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Infectious Disease 3 > HIV Dx and Management > Flashcards

HIV Dx and Management Flashcards

1
Q

Where is HIV spreading most rapidly?

A

-Asia

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2
Q

Epidemiology of HIV/AIDS

  • gender
  • race
  • sexual preference
  • age
  • age of testing?
  • largest infection rate?
A
  • male
  • black/hispanic
  • MSM
  • 25-44
  • require testing: 15-54
  • Africa
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3
Q

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

A
  • 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
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4
Q

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

A

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

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5
Q

Is there a cure for HIV? AIDS?

A
  • nope.

- nope.

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6
Q

Modes of HIV/AIDS transmission

A
  • Sex (oral, anal, P & V, digital…probabaly not.)
  • IV drug use
  • bodily fluids (breast milk, blood product, semen, vaginal fluids)
  • mother to baby (vertical)
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7
Q

How can mother spread HIV/AIDS to baby

  • before birth
  • during birth
  • after birth
A
  • placental aburpture: disruption of placenta from uterine wall, mixing of maternal and fetal blood.
  • mom bleed and baby aspirate
  • breastmilk
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8
Q

What are the stages of HIV/AIDS?

A
  • primary; Stage 1
  • asymptomatic; stage 2
  • symptomatic; stage 3
  • AIDS
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9
Q

Sx of primary stage 1 HIV/AIDS

A

-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.

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10
Q

Sx of asymptomatic Stage 2 HIV/AIDS

A
  • 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

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11
Q

Sx of symptomatic Stage 3 HIV/AIDS?

A
  • sx are mild
  • immune system deteriorates
  • emergence of opportunistic infections and cancers
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12
Q

Retrovirus infects what cells in the body?

A

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

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

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

A

-mixed immunodeficiency

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16
Q

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

A
  • immunodeficiency
  • autoimmunity; autoantibody production
  • Allergy/Hypersensitivity rxns: increased rates of hypersensitivity to medications/unknown allergens
17
Q

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

A

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
18
Q

Clinical presentation of Primary Infection Stage 1?

A
  • 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
19
Q

Clinical Presentation of Asymptomatic Phase, Stage 2

A
  • 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

20
Q

Clinical Presentation of Symptomatic Phase, Stage 3

A
  • 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.
21
Q

Dx of AIDS Stage 4?

A

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

22
Q

Clinical Presentation of AIDS stage 4?

A
  • 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.
23
Q

What is the most common opportunistic infection seen in AIDS?

A

Pneumocystis pneumonia is the most common.

24
Q

What are some other pulmonary OI’s in AIDS?

A
  • CAP (bacterial, mycobacterial, viral)
  • TB
  • Noninfectious causes of lung disease: Kaposi, non-hodgkins lymphoma, interstitial pneumonitis
  • Sinusitis (acute and chronic)
25
Q

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

A
  • 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
26
Q

What are some of the OI’s of the PNS?

A
  • 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
27
Q

What are some of the Rheumatologic OIs of AIDS?

A

-Arthritis

  • Severe inflammatory syndromes
  • -Reiters
  • -Psoriatic arthritis
  • -SICCA syndrome (dry eye and mouth)
  • -SLE

-avascular necrosis of femoral head

28
Q

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

A
  • complaints of visual changes
  • CMV Retinitis: perivascular hemorrhages and white fluffy exudates
  • Herpes infection
  • Toxoplasmosis
29
Q

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

A
  • 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.
30
Q

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

A
  • 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
31
Q

What are some of the Malignancies of HIV/AIDS?

A
  • Kaposis Sarcoma: lesions ANYWHERE.

- Non-hodgkins Lymphoma: usually b cell origin

32
Q

What are some GYN OIs of AIDS?

A
  • recurrent vaginal candidiasis
  • cervical dysplasia*
  • Cervical neoplasia* much more aggressive in HIV, most women die from their cervical cancer and not HIV
  • PID
33
Q

T-Cell activation: costimulation

  • what happens without costimulation?
  • what happens with costimuulation?
A
  • 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.
34
Q

T-cell Activation:

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

A

-1 week

35
Q

What is the role of Thelper cells?

A
  • 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.

36
Q

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

A

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.

Infectious Disease 3 (9 decks)

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