HIV SG Flashcards
When was AIDS first published
1981
What is HIV
a retrovirus; uses reverse transcriptase to turn RNS into DNA, integrate it’s genetic material into host DNA, and new virus is produced
What does HIV target
T cells (esp CD4 helper cells) Also, B lymphocytes and macrophages
What do lymphocytes do
WBC that defend against VIRUSES, fungi, some bacteria, and protozoa
What are B and T cells
- B cells make Abs to attack antigens
- CD4 T cells enhance immune response and tell B cells to make Abs
- CD8 killer cells destroy foreign agents
How does HIV replication occur
HIV particle fuses to CD4 component HIV incorporated into host cell by reverse transcriptase New copies of HIV released
How is HIV transmitted
Sexually: exchange of body fluids IVDU Needlestick injuries (occupational) Blood products (extremely low risk now) HIV infected mom to infant -Basically, requires infectious body fluid and portal of entry! Not spread via casual contact!
What is the risk of transmission
Insertive vaginal sex: 1/10K Receptive vaginal sex: 1/1K Needle stick: 1/300 Shared drug needle: 1/150 Receptive anal: 1/50
What is acute HIV
2-6 weeks after exposure, HIV initiates the attack and CD4 cells drop rapidly You develop mono or flu-like Sx that ;ast about 2 weeks, then resolve (this indicates your body initially fighting back at the disease) Patient is highly infectious
What do labs show in acute HIV
HIV antibody test is usually negative! it is too early for your body to have developed antibodies HIV RNA (viral load) is measurable, and extremely high (>100K) -Providers often only order the Ab test, which comes back negative, they tell the pt they are negative, and then they go infect others. -Elevated LFT’s, Leukopenia, anemia, thrombocytopenia
What does catching acute HIV allow
To stop the spread of disease to others But, once you have HIV, you can’t stop the disease progression
What are common manifestations of acute HIV
Fever adenopathy sore throat rash* upper trunk, neck, face Mucocutaneous ulcers myalgias arthralgias HA diarrhea N/V
What is clinical latency
It begins as immune system responds to infection (acute illness resolves)- lasts appx 10 years Patient seroconverts (serum becomes HIV antibody +) around 3 months after infection Viral load decreases to a set point and slowly rises over time (HIV is active in lymph nodes this whole time) CD4 slowly declines Patient is ASx usually
What happens during a symptomatic infection
Lymph nodes and tissue are damaged (burnt out) Virus may mutate and be more pathogenic Body fails to keep up with replacement of CD4 cells Viral load (HIV RNA) increases CD4 count decreases
What are HIV Sx
fever, night sweats LAD fatigue, malaise arthralgias weight loss *Hairy leukoplakia prolonged diarrhea cervical dysplasia (HPV) Molluscum, dermatophyte infection, seborrheic dermatitis *Kaposi Sarcoma recurrent HZV ITP
What is a normal CD4 count
600-1200 (then she says 500-1400)
What is usually the first Sx of HIV
Tuberculosis! immune system fails revealing TB Sx
What is AIDS
CD4 count <200 OR HIV + 1 of 27 AIDS defining conditions
What occurs at different CD4 counts
<200: P. jiroveci PNA, <100: Toxoplasmosis <50: MAC, CMV Any: Kaposi, Candida
What is pneumocystic jiroveci pneumonia
airborne fungus that reactivates when CD4 count is <200 Common opportunistic infx associated w/ AIDS Presents w/ nonspecific Sx (fever, cough, SOB) =/- hypoxemia CXR shows diffuse perihilar infiltrates
How do you diagnose and treat P. jirovecii PNA
Sputum sample; can also get LDH (elevated) Tx: Bactrim DS*** and supportive care
What is Toxoplasmosis
Parasite (toxoplasma gondii) that reactivates when CD4 <100 Causes encephalitis, IC lesions Acquired via cat feces, contaminated raw food or utensils If immunocompetent, you rarely show Sx
How does toxoplasmosis present in HIV
HA FND seizures AMS Retinitis Pneumonitis
How do you diagnose Toxoplasmosis
CT/MRI will show contrast enhancing lesions on brain Seropositive for toxoplasmosis
