Antivirals Flashcards Preview

CBSE Pharm > Antivirals > Flashcards

Flashcards in Antivirals Deck (84):
1

MOA of zanamivir and oseltamivir 

Inhibit influenza neuraminidase --> decrease Žthe release of progeny virus. 

2

Inhibit influenza neuraminidase --> decrease Žthe release of progeny virus. 

MOA of zanamivir and oseltamivir 

3

Use of zanamivir and oseltamivir 

Treatment and prevention of both influenza A and B. 

4

Treatment and prevention of both influenza A and B. 

Use of zanamivir and oseltamivir 

5

MOA of ribavirin

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase. 

6

Inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase. 

MOA of ribavirin

7

Use of ribavirin

RSV, chronic hepatitis C

8

RSV, chronic hepatitis C

Use of ribavirin

9

toxicity of ribavirin

Hemolytic anemia. Severe teratogen 

10

Hemolytic anemia. Severe teratogen 

toxicity of ribavirin

11

MOA of Acyclovir, famciclovir, valacyclovir 

  • Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells --> Žfew adverse effects.
  • Guanosine analog.
  • Triphosphate formed by cellular enzymes.
  • Preferentially inhibits viral DNA polymerase by chain termination. 

12

  • Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells --> Žfew adverse effects.
  • Guanosine analog.
  • Triphosphate formed by cellular enzymes.
  • Preferentially inhibits viral DNA polymerase by chain termination. 

MOA of Acyclovir, famciclovir, valacyclovir 

13

Use of Acyclovir, famciclovir, valacyclovir 

  • HSV and VZV. Weak activity against EBV. No activity against CMV.
  • Used for HSV- induced mucocutaneous and genital lesions as well as for encephalitis.
  • Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV.
  • Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
  • For herpes zoster, use a related agent, famciclovir.

14

  • HSV and VZV. Weak activity against EBV. No activity against CMV.
  • Used for HSV- induced mucocutaneous and genital lesions as well as for encephalitis.
  • Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV.
  • Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
  • For herpes zoster, use a related agent, famciclovir.

Use of Acyclovir, famciclovir, valacyclovir 

15

Toxicity of Acyclovir, famciclovir, valacyclovir 

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. 

16

Obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. 

Toxicity of Acyclovir, famciclovir, valacyclovir 

17

MOR to Acyclovir, famciclovir, valacyclovir 

Mutated viral thymidine kinase 

18

Mutated viral thymidine kinase 

MOR to Acyclovir, famciclovir, valacyclovir 

19

MOA of ganciclovir

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. 

20

5′-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. 

MOA of ganciclovir

21

Use of ganiciclovir

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability 

22

CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability 

Use of ganiciclovir

23

toxicity of ganiciclovir

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir. 

24

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir. 

toxicity of ganiciclovir

25

MOR of ganiciclovir

Mutated CMV DNA polymerase or lack of viral kinase. 

26

Mutated CMV DNA polymerase or lack of viral kinase. 

MOR of ganiciclovir

27

MOA of Foscarnet 

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

28

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

MOA of Foscarnet 

29

Use of foscarnet

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

30

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

Use of foscarnet

31

toxicity of foscarnet

Nephrotoxicity.

32

MOR of foscarnet

Mutated DNA polymerase 

33

MOA of cidofovir

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase. 

34

Preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase. 

MOA of cidofovir

35

Use of cidofovir

CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life. 

36

CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half-life. 

Use of cidofovir

37

toxicity of cidofovir

Nephrotoxicity (coadminister with probenecid and IV saline to decrease toxicity). 

38

HIV drug treatment

Highly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (< 500 cells/mm3), or high viral load. Regimen consists of 3 drugs to prevent resistance:

[2 nucleoside reverse transcriptase inhibitors (NRTIs)] +
[1 non-nucleoside reverse transcriptase inhibitor (NNRTI) OR 1 protease inhibitor OR 1

 

integrase inhibitor] 

39

Protease inhibitors

  • Atazanavir, Darunavir, Fosamprenavir, Indinavir, Lopinavir, Ritonavir, Saquinavir 
  • All protease inhibitors end in -navir. Navir (never) tease a protease. 

