The document discusses several neuromuscular disorders including poliomyelitis, amyotrophic lateral sclerosis, neuropathies, myopathies, myasthenia gravis, diseases of the neuromuscular junction, and botulism. Key points include that poliomyelitis and ALS affect motor neurons, neuropathies often present with weakness or foot drop and intact sensation, and myopathies cause generalized weakness while preserving sensation. Myasthenia gravis is due to antibodies against acetylcholine receptors. Diseases of the neuromuscular junction include myasthenia gravis and botulism.
The patient is a 40-year old woman with well-controlled myasthenia gravis scheduled for radical hysterectomy. An epidural anesthetic technique will be used with propofol for induction and maintenance to avoid muscle relaxants if possible due to MG. Non-depolarizing muscle relaxants may be used carefully at reduced doses if needed. The patient's arrhythmias may be treated with neostigmine. Post-operatively, criteria for extubation include VC > 10 ml/kg, RR <30, TV > 5ml, and inspiratory force > 25 cm.
Neuromuscular junction diseases interfere with the transmission of signals from nerves to muscles and can be acquired or inherited. Myasthenia gravis is an acquired autoimmune disorder where antibodies induce acetylcholine receptor deficiency at the neuromuscular junction, causing weakness that fluctuates with activity. Symptoms are tested using drugs like edrophonium, and treatment includes anticholinesterases, immunosuppressants, thymectomy, and plasmapheresis. Lambert-Eaton myasthenic syndrome is another autoimmune condition where antibodies affect calcium channels, and is associated with lung cancer. Certain drugs can also induce myasthenic syndrome symptoms.
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.
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 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.
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.
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.
Dr. Nishtha Jain provides an overview of Acute Inflammatory Demyelinating Polyneuropathy (AIDP). Key points include: AIDP is an immune-mediated disorder of the peripheral nervous system, often preceded by a respiratory or gastrointestinal infection. Diagnosis involves lumbar puncture showing elevated CSF protein without pleocytosis. Electrodiagnosis can show features of demyelination. Treatment involves plasma exchange or IV immunoglobulin to remove antibodies. Prognosis is generally good, with most patients achieving near-full recovery, though respiratory failure can occasionally occur. New variants beyond classic AIDP have been recognized.
The patient is a 40-year old woman with well-controlled myasthenia gravis scheduled for radical hysterectomy. An epidural anesthetic technique will be used with propofol for induction and maintenance to avoid muscle relaxants if possible due to MG. Non-depolarizing muscle relaxants may be used carefully at reduced doses if needed. The patient's arrhythmias may be treated with neostigmine. Post-operatively, criteria for extubation include VC > 10 ml/kg, RR <30, TV > 5ml, and inspiratory force > 25 cm.
Neuromuscular junction diseases interfere with the transmission of signals from nerves to muscles and can be acquired or inherited. Myasthenia gravis is an acquired autoimmune disorder where antibodies induce acetylcholine receptor deficiency at the neuromuscular junction, causing weakness that fluctuates with activity. Symptoms are tested using drugs like edrophonium, and treatment includes anticholinesterases, immunosuppressants, thymectomy, and plasmapheresis. Lambert-Eaton myasthenic syndrome is another autoimmune condition where antibodies affect calcium channels, and is associated with lung cancer. Certain drugs can also induce myasthenic syndrome symptoms.
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.
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 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.
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.
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.
Dr. Nishtha Jain provides an overview of Acute Inflammatory Demyelinating Polyneuropathy (AIDP). Key points include: AIDP is an immune-mediated disorder of the peripheral nervous system, often preceded by a respiratory or gastrointestinal infection. Diagnosis involves lumbar puncture showing elevated CSF protein without pleocytosis. Electrodiagnosis can show features of demyelination. Treatment involves plasma exchange or IV immunoglobulin to remove antibodies. Prognosis is generally good, with most patients achieving near-full recovery, though respiratory failure can occasionally occur. New variants beyond classic AIDP have been recognized.
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.
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.
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.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
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.
Anaesthetic Considerations in Neuromuscular diseaseHemant Ojha
This document discusses anaesthetic considerations for patients with neuromuscular disorders. It begins with an introduction to neuromuscular disorders and their classification. General considerations for pre-operative, peri-operative, and post-operative management are outlined. Specific guidance is provided for various disorders like Duchenne Muscular Dystrophy, Guillain-Barré syndrome, and Myasthenia Gravis. Key points are that depolarizing neuromuscular blocking agents should generally be avoided due to risk of hyperkalemia. Non-depolarizing agents may have prolonged effects. Careful monitoring is needed due to potential respiratory and cardiac involvement. Thorough pre-operative evaluation and planning of anaesthetic approach is important for
Myasthenia gravis (MG) is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscles.
The underlying defect is a decrease in the number of available acetylcholine receptors (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack
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.
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.
Myasthenia Gravis and Guillan Barre Syndrome (Acute Inflammatory Demyelinatin...Richard Brown
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.
