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PR3151 Finals > HIV > Flashcards

HIV Flashcards

1
Q

For HIV, there are 2 surrogate markers we can use:

  1. CD4 (Tcell) count
  2. Viral load

What is the CD4 count in a healthy person? Explain the significance of CD4 count.

A

Healthy person: 500-1200 cells/mm^3

Significance:
- Most important lab indicator of immune function in HIV pts
- Strongest predictor of disease progression
- Assess response to ART
- Assess need for initiating or discontinuing prophylaxis for opportunistic infections

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2
Q

For HIV, there are 2 surrogate markers we can use:

  1. CD4 (Tcell) count
  2. Viral load

Explain the significance of viral load

A
  • Measures amount of virus in plasma
  • Most important indicator of response to ART
  • Useful in predicting clinical progression
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3
Q

After initiating ART, how often do you monitor CD4 count?

How would you define ‘adequate response to Tx’?

A

Assessed at baseline, then every 3-6 months AFTER ART initiation.

Once adequate response (↑ in CD4 count by 50-150 cells/mm^3 within first year of Tx) achieved, assess every 12 months.

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4
Q

After initiating ART, how often do you monitor viral load?

A

Measured BEFORE ART initiation.

Measured 2-4w (not later than 8w) AFTER Tx initiation/ modification.

Then measured every 4-8w until viral load suppressed.

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5
Q

What are the 2 types of ART combinations?

A
  1. 2 NRTIs + 1 INSTI
  2. 1 NRTI + 1 INSTI
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6
Q

Name the medications under ‘2 NRTIs + 1 INSTI’ (3)

A
  1. Tenofovir + emtricitabine + bictegravir
  2. Tenofovir + emtricitabine + dolutegravir
  3. Abacavir + lamivudine + dolutegravir [Triumeq]
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7
Q

Name the medications under ‘1 NRTI + 1 INSTI’

A

Emtricitabine + dolutegravir

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8
Q

What are the contraindications for 1 NRTI + 1 INSTI?

A
  • HIV RNA > 500,000 copies/mL
  • HBV co-infection
  • Pt whose results of HIV genotypic resistance testing or HBV testing not available yet
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9
Q

Name all the NRTIs (TEALZ)

A

Tenofovir
Emtricitabine
Abacavir
Lamivudine
Zidovudine

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10
Q

MOA of NRTIs?

A

Inhibits reverse transcriptase, prevents HIV DNA replication

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11
Q

What are the disadvantages of NRTI?

A
  • ADEs include mitochondrial toxicity (rare but serious)
    s/sx: lactic acidosis, hepatic steatosis (fatty infiltrate), lipoatrophy (fat loss)
    (Z > T = A = L)
  • Requires dose adjustment in renally impaired (except Abacavir)
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12
Q

What are the ADEs of lamivudine, emtricitabine, tenofovir, abacavir and zidovudine?

Which are the 2 with ADEs to take more note of?

A

Lamivudine: minimal toxicity, n/v/d

Emtricitabine: minimal toxicity, hyperpigmentation, n/d

Tenofovir: n/v/d, renal impairment, decrease in bone mineral density (TAF < TDF)

Abacavir: n/v/d, hypersensitivity rxn in pts with HLA-B5701 (must test for HLA-B*5701 before initiating Tx, discontinue if occurs), possible association with MI (do not use for pts with high CV risk)

Zidovudine: n/v/d, myopathy, bone marrow suppression (anaemia, neutropenia) → monitor full blood count while on Tx

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13
Q

Name all the INSTIs (BRED)

A

Bictegravir, Raltegravir, Elvitegravir, Dolutegravir

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14
Q

MOA of INSTIs?

A

Inhibits integrase enzyme from combining viral DNA with host cell DNA

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15
Q

What are the advantages of INSTIs?

A
  • Bictegravir, Dolutegravir have good virologic effectiveness
  • High genetic barrier to resistance (B, D > R, E)
  • Generally well tolerated
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16
Q

What are the disadvantages of INSTIs?

