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Neuro Rehab 2 > HIV > Flashcards

HIV Flashcards

1
Q

what is the pathogenesis of contracting HIV

A

HIV is a RNA retrovirus that binds to receptor sites on CD4 (helper T or lymphocytes) cell surface, fuses and enters cell

HIV releases reverse transcriptase and instructs host DNA to copy and mass produce the virus –> lymph nodes (which have lots of CD4 receptors) quickly become site of massive viral replication

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2
Q

how is HIV most often spread today

A

through sharing contaminated needles in IV drug use

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3
Q

what are modes of transmission for HIV

A

sexual contact
blood or blood products
perinatal-mother to fetus

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4
Q

can a mother w HIV have a baby without passing it on? how?

A

yes

take antiretroviral meds (HAART drugs) during pregnancy
avoid breastfeeding

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5
Q

what are HIV prevention strategies

A

safe sex
screen blood
regular testing for high risk
avoid IV drug use
HAART drugs for pregnancy

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6
Q

what is needed to determine someone to be HIV (+)

A

(+) viral load test or (+) HIV antibody testing

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7
Q

what is viral load testing

A

tests for the presence of HIV RNA in blood plasma

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8
Q

what is HIV antibody testing

A

tests for HIV antibodies present in bloodstream after seroconversion

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9
Q

what is seroconversion

A

time it takes for our body to develop immune cells to fight infection

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10
Q

viral load testing vs HIV antibody testing: detection time

A

viral load = quick
- 2-12wks after infection

HIV antibody
- 3-12mo after infection

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11
Q

what are the 4 clinical stages of HIV

A
  1. acute infection
  2. asymptomatic HIV dz
  3. symptomatic HIV dz
  4. advanced HIV dz/ AIDS
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12
Q

what is the acute infection clinical stage defined by

A

initial infection until seroconversion
- usually w/i 12wks

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13
Q

what clinical manifestations are present at the acute infection clinical stage

A

often asymptomatic or flu-like sx (diarrhea, fever, swollen lymph nodes, fatigue, myalgias, sore throat)

less often: meningitis, encephalitis, sz, psychosis, cranial neuropathy

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14
Q

in developed countries, what is the most common clinical stage to encounter someone w HIV in

A

asymptomatic HIV
drugs are available to keep people asymptomatic and in this stage as long as possible

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15
Q

dx criteria for asymptomatic HIV dz

A

CD4 count >500ul

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16
Q

clinical manifestations for asymptomatic HIV dz clinical stage

A

periods of general lymphadenopathy but otherwise sx free

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17
Q

duration of asymptomatic HIV dz clinical stage

A

1-20yrs
- depends on medical management
- depends on virus subtype

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18
Q

what are the lab values for asymptomatic HIV dz clinical stage

A

(+) antibody test
slow decline in CD4 count
slow inc in viral load

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19
Q

dx criteria for symptomatic HIV dz

A

CD4 count: 201-499ul

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20
Q

dx criteria for advanced HIV dz /AIDS

A

CD4 count <200ul

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21
Q

clinical manifestations of symptomatic HIV dz

A

wt loss
fatigue
fever
night sweats
emergence of neuro sx

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22
Q

clinical manifestations of advanced HIV dz/AIDS

A

wasting syndrome
opportunistic infections
AIDS related dementia
AIDS defining illnesses

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23
Q

what are the 3 main categories of AIDS defining illnesses

A

lot are neurologic
cancers
pulmonary

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24
Q

CD4 count throughout the clinical stages

A

asymptomatic >500
symptomatic 201-499
AIDS <200

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25
Q

what are often responsible for neurologic sx seen in HIV

A

secondary processes including - infection
- med SE
- inflammation
- metabolic abnormalities

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26
Q

what is the most common neurologic sx seen

A

peripheral neuropathies
- DSP the most common

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27
Q

how can the ANS be impacted and what is the PT implication of this

A

tachycardic
abnormal HD response to activity

use RPE during PT for exertion

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28
Q

neuro sx in acute stages of HIV

A

aseptic meningitis
encephalitis
sz
myelopathy
peripheral neuropathy
HA

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29
Q

what is the only neuro manifestation that can be directly attributed to virus itself

A

AIDS dementia complex

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30
Q

what are CNS manifestations of HIV

A

AIDS dementia complex
cerebral toxoplasmosis
primary CNS lymphoma
PML
cryptococcal meningitis
CMV encephalitis
neurosyphilis
TB meningitis

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31
Q

what is the pathophys of AIDS dementia complex

A

HIV crosses BBB in infected microphages and CD4 cells

affinity toward subcortical brain structures like BG, thalamus, brainstem

==> subcortical dementia

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32
Q

what are s/sx of AIDS dementia complex

A

dec concentration
dec memory (implicit)
dec learning and motor skills
slow mvmts/bradykinesia (BG)
leg weakness
dulled personality

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33
Q

when does AIDS dementia complex present

A

usually late stages of dz

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34
Q

how is AIDS dementia complex dx?

