Pathophysiology, Signs And Symptoms, And Treatment Of Myasthenia Gravis

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Title of the Paper in Twelve Words or Less Myasthenia gravis (MG) is an autoimmune disease that affects nerve impulses to skeletal muscles. There are varying types of this disease and the symptoms can range from mild, a person having peripheral skeletal muscle weakness, to severe, a person having breathing problems (Sieb, 2014). Myasthenia gravis is diagnosed in 20 out of 100,000 people in the United States, and women are more likely than men to have the disease (Meriggioli and Sanders, 2012). This autoimmune disease can happen at any age, but women generally have an earlier onset than men; the mean age for females is 28 and 42 for males (Nair, Patil-Chhablani, Venkatramani, and Gandhi 2014). To better understand this disease this…show more content…
Pathology of Myasthenia Gravis Since MG has subtypes the pathology of this disorder needs to be analyzed by the autoantibody profile and the condition of the thymus (Meriggioli and Sanders, 2009). Pathologic antibodies target certain areas of the postsynaptic site of the skeletal muscle. In addition hyperplasia of the thymus or thymic tumors are vary influential in the disease process (Meriggioli and Sanders, 2012). Abnormalities of the thymus can lead to the development of the autoantibodies that target AChR, which ultimately triggers muscle weakness (Meriggioli and Sanders, 2012). . One pathological path of MG starts with antibodies against AChR, and this is the most prevalent type of MG. AChR myasthenia gravis occurs in 80% of patients that have this ocular or generalized disease, and the autoantibodies that disrupt AChR functions can arise from abnormalities in the thymus (Nacu, Anderson, Lisnic, Owe, Gilhus, 2015). Normal function of the postsynaptic receptor involves binding with acetylcholine, which causes depolarization and ultimately muscle contraction (Meriggioli and Sanders, 2012). In this autoimmune disorder several actions can occur involving antibodies that oppose normal function of AChRs and result in disruption and damage of the receptor. Anti-AChR antibodies can block acetylcholine by binding, cause complement lysis of motor endplate, or cause receptor degradation by triggering cross-linking (Meriggioli and Sanders, 2012).
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