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68 Cards in this Set
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SE is that it crystallizes in the kidney. need to keep pt well hydrated
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acyclovir
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this enzyme is needed to convert the drug into be activated to get through the 3 steps to prevent further elongation
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thymidine kinase
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DOC for CNS, visceral, disseminated infection
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acyclovir
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this is for acyclovir resistant HSV, then you would use this drug instead.
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foscarnet
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this is metabolized to penciclovir in the body but has same moa of acyclovir
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famcyclovir
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this is the valine prodrug of acyclovir
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valacyclovir
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this is used as a step down from IV acyclovir which is used to treat encephalitis
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PO valacyclovir
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what is the major SE of valacyclovir?
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thrombocytopenic purpura seen with high doses
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3 mechanisms that viruses gain resistance to acyclovir
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1. virus decreases TK
2. altered substrate specificty of TK, no longer recognizes acv 3. viruses with altered viral DNA pol enzymes |
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what is the treatment for keratoconjunctivitis?
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trifluridine - irreversibly inhibits thymidylate syntehtase. incorporates thymidine into viral DNA
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this is the DOC for CMV
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gangcyclovir
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T or F the MOA of gangcyclovir is the same as acyclovir
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false
instead of TK doing the phosphorylation, we use UL97 to phosphorylate |
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because of the SE we can't use ganciclovir very much. what are the SE?
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teratogenic
carcinogenic mutagenic contraindicated in pregnancy myelosuppression/neutropenia fever, rash, HA liver, and kidney dysfxn |
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ganciclovir is given via IV and PO. what is the oral prodrug of gangciclovir that is only given PO?
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valaganciclovir . converted in body to ganciclovir
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the SE are the same except for adding on what 2 things for valganciclovir?
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anemia
diarrhea |
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this is used only for resistant HSV, VZV and has poor bioavilability and GI intolerance
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foscarnet
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what is the MOA of foscarnet and how is it different than ganciclovir
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MOA is pyrophosphate analog. does NOT need phosphorylation
inhibits DNA, RNA polymerase and does NOT require TK |
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this is DOC for prevention of CMV in transplant and immunosuppressed pts
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foscarnet
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what are some SE of foscarnet
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nephrotoxicity
electrolyte disturbances gi upset bone marrow suppresion anemia |
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this is a competitive inhibitor for CMV dna polymerase. it can treat resistant HSV because it uses pyrukate kinase/monophosphate kinase and NOT thymidine kinase to phosphorylate its products
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cidovir
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how is cidovir given and what is it used for?
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IV only
compounded as topic cream for genital warts |
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how often is cidofovir given?
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Q 2 weeks
t 1/2 is 2.5 hrs BUT it lasts intracellularly for 60 hours |
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what 2 drugs do you ALWAYS give with cidofovir
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NS and probenecid
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this binds mrna and is given intravitreally Q 2-4 weeks
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formvirsen DOC for CMV retinitis
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this neuraminase inhibitor presents with hallucination, delirium, abnormal behavior, nausea and vomiting. it is also given PO within 36 hrs
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oseltamir
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this is inhaled within 48 hrs of sx and is a neuraminase inhibitor
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zanamivir
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who is NOT ALLOWED to use zanamivir?
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asthmatics because it can cause bronchospasm
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what is the MOA of m2 inhibitors?
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blocks m2 which impairs viral uncoating and therefore no viral RNA transcription
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what are the SE of m2 inhibitors
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anorexia
nausea nervousness anxiety confusion difficulty concentrating |
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hepatitis drugs are given which way?
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SC and IM
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peginterferon alfa 2a and 2b are used for what
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chronic hepatitis c
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if you're using IFN to treat HCV, what drug do you always give in conjunction?
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ribaviran
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what has flu like sx that occurs 3-4 hrs after injections and also has myalgias.
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IFN
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DOC for HPV
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imiquimod (cream)
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what is the monoclonal ab you give for RSV
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palivizumab (not a vaccine) given to high risk infants
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this is going to bind to gp41 and block conformational change, therefore not allowing the fusion of virus and host cell membrane. what drug am i?
