AntiViral V.txt

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AntiViral V.txt
2012-04-28 23:47:21

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  1. What is the MOA of acyclovir?
    • Guanosine analogue that is activated by viral thymidine kinase
    • Inhibits DNA synthesis by competing c dGTP
  2. How does resistance develop?
    ? viral thymidine kinase
  3. What are its pharmacokinetics?
    • Oral, IV, or topical
    • Excreted by kidney (adjust dose c impaired renal fxn)
  4. What is the preferred oral form of acyclovir?
    Valacyclovir (pro-Rx has higher bioavailability)
  5. What are the uses of acyclovir?
    • Genital herpes, herpes keratitis (ocular), herpes zoster
    • IV for herpes encephalitis and VZV
    • Prophylaxis in organ transplant and immunocompromise
  6. What are the acyclovir side effects?
    • Generally mild and safe in pregnancy
    • Nephrotoxic c high IV doses
    • Somnolence when given c zidovudine in HIV
  7. What are the alternatives for Tx of HSV?
    Famciclovir/Penciclovir (the oral pro-Rx form)
  8. What topical agent can be used?
    Docosanol (Abreva)
  9. What is its MOA?
    Inhibits viral fusion to cell membrane
  10. What is used for Tx of CMV?
    • Ganciclovir (IV)/Valganciclovir (oral)
    • -->they are also active against HSV
  11. What is the MOA?
    Inhibits DNA replication
  12. When is ganciclovir used?
    • Rx or prophylaxis of CMV in immunocompromised or transplant pt
    • CMV retinitis (give in ocular transplant)
  13. What are the toxic effects? (worse than acyclovir)
    • Neutropenia (especially when given IV c zidovudine in HIV)
    • Abnormal LFTs
  14. What Rx can be used in resistant CMV and HSV but are more toxic?
    • Cidofovir_renal toxicity (use probenecid and hydrate)
    • Foscarnet_renal toxicity
    • Inhibits DNA and RNA polymerase, reverse transcriptase
  15. What is the MOA of oseltamivir and zanamivir?
    Neuraminidase inhibitors_block release of virus from cell
  16. When are the used?
    For influenza A and B
  17. How are oseltamivir and zanamivir administered?
    • Start w/in 48hrs of onset
    • Oseltamavir_oral;
    • zanamivir_nasal or inhaled
  18. What are the adverse effects of zanamivir?
    • May worsen resp fxn in COPD
    • May cause bronchospasm in asthmatics
  19. Of oseltamivir?
    Nausea and vomiting, better if taken c food
  20. What are amantadine and rimantidine used for?
    Influenza A only
  21. What is their MOA?
    Blocks uncoating of virus
  22. What are the adverse effects of amantadine?
    Causes release of DA ? hallucinations (used in Parkinson's)
  23. How does rimantidine differ?
    Same mechanism, but doesn't cross BBB ? no hallucinations
  24. When is ribavirin used?
    RSV and Hep C
  25. What is its MOA?
    Purine analogue phosphorylated by virus that inhibits RNA polymerase and synthesis of GTP
  26. How is it given?
    Aerosol (for RSV), IV, and oral
  27. When is it give IV?
    Lassa fever and SARS
  28. How is it given in Hep C?
    combined c interferon
  29. What are the adverse effects?
    Dyspnea, anemia, depression, TERATOGENIC!
  30. What is the DOC for chronic Hep B?
    Lamivudine (don't treat acute Hep B)
  31. What is its MOA?
    Inhibits HBV polymerase and reverse transcriptase (HIV)
  32. What are other Rx used?
    • Adefovir_renal toxicity and lactic acidosis
    • Entacavir
    • Telbivudine_similar to lamivudine
  33. What are the antiviral mechanisms of the interferons?
    • A,B: blocks viral entry
    • 1: blocks transcription and translation of mRNA
    • 2: blocks viral replication
    • 3: blocks viral processing
    • 4,5: blocks viral assembly and release
  34. How is Hep C treated?
    Alfa-2b c ribavirin
  35. What are the side effects of interferon therapy?
    • Flu-like: aches, pains, nausea
    • Depression, suicide (use an antidepressant)
    • Anemia (worse when combined c ribavirin, telaprevir, or boceprevir)
  36. What are boceprevir and telaprevir?
    Protease inhibitors against Hep C
  37. When are they used?
    • For pts c type 1 Hep C genotype when interferon/ribavirin is not effective
    • What are their side effects?