An 8-year-old boy presented with difficulties chewing, swallowing, and drooling, as well as weakness in his limbs that worsened throughout the day. Investigations found a decremental response on repetitive nerve stimulation and increased acetylcholine receptor antibodies, leading to a diagnosis of juvenile myasthenia gravis. An MRI also revealed a thymoma. The patient underwent thymectomy and is now on anticholinesterase medication, showing improvement in symptoms. Thymoma is a rare tumor associated with myasthenia gravis due to autoimmune dysfunction at the neuromuscular junction.
This document summarizes disorders of the neuromuscular junction, including myasthenia gravis and other myasthenic syndromes. It describes the definition, aetiology, clinical features, investigations, management, and prognosis of myasthenia gravis. It also discusses other myasthenic syndromes such as Lambert-Eaton myasthenic syndrome and compares it to myasthenia gravis. The document further summarizes diseases of muscles including muscular dystrophies, spinal muscular atrophies, and neurofibromatosis.
Myasthenia gravis is a chronic autoimmune disorder that causes variable and fatigable weakness of the skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, preventing muscle contraction. Diagnosis involves testing for these antibodies as well as the Tensilon test, where edrophonium chloride is administered intravenously to temporarily improve muscle strength in those with myasthenia gravis. Common symptoms include drooping eyelids, double vision, and fatigue or weakness of muscles that worsens with activity.
Anaesthesia for neurological and neuromuscular disease2Kanika Rustagi
The document discusses various neurological and neuromuscular diseases relevant to anaesthesia including epilepsy, multiple sclerosis, Guillain-Barre syndrome, poliomyelitis, and cerebral palsy. It covers the pathophysiology, clinical features, diagnostic criteria, and anaesthetic considerations for managing patients with these conditions. Key points discussed include preoperative assessment and planning, choice of anaesthetic agents to avoid exacerbating symptoms, special monitoring needs, and postoperative care considerations.
The document summarizes myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. MG results from antibodies blocking acetylcholine receptors at the neuromuscular junction, inhibiting nerve signal transmission. Signs and symptoms include weakness of eye, facial, swallowing, and respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies. Treatment includes anticholinesterases, immunosuppressants, plasmapheresis, IV immunoglobulins, and sometimes thymectomy. While the immune system's role is clear, further research is still needed to develop more effective medical treatments without adverse effects.
Myasthenia gravis is an autoimmune disorder where antibodies block acetylcholine receptors at the neuromuscular junction, causing muscle weakness that worsens with use and improves with rest. Symptoms can include drooping eyelids, double vision, facial weakness, and limb fatigue. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and single fiber electromyography. Treatment includes anticholinesterase medications, immunosuppressants, plasmapheresis, intravenous immunoglobulin, and sometimes thymectomy.
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.
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.
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.
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.
The document outlines the curriculum for the Family and Community Medicine residency training program at Oman Medical Specialty Board, including objectives, structure, rotations, and evaluation methods. The 4-year program covers major rotations in family medicine, internal medicine, child health, and obstetrics/gynecology as well as minor rotations in other specialties. The family medicine rotation aims to develop residents' skills and knowledge to become effective primary care physicians through training in clinical practice, communication, management, and professional development.
This document discusses several neuromuscular disorders including poliomyelitis, amyotrophic lateral sclerosis, neuropathies, myopathies, myasthenia gravis, diseases of the neuromuscular junction, botulism, and other topics. It provides details on clinical presentation, pathogenesis, diagnostic testing, and management of these conditions.
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.
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.
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.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
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.
Anaesthetic Considerations in Neuromuscular diseaseHemant Ojha
This document discusses anaesthetic considerations for patients with neuromuscular disorders. It begins with an introduction to neuromuscular disorders and their classification. General considerations for pre-operative, peri-operative, and post-operative management are outlined. Specific guidance is provided for various disorders like Duchenne Muscular Dystrophy, Guillain-Barré syndrome, and Myasthenia Gravis. Key points are that depolarizing neuromuscular blocking agents should generally be avoided due to risk of hyperkalemia. Non-depolarizing agents may have prolonged effects. Careful monitoring is needed due to potential respiratory and cardiac involvement. Thorough pre-operative evaluation and planning of anaesthetic approach is important for
Myasthenia gravis (MG) is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscles.
The underlying defect is a decrease in the number of available acetylcholine receptors (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack
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.
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.
Myasthenia Gravis and Guillan Barre Syndrome (Acute Inflammatory Demyelinatin...Richard Brown
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.
An 8-year-old boy presented with difficulties chewing, swallowing, and drooling, as well as weakness in his limbs that worsened throughout the day. Investigations found a decremental response on repetitive nerve stimulation and increased acetylcholine receptor antibodies, leading to a diagnosis of juvenile myasthenia gravis. An MRI also revealed a thymoma. The patient underwent thymectomy and is now on anticholinesterase medication, showing improvement in symptoms. Thymoma is a rare tumor associated with myasthenia gravis due to autoimmune dysfunction at the neuromuscular junction.
This document summarizes disorders of the neuromuscular junction, including myasthenia gravis and other myasthenic syndromes. It describes the definition, aetiology, clinical features, investigations, management, and prognosis of myasthenia gravis. It also discusses other myasthenic syndromes such as Lambert-Eaton myasthenic syndrome and compares it to myasthenia gravis. The document further summarizes diseases of muscles including muscular dystrophies, spinal muscular atrophies, and neurofibromatosis.
