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HIV Flashcards

1
Q

Differences b/w HIV 1 & 2?

A

1: More prevalent and more pathogenic
2: Less pathogenic, resistant to NNRTI’s →(Western Africia)

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2
Q

What are the Cell Surface Receptors for HIV ?

A
  • CD4 receptors
  • Chemokine Receptors
    • CCR5-
      • dectable over entire course of infection
      • Found in majority of sexually transmitted HIV-1 infections
    • CXCR4-
      • Observed in pts with advanced AIDs
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3
Q

What is the Seroconversion window for HIV?

A
  • Time of infection to production of antibodies
    • average 3-4 weeks but up to 6 months
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4
Q

What HIV tests do we have? What does each one do?

A
  • Rapid (antibody tests)
    • Blood or oral fluid sample -can be done at home
      • Require confirmation though if test is reactive
  • Combination immunoassay -4th gen. test
    • detects HIV-1 and HIV-2 antibodies
    • detects HIV-1 protein 24 antigen
    • More sensitive in diagnosing early infection
  • PCR test
    • viral load tests to detect genetic material of HIV
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5
Q

Nucleoside and Nucleotide reverse transcriptase inhibitors (NRTI)→ “Nuke’s”

►What drugs do we have available?

►How do we normally use these drugs?

A

Generic names end in: ine

→Except: Tenofovir, Abacavir

  • Emtricitabine
  • Lamivudine
    • Can’t combine Emtricitabine & Lamivudine because they’re structurally similar
  • Tenofovir Disoproxil Fumarate (TDF)
    • Renal/Bone ADE’s -osteomalacia/porosis
  • Tenofovir Alafenamide (TAF)
    • Better tolerated version of TDF – less in blood = less systemic toxicity
    • Co-formulated with emtricitabine in Descovy for HIV & HBV
  • Abacavir
    • ABC

►How do we normally use these drugs?

→Generally: 2 NRTIs + Second class

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6
Q
  1. )Describe the HIV Lifecycle ? (5 steps)
  2. ) How do you prevent the development of HIV resistances to the medications?
A
  1. Virus identifies, binds and enters CD4+ cell
  2. Fuses and transcribes into DNA
  3. Integrated into nucleus
  4. Replicates, exits via protease
  5. Smaller pieces, gets out of cell and can infect new cells
  6. Must block the virus at 2 different steps to prevent the development of resistance
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7
Q

What combination NTRI products do we have available?

A

1.)

  • Truvada
    • Emtricitabine + TDF
  • Descovy
    • Emtricitabine + TAF
  • Epizicom
    • Lamivudine + Abacavir
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8
Q
  1. What is the MOA for NRTI’s ?
  2. What are the drug class side effects for NRTI’s?
A

1.)

  • Inhibit HIV-1 reverse transcriptase (RT) by competitive inhibition of the enzyme, as well as chain termination
    • Prevents replication/integration into the cell

2.)

  • Lactic acidosis
  • Hepatic steatosis
  • Lipodystrophy/lipoatrophy
    • accumulation or loss of body fat can be permamnent
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9
Q

►Specific ADE’s for Emtricitabine and Abacavir and TDF and TAF?

►If baseline liver test shows hyperlipidemia consider choosing what drug?

A
  • Emtricitabine
    • HA, GI issues, Rash
      • Hyperpigmentaiton of palms or soles of feet
        • rare-more popular in african americans
  • Abacavir
    • Hypersensitivity rxn (severe)
      • ​Associtaed with HLA B*5701→ if pt. is positive for this allele then don’t give drug, rare but test can be neg and rxn can still occur
    • Increased risk of MI***
  • TDF
    • Decreased bone mineral density- osteomalacia
    • Renal impairment- Fanconi syndrome
      • abnormal reabsorption of nutrients in kidneys
    • PK boosters increase risk of renal and BMD toxicity
  • TAF
    • reduced ADE’s
      • ​less renal and BMD issues then TDF

►TDF associated with lower lipid levels than TAF

If baseline hyperlipidemia, consider TDF

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10
Q
  1. What NRTI’s have activity against Hepatitis B virus?
  2. What dose adjustments do you need to make for NRTI’s?
A

1.)

  • Emtricitabine
  • Lamivudine
  • TDF
  • TAF

2.)

  • Most are renally excreted → renal dose adjustements
    • Abacavir is excreted through the liver via ADH
      • Alcohol drinkers can have INCREASED levels of this drug
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11
Q

What are the DDI’s with NRTI’s?

A
  • Substrates of P-glycoprotein
    • TAF>TDF
  • Do not give TAF with: →decrease TAF levels
    • Phenytoin, Oxcarbazepine, phenobarbital, rifampin, rifabutin, rifapentine, st. John’s wort
      • These are all cyp inducers
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12
Q
  1. What Non-nucleoside reverse transcriptase inhibitors do we have available? (NNRTI)?
  2. What is their MOA?
A
  • Doravirine
  • Rilpivirine
  • Efavirenz

2.) MOA: Inhibit reverse transcriptase by directly binding to it

→Non-competitive inhibition of reverse transcriptase

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13
Q
  1. What combination NNRTI products do we have available?
  2. What are the side effects of NNRTI’s?
A

1.)