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enfurvirtide (fusion inhibitor)
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what has its MOA as encoding for dummy building blocks and getting incorporated into viral DNA and therefore viral RNA can't produce functional DNA?
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NRTI
emtricitabine, tenofir |
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what is used first line and probably not toxic to mitochondria or causative of lipoatrophy but increases MI risk,
SE: rash, fever, fatigue, resp sx, GI sx |
abacavir
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what 2 NRTI increases MI risk
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abacavir and didanosine
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this is the only one where you have to take into account if you're going to eat or not
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didanosine
30 min before, 2 hrs afterwards |
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what has mitochondrial toxicity
lactic acidosis hepatic steatosis peripheral neuropathy pancreatitis lamivudine lipoatrophy |
NRTI
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what 2 drugs are never to be given together dt it causing lactic acidosis
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stauvudine and didanosine
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what especially causes mitochondrial toxicity
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stauvudine, didanosine, zalcitabine, zidovudine
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what will bind near the active site and doesn't compete with viral nucleosides but instead alters the active site and inactivates the enzyme and shuts it down
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efavirenz
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these have more drug interactions and cross resistance in class is common and usually used second line with NRTI
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NNRTIs
ex) efavirenz |
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what are some SE of efavirenz
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CNS effects: dizziness, HA, insomnia, vivid dreams, nightmares, hallucinations
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what are some SE of nevirapine
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severe hepatotoxicity
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this works AFTER viral replication has occurred (further down the line) they inhibit enzymes so that proteins can't be cleaved into functional proteins
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protease inhibitors
works further down the line |
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this has the most drug interactions of HIV meds
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protease inhibitors
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all PIs are substrates for what?
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CYP 3A4
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which one of the protease inhibitors lacks effects on cholesterol
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atazanavir
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which protease inhibitor do you NEVER give to a pregnant lady?
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efavirenz
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a single dose of this drug is used to prevent perinatal transmission
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nevirapine
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what is the best way to prevent perinatal transmittion?
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zidovudine + NRTI and PI or nevirapine
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what are some SE of protease inhibitors
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increased serum glucose/cholesterol/triglycerides/CAD risk/ fat deposition in back, abdomen,
hepatotoxicity |
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what is the only CCR5 antagonist
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maraviroc
reserved for resistant HIV infection SE: LFT elevation, cardiac events, cough, fever, dizziness, HA |
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when does raltegravir kick in and work?
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at step 5, integration..
before protease but after NRTI SE: CPK elevations, monitor muscle pain and weakness, nausea, diarrhea, fever, HA |
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what is the initial regimen in treating HIV?
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2 NRTI + NNRTI
zidovudine OR tenofovir + lamivudine OR emtricitabine + efavirenz didanosine + emtricitabine + efavirenz ATRIPLA is tenofovir + emtricitabine + efavirenz |
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what is influenza drug m2 inhibitor is hepatically metabolized before excretion so you must adjust dose?
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rimantadine
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resistance to M2 inhibitors develop in how many days?
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3-5 days
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by taking neuraminidase inhibitors, they decrease the duration of sx by how many days?
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1-2 days
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what are the SE of neuraminidase inhibitors?
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hallucination, delirium, abnormal behavior, nausea/ vomiting,
bronchospasm with zanamivir |
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what is the MOA of neuraminidase inhibitors?
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prevents the normal breaking bond that holds the virus to the outside of the infected cell therefore can't release new virus and prevents escape and is non infectious
**note that virion has already infected the host cell, but just can't escape |
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which IFN is used for hepatitis, which is used for MS
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IFN alpha = hepatitis
IFN B = MS |
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what lab tests do you have to get if taking IFN?
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baseline LFT, CBC, follow at 1 & 3 months
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what are some SE of IFN?
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muscle spasticity , flu like sx
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how can you treat the IFN SE
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start at low dose
give prophylactic ASA give at bedtime NSAIDs/ gc |
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what are some more common SE when giving IFN via injections:
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atrophy with necrosis
erythema skin lesions 2nd infection tx: rotate the sites, proper depth, massage, pretreat w/ ice, avoid the sun |
