MS & ALS (impaired physical mobility)

Question 1

MS: etiology, patho, classification scheme

Answer 1

etiology: unknown
but guessing: it develops in genetically susceptible ppl as a result of environmental exposure like infection
precipitating factors (promote the onset): infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health

pathphysiologuy: inflammation, demyelination, scarring

activated T cells travel from the blood to the brain

classification:
1. relapsing-remitting (MOST PPL diagnosed)
clearly defined relapses with a full reocovery or sight residual deficit upon recovery

2. primary-progressive
   accumulation of disability from disease onset
   slowly worsening neurons function but no distinct relapse (revery)
3. secondary progressive
   lapse remitting course, they start with relapse remitted then develop to progression w or w/o relapse occurs

clinically isolated syndrome
first clinical episode that is suggestive of MS. (subjective and obj info that suggest a demyelination.)
- develops with a duration of at least 24 hours, with or without recovery (in absence of fever or infection)

• shock, tingling etc

Question 2

MS , diagnosis, clinical manifestations, pseudo-relapse

Answer 2

Diagnosis -
- Hx
- clinical manifestations
- imaging studies process of elimination, ruling out all the things its not (MRI (will show plaques, inflammation, atrophy and tissue destruction), CSF analysis , evoked potentials (electrical events generated in the CNS by peripheral stimulation)

3 criteria for diagnosis:
- two inflammatory demyelinating lesions in 2 different locations
- damage/attack interval
- ruling out

Clinical manifestations -
Speech, Gait
Double vison
Scanning speech (words broken up)

Motor
Weakness or paralysis of limbs
stiffness or tightness of muscles (spascisity)

Sensory
numbness
tingling
blurred vision , patchy blindness
nerve root pain
tinnitus
dec hearing
Lhermities sign - electrical shock radiating down spine into the limbs

Cerebellar
- coordinates and regulates muscular activity, involuntary eye movement. lack of voluntary movement that would relate to gate instability
- difficulty swallowing

Fatigue
Bowel & Bladder
- constipation
- spastic bladder (urinary urgency, incontinence)
- flaccid bladder (no sensation to void)

possible severe cognitive dysfunction

Pseudo - relapse -
pseudo exasperation or flare

triggered by
STRESS
HEAT
ILLNESS
FATIGUE
not causing new damage

Question 3

What is the impact of pregnancy on a patient with MS

Answer 3

can exasterbate or be something that promotes the onset of it

Question 4

What are the goals of the Disease Modifying therapy (DONT NEED TO KNOW SPECIFIC DRUG NAME)

Answer 4

• dec relapse rate
• slower accumulation of brain lesions on MRI
  won’t heal scarring or heal current function but limits progression

Question 5

Adjunctive pharmacologic treatment , know categories for MLS

Answer 5

fro acute exacerbations:
- glucocorticoids (reduce edema and acute inflammation at site of demyelination)
- plasma exchange if not a good response to glucocorticoids

• anticholingerics : inc urine that the bladder can hold
• CNS stimulants for fatigue
• muscle relaxant for stascity
• nerve conduction enhancer - k+ channel blocker and improved nerve conduction in damaged segments (cautioned in seizure disorder or CKD)

Question 6

What are the functional limitations and patient teaching for people with MS

Answer 6

Not stating out in the sun because that can trigger a pseudo relapse

Longer breaks so your not wiped out at the end of shift (for her hairstylist)

help them learn to manage fatigue

help with lifestyle modifications

promote function through rehabilitation

PATIENT EDU:
identify triggers
rest
nutrition
treatment regimen
self-catheterization if necessary (bladder control)
monitor for side effects
adequate intake of fiber to aid in regular bowel habits
emotional adjustments

Question 7

Etiology & classifications of ALS

Answer 7

Rare and prpogressive
Characterised by loss of motor neurons and they’re unravel to send impulses to muscle fibers

A amyotrophic - no muscle nourishment
lateral area of spinal cord
sclerosis hardening

Classifications:
- Sporadic : most common
No family history , random

• Familial :
  one occurrence in family lineage

Question 8

Clinical manifestation UMN vs LMN

Answer 8

Upper Motor Neuron:
- loss of dexterity or ability to coordinate movements
-weakness
- spasticity (stiff or rigid muscles)
- hyperreflexia

vs
Lower Motor Neuron Symptoms
- weakness
- paralysis
HYPOreflexia
- fasciculation’s (twitches)
- flaccidity (not moving)
- muscle cramps

Question 9

How to diagnose ALS, what are known drug names and what do they do

Answer 9

Diagnosis:
difficult
neurological examination

diagnosis of exclusion
electrodiagnostic tests
blood and urie samples
spinal tap
x rays etc

Known drug names:
Riluzole - inhibits glutamate and slows progression of the disease but it doesnt cure it.
- when glutamate is continuously activated it causes muscles to breakdown

Radicava - slows functional deterioration

Question 10

4 Nursing invertions for ALS and prognosis

Answer 10

1. Facilitating communication :
   - have patient slow down and over articulate
   - limit distractions
   - use different methods: blinking, yes/no system
2. Aspiration Precautions
   - appropriate food consistency (honey or nectar consistency) small bites and eat slowly, position after eating to avoid reflux, small freq meals.

• coughing and deep breathing exercises
• secretion management
• incentive spirometer
• sucitoning airway or mouth if needed

3. Fall Precautions : bed alarm, bed in lowest position, lifts, wheelchair safety, promote safe mobility
4. Skin management
   turn q2 hours, nutrition, incontence management, reposition in wheelchair

Prognosis:
no cure
death occurs from a respiratory tract infection
2-6 years after diagnosis
- symptoms management
- hospice vs ventilator