HIV and AIDs Flashcards

1
Q

How is HIV transmitted?

A
Sexually 
IVDA 
Blood products (e.g. blood transfusion) 
Vertically (mother to child, transmission occurs at time of delivery) 
Organ transplant
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2
Q

Which two authorities provide information on infectious disease surveillance figures for England and Scotland?

A

PHE and PHS

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3
Q

How do we describe the risk of someone having HIV?

A

High risk and unknown risk

DON’T use term low risk

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4
Q

Does HIV testing require consent?

A

Yes - unless patient unconscious and considered to be in their best interest to have the test

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5
Q

Does a - HIV test affect insurance premiums?

A

No

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6
Q

Do you have to tell your work if you get a +ve HIV test?

A

Only if they req. HIV testing, e.g. in healthcare - and changes will be made to your work, e.g. avoiding exposure prone procedure (EPP)

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7
Q

What are three infections screened for during ANS?

A

HIV, syphilis, hep B

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8
Q

How do you diagnose HIV?

A

Combined Ag/Ig tests

4th generation ELISA assay allows simultaneous antigen/antibody detection

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9
Q

What is the issue with diagnostic tests for HIV?

A

Need to be aware of the diagnostic window!

This is the period of time during which infection markers are not detectable despite the patient being infected (length of window differs - about 1 month but can be p to 2)

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10
Q

What other may tests may you do after you have a diagnosis of HIV?

A

Viral load: measure of the effectiveness of Rx or diagnosis in the presence of maternal antibody (maternal Ig does not mean infection of the baby)

CD4 count

HIV resistance testing - polymerse and protease genes to identify specific mutations that confers resistance to ARTs (do for baseline diagnosis/suboptimal response/failure of Rx or need to change Rx

Subtype determination

Trophism testing - finding which receptors HIV are inclined to act on

Drug levels - ART reaching optimum?compliance?

Avidity test - gives info on timing of infection

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11
Q

What kind of virus is HIV?

A

Retrovirus

Contains 2 RNA strands

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12
Q

What kind of cells does HIV infect?

A

Infects CD4+ cells (especially T helper cells, but also macrophages, monocytes, brain and skin cells etc.)

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13
Q

How does HIV identify the cells it intends to infect?

A

HIV binds via its GP120 envelope glycoprotein to CD4 receptors

Chemokine receptors, e.g. CCR5 and CXCR4 may also be involved

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14
Q

What do infected cells do?

A

Migrate into lymphoid tissue

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15
Q

How does HIV lead to impaired immune function?

A

Viral replication and the release of new viruses –> new infections –> impaired CD4+ cells –> impaired immune function

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16
Q

What results of an impaired immune function?

A

Opportunistic infections, malignancy may arise as a result of inadequate immune response - AIDS (acquired immunodeficiency syndrome)

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17
Q

What are the two types of HIV?

A
HIV 1 (most common) 
HIV 2 (rare)
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18
Q

What is the major subtype of HIV?

A

M - responsible for global epidemic

Other minor subtypes include N, O and P

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19
Q

What is the natural history of HIV?

A

As dx progresses: CD4 count ↓ and HIV viral load ↑ –> ↑risk developing infections/tumours
The ↓ the CD4 count the ↑ the severity of illness

With initial infection, immune system may compensate for some time, but eventually CD4 v. low + viral load v. high  opportunistic infections + symptomatic HIV infection

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20
Q

What is a normal CD4 count?

A

> 500

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21
Q

At what CD4n count do most AIDS diagnoses (severe infections) occur at?

A

<200

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22
Q

Without treatment, what steps does HIV advance in?

A

Acute infection (seroconversion) –> asymptomatic –> HIV-related illness –> AIDS defining illness –> death

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23
Q

When does an acute HIV infection tend to occur?

A

2-4 weeks after infection

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24
Q

How long does the acute HIV infection tend to last for?

A

1-2 weeks

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25
Q

How does the acute HIV infection present?

A

‘Worst flu ever’
Occurs during seroconversion
80% get symptoms: flu-like illness, fever, malaise, lethargy, pharyngitis, lymphadenopathy, toxic exanthema (looks like EBV but serology -ve)

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26
Q

Why does the acute HIV illness/seroconversion occur?

