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77 Cards in this Set

  • Front
  • Back
Peripheral nervous system (PNS) consists of:
All nervous system structures outside the CNS.
Disorders of the PNS cause _________ of body systems.
Degeneration
Some disorders of the PNS are _____________.
Temporary
Neuromuscular disorders compose one group and may include _____ and _____disorders, or both.
Motor, sensory
Neuromuscular disorders involve:
Disruption of transmission between neurons and muscles that they stimulate.
Neuromuscular disorders can cause:
Muscle weakness and if respiratory system is affects= death.
What are some common neuromuscular disorders?
Multiple sclerosis (MS), myasthenia gravis (MG), amyotrophic lateral sclerosis (ALS), and Guillain-Barre syndrome (GBS)
Multiple Sclerosis
Chronic progressive degenerative disease that affects myelin sheath of neurons in CNS.

Degeneration in response to bodys immune system. Results in completely blocked nerve impulses and permanent loss of muscle function of that area.
If myelin sheath damaged?
Nerve impulses cannot be transmitted
Cause of MS
Viral infection, heredity
Age of onset for MS
20-50 (More in women)
S/S of MS
Muscle weakness, tingling sensations, numbness, visual disturbances, pain with eye movement.
What can trigger S/S of MS?
Extreme heat, cold, fatigue, infection, stress, hormone changes after pregnancy.
MS has...
Periods of exacerbation and remission. Intense fatigue causing immobility. Accidents and falls common. Muscle spasticity, bowel or bladder dysfunction, paralysis.

Death from resp infection typically after 20-35 years after DX.
MS DX tests
S/S and history. Analysis of CSF may show increase in IgG, MRI shows sclerotic plaques.
Therapeutic interventions for MS
No cure. Interferon therapy (Betaseron, Avonex) reduce exacerbations and delay disability.

ACTH (Prednisone) decrease inflammation.
Immunosupressants (Imuran, Cytoxan).
Anticonvulsants (Dilantin, Tegretol) releave neuro pain.
(Diazepam, Lioresal, Zanaflex) control muscle spasms.
(Urecholine, Ditropan) help with bladder problems.
Fatigue treated with antidepressants (Symmetrel)
Cholinesterase Inhibitors
Increase acetylcholine at synapses.

Prostigmin
S/E: Cholinergic toxicity (SLUDGE)
Atropine=antidote
Glucocorticoids
Reduce inflammation
Prednisone
S/E: Osteoporosis, infection, ^ BS, sodium/water retention, Cushings
Intervention: Provide calcium supplements
Immunosupressants
Supress immunity and antibody formation.
Imuran
S/E: Anorexia, hepatotoxicity, n&v, anemia
Intervent: Monitor blood counts, protect from bleeding, admin with meals
Antispasmodics/Muscle relaxants
Relax muscles, reduce pain.
Dantrium
S/E: CNS depression
Anticonvulsants
Treat nerve pain.
Dilantin
S/E: CNS depress
Intervent: Soft tooth brush, floss, gum massage
Glutamate Antagonist
Delays progression of ALS
Rilutek
S/E: Decreased strength, diarrhea, nausea, vomit
Intervent: Rest, monitor for resp depress, give on empty stomach
Plasmapheresis
Used to remove antibodies that may be attacking myelin from the blood.
Take 2-5 hours to complete
What is Myasthenia Gravis
"grave muscle disease"
Weakness of voluntary or skeletal muscles of the body. Disease of the neuromuscular junction.
Myasthenia Gravis is caused by
acetylcholine (ACh) from crossing synaptic cleft to contract muscle. The immune system attacks ACh
Cause of Myasthenia Gravis
Autoimmune process. A virus may initiate the disease. Disorders of the thymus gland are associated with MG.
Peak onset of Myasthenia Gravis
20-30 years. Men affects more than women after age 60. But more often in woman than men.
S/S of Myasthenia Gravis
Extreme muscle weakness, Hallmark: increased muscle weakness during activity and improvement in muscle strength after rest.
Muscles are strongest in the morning.
Activities affected by Myasthenia Gravis
Eye and eyelid movements, chewing, swallowing, speaking, breathing, skeletal muscle function.

Pt often have ptosis, masklike expression, fading voice

Exacerbations caused by stress, illness, trauma, temps, electrolye imbal.....
Complications of Myasthenia Gravis
Aspiration, resp infections, resp failure are leading cause of death.
Myasthenic crisis: sudden onset of weakness from not enough meds
Overmedication: can cause cholinergic crisis
***Both require medical attention
SLUDGE (cholinergic crisis s/s)
Salivation, lacrimation, urination, diarrhea, gi cramping, emesis

"liquid pouring out of ever body orifice"
DX tests for Myasthenia Gravis
History and symptoms and physical exam. Pt looks up 2-3 minutes (ptosis if MG is present will occur)

IV injection of Tensilon (antichol drug) if patient can suddenly open eyes wide= MG dx.
Interventions of Myasthenia Gravis
No cure.
Removal of thymus gland can decrease s/s in most pts.
Meds used: Prostigmin, Mestinon b/c they kill acetylcholinesterase that breaks down ACh

