Pathophysiology of Myasthenia Gravis

    When an action potential moves to motorneuron and reaches the motor end plate, the molecules of acetylcholine (ACh) is released from presynaptic vesicles, through the neuromuscular junction and then will interact with the ACh receptor (AchRs) in the membrane postsynaptic. AchRs canals open, allowing Na + and other cations into muscle fibers and cause depolarization. Persistent depolarization will converge into one, and if the accumulated depolarization is large enough, a meal will trigger an action potential, which moves along the muscle fibers to produce a contraction.

Neurojunction Normal
Neurojunction Normal

       In myasthenia gravis (MG), there is a reduction in the number AchRs available in the motor endplate or horizontal pleats on the post-synaptic membrane which causes a reduction in the number of receptors on the motor endplates, so depolarization that occurs in the motor endplate less, and not collected into action potentials. The end result is an inefficient neuromuscular transmission. Three mechanisms were obtained from the study include: autoantibodies against ACHR receptor and induces endocytosis, resulting in depletion of the membrane post-synaptic ACHR, autoantibodies alone cause it to malfunction ACHR by blocking the sites and the acetylcholine binding autoantibodies cause damage to the motor endplates, causing loss of ACHR.

Neuromuscular junction in patients with myasthenia gravis (MG)
Neuromuscular junction in patients with myasthenia gravis (MG)
Figure shows the chemical signaling, acetylcholine and acetylcholine receptors. Inverted Y-shaped molecules are antibodies that bound to the acetylcholine receptors that inhibit the action of acetylcholine

         Patients show symptoms after ACh receptors was reduced to approximately 30% of normal. This disease does not affect smooth muscle and heart because they have a different antigenicity cholinergic receptors. The role of the thymus in the pathogenesis of myasthenia gravis (MG) is not entirely clear, but 75% of patients myasthenia gravis (MG) have some degree of thymus abnormality (eg, hyperplasia in 85% of cases, thymoma in 15% of cases). Given the function of immune thymus and clinical improvement after thymectomy action, the thymus is thought to be where the formation of autoantibodies. However, the stimulus that initiates the autoimmune process has not been identified.


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