  • Most are single tablet with 3 drug combination
    • 1 NNRTI + 2 NRTIs

2.)

  • Rash
    • Toxic epidermal necrolysis
    • Steven-Johnson Syndrome
  • Liver Toxicity
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14
Q

What specfic ADR’s do we have for….

Doravirine?

Rilpivirine?

Efavirenz ?

A
  • Doravirine→less than efavirenz and rilpivrine**
    • abdominal pain
    • abnormal dreams
      • If you dream about dora thats abnormal
  • Rilpivirine -CNS side effects mainly
    • Depression (less than efavirenz)***
    • QTc prolongation
    • Rash
  • Efavirenz - efavirenZ “Z” as in Zzzz (sleep)⇒strongest ADR’s out of the class
    • sleepiness
    • insomnia
    • Depression
    • vivid dreams
    • Neural tube defects in 1st trimester
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15
Q

Pharmacokinetics of NNRTI’s

  • Absorption/food effects of …
    • Rilpivirine?
    • Efavirenz?
  • Metabolism of all NNRTI’s?
A
  • Absorption/food effects of ?
    • Rilpivirine
      • take w/ food
    • Efavirenz
      • ​take w/o food
  • Metabolism
    • Liver metabolis CYP 450-34A
    • Efavirenz-CYP2B6
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16
Q

DDI’s for NNRTI’s? (3 different bullent points of DDI’s)

A
  • NNRTI levels decrease with
    • Rifampin
    • Carbamazepine
    • Phenytoin
  • Efavirenz decreases levels of
    • Rifampin
    • Voriconazole
    • Methadone
    • Statins
  • Acid supressive therapy decrease absorption of rilpivirine and its combination products ***these drugs need to be spaced out from rilpivirine
    • PPI’s
    • H2-receptor antagonist
    • Antacids
17
Q
  1. What Protease Inhibitors do we have available?
  2. What is their MOA?
A

1.)

  • Darunavir*
    • DOC w/n the class
  • Ritonavir
  • Atazanavir*

*= given with a booster (Ritonavir or Cobicistat

2.)

  • MOA:
    • Inhibit HIV protease, preventing cleavage of proteins during replicaiton
      • Results in no active proteins
18
Q
  1. What combination protease inhibitor products do we have available?
  2. What are the class ADR’s of protease inhibitors? (six side effects)
A

1.)

  • PI + booster
    • booster = cobicistat or ritonavir
  • PI+ Booster + 2 NRTI’s

2.)

  • Hyperlipidemia
    • esp. with older pt’s – increase dose
  • possible caridovascular risk
  • blood glucose elevations -caution with diabetics
  • liver toxicity
  • bleeding risk- caution with hemophiliacs
  • body fat re-distribution (lipodystrophy)
19
Q

Drug-specific side effects of protease inhibitors….

A
  • Darunavir
    • skin rxn’s due to sulfonamide
      • can still give bactrim though
    • cardiovascular risk - higher than atazanavir
  • Atazanavir
    • hyperbilirubinemia
    • nephrolithiasis
20
Q

Aborption and Metabolism of Protease inhibitors?

A
  • Absorption*******
    • Acid supressive therapy interacts with atazanavir
      • ​DOES NOT interact with Darunavir
  • Metabolism
    • Substrates of CYP 450 and P-glycoprotein
      • most are also CYP 450 inhibitors-many DDI’s
    • Ritonavir -strongest metabolic inhibitor in class (b/c its a cyp booster)- boosts levels of other PI’s
21
Q
  1. What drugs do we have availble for Integrase Inhibitors (INSTI)?
  2. What is their MOA?
A

1.) favored as first line therapy

  • Raltegravir
    • doesn’t have a single tablet regimen
  • Dolutegravir
  • Elvitegravir*
    • only offered in combination products

2.) MOA: blocks insertion of HIV DNA into CD4 cell DNA

22
Q
  1. What combination integrase inhibitor (INSTI) products do we have available?
  2. What are the general drug class side effects of INSTI?
A
  • 2 NRTIs + INSTI
  • 2 NRTI’s + INSTI + Booster

2.)

  • Insomina
  • weight gain
  • increase in liver enzymes and creatine kinase
23
Q

What are the drug-specific side effects of INSTI agents…

A
  • Dolutegravir
    • neuropsychiatric effects -caused drug to be d/c
    • neural tube defects “Dolutegravir, neural tube defect is near”
      • avoid in women of childbearing age not on contraception or w/n 12 weeks of post conception
    • Increased CPK (phosphokinase)
  • Combination products → 2 NRTI’s + INSTI + Booster
    • GI issues
      • N/D
    • Renal impairment
    • Bone density loss
24
Q

Absorption and Metabolism of INSTI’s (integrase inhibitor)?

