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MULTIPLE SCLEROSIS

An immune-mediated,

progressive demyelinating disease of the CNS

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

Many believe it to be the result

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

In MS, sensitized T cells

remain in the CNS and promote the infiltration of other agents that damage the immune system

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

the myelinated axons, further interrupting the impulses

The areas most

frequently affected are the optic nerves, optic chiasm and tracts, the cerebrum, the brain stem, and cerebellum and the spinal cord

The axon

degenerates, resulting in permanent and irreversible damage.

CLINICAL MANIFESTATION

CLINICAL SYMPTOMS Fatigue Depression Weakness Numbness

Difficulty in

coordination Loss of balance Pain Blurring of vision

Diplopia

Patchy

blindness Total blindness

DIAGNOSTIC EXAMS MRI ELECTROPHORESIS OF CSF URODYNAMIC STUDIES

MRI OF MULTIPLE SCLEROSIS

MEDICAL MANAGEMENT

No cure exists for MS


Supportive measures

to relieve patients symptoms

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

management related to physical, psychological and social limits imposed by MS

MYASTHENIA GRAVIS
An autoimmune disorder

affecting the myoneural junction, is characterized by varying degrees of weakness of the voluntary muscles.

Women are affected more

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.

The acetylcholine attaches to

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.

In myasthenia gravis, antibodies directed at the acetylcholine

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)

Weakness of the muscles of

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

receptor antibody production and may be enlarged in myasthenia gravis

SINGLE FIBER ELECTROMYOGRAPHY

Detects a delay or failure of

neuromuscular transmission and is about 99% sensitive in confirming the diagnosis of myasthenia gravis

MEDICAL MANAGEMENT
Administration of anti cholinesterase medications and

immunosuppressive therapy Plasmapheresis-(plasma exchange) -to treat exacerbations

Thymectomy-removal of

thymus gland
No cure for myasthenia gravis,

treatment do not stop the production of acetylcholine receptor antibodies

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

manifestations - Prevention and management of complications

NURSING DIAGNOSES

Risk for

Aspiration Risk for Injury

Guillain- Barr Syndrome