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PHAR 557 > HIV - ARVs > Flashcards

HIV - ARVs Flashcards

1
Q

T or F: Antiretroviral therapy is essentially a fn’al cure for HIV

A

T

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2
Q

T or F: ARVs can be used in any combination to tx HIV

A

F

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3
Q

Six classes of HIV meds:

A

NRTIs (nucleoside reverse transcriptase inhibitors)

NNRTIs (non-nucleoside…)

Protease inhibitors

Integrase strand transfer inhibitors (INSTIs)

Fusion inhibitors

Chemokine receptor antagonist/entry inhibitors

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4
Q

What’re the standard NRTI combinations used in practice?

A
  1. TDF/FTC (tenofovir/emtricitabine)
  2. TAF/FTC (tenofovir/emtricitabine)
  3. ABC/3TC (abacavir/lamivudine)
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5
Q

MOA of NRTIs

A

phosphorylated to triphosphate form > competitively binds to HIV reverse transcriptase > terminates DNA chain elongation

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6
Q

Which NRTIs are also active against HBV?

A

3TC, FTC, and TDF/TAF (tenofovir)

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7
Q

What’s unique about TDF?

A

It’s a nucleotide, not a nucleoside (i.e. it’s already phosphorylated)

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8
Q

Notable AEs of TDF?

A
  1. Fanconi syndrome (proximal tubule reabsorption problems)
  2. renal failure
  3. decreased BMD
  4. HBV flareup if d/c’ed
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9
Q

T or F: TDF is hepatotoxic.

A

F

it’s nephrotoxic

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10
Q

What should be monitored in pts taking TDF?

A

SCr, urine protein, BMD

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11
Q

Why are TDF and TAF better than classic tenofovir?

A

because TDF and TAF are able to move from the gut into the blood and lymphoid cells, whereas classic tenofovir could not

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12
Q

What are some advantages of TAF over TDF?

A

Higher F and intracellular t1/2 > lower req’d dose and less plasma exposure to tenofovir

less renal tox (no Fanconi syndrome)

less eGFR effects

less BMD reductions

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13
Q

Why isn’t abacavir (ABC) used often

A

Convenience issues > ABC requires HLA-B testing to see if there’s a specific allele present (*5701) that increases risk of hypersensitivity rxn to it

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14
Q

ABC - If there is hypersensitivity to it, when would it show up?

A

At week 6 of ABC use

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15
Q

T or F: We should rechallenge ABC if hypersensitivity rxn occurs.

A

F > can result it death

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16
Q

Which two NRTIs are distinguished by a single fluorine atom?

A

3TC and FTC (the “F” is for fluorine)

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17
Q

NNRTIs: MOA?

A

binds to hydrophobic pocket of reverse transcriptase > active site changes shape > disrupts DNA chain elongation (prevents natural nucleosides from being incorporated into viral DNA)

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18
Q

NRTIs vs NNRTIs: which one is active against HIV-1? HIV-2? Both?

A

NRTIs: active against BOTH HIV-1/2

NNRTIs: active against HIV-1 only

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19
Q

What’s the issue w/ first gen NNRTIs?

A

low genetic barrier to resistance (single mutation in viral genome confers resistance)

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20
Q

Half life profile of NNRTIs?

A

They’re long (>24h)

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21
Q

Name 3 NNRTIs:

A

RPV (rilpivirine), efavirenz (EFV), doravirine (DOR)

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22
Q

How should rilpivirine be taken?

A

With foods that contain fat

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23
Q

What reduces rilpivirine absorption?

A

Protein shakes, higher pH

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24
Q

CI of rilpivirine?

A

PPIs, H2RAs, antacids (anything that reduces stomach acidity)

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25
Q

Important caution wrt RPV?

A

It prolongs QT interval > watch out when taking other drugs that do the same

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26
Q

Who should NOT receive RPV?

A

naive pts w/ viral loads >100,000 copies/mL > increased risk of tx failure

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27
Q

Major AEs of RPV?

A

severe rash, depression/mood changes, liver damange

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28
Q

How should efavirenz (EFV) be taken?

A

on an empty stomach

29
Q

How is efavirenz affected by food?

A

its absorption is increased by high fat meals (hence why it should be taken on an empty stomach)

30
Q

What kind of pts are given doravirine (DOR)?

