Pharmacology- Microbiology Antiviral Therapy

Front 1

Amantidine
-Mechanism

Back 1

Blocks viral penetration/ uncoating (M2 protein); may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals
A man to dine takes off his coat

Front 2

Amanitidine
-Clinical use

Back 2

Prophylaxis and treatment for Influenza A; Parkinson disease

"Amantadine blocks influenza A and rubella and causes problem with the cerebella

Front 3

Amantadine
-Toxicity

Back 3

Ataxia, dizziness, slurred speech

Front 4

Amantadine
-Mechanism of resistance

Back 4

Mutated M2 protein (90% of all influenza A strains are resistant to amantadine, so not used)

Front 5

Rimantidine
-What is it?

Back 5

Derivative of Amantadine with fewer CNS side effects. Does not cross the blood-brain barrier

Front 6

Zanamivir, oseltamivir
-Mechanism

Back 6

Inhibit influenza neuraminidase, decreasing release of progeny virus

Front 7

Zanamivir
-Clinical use

Back 7

Influenza A and B

Front 8

Ribavirin
-Mechanism

Back 8

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase

Front 9

Ribavirin
-Clinical use

Back 9

RSV, Chronic Hepatitis C

Front 10

Ribavirin
-Toxicity

Back 10

Hemolytic anemia, Severe teratogen

Front 11

Acyclovir
-Mechanism

Back 11

Monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog, triphosphate formed by cellular enzyme.
*Preferentially inhibits viral DNA polymerase by chain termination

Front 12

Acyclovir
-Clinical use

Back 12

HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephatlitis. Prophylaxis in immunocompromised patients. No effect on latent form of HSV and VZV

Front 13

Acyclovir
-Mechanism of resistance

Back 13

Lack of thymidine kinase

Front 14

Acyclovir
-Toxicity

Back 14

Generally well tolerated

Front 15

Ganciclovir
-Mechanism

Back 15

5'-Monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Tripohosphate formed by cellular kinases. Preferentially inhibits Viral DNA polymerase
As opposed to Acyclovir gets phosphorylated by the body thats why get side effects

Front 16

Ganciclovir
-Clinical use

Back 16

CMV, especially in immunocompromised patients

Front 17

Ganciclovir
-Toxicity

Back 17

Leukopenia, Neutropenia, Thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir

Front 18

Ganciclovir
-Mechanism of resistance

Back 18

Mutated CMV DNA polymerase or lack of viral kinase

Front 19

Foscarnet
-Mechanism

Back 19

Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase
FOScarnet= pyroFOSphate analog

Front 20

Foscarnet
-Clinical use

Back 20

CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSV

Front 21

Foscarnet
-Toxicity

Back 21

Nephrotoxicity

Front 22

Foscarnet
-Mechanism of resistance

Back 22

Mutated DNA polymerase

Front 23

Protease inhibitor
-Mechanism

Back 23

Used for HIV inhibits maturation of new virus by blocking protease in progeny virus

Front 24

Saquinavir
-Type of drug

Back 24

Protease inhibitor (-navir) Navir tease a protease

Front 25

Protease inhibitor
-Toxicity

Back 25

GI intolerance (nausea, diarrhea), hyperglycemia, lipodystrophy, thrombocytopenia (indinavir)

Front 26

Zidovudine
-Type of drug

Back 26

Nucleosides Reverse transcriptase inhibitors

Front 27

Stavudine (d4T)
-Type of drug

Back 27

Nucleosides Reverse transcriptase inhibitors

Front 28

Lamivudine (3TC)
-Type of drug

Back 28

Nucleosides Reverse transcriptase inhibitors

Front 29

Nevirapine
-Type of drug

Back 29

Non-nucleosides reverse transcriptase inhibitors

Front 30

Efavirenz
-Type of drug

Back 30

Non-nucleosides reverse transcriptase inhibitors

Front 31

Delavirdine
-Type of drug

Back 31

Non-nucleosides reverse transcriptase inhibitors
Never ever decline nucleosides

Front 32

Nevirapine
-Mechanism of action

Back 32

Non-nucleosides reverse transcriptase inhibitors
*Preferentially inhibit reverse transcriptase of HIV prevent incorporation of DNA copy of viral genome into host DNA RNA-dependent DNA polymerase

Front 33

Efavirenz
-Toxicity

Back 33

Non-nucleosides reverse transcriptase inhibitors
Bone marrow suppression (neutropenia, anemia), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), Megaloblastic anemia (ZDV)

Front 34

Non-nucleosides reverse transcriptase inhibitors
-Clinical use

Back 34

Highly active antiretroviral theraphy (HAART) generally entails combination therapy with protease inhibitors and reverse transcriptase inhibitors. Initiated when patients have low CD4 counts (<500 cells/mm3) or high viral load

Front 35

What is used as general prophylaxis and during pregnancy to risk transmission of HIV to fetus

Back 35

ZDV (Zidovudine)

Front 36

What can be given to prevent effects of reverse transcription inhibitors?

Back 36

GM-CSF and erythropoetin can be used to reduce bone marrow suppression

Front 37

Enfuvirtide
-Mechanism

Back 37

Fusion inhibitors, bind viral gp41 subunit; inhibit conformational change required for fusion with CD4 cells. Therefore block entry and subsequent replication

Front 38

Enfuvirtide
-Toxicity

Back 38

Hypersensitivity reactions, reactions at subcutaneous injection site, increase risk of bacterial pneumonia

Front 39

Enfuvirtide
-Clinical use

Back 39

In patients with persistent viral replications in spite of antiretroviral therapy. Used in combination with other drugs

Front 40

Interferons
-Mechanism

Back 40

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. Induce ribonuclease that degrades vital mRNA

Front 41

Interferons
-Clinical use

Back 41

IFN-alpha (Chronic Hep B and C, Kaposi's Sarcoma)
IFN-Beta - MS
IFN-Gamma- NADPH oxidase deficiency

Front 42

Interferons
-Toxicity

Back 42

Neutropenia