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Block 3 Pharm > Antiviral I > Flashcards

Antiviral I Flashcards

1
Q

Viruses are Obligate intracellular parasites… Enter living cells and take over cell’s synthetic machinery.
________core surrounded by protein sheath or lipid-protein envelope.

A

Nucleic acid

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2
Q

Viral latency—

A

some can integrate into host chromosome allowing for recurrence of
clinical infection without re-exposure to viral agent.

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3
Q

After virus is absorbed or penetrates, it has to

A

uncoat proteins from nucleic acids

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4
Q

Main point of attack for antivirals

A

Any of the stages of the viral life cycle, so long as agent is nontoxic/ adequately specific

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5
Q

In many viral infections viral replication is at maximum when

A

viral replication reaches a maximum near the time clinical symptoms first appear (influenza, poxviruses)

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6
Q

Drugs are most effective if administered

A

before onset of symptoms, except herpes bc replication continues after appearance of clinical signs

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7
Q

Key issues of viral infections

A

side effects/toxicity
occurance of resistant strains
latent (dormant form) and recurrent infections
carcinogenicty
need to have competent host immune system

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8
Q

Uses of passive immunization

A

injection of immune globulin will block viral penetration before disease
can modify course of disease if given early enough IV or IM

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9
Q

Viral replication rate is reduced by blocking viral entry into cells; may allow for
active immunity to develop.

A

passive immunization

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10
Q

Prophylaxis against influenza A but not influenza B

A

Amantidine

~ works about 70% time

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11
Q

Amantidine is given to pts w/ influenza A and will

A

Reduces fever in 50% of patients and illness

duration by 1-2 days if given within first 2 days of illness

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12
Q

Issue we’ve seen with amantidine in the past few years

A

influenzas have been resistant

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13
Q

Mech for amantidine

A

Blocks viral uncoating by interfering with influenza A M2 protein (an ion
channel

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14
Q

Blocks viral uncoating by interfering with influenza A M2 protein (an ion
channel

A

Amantidine

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15
Q

Metabolism and excretion in amantidine

A

90% excreated unchaged in urine and REDUCE dose in RENAL disease

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16
Q

Toxicity of Amantidine

A

CNS effects

slurred speech, anxiety, confusion, depression, headache

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17
Q

inactive prodrug …converted to active competitive inhibitor of influenza neuraminidases;

A

Oseltamivir

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18
Q

Oseltamivir is a prodrug that will inhibit neuramidase.. this is effective because

A

it interferes with viral release

from infected cells and viral penetration into respiratory epithelium

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19
Q

treatment of uncomplicated influenza A and B in patients ≥1 year old and prophy

A

Oseltamivir

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20
Q

Admin of Oseltamivir

A

2x day for 5 days with renal elimination

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21
Q

side effects in Oseltamivir

A

bronchitis, vomit, diahrrhea

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22
Q

decreases risk of serious influenza in 71% of adults and decrease chance of pnemonia in children

A

Oseltamivir

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23
Q

Interferes with DNA synthesis; thymidine analog.

A

Trifluridine

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24
Q

Trifluridine mech

A

interferes with DNA synthesis, thymidine analog

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25
Q

Uses of trifluridine

A

Ophthalmic herpes type 1 and 2 but not useful prophylactically

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26
Q

Ophthalmic herpes type 1 and 2 but not useful prophylactically

A

Trifluridine

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27
Q

guanosine derivative; inhibits DNA polymerase.
Phosphorylated form is produced 40-100x faster in infected cells by herpes thymidine kinase;
inhibits herpes DNA polymerase 10-30x more than host cell DNA polymerase; acts as a competitive inhibitor of dGTP and as a DNA chain terminator.

