Indendent Study Flashcards

1
Q
  • 25,000/yr
  • Females more than males
  • Age 20 - 40
  • Risk increases with family history
  • Seen during pregnancy/during labor
  • Families carry genetic defect
  • Only occurs in certain climates
  • Where one lives determines the risk of getting the disease
A

Etiology/predisposing factor MS

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2
Q

Primarily affecting the white matter/CNS
• s&s depend on location
•Inflammation destroys myelin sheath
•Plaques of sclerotic tissue

A

MS

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3
Q

1st exacerbation is asymptomatic
• Flu like s/s for 2-3 days – no numbness, no tingling
• 1 – 5 years pt exacerbates again for 3-4 days
• Pt feels sick with increase WBC
• Antibodies begin to attack myelin sheath
• Holes in myelin sheath
• Current is lost through holes
• During remission there will healing to nerve
• Appears to be multiple plaque AKA multiple sclerosis plaque find on nerve myelin

A

MS

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4
Q
  • Optic nerve
  • Chiasms and tracts
  • Cerebrum
  • Brain stem
  • Cerebellum – a big area to be found in
  • Spinal cord
  • Found in myelin sleeve with sclerotic patches
  • Affect all area in brain
  • MS drug Avonex, drug that works best $1,000 a dose
A

Areas of the CNS Affected

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5
Q

• – What disease does to body
o Double vision
o Clumsiness
o Ataxia

A

1 Clinical manifestations of MS

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6
Q
– complication related to it
o Foot drop
o Immobility
o Constipation/UTI/skin breakdown
o DVT/Pneumonia
A

Secondary Clinical manifestations of MS

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7
Q

o Loss of employment – lose job within 10 years
o Loss of independence
o Divorce Due to emotional peak/instability
▪ Due to breakdown of frontal lobe, causing impulsiveness and inappropriate behavior

A

Tertiary clinical manifestation of MS

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8
Q
  • visual problems
  • blurred, double-vision
  • memory deficits
  • personality changes
  • depression
  • seizures
  • hemiparesis
A

Cerebral Syndrome

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9
Q
  • fatigue
  • paresthesia
  • bowel/bladder problem
  • foot drop
  • heat intolerance (Uhthoff’s sign)
  • shooting/shock like pain
  • spasticity
A

Spinal Syndrome

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10
Q

is a condition most commonly observed multiple sclerosis and particularly in Optic Neuritis where small increases in body temperature (hyperthermia) caused by exercise, hot baths or showers or otherwise, cause a worsening of symptoms.
• Shooting /shock like pain
• Spasticity
• Pt is unable to experience heat or cold
• If pt gets to hot or cold they will exacerbate their disease
• Putting a patient in hot tub will create enough of a stress to create another exacerbation
• Pt should be careful with their environment, pt’s water should be warm not hot

A

Uhthoff’s symptom

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11
Q
•altered proprioception
•↓motor coordination
•ataxia/loss of balance
•spastic paralysis
•muscle spasm
•intentional tremors
With closed eye patient will fall over 
• Intentional tremors – developed tremors when they are going to pick something up
• Tremor gets worst all the time
A

Cerebellar Syndrome

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12
Q

CN- #3 and 12
•slurred speech
•eye pain
•nystagmus

A

Brain Stem Syndrome

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13
Q
• Corticosteroid
o Methylprednisolone – same as RA
o Iv dose for 3 days
o Followed by 6 weeks of oral prednisome
o Prednisone
• Immunostimulants (ABC&R)
o Avonex IM q wk – keep in remission
o Bestaseron SC QOD – immune stimulants
o Copaxone SC qam – immune stimulants
A

MS pharmacology

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14
Q
  • Use adaptive equipment
  • Moderate activity with rest periods
  • Avoid stress
  • Exercise – walking, biking, swimming
  • Intense exercise will exacerbate, due to emotional liability pt might engage in intense exercise
  • Gait training
  • Visualize extremities
  • Paint steps – provide fluorescent lit steps - less likely to fall
  • Use thermometer to test water – as disease progresses pt develops neuropathies, no feeling in finger tip and toes
A

MS NURSING INTERVENTION

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15
Q
  • Voiding schedule
  • Intermittent self cath
  • Decrease risk for UTI – watch for UTI
  • Depends
  • We do post-void residual
  • Use bladder scan to determine how much is in there
  • Known to have urinary retention
  • Urine retention is 50cc found in bladder post voiding
  • Begin cath when 250cc is left in bladder after voiding
  • Seen towards end of disease
  • Toward end pt will get urostomy in abdominal wall so pt can place cath directly into abodomen rather then ureter
A

Altered Urinary elimination

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16
Q

slowly, progressive disorder of movement
•degenerative changes
•basal ganglia region
•substantia nigra- destruction of neurons
•dopamine production decreases over time
•results in imbalance of neurotransmitters that affects voluntary movement

A

Parkinson’s

17
Q

50,000 new cases/year
•men more common
•ages 40 - 70
•1% of population has Parkinson’s
•Hispanic/Latinos/Whites highest incidence
•gradual onset
•symptoms progress slowly over a prolonged course

A

Parkinson’s

18
Q
  • genetics
  • atherosclerosis
  • viral infections
  • head trauma
  • chronic antipsychotic meds
  • environmental exposures
A