Myasthenia gravis is a chronic autoimmune disorder that causes variable and fatigable weakness of the skeletal muscles. It results from antibodies that block or destroy acetylcholine receptors at the neuromuscular junction, preventing muscle contraction. Diagnosis involves testing for these antibodies as well as the Tensilon test, where edrophonium chloride is administered intravenously to temporarily improve muscle strength in those with myasthenia gravis. Common symptoms include drooping eyelids, double vision, and fatigue or weakness of muscles that worsens with activity.
Anaesthesia for neurological and neuromuscular disease2Kanika Rustagi
The document discusses various neurological and neuromuscular diseases relevant to anaesthesia including epilepsy, multiple sclerosis, Guillain-Barre syndrome, poliomyelitis, and cerebral palsy. It covers the pathophysiology, clinical features, diagnostic criteria, and anaesthetic considerations for managing patients with these conditions. Key points discussed include preoperative assessment and planning, choice of anaesthetic agents to avoid exacerbating symptoms, special monitoring needs, and postoperative care considerations.
The document summarizes myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. MG results from antibodies blocking acetylcholine receptors at the neuromuscular junction, inhibiting nerve signal transmission. Signs and symptoms include weakness of eye, facial, swallowing, and respiratory muscles. Diagnosis involves testing for acetylcholine receptor antibodies. Treatment includes anticholinesterases, immunosuppressants, plasmapheresis, IV immunoglobulins, and sometimes thymectomy. While the immune system's role is clear, further research is still needed to develop more effective medical treatments without adverse effects.
Myasthenia gravis is an autoimmune disorder where antibodies block acetylcholine receptors at the neuromuscular junction, causing muscle weakness that worsens with use and improves with rest. Symptoms can include drooping eyelids, double vision, facial weakness, and limb fatigue. Diagnosis involves tests like the Tensilon test, repetitive nerve stimulation, and single fiber electromyography. Treatment includes anticholinesterase medications, immunosuppressants, plasmapheresis, intravenous immunoglobulin, and sometimes thymectomy.
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.
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.
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.
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.
The document outlines the curriculum for the Family and Community Medicine residency training program at Oman Medical Specialty Board, including objectives, structure, rotations, and evaluation methods. The 4-year program covers major rotations in family medicine, internal medicine, child health, and obstetrics/gynecology as well as minor rotations in other specialties. The family medicine rotation aims to develop residents' skills and knowledge to become effective primary care physicians through training in clinical practice, communication, management, and professional development.
This document discusses several neuromuscular disorders including poliomyelitis, amyotrophic lateral sclerosis, neuropathies, myopathies, myasthenia gravis, diseases of the neuromuscular junction, botulism, and other topics. It provides details on clinical presentation, pathogenesis, diagnostic testing, and management of these conditions.
The document describes a 50-year-old male who presented with a tender lump on his left shin and symptoms of fever and malaise for 5 days. The likely diagnosis is an abscess. Important investigations would include a blood sugar test. Management principles are adequate analgesia, antibiotics, adequate incision and drainage of the abscess under general anesthesia, cleaning and dressing of the wound.
1) Organ X is the vermiform appendix. A 67-year-old Malay woman presented with fever and right lower quadrant pain and was found to have a perforated appendix.
2) She underwent an appendectomy to remove the perforated appendix. Post-operatively, she is at risk for complications like an abdominal abscess.
3) Her management involved initial resuscitation, treatment of pain and fever, establishing the diagnosis of appendicitis, and an appendectomy followed by post-operative monitoring and treatment with IV antibiotics to prevent infection from the perforation.
1. The document describes an OSCE sample case involving an inguinoscrotal swelling. It provides differential diagnoses, classifications of hydrocele, and treatment approaches.
2. It also describes a case of undescended testes, including factors affecting testicular descent, treatment, and complications.
3. Additional cases include a hemangioma, hypospadias, and cleft lip, with descriptions of presentations, classifications, treatments and associated issues.
This document discusses OSCE (Objective Structured Clinical Examination), which is a clinical skills assessment used in medical education. OSCE involves candidates rotating through several stations to perform various clinical tasks within a time limit. Stations can be interactive, where an examiner observes and scores the candidate, or static, where the candidate answers questions without observation. Common interactive stations include history taking, clinical examination, and tag stations where the candidate interprets findings. The document provides examples of station profiles, checklists, and sample questions asked at different OSCE stations.
This document discusses several neuromuscular disorders including poliomyelitis, amyotrophic lateral sclerosis, neuropathies, myopathies, myasthenia gravis, diseases of the neuromuscular junction, botulism, tick paralysis, thyrotoxic periodic paralysis, and familial periodic paralysis. It provides details on clinical presentation, pathogenesis, diagnostic testing, and management for each condition.