A

dx of exclusion
- no way to test for it

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35
Q

what might an MRI show of someone w AIDS dementia complex

A

diffuse cerebral atrophy

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36
Q

what might a CSF sample show in someone w AIDS dementia complex

A

normal or slightly elevated protein levels

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37
Q

how is AIDS dementia complex treated

A

cocktail of 2 HAART drugs from different categories - depending on what the person tolerates

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38
Q

what is cerebral toxoplasmosis

A

CNS lesion secondary to dormant parasite toxoplasma gondii

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39
Q

what pt is at especially high risk for cerebral toxoplasmosis abscesses

A

if CD4 count <100ul

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40
Q

where do you find the parasite (toxoplasma gondii) that is responsible for cerebral toxoplasmosis

A

very common parasite

found in undercooked meat, cat and rodent feces - we are likely all carriers but have healthy enough immune systems to keep this in check

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41
Q

what are s/sx of cerebral toxoplasmosis

A

fever
HA
focal findings
- hemiparesis
- speech abnormalities
- hemianesthesia
- CN palsies

manifestations directly related to location in the brain

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42
Q

what is a common prophylactic treatment for cerebral toxoplasmosis and who is appropriate for this

A

bactrim or septra

if CD4 count <100

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43
Q

what would an MRI likely show in cerebral toxoplasmosis

A

mass lesions in corticomedullary junction and BG

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44
Q

when is a brain tissue biopsy warranted in cerebral toxoplasmosis

A

if 2 wks of anti-toxo therapy doesn’t produce clinical improvement

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45
Q

at what CD4 count does primary CNS lymphoma occur at

A

CD4 <50

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46
Q

what virus is primary CNS lymphoma associated with

A

EBV

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47
Q

what are s/sx of primary CNS lymphoma

A

HA
lethargy
mental status changes
occasionally focal sx
sz
fever

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48
Q

what is the preferred imaging for primary CNS lymphoma

A

MRI

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49
Q

what would primary CNS lymphoma look like on an MRI

A

diffuse, weakly enhancing lesions

classically found in deep white matter around ventricles

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50
Q

treatment options for primary CNS lymphoma

A

limited
- whole brain radiation therapy
- HAART

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51
Q

what is the prognosis for primary CNS lymphoma

A

poor
median <6mo
- often palliative radiation used for QOL

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52
Q

what virus is associated w PML

A

JC

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53
Q

who is PML seen in

A

CD4 count <100

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54
Q

what is PML

A

progressive multifocal leukoencephalopathy

demyelinating disorder caused by JC virus which results in rapid and aggressive destruction of subcortical white matter

55
Q

what are clinical s/sx of PML

A

subacute progressive hemiparesis
cog decline
visual disturbances

usually global sx w a rapid decline

56
Q

how will PML look on imaging

A

multifocal periventricular and subcortical white matter lesions on CT and MRI
- lesions in cerebellum and brainstem may occur

57
Q

what is able to make a definitive dx of PML

A

brain biopsy

58
Q

what treatment is available for PML

A

no specific antiviral meds available

use HAART for QOL

59
Q

what is the prognosis for PML

A

poor
death in weeks to months

60
Q

what lab could be taken to view the presence of JC virus in PML

A

CSF

61
Q

who is at inc risk for cryptococcal meningitis

A

CD4 <100

62
Q

clinical sx of cryptococcal meningitis

A

mild HA
nausea
change in mental status
maybe fever

may have focal deficits and/or seizures

63
Q

what is the hallmark of cryptococcal meningitis

A

inc ICP

64
Q

what is the pathophys of cryptococcal meningitis

A

inflammation of connective tissue in brain leading to swelling of meninges
–> widespread problems w CSF flow –> obstruction and inc ICP

65
Q

what does imaging often show of cryptococcal meningitis

A

often normal o may show hydrocephalus (from obstructed CSF flow)

