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Myasthenia Gravis is an autoimmune disorder characterized by weakness of skeletal muscles that worsens with exertion and improves with rest. It results from antibodies directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers. Clinically it presents with fluctuating weakness of extraocular muscles, facial muscles, bulbar muscles, limbs and respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies, repetitive nerve stimulation, edrophonium testing and imaging to identify thymomas. Treatment includes acetylcholinesterase inhibitors, immunomodulators like prednisone, plasmapheresis and thymectomy.
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Myasthenia gravis
Myasthenia Gravis is an autoimmune disorder characterized by weakness in skeletal muscles that worsens with exertion and improves with rest. Antibodies are directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and impairing signal transmission. Clinical presentation includes weakness of ocular, facial, bulbar, and limb muscles. Diagnosis involves testing for acetylcholine receptor antibodies, repetitive nerve stimulation, and response to edrophonium. Treatment focuses on acetylcholinesterase inhibitors, immunosuppression, and thymectomy in some cases.
Myasthenia Gravis - by MHR Corp
This document discusses myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. It begins with background on MG and outlines the anatomy of the neuromuscular junction which is affected. The pathology of MG involves antibodies blocking acetylcholine receptors, impairing muscle contraction. Clinical presentation includes fluctuating weakness worsened by exertion, especially in extraocular muscles. Diagnosis involves testing for acetylcholine receptor antibodies, with treatment including acetylcholinesterase inhibitors and immunomodulators.
Perioperative management in neuromuscular ds
Neuromuscular disorders affect the neuromuscular system and cause muscle weakness and fatigue. Anesthesia for patients with these disorders requires special considerations. Myasthenia gravis is an autoimmune disorder causing weakness through acetylcholine receptor destruction. Patients are sensitive to nondepolarizing neuromuscular blocking agents and need postoperative ventilation support. Periodic paralysis causes episodes of weakness triggered by various factors like potassium levels, exercise, or food intake. Anesthesia aims to prevent attacks through careful potassium monitoring and avoidance of certain medications.
Anesthetic management in Pediatric Neuromuscular disorders
This document summarizes the anesthetic management considerations for pediatric patients with various neuromuscular disorders. It discusses cerebral palsy, muscular dystrophies like Duchenne and Becker's, myotonias, mitochondrial myopathies, channelopathies, and malignant hyperthermia. Key points include increased sensitivity to medications, difficult airways, respiratory and cardiac issues, hypothermia risks, and triggering agents for malignant hyperthermia like succinylcholine and inhalational anesthetics. Close monitoring is important due to potential complications in the postoperative period.
Myasthenia gravis management guideline
This document provides guidelines for the management of myasthenia gravis (MG). It discusses the various subtypes of MG, diagnostic testing, and treatment options. For treatment, it recommends pyridostigmine as initial therapy in most cases, with corticosteroids or immunosuppressive drugs for those who do not respond adequately. It provides guidance on immunosuppressive agents, intravenous immunoglobulin and plasma exchange, treatment of myasthenic crisis and thymectomy. The guidelines aim to optimize treatment based on the subtype and severity of MG.
Myaesthenia gravis
Myasthenia gravis is an autoimmune disorder where antibodies reduce acetylcholine receptors at the neuromuscular junction, causing muscle weakness that increases with exertion. Anesthesia risks include worsening weakness from nondepolarizing muscle relaxants. The preoperative evaluation assesses respiratory and bulbar function. Anticholinesterases and plasmapheresis may be continued preoperatively. General anesthesia using propofol and inhaled agents without nondepolarizers aims to avoid intubation, but postoperative ventilation may be needed. Regional anesthesia requires reduced doses of amide local anesthetics. Postoperative care focuses on managing weakness, pain control without opioids, and resuming anticholinesterase therapy.
Exercise induced bronchoconstriction
This document discusses exercise-induced bronchoconstriction (EIB). It begins with a case presentation and then defines EIB. It reviews the epidemiology, pathophysiology, clinical presentations, diagnosis, and management of EIB. The key points are:
1) EIB is the transient narrowing of the lower airways that occurs after exercise, which can occur in both asthmatic and non-asthmatic individuals.
2) The pathophysiology involves osmotic and thermal mechanisms leading to the release of inflammatory mediators that cause bronchoconstriction.
3) Diagnosis involves objective exercise or surrogate challenge tests to demonstrate a drop in lung function following exercise.
Cell based therapy for traumatic brain injury
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Myasthenia gravis
Myasthenia Gravis is an autoimmune disorder characterized by weakness in skeletal muscles that worsens with exertion and improves with rest. Antibodies are directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and impairing signal transmission. Clinical presentation includes weakness of ocular, facial, bulbar, and limb muscles. Diagnosis involves testing for acetylcholine receptor antibodies, repetitive nerve stimulation, and response to edrophonium. Treatment focuses on acetylcholinesterase inhibitors, immunosuppression, and thymectomy in some cases.
Myasthenia Gravis - by MHR Corp
This document discusses myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. It begins with background on MG and outlines the anatomy of the neuromuscular junction which is affected. The pathology of MG involves antibodies blocking acetylcholine receptors, impairing muscle contraction. Clinical presentation includes fluctuating weakness worsened by exertion, especially in extraocular muscles. Diagnosis involves testing for acetylcholine receptor antibodies, with treatment including acetylcholinesterase inhibitors and immunomodulators.
Perioperative management in neuromuscular ds
Neuromuscular disorders affect the neuromuscular system and cause muscle weakness and fatigue. Anesthesia for patients with these disorders requires special considerations. Myasthenia gravis is an autoimmune disorder causing weakness through acetylcholine receptor destruction. Patients are sensitive to nondepolarizing neuromuscular blocking agents and need postoperative ventilation support. Periodic paralysis causes episodes of weakness triggered by various factors like potassium levels, exercise, or food intake. Anesthesia aims to prevent attacks through careful potassium monitoring and avoidance of certain medications.
