HIV Flashcards

1
Q

what is HIV

A

depletion CD4 lymphocytes- progressive immunosuppression, susceptibility to opportunistic infections and cancer

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2
Q

what is HIV

A

depletion CD4 lymphocytes- progressive immunosuppression, susceptibility to opportunistic infections and cancer

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3
Q

when does seroconversion occur

A

2-4 weeks after infection

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4
Q

what CD4 is when AIDs occurs

A
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5
Q

where does HIV bind

A

via gp120 glycoprotein to CD4 receptors on T helper, monocytes, macrophages, neural cells

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6
Q

signs seroconversion

A

primary infection. transient illness. fever, malaise, myalgia, pharyngitis, maculopapular rash, meningoencephalitis

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7
Q

what follows seroconversion

A

asymptomatic infection. 30% have persistent generalised lymphadenopathy

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8
Q

definition of AIDs

A

HIV + indicator of disease

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9
Q

definition of AIDs

A

HIV + indicator of disease

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10
Q

when does seroconversion occur

A

2-4 weeks after infection

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11
Q

what CD4 is when AIDs occurs

A
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12
Q

where does HIV bind

A

via gp120 glycoprotein to CD4 receptors on T helper, monocytes, macrophages, neural cells

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13
Q

If recent infection what tests can be done (if HIV Ab -ve)

A

HIV RNA or core p24 antigen; or check at 6 weeks and 3 months

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14
Q

what follows seroconversion

A

asymptomatic infection. 30% have persistent generalised lymphadenopathy

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15
Q

first line treatment TB

A

isoniazid, pyrazinamide, rifampicin, ethambutol

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16
Q

definition of AIDs

A

HIV + indicator of disease

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17
Q

time scale HIV to AIDs

A

8 years

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18
Q

timescale ARC to AIDs

A

2 years

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19
Q

time scale AIDs to death

A

2 years

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20
Q

diagnosis

A

serum or salivary HIV-Ab by ELISA

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21
Q

other pathogens affecting lungs in HIV

A

M avium intracellulare, CMV,HHV8 (Kaposis sarcoma), lymphoid intersititial pneumonitis

22
Q

in patient who is HIV +ve and cough, fever, night sweats, weight loss what is it until proven otherwise

A

TB

23
Q

first line treatment TB

A

isoniazid, pyrazinamide, rifampicin, ethambutol

24
Q

treatment CMV retinitis

A

ganciclovir containing intra ocular implants

25
Q

CNS complications

A

acute- transient menongoencaphelitis, myelopathy, neuropathy. chronic- dementia, encephalopathy

26
Q

treatment pneumocystis jiroveci

A

co trimoxazole

27
Q

diagnosis pneumocystis jiroveci

A

sputum or bronchoscopy and bronchoalveolar lavage

28
Q

primary prophylaxis pneumocystis jiroveci

A

if CD4

29
Q

other pathogens affecting lungs in HIV

A

M avium intracellulare, CMV,HHV8 (Kaposis sarcoma), lymphoid intersititial pneumonitis

30
Q

gut complications

A

candidiasis, HSV, aphthous ulcers, tumous, oesophageal dysphagia and retrosternal discomfort, anorexia, incr LFTs, hepatosplenomegaly, chronic diarrhoea, perianal disease, Kaposis sarcoma, lymphoma

31
Q

eye complications

A

CMV retinitis- fundoscopy- mozzarella pizza signs

32
Q

PEP

A

Truvada tab, 2 Kaleta tabs

33
Q

CNS complications

A

acute- transient menongoencaphelitis, myelopathy, neuropathy. chronic- dementia, encephalopathy

34
Q

indications for beginning antiretroviral therapy

A

CD4 200; pregnant women; if co infected with hep B and having treatment for hep B

35
Q

treatment toxoplasmosis

A

pyrimethamine

36
Q

benefits of earlier anti retrovirals

A

preservation immune function, prolonged survival, fewer adverse events, decreased transmission

37
Q

when should you start PEP

A

48-72hours after

38
Q

how long should PEP be given

A

28 days (4 weeks)

39
Q

follow up with PEP

A

12 and 24 weeks

40
Q

PEP

A

Truvada tab, 2 Kaleta tabs

41
Q

typical regimen for HIV1

A

efavirenz with 2 NRTIs- lamivudine and tenofovir disoproxil fumarate

42
Q

indications for beginning antiretroviral therapy

A

CD4 200; pregnant women; if co infected with hep B and having treatment for hep B

43
Q

potential risks of earlier anti retrovirals

A

drug toxicity, drug resistance, exhaustion of drug options

44
Q

benefits of earlier anti retrovirals

A

preservation immune function, prolonged survival, fewer adverse events, decreased transmission

45
Q

which virus is responsible for most HIV infections

A

HIV1

46
Q

what are the main classes of antiretrovirals

A

NRTIs (nucleoside reverse transcriptase inhibitor), PIs (protease inhibitor), NNRTIs (non nucleoside reverse transcriptase inhibitors)

47
Q

what can is HAART and what can it cause

A

highly active antiretroviral therapy- renal failure and insulin resistance

48
Q

what can PIs and NNRTIs interact with

A

drugs metabolised by cytochrome p450

49
Q

typical regimen for HIV1

A

efavirenz with 2 NRTIs- lamivudine and tenofovir disoproxil fumarate

50
Q

example of NRTI

A

tenofevir, lamivudine, zidovudine

51
Q

example PI

A

lopinavir

52
Q

example NNRTI

A

efavirenz