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Pase 2a Notes > HIV/ AIDS > Flashcards

HIV/ AIDS Flashcards

1
Q

UNAIDS goal to eliminate HIV by 2018 UK

A

90/90/90:

90% diagnosed
90% diagnosed on ART
90% viral suppression for those on ART by 2020

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2
Q

3 HIV transmission routes

A

Sexual
Blood
Vertical (35% from mother, but now 0 with tablets)

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3
Q

HIV prevention (sexual)

A

Voluntary male cirucmcision
Treatment of STIs
Male condoms
HIV counselling and testing
Tablets as prevention
Microbiocides
Pre or Post exposure prophylaxis

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4
Q

What is more effect pre or post explore prophylaxis?

A

Pre (injectable every 2 months)

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5
Q

Benefits to knowing HIV status

A

Access to treatment and care
Reduction in morbidity and mortality
Reduction in mother to child transmission
Reduction is sexual transmission
Public health
Cost effective

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6
Q

When is HIV tested?

A

Clinician triggered by clinical indicators
Routine screening in antenatal, high Prevelance locations and high risk groups
Patient requests

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7
Q

Risk factors for HIV

A

Sexual contact (MSM, Sub-Saharan, African, Thailand)
Multiple sexual partners
Rape in high Prevelance locations

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8
Q

Symptoms

A

Acute generalised rash
Glandular fever
Immune dysfunction indicators
Unexplained weight loss or night sweat
Recurrent bacterial infections
Oral candida
Generalised lymphadenopathy
Persistent diarrhoea

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9
Q

Learning points about testing

A

Patients may not remember or tell risk factors
Many departments routinely do
Early diagnosis reduces transmission, morbidity, mortality and costs
Pre-test counselling not required
= Normalise test

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10
Q

2 types of HIV screening test

A

Venous blood sample
Point of care finger prick - immediate but lower sensitivity and specificity

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11
Q

Positive vs negative results - what to do next

A

Negative = repeat if in window period
Positive/ not clear - explain need for further investigation and phone sexual health for advice

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12
Q

Where did HIV come from?

A

HIV-1 = simian immunodeficiency virus from chimpanzees
HIV-2 = West African sooty mangabey monkeys (diminishing)

and then through Bushmeat markets
= Worldwide

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13
Q

Genome structure of HIV

A

Small RNA retrovirus with 10 genes and uses reverse transcriptase to copy and integrate DNa into host cell DNA

Accessory genes to avoid immune

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14
Q

Mechanism of HIV replication in CD4-T cells

A
  1. ATTACHMENT to CCR5 receptors via glycoproteins
  2. CELL ENTRY of viral capsid of nucleic acid and associated proteins (uncoat)
  3. REPLICATION of DNA using reverse transcriptase and then integrated into host using integrase
  4. INTERACTION as host materials are used to transcript proteins and splice
  5. ASSEMBLY in nucleus / cytosol
  6. RELEASE by bursting or exocytosis
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15
Q

Who has genetic resistance to HIV?

A

1% Caucasian with mutant CCr5 gene

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16
Q

2 events that have major influence on long term outcomes

A

Acute infection - early treatment reduces symptoms and transmission

Immune response - determines disease progression and long term control

17
Q

HIV-1 pathogenesis

A

Can pass directly from cell to cell
= mainly CD4+ T cells
Helper, regulatory T cells, dendritic cells, macrophages etc

18
Q

Key driver of HIV disease?

A

T cell activation means dramatic loss of T cells in early infection increases gut mucosal permeability so bacteria leak into the blood
= chronic immune activation

19
Q

Expected survival on antiretroviral therapy

A

Life expectancy still reduced due to:
Adherence, side effect, resistance
non-AIDS defining illness
Size of latent HIV reservoir (resting)

STOPPING ART = revives previous load

20
Q

3 potential HIV cures

A

Sterilising cure - bone marrow transplant from HIV resistant
Functional cure
Shock and kill strategy - wake up virus and kill using cancer drugs

21
Q

Populations at risk of HIV?

A

Sex workers and clients
Injecting drug users
Heterosexual and gay men
Refugees, asylum seekers, migrants and displaced people
Criminals
Truck drivers

22
Q

Socio economic impact of HIV / AIDS in Africa

A

Life expectancy
Stigma
Loss of economically productive adults
Increased spending on ART
Change in social structure (carers)

23
Q

Who is at most risk of acquiring HIV?

A

50% of all new infections world wide are in 15-24 year olds:

STI cause inflammation
Sexual violence
Hormonal affects on mucosal immunity
Bacterial vaginosis alters pH

24
Q

When is early infant HIV screening done?

A

Before 6 weeks using blood PCR
= Allows ART before long term immune damage, smaller viral reservoirs

25
Q

Why are children less likely to have suppressed loads?

A

Not often tested as needs mothers consent
Services aren’t designed in mind
Chronic abnormalities not expected with HIV
Assumption that few would survive

26
Q

Prevention of HIV transmission

A

Condom use - in heterosexual hem
Needle and syringe programmes
Treatment as prevention = pre exposure prophylaxis ART

27
Q

Barriers to HIV vaccine

A

Live or attenuated pathogens too risky
HIV diversity increasing
No evidence of immunity if HIV cleared so don’t know if it can defend again

28
Q

2 markers used to monitor HIV infection

A

CD4 cell count
hIV viral load

29
Q

Describe CD4 and HIV concentration over time

A
  • First couple of weeks virus replicates quickly
  • Immune system decreases viral load
  • But since HIV replicates inside CD4, these are killed as immune defence increases
  • So viral load increases = immune system fails
30
Q

In a patient with glandular fever, rash and non-specific symptoms do what?

A

Ask about sexual history
Think of HIV seroconversion

31
Q

With what problems would we do a HIV test?

A

Unexpected patient
Recurring
No clear underlying cause

32
Q

Presentation of clinical latency

A

Persistent generalised lymphadenopathy

33
Q

Define AIDS

A

CD4 < 200

34
Q

What is the most common opportunistic infection in AIDS

A

Pneumocystis pneumonia (PCP)
= exertional drop in oxygen saturation

35
Q

All patients with what require a HIV test?

A

TB
(TB in HIV is always AIDS)

36
Q

There is a low threshold for what in a patient with HIV and headache?

A

Lumbar puncture
(Many CNS presentations)

37
Q

How does HIV affect risk of cancer?

A

Increases

38
Q

What is HAART?

A

Highly Active Anti-Retroviral Therapy
Usually 3+ drugs with 2 of the same class to act on different points of replication cycle

= HIV is entirely manageable with good prognosis on HAART

39
Q

Why is good drug adherence and avoidance of drug interactions key?

A

Suppress HIV replication
Avoid drug resistance

Pase 2a Notes (6 decks)

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