40

  • Atazanavir, Darunavir, Fosamprenavir, Indinavir, Lopinavir, Ritonavir, Saquinavir 
  • All protease inhibitors end in -navir. Navir (never) tease a protease. 

Protease inhibitors

41

MOA of protease inhibitors

  • Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. 

42

  • Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. 

MOA of protease inhibitors

43

use of Ritonavir

 can “boost” other drug concentrations by inhibiting cytochrome P-450. 

44

 can “boost” other drug concentrations by inhibiting cytochrome P-450. 

use of Ritonavir

45

toxicity of protease inhibitors

  • Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy.
  • Nephropathy, hematuria (indinavir). 

46

  • Hyperglycemia, GI intolerance (nausea, diarrhea), lipodystrophy.
  • Nephropathy, hematuria (indinavir). 

toxicity of protease inhibitors

47

NRTI's

Abacavir (ABC), Didanosine (ddI), Emtricitabine (FTC), Lamivudine (3TC), Stavudine (d4T), Tenofovir (TDF), Zidovudine (ZDV, formerly AZT) 

48

Abacavir (ABC), Didanosine (ddI), Emtricitabine (FTC), Lamivudine (3TC), Stavudine (d4T), Tenofovir (TDF), Zidovudine (ZDV, formerly AZT) 

NRTI's

49

MOA of NRTIs

  • Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group).
  • Tenofovir is a nucleoTide; the others are nucleosides and need to be phosphorylated to be active. 

50

  • Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3′ OH group).
  • Tenofovir is a nucleoTide; the others are nucleosides and need to be phosphorylated to be active. 

MOA of NRTIs

51

Use of Zidovudine

used for general prophylaxis and during pregnancy torisk of fetal transmission. 

52

used for general prophylaxis and during pregnancy torisk of fetal transmission. 

Use of Zidovudine

53

Toxicity of NRTIs

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV), pancreatitis (didanosine). 

54

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV), pancreatitis (didanosine). 

Toxicity of NRTIs

55

NNRTIs

Efavirenz, Nevirapine, Delavirdine 

56

Efavirenz, Nevirapine, Delavirdine 

NNRTIs

57

MOA of NNRTIs

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides. 

58

Bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides. 

MOA of NNRTIs

59

Toxicity of NNRTIs

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy. 

60

Rash and hepatotoxicity are common to all NNRTIs. Vivid dreams and CNS symptoms are common with efavirenz. Delavirdine and efavirenz are contraindicated in pregnancy. 

Toxicity of NNRTIs

61

integrase inhibitors

Raltegravir 

62

Raltegravir 

integrase inhibitors

63

MOA of raltegravir

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase. 

64

Inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase. 

MOA of raltegravir

65

toxicity of raltegravir

Hypercholesterolemia 

66

Hypercholesterolemia 

toxicity of raltegravir

67

fusion inhibitors

Enfuvirtide, Maraviroc 

68

Enfuvirtide, Maraviroc 

fusion inhibitors

69

MOA of Enfuvirtide 

Binds gp41, inhibiting viral entry. 

70

Binds gp41, inhibiting viral entry. 

MOA of Enfuvirtide 

71

Toxicity of enfuviritide

Skin reaction at injection sites. 

72

Skin reaction at injection sites. 

Toxicity of enfuviritide

73

MOA of maraviroc

Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120. 

74

Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120. 

MOA of maraviroc

75

MOA of interferons

Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties. 

76

Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties. 

MOA of interferons

77

Use of IFN-alpha

chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. 

78

chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. 

Use of IFN-alpha

79

use of IFN-beta

multiple sclerosis

80

multiple sclerosis

use of IFN-beta

81

Use of IFN-gamma

chronic granulomatous disease 

82

chronic granulomatous disease 

Use of IFN-gamma

83

toxicity of interferons

Neutropenia, myopathy. 

84

Neutropenia, myopathy. 

toxicity of interferons