They bind to the Agrin–LRP4–MuSK protein complex in the NMJ, whose primary function is the maintenance of the NMJ, including the n-ACh receptor distribution and clustering. In MusK MG and LPR4 MG, the antibodies are of the IgG4 subtype and do not have the complement activating property. They may also act by functionally blocking the binding of ACh to its receptor or by enhancing the endocytosis of the antibody-bound n-ACh receptor.
MUSCLE SYSTEM PRO III FOR MAC MAC
MAC brings about the final degradation of the receptors. They bind to the n-ACh receptor present in the postsynaptic membrane of the skeletal muscles and activate the complement system leading to the formation of the membrane attack complex (MAC). In n-AChR MG, the antibodies are of the IgG1 and IgG3 subtype. The pathophysiologic mechanisms in MG are dependent on the type of antibodies present. These include myasthenic crisis, an acute respiratory paralysis that requires intensive care, as well as adverse events due to long term medication treatment like opportunistic infections and lymphoproliferative malignancies.Ī complete understanding of the pathophysiologic mechanisms, clinical manifestations, treatment strategies, and complications of myasthenia gravis is necessary for better patient care and outcomes. Myasthenia gravis causes a significant number of complications. A wide variety of conditions can precipitate MG, such as infections, immunization, surgeries, and drugs. The reduced transmission of electrical impulses across the neuromuscular junction due to the formation of autoantibodies against the specific postsynaptic membrane proteins consequently causes muscle weakness.
It usually involves muscles of the eyes, throat, and extremities. The classic presentation is a fluctuating weakness that is more prominent in the afternoon.
Myasthenia gravis (MG) is the most common disorder affecting the neuromuscular junction (NMJ) of the skeletal muscles.
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