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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
How does the acute HIV infection present?
'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)
26
Why does the acute HIV illness/seroconversion occur?
The body makes the Ig against HIV, seroconversion occurs when the Ig and the HIV first meet
27
What is clinical latency in HIV?
Viral replication is slow therefore patients can be asymptomatic without treatment for a long time (up to 10y)
28
Is transmission still possible in clinical latency?
Yes if they are not on ARTs
29
Define AIDS
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
30
What is the clinical staging of HIV?
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
31
What is the relationship between HIV and AIDS?
Go between HIV and AIDS - treatment should bring AIDS patient back to HIV infected patient
32
What are opportunistic infections/tumours?
Certain infections/tumours developing due to weakness of the immune system (these are classified as AIDS illnesses)
33
List the AIDS defining conditions?
TB, pneumocystitis (PJP, PCP) Cryptosporidosis Kaposi's sarcoma, non-Hodgkin's lymphoma Toxoplasmosis, primary cerebral lymphoma, cryptococcal meningitis, PML CMV retinitis
34
In which conditions should you carry out HIV testing?
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
35
When should you start HIV treatment?
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
36
How many pills is involved in HIV treatment?
1
37
What is cART?
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)
38
How high must adherence to ART be to prevent disease progression?
>90%
39
When might you have to adjust cART?
If VL is not low enough after 4-6 weeks of starting treatment
40
How long does treatment take?
Treatment is lifelong (continuous treatment more successful than start stop)
41
What does poor adherence to cART lead to?
Viral mutation and resistance --> inadequate potency, drug levels --> selection of resistant quasispecies
42
What is the mechanism by which the HIV virus infects cells?
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
What do most drugs target?
Reverse transcriptase enzyme
44
What are the 4 classes of ART drugs?
Nucleoside reverse transcriptase inhibitors Non-nucleoside reverse transcriptase inhibitors Protease inhibitors Integrase inhibitors
45
What are the SEs of the nucleoside reverse transcriptase inhibitors?
Marrow toxicity, neuropathy, lipodystrophy
46
What are the SEs of the non-nucleoside reverse transcriptase inhibitors?
Skin rashes, hypersensitivity, DDIs
47
What are the SEs of the protease inhibitors?
DDIs, diarrhoea, lipodystrophy, hyperlipidaemia
48
What are the SEs of the integrase inhibitors?
Rashes
49
If lidodystrophy occurs due to the SEs of ART, what can we do?
Offer cosmetic surgery
50
What are the challenges of HIV care?
``` Osteoporosis Cognitive impairment Malignancy Cerebrovascular disease Renal disease IHD DM ```
51
How can we prevent HIV?
``` Behaviour change/condom use Circumcision Rx as prevention (VL undetectable = untransmissible) PrEP for high risk groups PEPSE ```
52
What is PEPSE?
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
Why can't we cure HIV?
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
Prognosis in HIV
Improving Early Rx = normal LE LE correlates with CD4 count
55
What is the risk of transmission with needle stick injury of HBV?
30%
56
What is the risk of transmission with needle stick injury of HCV?`
3%
57
What is the risk of transmission with needle stick injury of HIV?
0.3% Mucocutaneous exposure = 0.001%
58
What are the two PEP drugs?
Truvada and Kaltetra
59
If needle stick injury occurs what must you do?
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
When should testing for HIV be done in asymptomatic patients?
4 weeks after possible exposure | Repeat test at 12 weeks if this is negative
61
What two tests can be used to confirm a diagnosis of HIV?
HIV antibody test | p24 antigen test
62
What does the HIV antibody test consist of?
ELISA and Western blot assay
63
What is pneumocystis jiroveci?
Unicellular eukaryote
64
All patients with CD4 < what should have PCP prophyaxis
300
65
What are features of PCP pneumonia?
Dyspnoea Dry cough Fever V. few chest signs!!
66
What is a common complication of PCP?
Pneumothorax
67
What are some rarer extrapulmonary manifestations of PCP?
