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Infectious Disease > HIV > Flashcards

HIV Flashcards

1
Q

What is ART?

A

Antiretroviral therapy

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2
Q

What is AI?

A

Disease progression

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3
Q

What conditions increase the urgency of initiation of therapy?

A 
Pregnancy
AIDS-defining conditions, including HIV-associated dementia
Acute opportunistic infectoin
Lower CD4 counts
HIV-associated nephropathy
HIV-HBV co-infection
HIV/HCV co-infection
Acute/early infection
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4
Q

What are the goals of therapy?

A

Maximal and durable suppression of VL.
Restoration or preservation of immunologic function.
Improvement of QOL.
Reduction of HIV-related morbidity and mortality; prevention of opportunistic infections.
Avoidance of ADRs.
Prevent transmission.

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5
Q

What factors should be considered before selecting a regimen?

A 
Comorbid conditions
Potential ADRs
Potential drug interactions with other medications
Pregnancy or pregnancy potential
Results of genotypic drug resistance testing
HLA-B*5701 testing if considering ABC
Convenience
Financial stability
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6
Q

What is the MOA of NRTIs

A

Require intracellular phosphorylation of the 5’-triphosphate moiety to be active.
The 5’-triphosphate competes with endogenous deoxynucleotides for reverse transcriptase enzyme and prematurely terminates DNA elongation d/t modified 3’-hydroxyl group.

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7
Q

What is the BBW for NRTIs?

A

Lactic acidosis

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8
Q

How are NRTIs eliminated?

A

Renally (no CYP450 interactions or DDIs)

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9
Q

What are some ADRs of NRTIs?

A

Pancreatitis

Lipodystrophy/lipoastrophy

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10
Q

Which NRTIs have activity against Hep B?

A

3TC/FTC

TDF/TAF

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11
Q

How often are Combivir and Trizivir taken?

A

1 tab BID

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12
Q

How often are Epzicom, Truvada, and Descovy taken?

A

1 QD

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13
Q

What are the thymidine analogue NRTIs?

A

AZT/ZDV

d4T

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14
Q

Which NRTIs can be taken in pregnancy?

A

AZT/ZDV

Lamivudine

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15
Q

What are the side effects of 3TC?

A

None

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16
Q

What are the side effects of FTC?

A

Well tolerated

Skin hyperpigmentation

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17
Q

What drug should not be combined with d4T?

A

AZT/ZDV (both thymidine analogues)

ddI (similar toxicities)

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18
Q

What are the ADRs of ABC?

A

Hypersensitivity (2-9%) - flu like symptoms - happens in the morning - worsens progressively

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19
Q

Which drug do we do an HLA B*5701 test for?

A

ABC

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20
Q

How is ABC eliminated?

A

Renally as inactive metabolits

No adjustments needed

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21
Q

What are TDFs ADRs?

A

N/V
Decreased BMD, renal dysfunction, esp when used in boosted regimens (w/RTV/COBI)
Generally well tolerated

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22
Q

What are TAFs ADRs?

A

Well tolerated

Better safety profile (renal, bone) compared to TDF

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23
Q

What are NNRTIs MOA?

A

Bind non-competitively to RT and cause a conformational change.
Do not require intracellular phosphorylation and do not complete w/endogenous deoxynucleotides

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24
Q

How are NNRTIs metabolized?

A

By CYP450

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25
Q

What is the NNRTI half-life?

A

Very long

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26
Q

What is a common ADR of all NNRTIs?

A

Rash

LFT increases

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27
Q

What are the first generation NNRTIs?

A

EFV

NVP

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28
Q

What are the second generation NNRTIs

A

ETV

RPV

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29
Q

What are the ADRs for EFV?

A 
Rash (up to 10%)
CNS effects
Increased LFTs
Increased lipids
Neural tube defects if given in first 5-6 weeks of gestation.
Pregnancy category D
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30
Q

What are the ADRs for NVP?