Myasthenia gravis is an autoimmune disease characterized by weakness and fatigability of skeletal muscles caused by a decrease in acetylcholine receptors at the neuromuscular junction. Autoantibodies develop against acetylcholine receptors, impairing nerve conduction and ultimately destroying receptors. Symptoms include painless weakness that increases with activity and improves with rest, often affecting eye muscles first and sometimes spreading to other muscles. Diagnosis involves testing for acetylcholine receptor antibodies and responding to medication like Tensilon. Treatment options include anticholinesterase medications, immunosuppressants, thymectomy, plasmapheresis, IVIG, and in severe cases respiratory support.
Myasthenia gravis is an autoimmune disease characterized by weakness and fatigability of skeletal muscles caused by a decrease in acetylcholine receptors at the neuromuscular junction. Autoantibodies develop against acetylcholine receptors, impairing nerve conduction and ultimately destroying receptors. Symptoms include painless weakness that increases with activity and improves with rest, often affecting eye muscles first before spreading to other muscles. Diagnosis involves testing for acetylcholine receptor antibodies and responding to medication like Tensilon. Treatment options include anticholinesterase medications, immunosuppressants, thymectomy, plasmapheresis, IVIG, and steroids.
Myasthenia Gravis is a neuromuscular disorder characterized by fluctuating weakness that worsens with activity and improves with rest. It results from antibodies blocking or lessening the effects of acetylcholine at the neuromuscular junction. Symptoms often begin with weakness of the eye muscles or face. While treatments can help control symptoms, there is currently no cure. Management involves anticholinesterase medications, immunosuppressants, plasmapheresis, thymectomy, and ventilatory support during myasthenic crises.
Myasthenia gravis is an autoimmune disorder characterized by weakness and fatigability of skeletal muscles. It is caused by antibodies that block or destroy acetylcholine receptor sites in muscles, impairing nerve signal transmission and causing weakness. Symptoms often first affect ocular muscles and may progress to other areas. Treatment focuses on immunosuppression and thymectomy in some cases. Complications can include myasthenic crisis if respiratory muscles are affected.
Myasthenia Gravis is an autoimmune neuromuscular disorder characterized by muscle weakness and fatigability. It is caused by antibodies that block acetylcholine receptors at the neuromuscular junction, preventing muscle contraction. Symptoms vary widely and can include weakness of the eye muscles, facial muscles, limbs, and respiratory muscles. Diagnosis involves physical exams, blood tests to detect antibodies, and electrodiagnostic tests. Treatment options include acetylcholinesterase inhibitors, immunosuppressants, plasmapheresis, intravenous immunoglobulin, and thymectomy.
1. Acute flaccid paralysis (AFP) is defined as sudden onset of weakness or paralysis over 15 days in patients under 15 years old. It suggests involvement of the lower motor neuron complex.
2. Common causes of AFP include poliomyelitis, Guillain-Barré syndrome, transverse myelitis, botulism, and non-polio enteroviruses. Clinical features and investigations can help differentiate between these causes.
3. Treatment depends on the underlying etiology but may include supportive care, IV immunoglobulin, plasmapheresis, and corticosteroids. Prognosis ranges from full recovery to residual deficits or death, depending on the cause and extent of
1. Acute flaccid paralysis (AFP) is defined as sudden onset of weakness or paralysis over 15 days in patients under 15 years old. It suggests involvement of the lower motor neuron complex.
2. Common causes of AFP include poliomyelitis, Guillain-Barré syndrome, transverse myelitis, botulism, and non-polio enteroviruses. Clinical features and investigations can help differentiate between these causes.
3. Treatment depends on the underlying etiology but may include supportive care, IV immunoglobulin, plasmapheresis, and corticosteroids. Prognosis ranges from full recovery to residual deficits or death, depending on the cause and extent of
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.
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 is an autoimmune disorder where antibodies are formed against acetylcholine receptors in the neuromuscular junction, reducing their numbers and causing muscle weakness that worsens with repeated use and improves with rest. It most commonly affects the eye muscles and muscles of the face, throat, and limbs. While idiopathic in most cases, it has associations with certain genes and tumors of the thymus gland. Diagnosis involves testing muscle fatigue and response to medication, and treatment focuses on immunosuppressants, thymectomy, and supporting respiratory function to prevent crisis. Nurses monitor symptoms and respiratory status, educate on triggers and crisis response, and carefully manage medications and nutrition.
Guillain-Barré syndrome is a rare autoimmune disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and paralysis. It is considered a post-infectious disorder, often triggered by bacterial or viral infections. Clinically, it begins with pain, paresthesia, and weakness in the legs that ascends to the trunk and arms. Diagnosis involves lumbar puncture showing elevated proteins with normal cell counts and electrodiagnostic testing showing demyelination. Treatment focuses on supportive care like ventilation and immunotherapy using plasma exchange or IVIG. Recovery can take many months but most experience significant improvement.
Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy that results in demyelination and inflammation of the peripheral nervous system. It presents as rapidly progressive muscle weakness that peaks within 4 weeks. GBS is usually preceded by a bacterial or viral infection. The most common type is acute inflammatory demyelinating polyneuropathy, which involves demyelination of motor and sensory fibers. Treatment involves plasma exchange or intravenous immunoglobulin to modulate the immune response. Nursing management focuses on respiratory support, pain management, range of motion exercises, and prevention of complications.
