Exam 4 Neuro and Immune

what is MS

progressive autoimmune related demylination disease of CNS

s/s of MS

vary and have diff patterns
chronic pain
visual disturbances
numbness
fatigue
weakness
difficulty co-ordination
loss of balance
pain

what does MS distrupt

the flow of information within the brain and b/w brain and body

incidence of MS

20-50
common in women
genetic component

how do symptoms present?

exacerbations and recurrences of sym

Diagnosing MS

MRI of the brain and SC
LP
nerve conduction studies

what is LP

increase IgG antibodies and breakdown products of myelin

common disease course

characterized by clearly defined attacks of worsening neuro function
followed by partial or complete recovery period

During resmission in MS

symptoms improve partially or completely and there is no apparent progression of disease

meds to modify MS

Immunosupressants

examples of immunosuppressants used in MS

azathioprine
DMARDS

how to manage relapse of MS

solumedrol
prednisone

symptom management of MS

bladder and bowel incontinence
infection
dizziness and vertigo
fatigue
emotional changes
pain
muscle spascity in legs
tremors

other treatments for MS

rehab
exercise; improves mobility, reduce stiffnes, improve bowel and bladder function
stress management- stress can cause MS flares

Myasthenia Gravis

autoimmune disorder affecting myoneural junction
-antibodies directed at acetycholine- impairing transmission of impulses

blocking acetylcholine

prevents muscle contraction

theory of MG

thymus gland may give incorrect instructions to develop immune cells resulting in autoimmunity and produces acetylecholine receptor antibodies

s/s of MG

muscle weakness
increase weakness during periods of activity and improves after period of rest
see face and neck muscles effected
facial expression effected
breathing and neck muscles may be affected

NR considerations of MG

tell patient to do most things in morning b/c they had night to rest
aspiration risk

prevalence of MG

all ethnic groups both genders
not directly inherited
young adult women and old men

diagnosis of MG

impairment of eye movement or muscle weakness without any changes in individuals ability to feel
blood test
nerve conduction study
CT or MRI

blood test MG

detects presence of immune molecules or acH receptor antibodies

nerve conduction study in MG

shows gradual decrease of muscle action due to imparied nerve-muscle transmission

CT or MRI use in MG

detects thymona

Pharm therapy in MG

cholinesterase inhibitor
immunosupressants

cholinesterase inhibitor

medicines that block normal breakdown of acH

plasmapheresis

like dialysis
removes blood plasma from the body by withdrawing blood and seperating it into plasma and cells and transfusing cells back into the blood stream

what does plasmapheresis remove

removes antibodies in treating autoimmune conditions
plasma replaced by saline or albumin

management of MG - first line of treatment

thymectomy

complications of MG

myasthenia crisis

myasthenia crisis results in

break down in communication b/w nerves and muscles

s/s of myasthenia crisis

weakness in the arms and leg muscles
double vision
difficulties with speech and chewing

worst case scenario of myasthenia crisis

decreased ability to swallow and breath
aspiration and aspiration pneumonia risk

managing myasthenia crisis

ensure adequate ventilation, intubation and mechanical ventilation may be needed

patient edu. myasthenia crisis

make sure patient knows s.s of both myasthenia crisis and cholinergic crisis

assessment and supportive measures of myasthenia crisis

measures to ensure airway and resp support
if patient cannot swallow use an NG tube
avoid sedatives and tranquillizers that further relaxes muscles

prognosis of myasthenia crisis

most people can significantly improve their muscle weakness and lead normal lives
can go into remission temp or perm

goal of thymectomy

stable, long-lasting complete remissions

severe weakness of MG

resp failure
needs immediate emergency medical care

Parkinson's disease

decreased levels of dopamine due to destruction of cells

what does PD affect

neurotransmission of impulses

patho of PD

progressive disorder
steady decrease in function

s/s of PD

tremor at rest
rigidity- expressionless face- swallowing difficulty aspirations
bradykinesia
shuffling gait-imbalanced gait
depression and other psych changes
dementia
pill rolling
sleep disturbances