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This document summarizes the anesthetic management considerations for pediatric patients with various neuromuscular disorders. It discusses cerebral palsy, muscular dystrophies like Duchenne and Becker's, myotonias, mitochondrial myopathies, channelopathies, and malignant hyperthermia. Key points include increased sensitivity to medications, difficult airways, respiratory and cardiac issues, hypothermia risks, and triggering agents for malignant hyperthermia like succinylcholine and inhalational anesthetics. Close monitoring is important due to potential complications in the postoperative period.
Myasthenia gravis management guideline
This document provides guidelines for the management of myasthenia gravis (MG). It discusses the various subtypes of MG, diagnostic testing, and treatment options. For treatment, it recommends pyridostigmine as initial therapy in most cases, with corticosteroids or immunosuppressive drugs for those who do not respond adequately. It provides guidance on immunosuppressive agents, intravenous immunoglobulin and plasma exchange, treatment of myasthenic crisis and thymectomy. The guidelines aim to optimize treatment based on the subtype and severity of MG.
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Myasthenia gravis is an autoimmune disorder where antibodies reduce acetylcholine receptors at the neuromuscular junction, causing muscle weakness that increases with exertion. Anesthesia risks include worsening weakness from nondepolarizing muscle relaxants. The preoperative evaluation assesses respiratory and bulbar function. Anticholinesterases and plasmapheresis may be continued preoperatively. General anesthesia using propofol and inhaled agents without nondepolarizers aims to avoid intubation, but postoperative ventilation may be needed. Regional anesthesia requires reduced doses of amide local anesthetics. Postoperative care focuses on managing weakness, pain control without opioids, and resuming anticholinesterase therapy.
Exercise induced bronchoconstriction
This document discusses exercise-induced bronchoconstriction (EIB). It begins with a case presentation and then defines EIB. It reviews the epidemiology, pathophysiology, clinical presentations, diagnosis, and management of EIB. The key points are:
1) EIB is the transient narrowing of the lower airways that occurs after exercise, which can occur in both asthmatic and non-asthmatic individuals.
2) The pathophysiology involves osmotic and thermal mechanisms leading to the release of inflammatory mediators that cause bronchoconstriction.
3) Diagnosis involves objective exercise or surrogate challenge tests to demonstrate a drop in lung function following exercise.
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Traumatic brain injury (TBI) poses a major public health issue, costing over $76 billion annually in the US. While current management focuses on reducing secondary brain damage, cell-based therapy shows promise as an emerging treatment. Animal and early phase human trials have shown cell therapies using mesenchymal stem cells, neural progenitor cells, and bone marrow-derived cells can improve motor function, learning ability, and reduce inflammation following TBI. However, more research is still needed to determine the optimal cell type, route of delivery, timing of treatment, and safety monitoring methods to fully understand and maximize the therapeutic potential of cell-based therapies for TBI.
Myasthenia gravis
Myasthenia Gravis is an autoimmune disorder characterized by weakness of skeletal muscles that worsens with exertion. It results from antibodies directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and impairing signal transmission. Clinical presentation includes weakness of extraocular, facial, bulbar, and limb muscles. Diagnosis involves testing for acetylcholine receptor antibodies and electrodiagnostic studies. Treatment includes acetylcholinesterase inhibitors, immunomodulating therapies like prednisone, plasmapheresis, and thymectomy.
Myasthenia gravis
Myasthenia gravis is an autoimmune neuromuscular disease caused by antibodies against acetylcholine receptors at the neuromuscular junction. It causes muscle weakness and fatigability. It most commonly affects young women and older men. Symptoms include drooping eyelids, double vision, difficulty speaking and swallowing. Diagnosis involves testing for autoantibodies, electrophysiology and response to medication challenges. Treatment includes anticholinesterases, immunosuppression, thymectomy and management of exacerbations. Anesthetic management focuses on optimizing the patient, using regional techniques when possible and careful airway management and extubation planning due to risk of respiratory failure.
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Myasthenia gravis is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, reducing signal transmission from nerves to muscles. Common symptoms include ptosis, diplopia, and weakness of proximal limb muscles or bulbar muscles. Diagnosis involves history, physical exam, electrodiagnostic testing showing decremental response to repetitive nerve stimulation, and presence of acetylcholine receptor antibodies. Treatment options include anticholinesterase medications, immunosuppression, plasmapheresis, IVIg, and thymectomy.
Myasthenia Gravis
Myasthenia gravis is a disease characterized by fluctuating muscle weakness that worsens with exertion and improves with rest. It results from impaired signaling at the neuromuscular junction due to antibodies against acetylcholine receptors. Symptoms vary depending on the affected muscle groups but commonly involve eye and facial muscles. While the root cause is unknown, it is considered an autoimmune disease associated with changes in the thymus gland. Treatment aims to improve muscle strength and prevent worsening through acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and in some cases thymectomy.
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This document discusses Myasthenia Gravis (MG), a chronic autoimmune neuromuscular disease characterized by varying degrees of muscle weakness. MG is caused by autoantibodies that block neuromuscular transmission, reducing acetylcholine receptors. Symptoms include fatigable weakness of the eyes, face, neck, and limbs. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and antibody tests. Treatment includes anticholinesterases, immunosuppressants, plasma exchange, and sometimes thymectomy. The document also briefly discusses other myopathies and neuromuscular junction disorders like Lambert-Eaton myasthenic syndrome.
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This document provides information about Myasthenia Gravis (MG), including its epidemiology, clinical presentation, immunopathology, diagnostic procedures, treatment, and management of different subtypes. Some key points include:
- MG is an autoimmune disorder causing muscle weakness due to antibodies interfering with acetylcholine receptors at the neuromuscular junction.
