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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
Uses of trifluridine
Ophthalmic herpes type 1 and 2 but not useful prophylactically
26
Ophthalmic herpes type 1 and 2 but not useful prophylactically
Trifluridine
27
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.
Acyclovir
28
acts as a competitive inhibitor of dGTP and as a DNA chain terminator
Acyclovir
29
Acyclovir mech
inhibits DNA polymerase by activing like a competitive inhibitor of dGTP and as DNA chain terminator
30
IV Drug of choice for serious systemic herpes simplex virus (HSV), including HSV encephalitis
Acyclovir
31
IV, acyclovir is used for
Drug of choice for serious systemic herpes simplex virus (HSV), including HSV encephalitis and severe initial genital herpes
32
Oral drug to tx Primary herpetic gingivostomatosis
Acyclovir
33
______ used to tx primary genital herpes
acyclovir
34
Approved for chickenpox in children
Acyclovir
35
Side of Acyclovir
IG, well tolerated, rash, itch, nasuea | can be nephrotoxic or cause thrombophleibits
36
Similar to acyclovir; prodrug that is converted to penciclovir which is then phosphorylated—this is what inhibits viral DNA polymerase.
Famciclovir
37
Mech of Famciclovir
Similar to acyclovir; prodrug that is converted to penciclovir which is then phosphorylated—this is what inhibits viral DNA polymerase.
38
recurrent genital herpes and herpes zoster within 3 days of onset
Famciclovir
39
Oral; prodrug absorbed better than acyclovir | - less frequent dosing than acyclovir; renal elimination.
Famciclovir
40
Famciclovir sides:
Generally well-tolerated. - Rash, itching, nausea, vomiting, headache, fatigue
41
Penciclovir mech
simular to acyclovir
42
used for recurrent herpes of lips and face as topical cream
Penciclovir
43
similar to acyclovir, except the monophosphorylation is catalyzed byCMV protein kinase; virustatic.
Ganciclovir
44
Mech of ganciclovir
similar to acyclovir, except the monophosphorylation is catalyzed byCMV protein kinase; virustatic.
45
Used to tx CMV retinitis in AIDS and CMV prophy for transplant pts
Ganciclovir
46
Use of Ganciclovir
Used to tx CMV retinitis in AIDS and CMV prophy for transplant pts
47
Admin and exreation of Ganciclovir
IV or oral | unchanged in urine
48
Sides of Ganciclovir
Bone marrow suppression, leukopenia, thrombocytopenia, anemia. - May enhance bone marrow suppression when given with zidovudine (AZT)
49
Bone marrow suppression, leukopenia, thrombocytopenia, anemia. - May enhance bone marrow suppression when given with zidovudine (AZT)
Ganciclovir
50
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.
Foscarnet
51
Mech of Foscarnet
inhibits CMV DNA polymerase by bindint to pyrophostape binding ste to block viral DNA synthesis
52
Use of Foscarnet
AIDS patients with CMV (cytomegalovirus) retinitis and | acyclovir-resistant herpes simplex.
53
Drug to tx AIDS patients with CMV (cytomegalovirus) retinitis andacyclovir-resistant herpes simplex.
Foscarnet
54
Side effects of Foscarnet
Renal damage (30–50%), reversible (enhanced with amphotericin B). - Electrolyte imbalances - seizures
55
Nucleoside analog inhibitor of the reverse transcriptase domain of the hepatitis B DNA polymerase; must be phosphorylated by cell enzymes to be active.
Lamivudine
56
Mech of Lamivudine
Nucleoside analog inhibitor of the reverse transcriptase domain of the hepatitis B DNA polymerase; must be phosphorylated by cell enzymes to be active.
57
used to tx hep B
Lamivudine and Tenofovir
58
Use of Lamivudine and admin
Hep B and oral with 85% bioavailable
59
Side of Lamivudine
nausuea and diarrhea
60
esterified adenosine monophosphate analog phosphorylated by cell enzymes to the active nucleotide - inhibits the reverse transcriptase domain of the hepatitis B DNA polymerase
Tenofovir
61
Tenofovir ultimately will
inhibits the reverse transcriptase domain of the hepatitis B DNA polymerase
62
Tenofovir is for and it's admin
Hep B | 25% oral bioavailable
63
Sides of Tenofovir
GI upset
64
Mech of Ribavirin
interferes with viral mRNA synthesis | Mono-P form will inhibit inosine 5'P DH thus inhibits GTP synthesis
65
Tri-P form will inhibit: | for Ribivarin
Tri-P form inhibits GTP-dependent capping of viral mRNA
66
Mono-P form inhibits_________ and thus GTP synthesis
inosine-5’-P dehydrogenase
67
aerosol use in carefully selected infants and young children with documented severe lower respiratory syncytial virus (RSV) infections
Ribivarin
68
USed to tx Hepatitis C (oral) in combination with interferon-α
Ribivarin
69
Use of Ribavirin
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
used to tx Lower RSV infections
Ribavirin
71
Metabolsim of Ribavirin
hepatic metabolism; very slow clearance from blood; some metabolites and unmetabolized drug excreted in urine
72
Toxicity of Ribavirin in aerosol form
In aerosol form: Exercise caution with assisted ventilation (requires special aerosol equipment as drug may precipitate in and clog respiratory equipment)
73
CAn cause Pulmonary function deterioration (respiratory depression, lung inflammation) in aerosol use
Ribavirin
74
In IV form, Ribavirin can cause:
anemia and bone marrow suppresion
75
Induce host cells to produce enzymes that block translation of viral mRNA.
Interferon
76
Host produced proteins | Exert virus-nonspecific antiviral activities; active only in species in which they are produced
Interferon
77
EnZ induced by Interferons:
Protein kinase—phosphorylates elongation factor. Oligoisoadenylate synthetase—activates RNase that degrades viral mRNA. Phosphodiesterase—degrades terminal nucleotides of tRNA.
78
Treatment of hairy cell leukemia and AIDS-related Kaposi’s sarcoma
Interferon
79
2nd line for Condyloma acuminata (venereal warts)
Interferon alpha
80
Hepatitis B and C (improves disease course in 40–50%
Interferon alpha
81
PEG-alfa-2a and PEG-alfa-2b interferons in combination with ribavirin are specifically useful for
hepatitis C
82
Toxicity for interferon alpha
Flu-like syndrome. Leukopenia, bone marrow suppression. Neurotoxicity, myalgia.
83
Toxicity: Flu-like syndrome. Leukopenia, bone marrow suppression. Neurotoxicity, myalgia
Interferon A
84
reversible inhibitor of hepatitis C NS3 protease, thus blocking formation of infectious virus particles
Boceprevir
85
Boceprevir mech
reversible inhibitor of Hep C NS3 protease to block formation of infectious virus particles
86
Boceprevir works by reversible inhibitor of hepatitis C ______, thus blocking formation of infectious virus particles
NS3 protease
87
Uses of Boceprevir
hepatitis C genotype 1, in combination with PEG-interferon + ribavirin
88
Admin and elimiatino of Boceprevir
oral 3x day and metabolized by CYP3A

Block 3 Pharm (19 decks)

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