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18 Cards in this Set

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  • Back
What is the difference between NRTIs and NNRTIs
NRTIs - involved with the DNA process. interfere with and ultimately inhibit reverse transcriptase. Didanosine, Lamivudine, Tenofovir, Zidovudine, Emtricitabine

NNRTIs - do directly inhibit reverse transriptase. Efavirenz, Nevirapine
When should HIV therapy be started?
any one of the following:

HIV + plus:

AIDS defining illness
CD4 <350
HIV associated nephropathy
current hep B
pregnant
What should be used in HIV+ pregnant women?
2 NRTIs + 1 PI

lopinavir + zidovudine + lamivudine

Also need C-section
What is the treatment and prophylaxis for Pneumocystis?
TMP-SMX

Prophylaxis should be started if CD4 is <200 or if theres an oropharyngeal cadidiasis
What is the treatment and prophylaxis for Toxoplasmosis?
T - TMP-SMX or pyrimethamine + sulfadiazine or clindamycin + leucovorin

P - TMP-SMX
What is the prophylaxis against coccidioidomycosis?
Fluconazole or itraconazole

those living in an endemic area (southwest US), have positive IgM/IgG to Coccidioides immitis, and have CD4 <250
What is the prophylaxis of histoplasmosis?
Itraconazole

CD4 <150 or endemic area (eastern/central US)
When should PPV be administered?
CD4>200 who have not received the vaccine within the last 5 years.

Those with a CD4 count <200, vaccine can be considered in special circumstances
When do you use Inactivated influenza vaccine?
annually to all HIV+ pts. Live version is contraindicated
When would you use MMR?
all HIV+ pts with a CD4 >500
When do you use HBV vaccine?
all HIV+ pts who have never been exposed or have never been vaccinated.

Within 96 hours of exposure to chicken pox/shingles, those who have never been vaccinated, have no VZV history, have no VZV antibodies
When is interferon and ribavirin used?
Treatment of chronic hep C in general pts.

HIV+ pts with acute HCV to prevent chronic.
What are the 50s antibiotics? 30s?
50 - Chloramphenicol (static), Erythromycin (static - macrolides), Clindamycin (protein synthesis inhibitor)

30 - Tetracycline (static), Aminoglycosides (cidal)
What is the MOA of Aminoglycosides? Tetracyclines? Chloramphenicol? Erythromycin? Clindamycin?
A - block initial steps of protein synthesis causing misreading of mRNA code.

T - block the acceptor site for incoming aminoacyl tRNA. No AA are available for protein synthesis.

Ch - physically blocks the action of peptidyl transerase. The AA can't be joined to form a protein.

E - block translocation. The AA canot be shifted into their proper position to allow for peptide bond formation.

Cl - similar to chloramphenicol
What are sulfa antibiotics?
sulfonamides - inhibit folate synthesis by bacteria.

prophylaxis and treatment of Toxoplasma and Pneumocystis.

Combo with trimethoprim for empiric UTI.

sulfadiazine, sulfisoxazole, sulfamethoxazole
What are the differences between 6-mercaptopurine and cytarabine?
6 - inhibits de novo purine synthesis. Used especially for ALL

C - pyrimidine antagonist. Inhibits the redution of CDP to dCDP - DNA production ends. Used for non-lymphocytic leukemia.
How do fluoroquinolones work?
inhibit bacterial DNA gyrase. preventing the replication of the DNA. Bacterium cannot copy adn utilize its own DNA.

good against G+ and G-
What is rifampin?
transcription inhibitor.

bactericidal for intar- and extra-cellular Mycobacterium (especially TB)

contact prophylaxis from N. Meningitidis and H. influenzae

significant heptotox, bone marrow suppression, and thrombocytopenia.