Acute - Hiv/aids

Front 1

4 things AIDs is characterized by?

Back 1

Profound immunosuppression
Opportunistic infections
Secondary neoplasms
Neurologic manifestations

Front 2

How does a retrovirus work?

Back 2

Virus is carried in RNA. RNA enters a host cell, undergoes reverese transcriptase in the cytosol and produces viral DNA. Integrase than incorporates the viral DNA into the host chromosomal DNA

Front 3

How is HIV detected? What do they measure?

Back 3

Antibodies
Starting to use p24 capsid -- a particle on HIV that is elevated with infected pts

Front 4

Target tissues of HIV

Back 4

1. T Helpers Cells (CD4)
2. ther cells with CD4 receptors... macrophages, dendritic cells, NK, CD8 cells.
1 and 2 result in immune system dysfxt and opportunistic infections
3. Neurological cells (glial) -- particulalry CNS/brain

Front 5

9 steps in HIV infection

Back 5

1. HIV binding and fusion via CD4 receptors
2. Injection of viral core
3. uncoating
4. reverse transcriptase
5. DNA integration
6. Viral protein expression - transcription/translation (Use viral DNA as template to reproduce HIV RNA genome)
7. Protein modification (Use HIV RNA template to snythesize proteins)
8. Viral core assembly
9. Budding (infect other cells)

Front 6

Explain what goes on during the first phase of HIV infection?

Back 6

Early acute phase - 85% pts have s/s similar to mono (avg 2 wks)
Seroconversion illness (development of detectable ABs)
CD4 count decreased 3-6 wks after infection, but then return to normal

Front 7

Explain what goes on during the second phase of HIV infection?

Back 7

Middle chronic phase.
Apparent containment - immune system intact and patients are generally asymptomatic or develop mild opportunistic infections
Replication occurs for several years but body able to make a shit ton of CD4 cells so you look aiight

Front 8

Explain what goes on during the third phase of the HIV infection?

Back 8

Replacement mechanism can't do it = observable decline in CD4 and all that bad stuff happens.
You get A I D S

Front 9

When does the CDC classify a pt with A I D S?

Back 9

HIV+
CD4 < 200/microL
Opportunistic infections (unless already prone to it)

Front 10

When may you not be classified with A I D S even if you meet all the qualifications?

Back 10

1. High dose corticoid therapy or other immunosuppressive w/in 3 mo prior to onset of
2. Dx w/ WBC dx: lymphoma, lymphoyctic leukemia, cancers)
3. Genetic immunodeficiency atypical of HIV

Front 11

What does prognosis of AIDS vary with?

Back 11

Varies with viral subtypes and pt characteristics
Wasting syndrome - Cachexia (unintentional loss of >10% body mass)
Increased viral count --- both indicate poor prognosis

Front 12

5 categories and subgroups of Opportunistic Infections/Cancers

Back 12

1. Protozoa infection
2. Fungi infection
3. Bacterial infection (Pneumocystis Pneumonia, TB, Meningitis)
4. Viral Infection (herpes, CMV)
5. Neoplasms (Kaposi sarcoma, Non-Hodgkin Lymphoma, Primary Brain lymphoma, Invasive cancer of uterus)

Front 13

Difference between CD4 count and viral load? What do they tell you?

Back 13

CD4: determine's pts status at time measure was taken
Viral load: indicates the direction the infection is taking (>.5 log copies/mL is not good)

Front 14

3 main classes of HAART drugs

Back 14

1. Reverse transcriptase inhibiors = nuceloside RTI (NRTI) and non-nucleioside RTI (NNRTI)
2. Protease inhibitors (tries to prevent HIV RNA from forming proteins)
3. Fusion inhibitors (prevent HIV from binding to CD4)

Front 15

Benefits of HAART

Back 15

1. Improves immune fxt
2. Suppresses viral replication
3. Significant inc in life expectancy
4. Reductions in opportunistic infections and comorbidities
5. Substantial reductions in wasting syndrome (Preserved LBM)
ESSENTIALLY PROLONGS CHRONIC PHASE = 36 G'S/YEAR

Front 16

When do you put a patient on HAART?

