HIV and AIDS Flashcards

1
Q

State the modes of transmission of HIV

A

Sexual tranmission, IUD, Blood products, vertical transmission and organ transplantation

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2
Q

Describe the immunological mechanism of HIV

A

HIV infects and destroys cells of the immune system, especially the T-helper cells that are CD4+

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3
Q

Where are CD4 receptors present

A

Lymphocytes, macrophages, monocytes, brain, skin

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4
Q

Describe the natural history of HIV

A

CD4 count declines and HIV viral load increases over time.

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5
Q

Increased HIV viral load increases the risk of

A

Developing infections and tumours

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6
Q

The lower the CD4 count

A

The greater the severity of the disease

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7
Q

State the normal CD4 count

A

above 500

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8
Q

State when AIDS diagnosed

A

CD4<200

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9
Q

Clinical stage 1 HIV

A

Asymptomatic with persistent generalised lymphadenopathy

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10
Q

Clinical stage 2 HIV

A

Weight loss (<10% of body weight), minor muscocutaneous manifestations, HZV within the last 5 years, recurrent upper respiratory tract infections

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11
Q

Clinical stage 3 HIV

A

Weight loss >10% body weight, unexplained chronic diarrhoea >1mnth, unexplained fever >1mnth, oral candidiasis, oral hairy leukoplakia, pulmonary TB, severe bacterial infections and/or performance scale 3

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12
Q

Define performance scale 3

A

Bedridden, <50% of the day during the last month

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13
Q

Define clinical stage 4 HIV

A

HIV wasting syndrome, pneumonia, toxoplasmosis of the brain, CMV disease of any organ other than liver, spleen or lymph nodes, HSV, PML

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14
Q

State the natural history of progression of HIV

A

Acute infection (seroconversion), asymptomatic HIV, HIV related illness, AIDS defining illness and death

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15
Q

State the percentage of patients who get seroconversion illness

A

30-60%

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16
Q

State the symptoms of primary HIV

A

Flu, fever, malaise and lethargy, pharyngitis, lymphadenopathy, toxic exanthema

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17
Q

When is anti-retro-viral therapy started

A

CD4 350

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18
Q

What does combination antiretroviral therapy mean

A

At least 3 drugs from at least 2 groups

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19
Q

State the main side effect of cART

A

Lipodystrophy

20
Q

State the side effects of nuceloside reverse transcriptase inhibitors

A

Marrow toxicity, neuropathy, lipodystrophy

21
Q

State the side effects of non-nuceloside reverse transcriptase inhibitors

A

Skin rashes, hypersensitivity, drug interactions

22
Q

State the side effects of protease inhibitors

A

Drug interactions, diarrhoea, lipodystrophy, hyperlipidaemia

23
Q

State the side effects of integrase inhibitors

24
Q

What type of virus is HIV

A

Retrovirus

25
State the number of people estimated to be living with HIV worldwide
37 million
26
How does HIV destroy CD4 cells
It binds via GP120 envelope glycoprotein and these CD4 cell migrate to lymphoid tissue wher the virus replicates, producing millions of new virions
27
What is the result of infection of CD4 cells
Leads to decreased immune function
28
Describe post-exposure prophylaxis of HIV
Antiretroviral treatment given up to 72 hours after exposure. The first line is Truvada (tenofovir/emtricitabine) and raltegravir for 28 days
29
What should all pregnant women infected with HIV be commenced on by 24 weeks gestation
ART
30
How is the neonate treated
PEP given from birth to 4 weeks old with formula feeding
31
State the use of ELISA for HIV antibody and antigen
test for HIV antibody and p24 antigen. This is confirmed by confirmatroy assay
32
State the use of rapid point-of-care testing
Immunoassay kit which gives a rapid result from a finger prick or mouth swab but still needs serological confirmation
33
Describe the use of viral load testing in HIV
Used to monitor the response of ART.
34
When is nucleic acid testing/viral PCR used for the diagnosis of HIV
Neonates as placental transfer of maternal antibodies can affect ELISA antibody testing up to 18 months of age
35
List some opportunistic infections patients with HIV may get
Pneumocystis jirovecii, candidiasis, cryptococcus neoformas, toxoplasma gondii, CMV, cryptosporidium, kaposis sarcoma, lymphoma
36
State the aims of ART in the treatment of HIV
The reduction of the HIV viral load to a level undetectable by standard la techniques leading to recovery, reduced clinical progression, and reduced mortality
37
State the mechanism of CCR5 antagonists
Inhibit the entry of the virus into the cell by blocking the CCR5 co-receptor
38
State the mechanism of NRTIS
Inhibit reverse transcriptase and the conversion of viral RNA into DNa
39
State the mechanism of Integrase Stand Transfer Inhibitors
Inhibit integrase and prevent HIV DNA integrating into the nucleus
40
State the mechanism of protease inhibitors
Inhibit protease, an enzyme involved in the maturation of virus particles
41
State the mechanism of pharmacokinetic enhancers
Increase the effectiveness of antiretroviral drugs allowing lower doses
42
What should be started in the treatment of HIV
2 nucleoside reverse transcriptase inhibitors plus one of ritonavir-boosted protease inhibitor, non-nucleoside reverse transcriptase inhibitor or integrase inhibitor
43
State the main NRTI backbone drugs used in HIV treatment
Tenofovir and emtricitabine
44
State the main protease inhibitors used in HIV treatment
Atazanavir and darunavir
45
State the main NNTRIs used in HIV treatment
Rilpivirine
46
State the main Integrase inhibitors used in the treatment of HIV
Dolutegravir, elvitegravir, raltegravir