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IOS 11 Exam 4

Pharmacology of Anti-HIV agents

QuestionAnswer
Name the 8 Nucleoside analogs Abacavir,Didanosine,emtricitabine,lamivudine,stavudine,tenofovir,zalcitabine,zidovudine
Name the 3 Non-nucleoside analogs Delaviridine,efavirenz,nevirapine
Name the 9 protease inhibitors Fos-amprenavir,atazanavir,darunavir,indinavir,Lopinavir/ritonavir,nelfinavir,ritonavir,saquinavir,tipranavir
Name the Fusion inhibitor Enfuvirtide
Abacavir side effects Hypersensitivity reactions never rechallenge, extensive resistance
Didanosine side effects Second strongest affinsty for mitochondrial DNA- plus is acid labile must be taken on empty stomach watch pancreatitis,lactic acidosis
Emtricitabine side effects Hyperpigmentation of the palms and feet soles and is HBV active
Lamivudine side effects Well tolerated is active against HBV
Stavudine side effects 3rd strongest mitochondrial DNA killing, peripheral neuropathy, and body fat loss (face,appendages,buttocks
tenofovovir side effects Well tolerates potent against HBV, only nucleotide
Zalcitabile Side effects Very problematic-painful mouth ulcers
Zidovudine side effects Cytopenia,HA, nausea-caution in hepatic disease
Delaviridine Side effects Not really used due to poor activity
Efavarinz side effects CNS-abnormal dreams, somnolence, rash take at night
Nevirapine side effects Rash which can be very serious and lead to SJS there is a black box warning and must give half does lead in due to auto induction
Fosamprenavir side effects Circumoral parasthesias, rash (sulfa) contra in childrena and pregnancy
Protease inhibitors as a class cause -“The Laxatives” Class toxicities include hyperlipidemia, fat maldistribution (peripheral fat wasting/central fat accumulation), insulin resistance/hyperglycemia, GI complaints, and bleeding episodes in hemophilics.
Nucleoside Analogs as a class cause Lactic acidosis (inhibition of mitochondria DNA polymerase), and hetaptomegaly/steatosis
Non-Nucleoside Analog Reverse Transcriptase Inhibitors as a class cause All the agents in this drug class may cause a rash with potential SJS and hepatitis
Fusion Inhibitor as a class cause Injection site reactions are the main toxcitites. Painful welts, which maybe immune mediated.
Atazanavir side effects Hyperbilirubinemia via inhibition of UGT-1A1 and needs acid to be absorbed NO PPI
Darunavir side effects Cholesterol/lipids increased, GI distress, must be boosted with ritonavir, Best option for HIV resistant
Indinavir side effects Kidney stones-needs extra hydration to stay clear, dry skin, frequently boosted with ritonavir
Lopinavir/ritonavir side effects GI distress and increse in lipids and glucose also potent inhibitor
Nelfinavir side effects Diarrhea(Preemptively treat) must be taken with food, Rarely boosted with ritonavir No 3A4 routes
Ritonavir side effects Not used alone GI upset, Circumoral parasthesias, hypertriglceridemia, liver dysfunction, hyperinsulinemia
Saquinavir side effects Boosted with ritonavir GI upset, bloating
Tipranavir side effects Bad drug-GI upset, bloating, hyperlipidemia, liver toxcity, SULFA rash, MAJOR DI possible inducer of P-gP
P-glycoprotein All protease inhibitors are substrates and/or inhibitor/inducer of P-gP
Need food for absorption Indinavir(old), Tipranavir, atazanavir, nelfinavir, darunavir
Protease inhibitor boosting with ritonavir is required with (4) Darunavir,tipranavir,saquinavir, and lopinavir
Factors that determine Phamacological success Triple drug therapy, adverse drudrug or drug-food interactions, Adherence to therapy, gentatic metabolic differences, viral factos
Consequences of inadequate drug activity HIV resistance occurs due to high production, if reproduces in sub-optimal drug pressure, virus can efficently select for mutants (resistance) that have advantage in presence of drug
Created by: liza001
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