A

The body makes the Ig against HIV, seroconversion occurs when the Ig and the HIV first meet

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27
Q

What is clinical latency in HIV?

A

Viral replication is slow therefore patients can be asymptomatic without treatment for a long time (up to 10y)

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28
Q

Is transmission still possible in clinical latency?

A

Yes if they are not on ARTs

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29
Q

Define AIDS

A

CD4 count <200 or developed 1+ opportunistic infections

Treatment is now effective enough to prevent progression to AIDS

AIDS is the most severe form of HIV infection

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30
Q

What is the clinical staging of HIV?

A

Primary HIV Infection

Clinical stage 1 - persistent generalised lymphadenopathy (asymptomatic, normal activity)

Clinical stage 2 - wt loss <10% body wt, minor mucocutaneous manifestations, herpes zoster, recurrent URTIs (symptomatic, normal activity)

Clinical stage 3 - wt loss >10% body wt, unexplained chronic diarrhoea >1m, unexplained persistent fever >1m, oral candidiasis, oral hairy leukoplakia, pulmonary TB wi last yr, severe bacterial infections (bedridden <50% day in last mnth)

Clinical stage 4 - HIV wasting syndrome, PCP, toxoplasmosis, cryptospiridosis >1m, cryptococcosis, CMV (other than liver, lymph nodes, spleen), HSV infection, mucocutaneous >1m/visceral any duration, PML, disseminated endemic mycosis, candiasis of the oesophagus, trachea, bronchi/lungs, atypical mycobacteriosis, non-typhoid salmonella septicaemia, extrapulmonary TB, kapsoi’s sarcoma, HIV encephalopathy

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31
Q

What is the relationship between HIV and AIDS?

A

Go between HIV and AIDS - treatment should bring AIDS patient back to HIV infected patient

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32
Q

What are opportunistic infections/tumours?

A

Certain infections/tumours developing due to weakness of the immune system (these are classified as AIDS illnesses)

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33
Q

List the AIDS defining conditions?

A

TB, pneumocystitis (PJP, PCP)
Cryptosporidosis
Kaposi’s sarcoma, non-Hodgkin’s lymphoma
Toxoplasmosis, primary cerebral lymphoma, cryptococcal meningitis, PML
CMV retinitis

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34
Q

In which conditions should you carry out HIV testing?

A

Bacterial pneumonia, aspergillosis
Aseptic meningitis/encephalitis, cerebral abscess, space occupying lesion of unknown cause, GB syndrome, transverse myelitis, peripheral neuropathy, dementia, leucoencephalitis

Severe/recalcitrant seborrheic dermatitis/psoriasis, multidermatomal/recurrent herpes zoster
Oral candidiasis, oral hairy leukoplakia, chronic diarrhoea unknown cause, wt loss unknown cause, salmonella, shigella, campylobacter, Hep B/C
Anal cancer/anal intraepithelial dysplasia, lung cancer, seminoma, HN cancer, Hodgkin’s lymphoma, castleman’s disease
Unexplained blood dyscarasia incl. thrombocytopenia, neutropenia, lymphenia
Infective retinal disease (herpes virus/toxoplasmosis), unexplained retinopathy
Lymphadenopathy unknown cause, chronic parotitis, lymphoepithelial parotid cysts
Mononucleosis-like syndrome (primary HIV infection), PUO, STI

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35
Q

When should you start HIV treatment?

A

Advice is to start ART as soon as diagnosed

If CD4<200 start treatment ASAP

In pregnancy must start before the 3rd trimester to prevent vertical transmission

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36
Q

How many pills is involved in HIV treatment?

A

1

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37
Q

What is cART?

A

Combination anti-retroviral therapy

Must take at least 3 different drugs from at least 2 different groups (typically 2 nucleoside reverse transcriptase inhibitors + either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor)

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38
Q

How high must adherence to ART be to prevent disease progression?

A

> 90%

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39
Q

When might you have to adjust cART?

