HIV and AIDS Flashcards
State the modes of transmission of HIV
Sexual tranmission, IUD, Blood products, vertical transmission and organ transplantation
Describe the immunological mechanism of HIV
HIV infects and destroys cells of the immune system, especially the T-helper cells that are CD4+
Where are CD4 receptors present
Lymphocytes, macrophages, monocytes, brain, skin
Describe the natural history of HIV
CD4 count declines and HIV viral load increases over time.
Increased HIV viral load increases the risk of
Developing infections and tumours
The lower the CD4 count
The greater the severity of the disease
State the normal CD4 count
above 500
State when AIDS diagnosed
CD4<200
Clinical stage 1 HIV
Asymptomatic with persistent generalised lymphadenopathy
Clinical stage 2 HIV
Weight loss (<10% of body weight), minor muscocutaneous manifestations, HZV within the last 5 years, recurrent upper respiratory tract infections
Clinical stage 3 HIV
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
Define performance scale 3
Bedridden, <50% of the day during the last month
Define clinical stage 4 HIV
HIV wasting syndrome, pneumonia, toxoplasmosis of the brain, CMV disease of any organ other than liver, spleen or lymph nodes, HSV, PML
State the natural history of progression of HIV
Acute infection (seroconversion), asymptomatic HIV, HIV related illness, AIDS defining illness and death
State the percentage of patients who get seroconversion illness
30-60%
State the symptoms of primary HIV
Flu, fever, malaise and lethargy, pharyngitis, lymphadenopathy, toxic exanthema
When is anti-retro-viral therapy started
CD4 350
What does combination antiretroviral therapy mean
At least 3 drugs from at least 2 groups
State the main side effect of cART
Lipodystrophy
State the side effects of nuceloside reverse transcriptase inhibitors
Marrow toxicity, neuropathy, lipodystrophy
State the side effects of non-nuceloside reverse transcriptase inhibitors
Skin rashes, hypersensitivity, drug interactions
State the side effects of protease inhibitors
Drug interactions, diarrhoea, lipodystrophy, hyperlipidaemia
State the side effects of integrase inhibitors
rashes
What type of virus is HIV
Retrovirus
State the number of people estimated to be living with HIV worldwide
37 million
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
What is the result of infection of CD4 cells
Leads to decreased immune function
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
What should all pregnant women infected with HIV be commenced on by 24 weeks gestation
ART
How is the neonate treated
PEP given from birth to 4 weeks old with formula feeding
State the use of ELISA for HIV antibody and antigen
test for HIV antibody and p24 antigen. This is confirmed by confirmatroy assay
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
Describe the use of viral load testing in HIV
Used to monitor the response of ART.
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
List some opportunistic infections patients with HIV may get
Pneumocystis jirovecii, candidiasis, cryptococcus neoformas, toxoplasma gondii, CMV, cryptosporidium, kaposis sarcoma, lymphoma
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
State the mechanism of CCR5 antagonists
Inhibit the entry of the virus into the cell by blocking the CCR5 co-receptor
State the mechanism of NRTIS
Inhibit reverse transcriptase and the conversion of viral RNA into DNa
State the mechanism of Integrase Stand Transfer Inhibitors
Inhibit integrase and prevent HIV DNA integrating into the nucleus
State the mechanism of protease inhibitors
Inhibit protease, an enzyme involved in the maturation of virus particles
State the mechanism of pharmacokinetic enhancers
Increase the effectiveness of antiretroviral drugs allowing lower doses
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
State the main NRTI backbone drugs used in HIV treatment
Tenofovir and emtricitabine
State the main protease inhibitors used in HIV treatment
Atazanavir and darunavir
State the main NNTRIs used in HIV treatment
Rilpivirine
State the main Integrase inhibitors used in the treatment of HIV
Dolutegravir, elvitegravir, raltegravir