- Guillain-Barré syndrome (GBS) is an acute inflammatory neuropathy typically presenting with progressive ascending weakness, diminished reflexes, and possible respiratory/bulbar involvement.
- It is usually triggered by a preceding infection, most commonly by Campylobacter jejuni.
- Treatment involves supportive care and monitoring given risks of respiratory failure, as well as intravenous immunoglobulin (IVIG) or plasma exchange which can improve symptoms.
Guillain-Barré syndrome is an autoimmune disorder that causes damage to the peripheral nervous system, resulting in muscle weakness and sometimes paralysis. It is often preceded by a viral or bacterial infection. The immune system mistakenly attacks the myelin sheath surrounding nerves. Clinical manifestations include symmetric weakness, sensory changes, and autonomic dysfunction. Diagnosis involves neurological exam, CSF analysis showing elevated proteins, and electrophysiological testing. Treatment focuses on plasmapheresis, IV immunoglobulin, respiratory support, and rehabilitation. Prognosis is generally good but some experience long-term symptoms. Research shows Campylobacter jejuni, cytomegalovirus, and Epstein-Barr virus infections are
AN-MSN II 09.6.2020AN-GUILLAIN BARRE SYNDROME.pptxPrakash554699
This document discusses Guillain-Barré syndrome (GBS), an acute immune-mediated polyneuropathy that results in rapid progressive motor paralysis. GBS is characterized by acute onset muscle weakness that spreads throughout the body. It is caused by an autoimmune response triggered by bacterial or viral infections. Diagnosis involves neurological exams, cerebrospinal fluid analysis, electromyography, and nerve conduction studies. Treatment aims to prevent complications through respiratory support, physical therapy, intravenous immunoglobulins, and plasma exchange. Nursing care focuses on monitoring respiratory function, range of motion exercises, and managing symptoms like pain and impaired communication.
This document provides information on myasthenia gravis (MG), including:
- MG is an autoimmune neuromuscular junction disorder causing muscle weakness.
- Treatment involves immunomodulation with pyridostigmine, corticosteroids, immunosuppressants like azathioprine and mycophenolate, IVIG, or plasma exchange.
- Diagnosis is based on symptoms, serologic testing for acetylcholine receptor (AChR) or muscle-specific kinase (MuSK) antibodies, and electrodiagnostic testing showing decremental response on repetitive nerve stimulation.
Guillain-Barré syndrome is an acute inflammatory polyneuropathy that causes generalized paralysis. It is usually triggered by a viral or bacterial infection and causes the immune system to damage nerve cells. Common symptoms include progressive muscle weakness, numbness, and pain. Treatment involves immunotherapy to reduce immune response and support for breathing and other vital functions until recovery. Most patients recover fully but a small percentage have permanent nerve damage or die from respiratory failure.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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2. In MNL : Poliomyelitis is the protypicaldisease In Poliomyelitis weakness can be asymmetrical or more often symmetrical The cerebrospinal fluid analysis resembles that of aseptic meningitis. Patients initially have a clinical picture similar to that of viral meningitis
3. In MNL : Amyotrophic lateral sclerosis is the prototypical disease In Poliomyelitis weakness can be symmetrical or more often asymmetrical The cerebrospinal fluid analysis resembles that of viral meningitis. Patients initially have a clinical picture similar to that of viral meningitis…..
4. In Amyotrophiclateralsclerosis It affects the anterior horn cells and results in lower motor neuron disease without sensory involvement Results from a degeneration of the motor neuron with sensory involvement. complain of dysarthria or ptosis findings include hyporreflexia, muscle wasting, and fasciculation Pain is not a component of the clinical picture….
5. In Amyotrophiclateralsclerosis Poliomyelitis affects the anterior horn cells and results in lower motor neuron disease without sensory involvement Results from a degeneration of the motor neuron without sensory involvement. complain of dysarthria or dysphagia findings include hyperreflexia, muscle wasting, and fasciculation Pain is not a component of the clinical picture….
6. In MNL all are true except: lesions at the level of the brainstem or above produce bilateral weakness bilateral weakness caused by lesions above the spinal cord is associated with a change in mental status or cranial nerve involvement Lesions of the central nervous system result in spasticity, hyperreflexia, and extensor plantar reflexes bilateral upper motor neuron signs with normal mental status, neuroimagingshould focus on looking for a lesion in the spinal cord
7. In MNL : lesions at the level of the brainstem or above produceunilateralweakness bilateral weakness caused by lesions above the spinal cord is generally associated with a change in mental status or cranial nerve involvement Lesions of the central nervous system result in spasticity, hyperreflexia, and extensor plantar reflexes when bilateral upper motor neuron signs are found in conjunction with normal mental status, diagnostic testing including neuroimaging should focus on looking for a lesion in the spinal cord
8. In Neuropathies , all are true EXCEPT : a grip strength or foot-drop may be noted first patients usually note a slowly progressive course of symptoms. A disorder of transmission often leads to increased production of AChreceptors. Patients usually have intact sensation sensation.
