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IC18 HIV Flashcards

1
Q

What is the MEDIUM of transmission of HIV?

A

specific body fluids
* blood
* semen
* genital fluids
* breast milk

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2
Q

What are the modes of transmission of HIV?

A
  • unprotected sex with infected ppl
  • sharing infected needles & syringes
  • mother-to-child during pregnancy, childbirth, breastfeeding
  • transfusion of contaminated blood & blood products
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3
Q

In which population is it compulsory to screen for HIV in Singapore?

A

Pregnant women

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4
Q

How do we diagnose HIV?

A
  • seurm Ab detection HIV EIA test/Western blot
  • HIV RNA detection with PCR
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5
Q

What are the different stages of HIV?

A
  1. acute HIV infection
  2. asymptomatic
  3. persistent generalised lymphadenopathy
  4. AIDS
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6
Q

Describe the first stage of HIV

A

Stage 1: Acute HIV infection
- flu-like symptoms with swollen lymph nodes, fever, malaise rash for 2-3 weeks

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7
Q

Describe the second stage of HIV

A

Stage 2: Asymptomatic
- infected person may be asymptomatic for years

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8
Q

Describe the third stage of HIV

A

Stage 3: Persistent generalized lymphadenopathy
unexplained lymph node enlargement in neck, underarm, groin for >3 months

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9
Q

What is the definition of AIDS?

A

CD4 count < 200 cells/mm3
OR
presence of AIDS-defining diseases

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10
Q

What are the surrogate markers for HIV therapy?

A
  1. CD4 count
  2. Viral load (HIV RNA)
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11
Q

What is CD4 count an indicator of?

A
  • immune function
  • disease progression
  • response to treatment
  • when to initiate/discontinue prophylaxis for opportunistic infection
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12
Q

What is the normal CD4 count?

A

500-1200 cells/mm3

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13
Q

When do we measure CD4 count for a HIV infected person?

A
  1. baseline
  2. every 3-6 months after treatment initiation
  3. every 12 months after adequate response
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14
Q

What is the definition of “adequate response” in HIV therapy?

A

Increase in CD4 count by 50-150 cells/mm3 in the first year of therapy

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15
Q

What is an example of CD4 count being used to determine initiation/discontinuation of prophylaxis for opportunistic infections?

A

When CD4 < 200, initiate prophylaxis for pneumocystis pneumonia

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16
Q

What is viral load an indicator of?

A

Response to HIV therapy

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17
Q

When do we measure viral load for a HIV infected person?

A
  1. baseline before initiation of treatment
  2. 2-4 weeks after treatment initiation, max 8 weeks
  3. every 4-8 weeks until viral load suppression
  4. every 3-6 months/annually once stable + viral suppression
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18
Q

What is our target viral load?

A

Undetectable HIV RNA levels (ie. viral suppression) by 8-24 weeks

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19
Q

What are the goals of HIV therapy (ART)?

A
  • reduce morbidity & mortality
  • prolong duration & quality of survival
  • restore & preserve immune function
  • suppress HIV load for as long as possible
  • prevent transmission
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20
Q

When do we initiate ART for HIV infected persons?

A

ASAP regardless of CD4 count

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21
Q

What are the benefits of early HIV treatment?

A
  • maintain higher CD4 count & prevent potentially irreversible damage to immune system
  • ↓ risk for complications
  • ↓ risk of non-opportunistic conditions
  • ↓ risk of transmission
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22
Q

What are the limitations of early HIV treatment?

A
  • expensive
  • treatment fatigue
  • S/E & toxicities of ART
  • developing drug resistance
  • transmission of drug resistant virus
  • less time to prepare for ART (requires high adherence >95%)
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23
Q

Describe the steps in the replication of HIV

A
  1. attachment to CD4 receptor
  2. binding to CCR5/CXCR4 co-receptors
  3. fusion
  4. reverse transcription
  5. integration
  6. transcription
  7. translation
  8. cleavage of polypeptides & assembly
  9. viral release
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24
Q

Based on the steps in the replication of HIV, what are the targets of ART?

