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FM3 > Anti-virals > Flashcards

Anti-virals Flashcards

1
Q
  1. State the stage in the viral life cycle affected by each drug.
A

Antiviral drugs are all virustatic, they are active only against replicating viruses and do not effect latent virus

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2
Q
  1. Explain how each drug selectively interferes with viral rather than cellular processes.
A

.

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3
Q
  1. Explain why acyclovir and ganciclovir differ in their effectiveness toward HSV and CMV.
A

Acyclovir and ganciclovir are phosphorylated by different proteins, encoded by different viral genes

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4
Q

What viruses does Acyclovir address, what is it used for and how is it selective.

A

viruses: HSV, VZV
selectivity: affinity for the enzyme thymidine kinase encoded by HSV and VZV

  • Reduces duration and frequency of G-HSV outbreaks
  • decreases lesions, duration of symptoms and viral shedding of varicella patients
  • DOC with HSV encephalitis, neonatal
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5
Q

What is the MOA of acyclovir and what are concerns when using it as treatment.

A

requires 3 phosphorylation steps (first two by viral kinases), competes at viral DNA polymerase and results in chain termination

resistance is through alterations in TK or DNA polymerase

generally well tolerated and some renal or neurological toxicity, bioavailability is low

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6
Q

What viruses does Valacyclovir address, what is it used for and what are possible side effects

A

HSV, VZV, and HCMV

  • 1st and recurrent genital herpes, herpes labialis and acute zoster
  • topical penciclovir available for herpes libialis

Well tolerated, NV, rash; high doses cause confusion, hallucinations and seizures

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7
Q

What viruses does Famciclovir address, what is it used for and how is it selective?

A

HSV 1,2; VZV, EBV and HBV

  • 1st and recurrent genital herpes, herpes labialis and acute zoster
  • topical penciclovir available for herpes libialis
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8
Q

What is the MOA and mechanism of resistance. of Famciclovir?

A

Activation phosphor. Catalyzed by virus specific thymidine kinase; competitive inhibition of DNA polymerase (penciclovir does not cause chain termination)

Resistance: thymidine kinase-deficient

  • Bioavailability of penciclovir from PO famciclovir is 70%
  • generally well tolerated, ND, headache may occur
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9
Q

What is the MOA of Ganciclovir and what are methods of resistance?

A

required before inhibits DNA polymerase; competitively inhibits DNA polymerase and chain termination

Initial phosphorylation by protein kinase phophotranferase UL97, increases with duration of use or DNA polymerase (higher levels of resistance and potential cross-resist.)

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10
Q

What viruses does Ganciclovir address, what is it used for and what are possible side effects

A

HSV, VZV, EBV, HHV6,7 and HCMV

  • ocular:dual therapy with Foscarnet
  • CMV colitis, esophagitis, pneumonitis in ImmComp.
  • prevention of end organ CMV in AIDS
  • bioavailablity is low
  • myelosuppression esp. after IV
  • ND, fever, rash, headache, insomnia and peripheral neuropathy
  • CNS toxicity rarely
  • teratogenic and carcinogenic at high doses
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11
Q

What are the MOA, uses and side effects of Valgancivlovir.

A

L-valyl ester prodrug of ganciclovir

used in CMV retinitis in AIDS or prevention of CMV in high risk kidney and heart transplant

Initial phosphorylation by protein kinase phophotranferase UL97, increases with duration of use or DNA polymerase (higher levels of resistance and potential cross-resist.)

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12
Q

What viruses is Cidofovir used against?

A

HSV1,2; VZV, EBV, HHV 6, 8; HCMV

  • also against adenovirus, poxvirus, polyomaviruses and human papilloma virus
  • IV retinitis, given with probenecid, not directly injected
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13
Q

What are the method of action and resistance of Cidofovir? What are important concerns for adverse effects?

A

MOA: Potent inhibitor of and as an alternative substrate for viral DNA polymerase

agent is active independent of viral enzymes
-resistant strains retain susceptibility to foscarnet

  • long half-life
  • elimination by renal secretion
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14
Q

What viruses is Telbivudine used against and how is it used?

A

Hep B and C

tx of HBV by:

  • suppress HBC DNA to undetectable levels
  • seroconversion from neg to pos.
  • reduction in elevated transaminase levels
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15
Q

What is the MOA of Telbivudine and what are concerns regarding adverse effects?