- It can present with symptoms like ptosis, diplopia, limb or swallowing weakness.
- Diagnosis involves tests like repetitive nerve stimulation, serum acetylcholine receptor antibody levels, and single fiber electromyography.
- Treatment includes pyridostigmine, corticosteroids, immunosuppressants, IVIG, plasma exchange,
Myasthenia gravis guest_lecture[1]
This document provides information about Myasthenia Gravis from Harvard Medical School and Massachusetts General Hospital. It details the history, clinical classification, presentation, differential diagnosis, treatment, and pathophysiology of MG. Key points include that MG is caused by loss of acetylcholine receptors at the neuromuscular junction preventing signal transmission, most patients initially present with ocular or bulbar symptoms, treatment involves cholinesterase inhibitors and corticosteroids like prednisone, and acetylcholine receptor antibodies are present in many cases but their level does not correlate with severity.
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Myasthenia gravis is a neuromuscular disorder characterized by abnormal muscle fatigability that improves with rest. It is caused by circulating antibodies that damage acetylcholine receptors at the neuromuscular junction. Symptoms vary but commonly involve the eyes, face, neck and limbs. Treatment involves anticholinesterase medications and thymectomy, as the thymus gland is involved in pathogenesis. Thymectomy guidelines depend on a patient's age, symptoms, and response to medications, with early surgery generally recommended for adult patients. Complete removal of thymic tissue through a standard transternal incision is required for optimal surgical treatment of myasthenia gravis.
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This document summarizes Myasthenia Gravis (MG), a disorder of the neuromuscular junction caused by autoantibodies against acetylcholine receptors. It presents with fatigable weakness, especially of eye, face, neck and bulbar muscles. Diagnosis involves tests like tensilon/ice pack tests and repetitive nerve stimulation. Treatment includes acetylcholinesterase inhibitors, immunosuppression with steroids/azathioprine, plasma exchange and thymectomy. Prognosis varies but is generally good if confined to eye muscles and in young females after thymectomy. Other related conditions like Lambert-Eaton myasthenic syndrome and various muscular dystrophies are also briefly discussed.
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Myasthenia gravis
Myasthenia Gravis is an autoimmune disorder characterized by weakness of skeletal muscles that worsens with exertion. It results from antibodies directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and impairing signal transmission. Clinical presentation includes weakness of extraocular, facial, bulbar, and limb muscles. Diagnosis involves testing for acetylcholine receptor antibodies and electrodiagnostic studies. Treatment includes acetylcholinesterase inhibitors, immunomodulating therapies like prednisone, plasmapheresis, and thymectomy.
Myasthenia gravis
Myasthenia gravis is an autoimmune neuromuscular disease caused by antibodies against acetylcholine receptors at the neuromuscular junction. It causes muscle weakness and fatigability. It most commonly affects young women and older men. Symptoms include drooping eyelids, double vision, difficulty speaking and swallowing. Diagnosis involves testing for autoantibodies, electrophysiology and response to medication challenges. Treatment includes anticholinesterases, immunosuppression, thymectomy and management of exacerbations. Anesthetic management focuses on optimizing the patient, using regional techniques when possible and careful airway management and extubation planning due to risk of respiratory failure.
Exercise induced bronchoconstriction
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Myasthenia gravis
Myasthenia gravis is an autoimmune neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, reducing signal transmission from nerves to muscles. Common symptoms include ptosis, diplopia, and weakness of proximal limb muscles or bulbar muscles. Diagnosis involves history, physical exam, electrodiagnostic testing showing decremental response to repetitive nerve stimulation, and presence of acetylcholine receptor antibodies. Treatment options include anticholinesterase medications, immunosuppression, plasmapheresis, IVIg, and thymectomy.
Myasthenia Gravis
Myasthenia gravis is a disease characterized by fluctuating muscle weakness that worsens with exertion and improves with rest. It results from impaired signaling at the neuromuscular junction due to antibodies against acetylcholine receptors. Symptoms vary depending on the affected muscle groups but commonly involve eye and facial muscles. While the root cause is unknown, it is considered an autoimmune disease associated with changes in the thymus gland. Treatment aims to improve muscle strength and prevent worsening through acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and in some cases thymectomy.
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A 67-year-old woman with a history of myasthenia gravis presented with progressive muscle weakness, drooping eyelids, difficulty talking and swallowing, and an inability to walk more than a step or two. Tests at the hospital showed reduced vital capacity and inspiratory pressure. Her condition worsened over 24 hours despite treatment. Due to declining respiratory function and an arterial blood gas analysis showing respiratory acidosis, noninvasive ventilation was considered. The patient was intubated and put on mechanical ventilation. After two days of ventilation and treatment, her respiratory function improved enough that she could be successfully extubated.
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This document discusses myasthenia crisis, which is a life-threatening condition defined as weakness from myasthenia gravis that requires intubation or delays extubation after surgery. It presents information on the epidemiology, pathophysiology, clinical presentation, diagnosis, and management of myasthenia crisis. Key aspects of management include admission to the intensive care unit, assessment of respiratory function, elective intubation if needed, rapid immunomodulating therapy, careful weaning, and monitoring for complications.
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This document provides information on Myasthenia Gravis (MG), an autoimmune neuromuscular disease caused by antibodies against postsynaptic muscle membranes. It discusses the prevalence and classification of MG, clinical features including weakness and fatigability, diagnostic testing such as repetitive nerve stimulation and edrophonium testing, treatment including acetylcholinesterase inhibitors and immunotherapies, and management of symptoms. Key points covered include the fluctuating muscle weakness that worsens with exertion seen in MG, different classifications based on symptoms and severity, and first line treatment involving pyridostigmine and corticosteroids.
