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18 Cards in this Set
- Front
- Back
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name the 5 antiretroviral classes for HIV treatment
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-nucleoside analogue reverse transcriptase inhibitors (NRTI)
- non-nucleoside analogue reverse transcriptase inhibitors (NNRTI) - protease inhibitors - entry inhibitors (fusion inhibitors, CCR5 antagonist) - integrase inhibitors |
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diff in metabolism of NRTIs vs. NNRTIS's and why is this important?
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NRTI - excreted by kidneys
NNRTIs- metabolized by inducing the liver (P450 system) |
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toxicity diff bw NRTI vs. NNRTIs
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NRTI- mitochondrial toxicity (neuropathy, pancreatitis, hepatitis, lactic acidosis)
-bone marrow suppresion (AZT only) - hypersensitivty (abacavir only) NNRTI- -rash (don't use another NNRTI if history of severe rash) - hepatitis (early on in tx) |
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diff in mechanism b/w NRTI and NNRTIs
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NRTI - causes premature chain termination
NNRTIs- inhibit reverse transcriptase and prevent incorporatino of DNA copy of viral genome into host DNA |
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mechanism and metabolism of protease inhibitors (-navir)
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- inhibit protease so that defective viral proteins are produced
metabolized by liver's p450 system |
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what is special about the protease inhibitor, ritonavir?
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strongly INHIBITS P450 system, which dec metabolism of drug and increases level of drug in body as part of its mechanism; basis for ritonavir-booster effect (allows for inc serum concentrations)
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toxicity of protease inhibitors?
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hyperglycemia
hyperlipidemia hepatitis hyperbilirubinemmia |
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entry inhibitors include ____ and _____. what are their metabolism and toxicities?
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fusion inhibitors (enfuvirtide)
- hydrolysis - injection site rxn CCR5 antagonist (maraviroc) - liver P450 - heptatoxicity |
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name the integrase inhibitor.
when do you use them? how is it metabolized and whatare the toxicities? |
raltegravir
- only use integrase inhibitors when you have pt with resistant virus - metabolized by liver (glucuoronation) - minor non-specific Sx's |
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What are the goals of HIV Tx (2)?
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-drop in viral load <50 RNA copies/mL by 1 year of therapy (IMPORTANT!!)
- increase CD4 count by 100 per year of starting HAART (inc directly proportional to initial count) |
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what are some complications in HIV tx?
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-lipodystrophy syndrome (lipoatrophy, hyperadiposity)
-cardiovascular dz (inc artherogenic profile) - bone abnormalities YOO... YOU GOT PROBLEMS WITH YO FAT HEART BONE |
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what are drug resistance HIV most likely due to?
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lack of adherence to taking the drugs by the pts consistently
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what are the 2 types of ttests for drug resistance?
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phenotype- grow virus in presence of drugs (not common)
genotype- MOST COMMON in clinical practice (detect mutations associated w/ resistance to drugs) |
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how is failure defined in terms of HIV therapy?
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still having viral load greater than 50 RNA copies/mL after 1 year of HAART
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what are 3 lab tests to do during Tx for HIV? which is most important in indicating progression of Tx?
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-viral load (PCR) ==> MOST IMPORTANT INDICATOR OF PROGRESSION OF TX
- genotype (to check for drug resistance) - CD4 count |
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which populations do you go ahead with Tx for HIV?
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-AIDs pts (CD4<200)
- CD4 <350 -pregnant women who have HIV (to prevent transmission to their babies) - HIV associated nephropathy - HIV pts with Hep B co-infection |
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what are the drug combinations? what are the bad things about them?
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- boosted protease inhibitor + two NRTI (increased toxicity, lots of pills...)
- NNRTI + 2NRTI (can be just one pill, which is good... inc cross-resistance) just think, the better drug combination goes directly "where the money is" -- blocking the reverse transcriptase |
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which 2 drug classes affect p450 system? what does this mean?
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NNRTI and protease inhibitors; therefore, don't give those together
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