A

If VL is not low enough after 4-6 weeks of starting treatment

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40
Q

How long does treatment take?

A

Treatment is lifelong (continuous treatment more successful than start stop)

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41
Q

What does poor adherence to cART lead to?

A

Viral mutation and resistance –> inadequate potency, drug levels –> selection of resistant quasispecies

42
Q

What is the mechanism by which the HIV virus infects cells?

A

Virus attaches to CD4 receptor
Retrovirus codes for reverse transcriptase
RT converts viral RNA –> DNA
DNA integrates into host genome via integrase enzyme
More viral RNA produced
Virions assemble (protein formation req. proteases)

43
Q

What do most drugs target?

A

Reverse transcriptase enzyme

44
Q

What are the 4 classes of ART drugs?

A

Nucleoside reverse transcriptase inhibitors
Non-nucleoside reverse transcriptase inhibitors
Protease inhibitors
Integrase inhibitors

45
Q

What are the SEs of the nucleoside reverse transcriptase inhibitors?

A

Marrow toxicity, neuropathy, lipodystrophy

46
Q

What are the SEs of the non-nucleoside reverse transcriptase inhibitors?

A

Skin rashes, hypersensitivity, DDIs

47
Q

What are the SEs of the protease inhibitors?

A

DDIs, diarrhoea, lipodystrophy, hyperlipidaemia

48
Q

What are the SEs of the integrase inhibitors?

A

Rashes

49
Q

If lidodystrophy occurs due to the SEs of ART, what can we do?

A

Offer cosmetic surgery

50
Q

What are the challenges of HIV care?

A
Osteoporosis 
Cognitive impairment 
Malignancy 
Cerebrovascular disease Renal disease
IHD
DM
51
Q

How can we prevent HIV?

A
Behaviour change/condom use
Circumcision 
Rx as prevention (VL undetectable = untransmissible) 
PrEP for high risk groups 
PEPSE
52
Q

What is PEPSE?

A

Post-exposure prophylaxis for sexual exposure

28 day course of ART for those at high risk (should be started no later than 72h after exposure to dramatically reduce the risk of getting HIV)

53
Q

Why can’t we cure HIV?

A

HIV enters sanctuary sites where the drug can’t reach - if we were able to stimulate proliferation of the virus at these sites, the drugs may be able to identify the viruses more easily

54
Q

Prognosis in HIV

A

Improving
Early Rx = normal LE
LE correlates with CD4 count

55
Q

What is the risk of transmission with needle stick injury of HBV?

A

30%

56
Q

What is the risk of transmission with needle stick injury of HCV?`

A

3%

57
Q

What is the risk of transmission with needle stick injury of HIV?

A

0.3%

Mucocutaneous exposure = 0.001%

58
Q

What are the two PEP drugs?

A

Truvada and Kaltetra

59
Q

If needle stick injury occurs what must you do?

A

First aid - encourage bleeding, wash, wash out eyes, noses, mouth, report to OHS, senior manager/ doctor

PEP

Test source and exposed person (req. consent)

60
Q

When should testing for HIV be done in asymptomatic patients?

A

4 weeks after possible exposure

Repeat test at 12 weeks if this is negative

61
Q

What two tests can be used to confirm a diagnosis of HIV?

A

HIV antibody test

p24 antigen test

62
Q

What does the HIV antibody test consist of?

A

ELISA and Western blot assay

63
Q

What is pneumocystis jiroveci?

A

Unicellular eukaryote

64
Q

All patients with CD4 < what should have PCP prophyaxis

A

300

65
Q

What are features of PCP pneumonia?

A

Dyspnoea
Dry cough
Fever
V. few chest signs!!

66
Q

What is a common complication of PCP?

A

Pneumothorax

67
Q

What are some rarer extrapulmonary manifestations of PCP?

A

Hepatosplenomegaly
Lymphadenopathy
Choroid lesions

68
Q

What do you see on CXR with PCP?

A

Bilateral interstitial pulmonary infiltrates

69
Q

What investigation is needed to demonstrate PCP?

A

Bronchoalveolar lavage (silver stain shows characteristic cysts)

70
Q

How is PCP treated?

