AIDS Flashcards
HIV primarily targets
CD4+ lymphocytes, which are critical to proper immune system function.
diagnosis: depletion of CD4+ cells to** ≤200 cells/mL** or because of the development of new opportunistic infections
modes of transmission
Sexual: if unprotected
Parenteral:
Injectable drug use OR Receiving contaminated blood products
Perinatal: Mother-to-infant transmission during gestation, delivery, or breast-feeding
Occupational exposure via needle stick or exposure to eyes, nose, or open wound
Organ donation from an HIV infected donor
hiv is not transmissited by:
- Working or playing with an HIV positive person
- Closed mouth kissing
- Shaking hands
- Public pools
- Hugging
- Public toilet
Risk factors for HIV/AIDS infection
- Men who have sex with men (MSM)
- Unprotected sex with high-risk individuals
- History of or current IV drug use (needle or equipment sharing)
- Presence of other sexually transmitted infections (e.g., Chlamydia trachomatis or Neisseria gonorrhoeae)
- Persons with coagulation / hemophilia disorders
Previous blood product recipients
Pathophysiology
HIV is RNA virus, its contents include single-stranded RNA, reverse transcriptase and other enzymes.
types of hiv
There are two molecularly and serologically distinct but related types of HIV: HIV-1 and HIV-2.
HIV-1 is a retrovirus and member of the genus Lentivirus.
HIV-2 is a less common cause of the epidemic and is found primarily in West Africa.
These viruses have a prolonged latency period.
HIV lifecycle
- Binding
- Fusion
- Reverse transcriptase
- Integration
- Replication
- Assembly
- Budding
Q: Why is it so hard to cure AIDS completely?
A: The viral RT enzyme is highly error-prone, and many mutations occur in the conversion of RNA to DNA. This inefficient RT activity is responsible for HIV’s ability to rapidly mutate and develop drug resistance.
HIV infection stages
- The initial immune response against HIV is relatively effective, but it is unable to completely clear the infection
- Patient enters a latent, asymptomatic, or mildly symptomatic stage lasting 5 - 15 years (some references: 10 years).During this time, a high rate of viral replication can be seen in the lymph nodes.
- immune deficiency occurs when the body is no longer able to produce helper T cells at a rate equal to that at which HIV is destroying them.
acute HIV
rapid production of hiv
some poeple develope flu like symptoms
stage 2 chronic hiv
- asymtomatic
- slow reproduction of hiv
- gradual reduction of cd4 cells
- no symptoms
stage 3 aids
- symptomatic
- low levels of cd4 cells in the body
- appearance of oppurtunistic infection
Clinical presentation
Acute retroviral syndrome:
When the patient is present within (fever, myalgia, lymphadenopathy, pharyngitis, or rash)
Occur 2-6 weeks after initial infection and the symptoms last 2-4 weeks.
Diagnosis of HIV is made by either:
Positive HIV ELISA (enzyme linked immunosorbent assay)
Rapid test (e.g. OraQuick ADVANCE)
Diagnosis needs to be confirmed by a +ve HIV WB (Western Blotting) technique
A diagnosis of AIDS is made when an HIV positive patient has:
CD4 count ˂ 200 or 14% or the patient diagnosed with an AIDS indicating condition (pulmonary TB, recurrent pneumonia or cervical cancer)
Treatment response & disease progression is determined by:
CD4+ lymphocyte count (CD4+ count) and percentage
HIV RNA (viral load).
Treatment of efficacy and safety can be monitored by:
CD4+ lymphocyte count (CD4+ count) and percentage
HIV RNA (viral load)
Basic blood chemistry tests (U & E)
LFTs
CBC
Lipid profiles
Maximal suppression of viral replication
Maximal suppression of viral replication is defined as HIV RNA concentrations undetectable by the most sensitive assay available.
Combination antiretroviral therapy has increased both the length and quality of life of HIV-infected patients
Nucleoside \ nucleotide RT inhibitor (NRTI+NtRTI)
- Abacavir
- Lamivudine
Non-nucleoside RT inhibitor (NNRTI)
- Efavirenz
- Nevirapine
Protease inhibitor (PI)
- Atazanavir
- Indinavir
- Integrase strand transfer inhibitors (INSTI)
- Fusion inhibitors
- CCR5 inhibitors
raltegravir
Enfuvirtide
Maraviroc
Highly active antiretroviral therapy (HAART)
2 nucleoside \ nucleotide RT inhibitors
ONE NNRTI OR PI OR INSTI Abacavir and lamivudine
Causes of virologic failure should be identified if possible. These could be:
Poor compliance / adherence which might be due to medication SE / intolerance
Pharmacokinetic issues
Presence of drug resistance
HIV Treatment failure
Never add a new drug to a failing regimen to prevent the development of resistance, try to not initiate the regimen that failed in the past.If an agent in a given regimen must be stopped, it is recommended that all agents in the regimen be stopped and restarted simultaneously to prevent development of resistance.
Considerable cross resistance
can occur between medications within an antiretroviral class. Using drugs to which the patient has not been exposed may be insufficient
Complete cross-resistance
occurs within the first generation of NNRTIs, whereas the NRTIs and PIs have variable overlapping resistance patterns.
failure therapy Adherence and Resistance Testing
Question Adherence: Assess the patient’s adherence to the regimen and address any barriers.
Confirm Sample Adequacy: Ensure the plasma HIV RNA concentration in the resistance sample is adequate to accurately detect resistance mutations.
HIV Prophylaxis
- Tenofivir \ emtricitabine fixed-dose combination with safe sex.
Post-exposure prophylaxis
after exposure should contain 3 or more active ARVs and should continue for 4 weeks.
non-occupational post-exposure prophylaxis
s recommended for individuals seeking care within 72 hours to blood, genital secretions, or other infectious fluids from a known infected person.
