Figure 1. Normally, acetylcholine, a neurotransmitter (yellow) released by a neuron (turquoise), travels to the neurotransmitter receptors (green), leading to muscle contraction. Myasthenia gravis is an autoimmune disease where there are fewer receptors than normal. The few existing receptors are blocked by antibodies (purple).
MG develops as the result of autoantibodies that target components of the neuromuscular junction (NMJ), with various subtypes of MG classified by the antigen specificity of the autoantibody. The most common subtype of autoantibody-mediated MG, comprising approximately 85% of patients, is characterized by autoantibodies against the nicotinic AChR.
In other patients with MG, autoantibodies target MuSK or LRP4. A small proportion of patients with MG do not have detectable circulating autoantibody levels to known targets, and these patients are diagnosed as having seronegative MG. Congenital, presynaptic autoimmune, and thymoma-associated subtypes of MG exist, but their incidence is much rarer.
Learn more about the pathophysiology of MG.
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Cite this: Raghav Govindarajan. Fast Five Quiz: Pathophysiology of Myasthenia Gravis - Medscape - Oct 08, 2021.
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