Autoimmune Processes PPT Sept 6 2017

Autoimmune Processes
Educator: Naomi Palmer Mitchell

Presented to: Senior Nursing Students
Northern Caribbean University
September 6, 2017
Objectives
• Describe the pathophysiology of Multiple Sclerosis
• Identify the clinical manifestations of Multiple
Sclerosis
• Discuss the medical and nursing management of
Multiple Sclerosis
Objectives Cont’d
• Describe the pathophysiology of Myasthenia Gravis
• Identify the clinical manifestations of Myasthenia Gravis
• Discuss the medical and nursing management of Myasthenia
Gravis
• Describe the pathophysiology of Guillain-Barré Syndrome
• Identify the clinical manifestations of Guillain-Barré Syndrome
• Apply the nursing process as a framework for care of patients
with multiple sclerosis and Guillain-Barré syndrome.
Glossary
• Ataxia: impaired coordination of movements
• Dyskinesia: impaired ability to execute voluntary movements
• Dysphagia: difficulty swallowing, causing the patient to be
at risk for aspiration
• Paresthesia: a sensation of numbness or tingling or a
“pins and needles” sensation
• Spasticity: muscular hypertonicity with increased resistance to
stretch often associated with weakness, increased deep tendon
reflexes, and diminished superficial reflexes
• Diplopia: double vision
Multiple Sclerosis Background
• 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
• Age group mainly affected 20-40 years
• Women
Multiple Sclerosis Cont’d
• Cause (ongoing research)
• Researchers believe that some environmental
exposure at a young age may play a role in the
development of MS later in life.
• Genetic predisposition (increasing the susceptibility to

viruses)
Multiple Sclerosis Pathophysiology
• Sensitized T and B lymphocytes cross the blood–brain
barrier
• Their function is to check the CNS for antigens and
then leave
• Sensitized T cells remain in the CNS (other agents
infiltrate)
• Damage of the immune system
The process of demyelination. A and B depict a
Figure 64-2
normal nerve cell and axon with myelin. C and D show the slow
disintegration of myelin, resulting in a disruption in axon function.
Multiple Sclerosis Pathophysiology Cont’d
• Demyelination interrupts the flow of nerve impulses and
results in a variety of manifestations, depending on the
nerves affected.
• The axons themselves begin to degenerate, resulting in

permanent and irreversible damage
Clinical Manifestations
• Benign course:
• Symptoms are so mild that the patient does not
seek health care or treatment
• Between 80% and 85% of patients with MS have
a relapsing-remitting (RR) course. With each
relapse, recovery is usually complete
•Residual deficits
Clinical Manifestations Cont’d
• 15% develop secondary progressive course, in
which disease progression occurs with or without
relapses.
• 10% of patients have a primary progressive course,

