The nurse is teaching the female client with myasthenia gravis about the prevention of myasthenic and cholinergic crises. The nurse tells the client that this is most effectively done by:
a- Eating large, well-balanced meals.
b- Doing muscle-strengthening exercises.
c- Doing all chores early in the day while less fatigued.
d- Taking medications on time to maintain therapeutic blood levels.
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Myasthenia gravis (MG) is an autoimmune and chronic neuromuscular disease characterized by varying degrees of weakness of the skeletal muscles (volunteers) of the body. The denomination comes from Latin and Greek, and means "severe muscle weakness."
It begins with an insidious picture of loss of strength, which quickly recovers with rest but reappears upon restarting the exercise. It usually starts in the periocular muscles. In rare cases the onset is acute.
The main feature of myasthenia gravis is a muscle weakness that increases during periods of activity and decreases after periods of rest. Certain muscles - such as those that control the movement of the eyes and eyelids, facial expression, chewing, speech and swallowing (swallowing) - are often affected by this disorder. The muscles that control breathing and movements of the neck and extremities can also be affected, but, fortunately, with a medical control such disease can be controlled.
Etiology and pathophysiology:
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to the muscles. It occurs when normal communication between the nerve and muscle is interrupted in the neuromuscular junction, the place where nerve cells connect with the muscles they control.
Normally, when impulses travel through the nerve, nerve endings secrete a neurotransmitter substance called acetylcholine. Acetylcholine diffuses through the synaptic space at the neuromuscular junction, and binds to acetylcholine receptors, in the post-synaptic membrane. The receptors are activated and generate a muscular contraction.
In myasthenia gravis, antibodies block, alter, or destroy acetylcholine receptors in the neuromuscular junction, which prevents muscle contraction from occurring. These antibodies are produced by the body's own immune system. Therefore, myasthenia gravis is an autoimmune disease, because the immune system, which normally protects the body from external organisms, attacks itself by mistake. In addition, it has been shown that post-synaptic folds are flattened or "simplified", decreasing the efficiency of transmission. Acetylcholine is normally released, but the potentials generated are of less intensity than necessary.
The mechanisms by which antibodies decrease the number of receptors are three:
- Accelerated degradation by cross-linking and early endocytosis of the receptors.
- Blocking of the active site of the receiver.
- Post-synaptic muscle membrane injury by antibodies in collaboration with the complement system.
The antibodies are of the IgG type dependent on T lymphocytes, so the immunosuppressive treatment constitutes a therapeutic target.
On the other hand, repeated activity ends up decreasing the amount of acetylcholine released (what is known as presynaptic depletion). It also leads to less and less activation of muscle fibers by successive impulse (myasthenic fatigue). These mechanisms explain the increase in fatigue after exercise, and the decreasing stimulation in the electromyogram.
The thymus, an organ located in the upper chest area under the breastbone (bone in the center of the chest) exactly in the anterior mediastinum, plays an important role in the development of the immune system during the fetal stage. Your cells form a part of the body's normal immune system. The gland is quite large in children, it grows gradually until puberty and then reduces in size until it is replaced by fatty tissue with age. In adults suffering from myasthenia gravis, the thymus gland is abnormal. It contains certain clusters of immune cells characteristic of lymphoid hyperplasia, a condition that usually occurs only in the spleen and lymph nodes during an active immune response. 10% of patients suffering from myasthenia gravis develop thymomas. Thymomas are usually benign, but they can become malignant. They are usually due to the appearance of myoid cells (similar to myocytes), which can also act as autoantigen producers, and generate an autoimmune reaction against the thymus.
The relationship between the thymus gland and myasthenia gravis has not been fully understood. Scientists believe that it is possible for the thymus gland to generate incorrect instructions on the production of acetylcholine receptor antibodies, thus creating the perfect environment for a neuromuscular transmission disorder. However, it has been shown that 65% of myasthenic patients have an abnormal thymus, and 35% have hyperplastic.
a- Eating large, well-balanced meals.
b- Doing muscle-strengthening exercises.
c- Doing all chores early in the day while less fatigued.
d- Taking medications on time to maintain therapeutic blood levels.
