Myasthenia Gravis

Dr. Belal M. Hijji, RN. PhD

February 29, 2012

Learning Outcomes
By the end of this lecture, students will be able to:
Describe the pathophysiology, clinical manifestations, and
medical and nursing management of myasthenia gravis.

Introduction
Myasthenia gravis, an autoimmune disorder affecting the
myoneural junction, is characterized by varying degrees of
weakness of the voluntary muscles. Women tend to develop the
disease at an earlier age (20 to 40 years) compared to men (60 to
70).

Pathophysiology
Normally, a chemical impulse precipitates the release of
acetylcholine from vesicles on the nerve terminal at the
myoneural junction. The acetylcholine continuously bind to
the receptor sites on the motor end plate, for muscle
contraction to sustain.

 In myasthenia gravis, autoantibodies, produced in the thymus

gland, directed at the acetylcholine receptor sites impair
transmission of impulses across the myoneural junction.
Therefore, fewer receptors are available for stimulation, resulting
in voluntary muscle weakness that escalates with continued
activity. These antibodies are found in 80% to 90% of the cases.
In patients who are antibody negative, it is believed that the
offending antibody is directed at a portion of the receptor site
rather than the whole complex.

The thymus gland, a part of your immune system located in the upper
chest beneath the breastbone, may trigger or maintain the production
of antibodies that result in the muscle weakness common in
myasthenia gravis.
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Chemicals messengers, called neurotransmitters, fit precisely into

receptor sites on your muscle cells. In myasthenia gravis, certain
receptor sites are blocked or destroyed, causing muscle weakness.
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Clinical Manifestations
Involvement of the ocular muscles results in:
Diplopia (double vision) and ptosis (drooping of the
eyelids [next slide]).
Laryngeal involvement produces dysphonia (voice
impairment) and increases the patients risk for choking and
aspiration.
Patients experience weakness of the muscles of the face and
throat.
Generalized weakness affects all the extremities and the
intercostal muscles, resulting in decreasing vital capacity and
respiratory failure.

Assessment and Diagnostic Findings

Anticholinesterase test. Anticholinesterase agents stop the
breakdown of acetylcholine, thereby increasing its availability.
Edrophonium chloride, 2-10 mg, is injected IV. Thirty
seconds later, facial muscle weakness and ptosis should
resolve for about 5 minutes. This immediate improvement
usually confirms the diagnosis.
Keep atropine 0.4 mg ready to control the side effects of
edrophonium (convulsions and restlessness).
Acetylcholine receptor antibody titers.
MRI demonstrates thymus gland enlargement in 90% of cases.

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Medical Management
The aim of medical management is to improve function and
reduce and remove circulating antibodies. This could be
achieved through:
Anticholinesterase agents such as pyridostigmine bromide
and neostigmine bromide provide symptomatic relief by
increasing the concentration of available acetylcholine at
the neuromuscular junction.
Immunosuppressive therapy (corticosteroids,
cyclophosphamide, azathioprine ) aims to reduce the
production of the antibody.
Prednisone appears to be successful in suppressing the
disease.

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 Plasma exchange (plasmapheresis) is a technique used to

treat exacerbations by a temporary reduction in the titer of
circulating antibodies.
IV immune globulin (IVIG) is nearly as effective as
plasmapheresis. However, neither therapy is a cure as it
does not stop the production of the antibodies.
Thymectomy (surgical removal of the thymus gland) can
produce antigen-specific immunosuppression, resulting in
clinical improvement and decreasing or eliminating the
need for medication.

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Nursing Management
Nursing care focuses on patient and family teaching.
Educational topics include:
Medication management where emphasis is placed on
understanding their action, taking them on time,
consequences of delaying administration, and the signs
and symptoms of myasthenic and cholinergic crisis.
Energy conservation through identifying the best times
for rest periods throughout the day. The nurse is in
position to teach the patient various ways of conserving
energy. How? And to schedule activities to coincide
with peak energy and strength levels.

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 Strategies to help with ocular manifestations. To prevent

corneal damage, the nurse should instruct the patient to
tape the eyes closed for short intervals, regularly instil
artificial tears, and to patch one eye can help with double
vision.
Prevention and management of complications. To
minimize the risk of aspiration, the nurse instructs the
patient to plan the mealtimes with the peak effects of
medication, and to rest before meals. Further advice is
related to sitting upright during meals with the neck
slightly flexed to facilitate swallowing, and using soft
foods; if choking occurs frequently, the nurse can suggest
pureing ( ) food to a pudding consistency.
Suction should be available at home and usable.
Gastrostomy feedings may be necessary to ensure
adequate nutrition.
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 Finally the nurse should instruct the patient about factors that
will exacerbate symptoms and potentially cause crisis such as
emotional stress, respiratory infections, vigorous physical
activity, and high environmental temperature.

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