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| MOA: fusion inhibitor: preevents reeling in by preventing c and N terminal interactions of gp41, it is a decoy of part of gp41. Uses: works on HIV1 only Pharmacodynamis: administered via injection , bound by plasma protein. Adverse : 20,000 a year, skin rash at site of infection, pnuemonica inciidence higher, Resistance: altering of n terminal of gp41 |
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| MOA: fusion injhibitor: CCR5 binding, will not work for cxcr4 tropic virus, only 50 percent of patients are eligible. Pharmacodynamics: maybe used first line p450 metabolism, taken orally. Adverse events: URI, hepatotoxicity, cardiovascular evetns, and muscular events. Resistance: when viruses become CXCR4 tropic. |
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| MOA: poison RT chain elongation via missing 3 prim OH. Do not bind well to cellcular DNA poly. Drugs preventacute ifnection ,but little effect on ifnected cells . Pharmacodynamics: taken orally , prodrugs that are triphosghed by cytpolasmic enzymes- half life extended by this. Adverse rxns: mitochondrial polymerases are susceptible, leadsd to lactic acidsois. Resitance; mutation of RT active site. |
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| MOA: NRTI, fluorinated analog of lamivudine with longer t o.5 . No known drug interactions have been identified. |
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| MOA: NRTI, nucletoide technically (monophosphate). Few drug interactions as well. Make work on RT mutants with other NRTI resistance. Can be given in combo with emtricabin. |
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| Non0 nucleoside re verse transcriptase inhbitiors |
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Definition
| MOA: bind adjacent to nnrti active site, idnuce conformational change that blocks RT activity. HIV-1 activity.farmdynamics, taken orally. Resistance- develops rapidly. MetABOLISM-Cypra34, can inhibit and induce activity.Toxicity : Rash, elevated liver enzymes. : |
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| MOA: newset NNRTI , able to bind in pocket even after several mutations have accumulated in pocket. Reserved for patients resistant to firstline treatment. |
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| MOA:inhibitsstrand transfer actions performed by HIV itnegrase. Metabolism:glucorindationb, p450 not involved. Resistance:integrase. Toxicity: few |
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| MOA: reversibly bind to active site, resembles phelnyulanine, proline cleavage site TS. Resistance: in general protease inhibitors make many contacs with enzyme, increase resistance chances. Extremley effective when combined with two nucleoside analogs. Adverse: Changes in body fat distribution, hyperlipidemia, onset of diabetes farmacodynamics- administered orally, p450 cyp3a4 metabolized so lots of drug interactions, substrate of efflux pumps, limits cellular concentration. |
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| MOA: PI, less dosing required and improved lipid profiles. Processed by cyp3a4 still. |
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| MOA: active against virus resistant to other PIS. Tipranavir in particular is nonpeptide, so is reserved as 2nd line drug. Tipranivir, side effects generally worse than other PIS. Metabolzied via cyp3a4 |
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| typical HIV treatment regimen |
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Definition
| Two NNRTI plus drug from another class. |
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| 2 NRTIs for one month, three drugs if exposure is severe. Pregnancy start after fi rst trimester 3 drugs. Infant: zidovudine |
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| MOA: active against virus resistant to other PIS. Tipranavir in particular is nonpeptide, so is reserved as 2nd line drug. Tipranivir, side effects generally worse than other PIS. Metabolzied via cyp3a4 |
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