HIV Flashcards
what is the pathogenesis of contracting HIV
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
how is HIV most often spread today
through sharing contaminated needles in IV drug use
what are modes of transmission for HIV
sexual contact
blood or blood products
perinatal-mother to fetus
can a mother w HIV have a baby without passing it on? how?
yes
take antiretroviral meds (HAART drugs) during pregnancy
avoid breastfeeding
what are HIV prevention strategies
safe sex
screen blood
regular testing for high risk
avoid IV drug use
HAART drugs for pregnancy
what is needed to determine someone to be HIV (+)
(+) viral load test or (+) HIV antibody testing
what is viral load testing
tests for the presence of HIV RNA in blood plasma
what is HIV antibody testing
tests for HIV antibodies present in bloodstream after seroconversion
what is seroconversion
time it takes for our body to develop immune cells to fight infection
viral load testing vs HIV antibody testing: detection time
viral load = quick
- 2-12wks after infection
HIV antibody
- 3-12mo after infection
what are the 4 clinical stages of HIV
- acute infection
- asymptomatic HIV dz
- symptomatic HIV dz
- advanced HIV dz/ AIDS
what is the acute infection clinical stage defined by
initial infection until seroconversion
- usually w/i 12wks
what clinical manifestations are present at the acute infection clinical stage
often asymptomatic or flu-like sx (diarrhea, fever, swollen lymph nodes, fatigue, myalgias, sore throat)
less often: meningitis, encephalitis, sz, psychosis, cranial neuropathy
in developed countries, what is the most common clinical stage to encounter someone w HIV in
asymptomatic HIV
drugs are available to keep people asymptomatic and in this stage as long as possible
dx criteria for asymptomatic HIV dz
CD4 count >500ul
clinical manifestations for asymptomatic HIV dz clinical stage
periods of general lymphadenopathy but otherwise sx free
duration of asymptomatic HIV dz clinical stage
1-20yrs
- depends on medical management
- depends on virus subtype
what are the lab values for asymptomatic HIV dz clinical stage
(+) antibody test
slow decline in CD4 count
slow inc in viral load
dx criteria for symptomatic HIV dz
CD4 count: 201-499ul
dx criteria for advanced HIV dz /AIDS
CD4 count <200ul
clinical manifestations of symptomatic HIV dz
wt loss
fatigue
fever
night sweats
emergence of neuro sx
clinical manifestations of advanced HIV dz/AIDS
wasting syndrome
opportunistic infections
AIDS related dementia
AIDS defining illnesses
what are the 3 main categories of AIDS defining illnesses
lot are neurologic
cancers
pulmonary
CD4 count throughout the clinical stages
asymptomatic >500
symptomatic 201-499
AIDS <200
what are often responsible for neurologic sx seen in HIV
secondary processes including - infection
- med SE
- inflammation
- metabolic abnormalities
what is the most common neurologic sx seen
peripheral neuropathies
- DSP the most common
how can the ANS be impacted and what is the PT implication of this
tachycardic
abnormal HD response to activity
use RPE during PT for exertion
neuro sx in acute stages of HIV
aseptic meningitis
encephalitis
sz
myelopathy
peripheral neuropathy
HA
what is the only neuro manifestation that can be directly attributed to virus itself
AIDS dementia complex
what are CNS manifestations of HIV
AIDS dementia complex
cerebral toxoplasmosis
primary CNS lymphoma
PML
cryptococcal meningitis
CMV encephalitis
neurosyphilis
TB meningitis
what is the pathophys of AIDS dementia complex
HIV crosses BBB in infected microphages and CD4 cells
affinity toward subcortical brain structures like BG, thalamus, brainstem
==> subcortical dementia
what are s/sx of AIDS dementia complex
dec concentration
dec memory (implicit)
dec learning and motor skills
slow mvmts/bradykinesia (BG)
leg weakness
dulled personality
when does AIDS dementia complex present
usually late stages of dz
how is AIDS dementia complex dx?
