Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
|
Acyclovir
-what is it? -enzyme requirements -uses -SE |
-2 deoxyguanosine analogue (inhibits DNA synthesis)
-requires thymidine kinase activated by herpes infected cells -uses- HSV, VZV -SE: nephrotoxicity, neurotoxicity (more in IV than oral form) |
|
|
Valacyclovir (Valtrex)
-what is it? MOA -uses -Pk |
-prodrug of acycloviar (same MOA), converted to acyclovir by GI and first pass
-uses: herpes (genital, gingivostomatis esp in kids), VSV (higher dose), EBV -same as acyclovir but better PO absorption and longer half life |
|
|
Famciclovir/Penciclovir
-what is it? -uses -SE -Pk |
-guanosine analog
-uses: HSV, VZV, herpes zoster -few adverse effects -same as acyclovir but better PO absorption and longer half life |
|
|
Docosanol (Abreva)
-MOA -uses -only effective if . . . |
-inhibits cell entry (stops fusion b/n PM and HSV envelope)
-topical OTC cream for cold sores -only effective if started w/in 12 hrs of symptom onset |
|
|
Ganciclovir
-what is it? -Pk (enzyme affinity, cross reactivity) -SE -no acitivty vs. . . |
-guanosine analogue (inhibits DNA synthesis)
-higher affinity for phosphotransferase (so better CMV acitivty than acyclovir) -cross resistance with acyclovir -SE: bone marrow suppression (neutropenia, TCP) -teratongenic in animals -no activity vs. acyclovir-resistant HSV |
|
|
Foscarnet
-what is it? -uses |
-pyrophosphate analogue (inhibits DNAp)
-uses: CMV retinities, acyclovir and ganciclovir resistant virus -SE: nephrotoxic (direct damage to RT; hydrate with NS), BM suppression (sequestered in bone) |
|
|
Valgancicolovir
-what is it? -Pk |
-l-valyl ester prodrug of ganciclovir
-better PO bioavailibility |
|
|
Cidofovir
-what is it? -avoid using when . . . -uses |
-nucleotide analogue (inhibts DNAp)
-avoid CrCl <55mL/min (can be nephrotoxic) -uses: CMV retinitis (w/ probenicid and normal saline) |
|
|
Amantadine and Rimantadine
-MOA -Pk (elimination) -SE -DOC |
-affect influenza A viral uncoating (low pH is needed for uncoating)
-amantidine (renal elimination) vs. rimantadine (hepatic elimination) SE (A>R): increased dopamine effects (nevousness, insomnia, etc) -flu shot is DOC; must initiate tx w/in 48 hrs of symptoms onset |
|
|
Neuraminidase inhibitors
-MOA -examples and their routes of administration |
-analogues of sialic acid that block active site of neuraminidase; keep virus from releaseing from infected cell (aggregates at host surface)
-Oseltamivir (Tamiflu)-oral, Zanamavir (Relenza)-inhalation |
|
|
Interferon alpha
-MOA -Pk (form, route of administration) -SE (inc dose-limiting) -uses |
-may exert direct effect and/or modify immune response to infection
-pegylated form -IM or SQ administration -SE: flu-like syndrome common, BM suppression, CNS effects (dose-limiting)- including depression, confusion, fatigue -uses: chronic Hep B, chronic Hep C w/ ribavarin, genital warts (nonpegylated) |
|
|
Ribavirin
-MOA -SE -uses |
-guanosine nucleoside analogue (inhibits RNA synthesis)
-SE: anemia, teratogenic/embryonic/oncogenic effects -uses: comined with INF alpha for chronic Hep C, aerosolized for RSV (older tx) |
|
|
Lamivudine
-MOA -uses |
-pyrimidine (cytosine) nucleoside analogue; inhibits Hep B DNAp and HIV RT
-uses: chronic Hep B and HIV (in combo w/ other meds) |
|
|
Entecavir
-MOA -uses -not active against . . . |
-guanosine analog (inhibits Hep B DNAp)
-uses: Hep B -not active against lamivudine resistant virus |
|
|
Adefovir
-what is it? -MOA -improves . . . |
-adenine nucleotide
-reduces Hep B DNA -improves liver histology and normalizes AST (preventing cirrhosis and cancer secondary to hepatits) |
