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SBL > HIV Pharm > Flashcards

HIV Pharm Flashcards

1
Q

Antiretroviral therapy treatment goals

A

suppress HIV RNA, restore and preserve immune function, decrease morbidity and increase survival, prevent HIV transmission

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2
Q

HIV treatment interruption is associated with…

A

rebound viremia, worsening of immune function, increased morbidity and mortality

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3
Q

Drug combinations needed to achieve HIV viral suppression

A

3 active drugs from >/= 2 drug classes

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4
Q

How long does it take for ART to reduce viral load to below detection limit?

A

12 to 24 weeks

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5
Q

Predictors of virologic success

A

low baseline viremia, high potency of ARV regimen, and tolerability, convenience, and excellent adherence to regimen

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6
Q

MOA nucleoside reverse transcriptase inhibitors

A

binds to DNA chain and terminates production, inhibit incorporation of native nucleotides

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7
Q

What does the toxicity of NRTIs depend on?

A

ability to inhibit HIV RT without inhibiting host cell DNA pol

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8
Q

NRTIs most commonly used

A

emtricitabine, lamivudine, abacavir, tenofovir

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9
Q

Toxicities associated with NRTI

A

lactic acidosis, peripheral neuropathy, pancreatitis, anemia, myopathy

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10
Q

Zidovudine MOA

A

NRTI that interferes with thymidine incorporation

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11
Q

Clinical applications zidovudine

A

inhibits HIV-1, HIV-2, HTLV-1 and HTLV-2, mother-to-child transmission, prophylaxis for health care workers

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12
Q

Zidovudine toxicities

A

myalgia, nausea, anorexia, loss of limb fat, bone marrow suppression, skeletal muscle myopathy, hepatic steatosis

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13
Q

MOA stavudine

A

NRTI that interferes with thymidine incorporation

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14
Q

Clinical applications stavudine

A

inhibits HIV-1 and HIV-2

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15
Q

Stavudine toxicities

A

peripheral neuropathy, lipodystrophy, lactic acidosis, and hepatic steatosis

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16
Q

Emtricitabine MOA

A

NRTI, interferes with cytosine incorporation

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17
Q

Clinical applications emtricitabine

A

low barrier to resistance, treats HIV-1 and HIV-2, also active against HBV

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18
Q

Pharmacokinetics emtricitabine

A

long half life, excreted primarily unchanged in the urine

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19
Q

Emtricitabine toxicities

A

one of the least toxic, hyperpigmentation

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20
Q

Lamivudine MOA

A

NRTI, interferes with cytidine incorporation

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21
Q

Clinical applications lamivudine

A

treat HIV-1 and HIV-2, active against HBV

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22
Q

Pharmacokinetics lamivudine

A

long half life, excreted primarily unchanged as urine

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23
Q

Lamivudine toxicities

A

one of the least toxic agents, but may have HA, fatigue, N/D, rash, neutropenia, MSK pain, fever

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24
Q

Abacavir MOA

A

NRTI, interferes with guanosine analog

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25
Q

Clinical applications abacavir

A

treat HIV in combination

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26
Q

Who should abacavir not be given to?

A

patients with HLA-B*5701 genotype (causes an aberrant release of TNF)

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27
Q

Abacavir pharmacokinetics

A

long half life, not CYP substrate

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28
Q

Abacavir toxicities

A

unique hypersensitivity syndrome; fever, GI distress, rash, malaise, fatigue

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29
Q

Tenofovir disoproxil fumarate (TDF) MOA

A

NRTI, nucleoTide adenosine analog

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30
Q

Clinical applications TDF

A

treat HIV in combo, treat HBV

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31
Q

Pharmacokinetics TDF

A

10-50 hr half life, excreted unchange in urine

32
Q

TDF toxicity

A

generally well tolerated, nephrotoxicity with acute tubular necrosis, decreased bone mineral density