A

Activated by cellular kinases, competitively inhibits HBV DNA polymerase and chain termination (active independent of viral enzymes)

  • wide tissue distribution, excretion is renal
  • mild effects of fatigue, headache, abdominal pain, URI, increased creatine phosphokinase levels, NV
  • lactic acidosis, severe hepatomegaly with steatosis
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16
Q

What viruses and conditions are treated with interferons?

A

Hep B and C

HCV: sustained viral respons, absence of detectable viremia for 6mo, reduction in risk of hepatocellular carcinoma
-intralesional injection of condylomata acuminata

17
Q

What is the mechanism of action and adverse reactions associated with interferons?

A

Induction of intracellular signals, resulting in inhibition of viral penetration, translation, transcription, protein processing, maturation and release; increased MHC expression, enhanced pahogcytosis and proliferation of T cells

  • standard tx 1wk pegylated interferon alfa in combo with daily oral ribavirin
  • use of pegylated INF-a as a result of slower clearance and less frequent dosing
  • adverse effects: flu-like syndrome, transient liver enzymes, neurtoxicities, myelosuppression, profound fatigue, weight loss, rash, cough, alopecia, tinnitius, reversible hearing loss, retinopathy, pneumonitis, cardiotoxicity and depression; induction of autoimmune dysfunction; abortifacient
18
Q

What is Ribavirn used to treat?

A

Hep B and C

  • decreased mortality with Lassa fever, other hemorrhagic fevers
  • severe measles and other encephalopathies
  • inhibits replication in Flu A and B, parainfluenza, RSV, paramyxoviruses, HCV and HIV-1
19
Q

What is the MOA and adverse effects associated with Ribavirin?

A

Phosphorylated intracellularly , interferes with synthesis of guanosine triphosphate, to inhibit capping of viral messenger RNA, inhibit RNA-dependent polymerase (can be coadmin with INF-a)

conjunctiva or bronchial irritation

  • occupational protection against long-term exposure
  • bioavailability increased with high fat meals and decrease with antacids
  • excretion primarily renal
  • dose dependent hemolytic anemia, depression, fatigue, irritability, rash, cough, insomnia, nausea and pruritus
  • NOT USED with anemia, renal failure, ischemic vascular disease or pregnancy
20
Q

What is Boceprevir used to treat?

A

HCV genotype 1, sometimes administered with peg-interferon alfa and rebavirus in adult patients (do not use alone)

21
Q

What is the MOA of Boceprevir and its adverse reactions?

A

Covalently, yet reversibly binds to active site serine in HCV non structural protein 3/4A, required for cleavage of mature viral polyprotein

  • food enhances bioavailablity
  • adverse reactions: fatigue, anemia, nausea, headache and dysgeusia, worsening neutropenia and anemia
  • strong inhibitor of CYP3A4/5
22
Q

What is Amantadine used to treat?

A

influenza, 70-90% protective in prevention of clinical illness, and shortened duration of illness

23
Q

What is the MOA of Amantadine? What are the mechanisms of resistance? What are concerns for adverse reactions?

A

Block M2 proton channel of virus, inhibit uncoating of the viral RNA within cells, active against fluA only

-M2 proteinis mutation prone resulting in rapid development of resistance in 50% treated

  • rimantadine is 4-10x more active in vitro
  • amatadine excreted in urine, rimatadine metabolized before excretion in urine; require dose adjustment with liver or renal disease
  • adverse effects: GI, CNS are dose related
  • dopaminergic transmission changes
  • neurotoxicity with high plasma concentrations
  • teratogenic
24
Q

What is Oseltamivir used to treat? What are pertinent adverse reactions?

A

influenza

  • early admin is critical for decrease duration of the disease, severity decreased and frequency of complication decreased
  • once daily prophylaxis to those exposed 70-90% effective

activity against both flu A and B

  • dose adjustments for those with renal insufficiency
  • bioavailability is 80%
  • probenecid reduces renal clearance
  • adverse effects, NV, abdominal pain; tend to resolve spontaneously, headache, fatigue, diarrhea with prophylaxis use, rash is rare
25
Q

What are the mechanism of action and resistance in Oseltamivir?

A

Neuraminidase inhibitor, interfere with the release of influenza progeny,
competitively and reversibly interact with neuraminidase and destroy receptors recognized by viral hemagglutinin, PO prodrug is activated by hepatic esterases and widely distributed

Point mutations in the viral hemagglutinin or neuroaminidase genes; occurs most in immunocomp. Patients with prior oseltamivir exposure

FM3 (20 decks)

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