Advances in myasthenia gravis
Myasthenia gravis is a disease of skeletal muscle acetylcholine receptors caused by antibodies that prevent acetylcholine from binding to receptors, inhibiting nerve impulse transmission and muscle contraction. Symptoms vary in severity and commonly involve the eyes, face, throat, or limbs. Diagnosis involves the Tensilon test and repetitive nerve stimulation or single-fiber electromyography to confirm impaired neuromuscular transmission. Treatment includes acetylcholinesterase inhibitors, immunosuppression with corticosteroids and other drugs, immunomodulation therapies like plasmapheresis, and thymectomy in some cases.
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This document summarizes information about Myasthenia Gravis and Guillain-Barré Syndrome. Myasthenia Gravis is an autoimmune disorder causing muscle weakness due to a block of neuromuscular transmission. Symptoms include drooping eyelids, blurred vision, and limb weakness. Guillain-Barré Syndrome is an acute inflammatory disorder of peripheral nerves leading to progressive muscle weakness over days to weeks, often following a viral infection. It can cause respiratory failure and autonomic dysfunction in severe cases. Both disorders are treated with immunotherapies like intravenous immunoglobulin or plasmapheresis.
Exercise-induced bronchoconstriction
The document discusses exercise-induced bronchoconstriction (EIB). It defines EIB as a transient narrowing of the lower airways that occurs after vigorous exercise. The prevalence of EIB is 7-20% in the general population and up to 90% in asthma patients. The pathogenesis involves heat and water moving from the airway mucosa during exercise, leading to osmotic and thermal changes that cause bronchoconstriction. Diagnosis involves objective tests like exercise challenges, eucapnic voluntary hyperpnea, or inhaled mannitol challenges to detect a drop in lung function after exercise or hyperventilation. Treatment focuses on preventative bronchodilator medication use before exercise.
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This document discusses Myasthenia Gravis (MG), a chronic autoimmune neuromuscular disease characterized by varying degrees of muscle weakness. MG is caused by autoantibodies that block neuromuscular transmission, reducing acetylcholine receptors. Symptoms include fatigable weakness of the eyes, face, neck, and limbs. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and antibody tests. Treatment includes anticholinesterases, immunosuppressants, plasma exchange, and sometimes thymectomy. The document also briefly discusses other myopathies and neuromuscular junction disorders like Lambert-Eaton myasthenic syndrome.
Exercise-Induced Bronchoconstriction
Exercise-induced bronchoconstriction (EIB) is the transient narrowing of the lower airways that occurs after vigorous exercise in individuals both with and without asthma. It is triggered by factors like cold air, pollutants, and allergens during exercise. Diagnosis involves a history of acute symptoms after exercise and objective testing like exercise challenge tests, which measure any drop in lung function after exercise. Treatment focuses on preventing symptoms through proper warm-ups, medication, and avoiding triggers during exercise.
Myasthenia gravis
This document provides information about Myasthenia Gravis (MG), including its epidemiology, clinical presentation, immunopathology, diagnostic procedures, treatment, and management of different subtypes. Some key points include:
- MG is an autoimmune disorder causing muscle weakness due to antibodies interfering with acetylcholine receptors at the neuromuscular junction.
- It can present with symptoms like ptosis, diplopia, limb or swallowing weakness.
- Diagnosis involves tests like repetitive nerve stimulation, serum acetylcholine receptor antibody levels, and single fiber electromyography.
- Treatment includes pyridostigmine, corticosteroids, immunosuppressants, IVIG, plasma exchange,
Myasthenia gravis guest_lecture[1]
This document provides information about Myasthenia Gravis from Harvard Medical School and Massachusetts General Hospital. It details the history, clinical classification, presentation, differential diagnosis, treatment, and pathophysiology of MG. Key points include that MG is caused by loss of acetylcholine receptors at the neuromuscular junction preventing signal transmission, most patients initially present with ocular or bulbar symptoms, treatment involves cholinesterase inhibitors and corticosteroids like prednisone, and acetylcholine receptor antibodies are present in many cases but their level does not correlate with severity.
Timectomia
Myasthenia gravis is a neuromuscular disorder characterized by abnormal muscle fatigability that improves with rest. It is caused by circulating antibodies that damage acetylcholine receptors at the neuromuscular junction. Symptoms vary but commonly involve the eyes, face, neck and limbs. Treatment involves anticholinesterase medications and thymectomy, as the thymus gland is involved in pathogenesis. Thymectomy guidelines depend on a patient's age, symptoms, and response to medications, with early surgery generally recommended for adult patients. Complete removal of thymic tissue through a standard transternal incision is required for optimal surgical treatment of myasthenia gravis.
CNS myasthenia gravis davidson 10 MCQs.
This document summarizes Myasthenia Gravis (MG), a disorder of the neuromuscular junction caused by autoantibodies against acetylcholine receptors. It presents with fatigable weakness, especially of eye, face, neck and bulbar muscles. Diagnosis involves tests like tensilon/ice pack tests and repetitive nerve stimulation. Treatment includes acetylcholinesterase inhibitors, immunosuppression with steroids/azathioprine, plasma exchange and thymectomy. Prognosis varies but is generally good if confined to eye muscles and in young females after thymectomy. Other related conditions like Lambert-Eaton myasthenic syndrome and various muscular dystrophies are also briefly discussed.
Myasthenia gravis
HISTORY, DEFINITION, EPIDEMIOLOGY, ETIOLOGY, PATHOLOGY, PATHOPHYSIOLOGY, CLINICAL FEATURES, GENERAL CLASSIFICATION, CLINICAL CLASSIFICATION - MGFA, INVESTIGATION, DIFFERENTIAL DIAGNOSIS, MEDICAL MANAGEMENT
Pregnancy in a young girl with Myasthenia Gravis.
