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Myasthenia Gravis • Rapidly increasing weakness of extremities and

 A chronic autoimmune disorder affecting the trunk


neuromuscular transmission of impulses in the
voluntary muscles of the body. Management:

 The condition develops when there are • Atropine sulfate, plasmapheresis and IVIG
autoimmune attacks against the acetylcholine
receptors at the neuromuscular junction. • Cholinesterase inhibitors are stopped
temporarily until respiratory function improves
 Cardinal features: Muscle weakness and fatigue
Diagnostic Exams
Note:
• More common among women especially those • Serum test antibodies for Acetylcholine
between 20 - 40 years old receptors
• In men, 60 - 70 years old (Sherer, 2005) • Edrophonium (Tensilon) Test - IV injection
• 8o% of people with MG have either a thymic relieves the symptoms temporarily
hyperplasia or a thymic tumor with the thymus • Electrophysiologic Testing
gland as the site of antibody production
• CT Scan of the thymus
Pathophysiology • Other blood exams

Autoimmunity Management
/ Pharmacology
Depletion of acetylcholine receptors at the
neuromuscular junction • Anticholinesterase drugs like Pyridostigmine
/ bromide (Mestinon), NEOSTIGMINE to
Diminished amplitude of the end-plate potentials enhance neuromuscular transmission
/ • Immunosuppressive drugs like
Decreased muscle power PREDNISOLONE
/ • Plasmapheresis- to remove antibodies from the
Muscle weakness and fatigue blood
• IVIG
Manifestations
Surgery
• Diplopia and ptosis from ocular muscle
weakness • Thymectomy - for those with tumor or
hyperplasia of the thymus gland
• Extreme muscular weakness and fatigue
Crisis Management
• Mask - like facial expression
• Hospitalization
• Dysarthria and dysphagia • Edrophonium (Tensilon)
• Neostigmine
• Dysphonia from laryngeal muscle weakness • Aggressive respiratory support
• Plasmapheresis, IVIG
MG is purely a motor disorder with no effect on
sensation or coordination Note: Anticholinergic drug will be discontinued until
respiratory function improves; Atropine is given to
Myasthenic Crisis reduce excessive secretions during crisis

• Occurs with exacerbation and remission of the Complications


disease process
• Myasthenic crisis
• Severe generalized muscle weakness, respiratory
and bulbar weakness may result to respiratory • Aspiration from dysphagia
failure
• Decreased physical mobility causing pressure
• A crisis is commonly precipitated by respiratory ulcers, constipation urinary infection, etc.
infection, change in medication, pregnancy, or
drugs that can exacerbate MG • Respiratory failure

• Cholinergic Crisis or Brittle Crisis Nursing Management

• Occurs with overmedication with cholinesterase • Promote respiration


inhibitors • Prevent aspiration
• Minimize fatigue
Prior to Brittle Crisis: • Maintain social interaction
• Promote nutrition
• Sudden respiratory distress, dysphagia, • Maintain communication
dysarthria • Administer medications as prescribed

• Tachycardia and anxiety, ptosis and diplopia


Multiple Sclerosis Management
Generally palliative
• Also called “Disseminated Sclerosis"
• Corticosteroids or ACTH
• Involves randomly yattered patches of
demyelination in brainstem, cerebrum, • Baclofen for spasticity
cerebellum and spinal cord
• Interferon beta - 1b betaseron
• Is a chronic, debilitating, progressive disease
with periods of remissionand exacerbation • Physiotherapy and psychotherapy

Multiple Sclerosis • Carbamazepine for paresthesia and trigeminal


neuralgia
• Cause: unknown but viral and immunologic
causes have been implicated • Immunosuppressive drugs - cyclophosphamide,
azathioprine
• Onset: Early adult life (20 - 40 years old);
incidence higher in females, in Caucasians and Nursing Care
those living in cold climates
• Promote rest
Symptoms tend to increase with stress, fatigue and
heat • Avoid hot baths and exposure to hot
environment • Promote nutrition: small feedings,
Pathophysiology chew well, etc.
/
Sensitized T cells cross the blood-brain barrier • Promote mobility - avoid complications
/
T cells remain in CNS and do not leave (when normally • Encourage use of assistive devices with walking
they should)
/ • Provide health teachings
Infiltration of other agents that damage the immune
system is promoted • Promote self-esteem
/
Inflammation process takes place and destroy the myelin
/
Flow of nerve impulses, transmission of impulses are
interrupted
/
Destruction of CNS structures
/
Axons are degenerated
/
Permanent and irreversible damage occurs

Clinical Manifestations:
Subjective:

1. Paresthesia
2. Altered position sense
3. Ataxia
4. Fatigue, weakness
5. Blurred vision and diplopia
6. Altered emotional affect (depression, apathy,
euphoria)

Clinical Manifestations:
Objective:

1. Charcot's triad: intention tremor, nystagmus, scanning


speech (clipped)
2. Shuffling gait, in geased deep tendon reflexes, spastic
paralysis
3. Impaired bowel and bladder function
4 Impotence
5. Pallor of optic disk (later blindness)
6. Increased immunoglobulin levels in CSF
7. MRI - indicates demyelination
8. In advance stage: cognitive loss

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