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*B33VPI - Professionalism > Management of the patient with HIV and AIDs > Flashcards

Management of the patient with HIV and AIDs Flashcards

1
Q

How prevalent is HIV in the UK?

A
  • 91,500 people living with HIV in the UK (2010)
  • > 36 million living with HIV worldwide
  • 22 million deaths from HIV since 1981
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2
Q

Describe the typical progression of HIV infection WRT viral load and CD4.

A
  • Acute phase; asymptomatic or flu-like symptoms (Weeks 0-12), CD4 (white cells) fighting HIV infection; clearing viral load to 10^3 odd, CD4 count recovers slightly
  • Chronic phase; breakdown of immune system from HIV replication within it, viral load creeps up over time as immune system starts to break down - generally symptomatic, but then eventually develop AIDs syndrome
  • AIDs; lose a lot of weight, tired, fevers; if CD4 below 200 cells per micro litre, can present with various AIDs defining illnesses:
    • PCP (pneumonia)
    • Cytomegalovirus
    • Toxoplasmosis
    »> Infections that present in the immunocompromised
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3
Q

How many people with HIV present at the AIDs stage?

A
  • 30% of first-time HIV people present with a CD4 count below 200 cells per micro litre
  • Already at AIDs stage (advanced, not asymptomatic any more)
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4
Q

What is the aim of HAART therapy?

A
  • Undetectable viral load (in the blood etc)

- To slow down the progression line (chronic phase) into the full-blown AIDs syndrome

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5
Q

What is the treatment timeline for HIV?

A
  • Lifelong antiretroviral therapy (ARV/T) aka HAART (highly active antiretroviral therapy) or CART (combination antiretroviral therapy)
    »> No cure of preventive vaccine; aim is to prolong life and improve QoL (keep CD4 count up by keeping viral load down)
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6
Q

How is life expectancy affected if first diagnosed at 20 years of age? What is this similar to?

A
  • At least 2/3 of normal life expectancy, with it not being uncommon to live to full life expectancy (w/ARV/HAART/CART)
  • Same scenario as being diagnosed with T2DM at the same age
  • ‘Chronic illness’
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7
Q

What are the HAART treatment objectives?

A
  • Suppress viral load to undetectable (< 50 copies/ml)
  • Increase CD4 count (surrogate marker for immune system function)
  • Prevent opportunistic infections and progression to AIDs (vigilance)
    »> Saw opportunistic first in the 90s (diagnosing factor); but much rarer now
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8
Q

What are the different types of ARV (antiretroviral therapy) availible?

A

Reverse Transcriptase Inhibitors (13):
• Nucleoside analogues:
- Zidovudine (AZT, ZDV)
- Didanosine (ddI)

• Nucleotide analogues:
- Tenofovir (TFV)

• Non-nucleotide analogues:

  • Nevirapine (NVP)
  • Etravirine (ETV)

Integrase Inhibitors:

  • Raltegravir (RAL)
  • Elvitegravir

Fusion inhibitor:
- Fuzeon

Entry inhibitors (CCR5):
- Fuzeon (T20)

Protease inhibitors (10):

  • Saquinavir (SQV)
  • Darunavir (DRV)
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9
Q

What are the factors to consider WRT choosing first-line HAART therapy?

A
  • Patient’s willingness to commit to therapy (denial? compliance?)
  • Baseline resistance (10-11% in treatment naive patients in UK; HIV is already resistant to one or more medicines availible)
  • Efficacy data
  • Tolerability
  • Convenience
  • Efficacy data
  • Tolerability (S/Es)
  • Convenience
  • Commodities (drugs safe in DM/heart disease/CKD etc?)
  • Consequences of failure (resistance; designing regimen)
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10
Q

What is the first-line HAART for treatment-naive, non-resistant standard HIV patient?

A

BHIVA 2013 preferred:
- 2 NRTIs + efavirenz
E.g:
• Tenofovir + Emtricitabine (one nucleoside, one nucleotide)
• Abacavir + Lamivudine (older regimen)
»> Both + Efavirenz (non-nucleotide)
»> 3 drugs w/different mechanisms of action

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11
Q

If patient cannot take Efavirenz as part of first line HAART, what are they given instead to initiate HAART?

A

BHIVA 2013 alternative:
- 2 NRTIS + ritonavir-boosted protease inhibitor (e.g. lopinavir + ritonavir, saquinavir + ritonavir)
NRTI Example:
• Didanosine + Lamivudine (+ the above PI + ritonavir)

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12
Q

If a patient presents with a low CD4 count, what third antiretroviral is used in HAART instead of efavirenz?

A

Nevirapine

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13
Q

If a patient has cardiac disease, what are they given instead of the protease inhibitors of BHIVA 2013 Alternative HAART, and why?

A
  • Atazanavir (newer protease inhibitor)

- Lots of antiretrovirals can cause water retention and arrhythmias; bad for heart disease

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14
Q

How does when HAART first-line therapy is initiated affect 5-year survival?