dx of exclusion
- no way to test for it
what might an MRI show of someone w AIDS dementia complex
diffuse cerebral atrophy
what might a CSF sample show in someone w AIDS dementia complex
normal or slightly elevated protein levels
how is AIDS dementia complex treated
cocktail of 2 HAART drugs from different categories - depending on what the person tolerates
what is cerebral toxoplasmosis
CNS lesion secondary to dormant parasite toxoplasma gondii
what pt is at especially high risk for cerebral toxoplasmosis abscesses
if CD4 count <100ul
where do you find the parasite (toxoplasma gondii) that is responsible for cerebral toxoplasmosis
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
what are s/sx of cerebral toxoplasmosis
fever
HA
focal findings
- hemiparesis
- speech abnormalities
- hemianesthesia
- CN palsies
manifestations directly related to location in the brain
what is a common prophylactic treatment for cerebral toxoplasmosis and who is appropriate for this
bactrim or septra
if CD4 count <100
what would an MRI likely show in cerebral toxoplasmosis
mass lesions in corticomedullary junction and BG
when is a brain tissue biopsy warranted in cerebral toxoplasmosis
if 2 wks of anti-toxo therapy doesn’t produce clinical improvement
at what CD4 count does primary CNS lymphoma occur at
CD4 <50
what virus is primary CNS lymphoma associated with
EBV
what are s/sx of primary CNS lymphoma
HA
lethargy
mental status changes
occasionally focal sx
sz
fever
what is the preferred imaging for primary CNS lymphoma
MRI
what would primary CNS lymphoma look like on an MRI
diffuse, weakly enhancing lesions
classically found in deep white matter around ventricles
treatment options for primary CNS lymphoma
limited
- whole brain radiation therapy
- HAART
what is the prognosis for primary CNS lymphoma
poor
median <6mo
- often palliative radiation used for QOL
what virus is associated w PML
JC
who is PML seen in
CD4 count <100
what is PML
progressive multifocal leukoencephalopathy
demyelinating disorder caused by JC virus which results in rapid and aggressive destruction of subcortical white matter
what are clinical s/sx of PML
subacute progressive hemiparesis
cog decline
visual disturbances
usually global sx w a rapid decline
how will PML look on imaging
multifocal periventricular and subcortical white matter lesions on CT and MRI
- lesions in cerebellum and brainstem may occur
what is able to make a definitive dx of PML
brain biopsy
what treatment is available for PML
no specific antiviral meds available
use HAART for QOL
what is the prognosis for PML
poor
death in weeks to months
what lab could be taken to view the presence of JC virus in PML
CSF
who is at inc risk for cryptococcal meningitis
CD4 <100
clinical sx of cryptococcal meningitis
mild HA
nausea
change in mental status
maybe fever
may have focal deficits and/or seizures
what is the hallmark of cryptococcal meningitis
inc ICP
what is the pathophys of cryptococcal meningitis
inflammation of connective tissue in brain leading to swelling of meninges
–> widespread problems w CSF flow –> obstruction and inc ICP
what does imaging often show of cryptococcal meningitis
often normal o may show hydrocephalus (from obstructed CSF flow)
what is the gold standard for dx of cryptococcal meningitis
detection of organism on culture of CSF from LP
what is seen in a lumbar puncture of cryptococcal meningitis
elevated opening pressure
mild inc in CSF protein
detection of organism
how is cryptococcal meningitis treated
antifungal agents
aggressive mgmt of ICP w serial LPs and possible VP shunting
what is key in treating cryptococcal meningitis
managing ICP!!
- limit other neuro effects of compression of other neuro structures
who is CMV encephalitis seen in
people w HIV and CD4 <50
clinical presentation of CMV encephalitis
subacute to rapidly progressing mental status changes
sz
CN palsies
other organs infected (ex: retina, adrenal glands)
what provides the only definitive dx for CMV encephalitis
brain biopsy
how would CMV encephalitis show up on imaging
non-specific finding on MRI of periventricular lesions
what would a sample of CSF from CMV encephalitis show
may have polymorphonuclear pleocytosis
- overall inc in cell count
(not very specific)
what treatment for CMV encephalitis may be beneficial
HAART drugs
who is neurosyphilis seen in
in HIV, even if CD4 count isn’t low –> important to be tested for this if HIV+
what are possible CNS effects of neurosyphilis
meningitis
CN palsies (hearing, vision)
tabes dorsalis
sz
stroke
psychiatric disorders
what can imaging show for neurosyphilis
normal or:
- meningeal enhancement
- vasculitis
- brain infarct
what is used to confirm a neurosyphilis dx
blood serum testing for systemic syphilis + abnormal CSF
how is neurosyphilis treated
aqueous penicillin G
- good treatment
what is tuberculous meningitis caused by
mycobacterium tuberculosis
how is the risk of tuberculous meningitis related to CD4 count
risk is inversely related to CD4 count
- may be seen in people w CD4 of 500
what is a consideration with tuberculous meningitis differential dx
hard to tease out bc have lot of vague neuro sx and imaging will show nonspecific inflammation of connective tissue in brain
clinical presentation of tuberculous meningitis
subacute progression of:
- HA
- CN palsies
- mental status changes
- fever
- night sweats
- wt loss
also can see other systemic effects, ie pulmonary system
how might imaging present for tuberculous meningitis
meningeal enhancement and hydrocephalus
what does CSF for tuberculous meningitis show
lymphocytic pleocytosis
elevated protein
hypoglycorrachia
- low glucose form metabolism impact
how is tuberculous meningitis treated
same as pulmonary TB - isoniazid, rifampin, pyrazinamide, ethambutol
+ a corticosteroid to dec inflammation and neuro consequences
what are 3 types of peripheral neuropathy that can be seen
distal sensory polyneuropathy (DSP)
anti-retroviral drug-induced toxic neuropathies (ATN)
CMV subacute progressive polyradiculopathy
how does distal sensory polyneuropathy present
stocking glove
(most common)
how could you distinguish ATN from DSP
see onset of ATN in first few weeks from starting drugs
- otherwise indistinguishable from DSP
how does CMV subacute progressive polyradiculopathy present
more radiating nerve pain than stocking glove presentation
what does the incidence of DSP increase relative to
degree of person’s immunosuppression
what is the etiology of DSP
unclear
- not a direct HIV infection of peripheral nerves
- likely HIV causing other nutritional deficiencies
what are the primary sx of DSP
paraesthesias
dysaesthesias
what are risk factors associated with DSP
nutritional deficiencies
CMV
EtOH
DM
high viral load
low CD4 count
pathophysiology of DSP
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
what is a characteristic of treatment that makes DSP challenging to treat
pain is difficult to treat
PT intervention for DSP
ADs
uptrain other sensory
- vision and vestib
work on balance
treatment options for DSP
meds: NSAIDs, opioids, cannabinoids, etc.