This document describes the case of a 31-year-old woman with a history of myasthenia gravis who presented with amenorrhea. Myasthenia gravis is an autoimmune disorder causing muscle weakness due to antibodies against acetylcholine receptors at the neuromuscular junction. The patient had been experiencing symptoms of myasthenia gravis for 9 years and underwent thymectomy in 2008. She became pregnant after 6 months of marriage and had an uneventful pregnancy while continuing medication for myasthenia gravis. She delivered a baby girl via cesarean section due to failure to progress in labor. Both mother and baby were discharged in good condition.
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3. Symptoms vary widely and can include changes in sensation, vision problems, weakness, and balance issues. Diagnosis involves MRI imaging and ruling out other potential causes through blood and spinal fluid tests.
Mysthenia Gravis.ppt
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies destroy connections between nerves and muscles. Symptoms vary but can include drooping eyelids, blurred or double vision, difficulty swallowing and speaking, and weakness in arms or legs. While there is no cure, treatment aims to control symptoms through medications that enhance nerve-muscle communication or suppress the immune system.
Stroke Presentation Ms
A stroke occurs when the blood supply to the brain is interrupted or reduced, causing brain cells to die. It is a medical emergency. There are two main types of strokes: ischemic, caused by a blockage in a blood vessel, and hemorrhagic, caused by a ruptured blood vessel. Symptoms vary depending on the affected area of the brain but can include paralysis, confusion, and headaches. Diagnostic tests including CT scans and MRI images are used to determine the type and location of the stroke. Treatment options depend on the type of stroke but may include clot-busting drugs or surgery to repair damaged blood vessels. Prevention is key through controlling risk factors like high blood pressure, diabetes, and smoking.
Stroke (1)
This document provides an overview of strokes, including:
- Strokes are caused by a blockage or rupture of an artery to the brain, cutting off oxygen flow.
- Symptoms include weakness, paralysis, difficulty speaking or swallowing.
- Diagnosis involves medical imaging, blood tests, and physical exams to determine the type and location of blockage or rupture.
- Treatment depends on the type of stroke but may include clot-busting drugs, surgery, medication, and lifestyle changes to prevent future strokes.
Cerebrovascular disease (CVA / Stroke)
1) The document discusses strokes (cerebrovascular accidents or CVAs), their causes, types, symptoms, diagnosis and treatment.
2) Strokes are caused by disturbances in the vascular system and can be ischemic (caused by clot or blockage) or hemorrhagic (caused by bleeding).
3) Common symptoms of strokes include weakness or numbness on one side of the body, speech problems, and visual issues. The specific symptoms depend on the area of the brain affected.
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Lecture section...Myasthenia Gravis
Myasthenia Gravis is an autoimmune neuromuscular disorder characterized by weakness of skeletal muscles that worsens with exertion and improves with rest. It results from antibodies directed against acetylcholine receptors at the neuromuscular junction, reducing their numbers and impairing signal transmission from nerves to muscles. Diagnosis involves testing for antibodies, electrodiagnostic studies like repetitive nerve stimulation and single fiber EMG, and response to medications like edrophonium. Treatment focuses on acetylcholinesterase inhibitors, immunomodulators like corticosteroids, plasmapheresis, and thymectomy in cases involving thymoma.
vdocument.in_myasthenia-gravisppt.ppt
This document provides an overview of myasthenia gravis (MG), an autoimmune disorder characterized by muscle weakness and fatigability. It describes the anatomy of the neuromuscular junction where antibodies in MG interfere with signal transmission. Symptoms range from weakness of extraocular muscles to respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies and repetitive nerve stimulation studies. Treatment includes acetylcholinesterase inhibitors, immunomodulators like prednisone, plasmapheresis, and thymectomy for those with thymoma. Prognosis is good with treatment but respiratory failure remains a risk without proper management.
Myasthenia gravis
Myasthenia gravis is an autoimmune disorder characterized by fluctuating weakness of skeletal muscles. It results from antibodies directed against acetylcholine receptors at the neuromuscular junction, which decreases the number of receptors and impairs signal transmission from nerves to muscles. Symptoms include weakness of eye muscles, facial muscles, limbs, and respiratory muscles that worsens with exertion and improves with rest. Diagnosis involves testing for acetylcholine receptor antibodies in blood and repetitive nerve stimulation or single fiber electromyography. Treatment options include acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and thymectomy.
Myasthenia Gravis - Pathophysiology, Cl. Features, DD
Myasthenia Gravis - Pathophysiology, Cl. Features, DDStanley Medical College, Department of Medicine
Myasthenia gravis is an autoimmune disorder caused by antibodies that interfere with signal transmission at the neuromuscular junction. The antibodies are typically against acetylcholine receptors or muscle-specific kinase. This disrupts muscle contraction and causes weakness that fluctuates and worsens with activity. Symptoms usually start in extraocular muscles and may progress to other areas. Thymic abnormalities are seen in many cases and thymectomy can aid treatment.1 narrated myasthenia pp
Myasthenia Gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy acetylcholine receptors, interrupting communication between nerves and muscles. Symptoms include varying muscle weakness that worsens with activity. It commonly first affects eye muscles. Diagnosis involves tests showing improvement of symptoms with acetylcholinesterase inhibitors and presence of acetylcholine receptor antibodies. Treatment focuses on anticholinesterase medications, immunosuppressants, plasmapheresis, IVIG, and sometimes thymectomy. Patients require education on medication management and prevention of crisis.
Myasthenia-Gravis.pptx
Myasthenia gravis is an autoimmune disorder characterized by fatigue and weakness of skeletal muscles that worsens with exertion and improves with rest. It results from antibodies that block or destroy acetylcholine receptors in the neuromuscular junction, preventing muscle contraction. Symptoms often include drooping eyelids, double vision, facial weakness, and difficulty swallowing and speaking. Diagnosis involves testing for acetylcholine receptor antibodies and response to medication like edrophonium. Treatment includes anticholinesterases, corticosteroids, immunosuppressants, plasmapheresis, and sometimes thymectomy. Myasthenic crisis is a life-threatening exacerbation requiring ventilator support when respiratory muscles are severely
Myasthenia Gravis - Management
This document provides an overview of the diagnostic workup and treatment for myasthenia gravis. Key points include:
- Common symptoms include fluctuating weakness that worsens with exertion and improves with rest. Physical exam looks for muscle weakness and fatigability.