33
Q

Tenofovir alafenamide MOA

A

nucleoTide, adenosine analog

34
Q

Clinical applications tenofovir alafenamide

A

treat HIV and HBV

35
Q

ART drug combos

A

2 NRTIs targeting different bases and a drug from a different class

36
Q

NRTIs commonly combined

A

emtricitabine and tenofovir

37
Q

NRTIs not combined

A

emtricitabine and lamivudine; TDF and TA

38
Q

Lamivudine is given in combo with what INSTI

A

dolutegravir

39
Q

INSTI MOA

A

Integrase strand transfer inhibitors, blocks integration of the viral genome

40
Q

Raltegravir MOA

A

prevents formation of covalent bonds between viral and host DNA

41
Q

Toxicity raltegravir

A

“remarkably little” clinical toxicity, may have some hypersensitivities associated with it

42
Q

MOA Dolutegravir

A

prevents strand transfer, blocks chromosomal integration of viral CNA

43
Q

Toxicities dolutegravir

A

generally well tolerated, avoid in pregnancy

44
Q

INSTI metabolized by CYP3A4

A

elvitegravir

45
Q

Bictegravir MOA

A

prevents strand transfer, blocks chromosomal integration

46
Q

Protease Inhibitors MOA

A

prevents cleave of peptide and subsequent maturation of the virion; inhibit activity of aspartyl protease, which prevents proteolytic cleavage of gag and pol peptides

47
Q

Pharmacokinetics protease inhibitors

A

highly protein-bound, hepatic clearance, substrate for P-glycoprotein

48
Q

Toxicities protease inhibitors

A

nausea, vomiting, diarrhea; insulin resistance and lipodystrophy

49
Q

Saquinavir MOA

A

first protease inhibitor, prevents maturation of HIV particle

50
Q

Indinavir MOA

A

prevents maturation of HIV particle

51
Q

Indinavir toxicities

A

unique crystaluria/renal stones

52
Q

Darunavir MOA

A

non-peptidic protease inhibitor that prevents maturation of capsid

53
Q

Darunavir toxicities

A

Gi distress, increase triglycerides, rash and hypersensitivity reaction because it is a sulfa drug

54
Q

Atazanavir MOA

A

protease inhibitor that prevents maturation of capsid

55
Q

Toxicities atazanavir

A

GI distress, increase serum cholesterol, unconjugated hyperbilirubinemia not associated with hepatitis

56
Q

Lopinavir MOA

A

protease inhibitor that prevents maturation of HIV particle

57
Q

Ritonavir MOA

A

protease inhibitor but only used to block CYP3A4 and increase levels of more potent PIs

58
Q

Cobicistat MOA

A

CYP3A4 inhibitor used to boost levels of PIs

59
Q

NNRTI MOA

A

non-nucleoside reverse transcriptase inhibitors, inhibitor binds to reverse transcriptase and denatures it

60
Q

NNRTIs are only active against….

61
Q

Nevirapine MOA

A

NNRTI, prevents generation of DNA from viral RNA, induces CYP3A4

62
Q

Efavirenz MOA

63
Q

Efavirenz toxicities

A

CNS toxicity/psych side effects, rash

64
Q

Etravirine MOA

A

NNRTI, still works despite mutations

65
Q

Rilpivirine MOA

66
Q

Rilpivirine toxicities

A

more common in adolescents and children; CNS, endo and GI issues

67
Q

Doravirine MOA

68
Q

Entry inhibitor MOA

A

T20 peptides prevent conformational change allowing fusion of viral package to cell

69
Q

Enfuvirtide MOA

A

peptide that inhibits formation of protein critical for membrane fusion

70
Q

Enfuvirtide Clinical applications

A

only active against HIV-1

71
Q

Pharmacokinetics enfuvirtide

A

must be administered parenterally

72
Q

Entry blocker-CCR5 MOA

A

blocks CCR5, preventing fusion

73
Q

Maraviroc MOA

A

blocks binding of GP120 to CCR5, blocks HIV entry

74
Q

Maraviroc is not active against…

A

CXCR4 or mixed trophic viruses

75
Q

Pharmacokinetics maraviroc

A

CYP3A4, renal elimination

76
Q

Toxicities maraviroc

A

generally well tolerated, may experience cold-like symptoms, dizziness, GI upset

77
Q

HIV RNA viral load level that prevents sexual transmission

A

<200 copies/mL

SBL (21 decks)

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