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Microbiology > antiviral (not HIV and hepatitis) > Flashcards

antiviral (not HIV and hepatitis) Flashcards

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1
Q

antiviral therapy (except HIV) - only the groups according their action

A
  1. protein synthesis inhibitors
  2. Uncoating agents
  3. nucleic acid synthesis inhibitors
    4 release of progeny virus inhibitors
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2
Q

release of progeny virus inhibitors - agents and mechanism of action

A
  1. Oseltamivir
  2. zanamivir
    inhibit influenza neuraminidase
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3
Q

release of progeny virus inhibitors - clinical use

A

treatment and PREVENTION of both infleunza A and B

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4
Q

nucleic acid synthesis inhibitors - groups and agents

A
  1. Guanosine analogs: Acyclovir, famciclovir, valacyclovir, ganciclovir
  2. viral DNA polymerase inhibitors: Cidofovir, foscarnet
  3. Guanine nucleotide synthesis inhibitos: Ribavirin
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5
Q

nucleic acid synthesis inhibitors - Guanosine analogs - drugs

A
  1. Acyclovir
  2. famciclovir
  3. valacyclovir
  4. ganciclovir
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6
Q

Acyclovir, famciclovir, valacyclovir - mechanism of action

A

guanosine analog –> Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells (few adverse effects) –> Triphosphate formed by cellular enzymes –> preferentially inhibit viral DNA polymerase by chain termination

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7
Q

Acyclovir, famciclovir, valacyclovir - active against

A
  1. HSV
  2. VZV
  3. EBV (weak)
    NOT CMV
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8
Q

Acyclovir, famciclovir, valacyclovir - clinical use

A
  1. HSV-induced mucocutaneous lesion (hepres)
  2. HSV-induced genital lesion (hepres)
  3. HSV-encephalitis
  4. prophylaxis in immunocompromised
  5. Hairy cell leukoplakia
  6. hepres zoster (famciclovir)
    NO EFFECT ON LATENT STATE
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9
Q

Herpes zoster - treatment

A

famciclovir

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10
Q

Acyclovir vs valacyclovir according to bioavailability

A

Valaciclovir is a prodrug of acyclovir –> better oral bioavailability

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11
Q

Acyclovir, famciclovir, valacyclovir - toxicity

A
  1. obstructive cystalline neuropathy

2. acute renaL failure if not adequately hydrated

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12
Q

Acyclovir, famciclovir, valacyclovir - resistance

A

Mutated viral thimidine kinase

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13
Q

Ganciclovir - mechanism of action

A

5-Monophosphated formed by CMV viral kinase –> Triphosphate formed by cellular enzymes –> preferentially inhibits viral DNA polymerase by chain termination

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14
Q

Ganciclovir - clinical use

A

CMV, especially in immunocomprommised patients

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15
Q

Ganciclovir - oral

A

Valganciclovir, a prodrug of ganciclovir –> better oral bioavailability

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16
Q

acyclovir and ganciclovir - oral

A
  • Valaciclovir is a prodrug of acyclovir –> better oral bioavailability
  • Valganciclovir, a prodrug of ganciclovir –> better oral bioavailability
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17
Q

ganciclovir - toxicity

A
  1. leukopenia
  2. neutropenia
  3. thrombocytopenia
  4. Renal toxicity
18
Q

ganciclovir vs acyclovir according to toxicity on host cells

A

ganciclovir is more toxic to host enzymes than acyclovir

19
Q

ganciclovir - resistance

A

mutated viral kinase

20
Q

nucleic acid synthesis inhibitors - Guanosine analogs - drugs

A
  1. Acyclovir
  2. famciclovir
  3. valacyclovir
  4. ganciclovir
21
Q

viral DNA polymerase inhibitors - drugs

A
  1. Cidofovir

2. foscarnet

22
Q

Foscarnet - mechanism of action

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor. Binds to pyrophophate-binding site of enzyme. Does not require activation of viral kinase (PYROPHOSPHATE ANALOG)

23
Q

Foscarnet inhibits

A
  1. Viral DNA/RNA polymerase

2. HIV reverse transcriptase

24
Q

Foscarnet - clinical use

A
  1. CMV retinitis in immunocomporomised patients when gancyclovir fails
  2. Acyclovir resistant HSV
25
Q

Foscarnet - toxicity

A
  1. nephrotoxicity
  2. electrocyte abnormalities (hypo- hypercalcemia, hypo- hyperphosphatemia, hypokalemia, hypomagnesemia) –> can lead to seizures
26
Q

Foscarnet - mechanism of resistance

A

Mutated DNA polymerase

27
Q

viral DNA polymerase inhibitors - drugs

A
  1. Cidofovir

2. foscarnet

28
Q

Cidofovir - mechanism of action

A

Preferentially inhibits viral DNA polymerase. Does not require phosphoryation by viral kinase. LONG HALF LIVE

29
Q

Cidofovir - clinical use

A
  1. CMV retinitis in immunocompromised patients

2. Acyclovir-resistant HSV

30
Q

cidofovir vs foscarnet according to half live

A

Cidofovir has LONG HALF LIVE

31
Q

Cidofovir - toxicity

A

nephrotoxicity

32
Q

Cidofovir - toxicity - solution

A

coadminister with probenecid and IV saline to decrease toxicity

33
Q

antiviral therapy (except HIV) - only the groups according their action

A
  1. protein synthesis inhibitors
  2. Uncoating agents
  3. nucleic acid synthesis inhibitors
    4 release of progeny virus inhibitors
34
Q

antiviral - protein synthesis inhibitors - drugs

A

interderon-a

35
Q

interderon - α - mechanism of action as an antiviral

A

protein synthesis inhibitors

36
Q

Interferons as antivirals / types

A

Glycoproteins normaly synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties
α, β, γ interferons

37
Q

interferons - clinical use

A

Interferons - α: 1. chronic hepatitis B, C 2. Kaposi sarcoma 3. hairy cell leukemia 4. condyloma acuminatum 5. renal cell carcinoma 6. malignant melanoma
Interferons - β: multiple sclerosis
Interferons - γ: chronic granulomatous disease

38
Q

interferons - side effects

A
  1. neutropenia
  2. myopathy
  3. Flu-like symptoms
  4. depression
39
Q

antiviral therapy - uncoating agents - drugs - clinical use

A
  1. Amantadine
  2. Rimantadine
    no longer useful for influenza due to increased resistance
40
Q

amantadine - clinical use and side effect

A

clinical use: 1. antiviral (rubella, infl A) 2. Parkinson

side effects: 1. ataxia 2. livedo reticularis

Microbiology (25 decks)

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