9. In Neuropathies : a grip strength or foot-drop may be noted first patients usually note a slowly progressive course of symptoms. A disorder of transmission often leads to increased production of AChreceptors. Patients exhibit varying degrees of altered sensation
10. In Myopathies , all are true EXCEPT: Myopathies produce generalized, symmetrical weakness muscle tone is usually diminished, but sensation is preserved. Generally cause muscle pain and tenderness Reflexes are present but diminished
11. In Myopathies Myopathies produce generalized, symmetrical weakness muscle tone is usually diminished, but sensation is preserved. Metabolic disorders affecting muscle strength are painless in nature Reflexes are present but diminished
12.
13. In MG all the following are true except: Normally, vital capacity values range from 60 to 70 mL/kg. the forced vital capacity reaches 15 mL/kg, intubation is necessary Arterial blood gas is helpful as most of the patients have sufficient protective reserve and hypercapniadevelps early presence of swallowing and a strong cough suggests that the patient has sufficient protective and ventilatory reserve
14. In MG : Normally, vital capacity values range from 60 to 70 mL/kg. the forced vital capacity reaches 15 mL/kg, intubation is necessary Arterial blood gas is not necessarily helpful because functional reserve can be severely diminished by the time a patient develops either hypercarbia or hypoxia presence of swallowing and a strong cough suggests that the patient has sufficient protective and ventilatory reserve
15. In Diseases of the Neuromuscular Junction Repeated stimulation leads to diminishing motor strength, which is caused by : the blockage of the receptors as in organophosphate poisoning a decrease in the amount of ACh released as in botulism inactivating Ach by irreversibly binding with it as in MG Down regulation of the Ach receptors as in Atropinized patients
16. In Diseases of the Neuromuscular Junction Repeated stimulation leads to diminishing motor strength, which is caused by : the blockage of the receptors as in MG a decrease in the amount of ACh released as in botulism inactivating Ach by irreversibly binding with it as in organophosphate poisoning Down regulation of the Ach receptors as in Atropinized patients
17. decrease in the release of ACh may produceexcept decreased visual acuity low-grade fever dry, flushed skin Bradycardia urinary retention
18. decrease in the release of ACh may produce: decreased visual acuity low-grade fever dry, flushed skin Tachycardia urinary retention
19. All are true about Myopathies , except: generalized, symmetrical weakness Reflexes are present muscle tone is usually diminished sensation is lost Are always painful
20. All are true about Myopathies : generalized, symmetrical weakness Reflexes are present muscle tone is usually diminished sensation is preserved Are always painful
21. Lambert-Eatonmyasthenicsyndromeall are false except : 50% of cases are associated with non small cell carcinoma of the lung Clinically includes weakness that improves with use of muscles….. autonomic dysfunction, most commonly seen as flushed skin. Management with IVIG has been reported to be sufficient.
22. Lambert-Eatonmyasthenicsyndrome: 50% of cases are associated with small cell carcinoma of the lung Clinically includes weakness that improves with use of muscles autonomic dysfunction, most commonly seen asdry mouth. Management primarily focuses on treating the underlying neoplastic disorder
23. Regarding MG , all are true except: Age of onset is bimodal MG results from autoantibodies directed against the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction Ocular symptoms are often the first manifestation of MG Bulbar muscles are spared
24. Regarding MG : Age of onset is bimodal MG results from autoantibodies directed against the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction Ocular symptoms are often the first manifestation of MG Bulbar muscles may be involved
35. What is Icepacktest ? it is applied to the affected eye for approximately 2 minutes the distance between the lids is measured again prospective evaluation of the ice bag approach found the test result to be positive (an improvement in distance of at least 2 mm) in 80% of patients with MG and in no patients without MG.[7]
36. defined as respiratory failure leading to mechanical ventilation Occurs in 15 to 20% of patients with MG within the first 2 years of disease onset precipitant may not be found in 3 % of cases In MyasthenicCrisis all are true Except:
37. In MyasthenicCrisis : defined as respiratory failure leading to mechanical ventilation Occurs in 15 to 20% of patients with MG within the first 2 years of disease onset precipitant may not be found in 30% of cases
41. Regarding MG Management all are true EXCEPT: in the setting of acute exacerbation of MG , The use of intravenous pyridostigmine is recommended the initiation of corticosteroids in patients with moderate to severe weakness may improve the outcome Thymectomy is recommended for patients younger than 60 IVIG is preferred over PE due to the side effects of the later.
42. Regarding MG Management: in the setting of acute exacerbation of MG , The use of intravenous pyridostigmine is NOT recommended the initiation of corticosteroids in patients with moderate to severe weakness may improve the outcome Thymectomy is recommended for patients younger than 60 IVIG is preferred over PE due to the side effects of the later.
43. Regarding P.E in M.G : The fall in AChR levels is not associated with improvement in symptoms of MG. complications include hypotension or anticoagulation. It is safe in children. many case series showed long-term benefit in myasthenic crisis.
44. Regarding P.E in M.G : The fall in AChR levels is associated with improvement in symptoms of MG. There is a risk of complications from hypotension or anticoagulation. Because of safety concerns, clinical trials have not been done in children. Although there are no randomized controlled studies, a review yielded many case series with short-term benefit, especially in myasthenic crisis.
