HIV Dx and Management

Question 1

Where is HIV spreading most rapidly?

Answer 1

-Asia

Question 2

Epidemiology of HIV/AIDS

• gender
• race
• sexual preference
• age
• age of testing?
• largest infection rate?

Answer 2

• male
• black/hispanic
• MSM
• 25-44
• require testing: 15-54
• Africa

Question 3

What might be some reasons there is an increase in the number of HIV positive people in the US?

Answer 3

• 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

Question 4

HIV is what type of virus? How does this virus work?

Answer 4

-Retrovirus.
-viral RNA reverses transcribed to»>
DNA, DNA integrated into host cell genome»>RNA»>Polypeptide

Question 5

Is there a cure for HIV? AIDS?

Answer 5

• nope.

- nope.

Question 6

Modes of HIV/AIDS transmission

Answer 6

• Sex (oral, anal, P & V, digital…probabaly not.)
• IV drug use
• bodily fluids (breast milk, blood product, semen, vaginal fluids)
• mother to baby (vertical)

Question 7

How can mother spread HIV/AIDS to baby

• before birth
• during birth
• after birth

Answer 7

• placental aburpture: disruption of placenta from uterine wall, mixing of maternal and fetal blood.
• mom bleed and baby aspirate
• breastmilk

Question 8

What are the stages of HIV/AIDS?

Answer 8

• primary; Stage 1
• asymptomatic; stage 2
• symptomatic; stage 3
• AIDS

Question 9

Sx of primary stage 1 HIV/AIDS

Answer 9

-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.

Question 10

Sx of asymptomatic Stage 2 HIV/AIDS

Answer 10

• 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

Question 11

Sx of symptomatic Stage 3 HIV/AIDS?

Answer 11

• sx are mild
• immune system deteriorates
• emergence of opportunistic infections and cancers

Question 12

Retrovirus infects what cells in the body?

Answer 12

-CD4+ Tcells, Mfs, dendritic cells, B cells

Question 13

What causes a drop in your CD4 T cells during asymptomatic stage 2?

Answer 13

-CD 8 T cells- kill off all of the HIV infected CD4 cells

Question 14

T-cells become non-functional following infection, True or false? Why?

Answer 14

-True, there is a qualitative defect in T-cells that overshadows the simple quantitative defect.

Question 15

What results from infection of B-cells, T-cells, and mfs?

Answer 15

-mixed immunodeficiency

Question 16

The syndromes people develop in HIV/AIDS are a result from what 3 mechanisms?

Answer 16

• immunodeficiency
• autoimmunity; autoantibody production
• Allergy/Hypersensitivity rxns: increased rates of hypersensitivity to medications/unknown allergens

Question 17

How long is each phase/stage of HIV/AIDS?

Answer 17

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

Question 18

Clinical presentation of Primary Infection Stage 1?

Answer 18

• 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

Question 19

Clinical Presentation of Asymptomatic Phase, Stage 2

Answer 19

• 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

Question 20

Clinical Presentation of Symptomatic Phase, Stage 3

Answer 20

• 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.

Question 21

Dx of AIDS Stage 4?

Answer 21

-have aids defining illness regardless of CD4 count. OR opportunistic infection with CD4 count

Question 22

Clinical Presentation of AIDS stage 4?

Answer 22

• 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.

Question 23

What is the most common opportunistic infection seen in AIDS?

Answer 23

Pneumocystis pneumonia is the most common.

Question 24

What are some other pulmonary OI’s in AIDS?

Answer 24

• CAP (bacterial, mycobacterial, viral)
• TB
• Noninfectious causes of lung disease: Kaposi, non-hodgkins lymphoma, interstitial pneumonitis
• Sinusitis (acute and chronic)

Question 25

What are some CNS OI's in AIDS? Sx and Dx of each.

Answer 25

- 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

Question 26

What are some of the OI's of the PNS?

Answer 26

- 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

Question 27

What are some of the Rheumatologic OIs of AIDS?

Answer 27

-Arthritis - Severe inflammatory syndromes - -Reiters - -Psoriatic arthritis - -SICCA syndrome (dry eye and mouth) - -SLE -avascular necrosis of femoral head

Question 28

What are some of the Ocular OI's of AIDS?

Answer 28

- complaints of visual changes - CMV Retinitis: perivascular hemorrhages and white fluffy exudates - Herpes infection - Toxoplasmosis

Question 29

What are some of the Gastrointestinal OI's of AIDS?

Answer 29

- 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.

Question 30

WHat are some of the Skin OI's of AIDS?

Answer 30

- 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

Question 31

What are some of the Malignancies of HIV/AIDS?

Answer 31

- Kaposis Sarcoma: lesions ANYWHERE. | - Non-hodgkins Lymphoma: usually b cell origin

Question 32

What are some GYN OIs of AIDS?

Answer 32

- recurrent vaginal candidiasis - cervical dysplasia* - Cervical neoplasia* much more aggressive in HIV, most women die from their cervical cancer and not HIV - PID

Question 33

T-Cell activation: costimulation - what happens without costimulation? - what happens with costimuulation?

Answer 33

- 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.

Question 34

T-cell Activation: | -how long does it take for T-cell peak response after infection?

Answer 34

-1 week

Question 35

What is the role of Thelper cells?

Answer 35

- 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.

Question 36

How do Cytotoxic T cells kill? How about NK cells?

Answer 36

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.