    • Strong inhibition of CYP3A4_many Rx interactions
    • Pancytopenia, rash
  38. What is the MOA of the HIV reverse transcriptase inhibitors?
    Nucleoside analogs incorporated into DNA that inhibit viral reverse transcriptase and prevent conversion of RNA ? DNA
  39. What can happen if they inhibit human mitochondrial DNA polymerase?
    Anemia, peripheral neuropathy, and pancreatitis
  40. What are non-HIV uses of zidovudine?
    Psoriasis and T-cell leukemia
  41. What are its side effects?
    • Neutropenia, anemia-->caution if bone marrow is compromised
    • Lactic acidosis or hepatotoxicity-->STOP if these develop
  42. What are the Rx interactions?
    • Synergistic toxicity c neurotoxic, nephrotoxic, or myelosuppressive Rxs
    • Cimetidine, benzos inhibit metabolism
    • Probenecid ? elimination
    • Acetaminophen, ganciclovir ? risk of granulocytopenia
  43. What is the 1st choice combo in Tx of HIV?
  44. What is the 2nd choice?
  45. What is the MOA of lamivudine?
    Inhibits HIV RT and HBV polymerase (can be used as monotherapy in Hep B)
  46. What other antiretroviral is used for Hep B?
  47. Which anti-RVs cause peripheral neuropathy?
    Didanosine, stavudine, zalcitabine
  48. Which cause lactic acidosis?
    Didanosine, stavudine, zalcitabine, zidovudine
  49. Which cause anemia, agranulocytopenia?
    Zidovudine, didanosine
  50. What are the non-nucleotide RTIs?
    Efavirenz, nevirapine, delaviridine, etravirine
  51. What is their MOA?
    Bind directly to, and inhibit viral RT
  52. How are they given?
    ONLY c nucleoside analogues (rapid resistance occurs)
  53. What are the Rx interactions?
    Interact c protease inhibitors
  54. What is the preferred Rx?
  55. When is it NOT the 1st choice?
  56. Which other non-nucleotide RTI is teratogenic?
  57. Which non-nucleoside RTI can cause hepatitis and Stevens-Johnson syndrome?
  58. How are the protease inhibitors used?
    In combo c NRTIs
  59. What are their Rx interactions?
    • Metabolized by CYP3A4:
    • Rx that inhibit CYP3A4:
    • Rx that induce CYP3A5: St. Johns wort, rifampin, phenytoin, barbiturates
  60. What are their side effects?
    • Altered body fat distribution: buffalo hump, truncal obesity, facial atrophy
    • Insulin resistance and hyperglycemia
    • ? cholesterol, TGs, atherosclerosis, CVAs, MIs
    • Due to inhibition of CYP --> DO NOT combine c statins
  61. What is the 1st choice protease inhibitor and why?
    Atazanavir: dosed 1X/day, less effect on lipoproteins
  62. What is its major side effect?
    ? bilirubin due to inhibition of UGT-A1
  63. What is the PI of 2nd choice?
    Darunavir (combined c ritonavir)
  64. What effect does ritonavir have when combined c other PIs?
    ? their bioavailability
  65. What are the adverse effects?
    • Inhibits CYP3A4 --> many interactions
    • Contains EtOH --> caution when using c metronidazole
  66. What ? the bioavailability of saquinavir?
    High fat foods, grapefruit, ritonavir
  67. What are the adverse effects of indinavir?
    • Cross resistance c ritonavir
    • Nephrolithiasis, hyperbilirubinemia
  68. What are the side effects of amprenavir/fosamprenavir?
    • Contains propylene glycol --> avoid metronidazole
    • Stevens-Johnson syndrome
  69. What is the non-pepiditic protease inhibitor?
  70. What are the fusion inhibitors?
    Enfuviritide and maraviroc
  71. What is their MOA?
    Bind viral envelope and prevent fusion
  72. When are they used?
    In advanced disease when other Rx are beginning to fail
  73. How is enfuvirtide given?
  74. What is the major side effect?
    ? risk of pneumonia
  75. What is the only integrase inhibitor?
    Raltegravir (used when others stop working)
  76. What are the current Tx guidelines?
    • Tenofovir or emtricatibine
    • ZDV+lamivudine (2nd choice)
    • Efavirenz (switch to nevirapine in pregnancy)
    • Atazanavir