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antiviral pharmacology


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Viral adsorption and penetration into the cell is blocked by ---------.
Gama-globulins (non-specific).
Uncoating of the virus after its penetration into the cell is blocked by --------.
Amantadine (influenza A).
Antiviral chemotherapy: Early viral protein synthesis is blocked by --------.
Fomivirsen (CMV).
Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.
Purine, pyrimidine analogs; reverse transcriptase inhibitors.
Late viral protein synthesis and processing is blocked by --------.
Methimazole (variola); protease inhibitors.
Antiviral chemotherapy: Packaging and assembly of new viron is blocked by --------.
Rifampin (vaccinia).
Mechanism of action of Amantadine.
Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
Clinical uses of Amantadine.
Prophylaxis for influenza A; Parkinson's disease.
Symptoms of Amantadine toxicity.
Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.) "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."
Mechanism of action of Zanamivir.
Inhibits influenza neuraminidase.
Clinical use of Zanamivir.
Both influenza A and B.
Mechanism of action of Ribavirin.
Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
Clinical use of Ribavirin.
RSV (respiratory syncytial virus).
Symptoms of Ribavirin toxicity.
Hemolytic anemia. Severe teratogen.
Mechanism of aciton of Acyclovir.
Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.
Clinical use of Acyclovir.
HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.
Symptoms of Acyclovir toxicity.
Delirium, tremor, nephrotoxicity.
Mechanism of action of Ganciclovir.
Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
Clinical use of Ganciclovir.
CMV, especially in immunocompromised patients.
Symptoms of Ganciclovir toxicity.
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
Mechanism of action of Foscarnet.
Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
Clinical use of Foscarnet.
CMV retinitis in immunocompromised patients when ganciclovir fails.
Foscarnet toxicity.
Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
Protease inhibitor.
Mechanism of action of protease inhibitors.
Inhibit assembly of new virus by blocking protease enzyme.
Symptoms of protease inhibitor toxicity.
GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).
Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.
Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.
Mechanism of action of reverse transcriptase inhibitors.
Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.
Symptoms of reverse transcriptase inhibitor toxicity.
Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.
Protease inhibitors, reverse transcriptase inhibitors.
When should HIV therapy be initiated?
When patients have low CD4 counts (<500 cells/mm3) or high viral load.
Mechanism of action of Interferons.
Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.
Clinical use of Interferons.
Chronic hepatitis B and C, Kaposi's sarcoma.
Symptoms of Interferon toxicity.

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