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MS, MG, GBS Reviewer

The document discusses autoimmune neurological disorders, focusing on Multiple Sclerosis (MS) and Myasthenia Gravis (MG), detailing their symptoms, pathophysiology, diagnosis, and treatment options. MS is characterized by demyelination in the CNS leading to various neurological impairments, while MG affects neuromuscular transmission causing muscle weakness. Guillain-Barre Syndrome is also mentioned, highlighting its acute progression and treatment strategies, including plasmapheresis and supportive care.
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0% found this document useful (0 votes)
68 views5 pages

MS, MG, GBS Reviewer

The document discusses autoimmune neurological disorders, focusing on Multiple Sclerosis (MS) and Myasthenia Gravis (MG), detailing their symptoms, pathophysiology, diagnosis, and treatment options. MS is characterized by demyelination in the CNS leading to various neurological impairments, while MG affects neuromuscular transmission causing muscle weakness. Guillain-Barre Syndrome is also mentioned, highlighting its acute progression and treatment strategies, including plasmapheresis and supportive care.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Autoimmune Neurological Disorders -Visual problems and sensory impairment such

as numbness and tingling sensation


• Multiple sclerosis (MS)- A progressive (paresthesia).
immune-related demyelination of the
white matter of the CNS and damage to -Ocular disturbances (optic neuritis, diplopia,
the nerve fibers and their targets. ophthalmoplegia, blurred vision, and
nystagmus).
-Demyelination refers to the destruction of the
myelin, -the fatty and protein materials that -Muscle dysfunction (weakness, paralysis
surrounds nerve fibers in the brain and spinal ranging from monoplegia to quadriplegia,
cord. spasticity, hyperreflexia, intention tremor, and
gait ataxia.
-it results in impaired transmission of nerve
impulses. -Urinary disturbances (incontinence, urgency,
frequency and frequent infection).
-exact causes is “unknown”.
-Emotional lability (mood swings, irritability,
-but is related to slow-acting or latent viral euphoria, and depressions).
infection and autoimmune response.
-often, the disease relapses and remits,
-other theories suggests environmental and exacerbates, and symptoms recur including
genetic factors may also be linked to MS. fatigue, weakness, numbness, difficulty in
-emotional stress, overwork, fatigue, pregnancy, coordination, loss of balance, pain, and visual
and acute respiratory infection may precede the disturbances.
onset of illness.
MULTIPLE SCLEROSIS PATHOPHYSIOLOGY
-sensitized T-cells typically crosses the blood-
brain barriers.
-main function is to check the CNS for antigen
and then leave.
-however, in MS the T-cells remains and
promotes the infiltration of other agents that
damage the immune system.
-immune system initiates an inflammatory MULTIPLE SCLEROSIS: DIAGNOSIS:
response that attacks the myelin. ❖ MRI-detects MS lesions
MULTIPLE SCLEROSIS COMPLICATIONS: ❖ EEG
❖ LP-shows elevated gamma globulin
❖ Injuries from fall fractions in the CSF.
❖ UTI ❖ WBC count may rise
❖ Constipation ❖ Characteristics of relapse and remission
❖ Joint contracture of the disease or physical signs and
❖ Pressure ulcers symptoms.
❖ Rectal distention
❖ Pneumonia MULTIPLE SCLEROSIS: TREATMENT

MULTIPLE SCLEROSIS: SIGNS & SYMPTOMS: •Medical Management:

-depends on the site of myelin destruction.


-disease modifying therapies: interferon B-1a ❖ Impaired verbal communication
and interferon B-1b, glatiramer acetate ❖ Disturbed thought processes
(Copaxone), and IV methylprednisolone. ❖ Ineffective coping
❖ Impaired home maintenance
-symptom management of muscle spasms,
❖ Potential sexual dysfunction
fatigue, ataxia, and bowel and bladder control.
………………………………………
-those with relapse-remitting courses are placed
on immune modulating therapy, with interferons • Myasthenia Gravis (MG)-autoimmune
or glatiramer acetate. disorder affecting the myoneural
junction.
-steroids are used to reduce the associated
edema of the myelin sheaths during -a disorder of transmission at the
exacerbation. neuromuscular junction that affects
communication between the motor neuron and
-other drugs: baclofen, tizadine, or diazepam to
the innervated muscle cells.
relieve muscles spasticity.
-affects women than men, peaks at ages 20 and
-cholinergic agents to relieve urine retention and
30 years old.
minimize frequency and urgency.
-antibodies directed at acetylcholine at the
-Amantadine to relieve fatigue.
myoneural junction impair transmission of
-Anti-depressants-for mood swings and impulses, although the exact mechanism that
behavioral symptoms. triggers the autoimmune response is still
unclear, it is thought that t-cells have a key role.
-during exacerbation: supportive measures
include bed rest, comfort measures, massage, -75% of people with MG also have thymic
prevention of fatigue, pressure ulcers, bowels abnormalities such as thymoma (thymus tumor)
and bladder training. or thymic hyperplasia (increased thymus cells).
-antibiotics for bladder infection -Lambert-Eaton myasthenic syndrome is a
special type of MG that develops in association
-physical and speech therapy with neoplasm particularly small cell carcinoma
-counseling of the lungs.

