Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

19 Cards in this Set

  • Front
  • Back
What are the three varients of HIV-1 and why?
The varients of HIV-1 are responsible for most ocases of AIDS in the US
3 subgroups: M, O, N
What is subgorup M of HIV-1 divided into?
Divided into Clades (A-I)
What is the most common surgical emergency in HIV pts, and how does it result?
Due to CMV
Results in intestinal infaction/rupture. CMV goes into endothelial cells and results in obstructio of blood flow. Intestin becomes ischemic, infarction occurs, then ruptures
Presence of what HLA/MHC surface cells causes an accelerated progression of HIV?
B35 and CW4
What is the result of a immunosuppresed patient with Myocobacterium Avium Intracellulare?
Results in GI disturbance with water reabsorbtion and therefire watery diarrhea
What age, type of cell and what does the x-ray look like in HIV pt?
Infiltration due to CD8+, which is why lungs look white and not black
Why will x-ray of lungs look clean in a TB patient with HIV?
This is because you need CD4 cells to make granuloma, slide will look clean except for some lymphadenopathy
What is Immune Reconstitition Syndrome (IRS) and why does it happen?
When you are treating pt. with anti-retroviral therapy the pateint may get worse b/c you are rebuilding the immune system. Someone who has Hep. V while immuno-suppresed will not have jaundice, but give them the therapy and they will start to show the sympotoms
What causes NONbacterial thrombotic endocarditis and what can happen b/c of it?
Doe to increased production of fibrinogen (acute phase reactant) which results in clot development on valves. These can break off and go to brain to cause a stroke
What are some side effects of Protease Inhibitors?
Hepatic lipid synthesis, Increased triglycerides and VLDL, increase insunin resistance in Type II diabetes, can cause the buffalo hump on back, atheroscelrotic plaques, Acute MI
What is a direct clinical symptom of HIV in the CNS?
AIDS dementia complex, which is NOT opportunistic but direct cause of HIV virus
What virus causes Burkitts lymphoma?
Epstein Barr
What cells are present in Hodgkins lymphoma and not in Non-Hodgkins lymphoma?
Reed-Sternbrg cells
What is an example of an NRTI, what does it require, what does it do, and what is the cause of resistance?
Requires phosphorylation, much like Herpes but all three are from cellular enzymems
Binding to the RT inhibits the pol; incorporated into the DNA results in chain termination
Resistance is due to mutations in the HIV RT (pol)
What is an example of NNRI, what does it require for activation, how does it work, and how is resistance developed?
Does NOT require phosphorylation, binding to RT at a site distince from the active site
Inhibits HIV-1 RT but NOT HIV-2 RT
Resistance is due to mutaiotn in RT distince from those responsibe for NRTI
What is an example of a Protease Inhibitor, how does it work, and what causes resistance to it?
Small molecules that bind in the enzymatic pocket of HIV protease
Inhibition of the protease inhibits the maturation of the virus
Resistance is due to mutation in the protease (pol gene); cross resistance between protease inhibitors is common
What is an example of entry/fusion inhibitor, how does it work, and how is resistance developed?
Binds to gp41 which blocks the conformational change that occurs after gp120 binds to CD4; w/o this change gp41 cannot mediate fusion
Resistance happens when HIV mutates the binding site of Enfuvirtide
What is an example of an entry/CCR5 inhibititor, how does it work, and how is resistance developed?
Binds to CCRT and alters its conformation, inhibiting HIV binding to the co-receptor (ONLY ONE THE BINDS HOST)
Resistance will occur if HIV develops affinity for CXCR4 or HIV develops affinity for drug bound CCR5
What is an example of a Integrase inhibitor how does it work and how is resistance developed?
It inhibits the integrase catalase covalent joining or "strand transfer" of the viral DNA 3' ends to the cells genomic DNA