NSG 555 Quiz 3 - (Neuro module 7 + Hem Module
8): Questions With Definite Solutions
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Terms in this set (115)
lou gehrig's disease
incurable progressive muscle weakness and eventually
death
affects upper motor neurons and lower motor neurons.
ALS
age 55-75 is typical onset
sporatic, 5-10% familial. thought to be known gene
mutation
unknown. gene mutation SOD1 or C9orf72
may be due to oxidative stress/free radicals. eventually
pathophysiology of ALS
leads to denervation and atrophy of muscles b/c motor
neurons in brainstem and spinal cord die
neuro exam is essential.
ASYMMETRIC weakness in limbs first (usually arms)
foot drop, difficulty walking, weakness in liftin garms.
UMN (upper motor neuron) s/s: hyperreflexia, sapsticity,
babinski signs, incoordination and weakness
LMN (lower motor neuron) s/s: weakness, atrophy,
presentation of ALS
fasciculations (twitching)
BULBAR s/s ALS: dysarthria, dysphagia, siallorhea,
tongue atrophy and fasciculations
dementia may appear first.
bowel and bladder are spared
, widespread UMN, LMN s/s and absense of any other
disease process, absence of neuroimaging evidence of
other disease.
should get labs to rule out heavy metal poisoning, lyme
dx ALS
disease, HIV, hereditary d/o.
MRI, ESR, protein, immunofixation electrophoresis, CSF
analysis, b12, CK, EMG, nerve cond. studies and MRI,
chem, liver, thyroid tests
criteria for ALS diagnostics
EMG+clinical abnormalities (s/s LMN degeneration by
awaji-shima criteria clinical, electrophys and neuropath exam, s/s UMN by
clinical exam, progression of motor syndrome within a
region)
for ALS, improves survival
antiglutamate slows progression of ALS
riluzole
s/e: asthenia, dizzy, gi distress, low WBC, elevated liver
enzymes (check labs first and then q 3mos)
free radical scavenger to reduce oxidative stress:
decreases functional decline so reduces symptoms
progression)
Edaravone
INFUSION daily X14 days, then 14 days off, then daily X
10 days, 14 off, then repeat
s/s: contusion from injection, HA, gait change
improve depression, anxiety, and sleep s/s
SARI (trazadone). can improve emotional lability.
SSRI, SNRI for ALS
Benzos may also be used and may help with spasticity
and muscle cramps
TCAs, glycopyrrolate, atropine
anticholinergics for ALS
for sialorrhea (saliva increase), depression, anxiety,
sleep and pain
ALS: muscle relaxants (tizanidine, baclofen),
dextromethorphan/quinidine for emotional lability
other meds for ALS
modafinil--stimulant for fatigue
oxybutynin--bladder spasms
, acute unilateral weakness/paralysis of facial nerve with
Bells Palsy onset of <72 hours and unknown etiology.
CN VII (facial) affected
pregnancy, diabetes, URI, obesity, family hx, HTN. There
is usually a trigger like a URI or ischemia to a nerve.
Causes edema of facial nerve d/t inflammation. If not
increased incidence of alleviated then axonal demyelination and nerve
bells palsy with what? degeneration with varying degrees of s/s 3 days later.
HSV1 and 2
varicella possible.
acute and progressive onset, max paralysis within 48-72
hours and in all cases by day 5
IPSILATERAL (same side) pain in ear then facial paralysis
by 1-2 days
smooth forehead, inability to close eye, flattened
presentation and PE of
nasolabial fold, asymmetric smile. tinnitus and hearing
bells palsy
issues and drooling may occur.
altered taste and sensitivity to sound possible.
may be peripheral or central ns lesion source. CNS
would spare forehead and would be lower facial
weakness
exclude lyme disease (get a lyme titer if tick exposure or
if problem in the area)
Dx bells palsy
MRI to rule out MS, stroke and tumor with and without
contrast, esp if fails to recover within 3 mos
protect the eye is most important goal of care (prevent
exposure keratitis which can cause blindness also
protect from corneal abrasion)
mgt of bells palsy
glasses, tape shut at night, may need surgical
decompression but only in 6% of cases
massage and pt may help
8): Questions With Definite Solutions
Save
Terms in this set (115)
lou gehrig's disease
incurable progressive muscle weakness and eventually
death
affects upper motor neurons and lower motor neurons.
