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An immune-mediated,
DEMYELINATION
Refers to the destruction of
myelin, the fatty and protein material that surrounds certain nerve fibers in the brain and spinal cord, it results in impaired transmission of nerve impulses.
MULTIPLE SCLEROSIS
May occur in any age but
typically manifests in young adults between the ages of 20 to 40 years; It affects women more frequently than men
It is currently unknown
CAUSE OF MS
of a combination of genetic, environmental, and infectious origins. Not considered a hereditary or gene transmitted disease.
PATHOPHYSIOLOGY
Sensitized T and B
Lymphocytes cross the blood brain barrier, their function is to check the CNS for antigens and then leave
remain in the CNS and promote the infiltration of other agents that damage the immune system
attack leads to inflammation that destroys myelin and the oligodendroglial cells that produce myelin in the CNS
Demyelination
interrupts the flow of nerve impulses and results in variety of manifestations, depending on the nerve affected.
Plaques appear on
frequently affected are the optic nerves, optic chiasm and tracts, the cerebrum, the brain stem, and cerebellum and the spinal cord
The axon
CLINICAL MANIFESTATION
Difficulty in
Diplopia
Patchy
MEDICAL MANAGEMENT
PHARMACOLOGIC MNGT.
Interferon beta-1a (Rebif)and
Interferon beta 1-b (Betaseron) are administered subcutaneously Avonex(interferon 1-a) is administered intramuscularly Glatiramer Acetate (Copaxone) Methlprednisolone
NURSING DIAGNOSIS
Impaired bed and physical mobility related to weakness and muscle paresis
Impaired home maintenance
MYASTHENIA GRAVIS
An autoimmune disorder
affecting the myoneural junction, is characterized by varying degrees of weakness of the voluntary muscles.
frequently than men, and they tend to develop at an early age 20 to 40 years of age, versus 60 to 70 years for men.
PATHOPHYSIOLOGY
Normally, a chemical impulse
precipitates the release of acetylcholine from vesicles on the nerve terminal at the myoneural junction.
receptor sites on the motor endplate and stimulates muscle contraction. Continuous binding of acetylcholine to the receptor site is required for muscular contraction to be sustained.
receptor sites impair transmission of impulses across the myoneural junction. Fewer receptors are available for stimulation , resulting in voluntary muscle weakness that escalates with continued activity.
CLINICAL MANIFESTATIONS
Initial manifestation: Two thirds of patients involves the ocular muscles Diplopia (double vision) Ptosis (drooping of eyelids)
the face and throat (Bulbar symptoms) results in bland facial expression. Generalized weakness affects all extremities and intercostal muscles resulting in decreasing vital capacity and respiratory failure
Laryngeal involvement
produces dysphonia and increases the risk of choking and aspiration Myasthenia Gravis is purely a motor disorder with no effect on sensation or coordination.
DIAGNOSTIC TEST
ACETYL CHOLINESTERASE INHIBITOR TEST Used to diagnose myasthenia gravis Stops the breakdown of acetylcholine thereby increasing availability at the neuromuscular junction Edrophonium chloride (Tensilon) is administered IV
30 secs after injection, facial muscle weakness and Ptosis should resolve for about 5 minutes.
Improvement in muscle strength
represents a positive test and confirms the diagnosis. Atropine should be available to control the side effects of Edrophonium.
MRI SCAN
The enlargement of thymus gland maybe detected through this diagnostic test
The thymus gland is a site of Ach
neuromuscular transmission and is about 99% sensitive in confirming the diagnosis of myasthenia gravis
MEDICAL MANAGEMENT
Administration of anti cholinesterase medications and
Thymectomy-removal of
thymus gland
No cure for myasthenia gravis,
PHARMACOLOGIC THERAPY
Pyridostigmine bromide (Mestinon) First line of therapy Inhibits breakdown of Ach Increases relative concentration of Ach at the neuromuscular junction
NURSING MANAGEMENT
Educational management
- Medication management - Energy conservation - Strategies to help with ocular
NURSING DIAGNOSES
Risk for