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IHO Week 6 > HIV Drugs > Flashcards

Flashcards in HIV Drugs Deck (36):
1

What's the goal of therapy in HIV?

maximally inhibit viral replication and reduce viral RNA to undetectable levels

2

After therapy is initiated, an increase in viral load may indicate what?

drug resistance

3

What's the general strategy in terms of drug combo in adults who have never been treated for HIV before?

one of these: NNRTI, protease inhibitor, or integrase inhibitor
plus a dual combo of NRTIs

4

What are the four nucleoside reverse transcriptase inhibitors we know?

zidovudine (AZT)
lamivudine
emtricitabine
abacavir

5

What's the mechanism of the NRTIs?

they competitively inhibit reverse transcritase and can be incoporated into viral DNA chain and cause termination

6

What do the NRTIs need in order to become active?

they need to be phosphorylated by cellular enzymes to the trphosphate form in order to be active

7

What are the general adverse affects of the NRTIs?

you can get a potentially fatal syndrome of lactic acidosis with hepatis steatosis
this is likely due to mitochodnrial toxicity

they're also associated with fat redistribution and thus, hyperlipidemia

8

What are th emore specific side effects for zidovudine?

granulocytopenia and anemia - in up to 45% of patient!
also CNS disturbances: severe headache, insomnia, malaise
nausea

9

What's the specific side effect for abacavir?

hypersensitivity reactions

10

What's the one NUCLEOTIDE reverse transcriptase inhibitor

tenofovir

11

What's the mechanism of action for tenofovir?

same as the nucleosides - chain terminator

12

What's the adverse effects of tenofovir?

nausea, vomiting, diarrhea and potential for renal failure

fatal lactic acidosis has been reported

13

WHat are the two non nucleoside reverse transcriptase inhibitors?

efavirenz and etravirine

14

What's the mechanism for efavirenz and etravirine?

they bind directly to the reverse transcriptase enzyme at a distinct side and render it unable to produce viral DNA

15

True or false: the non nucleoside reverse transcriptase inhibitors do not require phosphorylation like the nucleoside RT inhibitors do.

true

16

Are the NNRTIs more effective against HIV1 or 2?

HIV-1

17

What are the general adverse effects of the NNRTIs?

severe rashes
metabolized by cyp450 - drug interactions

18

Which NNRTI has the specific side effect of vivid dreams, nightmares and hallucinations?

efavirenz

19

What are the more specific side effects for etravirine?

rash, nausea, peripheral neuropathy

20

What are the three protease inhibitors?

atazanavir
ritonavir
darunavir

21

What's the mechanism of the protease inhibitors?

they ihibit protease, so the pre-proteins don't get cleaves to the necessary proteins for the virus
this means the virus is no longer infectious because new viral particles cannot mature

22

What are the adverse effects of the protease inhibitors?

GI disturbances
hepatotoxicity
hyperglycemia
insulin resistance
hyperlipidemia
peripheral lipoatrophy and central fat accumulation
metabolized by/inhibit CYP3A4

23

Which protease inhibitor is poorly tolerated at high doses, so it's given to increase the serum concentrations of other protease inhibitors, thus decreaseing their dosage frequency?

ritonavir

24

HOW does ritonavir increase the serum concentrations of the other protease inhibitors?

it's a potent inhibitor of CYP3a4, which metabolizes the other proteases to decrease their effectiveness

25

What drug is the fusion inhibitor

enfuvirtide

26

How does efuvirtide work?

It binds to gp41 and prevents the conformational change necessary for HIV to fuse with the host cell membrane

27

How is efuvirtide administered?

subQ bid

28

What are the adverse effects of efuvirtide? What infection does it increase the risk for?

you have high incidence of local reactions - pain, erythema, induration, nodules, cysts

higher incidence of bacterial pneumonia

29

Why is efuvirtide such a great drug to have in our aresenal?

it works against HIV that is resistant to all other classes of antiretrovirals

30

What's the integrase inhibitor?

raltegravir

31

How does raltegravir work?

It inhibits integrase, so you don't get the DNA strand transfer necessary for provirus integration

32

WHat drug acts as a CCR5 antagonist?

maraviroc

33

What are the common side effects of maraviroc?

pyrexia, rash, postural dizziness

34

What term do we use for combo therapy with two RTIs and a PI?

highly active antiretroviral therapy = HAART

35

Long term use of HAART is associated with what adverse secodnary effect?

lipodystropy

36

What happens in lipodystorphy?

you get wasting of subcutaneous fat with central adiposity

leads to HL, insulin resistance and DM