- people often on a combo of multiple
hypnosis
meditation
guided imagery
biofeedback
acupuncture
what is clinically indistinguishable from DSP
ATN
- management will be similar
what is the likely etiology of ATN
mitochondrial toxicity d/t nuceloside-analogue reverse-transcriptase inhibitors
- energy/metabolic issue
what relationship can HAART drugs have w ATN sx
sx typically start 4-6mo after HAART
stopping HAART may dec sx after 1-2mo, or not at all
what will most patients opt for medical treatment w ATN
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
what is CMV neuropathy
distinct subacute progressive polyradiculopathy secondary to direct CMV infection of nerve roots
what is the pathophys of CMV neuropathy
lumbosacral nerve roots affected first , then ascends
CMV neuropathy sx
radiating pain
what will a CSF sample show of CMV neuropathy
pleocytosis w neutrophil predominance
can CMV neuropathy be treated
can be treated w antivirals
- which can partially reverse sx if caught early
why is regular screening for integ issues important in HIV
at risk for opportunistic infections
- kaposi’s can be rapidly fatal
- early intervention is key
what are examples of integumentary and neoplasm manifestations of HIV
kaposi’s sarcoma
non-hodgkin’s lymphoma
cervical cancer
other malignant cancers
what are examples of CP manifestations of HIV
TB
PCP
CMV
pericardial effusion
myocarditis
cardiomyopathy
endocarditis
coronary vasculopathy
what is lipodystrophy
fat redistribution to central visceral areas
what is HIV wasting syndrome
loss of >10% baseline BW
diarrhea
weakness
fever
what are common HAART therapy side effects
diarrhea
n/v –> can exacerbate other SE w poor nutritional status
what are some GI and nutritional manifestations
CMV
lipodystrophy
HIV wasting syndrome
HAART side effects
often a bloated abdomen and wasting in other areas
is MSK manifestations primary or secondary
secondary to neuro sx
- not primary to HIV
what are examples of MSK manifestations
polymyositis
myopathy
arthritic conditions
secondary biomechanical change
who is PreP appropriate for
pre-exposure prophylactics for those at high risk (gay and bi men)
what are general side effects of PreP
diarrhea
stomach pain
HA
fatigue (but usually subsides)
when is it indicated for HAART therapy to be started
CD4 <200
at what CD4 values can HAART be offered independent of viral load
CD4 200-350
HAART can be offered when CD4 values are _______ if viral load is ________
CD4 350-500
viral load >100K
when is HAART therapy not indicated and why
CD4 >500
pts not as high risk for opportunistic infections
what is the initiation of HAART therapy based on
clinical assessment
CD4 count
viral load
what does HAART stand for
highly
active
anti-retroviral
therapies
what are 2 main subclasses of HAART therapy
NRTIs
NNRTIs
how is HAART therapy often prescribed
as combinations of the NRTIs and NNRTIs (typically 2 at a time)
what are side effects of NRTI HAART drugs
“nasty side effects”
peripheral neuropathy
myopathy
anemia
GI disturbances
hepatomegaly
pancreatitis
what are side effects of NNRTI HAART drugs
rash
liver dysfunction
cog changes
lactic acidosis
what is the goal of HAART therapy
to dec HIV viral load to undetectable level
how does PT change in HIV
not really at all
- treat impairments
considerations for psychosocial support resources
what are PT components to address in PT
aerobic capacity
cog deficits
sensory impairments
pain
functional mobility
CP issues
occupational/recreational
what does the evidence say about PT and pain management
PT is a great option to dec pain and dec need for pharmacological mgmt
- good supports for physical modalities also
