pharm - ID HIV.txt

  1. CCR5 antagonists drugs
  2. CCR5 antagonists MOA
    Inhibits HIV entry into human cells by blocking HIV envelope glycoprotiens from interacting with chemokine co-receptors (specifically, CCR5 -- won't work if the HIV isn't using this mechanism but rather the CXCR4 or a combo of the two).
  3. CCR5 antagonists indication
    not first line -- HIV-1 pts who have failed prior therapies and have CCR5 tropism.
  4. CCR5 antagonists interactions
    metabolized by CYP3A4 (so decrease dose when given with an inhibitor)
  5. CCR5 antagonists SE
    orthostatic hypotension. rare hepatotoxicity, cardiovascular events.
  6. fusion inhibitors drugs
    enfuvirtide, PRO 140, ibalizumab
  7. fusion inhibitors MOA
    competitively inhibits HIV by binding CD4 flycoprotein targets (specifically gp41).
  8. fusion inhibitors kinetics
    IV (protein, so would be degraded if given PO)
  9. fusion inhibitors indications
    not first line -- MDR HIV as part of combination therapy
  10. fusion inhibitors SE
    peripheral neuropathy
  11. integrase inhibitors drugs
  12. integrase inhibitors MOA
    prevent the virus from incorporating its DNA into the host genome by inhibiting integrase (the enzyme that binds viral DNA and joins it to host DNA).
  13. integrase inhibitors kinetics
    metabolized by UGT1A1 (atazanavir is an inhibitor, rifampin is an inducer)
  14. single point mutations can knock out what classes?
    integrase inhibitors, NNRTIs :(
  15. NRTIs MOA
    Once incorporated to the cell, NRTIs are converted to nucleotides by host cell kinases. They then compete with endogenous nucleosides for incorporation into viral DNA (competitive inhibitors of reverse transcriptase).
  16. NRTIs kinetics
    zidovudine only IV, all are PO. short elimination half life, but life in cells are much longer than that (so don't overdose based on serum levels).
  17. NRTIs indications
    work for both HIV-1 and HIV-2
  18. NRTIs SE
    Also inhibit host cell DNA polymerase, likely contributing to their toxic effects (specifically linked to mitochondrial toxicities). MYALGIA, HA, diarrhea. Acidosis, peripheral neuropathy, toxicities (Pancreatitis, Hepatotoxicity, bone marrow supression).
  19. NNRTIs drugs
    efavirenz, nevirapine, 2G etravirine.
  20. NNRTIs MOA
    bind to a site on the reverse transcriptase molecule, inducing a conformational change and reducing its activity (so also inhibits viral RNA -> DNA transformation)
  21. NNRTIs contraindications
    pregnancy (efavirenz teratogenic)
  22. NNRTIs indications
    works for only HIV-1 (not HIV-2)
  23. NNRTIs SE
    rash, hepatits, transient CNS.
  24. protease inhibitors drugs
    things that end in NAVIR.
  25. protease inhibitors MOA
    Bind to viral proteases that typically cleave viral proteins during the maturation process. This results in the production of immature, noninfectious virus particles.
  26. protease inhibitors interactions
    protease inhibitors are CYP inhibitors, so significant interaction potential (ritonavir most potent CYP inhibitor, therefore often combined with other 3A4 substrates to prolong their half-lifes).
  27. protease inhibitors SE
    diarrhea, hyperlipidemia (less so with atazanavir).
  28. kaletra
    lopinavir/ritonavir. (ritonavir has significant GI toxicity alone).
  29. best for pregnancy
    nevirapine (NVP)
  30. best for HBV
    tenofovir (TDF) and efavirenz (EFV)
  31. NRTI AZT
  32. NRTI TDF
  33. NRTI 3TC
  34. NRTI FTC
  35. NRTI NVP
  36. NRTI EFV
Card Set
pharm - ID HIV.txt
pharm - ID HIV.txt