A

Acyclovir

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28
Q

acts as a competitive inhibitor of dGTP and as a DNA chain terminator

A

Acyclovir

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29
Q

Acyclovir mech

A

inhibits DNA polymerase by activing like a competitive inhibitor of dGTP and as DNA chain terminator

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30
Q

IV Drug of choice for serious systemic herpes simplex virus (HSV), including HSV encephalitis

A

Acyclovir

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31
Q

IV, acyclovir is used for

A

Drug of choice for serious systemic herpes simplex virus (HSV), including HSV encephalitis and severe initial genital herpes

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32
Q

Oral drug to tx Primary herpetic gingivostomatosis

A

Acyclovir

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33
Q

______ used to tx primary genital herpes

A

acyclovir

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34
Q

Approved for chickenpox in children

A

Acyclovir

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35
Q

Side of Acyclovir

A

IG, well tolerated, rash, itch, nasuea

can be nephrotoxic or cause thrombophleibits

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36
Q

Similar to acyclovir; prodrug that is converted to penciclovir which is then phosphorylated—this is what inhibits viral DNA polymerase.

A

Famciclovir

37
Q

Mech of Famciclovir

A

Similar to acyclovir; prodrug that is converted to penciclovir which is then phosphorylated—this is what inhibits viral DNA polymerase.

38
Q

recurrent genital herpes and herpes zoster within 3 days of onset

A

Famciclovir

39
Q

Oral; prodrug absorbed better than acyclovir

- less frequent dosing than acyclovir; renal elimination.

A

Famciclovir

40
Q

Famciclovir sides:

A

Generally well-tolerated. - Rash, itching, nausea, vomiting, headache, fatigue

41
Q

Penciclovir mech

A

simular to acyclovir

42
Q

used for recurrent herpes of lips and face as topical cream

A

Penciclovir

43
Q

similar to acyclovir, except the monophosphorylation is catalyzed byCMV protein kinase; virustatic.

A

Ganciclovir

44
Q

Mech of ganciclovir

A

similar to acyclovir, except the monophosphorylation is catalyzed byCMV protein kinase; virustatic.

45
Q

Used to tx CMV retinitis in AIDS and CMV prophy for transplant pts

A

Ganciclovir

46
Q

Use of Ganciclovir

A

Used to tx CMV retinitis in AIDS and CMV prophy for transplant pts

47
Q

Admin and exreation of Ganciclovir

A

IV or oral

unchanged in urine

48
Q

Sides of Ganciclovir

A

Bone marrow suppression, leukopenia, thrombocytopenia, anemia.
- May enhance bone marrow suppression when given with zidovudine (AZT)

49
Q

Bone marrow suppression, leukopenia, thrombocytopenia, anemia. - May enhance bone marrow suppression when given with zidovudine (AZT)

A

Ganciclovir

50
Q

inhibits CMV DNA polymerase by binding to its pyrophosphate-binding site; this blocks viral DNA synthesis
- Does not require conversion to triphosphate form to be active.

A

Foscarnet

51
Q

Mech of Foscarnet

A

inhibits CMV DNA polymerase by bindint to pyrophostape binding ste to block viral DNA synthesis

52
Q

Use of Foscarnet

A

AIDS patients with CMV (cytomegalovirus) retinitis and

acyclovir-resistant herpes simplex.

53
Q

Drug to tx AIDS patients with CMV (cytomegalovirus) retinitis andacyclovir-resistant herpes simplex.

A

Foscarnet

54
Q

Side effects of Foscarnet

A

Renal damage (30–50%), reversible (enhanced with amphotericin B).

  • Electrolyte imbalances
  • seizures
55
Q

Nucleoside analog inhibitor of the reverse transcriptase domain of the hepatitis B DNA polymerase; must be phosphorylated by cell enzymes to be active.

A

Lamivudine

56
Q

Mech of Lamivudine

A

Nucleoside analog inhibitor of the reverse transcriptase domain of the hepatitis B DNA polymerase; must be phosphorylated by cell enzymes to be active.

