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finals 3124 > HIV > Flashcards

HIV Flashcards

1
Q

mode of HIV transmission

A

transmitted from one person to another though specific body fluids - blood, semen, genital fluids, breastmilk

  • unprotected sex
  • sharing needles
  • pregnancy, childbirth, breast feeding
  • transfuse contaminated blood
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2
Q

goals of antiretroviral therapy ART in HIV infection

A
  1. reduce HIV associated morbidity
  2. prolong duration and quality of survival
  3. restore and preserve immunologic function
  4. maximally and durably suppress plasma HIV viral load
  5. prevent HIV transmission
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3
Q

use of CD4 cell count as surrogate markers

A
  • CD4 range: 500-1200 cells/ mm3
  • most important indicator and strongest predictor of subsequent disease progression and survival
  • use to determine urgency for initiating anti-retroviral therapy
  • use to assess response to antiretroviral therapy (assess @baseline every 3-6mo after tx started, 12mo after adequate response)
  • use to assess the need for initiating / discontinuing prophylaxis for opportunistic infections (eg. prophylaxis for pneumocystis pneumonia when CD4 cells <200cells/mm3)
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4
Q

use of HIV viral load as surrogate markers

A
  • amount of virus in plasma
  • most impt indicator of response to anti-retroviral therapy, can be useful in predicting clinical progression
  • measure before initiation and within 2-4 w (not later than 8w), after tx / modification, every 4-8w measure until viral load suppressed
  • effective regimen generally achieve viral suppresion (undetectable HIV RNA lvl)
  • in patients on stable regimen and suppressed viral load, monitoring can be done every 3-6 mth
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5
Q

when to start ART

A

recommended for all HIV infected individuals, regardless of CD4 cell count, to reduce morbidity and mortality associated with HIV infection and prevent transmission

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6
Q

limitations of earlier ART initiation

A
  1. development of tx-related SE and toxicities
  2. development of drug resistance because of incomplete viral suppression- loss of future tx options
  3. transmission of drug-resistant virus in pt who dont maintain full virologic suppression
  4. < time for pt to learn about HIV and its tx, hence < time to prepare for need for adherence
  5. increase total time on meds, hence greater chance of tx fatigue
  6. increase cost
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7
Q

benefits of earlier ART initiation

A
  1. maintenance of higher CD4 count and prevention of potentially reversible damage to immune system
  2. decrease risk for HIV-associated complications that can sometimes occur at CD4 counts >350cells/mm3 (eg. TB, non-Hodgkin’s lymphoma, Kaposi’s sarcoma, peripheral neuropathy, HIV associated cognitive impairment)
  3. decrease risk of transmission to others (positive public health implication)
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8
Q

who should be tested for HIV

A
  1. intravenous drug users
  2. person who have unprotected sex w multiple partners
  3. man x man
  4. treated for STD
  5. recipient of multiple blood transfusion
  6. sexually assaulted
  7. pregnant women (mandatory in sg)
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9
Q

diagnosis of HIV

A
  1. serum antibody detection (western blot; HIV enzyme immunoassay antibody test)
  2. HIV RNA detection/ quantification (viral load; PCR)
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10
Q

presentation of HIV

A
  1. acute primary HIV infection (flu like symptoms)
  2. asymptomatic stage (many years)
  3. persistent generalised lymphadenopathy (enlarged lymph node enlargement @neck/underarm/groin >3mth)
  4. AIDs / related conditions (advance, succumb to infection by unsual organisms that the uninfected person can resist; systemic symptoms- fever, weigh tloss, diarrhoea; rare cancers)
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11
Q

targets available for antiretroviral therapy

A
  1. nucleoside reverse transcriptase inhibitors NRTIs
  2. non-nucleoside reverse transcriptase inhibitors NNRTIs
  3. integrase strand transfer inhibitor INSTIs
  4. protease inhibitor PIs
  5. fusion/entry (inhibitor)
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12
Q

factors to consider when selecting initial regimen

A
  1. pt understanding of HIV
  2. cost and availability
  3. adherence (pill burden, freq, food & fluid consideration)
  4. virologic efficacy
  5. potential ADR (comorbidities, drug interactions)
  6. childbearing potential)
  7. genotypic drug resistance testing`
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13
Q

recommended combination for ART

A
  1. 2NRTI + 1INSTI
    (a) : tenofovir + emitricitabine + bictegravir
    (b) : tenofovir + emtricitabine + dolutegravir
    (c) : abacavir + lamivudine + dolutegravir
  2. 1NRTI + 1INSTI
    (a) : emtricitabine + dolutegravir
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14
Q

NRTIs suitable for HBV (hepatitis b virus)