Prednisone

Plasmapheresis can be used to remove antibodies from pts blood
Myasthenic Crisis caused by
Too LITTLE medication

S/S: ptosis, difficulty swallowing and speaking, dyspnea, weakness
Cholinergic Crisis caused by
Too MUCH medication

S/S: SLUDGE
Myasthenia Gravis patient teaching
Do activities like shopping at peak action of med.
Teach to conserve energy
Avoid infection
Dont use: D-penicillamine, alpha-interferon, botulinum toxin
Amyotrophic Lateral Sclerosis is
"Lou Gehrig's" disease
Degenerative condition that affects motor neurons responsible for control of voluntary muscles.
Within brain/spinal cord, upper and lower motor neurons begin to degenerate and form scar tissue or die, blocking trans of nerve impulses
Amyotrophic Lateral Sclerosis causes
atrophy of muscle tissue and muscle strength and corrdination decreases
Eventually muscles with breathing and swallowing become involved
Usual age of onset with Amyotrophic Lateral Sclerosis
40-70 (more in men than women)
S/S of Amyotrophic Lateral Sclerosis
Progressive muscle weakness, decreased coordination of arms, legs, and trunk. Fasciculations (muscle twitch), inappropriate emotional outbursts, bladder/bowel function remain intact
Complications of Amyotrophic Lateral Sclerosis
PE, CHF, death fro resp complications.

Death usually 3-5 years after DX
Diagnostic tests for Amyotrophic Lateral Sclerosis
Based on clinical symptoms.

EEG and EMG to rule out other conditions
Interventions for Amyotrophic Lateral Sclerosis
Baclofen and diazepam given to relieve muscle spasticity.
Quinine used for muscle cramps.
Riluzole to help reduce damage of motor neurons and prolong survival by several months.
***Prevent infection!
AAC for speech therapy
Person with ALS has an intact ___________ it is the _________ that is deteriorating.
mind, body
Gullain-Barre Syndrome
Aka: Acute inflammatory polyneuropathy.
Abrupt onset of symmetrical paresis that progresses to paralysis. Myelin in spinal and cranial nerves are destroyed by inflammation.
Peripheral nerves in Gullain-Barre Syndrome
Infiltrated by lymphocytes that cause edema and inflammation
Demyelination in Gullain-Barre Syndrome
Causes axonal atrophy resulting in slowed or blocked nerve conduction
Remyelination in Gullain-Barre Syndrome
Much slower process and occurs in descending pattern and is accompanied by a resolution of symptoms
Four variants to Gullain-Barre Syndrome
Ascending Gullain-Barre Syndrome (most common), descending Gullain-Barre Syndrome, Miller Fisher syndrome, pure motor Gullain-Barre Syndrome.
Ascending Gullain-Barre Syndrome
Most common
Progressive weakness and numbness that begins in the legs and ascends up the body. No deep tendon reflexes. In 50%, respiratory function compromised
Descending Gullain-Barre Syndrome
Less common
Affects the cranial nerves that originate in the brainstem first. Diff speaking and swallowing. Weakness progresses downward towards the legs. Respiratory compromise is rapid. Numbness problematic in hands more than feet.
Reflexes deminished or absent
Miller Fisher syndrome (variant of GBS)
RARE
No resp compromise or sensory loss.
Classis s/s are ataxia, absence of reflexes, paralysis of the extraocular muscles
Pure motor Gullain-Barre Syndrome
Mild form of ascending Gullain-Barre Syndrome.
S/S same except lack of numbness or paresthesias
Cause of Gullain-Barre Syndrome
Autoimmune response to viral infection or vaccination. Average age is 30-50
S/S of Gullain-Barre Syndrome
3 stages---------
1st stage: onset of symptoms and lasts until progressin of symptoms stop. Lasts 24hrs to 3 wks and characterized by rapid onset of muscle weakness and paralysis with little or no muscle atrophy.
May need to intube ascending/descending

2nd Stage: plateau stage s/s most sever but progression has stopped. Lasts 2-14 days

3rd Stage: Recovery stage. 6-24 months. GBS pts recover completely within a few months to a year
Complications of Gullain-Barre Syndrome
Resp failure, infection, depression, fatigue and paralysis of resp muscles, prone to pneumonia and UTIs, immobility
DX tests for Gullain-Barre Syndrome
Lumbar puncture to obtain CSF, shows ^ protein level. EMG and nerve conduction velocity tests to evaluate nerve function.
Interventions for Gullain-Barre Syndrome
During first stage patient is compeltely dependent for all needs. Plasmapheresis may be used to remove patients plasma and replace w/ fresh. Plasmapheresis should be started 7-14 days from the onset of s/s.
*Steroids not effective
Axonal regeneration and remyelination occur during recovery phase
Postpolio Syndrome
Affects pts 10-40 years after poliomyelitis virus.
S/S of Postpolio Syndrome
Weakening of muscles affected with first involvement with polio.
Fatigue, muscle weakness with atrophy, sleeping problems, jt pain, scoliosis, resp compromise
Peripheral neuropathies
Cranial nerve problems