Back 16

patient-oriented decision; weigh against patient status and imminent progression... you do start to adapt to drug cocktail and it becomes less efficient

Front 17

CD4 classifications

Back 17

>500/microL = asymptomatic
200-500 = early symptoms
<200 = severe immunosuppresion

Front 18

Why are NRTIs thought to cause mitochondrial dysfxt?

Back 18

NRTIs bind to DNA-polymerases and inhibit them in the mitochondria. This disrupts mictorchondrial DNA transcription. RESULT = fatigue

Front 19

Side effects of lipids with HAART and why?

Back 19

Dyslipidemia - protease inhibitor problem. inc. TGs, dec. TC, HDL, LDL
Insulin resistance
Great risk for type II diabetics

Front 20

Lipodystrophy

Back 20

Fat loss of face and limbs
Fat accumulation in belly, trunk and dorsal cerical area
Remember inc. belly fat = inc. risk for CVD (it's science). Caused by HAART - NOT HIV

Front 21

Explain why impaired aerobic capacity and limitations in physical function occur with HAART.

Back 21

Reduced/mutated mitDNA (NRTIs fault)
This is due to the drug cocktail itself - on top of the HIV.
MECHANISM: impared O2 extraction-utilization (a-vO2 dif)

Front 22

Why is CVD and PVD common with HAART?

Back 22

CVD = possible autonomic involvement
PVD = associated with lower CD4

Front 23

Primary complain of HIV folks?

Back 23

Fatigue - reductions in vigourous activity and high-level ADLs
30% in asmptomaric, 60% in symptomatic, 80% in A I D S

Front 24

Causes of neuropathy in HIV pt?

Back 24

1. Virus itself (Mechanism may be related to HIV gp120, which can activate neural receptors for inflammatory cytokines)
2. HIV drugs
3. Result of opportunistic infections or other complications

Front 25

Characteristics of HIV induced neuropathy

Back 25

Most are sensory, and can be asymptomatic
Many are painful (seen in palliative care seettings)

Front 26

Types of HIV induced neuropathy

Back 26

1. Distal Symmetric Polyneuropathy (DSP) most common
2. Autonomic neuropathy - inc. risk for CVD b/c inc. vessel stiffness
3. Motor neuropathies have been reported (sensory most common). At peripheral and spinal levels, contribute to weakness, and can mimic ALS

Front 27

Causes of dec. mm function in HIV pts (not due to HAART)

Back 27

1. mm wasting - reduced CSA (HAART reduces this)
2. Defecits in central activation - associated with viral load and past hx of AIDS defining illness (not related to HAART)

Front 28

Ragged red fibers (AZT fibers)

Back 28

Associated with mitochondrial dysfxt = shitty

Front 29

What is a 6MWD good for?

Back 29

An effective predictor of VO2, with or without HAART. It is also a good predictor of LE strength with pts NOT on HAART (relationship less strong with HAART)

Front 30

What should be included in your PT eval when you get an HIV pt?

Back 30

1. Functional aerobic status (6 MWD)
2. Ankle brachial index (PVD screen)
Neurological screening (Semmes-Weignstein Filaments)

Front 31

PT interventions for the HIV pt?

Back 31

1. Pain controls (TENS)
2. Pt. educ = insensate feet (custom shoes, orthoses), ADL/task modification, D/C planning
3. Exercise - consider pt goal

Front 32

What does the literature tell us about HIV and exercise?

Back 32

60% VO2max, 3x/wk is associated w/ slowed HIV progression pre-HAART
Phys activity inversly related to viral load
Can reduce fxt aerobic impairment
May improve arterial compliance (improve tissue elasticity, baro-reflex; shown in animals)

Front 33

Exercise for HIV pt if trying to inc LBM?

Back 33

8-12 reps, 50-80% 1RM. Effects more pronounced in patients with wasting.
Not always successful due to: nutritional status, central activation, testosterone levels

Front 34

What exercise protocol may be the best for HIV pt?

Back 34

combination of RT and aerobic. Reduce trunk fat mass and TGs and inc. strength/aerobic capacity