A
  1. Binding to CCR5/CXCR4 co-receptors
  2. Fusion
  3. Reverse transcription
  4. Integration
  5. Cleavage of polypeptide & assembly
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25
Q

What ART drug classes target the indicated steps?

  1. Binding to CCR5/CXCR4 co-receptors
  2. Fusion
  3. Reverse transcription
  4. Integration
  5. Cleavage of polypeptide & assembly
A

Binding to CCR5 –> CCR5 antagonist
Fusion –> Fusion inhibitor
[Both considered entry inhibitors]
Reverse transcription –> Nucleoside & non-nucleoside reverse transcription inhibitors [NRTIs, NNRTIs]
Integration –> Integrase strand transfer inhibitor [INSTIs]
Cleavage of polypeptides & assembly –> Protease inhibitors [PIs]

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26
Q

What are the two recommended ART regimens for patients naive to ART?

A
  1. 2 NRTI + 1 INSTI
  2. 1 NRTI + 1 INSTI
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27
Q

What are the possible combinations for the first regimen?

A

Tenofovir/Emtricitabine/Bictegravir [TEB]
Tenofovir/Emtricitabine/Dolutegravir [TED]
Abacavir/Lamivudine/Dolutegravir [Triumeq] [ALD]

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28
Q

What are the possible combinations for the second regimen?

A

Emtricitabine/Dolutegravir [ED]

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29
Q

When is the second regimen of 1 NRTI + 1 INSTI contraindicted?

A
  1. high HIV RNA count of > 500,000
  2. HBV coinfection
  3. initiating ART before HIV genotypic resistance testing & HBV testing results are available
30
Q

What drugs belong to the nucleoside reverse transcriptase inhibitor [NRTIs] class?

A

TEZLA (heh)
* Tenofovir
* Emtricitabine
* Zidovudine
* Lamivudine
* Abacavir

31
Q

What are the preparations of tenofovir available?

A

Tenofovir
* Alafanamide [TAF]
* Disoproxil fumarate [TDF]

32
Q

What are the side effects of tenofovir?

A
  • GI (N/V/D)
  • renal impairment
  • ↓ BMD (TAF < TDF)
33
Q

What are the side effects of emtricitabine?

A
  • minimal toxicity
  • hyperpigmentation
  • nausea, diarrhoea
34
Q

What are the side effects of lamivudine?

A
  • minimal toxicity
  • GI (N/V/D)
35
Q

What are the side effects of abacavir?

A
  • GI (N/V/D)
  • Hypersensitivity in genetically predisposed patients
  • MI
36
Q

Abacavir is contraindicated in what patient groups?

A
  • high cardiovascular risk (due to concern of MI)
  • patients positive for HLA-B*5701
37
Q

What are the side effects of zidovudine?

A
  • GI (N/V/D)
  • myopathy
  • bone marrow suppression
38
Q

What toxicity concern is associated with NRTIs?

A

mitochondrial toxicity

39
Q

Which drugs have a higher chance of causing the toxicity among all the NRTIs?

A

Z > T = A = L

40
Q

What drugs belong to the integrase strand transfer inhibitors [INSTIs] class?

A

DERB (heh)
* Dolutegravir
* Elvitegravir
* Raltegravir
* Bictegravir

41
Q

What are the general side effects of INSTIs?

A
  • weight gain
  • nausea, diarrhoea
  • headache
  • depression & suicidal thoughts in pts w preexisting psychiatric conditions
42
Q

What is the unique side effect of bictegravir and dolutegravir?

A

↑ SCr due to ↓ tubular secretion of Cr, not due to declining kidney function

43
Q

What are the unique side effects of raltegravir?

A
  • pyrexia (causes fever)
  • creatinine kinase elevation (risk of rhabdo)
44
Q

What are the advantages of INSTIs?

