Anti-Retroviral for HIV

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HUSOP2014
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136952
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Anti-Retroviral for HIV
Updated:
2012-02-24 00:13:21
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HUSOP DA EXAM2 HIV questions
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Lecture 2-20-12
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  1. What are the 3 non-nucleoside RT inhibitors approved for use?
    nevirapine, efavirenz, delavirdine
  2. T/F: Non-nucleoside RTI's induce a 3D structure change and competively reduce enzyme activity
    False: noncompetitive
  3. Are NNRTIs active against HIV-1, HIV-2, or both
    only HIV-1
  4. NNRTIs have no activity against mammalian _____________
    DNA polymerase
  5. which 2 hepatic enzymes eliminate NNRTIs
    CYP3A4 and CYP2B6
  6. How can resistance to NNRTI occur? How is it avoided?
    A single mutation can cause extensive resistance. To avoid use combinations of agents.
  7. What is the most frequent ADR for nevirapine and the organ most affected by this drug
    rash, liver (causes hepatitis)
  8. T/F Nevirapine is approved for monotherapy in adults but not children infected with HIV.
    False: combination only, adults AND children
  9. Efavirenz triple therapy with ______ and ______ showed 70% of patients with non-detectable levels.
    zidovudine, lamivudine
  10. Clicker Q:
    Which of the following is NOT a characteristic of NNRTIs
    a. metabolized by CYP 3A4 and 2B6
    b. binds to essential site
    c. shows no activity against mammalian DNA polymerase
    B
  11. What ADR is most common with efavirenz and can occur with the first dose
    CNS problems
  12. HIV protease inhibitors are peptidomimetic that inhibit what?
    HIV aspartyl protease
  13. HIV protease inhibitors prefer cleavage between what 2 amino acids?
    proline and phenylalanine
  14. Renin and pepsin are examples of what? are these inhibited by HIV protease inhibitors?
    Human aspartyl proteases, no
  15. inhibition of the protease prevents cleavage of which 2 polyproteins
    gag and pol
  16. Which enzyme is most responsible for HIV protease inhibitor elimination?
    CYP3A4
  17. which drug is often used to inhibit CYP3A4 to increase levels of other drugs?
    ritonavir
  18. T/F Resistance to one HIV protease inhibitor not cross-resistant to other protease inhibitors
    True
  19. What are the 7 HIV protease inhibitors from the lecture? (HINT: SARALIN)
    • saquinavir
    • atazanavir
    • ritonavir
    • amprenavir
    • lopinavir
    • indinavir
    • nelfinavir
  20. In general, HIV protease inhibitors have effectiveness against HIV-1, HIV-2, or both?
    both
  21. T/F Resistance to saquinavir can be achieved by a single nucleotide mutation
    False: requires multiple mutations
  22. what is the most common ADR for saquinavir?
    GI distress
  23. What is the dose-dependent ADR for ritonavir?
    high cholesterol, TG, lipodystrophy
  24. Food ____ oral bioavailability of indinavir, while food usually _____ bioavailability of HIV protease inhibitors
    decreases, increases
  25. A unique ADR of indinavir is ______ and ________ due to poor solubility of drug at neutral pH
    crystalluria and nephrolithiasis
  26. This drug's metabolite from CYP2C19 oxidation is active, unlike all other HIV protease inhibitors
    nelfinavir
  27. The prodrug of amprenavir is called what?
    fosamprenavir
  28. this HIV protease inhibitor is most likely to cause skin eruptions
    amprenavir
  29. This protease inhibitor is similar to ritonavir, but more potent against HIV-1 in vitro
    lopinavir
  30. Which 2 protease inhibitors may cause hyperbilirubinemia without clinical significance?
    indinavir and atazanavir
  31. Increase in circulating triglycerides can lead to what 3 effects?
    increased central fat, increased breast fat in women, insulin resistance
  32. what is the name of the only entry inhibitor, active against HIV-1
    enfuvirtide
  33. T/F enfuvirtide requires intramuscular injections 2x daily
    False: subcutaneous
  34. Enfuvirtide blocks interaction between N36 and C34 sequences of the _______
    gp41 glycoprotein

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