INF2 - A. MANAGEMENT OF HIV AND AIDS-COVERED Flashcards

1
Q

what is the main treatment of HIV

A

lifelong anti-retroviral therapy (HAART)/(CART)

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2
Q

is there a cure or a preventative vaccine

A

no

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3
Q

what is the objectives of HAART

A
  • suppress viral load to undetectable (<50 copies/ml)
    so can’t pass on to others
  • increase CD4 count (surrogate marker for immune system response) - fights off other infections
  • prevent opportunistic infections and progression to AIDS
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4
Q

when does AIDS develop

A

when immunity is so low (CD4 count is near 0)

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5
Q

examples of some reverse transcriptase inhibitors

A

nucleoside analogues:
- abacavir
- emtricitabine

nucleotide analogue:
- tenofovir

non-nucleoside analogues:
- efavirenz
- nevirapine

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6
Q

examples of some integrase inhibitors

A
  • raltegravir
  • dolutegravir
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7
Q

example of fusion inhibitor

A
  • enfuvirtide
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8
Q

example of entry inhibitor

A
  • maraviroc
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9
Q

examples of some protease inhibitors

A
  • ritonavir
    -saquinavir
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10
Q

what is HAARTs preferred first line of treatment

A

NRTIs +3rd drug

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11
Q

what is BHIVAs preferred regimen

A

NRTI:
- tenofovir + emtricitabine (Truvada)

+ one of:

NNRTI:
- rilpivirine

PI:
- atazanivir/ritonavir boosted
- darunavir/ritonavir boosted
- ritonavir

INI:
- dolutegravir
- elvitegravir
- raltegravir

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12
Q

what is BHIVAs alternative regimen

A

NRTI:
- abacavir + lamivudine (Kivexa)

+

NNRTI:
- efavirenz

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13
Q

what is regimen for if you get a new diagnosis of HIV during pregnant

A

NRTI:
- abacavir with emtricitabine or lamivudine

+ one of:

NNRTI:
- efavirenz

PI:
- atazanivir

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14
Q

when to use abacavir + lamivudine (Kivexa)

A

if viral load <100,000 (unless doloutegravir)
must be HLA B5701 negative

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15
Q

when to use rilpivirine

A

if viral load <100,000

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16
Q

when to start first line therapy

A

when CD4 count is still high (>350cells/micronL) ie-still have a good immune system

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17
Q

when to start HAART with a patient that has just had a AIDS diagnosis

A

within 2 weeks of starting opportunistic infection treatment depending on presenting complaint

18
Q

benefits of HAART

A
  • prevention of mother to child transmission
  • post exposure prophylaxis (ie - needle stick injury)
  • secondary prevention of HIV transmission (ie - to partner)
  • primary prevention (pre-exposure prophylaxis) ie - those at high risk
  • reduces HIV replication
  • increases or maintain CD4 numbers
  • maintain ‘less fit’ mutated HIV
  • delay progression to AIDS
  • infection at 20 years - near normal life expectancy
19
Q

short term harms of HAART

A
  • N&V
  • diarrhoea
  • abdominal bleeding
  • flatulence
  • headache
  • sleep disturbance
  • mild to moderate rash
20
Q

long term harms of HAART

A
  • changes in renal function
  • bone mineral density
  • hyperlipidaemia: can lead to high cholesterol and fatty plaques in arteries = heart attack and CVD
  • can develop diabetes and changes in glucose control
  • peripheral neuropathy (side effect of diabetes)
  • lipodystrophy and changes in body shape (thinning of arms and legs and redistribution to central region)
21
Q

what drugs do ARVs interact with

A
  • many ARVs are inducer, inhibitors or substrates of various cytochrome P450 isoenzymes (except nucleoside analogues, integrate inhibitors, enfuvirtide)
22
Q

what is the problem with enzyme induction

A

can take 2 weeks to manifest or stop so if you stop the drug, enzyme induction can still occur for 2 more weeks and drug interactions can continue even when interacting medicine stopped

23
Q

what drugs should be avoided with HAART

A
  • PPIs
  • Simvastatin
  • St Johns Wort
  • MDMA
  • Fluticasone
24
Q

when should you switch ARV drugs

A
  • side effects causing life limitations/will become non-adherent
  • pregnancy (actual or potential)
  • avoid potential toxicity
  • drug interactions
  • co-morbidities
  • new trial data/guidelines
  • viral resistance
25
Q

what is viral resistance with ARV and how to treat it

A
  • failure to achieve viral load <50 within 6 months
  • consecutive VL > 200 after VL <50 (ie - developed resistance)
  • resistance test to identify new active drugs
  • aim for 2 or more new active drugs
  • include a protease inhibitor
  • maintain resistance mutations that impair viral fitness
26
Q

who is 2nd line therapy for

A
  • those with resistant HIV
  • highly individual
  • more complex regime with higher pill burdens
  • drugs from newer classes
  • may need to use expanded access or clinical trial drugs
27
Q

what to consider before switching

A
  • effects of drug half-life, enzyme indiction and inhibiton
  • if an enzyme inducer, need to taper off that drug and taper onto new one so don’t get toxicity from a high dose of 2 drugs for overlap period (efavirenz - long half-life and enzyme inducer)
28
Q

how to taper off efavirenz and what to switch to

A

slowly taper off
- lower levels of etravirine, rilpivirine, nevirapine, maraviroc after switch

