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Pharmacology > Antiviral Drugs > Flashcards

Antiviral Drugs Flashcards

1
Q

Respiratory Viral infection Treatment:
Infuenza A, B and Respiratory Syncytial Virus (RSV)

Neuraminidase inhibitors

Inhibitors of Viral uncoating

Synthetic Guanosine Analogue

A

Neuraminidase inhibitors:

  • Oseltamivir
  • Zanamivir

Inhibitors of Viral uncoating:

  • Amantadine,
  • Rimantadine

Synthetic Guanosine Analogue:
- Ribavirin

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2
Q

Neuraminidase inhibitors - MOA

  1. Effective against
  2. When is administration best
A

Neuraminidase inhibitors: Oseltamivir, Zanamivir

  • Analogs/inhibitors of sialic acid substrate for neuramindase*
  • Inhibit release of virus
  • Effective against BOTH Type A and B Infuenza*
  • Administration is best prior to exposure as prophylaxis
  • Admin within 24-48hrs after infection - modest effect on symptoms.

NOTE: 2015-2016 influenza season
- Osetamivir and zanamivir are the only twi agents recommended for use!!

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3
Q

Neuraminidase Inhibitors PK/AE:

A

Oseltamivir: orally active prodrug (hydrolyzed in Liver)
Zanamivir: Not orally active (inhaled, intranasal)

AE:

  • Oseltamivir: GI discomfort, nausea due to oral route (alleviated when taken with food)- 1 year up
  • Zanamivir: airway irritation (avoid in severe asthma, COPD)- 7 years up
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4
Q

Ion channel blockers MOA

  1. Effective against
  2. When is administration best
A

Amantadine - widely distributed and crosses BBB not extensively metabolized and excreted into urine where it may accumulate
Rimantadine - not widely distributed, metabolized and eliminated in urine.
- Block viral membrane protein, M2 (H+ channel)
- channel is required for fusion of viral with cell
membrane to endosome (requirement for viral uncoating)
- oral
1. Exclusively active against Influenza A virus
2. Equally effective in prophylaxis and treatment

NOT effective for treatment of current strains and not. used

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5
Q

Ion channel blockers AE/CI:

A

Amantadine: CNS - insomnia, dizziness, ataxia, leading ti hallucinations, seizures
Rimantidine: fewer problems
Both: GI intolerance

CI:

  • Monitor amantadine in psychiatric patients, cerebral atherosclerosis, renal impairment, epilepsy
  • Pregnancy, nursing (FDA Category C)

upto 50% people are naturally resistant

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6
Q

Purine/pyrimidine analogs MOA

  1. Active against?
  2. Combo’d with?
A

Ribavirin (Nucleoside anolgue GUANOSINE)
- Converted to Ribavirin-triphosphate which inhibits guanosine triphosphate formation nd prevents viral mRNA capping.

  • Inhibits RNA-dependent RNA polymerase resulting in inhibition of viral protein synthesis
  • Active against broad spectrum of RNA and DNA viruses (eg RSV, HCV, Lassa fever)
  • used in combo with IFNa for HCV Tx.
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7
Q

Ribavirin PK/AE

A

Oral IV and aerosolized
Distrbution significantly prolonged in RBC (16-40 days)

AE:

  • Dose dependent transient hemolytic anemia (can bind to RBC).
  • GI (nausea, anorexia)
  • CNS (fatigue, headache, insomnia)
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8
Q

Ribavirin CI:

A

Pregnancy (Cat. X) extrememly teratogenic

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9
Q

Tx for Hepatic Viral infections Hep A,B,C,D, and E:
Interferon

Nucleotide/Nucleoside analogs

Protease Inhibitors

A 
Interferon
- IFNa
Nucleotide/Nucleoside analogs
- Lamivudin, Entecavir, Ribavirin
Protease Inhibitors
- Boceprevir, Teleprevir
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10
Q

INFa MOA:

A
  • Naturally occuring, inducible glycoproteins/ cytokines
  • Do Not target viral gene products directly
  • Inhibit RNA and DNA synthesis by activating / Inducing protein expression that inhibit virus infection eg, PKR
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11
Q

INFa PK/AE

A

Not orally active because its naturally occuring
uptake and metabolism by liver and kidney
usually pegylated to improve PK profile

AE:

  • Flu like (fever, chills, myalgias and GI disturbances)
  • Fatigue and mental depression
  • interferes w/ hepatic drug metabolism. Can cause toxic accumulation of theophylline
  • May potentiate zidovudine induced myelosuppression
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12
Q

INFa

Clinical Applications: Diseases it treats?

A
  • HCV (combo w/ ribavirin)

- HBV, condyloma acuminata, hairy cell leukemia, kaposi’s sarcoma

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13
Q

Hepatic Anti-viral drugs

Nucleoside / Nucleotide Analogs

A

Lamivudine
Entecavir
- Must be phosphorylated by cellular enzymes to triphosphate (active) form.
- Actions are suppressive rather than curative

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14
Q

Lamivudine
Active against:
MOA:

A

Hep B and HIV

  • Triphosphate form inhibits HBV and HIV reverse transcriptase.
  • Monophosphate for incorporates into DNA (by HBV polymerase) resulting in chain termination.
  • well tolerated
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15
Q

Entercavir
Active against:
MOA:

A
  • effective against Lamivudine-resistant strains of HBV and HIV*
  • phosporylated form competes w/ natural substrates for viral polymerase.
  • Subsquent inhibition of polymerase blocks reverse transcriptase activity.