66
Q

what is the gold standard for dx of cryptococcal meningitis

A

detection of organism on culture of CSF from LP

67
Q

what is seen in a lumbar puncture of cryptococcal meningitis

A

elevated opening pressure
mild inc in CSF protein
detection of organism

68
Q

how is cryptococcal meningitis treated

A

antifungal agents
aggressive mgmt of ICP w serial LPs and possible VP shunting

69
Q

what is key in treating cryptococcal meningitis

A

managing ICP!!
- limit other neuro effects of compression of other neuro structures

70
Q

who is CMV encephalitis seen in

A

people w HIV and CD4 <50

71
Q

clinical presentation of CMV encephalitis

A

subacute to rapidly progressing mental status changes
sz
CN palsies

other organs infected (ex: retina, adrenal glands)

72
Q

what provides the only definitive dx for CMV encephalitis

A

brain biopsy

73
Q

how would CMV encephalitis show up on imaging

A

non-specific finding on MRI of periventricular lesions

74
Q

what would a sample of CSF from CMV encephalitis show

A

may have polymorphonuclear pleocytosis
- overall inc in cell count

(not very specific)

75
Q

what treatment for CMV encephalitis may be beneficial

A

HAART drugs

76
Q

who is neurosyphilis seen in

A

in HIV, even if CD4 count isn’t low –> important to be tested for this if HIV+

77
Q

what are possible CNS effects of neurosyphilis

A

meningitis
CN palsies (hearing, vision)
tabes dorsalis
sz
stroke
psychiatric disorders

78
Q

what can imaging show for neurosyphilis

A

normal or:
- meningeal enhancement
- vasculitis
- brain infarct

79
Q

what is used to confirm a neurosyphilis dx

A

blood serum testing for systemic syphilis + abnormal CSF

80
Q

how is neurosyphilis treated

A

aqueous penicillin G
- good treatment

81
Q

what is tuberculous meningitis caused by

A

mycobacterium tuberculosis

82
Q

how is the risk of tuberculous meningitis related to CD4 count

A

risk is inversely related to CD4 count
- may be seen in people w CD4 of 500

83
Q

what is a consideration with tuberculous meningitis differential dx

A

hard to tease out bc have lot of vague neuro sx and imaging will show nonspecific inflammation of connective tissue in brain

84
Q

clinical presentation of tuberculous meningitis

A

subacute progression of:
- HA
- CN palsies
- mental status changes
- fever
- night sweats
- wt loss

also can see other systemic effects, ie pulmonary system

85
Q

how might imaging present for tuberculous meningitis

A

meningeal enhancement and hydrocephalus

86
Q

what does CSF for tuberculous meningitis show

A

lymphocytic pleocytosis
elevated protein
hypoglycorrachia
- low glucose form metabolism impact

87
Q

how is tuberculous meningitis treated

A

same as pulmonary TB - isoniazid, rifampin, pyrazinamide, ethambutol

+ a corticosteroid to dec inflammation and neuro consequences

88
Q

what are 3 types of peripheral neuropathy that can be seen

A

distal sensory polyneuropathy (DSP)

anti-retroviral drug-induced toxic neuropathies (ATN)

CMV subacute progressive polyradiculopathy

89
Q

how does distal sensory polyneuropathy present

A

stocking glove
(most common)

90
Q

how could you distinguish ATN from DSP

A

see onset of ATN in first few weeks from starting drugs
- otherwise indistinguishable from DSP

91
Q

how does CMV subacute progressive polyradiculopathy present

A

more radiating nerve pain than stocking glove presentation

92
Q

what does the incidence of DSP increase relative to

A

degree of person’s immunosuppression

93
Q

what is the etiology of DSP

A

unclear
- not a direct HIV infection of peripheral nerves
- likely HIV causing other nutritional deficiencies

94
Q

what are the primary sx of DSP

A

paraesthesias
dysaesthesias

95
Q

what are risk factors associated with DSP

A

nutritional deficiencies
CMV
EtOH
DM
high viral load
low CD4 count

96
Q

pathophysiology of DSP

A

distal to prox axonopathy and distal axonal degen

small, unmyelinated sensory fibers are lost early
-> progresses to destruction of larger myelinated fibers w dz progression –> macrophages and inflammatory cytokines infiltrate peripheral nerve and dorsal root ganglion