A

Do not start in women w/ >250 CD4 or men w/ > 400 d/t hepatotoxicity

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31
Q

How is EFV metabolized?

A

It is a P-450 substrate and inducer

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32
Q

How is NVP metabolized?

A

It is a P-450 autoinducer and inducer of other drugs

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33
Q

What are the DDIs of ETV?

A

Multiple drug interactions

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34
Q

What enzymes are ETV a substrate for?

A

3A4
2C9
2C19

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35
Q

What enzymes are ETV an inducer for?

A

3A4

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36
Q

What enzymes are ETV an inhibitor for?

A

2C9

2C19

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37
Q

What is ETV currently approved for?

A

Anti-retroviral experienced patients only

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38
Q

What are the ADRs for RPV?

A 
Rash
Depression
Insominia
HA
Increased QT interval
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39
Q

Which NNRTI must be taken with a meal?

A

RPV

Meal must be > 500 cal

40
Q

Which NNRTI has acid dependent absorption?

A

RPV

DDI with acid-reducing agents

41
Q

How does RPV affect CYP enzymes?

A

It is a substrate

42
Q

When should RPV NOT be started?

A

> 100,000 HIV-1 RNA copies
or
< 200 CD4

43
Q

What is RPV approved for?

A

Anti-retroviral naive patients only

44
Q

How should Atripla be taken?

A

1 QHS

45
Q

How should Complera and Odefsey be taken?

A

1 QD

46
Q

What are the ADRs of COBI?

A

Acute renal failure and Fanconi syndrome (when used with tenofovir)

47
Q

What is COBI approved for?

A

Only to boost atazanavir and darunavir

48
Q

Is COBI interchangable?

A

Not with ritonavir for all other PIs

49
Q

What are the PK enhancers?

A

COBI

Ritonavir

50
Q

What are PIs MOAs?

A

Block the maturation process, thereby resulting in the production of immature, noninfectious virions

51
Q

How are PIs metabolized?

A

CYP-450

52
Q

What are the GI ADRs of PIs

A 
Lipodystrophy
Hyperlipidemia
Hyperglycemia
Pancreatitis 
LFT increases
53
Q

Why are PKs used with PIs?

A

PIs are poorly absorbed

54
Q

What are the ADRs of RTV?

A

GI: loose stools, maybe diarrhea 1st couple of weeks then it goes away

55
Q

How is RTV involved with CYP enzymes?

A

Very potent CYP450 inhibitor

56
Q

What are the ADRs of ATV?

A

GI
Hyperbilirubinemia
Nephrolithiasis

57
Q

Which PIs have a sulfa moiety?

A

DNV
FPV
TPV

58
Q

What are DNVs ADRs?

A

GI

rash

59
Q

Which PIs are preferred in pregnancy?

A

ATV

DNV

60
Q

How is evotaz taken?

A

1 QD

61
Q

How is Prezcobix taken?

A

1 QD

62
Q

What is needed in addition to Evotaz and Prezcobix?

A

Still need 2 other agents

63
Q

What is the MOA of entry inhibitors?

A

Inhibit the various steps of HIV with CD4 cells

64
Q

What is the fusion inhibitor?

A

T-20

65
Q

What are the ADRs of T-20?

A

Injection site reaction

66
Q

How is T-20 administered?

A

SQ BID

67
Q

Who can receive T-20?

A

ART experienced patients only

68
Q

What is the CCR5 receptor antagonist?

A

Maraviroc

69
Q

What are the ADRs of Maraviroc?

A

Hepatotoxicity +/- systemic allergic reaction (pruritic rash, eosinophilia or elevated IgE)

70
Q

Who is Maraviroc approved for?

A

Patients who have CCR5 tropic virus

71
Q

Which CYP enzyme is Maraviroc a substrate for?

A

3A4

72
Q

What does Maraviroc dosing depend on?

A

Co-administered agents

73
Q

What is the MOA of integrase inhibitors?

