HIV Flashcards

1
Q

Where did HIV arise from?

A

HIV 1 - Related to simian immunodeficiency virus in chimpanzees and gorillas.
HIV 2 which is slower to progress and harder to transmit - Closely related to SIV found in other primates
Thought to have jumped species from many mechanisms including bush meat

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2
Q

How is HIV transmitte?

A
  • Enters the body through mucous membranes, direct injections or via open wounds. So some activities that allow for HIV transmission are as follows:
  • Anal or vaginal intercourse (oral sex isn’t efficient route)
  • Injecting drugs/sharing equipment,
  • Mother to child transmission
  • Transmission in healthcare settings
  • Transmission via donated blood/clotting factors
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3
Q

Explain the pathogenesis of HIV

A
  • Infects immune cells which carry CD4 receptors such as T helper cells, macrophages and dendritic cells.
  • HIV then causes depletion of CD4 T helper cells by direct killing of cells, apoptosis of uninfected cells and CD8 cytotoxic T cells killing infected CD4 cells.
  • Causes abnormal B cell activation resulting in excessive immunoglobulin production.
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4
Q

What is the critical level of CD4 cells that increase risk of opportunistic infections?

A

Equal to, or below 200

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5
Q

What are the important HIV enzymes and some potential drug targets

A

Important enzymes - Integrase, protease and reverse transcriptase.
- Targers for drug treatments include: Fusion inhibitor (enfurvitide) (prevents binding to CD4 cells), nucleoside reverse transcriptase inhibitors (abacavir/tenoforvir), non-nucleoside reverse transcriptase inhibitors (efavirenz), integrase inhibitors (Dolutegravir) and protease inhibitors (Darunavir)

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6
Q

Describe features of HIV latency

A
  • It is the state of reversibly non-productive infection of individual cells. This is the asymptomatic period between initial infection and advanced HIV (can be 10-15 years)
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7
Q

What can cause HIV drug resistance?

A
  • Inconsistent HIV medication use.
  • Infection from an HIV drug resistant strain
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8
Q

What are the two approaches currently being researched for an HIV vaccine

A
  • Active vaccination which aims to induce immune response against HIV.
  • Passive vaccination in which preformed antibodies against HIV are administered.
  • Live attenuated vaccines are not being used ass there is risk of the HIV becoming live and infectious.
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9
Q

What population groups are at highest risk of contracting HIV

A
  • Sub Saharan Africa,
  • MSM,
  • Children of people living with HIV,
  • People who inject drugs,
  • People who have transactional sex
  • But really anybody
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10
Q

What is the method of HIV testin

A

4th generation testing tests for p24 antigen/HIV antibody. However has a window period of 45 days.
Can do point of care tests and can do home testing.

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11
Q

What are the symptoms of primary HIV infection or ‘seroconversion’

A
  • Rash,
  • Lymphadenopathy,
  • Fever, weight loss,
  • Malaise
  • Headaches, neuropathy,
  • Mouth sores and oral thrush,
  • Myalgia,
  • Hepatosplenomegaly,
  • Nausea and vomiting
    Top 4 are main ones
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12
Q

What are the possible differentials for primary HIV infections

A
  • Infectious mononucleosis,
  • Secondary syphilis
  • Drug rash,
  • Other viral infections, eg, CMV or influenza
  • ALWAYS DO HIV TEST
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13
Q

What are some HIV indicator conditions

A
  • Pneumocystis pneumonia,
  • Oral hairy leucoplakia,
  • Oesophageal candida,
  • TB,
  • Kaposi’s Sarcoma,
  • Chronic diarrhoea,
  • Bacterial pneumonia,
  • Dementia,
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14
Q

What are the two blood markers investigated for in HIV

A
  • HIV viral load. Undetectable is below 200 copies, in Scotland the aim is for below 20 copies/ml as this prevents transmission and improves health of patient.
  • CD4. This is calculated from total lymphocyte count. There is high risk of opportunistic infection if below 200/mm cubed.
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15
Q

What is the treatment for HIV, its challenges and when should it be started?

A
  • Highly active antiretroviral treatment (HAART) which should be started asap.
  • This usually involves triple therapy with 2 nucleoside reverse transcriptase inhibitors and 1 drug from another class.
  • Challenges include: Need for good adherence, the psychological impact the short and long term side effects and the many drug to drug interactions
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16
Q

What are the short and long term toxicities associated with antiretroviral treatment

A

Short - Rash, hypersensitivity (eps. Abacavir), CNA side effects, GI side effects, renal and hepatic toxicity.
Long term - Body shape changes (lipoatrophy, weight gain), renal toxicity with commonly used drug called tenofovir disoproxil, hepatic toxicity, lipid and bone toxicity.

17
Q

What are some common drug interactions with antiretroviral therapies

A

It is often mediated by CYP450 enzymes. Examples of interactions include; PPIs, statins, antipsychotics, topical or inhaled drugs. So always check

18
Q

Describe features of HIV partner notification and what are some HIV prevention methods

A
  • Should be carried out by specialist HIV team.
  • Prevention methods include:
  • Condoms,
  • Treatment as prevention (TasP)
  • Pre-exposure Prophylaxis (PrEP),
  • Post-exposure Prophylaxis (PEP),
  • Prevention of Mother to Child Transmission (PMTCT)
  • Harm reduction via needle exchange.
19
Q

Describe features of PrEP/PEP (HIV - using antiretrovirals as prevention)

A

PEP - Is taken within 72 hours after exposure. It should be taken for 28 days and is available from sexual health/A&E.
PrEP - Available from sexual health for people at high risk of HIV through sexual transmission. Cheap and effective intervention but must emphasise condom use.

20
Q

Explain some features of prevention of mother to child HIV transmission

A
  • Transmission has fallen due to antenatal HIV screening. If mother is HIV positive then following measures are put in place:
  • ARVs for mother during pregnancy,
  • Minimise risk at delivery, maybe via C-section.
  • PEP for baby
  • Avoid breast feeding.