Antivirals Flashcards

1
Q

Influenza drugs

A

Amantadine
Oseltamivir
Zanamivir
Baloxavir marboxil

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2
Q

Herpesvirus drugs

A

Acyclovir/valacyclovir
Ganciclovir/valganciclovir
Cidofovir (+ probenecid)
Foscarnet

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3
Q

Hemagglutatin

A

Binds to sialic acid to initiate infection

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4
Q

Neuramidiase

A

Cleaves/releases virions so other cells can be infected

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5
Q

M2 protein

A

Influenze protein channel
Incoating and release of viral contents

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6
Q

Chemotherapy

A

Not a substitute for vaccination
Must be stated within 48 hours for patients with high risk of influenza complications

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7
Q

Amantidine (Adamatases) mechanism

A

blocks influenza A M2 channel proteins
does not work on influenza B

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8
Q

amantadine resistant

A

nearly 100% due to mutations in M2 protein

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9
Q

amantidine uses

A

parkinsons

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10
Q

amantidine adverse effects

A

mild CNS effects (tremor, diziness, ataxia)

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11
Q

neuramidase inhibitors (oseltamivir, zanamivir) mechanism

A

competitive inhibitor or viral neuramiinidase

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12
Q

Oseltamivir pharmacokinetics

A

orally avaliable

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13
Q

zanamivir pharmacokinetics

A

Given as dry powder for oral inhalation directly to side of infection

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14
Q

Neuramidase inhibitor resistance

A

Very low

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15
Q

Neuramidase inhibitor uses

A

Prophylaxis (pre and post exposure to influenza A or B in high-risk or unvaccinated patients)
Given within 48 hours of symptom onset

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16
Q

Oseltamivir adverse effects

A

Mild nausea and vomiting

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17
Q

Zanamivir adverse effects

A

Not for use in people with asthma/COPD due to risk of bronchospasm

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18
Q

Cap dependent endonuclease inhibitors (baloxavir marboxil) mechanism

A

Inhibits cap dependent nucleus

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19
Q

Cap dependent endonuclease inhibitors (baloxavir marboxil) pharmacokinetics

A

Reduced availability when taken with dairy products

20
Q

Cap dependent endonuclease inhibitors (baloxavir marboxil) uses

A

Alternative for oseltamivir for post expoure prophylaxis and treatment of influenza A and B (used within 48 hours)

21
Q

Cap dependent endonuclease inhibitors (baloxavir marboxil) adverse effects

A

Mild GI symptoms and headaches

22
Q

_ herpesvirus is not eradicated by antiviral drugs

A

Latent

23
Q

Nucleoside analogues for HSV and VZV (acyclovir, valacyclovir) uses

A

HSV»VZV
CMV is resistant

24
Q

Valacyclovir compared to acyclovir

A

Greater oral bioavaliability

25
Q

Nucleoside analogues for HSV and VZV (acyclovir, valacyclovir) mechanism

A

Convirted to acyclo-GMP by viral thymidine kinase in the cytosol of infected cells
Host kinases convert mono to triphosphate which is transported to the nucleus and inhibits viral DNA polymerase or causes DNA chain termination

26
Q

Resistance to Nucleoside analogues for HSV and VZV

A

Viral TK defiencu

27
Q

Nucleoside analogues for HSV and VZV uses

A

Genital herpes
Primary herpetic gingivostomatitis
Mucocutaneous HSV
HSV encephalitis
VZV infections

28
Q

Nucleoside analogues for HSV and VZV adverse effects

A

Occur with IV use
Renal dysfunction from crystalline neuropathy (Minimalized by hydration and slow IV infusion)
Neurotoxicity

29
Q

Nucleoside analogues for CMV

A

Ganciclovir
Valganciclovir

30
Q

Nucleoside analogues for CMV are used for

A

All herpesviruses but especially CMV

31
Q

Ganciclovir and calganciclovir mechanism

A

Same as acyclovir
Converted to monophosphate by CMV UL97 kinase then die and try phosphorylated by host kinases
anti-try phosphates inhibit CMV UL54 DNA polymerase and terminates DNA chain elongation

32
Q

Nucleoside analogues for CMV reistance

A

Mutations in UL97 kinase, UL54 DNA polymerase

33
Q

Valganciclovir compared to ganciclovir

A

Higher oral bioavaliability

34
Q

Valganciclovir and ganciclovir uses

A

Restricted due to toxicity
HSV herpetic keratitis
CMV retinitis
Prophylaxis of CMV infection and organ transplant patients

35
Q

Valganciclovir and ganciclovir Adverse effects

A

Lower therapeutic index than acyclovir/valacyclovir
Black box warning for myelosuppression
Renal insufficiency

36
Q

Nucleotide analogs for CMV

A

Cidodovir (cytidine nucleotide analogs)
Active against Kinase deficient herpes virus is because they don’t need to be phosphorylated by viral tyrosine kinase

37
Q

Cidofovir mechanism

A

Converted to active diphosphate by host kinesis
Inhibits viral DNA polymerase and terminates DNA chain

38
Q

Cidofovir pharmacokinetics

A

IV only
Excreted by OAT1

39
Q

Cidofovir use

A

Black box warning only for use for CMV retinitis and HIV/AIDS patients
Alternative to ganciclovir, foscarnet

40
Q

Cidofovir adverse effects

A

Black box warning for nephrotoxicity
Given with probenecid
Black box warning for neutropenia
Black box warning for carcinogen and teratogen

41
Q

Non-nucleoside analog for drug resistant HSV and CMV

A

Foscarnet

42
Q

Foscarnet uses

A

All herpesvirures
Hepatitis B
HIV

43
Q

Foscarnet mechanism

A

Inhibits DNA polymerase and HIV reverse transcriptase (not used for HIV treatment

44
Q

Foscarnet use

A

Black box warning for appropriate use
Ganciclivir-resistane CMV retinitis in HIV/AIDS patients or organ transplant recipients
Acylovar-resistant HSV mucocutaneous infections

45
Q

Foscarnet adverse effects

A

Black box warning for nephrotoxicity
Pronounced electrolyte disturbances- Symptomatic hypocalcemia
Blackbox warning for seizures due to electrolyte imbalance