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Pharmacology > Antiviral Drugs > Flashcards

Antiviral Drugs Flashcards

1
Q

How would you administer Acyclovir for someone who presents with genital herpes (HSV-2)?

A

orally

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2
Q

How would you administer Acyclovir for someone who presents with herpes infection of face and mouth?

A

orally; usually reserved for immunocompromised patients

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3
Q

When is IV acyclovir used?

A

for immunosuppressed patients with chicken pox or with shingles

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4
Q

MOA for Acyclovir

A
  1. prodrug converted to acyclo-guanidine triphosphate (active) by thymidine kinase
  2. sequential phosphorylation by cellular enzymes to acyclo-GTP
  3. acyclo-GTP inhibits viral DNA polymerase, and is incorporated into viral DNA resulting in chain termination –> replication is blocked
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5
Q

Is acyclo-GTP more selective for viral or human DNA polymerases?

A

viral

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6
Q

What are 3 mechanisms of drug resistance for acyclovir?

A
  1. thymidine kinase mutation (viruses that do not activate acyclovir)
  2. decreased viral expression of thymidine kinase
  3. mutation and selection of viral DNA pol that are not inhibited as well by acyclo-GTP
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7
Q

What are adverse effects of topical and oral administration of acyclovir? IV?

A
  1. topical - transient burning sensation
  2. oral - nausea, diarrhea, HA, vertigo
  3. reversible kidney damage that presents with high creatine and urea levels
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8
Q

How can kidney damage be minimized during IV administration of acyclovir?

A
  1. slow infusion (1hour)
  2. adequate hydration
  3. avoiding co-administration with other nephrotoxic drugs
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9
Q

What is a contraindication for acyclovir administration?

A

avoiding IV co-administration with other nephrotoxic drugs

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10
Q

What is the active form of acyclovir?

A

acyclovir triphosphate

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11
Q

What are 2 other drugs for herpes that are prodrugs of acyclovir?

A
  1. valacyclovir
  2. famiciclovir

*both have better oral availability

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12
Q

What are topical drugs for ocular herpes?

What do they all have in common?

A
  1. ganciclovir or acyclovir
  2. trifluridine
  3. brivudine
  4. vidarabine

inhibit viral DNA synthesis

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13
Q

When would you administer vidarabine?

A

acute kertoconjunctivitis and recurrent keratitis caused by HSV 1 or 2

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14
Q

Which topical drug for ocular herpes causes edema of the eyelid in 3% of patients and is not absorbed systemically?

A

trifluridine

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15
Q

Ganciclovir is a drug for _____. Availability? Adverse effects?

A

cytomegalovirus

available orally and IV

granulocytopenia and thrombocytopenia; should not be used during pregnancy

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16
Q

Ganciclovir is approved for prophylactic use in _____.

A

organ transplant patients

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17
Q

Describe the MOA of ganciclovir.

A
  1. converted to monophosphate by viral deoxyguanosine kinase (in CMV infected cells)
  2. cellular kinases convert to triphosphate
  3. ganciclovir triphosphate inhibits viral DNA polymerase (more selectively the human pol) and incorporates into the DNA resulting in chain termination —> viral replication blocked
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18
Q

What are contraindications of ganciclovir?

A
  1. coadministration with zidovudine exacerbates granulocytopenia and thrombocytopenia
  2. coadministration with G-CSF can reduce granulocytopenia
19
Q

What are other drugs for CMV? (x3) Give some facts about each.

A
  1. valganciclovir (prodrug of ganciclovir)
    - better oral availability; just as effective for CMV retinitis as IV ganciclovir
  2. cidofovir
    - approved for only one indiction (CMV retinitis in AIDS patients)
    - MOA converted to diphosphate and inhibits viral DNA pol
  3. foscarnet
    - approved uses are CMV retinitis in AIDS patients
    - nephrotoxic
20
Q

What is the clinical use of Fomivirsen?

A

CMV retinitis in patients that do not respond to another drug

21
Q

MOA for Fomivirsen

A

antisense drug

inhibits the replication of CMV by binding to the complimentary sequence of mRNA transcribed by CMV; inhibits synthesis of proteins that are essential for production of infection CMV

22
Q

What an adverse effect of Fomivirsen

A

ocular inflammation

23
Q

For which Hepatitis is there not a vaccine for?

A

Hep C

24
Q

What is the preferred drug for Hep B?

A

Entecavir

25
Q

Drugs for Hep B are ______ and inhibit _______.

A

nucleoside analogs that inhibit Hep B reverse transcriptase

26
Q

What are the effects of Lamivudine on Hep B infections?

A
  1. suppresses viral réplication (but is not a cure)
  2. reduces liver inflammation
  3. long term use leads to resistance
27
Q

What is the active form of entecavir and what does it do?

A

lamivudine triphosphate - incorporates into viral DNA by HBV reverse transcriptase resulting in DNA chain termination

28
Q

What is the prodrug of tenofovir for Hep B?

A

tenofovir disoproxil

29
Q

Tenofovir is an NRTI. What does NRTI stand for?

A

nucleotide analog reverse transcriptase inhibitor

30
Q

_______ is used for both HIV and Hep B

A

tenofovir

31
Q

Hep C and HIV require _____ drug treatment for two reasons:

A

combination drug treatment bc:

  1. better blocking of viral replication - wha the first drug doesn’t block may be blocked by the second drug
  2. drug resistance is less likely to arise
32
Q

What are the 3 current drugs for Hep C? (older ones were PEG-IFN and ribavirin)

which step in replication does each drug inhibit?

A
  1. viral protease inhibitors (Simeprevir)
    • inhibits translation/processing
  2. Viral RNA polymerase inhibitors / chain termination (Sofosbuvir)
    • inhibits replication
  3. NS5a protein inhibitor (Ledipasvir)
    • inhibits morphogenesis; NS5A protein plays important role in viral rep, assembly, secretion
33
Q

What is the adverse effect of PEG-IFN?

A

flu like sxs (bc interferon alpha binds to receptors of infected cells) and depression

34
Q

What is an adverse effect of ribavirin?

A

hemolytic anemia

35
Q

What are the two types of vaccines available for influenza A and B?

A

inactivated influenza vaccine

attenuated live vaccine (intranasal spray)

36
Q

What are the two classes of drugs for influenza?

A
  1. Adamantanes
    - amantadine and rimantadine
  2. neuraminidase inhibitors
    - oseltamivir (tamiflu) and zanamivir (relenza)
37
Q

In the influenza virus, amantadine blocks ____ and neuraminidase blocks ______.

A

amantadine blocks proton channel

neuraminidase blocks budding

38
Q

True or false: amantadine and rimantadine are active against Influenza A but not against Influenza B.

A

true

39
Q

What is the MOA for amandine/rimantadine

A

inhibit viral M2 proton channels, virus taken up by endosomes - viruses cannot acidify and uncoat

40
Q

Which neuraminidase inhibitor should not be used in asthma patients to treat influenza?

A

zanamavir

41
Q

What are used for prophylaxis of family members/nursing home patients?

A

neuraminidase inhibitors such as oseltamivir (tamiflu) and zanamivir (relenza)

42
Q

What is the MOA for neuraminidase inhibitors?

A

normally, neuraminidase catalyzes cleavage of silica acid residues on the surface of host cells and influenza virus - required for release of viral progeny

neuraminidase inhibitors block this - inhibitors are analogs of silica acid

43
Q

Must begin treatment of neuraminidase inhibitors within _______ of sxs to improve outcomes.

A

within 2 days of symptoms

Pharmacology (5 decks)

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