Beruflich Dokumente
Kultur Dokumente
Antiretrovirals
Maraviroc CCR5 Antagonist CCR5 Tropism assay required BBW: hepatotoxity -Tropism switching
before use -severe rash/ systemic (CXCR4 instead of CCR5
CYP 3A4 metabolism anaphylaxis rxn can occur for entry) CXCR4 tropic
before hepatotoxicity virus faster disease
progression
infectious diseases/ URI due to -Increased affinity for the
pt being immunocompromised co-receptor
-Utilization of inhibitor-
bound receptor for entry
-Faster rate of entry
Enfuvirtide: fusion Gp41 fusion inhibitor -SubQ injection not a first- injection site reaction -Mutation in gp41 dec
inhibitor (-fu) line therapy drug affinity (also lead to
No CYP metabolism just -used in treatment-experienced pt dec fusion by virus
degraded who have a relapse affect viral fx)
MOA/ Metabolism Overall SE Drug-specific SE Resistance
NRTIs Act like a nucleotide, but lack -Lactic acidosis Abacavir: rash, -ATP-dependent
3 hydroxyl group chain -hepatic steatosis hypersensitivity reaction pyrophosphorolysis
Abacavir; ABC termination -Lipodystrophy screen for HLA-B*5701 (removal from the 3 end
Didanosine; ddl -T-cells recognize abacavir- of the nascent chain)
Emtracitabine; Oral small molecular weight -mitochondrial DNA problems altered HLA-B*5701 MHC Class Prevention of NRTI
FTC drugs, need - B-oxidation, the Kreb's cycle I incorporation into DNA
Lamivudine; 3TC phosphorylation to be and inh DNA pol affects Didanosine & Stavudine:
Stavudine; d4T active enzymes for ATP production pancreatitis and peripheral
Tenofovir DF; TDF -buildup of triglycerides neuropathy
Zidovudine; AZT, *NO CYP3A4 no drug (hepatic steatosis) and lactic Emtracitabine:
ZDV interations acid build up (lactic acidosis) hyperpigmentation
-virus and drugs cause increase in Emtracitabine & Lamivudine:
VLDL lipodystrophy exacerbation of HBV infection
if HBV Tx discontinued
Stavudine & Zidovudine:
lipoatrophy
Tenofovir TDF: renal
impairment
Zidovudine: bone marrow
suppression drug-induced
anemia
NNRTIS -vir in the Oral small molecular weight Rash Efavirenz & Rilpivirine -AA substitutions in drug
middle drugs Hepatoxicity neuropsychiatric issues, binding pocket cross
Delavirdine; DLV * CYP3A4 potential for drug -(both are worst with insomnia resistance among
Efavirenz; EFV problems Nevirapine) Efavirenz : fetal risk, different NNRTIs
Etravirine; ETR -Delavirdine: inhibits 3A4 dyslipidemia *rapid resistance if used
Nevirapine; NVP -Efavirenz, Etravirine & Etravirine : nausea alone!!
Rilpivirine; RPV Nevirapine: induce 3A4 Nevirapine : hepatotoxicity
Integrase inhibitors- Metabolized by Raltegravir: inhibition of renal -Mutations in integrase
gravir glucuronidation tubular secretion Elevation gene
Dolutegravir; NOT CYP of serum creatine kinase
DTG
Elvitegravir; EVG
Raltegravir; RAL
Protease Inhibitors -protease inhibitor blocks Gag - insulin resistance Atazanavir, Indinavir, -mutations in protease
-navir and Gag- Pol -INCREASED lipids & glucose Tipranavir: inh UGT1A1 active site
Atazanavir; ATV -hepatically cleared via CYP -Cushingoid appearance
Darunavir; DRV DRUG INTERACTIONS ARE -hepatotoxicity
Fosamprenavir; THE MAIN ISSUE -GI intolerance; N/V/D
FPV -inh GLUT 4 in adipocytes
-inh SREBP protein
Lopinavir/Ritonavir
Nelfinavir; NFV
Tipranavir; TPV