HIV Dx and Management Flashcards
Where is HIV spreading most rapidly?
-Asia
Epidemiology of HIV/AIDS
- gender
- race
- sexual preference
- age
- age of testing?
- largest infection rate?
- male
- black/hispanic
- MSM
- 25-44
- require testing: 15-54
- Africa
What might be some reasons there is an increase in the number of HIV positive people in the US?
- infected are living longer d/t HARRT (medication use increases life span, more likely to live a normal life span) (highly active anti-retroviral therapy)
- sex practices among high risk groups are worsening again
- percentage of new infections is growing fastest in females compared with males
HIV is what type of virus? How does this virus work?
-Retrovirus.
-viral RNA reverses transcribed to»>
DNA, DNA integrated into host cell genome»>RNA»>Polypeptide
Is there a cure for HIV? AIDS?
- nope.
- nope.
Modes of HIV/AIDS transmission
- Sex (oral, anal, P & V, digital…probabaly not.)
- IV drug use
- bodily fluids (breast milk, blood product, semen, vaginal fluids)
- mother to baby (vertical)
How can mother spread HIV/AIDS to baby
- before birth
- during birth
- after birth
- placental aburpture: disruption of placenta from uterine wall, mixing of maternal and fetal blood.
- mom bleed and baby aspirate
- breastmilk
What are the stages of HIV/AIDS?
- primary; Stage 1
- asymptomatic; stage 2
- symptomatic; stage 3
- AIDS
Sx of primary stage 1 HIV/AIDS
-short, flu-like illness; occurs 1-6weeks after infection
- may have no sx
- during this time your opportunity to infect others is the highest.
-virus is rapidly replicating within the blood.
Sx of asymptomatic Stage 2 HIV/AIDS
- free of sx, may have swollen glands
- last approx 10 years
- very low levels of HIV in blood, the virus is replicating in the T cells, its found a home and having fun.
- most replication takes place in the gut.
-HIV abys are detectable in blood
Sx of symptomatic Stage 3 HIV/AIDS?
- sx are mild
- immune system deteriorates
- emergence of opportunistic infections and cancers
Retrovirus infects what cells in the body?
-CD4+ Tcells, Mfs, dendritic cells, B cells
What causes a drop in your CD4 T cells during asymptomatic stage 2?
-CD 8 T cells- kill off all of the HIV infected CD4 cells
T-cells become non-functional following infection, True or false? Why?
-True, there is a qualitative defect in T-cells that overshadows the simple quantitative defect.
What results from infection of B-cells, T-cells, and mfs?
-mixed immunodeficiency
The syndromes people develop in HIV/AIDS are a result from what 3 mechanisms?
- immunodeficiency
- autoimmunity; autoantibody production
- Allergy/Hypersensitivity rxns: increased rates of hypersensitivity to medications/unknown allergens
How long is each phase/stage of HIV/AIDS?
dependent on host and virus
-use of antiretroviral therapy, use of chemopropophylaxis for opportunistic infections.
Generally speaking:
- Primary is 3-14 days
- Asymptomatic is 4-8years
- Symptomatic is 4-8years
- AIDS is 2-20years
Clinical presentation of Primary Infection Stage 1?
- brief, sudden, mono type illness
- fever
- sweats
- malaise
- HA*
- Athralgias
- Photophobia*
- Lymphadenopathy**
- truncal maculopapular rash
- most common neuro sx
- *most commonly seen in ALL HIV patients
Clinical Presentation of Asymptomatic Phase, Stage 2
- longest of the 4 phases
- lack of overt evidence of HIV disease, only evidence is sero-positivity (have aby to RNA retrovirus?/HIV?)
*can easily spread because they are asymptomatic
Clinical Presentation of Symptomatic Phase, Stage 3
- persistent generalized lymphadenopathy
- localized fungal infections: toes, fingernails, mouth, vaginal candidiasis or trichomonal infections.
- oral hairy leukoplakia (in mouth)
- warts, molluscum, multidermatomal zoster*, and herpes simplex.
- Night sweats, weight loss, diarrhea.
Dx of AIDS Stage 4?
-have aids defining illness regardless of CD4 count. OR opportunistic infection with CD4 count
Clinical Presentation of AIDS stage 4?
- PE is often normal, abnormal findings are non-specific
- fever, night, sweats, and weight loss
- persistent fever requires work up, weight loss can be quite severe and is generally muscle mass loss. Increased metabolic rate d/t virus compounds the problem.
What is the most common opportunistic infection seen in AIDS?
Pneumocystis pneumonia is the most common.
What are some other pulmonary OI’s in AIDS?
