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

A

rashes

24
Q

What type of virus is HIV

A

Retrovirus

25
Q

State the number of people estimated to be living with HIV worldwide

A

37 million

26
Q

How does HIV destroy CD4 cells

A

It binds via GP120 envelope glycoprotein and these CD4 cell migrate to lymphoid tissue wher the virus replicates, producing millions of new virions

27
Q

What is the result of infection of CD4 cells

A

Leads to decreased immune function

28
Q

Describe post-exposure prophylaxis of HIV

A

Antiretroviral treatment given up to 72 hours after exposure. The first line is Truvada (tenofovir/emtricitabine) and raltegravir for 28 days

29
Q

What should all pregnant women infected with HIV be commenced on by 24 weeks gestation

A

ART

30
Q

How is the neonate treated

A

PEP given from birth to 4 weeks old with formula feeding

31
Q

State the use of ELISA for HIV antibody and antigen

A

test for HIV antibody and p24 antigen. This is confirmed by confirmatroy assay

32
Q

State the use of rapid point-of-care testing

A

Immunoassay kit which gives a rapid result from a finger prick or mouth swab but still needs serological confirmation

33
Q

Describe the use of viral load testing in HIV

A

Used to monitor the response of ART.

34
Q

When is nucleic acid testing/viral PCR used for the diagnosis of HIV

A

Neonates as placental transfer of maternal antibodies can affect ELISA antibody testing up to 18 months of age

35
Q

List some opportunistic infections patients with HIV may get

A

Pneumocystis jirovecii, candidiasis, cryptococcus neoformas, toxoplasma gondii, CMV, cryptosporidium, kaposis sarcoma, lymphoma

36
Q

State the aims of ART in the treatment of HIV

A

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
Q

State the mechanism of CCR5 antagonists

A

Inhibit the entry of the virus into the cell by blocking the CCR5 co-receptor

38
Q

State the mechanism of NRTIS

A

Inhibit reverse transcriptase and the conversion of viral RNA into DNa

39
Q

State the mechanism of Integrase Stand Transfer Inhibitors

A

Inhibit integrase and prevent HIV DNA integrating into the nucleus

40
Q

State the mechanism of protease inhibitors

A

Inhibit protease, an enzyme involved in the maturation of virus particles

41
Q

State the mechanism of pharmacokinetic enhancers

A

Increase the effectiveness of antiretroviral drugs allowing lower doses

42
Q

What should be started in the treatment of HIV

A

2 nucleoside reverse transcriptase inhibitors plus one of ritonavir-boosted protease inhibitor, non-nucleoside reverse transcriptase inhibitor or integrase inhibitor

43
Q

State the main NRTI backbone drugs used in HIV treatment

A

Tenofovir and emtricitabine

44
Q

State the main protease inhibitors used in HIV treatment

A

Atazanavir and darunavir

45
Q

State the main NNTRIs used in HIV treatment

A

Rilpivirine

46
Q

State the main Integrase inhibitors used in the treatment of HIV

A

Dolutegravir, elvitegravir, raltegravir