Myasthenia gravis: Nursing

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Myasthenia gravis is a chronic, progressive autoimmune disease caused by antibodies that bind to and destroy neuromuscular communication, where nerves send impulses to trigger skeletal muscle contraction. Over time, this results in fatigue and muscle weakness due to impaired muscle contractions.

Now, to better understand myasthenia gravis, let's review the normal physiological process of muscle contraction that occurs at cellular level. Muscle contraction is initiated at the neuromuscular junction, which is basically a connection between the axonal end of a motor neuron and a skeletal muscle fiber. So, the end of the neuron is called the presynaptic membrane, while the muscle cell is called the postsynaptic membrane.

Now, to trigger muscle contraction, the axonal end of the motor neuron releases the neurotransmitter acetylcholine, also called ACh, at the neuromuscular junction. Acetylcholine then binds to the nicotinic acetylcholine receptors present on the muscle cell membrane. The binding of acetylcholine to its receptor activates a chain reaction within the muscle cell, which ultimately results in voluntary muscle contraction.

Now, myasthenia gravis is caused by autoantibodies that target the neuromuscular junction. In a minority of cases, this occurs as a paraneoplastic syndrome, where an underlying cancer like thymoma or bronchogenic carcinoma can result in the production of autoantibodies. However, in the majority of cases, myasthenia gravis does not have a clear underlying cause. Clients at risk are those who are assigned female at birth in their 20s and 30s, or clients assigned male at birth in their 60s and 70s.

So, in myasthenia gravis, the client's own B cells generate autoantibodies, setting in a type II hypersensitivity reaction. These autoantibodies specifically bind with the postsynaptic acetylcholine receptor, or AChR for short, in 90% of clients, or sometimes target the muscle-specific tyrosine kinase receptors, or MuSK for short, in 10% of clients, both of which ultimately lead to loss of acetylcholine receptor function. In addition, binding of autoantibodies to acetylcholine receptors activates the classical pathway of the complement, which triggers inflammation and damage of the postsynaptic membrane of muscle cells, ultimately decreasing the number of available acetylcholine receptors on the muscle membrane. As a result of all these, initiation of a muscle contraction becomes less effective over time.


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