autoimmune disorders(1)

7/31/2019 Autoimmune Disorders(1)

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MULTIPLE SCLEROSISAn immune-mediated,

progressivedemyelinating diseaseof the CNS


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DEMYELINATIONRefers to the destruction ofmyelin, the fatty and proteinmaterial that surrounds certainnerve fibers in the brain and

spinal cord, it results inimpaired transmission of nerveimpulses.


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MULTIPLE SCLEROSISMay occur in any age but

typically manifests in youngadults between the ages of 20to 40 years;

It affects women morefrequently than men


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CAUSE OF MSIt is currently unknown Many believe it to be the result

of a combination of genetic,environmental, and infectiousorigins.

Not considered a hereditary orgene transmitted disease.


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PATHOPHYSIOLOGY

Sensitized T and BLymphocytes cross theblood brain barrier, theirfunction is to check theCNS for antigens and thenleave


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In MS, sensitized T cellsremain in the CNS and

promote the infiltrationof other agents that

damage the immunesystem


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The immune system

attack leads toinflammation that

destroys myelin and theoligodendroglial cells

that produce myelin inthe CNS


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Demyelinationinterrupts the flow ofnerve impulses andresults in variety ofmanifestations,depending on the nerve

affected


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Plaques appear onthe myelinated

axons, furtherinterrupting theimpulses


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The areas most

frequently affected are theoptic nerves, optic chiasm

and tracts, the cerebrum,the brain stem, andcerebellum and the spinalcord


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The axondegenerates,resulting in

permanent andirreversible damage.


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CLINICAL

MANIFESTATION


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CLINICAL SYMPTOMSFatigue

Depression

WeaknessNumbness


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Difficulty incoordination

Loss of balancePain

Blurring of vision


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Diplopia

Patchyblindness

Total blindness


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DIAGNOSTIC EXAMS

MRI

ELECTROPHORESIS OFCSF

URODYNAMICSTUDIES


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MRI OF MULTIPLE SCLEROSIS


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MEDICAL MANAGEMENT

No cure exists for MS

Supportive measures

to relieve patientssymptoms


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PHARMACOLOGIC MNGT.Interferon beta-1a (Rebif)and

Interferon beta 1-b (Betaseron) are

administered subcutaneouslyAvonex(interferon 1-a) is administered

intramuscularly

Glatiramer Acetate (Copaxone)

Methlprednisolone


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NURSING DIAGNOSIS

Impaired bed and physical mobilityrelated to weakness and muscle

paresis

Impaired home maintenance

management related to physical,psychological and social limitsimposed by MS


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MYASTHENIA GRAVISAn autoimmune disorder

affecting the myoneuraljunction, is characterized by

varying degrees of weaknessof the voluntary muscles.


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Women are affected morefrequently than men, and

they tend to develop at anearly age 20 to 40 years ofage, versus 60 to 70 years formen.


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PATHOPHYSIOLOGY

Normally, a chemical impulseprecipitates the release ofacetylcholine from vesicles onthe nerve terminal at themyoneural junction.


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The acetylcholine attaches to

receptor sites on the motorendplate and stimulates musclecontraction.

Continuous binding ofacetylcholine to the receptor

site is required for muscularcontraction to be sustained.


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In myasthenia gravis, antibodies

directed at the acetylcholinereceptor sites impair transmissionof impulses across the myoneural

junction.Fewer receptors are available for

stimulation , resulting in voluntarymuscle weakness that escalateswith continued activity.


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CLINICAL MANIFESTATIONS

Initial manifestation:

Two thirds of patients involves the ocular muscles

Diplopia (double vision)

Ptosis (drooping of eyelids)


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Weakness of the muscles of

the face and throat (Bulbarsymptoms) results in blandfacial expression.

Generalized weakness affectsall extremities and intercostal

muscles resulting in decreasingvital capacity and respiratory

failure


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Laryngeal involvement

produces dysphonia andincreases the risk of choking

and aspirationMyasthenia Gravis is purely

a motor disorder with noeffect on sensation orcoordination.


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DIAGNOSTIC TEST

ACETYL CHOLINESTERASE

INHIBITOR TEST

Used to diagnose myasthenia gravisStops the breakdown of acetylcholine

thereby increasing availability at the

neuromuscular junctionEdrophonium chloride (Tensilon) is

administered IV


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30 secs after injection, facialmuscle weakness and Ptosis shouldresolve for about 5 minutes.

Improvement in muscle strength

represents a positive test andconfirms the diagnosis.

Atropine should be available tocontrol the side effects ofEdrophonium.


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MRI SCAN

The enlargement of thymus glandmaybe detected through this

diagnostic testThe thymus gland is a site of Ach

receptor antibody production andmay be enlarged in myastheniagravis


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SINGLE FIBER

ELECTROMYOGRAPHY

Detects a delay or failure of

neuromuscular transmissionand is about 99% sensitive in

confirming the diagnosis ofmyasthenia gravis


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MEDICAL MANAGEMENT

Administration of anticholinesterase medications andimmunosuppressive therapy

Plasmapheresis-

-(plasma exchange)-to treat exacerbations


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Thymectomy-removal of

thymus gland

No cure for myasthenia gravis,treatment do not stop the

production of acetylcholinereceptor antibodies


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PHARMACOLOGIC THERAPY

Pyridostigmine bromide (Mestinon)

First line of therapy

Inhibits breakdown of Ach

Increases relative concentration of

Ach at the neuromuscular junction


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NURSING MANAGEMENT

Educational management

- Medication management

- Energy conservation

- Strategies to help with ocular

manifestations- Prevention and management of

complications


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NURSING DIAGNOSES

Risk forAspiration

Risk for Injury


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Guillain- Barr Syndrome


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autoimmune disorders(1)

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