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Flashcards in HIV Deck (21):
1

When would we be worried about opportunistic infections in a HIV patient?

CD4 count of <200

2

Risk factors for HIV?

M2M sex; anal sex; immunosuppression

3

Timeline of HIV infection?

• Infects and destroys CD4 + immune cells
• Gradually CD4+ cells deplete faster than they are produced
• Cell mediated immunity is weakened
• In the earlier stages CD4 200-500 cells/uL, patients are often asymptomatic or they may notice worse than usual skin or oral conditions e.g. tinea pedis, warts, genital herpes
• AIDS defining illnesses are rare at CD4 counts above 200 and more common <100
• AIDS is usually only seen when HIV is undiagnosed and anti-retroviral therapy is not taken

4

Sero-conversion illness?

Will give us a clue about the duration of the infection. Usually presents like a flu!
Has the patient noticed:
1. Rash
2. Lymphadenopathy
3. Fever
4. Weight loss
5. Sweats

Sero-conversion= HIV antibody test converts from negative to positive 3-5 weeks after transmission.

5

What happens if the patient has no recollection of sero-conversion symptoms? What tests would you like to do?

1. T cell count
2. HIV viral load and genotype sequencing for drug resistance mutation

6

What are some other diseases/conditions up on the wards would make you think of HIV?

• Mycobacteria avian complex (MAC) ** MAC lymphadenitis
• TB (every patient with TB should be tested for HIV)
• Toxoplasma --> cerebral toxoplasmosis.
• Candidiasis
• Pneumocystis jiroveci pneumonia!! (PCP) (T cells s sarcoma
- kaposis sarcoma

7

Principles of HAART?

1. Suppress viral replication to prevent viral infection of CD4 cells
2. Allow reconstitution of cell mediated immunity
3. Stop reverse transcription generating random drug resistant mutations

8

What does a rising viral load while taking HAART therapy indicate?

non adherence, drug resistance or both

9

what are some appropriate tests you should do prior to starting HAART therapy?

-CD4 cell count
-plasma HIV RNA
-genotypic resistance
-screen for hep b and c
-FBE etc
-Fasting blood glucose and lipids

10

what is the standard HIV medical therapy?

2 x Nucleotide reverse transcription inhibitor PLUS either a integrase inhibitor or a Non nucleotide reverse transcription inhibitor or a protease inhibitor

11

how many WHO stages are there for HIV classification?

4

12

what are the 3 characteristic retroviral genes associated with HIV

gag- structural proteins
pol- enzymes RT, integrase and protease
env- envelope proteins

13

Why is ART therapy unable of eradicating HIV infection?

Due to survival of HIV infection in latent, long living CD4+ cells which the drugs can't target.
Also, the highly conserved regions of gp120 and gp41 that are necessary for viral attachment are covered by highly variable proteins that change over time.

14

what sort of therapies can you offer contacts for HIV infection?

Pre-prophylaxis and Post exposure therapy (medical therapy)

15

what are the drug classes that we can use for HIV?

1. Nucleoside reverse transcription inhibitors
2. protease inhibitors
3. integrase inhibitors
4. Non nucleotide reverse transcription inhibitors
5. chemokine receptor inhibitor

16

give some examples of NRTIs

abacavir, tenofovir, lamivudine

17

give some examples of NNRTIs?

efavirenz, nevirapine

18

give some examples of integrase inhibitors

raltegravir

19

give some examples of protease inhibitors

atazanavir, lopinavir

20

describe the steps in HIV infection. Indicate which steps we can target with drugs

1. attachment to CD4 receptor
2. binding to coreceptor CCR5 CXCR4 --->
3. fusion with cell membrane -->
4. reverse transcription -->
5. integration -->
6. transcription
7. translation
8. cleavage of polypeptides and assembly -->
9.viral release

21

empirical treatment of toxoplasmosis

sulphadiazine-pyremethamine + folinic acid