A
  • Initiate with a CD4 count of > 200 cells/mm^3
  • If starting HAART < 200 cells/mm^3 CD4, risk of death/progression to AIDs is 12%; DOUBLE that of if starting between 351-500 cells (6%)
  • 201-350 cells CD4 = 7% risk at 5 years
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15
Q

What are the reasons for delayed vs earlier initiation of HAART therapy?

A

For delayed:

  • Drug toxicity
  • Preservation of limited Rx options (later before you develop resistance)
  • Cost

For earlier:

  • Potency, durability, simplicity and safety of current regimens (compared to OG antiretrovirals)
  • Improves formulations and PK (don’t have to take drugs five times a day for example)
  • New classes of drugs
  • Excess morbidity/mortality at lower CD4 (risk of death doubles)
  • Public health; if patient does not get treated down to an undetectable viral load, they are much more likely to transmit the infection
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16
Q

When is HAART first-line therapy initiated in patients with a primary (first-time) HIV infection? What other circumstances mirror this approach?

A
  • Treat in clinical trial (evidence not clear)

Same in:

  • Neurological involvement (HIV in the CNS)
  • < 200 CD4 cell/micro L for > 3 months
  • AIDs defining illness
17
Q

For an established HIV infection, when is HAART first-line therapy initiated in patients with varying CD4 counts?

A

CD4 cells/micro L:

  • < 200 = Treat
  • 201-350 = Treat ASAP when patient is ready (counsel)
  • 351-500 = Treat in specific situations e.g. Hep B (develop symptoms more early)
  • > 500 = Consider enrolment in ‘when to start trial’
  • AIDS diagnosis = Treat
18
Q

Describe the importance of early HIV diagnosis.

A
  • Late diagnosis is most important predictor of dying of AIDs (OR 10.55; 10x more likely to die from AIDs)
  • 1-year mortality rate: 31.6 per 1000 persons diagnosed in 2010:
    • Adults diagnosed late: 40.3/1000
    • Prompt diagnosis: 5.2/1000 (w/high CD4 count)
19
Q

What is a ‘late diagnosis’ of HIV WRT CD4?

A

Diagnosed/presenting with a CD4 < 350.

20
Q

Which groups are more liable to presenting later/being diagnosed with HIV later? (asymptomatic for longer?)

A
  • > 50 years or older (67%) vs. 15-24 years (31%)
  • Heterosexual men (64%) vs. Women (46%), Homoesexual men (36%)
  • Black African adults (66%)
  • Black African adults born abroad (96%)
21
Q

What are the public health implications of not knowing you’re HIV+? (asymptomatic etc.)

A
  • If 25% of the HIV infected populace were unaware they were infected, they go on to be the root cause of 54% (more like 70%) of new HIV infections
  • Compared to the remaining 75% who are aware, who cause 46% of new infections
22
Q

What are meant by ‘indicator diseases’?

A

The range of diseases that are more common among people that are HIV+; patient should be tested for HIV as a precautionary measure.

23
Q

List some common indicator diseases for HIV.

A

Respiratory:

  • Bacterial pneumonia
  • Aspergillosis (fungal)

Neurology:

  • Aseptic meningitis/encephalitis
  • Cerebral abscess
  • Lesion of unknown cause
  • GBS; Guillain-Barré syndrome (immune system attacks myelin sheath of PNS)
  • Peripheral neuropathy
  • Dementia

Dermatology:

  • Severe/recalcitrant seborrhoeic dermatitis/psoriasis
  • Recurrent herpes zoster

Gastroenterology:

  • Oral candidiasis/hairy leukoplakia
  • Chronic diarrhoea/weight loss of unknown cause
  • Salmonella, shigella or campylobacter
  • Hep B/C
Oncology:
- Anal cancer or anal intraepithelial dysplasia
- Lung cancer
- Seminoma
- H&amp;N cancer
- Hodgkin's lymphoma 
(HIV may be trigger of CAN)

Gynaecology:
- Vaginal/cervical intraepithelial neoplasia Grade II or above

Haematology:

  • Thrombocytopenia
  • Neutropenia
  • Lymphopenia

Ophthalmology

  • Infective (herpes, toxoplasma)
  • Unexplained retinopathy

ENT:

  • Lymphadenopathy of unknown cause
  • Chronic parotitis

Other:

  • Mononucleosis-like syndrome (primary HIV)
  • Pyrexia
  • Lymphadenopathy of unknown cause
  • Any STI
24
Q

What are the benefits of HAART?

A
  • Prevention of mother to child transmission (if undetectable viral load)
  • Post exposure prophylaxis (PEP)
  • Secondary prevention of HIV transmission
  • Primary prevention (PrEP)
  • Clinical management of patients with HIV

Main points:
• Reduces HIV replication
• Increase or maintain CD4 numbers
• Maintain ‘less fit’ mutated HIV
• Delay progression to AIDs (becomes terminal then)
• Infection at 20 years of age; 2/3 normal life expectancy

25
Q

What are the short-term S/Es of HAART?

