Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
46 Cards in this Set
- Front
- Back
|
Can HIV be eradicated with an antiretroviral regimen?
|
No
|
|
|
Why can't HIV be eradicated with antiretrovirals?
|
Latent CD4+
|
|
|
What should antiretroviral regimens contain?
|
At least two active drugs from multiple drug classes
|
|
|
Why does ARV therapy include multiple drug classes?
|
Decrease failure due to resistance
|
|
|
When should ARV therapy be initiated?
|
When HIV infected (even if CD4 > 500)
|
|
|
Is compliance needed for ARV therapy success?
|
Yes, at least 90-95%
|
|
|
What is a standard NNRTI based regimen?
|
One NNRTI + two NRTI
|
|
|
Major side effects of NNRTI efavirenz?
|
Teratogenicity in first trimester, CNS effects, rash
|
|
|
Alternative for efavirenz?
|
Nevirapine
|
|
|
Major side effects of nevirapine?
|
Hepatotoxicity, rash
|
|
|
Mechanism of NNRTIs?
|
Non-competitive inhibitors of reverse transcriptase
|
|
|
Disadvantage of NNRTIs?
|
Low genetic barrier to resistance
|
|
|
Contents of protease inhibitor based regimen?
|
One PI + two NRTI
|
|
|
Mechanism of PI?
|
Binds to HIV protease
|
|
|
Why is ritonavir added to PI based regimens?
|
Boosts effect via CYP3A4 inhibition
|
|
|
Major side effects of protease inhibitors?
|
Dyslipidemia, fat maldistribution, insulin resistance
|
|
|
Major drug interactions for PIs?
|
Drugs with CYP3A4 metabolism (inhibitors)
|
|
|
Advantages of PIs?
|
Higher genetic barrier to resistance
|
|
|
Backbone of all HAART regimens?
|
Dual NRTIs
|
|
|
Major class adverse events for NRTIs?
|
Lactic acidosis and hepatic steatosis/lipoatrophy
|
|
|
Major side effect for NRTI abacavir, and what can be tested to avoid this?
|
Hypersensitivity, HLA-B5701
|
|
|
Common side effects of NRTIs stavudine and didanosine?
|
Pancreatitis, peripheral neuropathy
|
|
|
Zidovudine, formerly AZT, has what major side effect?
|
Bone marrow suppression
|
|
|
What NRTIs does truvada include?
|
Emtricitabine + tenofovir
|
|
|
What NRTIs does combivir include?
|
Lamivudine + zidovudine
|
|
|
When are fusion inhibitors used?
|
When patients have side effects or resistance to other ARVs like NNRTIs
|
|
|
Only fusion inhibitor so far?
|
Enfuviritide
|
|
|
When is maraviroc useful?
|
For HIV strains that use CCR5 for entry into cell
|
|
|
Major side effects for maraviroc?
|
Hepatotoxicity, dizziness, rash
|
|
|
Why should maraviroc not be used with PIs?
|
PIs inhibit CYP3A4, and maraviroc is a CYP3A4 substrate
|
|
|
Primary integrate inhibitor?
|
Raltegravir
|
|
|
Side effects of raltegravir?
|
CPK elevations, rhabdomyolysis
|
|
|
How should raltegravir dosage be changed when given with rifampin?
|
Dose should double, rifampin induces CYP metabolic enzymes
|
|
|
Strobilid, containing the integrate inhibitor elvitegravir, should be avoided in what patients?
|
Patients with creatinine clearance <70
|
|
|
Most common treatment and prophylaxis for Pneomocystitis jirovecii, aka PCP?
|
TMP/SMX, high dose, three weeks
|
|
|
When should patients receive pneumocystis prophylaxis?
|
When CD4 < 200
|
|
|
Mechanism of pentamidine in PCP treatment?
|
Interference with protozoal RNA/DNA protein synthesis
|
|
|
Why are drug interactions possible with pentamidine?
|
CYP2C19 substrate
|
|
|
When should MAC prophylaxis be initiated?
|
When CD4 < 50
|
|
|
When should MAC prophylaxis be discontinued?
|
When CD4 < 100 for 3 months
|
|
|
What drugs should be used for MAC treatment and why?
|
Clarithromycin + ethambutol, two drugs to prevent/delay resistance
|
|
|
When is a patient at the greatest risk for cryptosporidiosis infection?
|
When CD4 < 100
|
|
|
Best prophylaxis for crypto?
|
HAART (only need CD4 restoration)
|
|
|
When is prophylaxis for Toxoplasmosis gondii recommended?
|
When CD4 < 100
|
|
|
Prophylaxis treatment for T. gondii?
|
Pyrimethamine + sulfadiazine + leucovorin
|
|
|
Why is leucovorin part of T. gondii prophylaxis?
|
Decrease bone marrow suppression
|