-exercise program to maintain muscle tone -neonatal myasthenia gravis is caused by


placental transfer of Ach receptors antibody.
NURSING PROCESS-ASSESSMENT OF THE
PATIENT WITH MS: MYASTHENIA GRAVIS: SIGNS & SYMPTOMS:

-Neurologic deficits ❖ Progressive skeletal muscle weakness


❖ Fatigability
-Secondary complications ❖ Weak eye closure
-Impact of disease on physical, social, and ❖ Ptosis
emotional function and on lifestyle. ❖ Diplopia
❖ Blank and expressionless faces and nasal
-patient and family coping. vocal voices impairment (dysphonia).
NURSING PROCESS-DIAGNOSIS OF THE ❖ Frequent nasal regurgitation and difficulty
PATIENT WITH MULTIPLE SCLEROSIS: chewing and swallowing.
❖ Weakened respiratory muscles with
❖ Impaired physical mobility decreased tidal volume and vital
❖ Risk for injury capacity.
❖ Impaired bowel and bladder function
MYASTHENIA GRAVIS: DIAGNOSIS:
❖ History and physical examination MANAGEMENT OF MYASTHENIC CRISIS:
❖ Anticholinesterase test- uses drugs that
-Patient instruction in signs and symptoms of
inhibit acetylcholinesterase (e.g. tensilon
myasthenic crisis and cholinergic crisis.
test- edrophonium chloride).
❖ Nerve stimulation studies -Ensuring adequate ventilation; intubation and
❖ Immunoassay test- detects the presence mechanical ventilation may be needed.
of Ach receptor antibodies in the blood.
❖ Single-fiber electromography- detects -Assessment and supportive measures include:
delayed or failed neuromuscular − Ensure airway and respiratory support
transmission in muscle fibers supplied. − Take ABGs. Serum electrolytes, I&O, and
MEDICAL MANAGEMENT (M.G): daily weight.
− If patient cannot swallow, nasogastric
•Pharmacologic therapy: feeding may be required.
− Immunosuppresive (corticosteroids, − Avoid sedatives and tranquilizers
azathioprine and cyclosporine). NURSING PROCESS: THE CARE OF THE
− Pyridostigmine and neostigmine- inhibits PATIENT WITH MYASTHENIA GRAVIS:
breakdown of Ach at the neuromuscular
junction by acetylcholinesterase. ❖ Focus on patient and family teaching.
❖ Provide medication teaching and
•Plasmapheresis- is the removal of antibodies management.
from the circulation and provides short term ❖ Implement energy conservation
clinical improvement. measures.
-used to stabilize the condition of persons in ❖ Implement strategies to help with ocular
myasthenic crises or for short-term treatment in manifestations.
undergoing thymectomy. ❖ Prevent and/or manage complications
and avoid crisis.
-Thymectomy ❖ Implement measures to reduce risk of
aspiration.
-Intravenous immunoglobulin therapy
❖ Avoid stress, infections, vigorous physical
-Note: aminoglycoside antibiotic should be activity, some medications, and high
avoided due to exacerbation of the disease. environmental temperatures.
•Myasthenic Crisis: result of disease INTERVENTIONS:
exacerbation or a precipitating event, most
❖ Utilize a collaborative approach
commonly a respiratory infection.
❖ Coordinate and refer as needed to health
-severe generalized muscle weakness with care services, social services, speech
respiratory and bulbar weakness. therapy, physical therapy, counseling
services, home care services.
-patient may develop respiratory compromise
❖ Activity and rest:
failure.
o Implement program of activity and
•Cholinergic Crisis: caused by over medication daily exercise.
with cholinesterase inhibitors. o Implement relaxation,
coordination, and muscle
-severe muscle weakness with respiratory and stretching exercises and walking.
bulbar weakness. o Avoid very strenuous activity and
-patient may develop respiratory compromise extreme fatigue.
and failure. INTERVENTIONS (CONT.):
❖ Bowel and bladder control: GUILLAIN-BARRE SYNDROME: CAUSES:
o Instruction or administration of
-The precise cause in unknown but it may be a
prescribed medications.
cell-mediated immune response with attack on
o Voiding schedule
the peripheral nerves in response to a virus
o Bowel training program
(cytomegalovirus and Epstein-Barr virus).
o Adequate fluid and fiber to prevent
constipation. -Campylobacter jejuni
❖ Reinforce and encourage swallowing
instructions. -Precipitating factors: minor febrile illness,
❖ Strategies to reduce risk of aspiration. respiratory tract infection, gastroenteritis,
❖ Memory aids, structured environment, surgery, rabies, systemic lupus erythematosus,
and daily routine to enhance cognitive vaccinations, and viruses.
function.