A
  • N&V, diarrhoea (to the point of dehydration), abdominal bloating & flatulence (real bad)
  • Headaches ‘banging headaches’
  • Mild to moderate rash; rarely leading to Steven-Johnson syndrome
26
Q

What are the long-term S/Es of HAART?

A
  • Osteopenia; changes in bone mineral density (lower)
  • Changes in renal function (dropping)
  • Dyslipidemia (atherosclerosis)
  • DM and changes in glucose control
  • Peripheral neuropathy
  • Lipodystrophy & changes in body shape (random depositions of fat in the body)
    »> Newer antiretrovirals have fewer of these though
27
Q

What are the issues of antiretrovirals and potential drug interactions?

A
  • Most ARVs are enzyme inducers/inhibitors/substrates of various Cytochrome P450 isoenzymes
  • Clinical significance not always known; weighing up reduced efficacy vs. increased toxicity (juggle interacting drug regimens)
  • Interactions are not class-based; one protease inhibitor may be fine, whilst another may cause a major interaction
28
Q

How does the effect on CYP450 enzymes vary with if their induced or inhibited by antiretrovirals?

A
  • Enzyme induction; can take 2 weeks to manifest, or 2 weeks to stop
  • Enzyme inhibition; occurs quickly
    »> Drug interactions have potential to continue even after interacting medicine has been stopped.
29
Q

Why can’t the ARVs atazanavir and rilpivirine be taken w/acid suppressing drugs e.g. PPIs?

A

Both rely on an acidic environment for absorption

30
Q

Why are Ritonavir and Cobicistat potentially a problem for asthmatics?

A
  • Powerful enzyme inhibitors
  • Can cause v. elevated levels of other other drugs resulting in toxicity e.g. Cushing’s disease w/steroid inhalers (like Fluticasone), and joint injections
31
Q

What are some important, common drug interactions with ARVs, and the actions required?

A

Clarithromycin:
- Decrease dose in renal failure, consider azithromycin

Rifampicin:
- Increase efavirenz (w/TDM), increase other ARV doses

H2-receptor blockers:
- Give 2-12 hours after atazanavir; not within 12 hours before

PPIs:
- Avoid, use alternative

Simvastatin:
- Avoid, use alternative

St. John’s Wort:
- Avoid

MDMA:
- Avoid

Methadone:
- Monitor for withdrawal and increase dose slowly

Warfarin:
- Frequent INR monitoring (high variance in patients)

Fluticasone:
- Avoid, use alternative (can lead to steroid syndrome)

32
Q

Why is medicine adherence paramount for ARV therapy?

A
  • Very high levels of adherence essential to delay development of resistance; to maintain therapeutic level
  • Need at least 95% of regimen
33
Q

What are common reasons for non-adherence of ARVs?

A
  • Failure to acknowledge need for treatment (denial?)
  • Not understanding the benefits of treatment
  • Perceived harm from taking ARVs and fear of stigmatising S/Es (e.g. lipodystrophy, debilitating diarrhoea)
  • Intolerance to S/Es
  • Complex regimens leading to misunderstanding how to take ARV and forgetting to take ARV (but loads of new combination therapies now)
  • Fear of disclosure of HIV status
  • Cost of ARV (especially in sub-Saharan Africa etc. where there is poor access)
34
Q

Describe how ARV regimens have changed from 1996 to 2006.

A 
1996:
- Didanosine + stavudine + saquinavir
• 24 pills/dose, 5 times a day
• Saquinavir; 6 Q8H w/fatty food
• Didanosine; 2 BD 30 mins AC or 2 hours PC
• Stavudine; 1 tab BD

2006:
- Emtricitabine/tenofovir DF + efavirenz (Atripla)
• 1 tablet OD
• No food restrictions, though taking with high fat meals increases absorption and S/Es

35
Q

How doe HIV co-infection w/TB infect the patient?

A
  • HIV+ people 30x more likely to develop TB (immunocompromised)
  • TB most common cause of AIDS related death (26%, especially in sub-Saharan Africa)
  • Extrapulmonary TB common; spread from lungs to bones etc.
36
Q

How prevalent is TB/TB + HIV coinfection?

A
  • > 1 million people in the world with HIV and TB coinfection
  • 1/3 world population may have latent TB infection
37
Q

In TB + HIV coinfection, why is TB treated first, then HIV?

A
  • Treating both at the same time can lead to IRIS (Immune Reconstitution Inflammatory Syndrome)
  • TB and ARVs put immune system into overdrive
  • Thus TB treated first, then ARV once eradicated
    »> Unless CD4 count already < 200
    »> Rifampicin is also an enzyme inducer (erythromycins)
38
Q

How is HIV/TB co-infection treated?

A
  • Treat TB immediately w/rifampicin-containing regimen
  • OR, treat HIV immediately (2 weeks - 2 months after starting TB therapy) if CD4 < 200 cells/micro L
  • CD4 201 < 350; treat after initial TB treatment phase
  • Complex drug interactions and additive toxicities

*B33VPI - Professionalism (2 decks)

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