29
Q

what is an example of an opportunistic infection caused by HIV

A
  • AIDS (when CD4 count <200)
  • atypical presentations of infections ie -with a chest infection might present with a high temp as immune system is impaired
30
Q

HIV and TB

A
  • HIV people 30x more likely to develop TB
  • TB is most common cause of AIDS related death
  • extra pulmonary TB very common
  • TB and ARVs can lead to immune reconstitution inflammatory syndrome
31
Q

treatment for those with co-infection of TB and HIV

A
  • treat TB immediately with rifampicin containing regime (interacts with HIV drugs)
  • CD4 <200: treat HIV immediately (2 weeks - 2 months after starting TB therapy)
  • CD4 >201: treat after initial TB treatment phase (2 months)
32
Q

what is PCP

A
  • Pneumocystis jirovecii pneumonia
  • uncommon in all but those that have HIV
  • exertional dyspnoea over weeks, malaise, dry cough, fevers, interstitial shadowing on chest x-ray
33
Q

treatment for PCP

A

21 days
- IV co-trimoxazole 30mg/kg ads 3/7 then tds and
- prednisolone 40mg bd 5 days then wean

prophylaxis for all patient with CD4<200
- co-trimoxazole 480mg od or
- dapsone 100mg od

34
Q

what is toxoplasma gondii

A
  • similar to PCP
  • ingestion of soil/veg/water contaminated with cat faeces
  • primary infection asymptomatic
  • reactivation occurs when CD4 <200
  • cerebral abscess, ring enhancing lesions on CT, focal neurology, seizures
35
Q

treatment for toxoplasma gondii

A
  • pyrimethamine, sulfadiazine (or clindamycin) and colonic acid for 6 weeks then maintenance

co-trimoxazole prophylaxis for PCP covers toxoplasmosis or:
- dapsone 50mg daily + pyrimethamine 50mg/weekly + folinic acid 15mg/weekly

36
Q

how does pregnancy affect HIV treatment

A
  • all women screened for HIV at start of pregnancy
  • woman conceiving on an effective CART regimen should continue this treatment

exceptions:
- non-standard regimens ie - PI mono therapy
- regimens which show lower PK in pregnancy ie - darunavir/cobicistat and elvitegravir/cobicistat

  • avoid newer agents
37
Q

what if a pregnant woman is pregnant and contracts HIV

A
  • commence CART as soon as they can in 2nd trimester where baseline VL ≤30,000 HIV RNA copies/mL
  • start at start of 2nd trimester when baseline VL 30,000-100,000 HIV RNA copies/mL
  • within 1st trimester is VL >100,000 HIV RNA copies/mL and/or CD4 <200 cells/mm3 (risk to woman > toxicity to baby)
  • all need to have commenced CART by week 24 of pregnancy
  • start on tenofovir DF or abacavir with emtricitabine or lamivudine as a nucleoside backbone
  • 3rd agent = efavirenz or atazanavir/ritonavir as most safety data
38
Q

is there a risk of baby getting HIV

A
  • in womb - no as bloods don’t mix
  • birth canal in delivery - yes
  • want mother’s VL to be undetectable
  • may need to increase doses in 3rd trimester
  • VL <50 HIV RNA copies/mL (undetectable) at 36 weeks - planned vaginal delivery
  • VL 50-399 HIV RNA copies/mL at 36 weeks - pre-labour CS
  • IV zidovudine if HIV untreated at time of delivery of VL>50
  • avoid breastfeeding
39
Q

post-exposure prophylaxis for baby

A
  • Zidovudine 2/52 if maternal VL< 50 copies/mL
  • triple therapy (zidovudine, lamivudine, nevirapine) if VL >50 copies/mL on day of birth
40
Q

post-exposure prophylaxis

A
  • needle stick, laceration, puncture
  • remove virus before systemic dissemination action and infection is established (with 72 hours)
  • start within an hour for occupational exposure
41
Q

treatment for post-exposure prophylaxis

A
  • Truvada 1 od and
  • Raltegravir 400mg bd
  • 1 month treatment
  • off-label use but evidence-based
42
Q

pre-exposure prophylaxis

A
  • recommended for MSM at risk of HIV
  • trans women at risk
  • heterosexualmen/women whose partner has HIV (unless partner on ART, VL<200)
  • tenofovir and emtricitabine (Truvada)