HIV infection and AIDS Flashcards

1
Q

HIV staging

A

stage1
asymptomatic
generalised lymphadenopathy

stage 2
moderate weight loss
recurrent URTIs
herpes
ulcerations oral
seborrheic dermatitis
fungal nail infection
stage 3
unexplained severe weight loss
chronic diarrhoea
unexplained fever
oral candidiasus
pulmonary tuberculosis
stage 4
Candidiasis of oesophagus, trachea
cervical carcinoma
cryptococcosis
Herpes simplex chronic
HIV encephalopathy
HIV wasting syndrome
lymphoma
pneumonia, recurrent bacterial
toxoplasmosis cerebral

much more

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2
Q

HIV vs AIDs

A

Certain infections and tumours that develop due to a weakness in the immune system are classified as AIDS illnesses. If you have no symptoms then you have HIV infection only

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3
Q

immunology

A

infects and destroys cells of the immune system especially the T-Helper cells that are CD4+
also present on the surface of macrophages and monocytes, cells in the brain, skin, and probably many other sites
-increasing risk of developing infections and tumours

opportunistic infection are
consequence of impaired cell mediated rather than antibody mediated immunity

However, B lymphocyte defect with impaired antibody production to new antigens increased risk of infection with encapsulated bacteria, notably strep pneumoniae

o Most AIDS diagnoses occur at CD4 count <200

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4
Q

oppurtunistic infections in HIV disease

A

pneumocystic jiroveci pneumonia
PCP
caused by the yeast-like fungus Pneumocystis jirovecii
Candidiasis
cryptosporidiosis
cryptococcus neoformans most common cause of meningitis in AIDS

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5
Q

natural history of HIV

A

acute infection- seroconversion
o Approx. 30-60% of patients have a seroconversion illness (when HIV antibodies first develop)
o Abrupt onset 2-4 weeks’ post exposure, self-limiting 1-2 weeks
o Symptoms generally non-specific and differential diagnosis includes a range of common conditions
• Asymptomatic
• HIV related illnesses
• AIDS defining illness – usually CDC category C
Death

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6
Q

diagnosis

A

• If no seroconversion illness then the most accurate way of telling how long HIV has been present is to test stored samples of blood (if available).
o HIV is diagnosed by detecting host antibodies by using rapid point-of-care tests or in the laboratory, where ELISA tests are usually done.
o Most tests detect antibodies to both HIV-1 and HIV-2.

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7
Q

monitoring disease

A
CD4 lymphocyte count
500-1500 cells/mm3. 
HIV viral load
quantitative PCR of HIV-RNA, 
clinical features
o	Persistent generalised lymphadenopathy with nodes typically < 2 cm diameter is a common finding. Eventually the lymph nodes regress, with destruction of node architecture as disease advances.
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8
Q

Anti retroviral therapy

A

• Combination antiretroviral therapy (cART) means at least 3 drugs from at least 2 groups
adherence needs to be over 90%
can lead to normal life but side effects significant

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9
Q

life expectancy according to CD4 nadir prior to treatment

A

<100 52 yrs
100-200 62 yrs
>200 70+yrs

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10
Q

side effects of antiviral drugs

A

nucleside reverse transcriptase inhibitors
-marrow toxicity, neuropathy, lipodystrophy
Non nucleoside RT inhibitors
-skin rashes, hypersensitivity, drug interactions
Protease inhibitors
-Drugs interact, diarrhoea, lipodystrophy, hyperlipidaemia
integrase inhibitors
-rashes

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11
Q

CVD

A

hyperlipidaemias, insulin resistance, increased incidence of MI in HIV patients (mechanism unknown)
HIV increases risk of osteoporosis, cognitive impairment

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12
Q

prevention

A

• Behaviour change and condoms
• Circumcision
• Treatment as prevention
o VL undetectable = transmission risk of 1 in 100,000
• Pre-exposure prophylaxis (PrEP)
• Post-exposure prophylaxis for sexual exposure (PEPSE)
o 3 drugs, 4 weeks.

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13
Q

Kaposi sarcoma

A

vascular tumour arising from endothelium
-manifestation of HIV
skin is the commonest site but it also frequently develops on the hard palate, in the gut or in the bronchi.
The cause of KS is now known to be a herpes virus which has been named the Kaposi’s-associated virus (KAV).

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