Hepatosplenomegaly Lymphadenopathy Choroid lesions
68
What do you see on CXR with PCP?
Bilateral interstitial pulmonary infiltrates
69
What investigation is needed to demonstrate PCP?
Bronchoalveolar lavage (silver stain shows characteristic cysts)
70
How is PCP treated?
Co-trimoxazole IV pentamidine in severe cases Steroids if hypoxic
71
What are common opportunist infections/disorders that develop with a CD4 count of 200-500cells/mm3?
``` Oral thrush (candida albicans) Shingles (HZV) Hairy leukoplakia (EBV) Kaposi sarcoma (HHV8) ```
72
What are common opportunist infections/disorders that develop with a CD4 count of 100-200cells/mm3?
``` Cryptosporidiosis Cerebral toxoplasmosis PML (JC virus) PCP HIV dementia ```
73
What are common opportunist infections/disorders that develop with a CD4 count of 50-100cells/mm3?
Aspergillosis (A. fumigatus) Oesophageal candidiasis Cryptococcal meningitis Primary CNS lymphoma (EBV)
74
What are common opportunist infections/disorders that develop with a CD4 count of <50cells/mm3?
CMV retinitis | Mycobacterium avium-intracellulare infection
75
What organism accounts for 50% of cerebral lesions in HIV patients?
Toxoplasmosis
76
What are symptoms of toxoplasmosis?
Constitutional symptoms, headache, confusion, drowsiness
77
What do you see on CT in toxoplasmosis?
Usually single/multiple ring enhancing lesions, mass effect may be seen
78
How is toxoplasmosis treated?
Sulfadiazine and pyrimethamine
79
How can you differentiate between primary CNS lymphoma and toxoplasmosis?
Toxoplasmosis - multiple lesions, ring/nodular enhancement, thallium SPECT negative Lymphoma - single lesion, solid enhancement, thallium SPECT positive
80
What usually causes encephalitis in HIV patients?
CMV or HIV itself
81
What do you see on CT in encephalitis?
Oedematous brain
82
What is the most common fungal infection of the CNS?
Cryptococcus
83
How does cryptococcal infection present?
Headache, fever, malaise, NV, seizures, focal neurological deficit
84
What do you see on the CSF of someone with a cryptococcal infection?
High opening pressure | India ink test positive
85
What do you see on the CT of someone with a cryptococcal infection?
Meningeal enhancement, cerebral oedema
86
What is progressive multifocal leukoencephalopathy?
Widespread demyelination
87
What causes PML?
Infection of oligodendrocytes by JC virus
88
What are symptoms of PML?
Subacute onset of behavioural changes, speech, motor and visual impairment
89
What do you see on CT in PML?
Single/multiple lesions, no mass effect
90
What do you see on MRI in PML?
High-signal demyelinating white matter lesions
91
What causes AIDS dementia?
HIV virus itself
92
What are symptoms of AIDS dementia?
Behavioural changes, motor impairment
93
What can you see on the CT of someone with AIDS dementia?
Cortical and subcortical atrophy
94
What is the most common cause of infective diarrhoea in HIV?
Cryptosporidium
95
What are other possible causes of diarrhoea in HIV?
CMV Mycobacterium avium intracellulare Giardia
96
What kind of organism is Cryptosporidium?
Intracellular protozoa
97
What investigation can be used to identify the Cryptosporidium?
Modified ZN stain of stool which shows characteristic red cysts
98
What is the treatment of Cryptosporidium?
Supportive
99
When is Mycobacterium avium intracellulare infection typically seen?
CD4 <50
100
What are typical features of Mycobacterium avium intracellulare infection?
Fever, sweats, ab pain, diarrhoea May be hepatomegaly and derranged LFTs
101
How is Mycobacterium avium intracellulare infection diagnosed?
Blood cultures + bone marrow examination
102
What is the treatment of Mycobacterium avium intracellulare infection?
Rifabutin, ethambutol, clarithromycin

Infection (22 decks)

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