A

Prevent covalent bonds from forming between integrase and host DNA -> HIV integrase unable to incorporate the viral DNA into the CD4 cell chromosome -> prevention of strand transfer and viral replication

74
Q

What are RALs ADRS?

A

None in clinical trial

Post marketing reports: skin rashes and severe hypersensitivity

75
Q

Which integrase inhibitor is preferred in pregnancy?

A

RAL

76
Q

How is RAL metabolized?

A

No p450 metabolism

Glucuronidated by UGT 1A1

77
Q

What is EVGs ADRs?

A

Diarrhea

78
Q

How is EVG used?

A

In combination with ARVs (PIs) in treatment experienced patients

79
Q

What are DTGs ADRs?

A

Well tolerated
Insomnia
H/A

80
Q

How is DTG metabolized?

A

Primarily metabolized by UGT 1A1

81
Q

What are the current guideline regimen for an ART naive patient?

A 
NNRTI + 2 NRTIs
OR
PI (booster) + 2 NRTIs
OR
INSTI + 2 NRTIs
82
Q

What is the preferred PI regimen for an ART naive patient?

A

Darunavir/ritonavir + FTC/TDF
OR
Darunavir/ritonavir + FTC/TAF

83
Q

What are the preferred integrase inhibitor regimen for an ART naive patient?

A 
Raltegravir + FTC/TDF or FTC/TAF
OR
Elvitegravir/cobi/FTC/TDF
OR
Elvitegravir/cobi/FTC/TDF
OR
Dolutegravir + FTC/TDF
OR
Dolutegravir/abacavir/lamivudine
84
Q

Which integrase inhibitor regimens can you not use if CrCl < 70?

A

Stribild and Genvoya

85
Q

What labs do you get at baseline?

A 
Plasma HIV RNA (viral load), CD4 count
Chem-7, LFTs, CBC/diff
Fasting lipids
Other serologies (CMV, Toxo, Crypto, RPR, Hep A/B/C
HLA B*5701 genetic screening
86
Q

What do we monitor for at 2 weeks after treatment initiation?

A

Side effects
Adherence
Can obtain VL and CD4 count

87
Q

What do we monitor at 4-6 weeks?

A

Side effects
Adherence
VL (should decrease by at least 1 log)
CD4 count

88
Q

How often should the patient be checked once stable and what is monitored?

A 
Every 3-6 months
VL
CD4
Chem-7
CBC
U/A (if on tenofovir)
89
Q

What is virologic suppression?

A

A confirmed HIV RNA level below the limit of assay detection

90
Q

What is virologic failure?

A

The inability to achieve or maintain suppression of viral replication (< 200 HIV RNA level)

91
Q

What is incomplete virologic response?

A

Two consecutive plasma HIV RNA levels > 200 after 24 weeks on an ARV regimen. Baseline HIV RNA may affect the time course of response, and some regimens willl take longer than others to suppress HIV RNA levels.

92
Q

What is virologic rebound?

A

Confirmed detectable HIV RNA (to > 200) after virologic suppression

93
Q

What is persistent low-level viremia?

A

Confirmed detectable HIV RNA levels that are < 1000

94
Q

What is virologic blip?

A

After virologic suppression, an isolated detectable HIV RNA level that is followed by a return to virologic suppression.

95
Q

When do you consider switching the drug regimen of a patient?

A

When adherence, tolerability, and PK causes of treatment failure have been ruled out consider the following:

  • Virologic failure
  • Immunologic Failure
  • Clinical Failure
  • Intolerable toxicity
96
Q

What is immunologic failure?

A

The failure to achieve and maintain an adequate CD4 response despite virologic suppression.
Increases in CD4 counts in ARV-naive patients with intial ARV regimens are approximately 150 over the first year

97
Q

What is clinical failure?

A

Occurence or recurrence of HIV-related events (after at least 3 months on HAART)

Infectious Disease (19 decks)

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