- CAP (bacterial, mycobacterial, viral)
- TB
- Noninfectious causes of lung disease: Kaposi, non-hodgkins lymphoma, interstitial pneumonitis
- Sinusitis (acute and chronic)
What are some CNS OI’s in AIDS? Sx and Dx of each.
- Toxoplasmosis: most space occupying common lesion.
- -Sx: HA, focal neuro deficit, sz, AMS
- -Dx: CT, MRI
- CNS Lymphoma: 2nd most common space occupying lesion.
- -Dx:brain biopsy
- AIDS Dimentia Complex
- -Sx: decreased cognitive skills and motor speed, sx wax and wane
- -Dx: of exclusion based on brain imaging and CSF evaluation.
- Cyptococcal Meningitis
- -Sx: fever, HA
- -Dx: +latex agglutination of CSF
- HIV myelopathy
- -Sx: leg weakness, incontinence d/t spinal cord impairment, spastic paresis, ataxia
- -Dx: of exclusion, LP, and MRI
- Progressive Multifocal Leukoencaphalopathy (PML)
- -Sx: aphasia, hemiparesis, and cortical blindness
What are some of the OI’s of the PNS?
- Inflamm Demyelinating Polyneuropathy (similar to Guillian-Barre)
- Transverse myelitis d/t Herpes Zoster of CMV
- peripheral neuropathy
- CMV can cause an ascending polyradiculopathy: lower extremitcy weakness
What are some of the Rheumatologic OIs of AIDS?
-Arthritis
- Severe inflammatory syndromes
- -Reiters
- -Psoriatic arthritis
- -SICCA syndrome (dry eye and mouth)
- -SLE
-avascular necrosis of femoral head
What are some of the Ocular OI’s of AIDS?
- complaints of visual changes
- CMV Retinitis: perivascular hemorrhages and white fluffy exudates
- Herpes infection
- Toxoplasmosis
What are some of the Gastrointestinal OI’s of AIDS?
- Candidal Esophagitis (if you have this you REALLY should expect aids)
- Hepatic Disease, co-infection of hep B and C. Liver is frequent site for neoplasms.
- Biliary disease
- Enterocolitis: VERY common in HIV patient.
- -due directly to HIV mf infection, secondary cause include: bacteria, virus, protozoans
- sx for >mo and no identifiable cause, presumptive for AIDS enteropathy.
WHat are some of the Skin OI’s of AIDS?
- HSV Infection; d/t risk of dissemination all treated with oral meds.
- Herpes Zoster: d/t risk of dissemination all must be treated w/ oral meds.
- Molluscum contagiosum
- -tx w/ liquid nitrogen
- Folliculitis/furuncles
- -staphylococcus most common bacterial cause of skin infection in HIV pt
- always assume its MRSA and tx accordingly
- Bacillary angiomatosis
- -bartonella henselae and bartonella quintana
- -zoonotic infection from flea and domesticaed cats
- -red raised, highly vascular lesions that can mimic kaposis
- -fever is common w/ bone LN and liver involvement
What are some of the Malignancies of HIV/AIDS?
- Kaposis Sarcoma: lesions ANYWHERE.
- Non-hodgkins Lymphoma: usually b cell origin
What are some GYN OIs of AIDS?
- recurrent vaginal candidiasis
- cervical dysplasia*
- Cervical neoplasia* much more aggressive in HIV, most women die from their cervical cancer and not HIV
- PID
T-Cell activation: costimulation
- what happens without costimulation?
- what happens with costimuulation?
- Require t cell binding to APC
- -DC and MF produce surface B7 proteins that bind with CD28 receptor on T cell, leading to crucial co-stimulatory signal. This leads to cytokine release (IL1 & 2) from APC or T cell and triggers proliferation and differentiation of activated T cell.
- No costimulation=anergy. there is no rxn to the Ag, the body doesnt stimulate a response. T cells become tolerant to that AG and do not secrete cytokines.
- Costimulation leads to T cell activation, they enlarge, proliferate, and from clones.
T-cell Activation:
-how long does it take for T-cell peak response after infection?
-1 week
What is the role of Thelper cells?
- once they have been primed by APC presentation of ag they,
- activate T and B cells
- Induce T and B cell proliferation
- activate mf and recruit other immune cells
**Without Thelper there is no immune response.
How do Cytotoxic T cells kill? How about NK cells?
secretes perforins and granzymes that insert into the target cell membrane forming pores leading to apoptosis.
-same as Tcytotoxic, they recognize cellls w/o MHC I, aby coated target cell, or diffferent surface markers on stressed cells and secrete perforin/granzymes.