A
  • Absorption**********
    • Anything with Elvitegravir in it: take with food
  • Metabolism
    • All INSTI’s are substrates of UGT1A1
    • CYP34A substrates-everyone except RALTEGRAVIR
      • Bictegravir
      • Dolutegravir
      • Elevitegravir → requires PK boosting through CYP 3A4 (give with Cobicistat)
    • Some are substrates of Pg-p
      • Raltegravir
25
Q

DDI’s of INSTI’s? (4 different bullet points)

A

** all interact w/ chelating agents: require spacing dose

  • Polyvalent cations: calcium or iron supplements, cation containing antacids or laxatives
    • decrease INSTI absorption
      • require spacing from dosing
  • Rifampin, Carbmazepine, Phenytoin, St, Johns wort
    • reduce plasma level of integrase inhibitors
  • Metformin
    • Dolutegravir increases metformin levels
    • Biktarvy (2 NRTI’s + INSTI)
      • increases metformin levels
  • Stribild and Genvoya
    • similar DDI’s as boosted PI’s due to cobicistat
26
Q
  1. What combination product of NNRTI and INSTI do we have?
  2. Why would pt’s take this product aka Indication?
  3. CI’s and DDI’s?
A
  1. Juluca (NNRTI + INSTI)
  2. Indication: Maintenance HIV therapy→ not 1st line therapy- for pts who have issues with NRTI’s
  3. C/I with PPI’s and dofetilide (anti-arrhythmic)
    1. ​DDI’s w/ anatacids and H2-antagonists
27
Q
  1. What CCR5 Inhibitor agents do we have available?
  2. What must you do prior to administering this drug?
  3. What type of pt’s is this drug given to?
  4. ADR’s?
A
  1. Maraviroc
  2. Patient must have expression of CCR5 inhibitor -tropic HIV
    1. CCR5 tropism test must be adminstered prior to administeration
  3. Indication: For experienced patients with resistance
  4. ADR’s: Liver toxicity - black box warning
28
Q
  1. What fusion inhibitor agent do we have available?
  2. MOA?
A
  1. Agent: Enfuvirtide
  2. MOA: Inhibits function of transmembrane gp 41
29
Q
  1. What Post-attachment inhibitor agent do we have available?
  2. MOA?
  3. Indication?
A
  1. Ibalizumab
  2. MOA: binds to host CD4 cell and prevents post attachment steps ( cell to cell fusion)
  3. Indication: heavily treament-experienced pts with multi drug resistance HIV-1 that is failing current regimen
    1. EX: pt that is born with HIV
30
Q
  1. Antiretroviral Therapy (ART) is recommended for ?
  2. What test is recommended prior to starting ART?
A
  1. Treatment and Prevention of HIV
  2. Pregnancy test
31
Q
  1. What is the intial ART regimen for most people with HIV?
  2. When might you use Epzicom and Triumeq specifically?
A
  1. INSTI + 2 NRTI’s
  2. Epzicom and Triumeq- (both are– INSTI + 2 NRTI’s) may be used if the patient is HLA-B*5701 negative and HIV viral load is LESS THAN 100,000 copies *** combination product must contain abacavir
32
Q

What Antiretroviral treatments (ART) are NOT recommended?

A
  • Monotherapy
  • Dual NRTI regimens
  • Triple NRTI regimens
  • 2-NNRTI combinations
  • 2 boosters combos
    • ​one booster is enough
33
Q

If your patient is HLA-B*5701 postive what drug should you avoid?

A
  • avoid abacavir
    • use abacavir if VL is greater than 100,000
34
Q
  1. What is the current CDC recommended HIV prophylaxsis medication?
  2. When is it the most effective?
  3. What doesn’t it protect against?
  4. What is the indication for this medication?
  5. What are the requirements for taking this?
A
  1. Truvada ( Emtricitabine/TDF)
  2. Effective if taken daily
  3. Doesn’t protect against STD’s
  4. Intended in combo with other HIV prevention methods for sexually active people at substantial risk for HIV -prostitutes, druggies, homosexual sex
  5. Greater than 18 years old and must weigh at least 35kg (77lbs)
35
Q

What are the CDC guidelines before prescribing Truvada? (7 bullet points)

A
  • Neg HIV test
  • No signs or symptoms of acute HIV
  • Normal renal function
  • No C/I’s to truvada
  • Documented Hepatitis B virus infection and immunization status
  • Test for HCV infection
  • Screen for STD’s
36
Q
  1. Patient monitoring while on Truvada?
  2. Side effects of Truvada
  3. How long can drug be taken for?
A
  1. PT must be reassesed every 90 days while on med- labs, continued HIV risk, adherence, tolerability, etc.
  2. Can be taken indefinitely
  3. Short term- HA, abd. pain/nausea, weight loss
    1. Long term- potential bone and renal side effects
37
Q
  1. What steps should you take for for POST-exposure of HIV?
  2. What drugs should you give?
A
  1. administer antiretrovirals w/n hours of exposure for 28 days
    1. optimal w/n 72 hours
  2. If you were exposed in healthcare setting: (raltegravir + truvada)
    1. If you were exposed in non-healthcare setting: (raltegravir + truvada OR dolutegravir + truvada)
38
Q

What do HIV therapy do you give to pregnant women?

A
  • Darunavir + Ritonavir -BID

Pharm II (12 decks)

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