myasthenia gravis endocrinology

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MYASTHENIA GRAVIS Arun jose m Tbilisi state medical university

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Myasthenia gravis ( m.g pseudoparalytica ) autoimmune neuromuscular disease leading to fluctuating muscle weakness & fatiguability . Caused by circulating antibodies that block acetylcholine receptors at the post-synaptic N-M junction, inhibiting the stimulative effect of acetylcholine . few receptors are spared and the muscles can no longer be sufficiently excited by the nerves that innervate them.

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Epidemiology It most commonly affects women under 40 - and people from 50 to 70 years old of either sex, Neonatal:12% Congenital Juvenile myasthenia gravis: myasthenia occurring in childhood but after the peripartum period. Risk factors the female gender with ages 20 – 40, familial myasthenia gravis, D- penicillamine ingestion (drug induced myasthenia), and having other autoimmune diseases.

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Classification Class I: Any eye muscle weakness, possible ptosis , no other muscle weakness. Class II: Eye muscle weakness of any severity, mild weakness of other muscles Class III: Eye muscle weakness of any severity, moderate weakness of other muscles Class IV: Eye muscle weakness of any severity, severe weakness of other muscles Class V: Intubation needed to maintain airway

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Clinical Presentation fatigability ,muscles become weak during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement , chewing , talking, facial expression and swallowing are especially susceptible paralysis of the respiratory muscles.

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Extraocular muscle weakness . Ptosis is present initially in 50% of patients and during the course of disease in 90% of patients. Head extension and flexion weakness. Muscles tht control breathing are also affected. diplopia , an unstable gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia ,shortness of breath and dysarthria .

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PATHOPHYSIOLOGY auto-antibodies develop against the nicotinic acetylcholine receptor . myasthenia gravis is closely associated with thymoma . People treated with penicillamine can develop MG symptoms. MG is more common in families with other autoimmune diseases. familial predisposition is found in 5% of the cases . This is associated with certain genetic variations such as an increased frequency of HLA-B8 and DR3.

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thymoma

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Diagnosis Physical examination Muscle fatigability can be tested for many muscles. Blood tests serology can be performed in a blood test to identify certain antibodies against the acetylcholine receptor . A proportion of the patients without antibodies against the acetylcholine receptor have antibodies against the MuSK protein . repetitive nerve stimulation test repeatedly stimulating a muscle with electrical impulses, the fatiguability of the muscle can be measured.

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single fiberelectromyography , is the most sensitive ( not the most specific) test for MG, shows increased jitter in some muscles in almost all patients with myasthenia gravis. Jitter is greatest in weak muscles. Imaging Pulmonary function test : spirometry Pharmacological testing Tensilon test Before After

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Single fiber EMG

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Treatment medication Medication consists mainly of cholinesterase inhibitors to directly improve muscle function and immunosuppressant drugs to reduce the autoimmune process. Thymectomy is a surgical method to treat MG. For emergency treatment, plasmapheresis can be used as a temporary measure to remove antibodies from the blood circulation Immunosuppressive drugs: treated with a combination of these drugs with a cholinesterase inhibitor. Treatments with some immunosuppressives take weeks to months before effects are noticed. With treatment, patients have a normal life expectancy, except malignant thymoma

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Thank you 

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