A
  1. tenofovir
  2. emtricitabine
  3. lamivudine
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15
Q

class advantage of NRTIs

A
  1. established dual backbone of combi ART

2. renal elimination, little concerns for drug interactions

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16
Q

class disadvantage of NRTIs

A
  1. ADR related to mitochondrial toxicity (rare but serious)
  2. lactic acidosis and hepatic steatosis (fatty infiltrate)
  3. lipoatrophy (loss of fat)
    level of seriousness: zidovudine > tenofovir = abacavir = lamivudine
  4. all but abacavir requires dose adjustment
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17
Q

types of NRTIs

A
  1. tenofovir
  2. emtricitabine
  3. abacavir
  4. lamivudine
  5. zidovudine
18
Q

which NRTI suitable for pregnancy

A

zidovudine

19
Q

which NRTI have minimal toxicities

A
  1. lamivudine: minimal toxicity, ADR: N/V/D

2. emtricitabine: minimal toxicity; ADR- hyperpigmentation, N/D

20
Q

ADR of abacavir

A
  1. NVD
  2. hypersensitivity rxn in HLAB*5701 pt
  3. rashes, fever, malaise, fatigue, loss appetite, cough, SOB
  4. concern for association with myocardial infarction (not to be used in high CV risk patients)
21
Q

ADR of zidovudine

A
  1. NVD

2. bone marrow suppression causing anemia/neutropenia

22
Q

ADR of tenofovir

A
  1. NVD

2. renal impairment, decrease bone mineral density

23
Q

types of INSTI

A
  1. bictegravir
  2. dolutegravir
  3. raltegravir
  4. elvitegravir
24
Q

class advantages of INSTI

A
  1. bictegravir and dolutegravir have good virologic effectiveness
  2. high genetic barrier to resistance (B=D >R=E)
  3. generally well tolerated
25
Q

class disadvantage of INSTI

A
  1. ADR: weight gain, diarrhoea, N, HA, depression (but rarely reported in pt w pre-existing psychiatric conditions)
  2. DDI: F lowered by concurrent administration of polyvalent cations (B,D,E are CYP3A4 substrates)
26
Q

INSTI ADR

A
  1. bictegravir: increase SCr
  2. Raltegravir: Pyrexia, Cr kinase elevation (rhabdomyolysis)
  3. dolutegravir: increase SCr by inhibiting tubular secretion
27
Q

types of NNRTIs

A
  1. Efavirenz

2. Rilpivirine

28
Q

class advantage of NNRTIs

A
  1. long half life

2. less metabolic toxicity (hyperlipidaemia, insulin resistance) than PIs

29
Q

class disadvantage of NNRTIs

A
  1. low genetic barrier to resistance
  2. cross resistance among approved NNRTIs
  3. skin rash, SJS (R
30
Q

ADR of NNRTIs

A
  1. efavirenz: rashes, hyperlipidaemia (due to increase LDL-C); neuropsychiatric SE (dizziness, depression, insomnia)
  2. Rilpivirine: depression, HA
31
Q

CYP activities for NNRTIs

A
  1. Efavirenz: 3A4 substrate, 2B6 & 2C19 inducer

2. Rilpivirine: 3A4 substrate; lower absorption with high gastric pH, CI with PPIs

32
Q

types of PIs

A
  1. Ritonavir
  2. Lopinavir
  3. Atazanavir
  4. Daruncavir
  5. Fosamprenavir
33
Q

class advantage of PIs

A
  1. high genetic barrier to resistance

2. PI resistance less common

34
Q

class disadvantage of PIs

A
  1. metabolic complications (dyslipidemia, insulin res.)
  2. GI SE (NVD)
  3. liver toxicity (esp chronic Hep B/C)
  4. CYP3A4 inhibitor and substrates (DDI)
  5. fat maldistribution (lipohypertrophy)
  6. increased risk of osteopenia/ osteoporosis
35
Q

ADR of PIs

A
  1. ritonavir: potent CYP3A4, 2D6 inhibitor, used with other PI (L/R) to boost levels
  2. Darunavir: good GI tolerability, less lipid SE; SJS
    (sulfonamide)
  3. atazanavir: good GI tolerability, less lipid SE, CI with concurrent use of PPI, hyperbilirubinemia, prolong QT interval, skin rash
36
Q

types of fusion inhibitor

A
  1. enfuvirtide (subscu injection BD)
37
Q

ADR of enfuvirtide

A

fusion inhibitor

  1. erythema/ induration, nodules/ cyst, pruritis
  2. rare hyper sensitivity
  3. increase bacterial pneumonia
38
Q

types of CCR5 antagonist

A
  1. maraviroc (selzentry) - is a CYP3A4 sub
39
Q

when to use CCR5

A

only on those whose strain of HIV uses the CCR5 receptor to enter CD4 cells

  • need do co-receptor tropism assay before initiation
  • must be CCR5 predominant to use (if not use CXCR4 or dual mixed tropism)
40
Q

ADR of maraviroc

A

CCR5

  1. abdominal pain
  2. cough
  3. musculoskeletal symptoms
  4. rashes, pyrexia
  5. dizziness
  6. URTI
  7. hepatotoxicity
  8. orthostatic hypotension
41
Q

reasons of failure of HIV tx

A
  1. drug toxicity
  2. dosing frequency and requirements
  3. DDI
  4. viral resistance
  5. regimen potency
  6. provider experience
  7. adherence not >95%
42
Q

strategies to improve adherence to ART

A
  1. establish readiness to start therapy
  2. provide education on medication dosing
  3. review potential SE
  4. anticipate and treat SE
  5. engage family & friends
  6. utilise educational aids (picture, pillboxes, calendar)
  7. simplify regimens, dosing and food requirements (taking ARV w or w/o food)
  8. provide accessible trusting healthcare team

finals 3124 (7 decks)

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