May affect sensory, motor or both branches of a single nerve
Cause of cranial nerve disorders include
tumors, infections, inflammation, trauma
Trigeminal Neuralgia (Cranial Nerve V)--trigeminal nerve

****SENSORY DISORDER
Sometimes called tic douloureux, involved 5th cranial nerve (trigeminal).
Affects sensory portion of nerve.
Chronic compression of nerve is suspected to initiate onset of s/s usually in women at age 50-60
S/S of Trigeminal Neuralgia
Pain that begins and ends suddenly, some have hundreds of attacks a day and others only a couple a year, pain felt in the skin on one side of the face.
Areas affected: lips, upper lower gums, cheeks, forehead, side of nose.
Pt may not wash fash or brush teeth to avoid pain.
Treatment of Trigeminal Neuralgia
Anticonvulsants like Dilantin and Tegretol to reduce nerve impulses.
Nerve block offers 8-16 months of releif
If corneal sensation is lots, goggles or eye path or artificial tears may be necess.
Complications of Trigeminal Neuralgia
Corneal damage, poor nutrition, depression
Bell's Palsy (Cranial Nerve VII)-facial nerve

***MOTOR DISORDER
Facial nerve becomes inflamed and edematous causing interruption of nerve impulses. Thought to be nerve trauma from viral or bacterial infection. Loss of motor control on one side of the face. (Bilater is less than 1%)
Contracture of facial muscles may occur if recovery is slow.
More common in third trimester of pregnancy in pts w/ HIV or DM.
S/S of Bell's Palsy
May be sudden or over 2-5 day period. Severity peaks within several days of onset.
Dry eye, tingling around lips, unable to close eyelid, close lips, mouth pulled toward affected side, cant smile or raise eyebrows, drooling, lost sense of taste on affected side of tongue, 50% full recovery in short time, 35% fully recover <1year
Treat Bell's Palsy
Prednisone 7-10 days to decrease edema. Analgesics for pain and antiviral. Moist heat with gentle massage to face and ear also eases pain
Complications of Bell's Palsy
Corneal damage, poor nutrition, depression
A patient with TN asks the nurse why she was started on carbamazepine (tegretol). Which response is best? A)"It will help decrease the inflammation in your nervous system." B) "It will depress your immune system, which can slow the pregression of the disease." C) "It can help relieve nerve pain." D) "It relaxes the bladder to help control bladder spasms
C) It can help relieve nerve pain
A patient with ALS asks why he doesnt seem to have enough breath to sing anymore. Which explanation by the nurse is best? A) ALS can damage the nerve to your bronchi and bronchioles, causing contriction and reduced airflow." B)The demyelination of your nerves caused by ALS causes confusion in the impulses to your lungs." C) "ALS can affect your coval cords, making it diffucult to form sounds as you speak or sing." D) " ALS may be affecting the nerves that go to your resp muscles, making the weak."
D) ALS may be affecting the nerves that go to your resp muscles, making them weak.
A pt who is newly dx with ALS says to the nurse, "I do not want to be kept alive on machines." Which nursing action is best in response? A) Ask if pt has advance directives and provide info about preparing them. B) Reassure the pt that he will not need to make decisions about machines for a long time. C) Inform pt that individuals with ALS are not candidates for artificial ventilation D) Explain to the pt that a ventilator will be necessary to keep hi breathing as his disease progresses.
A) Ask if pt has advance directives and provide info about preparing them.
When caring for a patient admitted with dx of Guillain-Barre syndrome, which nursing dx should take priority?
A) Anxiety B) Imbalanced nutrition C) Impaired gas exchange D) Impaired mobility
C) Impaired gas exchange
Which nursing interventions are appropriate for the patient with Bell's palsy? Select all that apply.
A) Admin moisturizing eye drops B) Apply an eye patch C) Avoid touching the patients face D) Apply warm compresses E) Provide facial massage F) Teach pt to protect her face from cool breezes
A)Admin moisturizing eye drops
B)Apply an eye patch
D)Apply warm compresses
E)Provide facial massage
Which meal would be the best choice for a pt with myasthenia gravis?
A) Baked chicken sandwich, fresh carrots, apple
B) Meatloaf, mashed potatoes, canned green beans
C) Steak, baked potato, green salad
D) Tacos, fresh veggies, sliced peaches
B) Meatloaf, mashed potatoes, canned green beans
How will the visiting nurse caring for a pt with myasthenia gravis and sever muscle weakness know if interventions have been effective?
A) Pt verbalizes satisfaction with the plan on care
B) Pt states understanding of the medication regimen
C) Pt and family state that no further home visits are needed.
D) Pt is able to perform ADLS with Sa02 remaining at 95%
D) Pt is able to perform ADLS with Sa02 remaining at 95%