Ch 43 Flashcards
herpes viruses
- herpes simplex
- varicella zoster
- cytomegalovirus
nucleoside analogue (acyclovir family) MOA
compete with endogenous nucleosides, competitively inhibits viral DNA polymerase, prevent synthesis of viral DNA
acyclovir
- IV is DOC for serious HSV infections
- oral is more effective than topical for genital herpes
nucleoside analogues ADE
- GI disturbances
- headache
- rash
- IV acyclovir can cause phlebitis and reversible renal dysfunction
penciclovir
-topical for herpes labialis (cold sore)
ganciclovir
- DOC for cytomegalovirus
- ophthalmic gel for HSV keratitis
ganciclovir ADE
- leukopenia
- thrombocytopenia
- myelosuppression
- retinal detachment
- liver/renal dysfunction
cidofovir
- reserved for infections resistant to ganciclovir and other drugs due to more serious ADE
- nephrotoxicity, neutropenia, metabolic acidosis
trifluridine
ophthalmic topical for ocular HSV infection
foscarnet
- IV only
- used for CMV retinitis in AIDS
- acyclovir resistant HSV and shingles
foscarnet ADE
- renal impairment and acute renal failure
- hematologic toxicity
- cardiac arrhythmia
- heart failure
- seizure
- pancreatitis
HAART
- highly active antiretroviral therapy
- concept of multidrug use that has markedly reduced viral loads and improved survival
HIV
-RNA retrovirus that enters the cell and acts as a template to produce viral DNA via reverse transcriptase
nucleoside reverse transcriptase inhibitors (NRTIs)
- 1st class of drugs for HIV+ and included in almost all HIV regimen
- use of multiple is synergy, not duplication, due to each drug focusing on different DNA base
nonnucleoside reverse transcriptase inhibitors (NNRTIs)
- efavirenz is most potent and preferred
- viral resistance happens quickly and must be combined with other drugs
nonnucleoside reverse transcriptase inhibitors (NNRTIs) MOA
bind directly to reverse transcriptase and disrupt the catalytic site
nonnucleoside reverse transcriptase inhibitors (NNRTIs) ADE
- rash
- possible Stevens Johnson
- teratogenic
- neuropsychiatric reaction
protease inhibitor MOA
bind to the protease enzyme and inhibit proteolytic activity, resulting in immature and noninfectious viral particles
ritonavir
inhibits metabolism of other protease inhibitors which raises plasma levels and duration of action
fusion and entry inhibitors
- inhibit the fusion and entry of HIV
- active for HIV resistant to reverse transcriptase inhibitors and protease inhibitors
integrase strand transferase inhibitor MOA
- incorporates viral DNA formed by reverse transcriptase into the DNA of CD4 cells
- effective against resistant strands
integrase strand transferase inhibitor ADE
- headache
- N/V/D
preferred initial HIV treatment regimen
2 NRTI + NNRTI or PI
- change therapy due to treatment failure (decrease CD4 or increase viral load) or drug toxicity
- failure to respond to regimen needs at least 2 new drugs for alternate regiment
neuraminidase inhibitors MOA
- inhibits neuraminidase that catalyzes reaction that causes viral spread in influenza A and B
- most effective less than 3 days after onset with less than 2 days preferred
neuraminidase inhibitor indications
- hospitalized for influenza
- severe, complicated, progressive illness
- higher risk of complication
neuraminidase inhibitor prophylaxis
- routine prophylaxis not advised due to viral resistance
- requires therapy throughout period of potential exposure and 7 days afterward
amantanes
-no longer used clinically for flu due to resistant strains
endonuclease inhibitor (baloxavir)
-single dose within 48 hours of onset of flu symptoms
tenovir
DOC for chronic hepatitis B
ribavarin
- aerosol treatment for RSV
- oral treatment for hepatitis C
ribavarin ADE
- apnea, pneumothorax, cardiac arrest
- hemolytic anemia
- teratogenic
