Myasthenia+Gravis

· MG is a disorder of transmission at the neuromuscular junction that affects communication between the motor neuron and the innervated muscle cell. Can occur at any age but usually between 20 and 30. 3x more common in women. · Pathophysiology: Autoimmune disease. Caused by antibody mediated destruction of acetylcholine receptors in the neuromuscular junction. Exact mechanism trigger is unclear, but thought to be related to T-lymphocytes function. 75% of people with MG also have thymic abnormalities (for example thymus tumor, etc.). Neonatal MG occurs in 10% of infants born to mothers with MG. · Clinical Manifestations: This is tricky: In persons with myasthenia gravis who have fewer acetylcholine receptors in the postsynaptic membrane, each release of acetylcholine from the presynaptic membrane results in a lower endplate potential. This results in muscle weakness and fatiguability with sustained effort. Most common areas are eye and periorbital muscles. Early symptom: ptosis due to eyelid weakness or diplopia due to weakness of the extraocular muscle weakness. Progresses to generalized weakness, including respiratory. Chewing and swallowing are difficult, weakness in limbs, hard to climb stairs and lifting objects. As the disease progresses: muscles of lower face, speech impairment. Interestingly, symptoms are decreased in morning but increases as the day and activity continues. · Myasthenia crisis: a sudden exacerbation of symptoms and weakness. Occurs when muscle weakness is so severe that it compromises ventilation to the extent that ventilary support and airways protection are needed, Usually stress, illness, cold, emotional upset, after surgery, etc.. brings this on. Or from inadequate or excessive dose of the anticholinesterase drug used in treatments of the disorder. · Diagnoses and treatment: Anticholinesterase test. Nerve stimulation studies, immunoassay test for ACT receptor antibodies. Treatment methods include pharmacologic agents (anticholinerasterase drugs: pyridostigmine and neostigmine) and immunosuppressant therapy: corticosteroids, azathioprine, cyclosporine; management of myasthenic crisis; thymectomy; and plasmapheresis or intravenous immunoglobulin. Medications that exacerbate MG should be avoided such as aminoglycoside antibodies. · Plasmatherisis remove antibodies from circulation and provide short term clinical improvement. Used primarily to stabilize the condition of those in the MG crisis. · A Thymectomy (surgical removal of the thymus) may be used as a treatment of MG but the mechanism is unknown and the surgery is controversial · // It is not written in the textbook whether or not this is a degenerative disease and if it gets worse with age but it seems to me that it comes and goes throughout the lifespan and can be handled somewhat with medications and treatments //
 * ryssa Brainerd N316B P/PH Exam I Study Guide **
 * __ Myasthenia Gravis __**