GUILLAIN-BARRE SYNDROME: TYPES:


INTERVENTIONS (CONT.): • Acute inflammatory demyelinating
❖ Implement measures to minimize stress. polyradiculoneuropathy (AIDP)
❖ Maintain temperate environment: air • Miller fisher syndrome (MFS)
conditioning to avoid excessive heat and • Acute motor axonal neuropathy (AMAN)
avoidance of exposure to extreme cold. • Acute motor-sensory axonal
❖ Use assistive devices and modify home neuropathy (AMSAN).
care management and independence in
ADLs.
❖ Support coping ability
………………………………………
• Guillain-Barre Syndrome- aka:
infectious polyneuritis, Lady-Guillain-
Barre syndrome.
-autoimmune disorder with acute attack of
peripheral nerve myelin.
-is an acute, rapidly progressive, and potentially
fatal form of polyneuritis that causes muscle GUILLAIN-BARRE SYNDROME: SIGNS &
weakness and mild distal sensory loss. SYMPTOMS:
•Muscle Weakness:
− Dyskinesia (inability to execute to
voluntary movement).
− Hyporeflexia
− Paresthesia (numbness)
•Manifestation is variable and include
weakness, paralysis, paresthesias, pain,
diminished or absent reflexes starting with the
lower extremities and progressing upward,
bulbar weakness, cranial nerve symptoms,
tachycardia, bradycardia, hypertension, or − Requires intensive care management
hypotension. with continuous monitoring and
respiratory support.
THREE-PHASE COURSE: GUILLAIN-BARRE
− Plasmapheresis and IVIG are used to
SYNDROME:
reduce circulating antibodies.
• Initial Phase- begins when the first
•Recovery rates vary but most patients recover
definitive symptom develops; ends 1 to 3
completely.
weeks later, when no further
deterioration noted. NURSING PROCESS-PLANNING THE CARE OF
• Plateau phase- lasts for several days to 2 THE PATIENT WITH GUILLAIN-BARRE
weeks. SYNDORME:
• Recovery phase- remyelination and
•Major goals include:
axonal process regrowth, lasts for 6
months to two years. − Improved respiratory function
− Increased mobility
COMPLICATIONS: GUILLAIN-BARRE
SYNDROME: − Improved nutritional status
− Effective communication
− Mechanical ventilation failure − Decreased fear and anxiety
− Aspiration − Effective patient and family coping
− Pneumonia − Absence of complications
− Sepsis
− Joint contractures INTERVENTIONS:
− Deep vein thrombosis •Enhance physical mobility and prevent DVT:
− Tachycardia
− Support limbs in a functional position.
− Loss of bowel/sphincter control
− Perform passive ROM at least twice daily
GUILLAIN-BARRE SYNDROME: DIAGNOSTICS: − Initiate position changes at least every 2
hours.
• History of preceding febrile illness
− Provide elastic compression hose and/or
• Increased protein level and WBC of the
sequential compression boots
CSF due inflammatory disease-more
definitive diagnosis of condition. − Provide adequate hydration
• Symmetric body weakness •Administer IV and parenteral nutrition as
• Diminished reflexes noted prescribed.
GUILLAIN-BARRE SYNDROME: TREATMENT: •Carefully assess swallowing and gag reflex and
take measures to prevent aspiration.
• Pallative
• Endotracheal tube or tracheotomy for
patient with difficulty clearing out
secretions.
• A trial dose of prednisone on the initial
phase of the disease and is discontinued
if no effect.
• Plasmapheresis is also useful during
initial phase.
GUILLAIN-BARRE SYNDROME: (CONT.):
•Medical management:

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