|
|
Telbivudine
-MOA -no activity against . . . |
-innhibits Hep B DNAp
-no activity against HIV |
|
|
Hep B tx
-goal -markers -initial therapy -end treatment |
-viral suppression, not eradication
-HBeAg +, HBV DNA, elevated ALT; AntiHBe = resistance -INFalpha, lamivudine, entacavir, telbivudine, tenofovir, adefovir (lam and telb have high resistance rates; INF is difficult to tolerate) -16-48wks INFs; others a min of 1 yr |
|
|
Hep C tx
-goals -tx |
-eradicate virus, prevent progression of liver disease, reduce risk for cancer
-pegINFalpha + ribavarin for 24-48wks (depending on genotype) |
|
|
What 6 clinical conditions indicate HIV tx should be initiated
|
1. hx of AIDS defining illness
2. CD4 <200 3. CD4 200-350 4. pregnancy 5. HIV nephropathy 6. coinfection with HBV |
|
|
Potential sites of action of anti-HIV drugs
|
-reverse transcriptase: transcribes complementary DNA from viral RNA
-integrase: integrates viral dsDNA into host chromosome -protease: cleaves gag-pol polyprotein that allows maturation of virions |
|
|
Antiretroviral Tx
1) pick 2 NRTI's 2) Pick one NNTRI or PI |
1) abacavir, lamivudine, tenofovir, emtricitabine, didanosine, stavudine, zidovudine
2) Efavirenz, Nevirapine, Delaviridine (NNRT), atazanavir, fosamprenavir, lopinavir, all with or without ritonavir (PIs - others end in "navir") |
|
|
RT inhibitors: MOA
1) NRTIs (nucleoside reverse transcriptase inhibitors) 2) NNRTI's 3) PI's (protease inhibitors) 4) entry inhibitors |
-nucleoside analogues inhibit DNAp (RT)
- non competitive inhibition of RT -prevent cleavage of precursor protein necessary for HIV maturation -bind gp41 or CCR5, preventry fusion/entry |
|
|
potentiall life threatening SE of Anti Retrovirals (due to inhibition of similar human enzymes
-lactic acidosis -hypersentivity rxn -bleeding events -BM suppression -nephrolithiasis/nephrotoxicity -pancreatitis -peripheral neuropathy -teratogen -CNS effects -CAD/hyperlip/DM/fat maldistribution -osteonecrosis |
-lactic acidosis (didanosine, zidovudine, stavudine)
-hypersensitivity rxn (abacovir) -bleeding events (tipranivir) -BM suppression (zidovudine) -nephrolithiasis and toxicity (Idinivir, Tenofovir) -pancreatitis (didanosine*, stavudine, tenofovir) -peripheral neuropathy (didanosine, stavudine) -teratogen (efavirenz) -CNS effects (efavirenze) -CAD/hyperlip/DM/Fat maldistribution: PIs -osteonecrosis: PI |
|
|
Ritonavir
|
-given with protease inhibitor
-helps slow metabolsm of PI |
|
|
Should not give anti-retrovirals with . . .
|
-simvustatin/lovastatin (use pravastatin or atorvastatin instead)
-rifampin -also monitor: azoles, oral contraceptives, anticonvulsnats, methadone, sildenafil |
|
|
Drug interactions with PIs
|
-ritonavir, aozles increase activity
-efavirenz/nevirapine, rifampin, rifabutin may decrease activity (Adjust dose) |
|
|
Acquisition of resistance
|
-unavoidable with monotherapy
-cross resistance w/in classes (same MOA) -point mutations in RT and protease (1 pt mutation at 103 causes 99% resistance to NNRTIs) |
|
|
Nephrotoxicity is associated with . . .
|
foscarnet, acyclovir (give IV NS to hydrate), famciclovir, cidofovir, indinavir (lithiasis)
|
|
|
SE matching
1. ganciclovir 2. acyclovir 3. cidofovir 4. foscarnet 5. amantadine 6. INF alpha |
1. nephrotoxic, BM suppression
2. nephrotoxic 3. nephrotoxic 4. Anemia, BM suppression, nephrotoxic 5. CNS side effects 6. flu like, CNS side effects, BM suppression |
|
|
SE matching:
2. abacavir 3. zidovudine 4. Efavirenz |
1.
2. serious hypersensitivity rxn 3. lactic acidosis, BM suppression 4. teratogen, CNS effects |