Diagnostics of PD

diagnosis is based of s/s
no scan or blood test

management of PD

exercise to release dopamine
ROM

pharm treatment for PD

combo pill of carbidopa/levodopa

carbidopa

decarboxylase inhibitor
- prevents levodopa from being broken down before reaching the brain

levodopa

Dopamine precursor

Carbidope/Levodopa

are given together to lower dose of levodopa causing less N/V

surgical procedures for PD

deep brain stimulation
pacemaker in brain once meds lose effectiveness

ALS occur in

men age 55

ALS

degenerative nerve cells in brain and spinal cord
- progressive muscle weakness, paralysis and muscle wasting -> everything slows down
RESP PARALYSIS
COGNITIVE function not typically affected

cause of ALS

unknown

cure of ALS

none

s/s of ALS

painless, gradual onset of muscle weakness or slurred speech
fatigue
twitching and cramping in muscles
muscle weakness
muscle atrophy
dysphagia
dysarthria
hyperreflexia
constipation
cognitive function remains intact

care for ALS patient

remain patent airway, suctioning, intubation, CPAP, Bipap
communication
swallow eval - aspiration risk

medications for ALS

baclofen(Lioresal)
diazepam (valium)

baclofen(Lioresal)
diazepam (valium)

antispasmotics
muscle relaxers

what does a cerebral angiography look like?

looks at cerebral vasculature
- needs contrast dye

where does a cerebral angiography go through

groin and neck, PCI of brain through to the cerebral artery
no stent is places

what does a cerebral angiography Dx?

aneurysms, hemorrhages, removed blood clot to admin chemo

NR considerations for cerebral angiography

do neuro checks
increase fluids to flush dye

EEG

measures brain waves

diagnoses of EEG

seizures or monitoring them
- to confirm brain death
camera on patient

lumbar puncture

CSF with drawn from spinal cord

Dx LP

MS syphili menigistis other infections, malignany's, increased ICP

contraindications of LP

if on anticoagulant must be reversed

risks of LP

HA increased ICP bleeding

GCS

assess pt. with neuro deficits
concerned when pt cant protect their own airway

lowed the GCS score

worse the outcome

comotose patient GCS scale

8 or less

what are seizures

abnormal episodes of motor sensory autonomic or psychic activity due to sudden abnormal, uncontrolled electrical discharge from CN

generalized seizure

whole brain

focal seizures

starts in 1 hem

unknown seizures

half of all seizures

cause of seizures

CVA disease
hypoxemia
fever
head injury
HTN
brain tumor
alchol withdrawl

tonic clonic seizures

whole body seizures

NR for seizures

sit and wait for seizures to stop
get sharp objects out of the way
bed flat , monitor airway, untie gown, turn to side
note time and when ends
symptoms before during and after seizures

s/s of seizures

pt have an aura
presents focal; handshaking or mouth jerking
extensive like tonic clonic- incontinence

if a seizure is over 5 mins

call a rapid
protect airway

post ictal phase

confusion
drowsiness
increase HOB

NR after a seizure

check vitals
GCS
check pupils
reorient

how to diagnose seizures

EEG
video recording with the EEG
serum and urine test- drugs, ETOH, seizure med levels

anticonvulsant

increased levels toxic
decreased levels not therapeutic
- NEVER ABPRUPLTY STOP

epilepsy

recurring seizures

primary cause of epilepsy

idiopathic

secondary cause of epilepsy

brain tumor, birth trauma, infections, ETOH witdrawal

goal of epilepsy therapy

control seizure with minimal SE, meds to control seizures

prevention for seizure meds

phenytoin (Dilantin)
Carbanazepine (Tegretol)
valproic acid (Depakote)
levetiracetam (Keppra)

meds to stop active seizure

Diazpam (Valium)
Lorazepam (Ativan)

SE of benzodiazepines

drowsiness
sedative, controlled substance

Reversal of benzodiazepines

Flumazenil

daily prevention of seizures

therapeutic serun drug levels
monitor LFT

Cerebrovascular disorders

abnormality of the CNS when blood supply is disrupted

non-modifiable risks for a CVA

55 or older, male and AA

modifiable risks for a CVA

HTN,Afib
increased cholestrol
obesity
diabetes

stroke

sudden loss of function from a distruption of the blood supply to the brain

ischemic stroke

blood clot or piece of plaque cuases ischemia

hemorrhagic stroke

rupture blood vessel due to increased Bp is the most common

cerbellum stroke

ataxia, dizzy, unbalanced