- Diagnostic tests include acetylcholine receptor antibodies, repetitive nerve stimulation, and single fiber electromyography to confirm diagnosis.
- Treatment involves anticholinesterase medications to increase acetylcholine levels, immunosuppressants like prednisone and azathioprine to reduce antibody production, and sometimes thymectomy to remove the thymus gland.
Myasthenia gravis
This document summarizes key information about Myasthenia Gravis (MG), an autoimmune disorder characterized by muscle weakness and fatigue. It discusses the epidemiology of MG, noting peaks in incidence among younger females. The pathophysiology involves antibodies interacting with acetylcholine receptors at the neuromuscular junction, reducing receptor numbers. Diagnosis involves testing for antibodies and response to cholinesterase inhibitors. Treatment focuses on immunomodulation including plasmapheresis, IVIG, thymectomy and immunosuppressive drugs.
Myasthenia gravis,
Myasthenia gravis is an autoimmune disorder characterized by fluctuating muscle weakness and fatigability caused by antibodies attacking acetylcholine receptors at the neuromuscular junction. It is diagnosed through tests like the edrophonium test, repetitive nerve stimulation, bloodwork detecting antibodies, and electromyography. Treatment involves acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, and sometimes thymectomy to manage symptoms and weakening. Nursing care focuses on maintaining breathing and mobility, preventing aspiration, and educating patients.
Myasthenia gravis sh
Myasthenia Gravis is a neuromuscular junction disorder characterized by skeletal muscle weakness and fatigability. It is caused by antibodies that interfere with acetylcholine receptor function, reducing the efficiency of nerve impulse transmission and causing muscle weakness. Symptoms include weakness of eye muscles, facial muscles, and limbs which worsens with repeated use and improves with rest. Diagnosis involves tests like repetitive nerve stimulation, blood tests for antibodies, and response to medication. Treatment options include anticholinesterase medications, immunosuppressants, plasmapheresis, IVIG, and sometimes thymectomy. With current treatments prognosis is generally good though exacerbations can occasionally cause life-threatening crises requiring respiratory support.
Cns Mg Davidson 07.
Myasthenia gravis is a disorder of the neuromuscular junction caused by autoantibodies that block signal transmission. It causes progressive weakness of voluntary muscles, especially those of the eyes, face, neck, and limbs. Symptoms worsen with activity and improve with rest. Diagnosis involves tests like the Tensilon test and repetitive nerve stimulation. Treatment focuses on improving acetylcholine activity and suppressing the immune response, using medications, thymectomy, or other immunotherapies. Prognosis depends on which muscles are affected, with ocular-only forms having an excellent prognosis.
Neuro pain 60 mins
Neuropathic pain poses a challenge to effective rehabilitation. Best practice, considerations & the use of Action Potential Simulation therapy to effectively treat neuropathic pain, sharing our results from a 2 year research project in people with MS.
Neuro pain 60 mins
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Myasthenia gravis
Myasthenia Gravis is an autoimmune neuromuscular disease causing muscle weakness that worsens with activity and improves with rest. Antibodies attack acetylcholine receptors at the neuromuscular junction, reducing muscle stimulation. Symptoms include drooping eyelids, double vision, difficulty speaking and swallowing. While there is no cure, treatment aims to reduce antibodies and improve transmission at the neuromuscular junction through immunosuppressants and acetylcholinesterase inhibitors. Patients require education on exacerbating/alleviating factors and signs of crisis to safely manage the fluctuating nature of the disease.
Medicine 5th year, 3rd lecture (Dr. Mohammad Shaikhani)
Myasthenia gravis is an autoimmune disorder causing fatigue and weakness of voluntary muscles. It is usually caused by antibodies against acetylcholine receptors at the neuromuscular junction, impairing signal transmission. Most patients have thymic hyperplasia or thymoma. Diagnosis involves tests like the Tensilon test and checking for acetylcholine receptor antibodies. Treatment focuses on acetylcholinesterase inhibitors and immunosuppression with corticosteroids, azathioprine or plasma exchange to reduce antibodies. Prognosis depends on factors like age of onset and presence of thymoma.
Anaesthesia management of patient posted for scoliosis correction
This document discusses the anesthetic considerations for scoliosis surgery. It begins with definitions and classifications of scoliosis. It then discusses epidemiology, measurement of severity, pre-anesthetic assessment, anesthesia techniques used, and conclusions. Key points include the need for careful preoperative pulmonary and cardiac evaluation given the risks of respiratory impairment. Intraoperatively, neuromuscular monitoring is important to detect any spinal cord issues, and total intravenous anesthesia is typically used. Postoperatively, close monitoring and respiratory care are essential to address issues like pain management and pulmonary complications.
Myasthenia gravis (Ascending Disease)
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, trouble talking, and trouble walking.
microvascular angina.pptx
Dr. Rikesh Tamrakar's document discusses two types of chest pain conditions: Prinzmetal angina and microvascular angina. Prinzmetal angina, also known as variant angina, is caused by transient spasms of the coronary arteries and presents with chest pain at rest, often between midnight and dawn. Microvascular angina presents with chest pain on exertion despite no blockages in the coronary arteries, and may be caused by endothelial dysfunction or small vessel disease. Both conditions can cause ischemia and be diagnosed through ECG changes and stress testing, and are generally treated with calcium channel blockers, nitrates, and lifestyle modifications.
Anesthesia for spine surgery
1. Anesthesia for spine surgery presents several challenges including patient positioning, increased blood loss, and spinal cord protection.
