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Myasthenia gravis yashwant kumar

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Myasthenia gravis yashwant kumar

  1. 1. Myasthenia GravisMyasthenia Gravis “Grave muscle weakness”“Grave muscle weakness” YASHWANT KUMAR DILLI BABU-GROUP:8YASHWANT KUMAR DILLI BABU-GROUP:8
  2. 2. Myasthenia Gravis • Autoimmunediseaseaffecting theneuromuscular junction • Not abrain disorder – brain functionsnormally • Characterized by fluctuating muscleweaknessand fatigability • Diseasemay begeneralized or ocular specific
  3. 3. NeuroMuscularJunction(NMJ)
  4. 4. Pathophysiology • Antibodiesattack Acetylcholine(ACH) receptorsat the motor end plate • Decreased number of (ACH) receptor sitesat neuromuscular junction • Preventsneurotransmitter (ACH) from attaching and stimulating musclecontraction • Resulting in lossof musclestrength
  5. 5. Causes • No singlecausehasbeen identified • Abnormal thymustissuefound in most patientswith MG • Thymic tumorsfound in 15% of patients • Virusinfectionshavebeen found in somecasesand areasuspected cause
  6. 6. Genetic Factors • MyastheniaGravisisnot agenetically inherited disease • Somefamiliesappear to carry agenethat increasesthe risk for developing thedisease • No specific genehasbeen identified and thereareno tests for genetic screening
  7. 7. Signs and Symptoms • Affectsany of themusclesthat can be controlled voluntarily, certain musclegroupsaremorecommonly affected than others • Eye, face, throat, neck, limb muscles • Difficulty speaking (dysarthria) • Difficulty swallowing (dysphagia), • Drooping eyelids(ptosis)
  8. 8. Signs and Symptoms • Doublevision (diplopia) • Nasal-sounding speech and weak neck musclesthat give thehead atendency to fall forward or backward.  • Symptomstend to progressover time, usually reaching their worst within afew yearsafter theonset of the disease • Worsening muscleweaknesswith repeat activity
  9. 9. Complications  Myasthenic crisis: A life-threatening condition, which occurs when the muscles that control breathing become too weak to do their jobs. Emergency treatment is needed to provide mechanical assistance with breathing. Medications and blood-filtering therapies help people recover from myasthenic crisis, so they can again breatheon their own.  Thymus tumors: About 15 percent of the people who have myasthenia gravis have a tumor in their thymus, a gland under the breastbone that is involved with the immune system. Most of thesetumorsarenoncancerous.
  10. 10. Underactive or overactive thyroid: The thyroid gland, located in the neck, secretes hormones that regulate metabolism. If thyroid is underactive, body uses energy more slowly. An overactive thyroid makes body use energy too quickly. Lupus: Disease of immune system. Common symptoms include painful or swollen joints, hair loss, extreme fatigue and ared rash on theface. Rheumatoid arthritis: Caused by problems with immune system. It is most conspicuous in the wrists and fingers, and can result in joint deformities that make it difficult to use hands. Complications
  11. 11. Prognosis • Chronic diseasewith periodsof exacerbation and sometimesremissions • Diseasecourseishighly variable • Symptomsrespond well to treatment and in most cases thepatient can liveanormal or nearly normal life • Ocular Myastheniahasthebest prognosis
  12. 12. Diagnosis •Edrophonium test (Tensilon) •Blood analysis •Repetitivenervestimulation •Single-fiber electromyography (EMG) •Imaging scans
  13. 13. Edrophonium test: Injection of the chemical edrophonium (Tensilon) may result in a sudden, although temporary, improvement in muscle strength — an indication that you may have myasthenia gravis. Edrophonium acts to block an enzyme that breaks down acetylcholine, the chemical that transmits signals from nerve endingsto musclereceptor sites. Blood analysis: A blood test may reveal the presenceof abnormal antibodies that disrupt the receptor sites where nerve impulses signal musclesto move.
  14. 14. Repetitive nerve stimulation: Is a type of nerve conduction study, in which electrodes are attached to skin over the muscles to be tested. Small pulses of electricity are sent through the electrodes to measure the nerve's ability to send a signal to muscle. To diagnose MG, the nerve will be tested many times to see if its ability to send signals worsens with fatigue. Single-fiber electromyography (EMG): EMG measures the electrical activity traveling between brain and muscle. It involves inserting a very fine wire electrode through skin and into a muscle. In single-fiber EMGs, asinglemusclefiber istested. Imaging scans: CT scan or an MRI to confirm a tumor or other abnormality in thymus.
  16. 16. Exacerbation Trigger Factors • Infection • Stress • Fatigue • Cathartics(laxatives) • Heat (sauna, hot tubs, sunbathing)
  17. 17. Medications/Treatment •Plasmapheresis •Immunoglobulin Therapy •Thymectomy •Corticosteroids •Yogaexercises(Pranayama)
  18. 18. Medications/Treatment • ImmunosuppressiveTherapy • Prednisone • Azathioprine • AcetylcholinesteraseInhibitors • First lineof therapy • Neostigminebromide(Pyridostigmine) • Edrophonium chloride(Tensilon)
  19. 19. Thymectomy - surgical removal of the thymusgland. Theroleof thethymusgland in MG isnot fully understood, and thethymectomy may or may not improveapatient'ssymptoms. Plasmapheresis- aprocedurethat removes abnormal antibodiesfrom theblood and replaces thepatient'sblood with normal antibodies through donated blood. Extent of theproblemsisdependent on the severity of thecondition and thepresenceof other problemsthat could affect thepatient. Surgery