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9 Cards in this Set

  • Front
  • Back
HSV
- genital herpes infection
- infection of the mouth and lips
- anorectal mucocutaneious diseae
- esophagus
- keratoconjunctivitis
- Encephalitis
Varicella Zoster Virus
Cytomegalovirus
- Chicken pox and shingles
- CMV retinitis, colitis, esophagitis, hepatitis, (immunocompromised pt)
MOA OF acyclovir:
- cellular uptake and initial phosphorylation by HSV thymidine kinase
- selective toxicity - the affinity for HSV kinase is 200 fold > than for mammalian enzyme.
- competitive inhibition w/ dGTP for the VIRAL DNA. -- as a CHAIN TERMINATOR.
Resistance to Acyclovir:
- 1. Absence or partial production of V tk.
2. Altered thymidine kinase substrate specificity (phosphorylation of thymidine not acyclovir)
3. Altered viral DNA polymerase.

CAUSED BY point mutation, base insertions, or deletions.
Acyclovir: (wide distribution)
- ROUTE of excretion:
- Route of excretion: glomerular filtration and tubular secretion.
Half life of acyclovir with normal kidney vs. anuria.
normal kidney: 3 hours
anuria: 20 hours.

METABOLISM 10-30%
Adverse Effect of acyclovir:
- Nausea, diarrhea, malaise
- Precipitation of crystals in renal tubule.
- decreased CrCl
- Injection site reactions.
- CNS side effects (Altered sensorium, tremor, myoclonus, delirium, seizures, coma)
Valacylovir converted to acyclovir:
- 1st pass intestinal and hepatic metabolism

- increase p.o. bioavailability to 70%
Valacyclovir Adverse Effects:
- thrombotic thrombocytopenic purpura.
- nausea, ha, diarrhea.

High Doses: hallucinations, confusions, nephrotoxicity.