A

Co-trimoxazole
IV pentamidine in severe cases
Steroids if hypoxic

71
Q

What are common opportunist infections/disorders that develop with a CD4 count of 200-500cells/mm3?

A
Oral thrush (candida albicans) 
Shingles (HZV)
Hairy leukoplakia (EBV)
Kaposi sarcoma (HHV8)
72
Q

What are common opportunist infections/disorders that develop with a CD4 count of 100-200cells/mm3?

A
Cryptosporidiosis
Cerebral toxoplasmosis
PML (JC virus) 
PCP
HIV dementia
73
Q

What are common opportunist infections/disorders that develop with a CD4 count of 50-100cells/mm3?

A

Aspergillosis (A. fumigatus)
Oesophageal candidiasis
Cryptococcal meningitis
Primary CNS lymphoma (EBV)

74
Q

What are common opportunist infections/disorders that develop with a CD4 count of <50cells/mm3?

A

CMV retinitis

Mycobacterium avium-intracellulare infection

75
Q

What organism accounts for 50% of cerebral lesions in HIV patients?

A

Toxoplasmosis

76
Q

What are symptoms of toxoplasmosis?

A

Constitutional symptoms, headache, confusion, drowsiness

77
Q

What do you see on CT in toxoplasmosis?

A

Usually single/multiple ring enhancing lesions, mass effect may be seen

78
Q

How is toxoplasmosis treated?

A

Sulfadiazine and pyrimethamine

79
Q

How can you differentiate between primary CNS lymphoma and toxoplasmosis?

A

Toxoplasmosis - multiple lesions, ring/nodular enhancement, thallium SPECT negative

Lymphoma - single lesion, solid enhancement, thallium SPECT positive

80
Q

What usually causes encephalitis in HIV patients?

A

CMV or HIV itself

81
Q

What do you see on CT in encephalitis?

A

Oedematous brain

82
Q

What is the most common fungal infection of the CNS?

A

Cryptococcus

83
Q

How does cryptococcal infection present?

A

Headache, fever, malaise, NV, seizures, focal neurological deficit

84
Q

What do you see on the CSF of someone with a cryptococcal infection?

A

High opening pressure

India ink test positive

85
Q

What do you see on the CT of someone with a cryptococcal infection?

A

Meningeal enhancement, cerebral oedema

86
Q

What is progressive multifocal leukoencephalopathy?

A

Widespread demyelination

87
Q

What causes PML?

A

Infection of oligodendrocytes by JC virus

88
Q

What are symptoms of PML?

A

Subacute onset of behavioural changes, speech, motor and visual impairment

89
Q

What do you see on CT in PML?

A

Single/multiple lesions, no mass effect

90
Q

What do you see on MRI in PML?

A

High-signal demyelinating white matter lesions

91
Q

What causes AIDS dementia?

A

HIV virus itself

92
Q

What are symptoms of AIDS dementia?

A

Behavioural changes, motor impairment

93
Q

What can you see on the CT of someone with AIDS dementia?

A

Cortical and subcortical atrophy

94
Q

What is the most common cause of infective diarrhoea in HIV?

A

Cryptosporidium

95
Q

What are other possible causes of diarrhoea in HIV?

A

CMV
Mycobacterium avium intracellulare
Giardia

96
Q

What kind of organism is Cryptosporidium?

A

Intracellular protozoa

97
Q

What investigation can be used to identify the Cryptosporidium?

A

Modified ZN stain of stool which shows characteristic red cysts

98
Q

What is the treatment of Cryptosporidium?

A

Supportive

99
Q

When is Mycobacterium avium intracellulare infection typically seen?

A

CD4 <50

100
Q

What are typical features of Mycobacterium avium intracellulare infection?

A

Fever, sweats, ab pain, diarrhoea

May be hepatomegaly and derranged LFTs

101
Q

How is Mycobacterium avium intracellulare infection diagnosed?

A

Blood cultures + bone marrow examination

102
Q

What is the treatment of Mycobacterium avium intracellulare infection?

A

Rifabutin, ethambutol, clarithromycin