45. Regarding Botulism , all are true except: Most common type is infant Botulism Clostridium botulinum is an anaerobic, spore-forming bacterium types A, B, and C toxins cause human disease…. botulinum toxin works by binding irreversibly to the presynaptic membrane of peripheral and cranial nerves, inhibiting the release of ACh at the peripheral nerve synapse
46. Regarding Botulism : Most common type is infant Botulism Clostridium botulinum is an anaerobic, spore-forming bacterium types A, B, and E toxins cause human disease…. botulinum toxin works by binding irreversibly to the presynaptic membrane of peripheral and cranial nerves, inhibiting the release of ACh at the peripheral nerve synapse
47. In Botulism , all are true except : There is no pain The onset of symptoms is 6 to 48 hours after the ingestion of tainted food descending, symmetrical, flaccid paralysis diplopia, dysarthria, and dysphagia are the first signs Pupils are often fixed and reactive to light…
48. In Botulism : There is no pain The onset of symptoms is 6 to 48 hours after the ingestion of tainted food descending, symmetrical, flaccid paralysis diplopia, dysarthria, and dysphagia are the first signs Pupils are often dilated and not reactive to light…
49. Regarding Botulisim antitoxin there is a risk of anaphylaxis and serum sickness It is known to decrease ventilator dependence the antitoxin should be administered once the toxin can be identified in serum and stool the antitoxin should be administered as soon as possible An intravenous human botulism immune globulin (BIG-IV) has been developed for treatment of wound related botulism
50. Regarding Botulisim antitoxin there is a risk of anaphylaxis and serum sickness although it is not clear that the antitoxin decreases ventilator dependence the antitoxin should be administered as soon as possible (clinical findings and exclusion of other processes) An intravenous human botulism immune globulin (BIG-IV) has been developed for treatment of infantile botulism
51. In TickParalysis, all are true except an acute, ascending, flaccid motor paralysis Usually starts after 6-12 days from female tick has attached and begun to feed fixed and dilated pupils associated with the disease. Intubation may be necessary after tick removal
52. In TickParalysis an acute, ascending, flaccid motor paralysis Usually starts after 1-2 days from female tick has attached and begun to feed fixed and dilated pupils associated with the disease. Intubation may be necessary after tick removal
53. In ThyrotoxicPeriodicParalysis , all are true EXCEPT: It is due to decreased sodium-potassium adenosine triphosphatase activity Treatment of the hyperthyroid symptoms helps the treatment of the paralysis There is probably a genetic feature underlying this disorder all patients have thyroid function testing done after a first episode of hypokalemic paralysis
54. In Thyrotoxic Periodic Paralysis It is due to increased sodium-potassium adenosine triphosphatase activity Treatment of the hyperthyroid symptoms helps the treatment of the paralysis There is probably a genetic feature underlying this disorder all patients have thyroid function testing done after a first episode of hypokalemic paralysis
55. In Familial Periodic Paralysis all are true EXCEPT: autosomal-dominant disorders of ion channels intermittent attacks of flaccid extremity weakness associated with either hyperkalemia or hypokalemia bulbar and respiratory muscles may be affected. The onset of symptoms often follows a high carbohydrate intake and a period of rest. An electrocardiogram, which should be done immediately
56. In Familial Periodic Paralysis: autosomal-dominant disorders of ion channels intermittent attacks of flaccid extremity weakness associated with either hyperkalemia or hypokalemia bulbar and respiratory muscles not affected. The onset of symptoms often follows a high carbohydrate intake and a period of rest. An electrocardiogram, which should be done immediately
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63. Which of the following statements is true? a. Herpes zoster is often associated with motor dysfunction with or without a rash. b. Acute rabies infection typically begins as a Ramsay-Hunt syndrome before progressing to severe throat spasm and to cardiac and renal failure. c. Weakness or diplopia when fatigued may be the only complaint with multiple sclerosis. d. Treatment for polymyositis is early administration of systemic steroids. e. Serum calcium should be measured in patients with recurrent generalized weakness that follows periods of heavy exertion or that is present upon awakening.
64. The answer is c. Ramsay-Hunt syndrome refers to herpes zoster involving the tympanic membrane, ear canal, and other areas in the distribution of the sensory branches of the facial nerve. Herpetic zoster may result in motor abnormalities in up to 25% of cases. Weakness or diplopia only on exertion is a common complaint in early cases of multiple sclerosis. Another early presenting sign is retrobulbar neuritis; in fact, 50–75% of cases occur in patients who develop multiple sclerosis. Steroids may transiently exacerbate weakness in patients with polymyositis and should not be started on patients who will be discharged from the ED. Acute periodic paralysis appears to involve abnormalities in cellular function, possibly related to potassium transport. The disease is most common in young men. No specific physical findings may be found and it is often misdiagnosed as hysterical in origin
65. 2. A 34-year-old woman with known myasthenia gravis presents in respiratory distress. She is unable to move without assistance. Her vital signs are: temperature 36◦C (96.8◦F), heart rate 50/min, blood pressure 100/60 mm Hg, respiratory rate 35/min and shallow. She is drooling and has upper airway rhonchi and bilateral wheezing. Her respiratory rate appears to be decreasing. You immediately: a. Administer 2–4 mg of intravenous edrophonium. b. Perform endotracheal intubation. c. Administer 1 mg of atropine; if there is an improvement in her wheezing, administer pralidoxime. d. Start an intravenous atropine drip. e. Arrange emergent hyperbaric therapy.