A
  • high genetic barrier to resistance (B, D > E, R)
  • good virologic eeffectiveness (B, D)
  • generally well tolerated
45
Q

What are the disadvantages of INSTIs?

A

DDI
* polyvalent cations ↓ F
* CYP450 DDI

46
Q

Why do INSTIs have CYP450 DDI?

A

D, E, B are 3A4 substrates

47
Q

What drugs belong to the non-nucleoside reverse transcription inhibitors [NNRTIs] class?

A

ER
* Efavirenz
* Rilpivirine

48
Q

What are the general side effects of NNRTIs?

A
  • skin rash, SJS (E>R)
  • QTc prolongation
49
Q

What are the unique side effects of efavirenz?

A
  • rash
  • hyperlipidemia
  • ↑ LDL-C & TG
  • hepatotoxicity
  • neuropsychiatric S/E (dizziness, depression, insomnia, abnormal dreams, hallucination)
50
Q

What are the unique side effects of rilpivirine?

A
  • depression
  • headache
51
Q

What drugs are contraindicated with rilpirivine and why?

A

PPI - higher gastric pH = ↓ oral F

52
Q

What CYP enzymes is efavirenz metabolized by?

A

3A4

53
Q

What CYP enzymes does efavirenz have an inducing effect on?

A

2B6
2C19

54
Q

What CYP enzyme is rilpivirine metabolized by?

A

3A4

55
Q

What are the advantages of NNRTIs?

A
  • long half lives (OD dosing)
  • less metabolic toxicities than some PIs
56
Q

What are the disadvantages of NNRTIs?

A
  • low genetic barrier to resistance
  • cross-resistance
  • CYP450 DDI
57
Q

What drugs belong to the protease inhibitors [PIs] class?

A

drugs ending with ‘vir’
* ritonavir
* darunavir
* lopinavir
* atazanavir
* fosamprenavir

58
Q

What are the general side effects of PIs?

A
  • GI (N/V/D)
  • hepatic toxicity (esp w chronic hep B/C)
  • fat maldistribution (lipohypertrophy)
  • ↑ risk of osteopenia/osteoporosis
59
Q

What are the unique side effects of ritonavir?

A

paresthesia (“pins & needles” feeling)
taste perversion

60
Q

What are the unique side effects of atazanavir?

A
  • hyperbilirubinemia
  • QTc prolongation
  • skin rash
61
Q

What are the unique side effects of darunavir?

A
  • skin rash
  • SJS (as it is a sulfonamide)
62
Q

What are the advantages of PIs?

A
  • high genetic barrier to resistance
  • resistance to PIs is less common
63
Q

What are the disadvantages of PIs?

A
  • metabolic complications
  • CYP450 DDI
64
Q

Why do PIs have CYP450 DDI?

A

ritonavir is a potent 3A4 + 2D6 inhibitor

65
Q

What drug classes are considered entry inhibitors?

A

CCR5 antagonists
Fusion inhibitors

66
Q

What drug belongs to the CCR5 antagonist class?

A

Maraviroc (Selzentry)

67
Q

Who can use CCR5 antagonists?

A

in patients whose HIV strain is CCR5 predominant

68
Q

What test is needed to determine that?

A

co-receptor tropism essay

69
Q

What hepatic enzyme metabolizes maraviroc?

A

3A4

70
Q

What are the side effects of maraviroc?

A
  • abdominal pain
  • cough
  • dizziness
  • musculoskeletal symptoms
  • pyrexia
  • rash
  • URTI
  • hepatotoxicity
  • orthostatic hypotension
71
Q

What drug is in the fusion inhibitors class?

A

Enfuvirtide

72
Q

What are the side effects of enfuvirtide?

A
  • injection site reactions (erythema/induration, nodules/cysts, pruritus, ecchymosis)
  • bacterial pneumonia
  • hypersensitivity (rare)

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