myasthenia gravis in present era

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myasthenia gravis in present era

  1. 1. A SEMINAR PRESENTATION BY G. HARISH, 091D1R0014,UNDER THE SUPERVISION OFDr. BIGALA RAJKAMAL. M.Pharm, PhD, FAGE.PRINCIPALGANGA PHARMACY COLLEGE,DASNAGAR,NIZAMABAD. 1
  2. 2. 1. INTRODUCTION2. ETIOLOGY3. PATHOPHYSIOLOGY4. SIGNS& SYMPTOMS5. DIAGNOSIS6. TREATMENT7. CONCLUSION8. REFERENCES 2
  3. 3. 1. INTRODUCTION: Myasthenia gravis (MG) is an autoimmune syndrome caused by the failureof neuromuscular transmission, which results from the binding of auto antibodies toproteins involved in signaling at the neuromuscular junction (NMJ) MG is caused by a decrease in the numbers of postsynaptic acetylcholinereceptors at the neuromuscular junction, which decreases the capacity of theneuromuscular end-plate to transmit the nerve signal. Normally, in response to a stimulus resulting in depolarization, acetylcholineis released presynaptically and acts on the motor end plate to initiate a muscle actionpotential. In MG, the number of activated postsynaptic receptors may be insufficientto trigger an action potential. 3
  4. 4. 2. ETIOLOGY:(1) Acquired autoimmune.(2) Transient neonatal caused by the passive transfer of maternal anti-AChRantibodies(3) Drug induced: D-penicillamine is the prototype of drug induced myastheniagravis. Clinical presentation may be identical to typical acquired autoimmunemyasthenia gravis and the antibody to AChR may be found.(4) Congenital myasthenic syndromes (AChR deficiency, slow channel syndrome, andfast channel syndrome) are distinct heritable disorders of postsynaptic neuromusculartransmission with characteristic age of onset, pathology, electrophysiology, andtreatment. 4
  5. 5. 3. PATHOPHYSIOLOGY: A. Normal Neuromuscular Transmission Acetylcholine (ACh) is synthesized in the nerve terminal by action of the enzyme choline acetyltransferase. ACh is then stored in vesicles ACh then binds to the post-synaptic ACh receptor, resulting in a transient increase in membrane permeability to Na, K, Ca, and Mg, leading to an Endplate potential (EPP).Acetycholinesterase and diffusion deactivates the Ach and terminates neuromusculartransmission. 5
  6. 6. B. Acetylcholine Receptor Antibody:The antibody blocks neuromuscular transmission by several mechanisms -blockade of receptor sites by steric hindrance, destruction of AChR(complement mediated), and cross linking of AChR which causes increasedturnover by endocytosis 6
  7. 7. C. Structural Changes The chronic inflammation of Myasthenia gravis causes several changes in the structure of the Neuromuscular Junction which also inhibit transmission and contribute to weakness 7
  8. 8. D. Genetic factors: Certain HLA types associated with MG (HLA-DR3 and DQ2)E. Role of Thymus: 8
  9. 9. 4. SIGNS& SYMPTOMS: 9
  10. 10. A.Eye Muscles:  Diplopia.  Photophobia.  Ptosis.B.Facial Muscles weakness:C.Orbicularis Oculi Weakness.D. Orbicularis Oris WeaknessE.Oropharyngeal Muscles.  Tongue Weakness.  Weakness in Chewing.  Dysphagia.F.Respiratory Muscle WeaknessG.Pelvic Floor Muscle Weakness 10
  11. 11. 5. DIAGNOSIS: 11
  12. 12. 6. TREATMENT: 12
  13. 13. 1. Anticholinesterases: Neostigimine pyridostigmine 13
  14. 14. 2. EPHEDRINE Ephedrine may be useful as an ancillary medication, added to anticholinesterases, for those Myasthenia gravis patients who need a little extra strength and are not bothered by its possible side effects of nervousness, heart palpitations, or insomnia. For adult Myasthenia gravis it is taken as a 25-mg capsules two to three times a day.3. PLASMAPHERESIS. 14
  15. 15. 4. INTRAVENOUS IMMUNOGLOBULIN’S5. IMMUNOSUPPRESSIVE DRUG THERAPY A. CORTICOSTEROIDS B. AZATHIOPRINE: 15
  16. 16. C.CYCLOSPORINESURGICAL THYMECTOMY: 16
  17. 17. 7. CONCLUSIONIn the management of myasthenia gravis, no standard measure of disease severityand no medical treatment approach has been proven efficacious by rigorous,prospective, controlled studies. The preponderance of evidence certainly links a“connection” between the immune system and the central nervous system beyond areasonable doubt. However the latest techniques like intra venous immunoglobulins, plasmapheresis and surgical thymectomy were found to be effective. But research is goingon to findout the effective medical treatment for myasthenia gravis. May be infuture we can treat the myasthenia gravis without any adverse effects. 17
  18. 18. 8. BIBLIOGRAPHY:1. A text book of pharmacology by rang and dales, sixth edition, published bychurchill livingstone, page numbers 52,166,745.2. A text book of pharmacology by tripati, sixth edition, jaypee publications, pagenumber 102-1043. A text book of pharmacology by goodman&gillman, chapter 524. Journal of neurosurg psychiatry 2012 july, masuda.j, motmura.m et.al..5. International journal of padiatric ortorhniolarynglogy19(1990)273-276, elsevier.6. The journal of clinical investigation volume 116, number 11, nov 20067. The journal of clinical evaluation and management of myasthenia gravis by john c.,keesey.md et. al.. 18
  19. 19. 19

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