97
Q

what is a characteristic of treatment that makes DSP challenging to treat

A

pain is difficult to treat

98
Q

PT intervention for DSP

A

ADs
uptrain other sensory
- vision and vestib
work on balance

99
Q

treatment options for DSP

A

meds: NSAIDs, opioids, cannabinoids, etc.
- people often on a combo of multiple

hypnosis
meditation
guided imagery
biofeedback
acupuncture

100
Q

what is clinically indistinguishable from DSP

A

ATN
- management will be similar

101
Q

what is the likely etiology of ATN

A

mitochondrial toxicity d/t nuceloside-analogue reverse-transcriptase inhibitors
- energy/metabolic issue

102
Q

what relationship can HAART drugs have w ATN sx

A

sx typically start 4-6mo after HAART

stopping HAART may dec sx after 1-2mo, or not at all

103
Q

what will most patients opt for medical treatment w ATN

A

most will stay on HAART therapy anyway, maybe be put on another drug
- people would rather tolerate ATN SE than go off and potentially have poorer QOL

104
Q

what is CMV neuropathy

A

distinct subacute progressive polyradiculopathy secondary to direct CMV infection of nerve roots

105
Q

what is the pathophys of CMV neuropathy

A

lumbosacral nerve roots affected first , then ascends

106
Q

CMV neuropathy sx

A

radiating pain

107
Q

what will a CSF sample show of CMV neuropathy

A

pleocytosis w neutrophil predominance

108
Q

can CMV neuropathy be treated

A

can be treated w antivirals
- which can partially reverse sx if caught early

109
Q

why is regular screening for integ issues important in HIV

A

at risk for opportunistic infections
- kaposi’s can be rapidly fatal
- early intervention is key

110
Q

what are examples of integumentary and neoplasm manifestations of HIV

A

kaposi’s sarcoma
non-hodgkin’s lymphoma
cervical cancer
other malignant cancers

111
Q

what are examples of CP manifestations of HIV

A

TB
PCP
CMV
pericardial effusion
myocarditis
cardiomyopathy
endocarditis
coronary vasculopathy

112
Q

what is lipodystrophy

A

fat redistribution to central visceral areas

113
Q

what is HIV wasting syndrome

A

loss of >10% baseline BW
diarrhea
weakness
fever

114
Q

what are common HAART therapy side effects

A

diarrhea
n/v –> can exacerbate other SE w poor nutritional status

115
Q

what are some GI and nutritional manifestations

A

CMV
lipodystrophy
HIV wasting syndrome
HAART side effects

often a bloated abdomen and wasting in other areas

116
Q

is MSK manifestations primary or secondary

A

secondary to neuro sx
- not primary to HIV

117
Q

what are examples of MSK manifestations

A

polymyositis
myopathy
arthritic conditions
secondary biomechanical change

118
Q

who is PreP appropriate for

A

pre-exposure prophylactics for those at high risk (gay and bi men)

119
Q

what are general side effects of PreP

A

diarrhea
stomach pain
HA
fatigue (but usually subsides)

120
Q

when is it indicated for HAART therapy to be started

A

CD4 <200

121
Q

at what CD4 values can HAART be offered independent of viral load

A

CD4 200-350

122
Q

HAART can be offered when CD4 values are _______ if viral load is ________

A

CD4 350-500
viral load >100K

123
Q

when is HAART therapy not indicated and why

A

CD4 >500
pts not as high risk for opportunistic infections

124
Q

what is the initiation of HAART therapy based on

A

clinical assessment
CD4 count
viral load

125
Q

what does HAART stand for

A

highly
active
anti-retroviral
therapies

126
Q

what are 2 main subclasses of HAART therapy

A

NRTIs
NNRTIs

127
Q

how is HAART therapy often prescribed

A

as combinations of the NRTIs and NNRTIs (typically 2 at a time)

128
Q

what are side effects of NRTI HAART drugs

A

“nasty side effects”

peripheral neuropathy
myopathy
anemia
GI disturbances
hepatomegaly
pancreatitis

129
Q

what are side effects of NNRTI HAART drugs

A

rash
liver dysfunction
cog changes
lactic acidosis

130
Q

what is the goal of HAART therapy

A

to dec HIV viral load to undetectable level

131
Q

how does PT change in HIV

A

not really at all
- treat impairments

considerations for psychosocial support resources

132
Q

what are PT components to address in PT

A

aerobic capacity
cog deficits
sensory impairments
pain
functional mobility
CP issues
occupational/recreational

133
Q

what does the evidence say about PT and pain management

A

PT is a great option to dec pain and dec need for pharmacological mgmt
- good supports for physical modalities also

Neuro Rehab 2 (48 decks)

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