Monitor after discontinuation in case of exacerbation of severe hepatitis***

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16
Q

Protease inhibitors

A

Boceprevir, Teleperir

  • Tx of HCV in adult patients who have been previously untreatd or failed tx. w/ IFNa and ribavirin
  • Combo’d wt, IFNa and ribavrin

MOA: Bind reversibly to nonstructural protein 3 (NS3) serine protease and inhibit replication of HCV

17
Q

Commonly reported AE reactions in adults due to protease inhibitors:

A 
fatigue
anemia
nausea
headache
dysgeusia
18
Q

Tx of herpes viral infections

A

Herpes can form latent infection. Available drugs are for replicating virus only

Purine and pyrimidine analogs:
-ovir [acyclovir, valacyclovir, cidofovir, Ganciclovir, Valganciclovir, Penciclovir, Trifluridine

Foscarnet

19
Q

Acyclovir
DOC?
commonly used for?

A

Prototypic antiherpetic therapeutic agent
Activity against: herpes simplex virus (HSV) Types 1 and 2, VZV, EBV (HSV4).

DOC in HSV Encephalitis*

  • Commonly used for genital herpes infections and prophylactically in immuncompromised and transplant patients.
  • CMV is resistant at clinically achievable levels (does not encode thymidine Kinase)
  • Valacyclovir = Prodrug of acyclovir
20
Q

Acyclovir MOA

A
  • 3 phosphorylation steps for activation
  • Monophosphorylated by herpes virus-encoded enzyme (thymidine kinase)
  • Host cell enzymes complete phosporylation to di and triphosphate forms.
  • Competes w/ GTP; once incorporated into DNA causes chain termination and inhibition of viral DNA polymerase

Resistance is rare in immunocompetent hosts. occurs by

  • deficient thymidine kinases
  • altered viral DNA polymerase w/ decreased affinity for acyclovir.
21
Q

Acyclovir - PK

A
  • IV, oral or topical
  • Valacyclovir has greater oral bioavailability than acyclovir
  • Partially metabolized thus can accumulate w/ renal failure.
22
Q

Acyclovir AE

A

topical: local irritation
oral: headache, diarrhea, nausea and vomiting
IV: acute renal failure. Risk can be minimized by slow infusion and prioir hydration of patient.

23
Q

Gancyclovir

DOC?

A
  • Valganciclovir = pro-drug w/ greater oral bioavailability
  • analog of acyclovir (8-20 X activity against CMV)
  • DOC for CMV retinitis and CMV prophylaxis in immunocompromised

MOA:
Phosphorylated by viral (UL97) and cell kinases
DNA chain terminator and DNA polymerase inhibitor

24
Q

Gancyclovir PK

A

Gancyclovir (IV)
Valgancycovir (oral) undergoes rapid hydrolysis in intestines and liver to gancyclovir
Urine excretion

25
Q

Gancyclovir AE/CI

A

Myelosuppresion
Severe dependent neutropenia

CI:
Pregancy (FDA Cat. C)

26
Q 
Cidofovir
whats special about it?
Major use?
Activation?
MOA?
A

Special because does not require phosphorylation by viral kinases.

  • Major use is tx. of CMV-induced retinitis in HIV/AIDS
  • Require activation by host cell kinases
  • effective against HSV and gancyclovir resistant HSV.

MOA:
- DNA chain terminator and DNA polymerase inhibitor

27
Q

Cidofovir PK/AE

A

IV, intravitreal and topical
must be co-administered with probenecid (blocks renal tubular secretion)–> increased time for effects

AE: Nephrotoxicity

28
Q

Penciclovir

A

Active against HSV 1-2 and VZV (cold sores)

Used for the topical tx of HSV (cold sores)

29
Q

Penciclovir

MOA?

A

penciclovir
MOA: monophosporylated by viral thymidine kinase
- further phosphorylation occurs to give active triphosphate form.
- Inhibits HSV DNA polymerase/ chain terminator
- active against HSV-1, 2 and VZV
- Used for the topical tx. of HSV (cold sores)

30
Q

Penciclovir PK/AE

A

topical only
AE:
Dermatologic: mild erythema

31
Q

Trifluridine
DOC
MOA?

A

Effective against HSV-1, 2 and vaccina virus.

DOC for HSV keratoconjunctivitis and recurrent epithelial keratitis

MOA: Triphosphate form incorporated into viral DNA causing fragmentation

32
Q

Trifluridine - PK/AE

A 
Ophthalmic ointment (too toxic for systemic)
t1/2=12min (apply frequently)

AE: Transient irritation of eye and palpebral (eyelid) edema

33
Q

Foscarnet

A

Organic analog of inorganic pyrophosphate
Does not require phosphorylation!!

Used for CMV retinitis in immunocompromised patients, acyclovir-resistant HSV and SMV retinitis and gancilovir-resistant CMV and VZV.

34
Q

Fodscarnet MOA

resistance?

A

Structural analog of anion pyrophosphate that selectively inhibits the pyrophosphate binding site on viral DNA polymerases

resistance:
point mutation in polymerase

35
Q

Foscarnet PK/AE

A

IV only
-LAST RESORT

AE:
Nephrotoxicity*
Electrolyte disturbances (Ca+2, Mg+2, K+, PO4)*
Anemia
Genital ulceration (mainly men)
CNS: Hallucinations, seizures, headache (25%)

Pharmacology (27 decks)

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