Download Free Medical Myasthenia Gravis PowerPoint Presentation

Myasthenia Gravis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : PPt about myasthenia gravis include definition and epidimiology of myasthenia gravis, also i disscussed tratment previntion for myasthenia gravis

Tags : myasthenia gravis,disorders of neurotransmission,neurotransmission

Published on : Oct 29, 2023 | Views : 2494 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Penza State University Medical Institute Department of Neurology, Neurosurgery and Psychiatry Myasthenia gravis Speaker : Ragab Mahmoud
Slide 2-

DEFINITION Myasthenia gravis (MG) is the most common of the disorders of neurotransmission. MG is an autoimmune disorder, with antibodies directed against postsynaptic targets. It is heterogeneous with respect to age of onset, severity, involvement of specific muscle groups, and thymic changes. MG should be distinguished from some rarer disorders of neuro-transmission in which other autoimmune, genetic, or toxic aetiolo-gies are responsible. An overview of the differential diagnosis will be discussed later, with congenital myasthenia outlined
Slide 3-

Etiology Myasthenia gravis is not inherited and it is not contagious. It generally develops later in life when antibodies in the body attack normal receptors on muscle. This blocks a chemical needed to stimulate muscle contraction. The majority of patients with MG have antibodies directed against the nicotinic AChR with a variable proportion of the remaining cases having antibodies directed against MuSK. Both antibodies bind to the extracellular domains of the native molecule.
Slide 4-

Etiology Both AChR and MuSK antibodies are directly pathogenic and not just markers of the disease. They satisfy the strict criteria for causation in antibody-mediated diseases: Both antibodies are specific to MG, with autoantigens on postsynaptic muscle membrane that are involved in neurotransmission. Passive transfer of immunoglobulin G (IgG) from MG patients to mice produces weakness and evidence of impaired neurotransmission Similarly, transient maternal–fetal transfer of disease has been reported in both serological forms of MG Active immunization in animals with the respective autoantigen is capable of replicating the human disease with similar clinical and electrophysiological features
Slide 5-

Epidemiology Incidence In 55 studies conducted from 1950 to 2007, the incidence rate of MG varied between 1.7 and 21.3, resulting in a global pooled incidence rate of 5.3 per 1,000,000 persons per year.2 Another 29 studies between 2007 and 2019 reported an incidence rate of MG ranging from 0.15 to 61.33 per 1,000,000 persons per year.3 A 2021 study cites the incidence rate of MG as 4.1 to 30 cases per 1,000,000 persons per year. Prevalence The reported prevalence of MG over the past 50 years is increasing and varies based on location.1,2,5 Global prevalence rates range from 150 to 200 cases per 1,000,000 people.
Slide 6-

Clinical features Ocular MG Ptosis ophthalmoplegia happen to people from age 4-90 , more common in males than females Generalized MG Ptosis ophthalmoplegia generalized weakness Predominant ocular, facial & bulbar weakness happen to people from age 10-70 , more common in females than males
Slide 7-

Diagnostic studies ice-pack test Application of crushed ice in a latex glove over the ptotic eyelid, leading to eyelid opening Edrophonium (Tensilon®) test Transient improvement in objective muscle weakness after intravenous injection of the acetylcholinesterase inhibitor However, both tests give false positive and false negative results, particularly in inexperienced hands, and edrophonium has the potential to cause serious bradycardias (hence atropine, a cardiac monitor, and resuscitation equipment should be readily available). Neither test should be needed in the vast majority of patients.
Slide 8-

Diagnostic studies Neurophysiological examination Neurophysiological examination is most informative when performed by an experienced clinician. False negative results are common, especially in OMG, and over-interpretation of minor decrement leads to false positive results. Repetitive nerve stimula tion (RNS) at 3–10 Hz may produce a decrement of more than 10% in over 50% of patients with generalized MG . RNS has particu-larly low sensitivity in OMG Up to 85% of patients with generalized MG and 50% of OMG patients have antibodies against AChR as measured by standardradioimmunoprecipitation (using 125 I-labelled bun garotoxin) or enzyme-linked immunosorbent assay (ELISA)techniques. LRP4 is a newly identified receptor for agrin and is needed for the formation of NMJs Recently, antibodies against LRP4 have been described in a variable number of patients with MG with out antibodies to AChR or MuSK (i.e. the ‘double seronegatives’) They can be seen in 2–45% of patients who are negative for AChR and MuSK antibodies, but the true incidence is unknown because of limited studies.
Slide 9-

TREATMENT Cholinesterase inhibitors. Medicines such as pyridostigmine (Mestinon, Regonal) improve communication between nerves and muscles. These medicines aren't a cure, but they can improve muscle contraction and muscle strength in some people. Possible side effects include gastrointestinal upset, diarrhea, nausea, and too much salivation and sweating. Corticosteroids. Corticosteroids such as prednisone (Rayos) block the immune system, making it less able to produce antibodies. Use of corticosteroids over a long period of time, however, can lead to serious side effects. These include bone thinning, weight gain, diabetes and higher risk of some infections. Immunosuppressants. These medicines could include azathioprine (Azasan, Imuran), mycophenolate mofetil (Cellcept), cyclosporine (Sandimmune, Gengraf, others), methotrexate (Trexall) or tacrolimus (Astagraf XL, Prograf, others). These medicines, which can take months to work, might be used with corticosteroids. Side effects of immunosuppressants, such as higher risk of infection and liver or kidney damage, can be serious.
Slide 10-

TREATMENT Intravenous therapy : 1- Plasmapheresis (plaz-muh-fuh-REE-sis). This procedure uses a filtering process that's like dialysis. Your blood is put through a machine that removes the antibodies that block transmission of signals from your nerve endings to your muscles. However, the good effects from this procedure usually last only a few weeks. Having several procedures can lead to problems finding veins for the treatment. Risks of plasmapheresis include a drop in blood pressure, bleeding, heart rhythm problems or muscle cramps. Some people have an allergic reaction to the solutions used to replace the plasma. 2- Monoclonal antibody. Rituximab (Rituxan) and eculizumab (Soliris) are medicines given by vein for myasthenia gravis. These medicines are usually used when other treatments don't work. They can have serious side effects.
Slide 11-

Surgery Intravenous therapy : 1- Video-assisted thymectomy. In one form of this surgery, surgeons make a small opening in the neck or a few small openings in the side of the chest. They then use a long, thin camera, called a video endoscope, and small instruments to see and remove the thymus gland. 2- Robot-assisted thymectomy. In this form of thymectomy, surgeons make several small openings in the side of the chest. They use a robotic system to remove the thymus gland. This system includes a camera arm and mechanical arms.
Slide 12-

THANK YOU FOR YOUR ATTENTION