in which disabling symptoms steadily increase,
with rare plateaus and temporary improvement
Clinical Manifestations Cont’d
Secondary complications of MS
Primary Symptoms • urinary tract infections,
constipation, pressure
• Spasticity ulcers, contracture
deformities,
• Ataxia
• dependent pedal edema,
pneumonia, reactive
depression, osteoporosis.
Primary Progress MS
• Quadriparesis
• Cognitive dysfunction
• Paresthesias
• Dysesthesias
• Proprioception loss
Characteristics of MS
Exacerbation Remission
New symptoms appear • Symptoms decrease or
and existing ones disappear
worsen
Diagnostic Methods
• MRI
• Electrophoresis of CSF
• Urodynamic studies
• Neuropsychological testing
Medical Management of Multiple Sclerosis
• No cure exists for MS.
• Daily analgesic medications
• Opioids, antiseizure medications, or antidepressants
• Perimenopausal women
• Estrogen loss, immobility and corticosteroid therapy
play a role in the development of osteoporosis among
women with MS
• The goals of treatment are to delay the progression of
the disease, manage chronic symptoms, and treat acute
exacerbations
• Symptoms requiring intervention include spasticity,
fatigue, bladder dysfunction and ataxia
• MS include immunomodulating therapies and
immunosuppressive agents (Disease Modifying
Therapy)
• Interferon
• Acetaminophen and ibuprofen
• Glatiramer acetate (Copaxone)
• IV methylprednisolone
• Gamma-aminobutyric acid (GABA) agonist (treating
spasticity)
• Benzodiazepines (treating spasticity)
• Anticholinergic, agents, alpha-adrenergic blockers,
antispasmodic agents (bladder and bowel issues)
NURSING PROCESS for MULTIPLE
SCLEROSIS
• Assessment
• Diagnosis
• Plan/Goal
• Intervention
• Evaluation
Myasthenia Gravis
Myasthenia Gravis
• An autoimmune disorder affecting the myoneural
junction, is characterized by varying degrees of
weakness of the voluntary muscles
• Women are affected more - 20 to 40 years of age,
versus 60 to 70 years for men
Myasthenia Gravis Pathophysiology
Normal Function During Myasthenia Gravis
Chemical Impulse
Chemical Impulse
↓
↓
Release of acetylcholine
Release of acetylcholine
↓
↓
Acetylcholine (Ach) receptor sites
Acetylcholine attaches to receptor weakened or destroyed by
sites ↓ antibodies and block Ach
Stimulates muscle contraction reception↓
No muscle contraction
Clinical Manifestation of Myasthenia
Gravis
Diagnostics for Myasthenia Gravis
• Acetylcholinesterase inhibitor test
Stops the breakdown of acetylcholine, thereby
increasing availability at the neuromuscular junction
• For example, Edrophonium chloride (Tensilon)
• MRI scan
• Electromyography (EMG)
Medical Management of Myasthenia
Gravis
• Improving function and reducing and removing circulating
antibodies.
• Anticholinesterase medications -Pyridostigmine bromide
(Mestinon),
• Immunosuppressive therapy,
• Plasmapheresis
• Thymectomy
• Intravenous immune globulin (IVIG)
• THERE IS NO CURE
Nursing Management of Myasthenia
Gravis
• Patient and family teaching
• Medication management- strict schedule
• Keep a diary and learn when the medication of wearing off
• Energy conservation
• To minimize the risk of aspiration, mealtimes should coincide
with the peak effects of anticholinesterase medication
• Suction available at home
Nursing Management Cont’d
• Meals with soft consistency
• Tape eye lids together
• Instill artificial tears
• Patching of one eye helps with diplopia
Guillain-Barre Syndrome
GBS
Definition and Background of GBS
• Autoimmune attack on the peripheral nerve myelin
• Acute, rapid segmental demyelination of peripheral nerves
and some cranial nerves, producing ascending weakness
• Campylobacter jejuni, cytomegalovirus, Epstein-
Barr virus, Mycoplasma pneumoniae, H.
influenzae, and HIV are the most common
infectious agents that are associated with the
development of Guillain-Barré syndrome
Diagnostic Findings
• A history of a viral illness in the previous few weeks
suggests the diagnosis
• Lung Function Tests
• CSF
Medical Management for Guillain-Barre
Syndrome
• Medical emergency
• ICU- Respiratory therapy or mechanical ventilation
• Preventing the complications of immobility-
anticoagulant
agents and anti-embolism stockings
• Plasmapheresis
NURSING PROCESS FOR Guillain
Barre-Syndrome
• Assessment
• Nursing Diagnosis
• Plan/Goal
• Intervention
• Evaluation
References
• Hinkle, J.L. & Cheever, K.H. (2017). Brunner & Suddarth's
Textbook of Medical-Surgical Nursing (14th ed.). China:
Lippincott Williams & Wilkins.
• Hinkle, J.L. & Cheever, K.H. (2014). Brunner & Suddarth's

Textbook of Medical-Surgical Nursing (13th ed.). China:
Lippincott Williams & Wilkins.

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Autoimmune Processes

Educator: Naomi Palmer Mitchell

• Genetic predisposition (increasing the susceptibility to

• The axons themselves begin to degenerate, resulting in

• 10% of patients have a primary progressive course,

• Hinkle, J.L. & Cheever, K.H. (2014). Brunner & Suddarth's

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