----------------------------
Myasthenia gravis (MG) is an autoimmune and chronic neuromuscular disease characterized by varying degrees of weakness of the skeletal muscles (volunteers) of the body. The denomination comes from Latin and Greek, and means "severe muscle weakness."
It begins with an insidious picture of loss of strength, which quickly recovers with rest but reappears upon restarting the exercise. It usually starts in the periocular muscles. In rare cases the onset is acute.
The main feature of myasthenia gravis is a muscle weakness that increases during periods of activity and decreases after periods of rest. Certain muscles - such as those that control the movement of the eyes and eyelids, facial expression, chewing, speech and swallowing (swallowing) - are often affected by this disorder. The muscles that control breathing and movements of the neck and extremities can also be affected, but, fortunately, with a medical control such disease can be controlled.
Etiology and pathophysiology:
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to the muscles. It occurs when normal communication between the nerve and muscle is interrupted in the neuromuscular junction, the place where nerve cells connect with the muscles they control.
Normally, when impulses travel through the nerve, nerve endings secrete a neurotransmitter substance called acetylcholine. Acetylcholine diffuses through the synaptic space at the neuromuscular junction, and binds to acetylcholine receptors, in the post-synaptic membrane. The receptors are activated and generate a muscular contraction.
In myasthenia gravis, antibodies block, alter, or destroy acetylcholine receptors in the neuromuscular junction, which prevents muscle contraction from occurring. These antibodies are produced by the body's own immune system. Therefore, myasthenia gravis is an autoimmune disease, because the immune system, which normally protects the body from external organisms, attacks itself by mistake. In addition, it has been shown that post-synaptic folds are flattened or "simplified", decreasing the efficiency of transmission. Acetylcholine is normally released, but the potentials generated are of less intensity than necessary.
The mechanisms by which antibodies decrease the number of receptors are three:
- Accelerated degradation by cross-linking and early endocytosis of the receptors.
- Blocking of the active site of the receiver.
- Post-synaptic muscle membrane injury by antibodies in collaboration with the complement system.
The antibodies are of the IgG type dependent on T lymphocytes, so the immunosuppressive treatment constitutes a therapeutic target.
On the other hand, repeated activity ends up decreasing the amount of acetylcholine released (what is known as presynaptic depletion). It also leads to less and less activation of muscle fibers by successive impulse (myasthenic fatigue). These mechanisms explain the increase in fatigue after exercise, and the decreasing stimulation in the electromyogram.
The thymus, an organ located in the upper chest area under the breastbone (bone in the center of the chest) exactly in the anterior mediastinum, plays an important role in the development of the immune system during the fetal stage. Your cells form a part of the body's normal immune system. The gland is quite large in children, it grows gradually until puberty and then reduces in size until it is replaced by fatty tissue with age. In adults suffering from myasthenia gravis, the thymus gland is abnormal. It contains certain clusters of immune cells characteristic of lymphoid hyperplasia, a condition that usually occurs only in the spleen and lymph nodes during an active immune response. 10% of patients suffering from myasthenia gravis develop thymomas. Thymomas are usually benign, but they can become malignant. They are usually due to the appearance of myoid cells (similar to myocytes), which can also act as autoantigen producers, and generate an autoimmune reaction against the thymus.
The relationship between the thymus gland and myasthenia gravis has not been fully understood. Scientists believe that it is possible for the thymus gland to generate incorrect instructions on the production of acetylcholine receptor antibodies, thus creating the perfect environment for a neuromuscular transmission disorder. However, it has been shown that 65% of myasthenic patients have an abnormal thymus, and 35% have hyperplastic.
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Neurologic Practice