A

Naive pts only

31
Q

Name all NRTIs?

A

3TC, FTC, TAF, TDF, ABC

32
Q

Protease inhibitor (PI) MOA?

A

inhibits the action of HIV-1/2 protease, an enzyme that cleaves two precursor proteins into smaller fragments.

33
Q

Resistance profile of PI’s?

A

Resistance is RARE (high genetic barrier to resistance)

34
Q

What kinds of pts should use protease inhibitors?

A

pts who fail other regimens due to resistance, and pts who have poor adherence

35
Q

What do PI’s require to be taken concomitantly?

A

Pharmacokinetic booster

36
Q

Name two PK boosters that may be used w/ PIs

A

ritonavir (RTV, /r), cobicistat (/c) (note: ritonavir is also a PI)

37
Q

T or F: PIs can cause DM

A

T

38
Q

RTV (/r, ritonavir) - How is absorption affected by food?

A

Its absorption is INCREASED by food

39
Q

T or F: Cobicistat is used as a PI booster.

A

T

40
Q

Cobicistat MOA:

A

CYP3A4 inhibitor (NOT a PI like ritonavir)

41
Q

T or F: Cobicistat, like ritonavir, is a PI

A

F (it’s a 3A4 inhibitor)

42
Q

What may be observed while taking cobicistat?

A

Increased serum creatinine by 10-15 µmol/L

43
Q

If an increase of creatinine is observed while taking cobicistat (/c), when should it be this med be stopped?

A

if SCr rises higher than 10-15 µmol/L

44
Q

Which PI has the highest genetic barrier to resistance?

A

Darunavir (DRV)

45
Q

Which PI is the most preferred?

A

Daruavir (DRV)

46
Q

How should DRV be taken?

A

With food (reduces GI irritation + increases absorption)

47
Q

How should atazanavir (ATV) be taken?

A

With food (NOT on an empty stomach)

48
Q

What does atazanavir require for it to be absorbed?

A

acidic envir

49
Q

What is an important AE of ATV (a PI)?

A

Hyperbilirubinemia (jaundice and scleral icterus)

50
Q

Name the PIs:

A

darunavir (DRV), atazanavir (ATV), cobicistat (/c) (technically NOT a PI), and ritonavir (RTV, /r)

51
Q

MOA of integrase strand transfer inhibitors (INSTIs)?

A

Inhibits translated retroviral DNA strand from being inserted into host cell genes

52
Q

Which HIV types are targeted by INSTIs?

A

HIV-1 and 2

53
Q

T or F: Currently, ALL first-line regimens are INSTI based.

A

T

54
Q

T or F: INSTIs have few DIs and are better tolerated relative to other ARVs.

A

T

55
Q

T or F: Despite their better AE profile, INSTIs reduce viral load v. slowly.

A

F

quickly

56
Q

List the INSTIs:

A

raltegravir (RAL)
elvitegravir (EVG)
dolutegravir (DTG)
bictegravir (BIC)

57
Q

How should RAL be taken?

A

w/o respect to meals (absorption is higher w/ high fat meal, however)

58
Q

Important DI w/ RAL

A

Avoid Al and Mg salts > chelation > reduced absorption

59
Q

How should elvitegravir be taken?

A

with food (increases absorption) and with cobicistat

60
Q

EVG should be separated from _____ by at least 2h

A

antacids

61
Q

Which INSTI has a lower barrier to resistance?

A

EVG (elvitegravir)

62
Q

How should dolutegravir (DTG) be taken?

A

without respect to meals (food increases extent and slows rate of absorption, but not sig)

63
Q

Important DI of DTG

A

Avoid cations (Al, Ca, Mg, Fe, Zn salts) > take DTG 2h before or 6h after

64
Q

Important AE of DTG?

A

Increased ALT and AST > may result in acute hepatitis

65
Q

Which population should avoid DTG?

A

Pregnant women (possible neural tube defects)

66
Q

Which INSTI do we often put pts on?

A

bictegravir (BIC)

67
Q

How should bictegravir be taken?

A

w/o regard to meals

68
Q

Important DI involving bictegravir

A

Interaction w/ cations (Ca, Mg, Al, Fe, sucralfate)

69
Q

Why is bictegravir usually the new standard tx?

A

Due to it being a small, single tablet

PHAR 557 (36 decks)

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