTIs
NNRTIs
PI
Entry Inhibitor
6 NRTIs
Azidothymidine (zidovudine)- BM
Stavudine- P & PN
Lamivudine (3-thiacytidine)- P & PN
Dideoxyinosine- P & PN
Abacavir- allergies
Tenofovir- (SEs like PIs)
Azidothymidine MOA
RTI & chain terminator- cell becomes deficient in thymidine
Azidothymidine SEs
Severe:
BM, granulocytopenia, anemia, neurotoxic, NVHA, insomnia, myalgia
25% of patients can't tolerate
Stavudine MOA
RTI & chain terminator
Stavudine SEs
interferes w/mitochondrial DNA
contraindicated w/AZT
pancreatitis
Lamivudine MOA
less active & less toxic than AZT

Prevents resistance to AZT
Lamivudine SEs
less severe than AZT
no BM, no neuro
resistance quickly w/cross resistance to ddI, ddC & abacavir
3TC
Lamivudine
d4T
Stavudine
Prevents resistance to AZT
Lamivudine
Dideoxyinosine MOA
RTI
Dideoxyinosine SEs
pancreatitis & mitochondrial
Abacavir MOA
guanosine analog, RTI
Abacavir SEs
allergies, fever, rash, respiratory
Tenofovir MOA
RTI-
Tenofovir SEs
Unique- GI, glycosuria, hyperglycemia & triglyceridemia, renal, neutropenia
3 NNRTIs
Nevirapine
Delavirdine
efavirenz
NNRTIs MOA
RTI not nucleoside analog
NNRTIs SEs
fever, nausea, CNS, hepatotoxicity
rash to Stevens-Johnson
Protease Inhibitors Names
saquin-
indin-
riton-
melfin-
ampren-
lopin- avir
PIs MOA
prevent cleavage of HIV protein precursors
PIs SE
diabetes & diabetic like syndrome, cholesterol & TGs increased, fat wasting, asthenia,
Treatment guidelines for HIV
2 NRTIs & a PI
2 NRTIs & a NNRTI
1 NRTI & 1 NNRTI & 2 PIs
Enfuvirtide MOA
entry inhibitor
prevents HIV binding to CD4