2. Pre-operative assessment focuses on airway evaluation, neurological and cardiovascular status, and determining risk factors for complications.
3. During surgery, careful positioning, maintenance of stable anesthesia and hemodynamics, and monitoring for changes like abnormal SSEPs are important considerations.
4. Post-operative care involves managing pain, monitoring for complications, and addressing issues like respiratory function, neck edema, and injury risks from prolonged prone positioning.
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Myasthenia Gravis - Pathophysiology, Cl. Features, DD
Myasthenia Gravis - Pathophysiology, Cl. Features, DD
Medicine 5th year, 3rd lecture (Dr. Mohammad Shaikhani)
Medicine 5th year, 3rd lecture (Dr. Mohammad Shaikhani)
Anaesthesia management of patient posted for scoliosis correction
Anaesthesia management of patient posted for scoliosis correction
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Mapleson breathing systems
There are several types of Mapleson breathing systems classified based on the position of the reservoir bag. Mapleson A has an afferent reservoir with the bag attached to the fresh gas inlet. Mapleson D has an efferent reservoir with the bag attached to the patient outlet. Both systems allow for spontaneous or controlled ventilation but Mapleson D is more efficient due to continuous mixing of fresh gas and exhaled gases. The systems are tested for leaks and proper functioning using various occlusion and pressurization techniques.
Lower limb blocks
1) Lower limb nerve blocks provide post-operative pain relief and are safer than complete sympathectomy, though they are technically more difficult than upper limb blocks or central neuraxial blocks.
2) The lumbar and sacral plexuses give rise to various nerves that can be blocked individually or as combinations to anesthetize the lower limb, including the femoral, lateral femoral cutaneous, and obturator nerves.
3) The 3-in-1 block anesthetizes the femoral, obturator, and lateral femoral cutaneous nerves via a single injection into the femoral sheath above the inguinal ligament.
Laser
Anesthesia considerations for laser surgery include managing hazards from atmospheric contamination, laser-tissue interactions, and endotracheal tube fires. Various laser wavelengths are used in procedures like dermatology and ophthalmology. Endotracheal tubes must be protected to prevent fires, and techniques like intermittent apnea and helium-oxygen mixtures reduce risks. Post-operative monitoring is also important due to potential complications from the laser effects. Safety policies and protocols help minimize risks from laser use in surgery.
Koshy
This patient has a history of myocardial infarction, triple vessel coronary artery disease, and is scheduled for elective non-cardiac surgery. Based on his positive stress test results and coronary angiogram showing severe blockages, the cardiologist recommends coronary artery bypass graft surgery prior to the planned surgery to improve his long-term prognosis and reduce perioperative cardiac risks.
Iv induction agents
1. Ketamine, thiopentone, and propofol are common intravenous anesthetic agents that differ in their chemical structure, pharmacokinetics, and mechanisms of action.
2. Ketamine is a non-competitive NMDA receptor antagonist, thiopentone enhances GABA activity, and propofol directly activates GABA receptors.
3. All three agents cause sedation, but ketamine can also induce dissociative anesthesia and has analgesic properties while propofol is commonly used for sedation and induction.
Introduction 2
The document summarizes a study on the effect of preemptive gabapentin on postoperative pain and opioid requirement following head and neck surgeries. The study involved 60 patients divided into a gabapentin group and a control group. Pain scores and opioid requirements were significantly lower in the gabapentin group compared to the control group over 24 hours post-surgery. Heart rate, blood pressure and nausea were also lower in the gabapentin group. The study concludes that preemptive gabapentin effectively reduces postoperative pain and opioid needs following head and neck surgeries.
Inhalational anes
The document compares the commonly used inhalational anesthetics nitrous oxide, isoflurane, sevoflurane, halothane, and desflurane. It discusses their physical and chemical properties, effects on organ systems like cardiovascular, respiratory, central nervous system, hepatic, renal, and skeletal muscle. Nitrous oxide is also described in detail regarding its history of use, pharmacokinetics, and clinical applications.
Inhalational anaesthetic agents
The document discusses the history of inhalational anesthetic agents and the concept of minimum alveolar concentration (MAC). It describes how MAC was defined by Eger in the 1960s as the concentration of an inhaled anesthetic that prevents movement in 50% of subjects exposed to a painful stimulus. MAC allows comparison of potency between agents and provides a standard measure. Factors like age, drugs, and medical conditions can impact MAC values.
Icu care after acute head injury
This document discusses the management of intensive care for patients with acute head injuries. It outlines factors that influence patient outcomes, such as the severity of the primary and secondary injuries. It emphasizes the importance of monitoring patients to avoid physiological insults that can exacerbate secondary brain injury, including intracranial hypertension, hypoxia, hypotension, and fever. A variety of monitoring modalities are described to optimize cerebral perfusion pressure and oxygenation in order to minimize ischemia. Both general and specific medical management strategies are covered, such as surgical intervention, ventilation, fluid management, and use of pharmacological agents to reduce intracranial pressure.
Hypoxia and oxygen therapy 3
There are several types of hypoxia that can occur depending on the underlying cause of inadequate oxygen delivery or utilization in the body's tissues. Arterial (hypoxic) hypoxia results from problems getting oxygen into the bloodstream, such as inadequate ventilation, diffusion limitations, or shunts. Stagnant (ischemic) hypoxia occurs when blood flow to tissues is inadequate. Anemic hypoxia is due to insufficient hemoglobin to carry oxygen. Histotoxic hypoxia involves the tissues' inability to utilize oxygen. Symptoms and signs depend on the severity and rapidity of hypoxia onset. Oxygen therapy aims to improve oxygen delivery and is indicated for documented hypoxia from various acute conditions. Delivery methods include low
Fire in ot
The document discusses fire safety in operating theaters. It outlines the fire triad of fuel, oxidizer, and ignition source and emphasizes prevention by separating these elements. It describes typical fuels and ignition sources in operating rooms and recommendations to reduce risks, such as using laser-resistant endotracheal tubes. The document also covers management of different types of fires and the importance of safety education for appropriate responses to fires.