(general ADEs, ADEs specific to bictegravir & dolutegravir and raltegravir and DDIs)

A

General ADEs: Weight gain, n/d, headache, depression (rare)

Bictegravir and Dolutegravir: ↑ SCr

Raltegravir: pyrexia, creatine kinase elevation (rhabdomyolysis)

DDIs: ↓ bioavailability with concurrent administration of polyvalent cations; Bictegravir, Dolutegravir and Elvitegravir are CYP3A4 substrates

17
Q

Name the NNRTIs (ER)

A

Efavirenz, Rilpivirine

18
Q

MOA of NNRTIs?

A

Also targets reverse transcriptase enzyme but at a different binding site than NRTIs

19
Q

Advantages of NNRTIs?

A
  • Long t1/2
  • Less metabolic toxicity (hyperlipidemia, insulin resistance) than some PIs
20
Q

Disadvantages of NNRTIs?

A
  • Low genetic barrier to resistance
  • Cross resistance among NNRTIs
  • Skin rash, SJS (R < E)
  • Potential for CYP450 DDIs (some are inducers, some inhibitors)
  • QTc prolongation
21
Q

ADEs of NNRTIs? (specific)

A
  • Efavirenz: rash, hyperlipidemia, neuropsychiatric (dizziness, depression, insomnia, abnormal dreams, hallucination), ↑ in LDL-C and TGs, hepatotoxicity
  • Rilpivirine: depression, headache
  • Mixed CYP inducer/ inhibitor: Efavirenz CYP3A4 substrate, induces CYP2B6 and 2C19; Rilpivirine CYP3A4 substrate, oral absorption ↓ with ↑ gastric pH (use with PPIs contraindicated)
22
Q

Name all the protease inhibitors (FRALD)

A

Fosamprenavir, Ritonavir, Atazanavir, Lopinavir, Darunavir

23
Q

Advantages of PIs?

A
  • High genetic barrier to resistance
  • Resistance less common
24
Q

Disadvantages of PIs? (ADEs and DDIs)

A
  • ADEs: metabolic complications (dyslipidemia, insulin resistance), GI SEs (n/v/d), liver toxicity (esp with chronic hep B, C), lipohypertrophy, ↑ risk of osteopenia/ osteoporosis
  • CYP3A4 inhibitors and substrates → potential DDIs
25
Q

What are ADEs of PIs? (specific)

A
  • Ritonavir: potent CYP3A4, 2D6 inhibitor; PK enhancer (frequently combined with Lopinavir)
    Additional SEs: paresthesia* (numbness of extremities), taste perversion
  • Darunavir: good GI tolerability, less lipids effects, skin rash (10%), concern for SJS (sulphonamide)
  • Atazanavir: good GI tolerability, less lipids effects*
    Additional SEs: hyperbilirubinemia*, prolonged QTc interval, skin rash, use with PPIs contraindicated (oral absorption ↓)
26
Q

Name a fusion inhibitor (E)

A

Enfuvirtide

27
Q

What are the ADEs of FIs?

A
  • Injection site reaction (erythema/ induration, nodules/ cyst, pruritus, ecchymosis in 98%)
  • ↑ bacterial pneumonia
  • rare hypersensitivity reaction reported (fever, rash, chills, ↓ BP)
28
Q

Name a CCR5 antagonist (M)

A

Maraviroc

29
Q

In which type of pt can we use CCR5 antagonist?

What must we do before Tx initiation?

A

Only use in pts whose HIV strain uses predominantly CCR5 receptor to enter CD4 cells.

Need co-receptor tropism assay BEFORE initiation of Tx

30
Q

How is CCR5 antagonist metabolised? (DDIs)

A

CYP3A4 substrate → potential DDIs

31
Q

What are the ADEs of CCR5 antagonists?

A
  • Abdominal pain
  • Cough
  • Dizziness
  • Musculoskeletal symptoms
  • Pyrexia
  • Rash
  • URTI
  • Hepatotoxicity
  • Orthostatic hypotension

PR3151 Finals (11 decks)

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