ALS
age 55-75 is typical onset
sporatic, 5-10% familial. thought to be known gene
mutation
unknown. gene mutation SOD1 or C9orf72
may be due to oxidative stress/free radicals. eventually
pathophysiology of ALS
leads to denervation and atrophy of muscles b/c motor
neurons in brainstem and spinal cord die
neuro exam is essential.
ASYMMETRIC weakness in limbs first (usually arms)
foot drop, difficulty walking, weakness in liftin garms.
UMN (upper motor neuron) s/s: hyperreflexia, sapsticity,
babinski signs, incoordination and weakness
LMN (lower motor neuron) s/s: weakness, atrophy,
presentation of ALS
fasciculations (twitching)
BULBAR s/s ALS: dysarthria, dysphagia, siallorhea,
tongue atrophy and fasciculations
dementia may appear first.
bowel and bladder are spared
, widespread UMN, LMN s/s and absense of any other
disease process, absence of neuroimaging evidence of
other disease.
should get labs to rule out heavy metal poisoning, lyme
dx ALS
disease, HIV, hereditary d/o.
MRI, ESR, protein, immunofixation electrophoresis, CSF
analysis, b12, CK, EMG, nerve cond. studies and MRI,
chem, liver, thyroid tests
criteria for ALS diagnostics
EMG+clinical abnormalities (s/s LMN degeneration by
awaji-shima criteria clinical, electrophys and neuropath exam, s/s UMN by
clinical exam, progression of motor syndrome within a
region)
for ALS, improves survival
antiglutamate slows progression of ALS
riluzole
s/e: asthenia, dizzy, gi distress, low WBC, elevated liver
enzymes (check labs first and then q 3mos)
free radical scavenger to reduce oxidative stress:
decreases functional decline so reduces symptoms
progression)
Edaravone
INFUSION daily X14 days, then 14 days off, then daily X
10 days, 14 off, then repeat
s/s: contusion from injection, HA, gait change
improve depression, anxiety, and sleep s/s
SARI (trazadone). can improve emotional lability.
SSRI, SNRI for ALS
Benzos may also be used and may help with spasticity
and muscle cramps
TCAs, glycopyrrolate, atropine
anticholinergics for ALS
for sialorrhea (saliva increase), depression, anxiety,
sleep and pain
ALS: muscle relaxants (tizanidine, baclofen),
dextromethorphan/quinidine for emotional lability
other meds for ALS
modafinil--stimulant for fatigue
oxybutynin--bladder spasms
, acute unilateral weakness/paralysis of facial nerve with
Bells Palsy onset of <72 hours and unknown etiology.
CN VII (facial) affected
pregnancy, diabetes, URI, obesity, family hx, HTN. There
is usually a trigger like a URI or ischemia to a nerve.
Causes edema of facial nerve d/t inflammation. If not
increased incidence of alleviated then axonal demyelination and nerve
bells palsy with what? degeneration with varying degrees of s/s 3 days later.
HSV1 and 2
varicella possible.
acute and progressive onset, max paralysis within 48-72
hours and in all cases by day 5
IPSILATERAL (same side) pain in ear then facial paralysis
by 1-2 days
smooth forehead, inability to close eye, flattened
presentation and PE of
nasolabial fold, asymmetric smile. tinnitus and hearing
bells palsy
issues and drooling may occur.
altered taste and sensitivity to sound possible.
may be peripheral or central ns lesion source. CNS
would spare forehead and would be lower facial
weakness
exclude lyme disease (get a lyme titer if tick exposure or
if problem in the area)
Dx bells palsy
MRI to rule out MS, stroke and tumor with and without
contrast, esp if fails to recover within 3 mos
protect the eye is most important goal of care (prevent
exposure keratitis which can cause blindness also
protect from corneal abrasion)
mgt of bells palsy
glasses, tape shut at night, may need surgical
decompression but only in 6% of cases
massage and pt may help