66. The answer is b You should be able to differentiate a myasthenic crisis from a cholinergic crisis. Both can present with progressive muscle weakness and respiratory depression, dysphagia, and other physical signs. Bradycardia, wheezing, and salivation suggest cholinergic crisis. A common error is to mistake a cholinergic as a myasthenic crisis and administer additional acetylcholinesterase inhibitor. The immediate treatment for either type is ABCs and intubation at the first clinical signs of respiratory failure. In a cholinergic crisis, atropine can be used for the muscarinic symptoms, but it is not a substitute for airway management and ventilatory assistance.
67. A 13-year-old girl presents with a 3-day history of malaise, low-grade fever, and double vision with unilateral ptosis. The potential diagnosis of botulism is best supported by finding: a. Acute renal failure. b. Cardiac failure. c. Bilateral numbness of hands and feet. d. Acute urinary retention. e. Pseudomembranouspharyngitis.
68. The answer is d Both botulism and diphtheria may present with acute bulbar nerve palsies, weakness of any or all extremities, and cholinergic manifestations, such as urinary retention and colicky pain. In both diseases, the most common early neurologic findings are ptosis, double vision, and difficulty in accommodation. Diphtheria is an acute febrile illness. A primary symptom is a severe pseudomembranouspharyngitis presenting with severe throat pain and excessive saliva production. In diphtheria, cardiotoxic and renal abnormalities are direct results of the elaborated bacterial toxin.
69. A 34-year-old woman with myasthenia gravis presents with flank pain and fever of 103.4◦F. She is allergic to penicillin, and despite boluses of intravenous fluid and antibiotic therapy, she becomes hypotensive. A medicine that you can safely use in her management is: a. Gentamicin. b. Vecuronium. c. Lidocaine. d. Procainamide. e. Succinylcholine.
70. The answer is c Aminoglycoside antibiotics have some curare-type effects on the motor endplate; if they are used in the myasthenic patient, the physician should be prepared to treat paralysis and respiratory arrest. Obviously, these patients are more susceptible to muscle-paralyzing agents as well. Phenytoin, quinidine, procainamide, and lithium can also adversely affect patients with myasthenia gravis.
73. An extract from the bark and stems is the source of a potent isoquinoline alkaloid used in the deadly poison curare. Amazonian Indians use the gummy extract to coat the poison darts of their blowguns. The alkaloid D-tubocurarine blocks acetylcholine receptor sites at neuromuscular junctions, causing relaxation and paralysis of muscles, including respiratory organs and the heart.
74. In fact, D-tubocurarine has been used to relax the heart muscle during open heart surgery.
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76. The answer is a Neuropathies tend to have the following characteristics: proximal progression of symptoms sensory deficits often in a stocking glove distribution early loss of DTRs. Myopathiescharacteristically present with proximal motor weakness myalgias delayed loss of DTRs CPK enzymes may be elevated. There are exceptions to these generalizations.
77. Lambert-Eaton MyasthenicSyndrome results from an autoimmune attack directed against the voltage-gated calcium channels (VGCCs) on the presynaptic motor nerve terminal. This results in a loss of functional VGCCs at the motor nerve terminals. The number of quanta released by a nerve impulse is diminished. However, because presynaptic stores of ACh and the postsynaptic response to ACh remain intact, rapid repetitive stimulation or voluntary activation that aids in the release of quanta will raise the endplate potential above threshold and permit generation of muscle action potential. As neuromuscular transmission is completed at additional neuromuscular junctions, a transient increase will occur in the strength of the muscle. Parasympathetic, sympathetic, and enteric neurons are all affected. Clinically, this phenomenon is noted by the appearance of previously absent tendon reflexes following a short period of strong muscle contraction by the patient.
78. Myasthenia Gravis Autoantibodies (immunoglobulin G [IgG]) develop against ACh nicotinic postsynaptic receptors for unknown reasons, although certain genotypes are more susceptible.2 Cholinergic nerve conduction to striated muscle is impaired by a mechanical blockage of the binding site by antibodies and, ultimately, by destruction of the postsynaptic receptor.Patients become symptomatic once the number of ACh receptors is reduced to approximately 30% of normal. The cholinergic receptors of smooth and cardiac muscle have a different antigenicity than skeletal muscle and are not affected by the disease.The role of the thymus in the pathogenesis of myasthenia gravis is not entirely clear, but 75% of patients with myasthenia gravis have some degree of thymus abnormality (eg, hyperplasia in 85% of cases, thymoma in 15% of cases). Given the immunologic function of the thymus and the improvement in the clinical condition of patients following thymectomy, the thymus is suspected to be the site of autoantibody formation. However, the stimulus that initiates the autoimmune process has not been identified