57
Q

used to tx hep B

A

Lamivudine and Tenofovir

58
Q

Use of Lamivudine and admin

A

Hep B and oral with 85% bioavailable

59
Q

Side of Lamivudine

A

nausuea and diarrhea

60
Q

esterified adenosine monophosphate analog phosphorylated by cell enzymes to the
active nucleotide
- inhibits the reverse transcriptase domain of the hepatitis B DNA polymerase

A

Tenofovir

61
Q

Tenofovir ultimately will

A

inhibits the reverse transcriptase domain of the hepatitis B DNA polymerase

62
Q

Tenofovir is for and it’s admin

A

Hep B

25% oral bioavailable

63
Q

Sides of Tenofovir

A

GI upset

64
Q

Mech of Ribavirin

A

interferes with viral mRNA synthesis

Mono-P form will inhibit inosine 5’P DH thus inhibits GTP synthesis

65
Q

Tri-P form will inhibit:

for Ribivarin

A

Tri-P form inhibits GTP-dependent capping of viral mRNA

66
Q

Mono-P form inhibits_________ and thus GTP synthesis

A

inosine-5’-P dehydrogenase

67
Q

aerosol use in carefully selected infants and young children with documented severe
lower respiratory syncytial virus (RSV) infections

A

Ribivarin

68
Q

USed to tx Hepatitis C (oral) in combination with interferon-α

A

Ribivarin

69
Q

Use of Ribavirin

A

aerosol use in carefully selected infants and young children with documented severe
lower respiratory syncytial virus (RSV) infections
• Hepatitis C (oral) in combination with interferon-α

70
Q

used to tx Lower RSV infections

A

Ribavirin

71
Q

Metabolsim of Ribavirin

A

hepatic metabolism; very slow clearance from blood; some metabolites and
unmetabolized drug excreted in urine

72
Q

Toxicity of Ribavirin in aerosol form

A

In aerosol form: Exercise caution with assisted ventilation (requires special aerosol equipment as drug may precipitate in and clog respiratory equipment)

73
Q

CAn cause Pulmonary function deterioration (respiratory depression, lung inflammation) in aerosol use

A

Ribavirin

74
Q

In IV form, Ribavirin can cause:

A

anemia and bone marrow suppresion

75
Q

Induce host cells to produce enzymes that block translation of viral mRNA.

A

Interferon

76
Q

Host produced proteins

Exert virus-nonspecific antiviral activities; active only in species in which they are produced

A

Interferon

77
Q

EnZ induced by Interferons:

A

Protein kinase—phosphorylates elongation factor. Oligoisoadenylate synthetase—activates RNase that degrades viral mRNA.
Phosphodiesterase—degrades terminal nucleotides of tRNA.

78
Q

Treatment of hairy cell leukemia and AIDS-related Kaposi’s sarcoma

A

Interferon

79
Q

2nd line for Condyloma acuminata (venereal warts)

A

Interferon alpha

80
Q

Hepatitis B and C (improves disease course in 40–50%

A

Interferon alpha

81
Q

PEG-alfa-2a and PEG-alfa-2b interferons in combination with ribavirin are specifically useful for

A

hepatitis C

82
Q

Toxicity for interferon alpha

A

Flu-like syndrome. Leukopenia, bone marrow suppression. Neurotoxicity, myalgia.

83
Q

Toxicity: Flu-like syndrome. Leukopenia, bone marrow suppression. Neurotoxicity, myalgia

A

Interferon A

84
Q

reversible inhibitor of hepatitis C NS3 protease, thus blocking formation of infectious
virus particles

A

Boceprevir

85
Q

Boceprevir mech

A

reversible inhibitor of Hep C NS3 protease to block formation of infectious virus particles

86
Q

Boceprevir works by reversible inhibitor of hepatitis C ______, thus blocking formation of infectious
virus particles

A

NS3 protease

87
Q

Uses of Boceprevir

A

hepatitis C genotype 1, in combination with PEG-interferon + ribavirin

88
Q

Admin and elimiatino of Boceprevir

A

oral 3x day and metabolized by CYP3A

Block 3 Pharm (19 decks)

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