Fiberoptic
The document discusses the physics and principles of fiberoptic image transmission using total internal reflection within glass fibers. It describes the components, optical and mechanical systems, working channels, and cleaning/sterilization of flexible fiberoptic laryngoscopes. The goal of fiberoptic intubation is to provide well-illuminated and magnified images of the airway for safe endotracheal intubation.
Electrolyte disturbances
This document summarizes electrolyte disturbances, specifically disorders of sodium and potassium balance. It discusses the causes, types, clinical features, diagnosis, and treatment of hyponatremia, hypernatremia, hypokalemia, and hyperkalemia. The key points covered include normal sodium and potassium levels, how they are regulated, complications that can arise from imbalances, and goals and principles of correcting electrolyte abnormalities.
Ecg presentation
The document provides an overview of electrocardiogram (ECG) interpretation including basics of normal ECG features, measurements of intervals, axis determination, identification of chamber enlargement, types of heart blocks, signs of ischemic heart disease, ectopic beats, tachyarrhythmias, bradyarrhythmias, and other common ECG abnormalities. It describes the typical appearance of P, QRS, and T waves as well as the durations of normal intervals and how to assess cardiac axis. It also outlines characteristics of atrial and ventricular enlargement, various grades of atrioventricular block, bundle branch blocks, ischemic changes, premature beats, tachycardias, bradycardic rhythms, and effects of electroly
Difficult airway guidelines
1. The document outlines a 4 plan approach for managing difficult or failed tracheal intubation during anesthesia induction.
2. Plan A involves initial direct laryngoscopy and use of introducers or alternative laryngoscopes if poor view is obtained.
3. Plan B involves use of supraglottic airway devices like ILMA or LMA if Plan A fails, with fiberoptic intubation through the device.
4. Plan C maintains oxygenation and ventilation by reverting to a face mask if intubation fails via Plan B, postponing surgery and awakening the patient.
5. Plan D involves rescue techniques if ventilation and oxygenation cannot be maintained as
Congenital heart disease
1. The document discusses two congenital heart defects, Tetralogy of Fallot and Transposition of the Great Vessels. Tetralogy of Fallot is characterized by four features and leads to cyanosis if left untreated.
2. Transposition of the Great Vessels involves the transposition of the aorta and pulmonary artery, which prevents oxygenated blood from reaching the body. It requires measures to maintain ductal flow or creation of communications between ventricles.
3. The document outlines evaluations, investigations, surgical procedures, and goals/risks of management for both conditions.
Complete fiberoptic
This document discusses fiberoptic intubation, including:
1. Indications for fiberoptic intubation such as difficult airway cases or cervical spine injuries
2. Topical anesthesia techniques for awake fiberoptic intubation, including nerve blocks to anesthetize the nasal passages, pharynx, and larynx
3. Proper setup and positioning for fiberoptic intubation, including devices to aid visualization and intubation
Cholecytectomy
An 80-year-old woman presented with right upper abdominal pain and nausea/vomiting. She had a history of hypertension, hypothyroidism, obstructive sleep apnea, and recurrent urinary tract infections. Examination and investigations revealed acute obstructive cholecystitis. She underwent an open cholecystectomy with combined spinal-epidural anesthesia and was managed post-operatively with epidural analgesia and intravenous fluids. She recovered well and was discharged on the third post-operative day.
Breathing mechanics
The document discusses the mechanics of breathing and factors that influence gas exchange in the lungs. It describes how the diaphragm and external intercostal muscles cause the chest cavity to expand and contract. This creates pressure differences that allow air to flow into and out of the lungs down a pressure gradient. Resistance to airflow is determined by properties of the airways like their size, branching patterns, and surface properties. Lung compliance and alveolar surface tension also impact gas exchange efficiency in the lungs.
Brachial block
Upper limb nerve blocks provide anesthesia for surgeries on the arm and hand. The brachial plexus supplies sensation and movement to the upper limb and can be blocked at different levels, including supraclavicular, interscalene, axillary, and infraclavicular. Nerve stimulators can help locate nerves more accurately than paresthesia alone. Potential complications depend on the specific block but may include pneumothorax, phrenic nerve block, and accidental spinal or epidural injection.
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
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Editor's Notes
- Induciton of a myasthenic-like syndrome in mice by injecting a large quantitiy of immunoglobulin G from MG patients
- Induciton of a myasthenic-like syndrome in mice by injecting a large quantitiy of immunoglobulin G from MG patients Top photo shows a rabbit with "floppy" ears after an injection of receptor antigens. Bottom shows the same rabbit after receiving edrophonium. http://www.aneuroa.org/html/c20html/1970_1979.htm
- Induciton of a myasthenic-like syndrome in mice by injecting a large quantitiy of immunoglobulin G from MG patients
- Onset from mild to maximal weakness is less than 36 months in 83% of patients
- Lambert-Eaton myasthenic syndrome (LEMS) is a rare condition in which weakness results from an abnormality of acetylcholine (ACh) release at the neuromuscular junction. Recent work demonstrates that LEMS results from an autoimmune attack against voltage-gated calcium channels (VGCC) on the presynaptic motor nerve terminal.
- Positive RNS test features Decrement in CMAP amplitude Size: More than 10% in reduction in CMAP amplitude Measure from 1st to 4th or 5th potential in train Smallest CMAP is often 2nd or 3rd potential in train Post-exercise exhaustion Exercising muscle briefly before testing exacerbates decremental response Occurs rapidly after initial stimulation Post-tetanic potentiation Reduction in decrement in minutes after exercise Occurs after post-exercise exhaustion
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