Parkinson’s risk factors

19
Q

tremor,
ridgidity,
bradykinesia,
and postural instability

A

4 Classic Signs:

20
Q
  • slowness of movement
  • freezing phenomenon
  • shuffle
  • micrographia
  • dysphonia
A

Bradykinesia

21
Q
  • Aspiration – when eating
  • Respiratory infection
  • UTI
  • Injury
  • Skin breakdown
  • Pt run risk of being ABC pt
  • Disabling disease which leads to death
A

Parkinson’s Complications

22
Q
  • Pet Scan – evaluate levodopa
  • SPECT
  • CT/MRI
  • Urine/CSF – decreased homovanillic acid (abnormal breakdown of dopamine)
  • Non of these will diagnose parkinsons,
  • To diagnose: all pieces are put together, symptoms, complaints, diagnostic
A

Parkinson’s diagnosis

23
Q
  • 0 = no sign of disease
  • 1 = unilateral disease
  • 2 = bilateral disease without impairment of balance
  • 3 = mild/moderate bilateral with postural instability
  • 4 = severe disability but able to stand and walk
  • 5 = wheelchair = dependent or bedridden

1- 2 = Start with cogentin, - drug to reduce tremors
2- 3 = sinemet (cardopa-levodopa)– the problem with

A

Unified Parkinson Disease Rating Scale

24
Q
Risk for aspiration
o Semisolid diet
o Chin tuck
o Be careful with liquid
o Perform swallowing test
o No crumbly food
o Check mouth frequently for residue
o Might have to put GI tube
• Impaired physical mobility
o Postural/balance exercises
• Self care deficits
• Impaired verbal communication
A

Nursing Diagnosis for Parkinson’s

25
progressive weakness/fatigue of skeletal muscles •autoimmune disorder affecting neuromuscular junction due to ineffective release of acetylcholinine • Hallmark is muscle weakness
Mysthenia gravis
26
* Insufficient Acetylcholine | * Excessive cholinesterase (enzyme that eats acetylcholine, destruction of actylcholine receptors by autoimmune process
Pathophysiology of MG
27
``` •begins with ocular difficulties (diplopia, ptosis) •weakness/fatigue- face/throat •difficulty chewing •mask-like facial expressions •bulbar- weak voice, dysphagia, dysarthria, •can progress to generalized weakness and eventual respiratory failure •exacerbation & remission common •muscles most involved: face (eye- drooped lid, mouth- swallowing, chewing) ```
Clinical Manifestations for MG
28
``` • Ocular o Diplopia o Pitosis o Ocular: Difficulty with vision, unable to focus, difficulty with accomodation • Facial muscles o Mask like facial expressions – little or no emotion • MS o Extreme muscle weakness • Bulbar o Weak voice o Dysphagia / dysarthria o Difficulty swallowing • Respiratory weakness o SOB, dypnea, hypoxia o A problem when it effects respiratory system o Pt might have difficulty breathing since there is not enough acethycholine for breathing o Pt will require respiratory support o In elderly illness progresses quickly ```
Assessment Findings MG
29
* give exactly on time (lasts 3-4 hrs) * with milk or food to decrease GI upset * give 3-4x day to increase muscle strength * always assess muscle strength before eating * avoid morphine, quinidine, curare, procainamide, neomycin, animoglycosides, strong sedatives
Mestinon
30
edrophonium (Tensilon) * 30 seconds after IV injection, facial weakness and ptosis resolve for 5 minutes * Reaction confirms diagnosis
MG Drug challenge:
31
``` – remove anti-acetylcholine o Take out unit of blood o Clean out antibodies o Give back to the pt o 4-6 units over period of time o Makes pt come out of exarcerbation • Thymectomy – thymus is responsible for producing the anti-acetychole antibodies o Removal of thymus can cure MG – takes 4-10 years to work ```
Plasmapheresis for MG
32
* too little medication * infection, stress or trauma * Edrophonium IV = improves * severe, muscle weakness with inability to speak, swallow, or breathe
Myasthenic –
33
* too much medication * Edrophonium IV = worsen * similar to myasthenic crisis and include excessive salivation, sweating, N/V/D * Antidote - atropine
Cholinergic
34
* Monitor pt ability to clear secretions * Small bites at 30 degrees * Supervise meals * Sit upright
NI for MG
35
``` progressive degeneration and loss of both upper and lower motor neurons •known as Lou Gehrig’s disease •affects 1.5 in 100,000 •males more than females •onset usually 40-70 yrs •results in progressive muscle loss •survival rate average 2- 3 years •death usually respiratory ```
ALS
36
* diagnostic * EMT * muscle biopsy * serum creatinine levels * pulmonary function tests
ALS DIAGNOSTIC
37
* muscle weakness/fatigue * muscle atrophy * hyper-reflexia; fasciculation; spasticity * difficulty chewing, & speaking * dyspnea leads to respiratory suppression * No sensory or cognitive loss
Clinical manifestations of ALS
38
* supportive/palliative * Prepare for ventilatory involvement * medications: muscle relaxants; control muscle spasticity; anticholinergic (reduce oral secretions); anti-seizure * Rilutek (riluzole) effective in the Rx of ALS to extent survival time
ALS management
39
Chronic, progressive demyelinating disease of the CNS
MS