Emg is used to diagnose primary muscle disorders and

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EMG is used to diagnose primary muscle disorders and disorders that affect the neuromuscular junction The function of muscles is indicated by the strength and pattern of their electrical activity. Normally, there is no electrical activity in a muscle at rest. If a muscle disease is present, there may be electrical activity in the rested state and abnormal activity when the muscle contracts. Repetitive stimulation can result in muscle becoming fatigued Acetylcholinersterase is a naturally-occurring chemical that breaks up the acetylcholine in the synaptic cleft after impulse transmission. An anticholinesterase drug will prevent release of acetylcholinesterase, so the acetylcholine in the synaptic cleft will not be broken down. Having the acetylcholine linger in the gap will increase the chance of contraction impulse being transmitted in the presence of fewer functioning acetylcholine receptors on the muscle fiber.
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Blood testing revealed high levels of an anti- acetylcholine receptor antibody in her plasma. Blood tests are performed to determine serum levels of certain antibodies (e.g., AChR-binding antibodies, AChR-modulating antibodies, antistriational antibodies). High levels of these antibodies may indicate MG Differential diagnosis Supporting or refuting information Myasthenia gravis Botulism Idiopathic inflammatory myopathies It is an autoimmune disease in which the patients have developed immunity against their own acetylcholine-activated ion channels. The end plate potentials that occur in the muscle fibers are mostly too weak to stimulate the muscle fibers. If it is intense enough, patients die of paralysis of the respiratory muscles. A paralytic illness caused by the neurotoxin produced by Clostridium botulinum, which is a large, gram-positive anaerobic bacillus. Symptoms similar to myasthenia gravis (MG) but there may be hypotension, bradycardia, diarrhea followed by constipation, and urinary retention Heterogeneous group of muscular disorders characterised by progressive muscle weakness. Presentation is sub-acute or chronic and rarely acute. May be associated with dysphagia, fatigue, difficulties with breathing, and skin lesions QUESTIONS 1. What effect would an AChE inhibitor have at the neuromuscular junction? 2. How would a large reduction in extracellular [Ca2+] affect synaptic transmission at the neuromuscular junction?
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3. What is the ionic mechanism that underlies the endplate potential (EPP) produced by acetylcholine (ACh) release? ANWERS 1. AChE inhibitor will prevent the release of AChE which degrades acetylcholine in the synaptic cleft after impulse transmission leading to increased level of Ach at the neuromuscular junction which will increase muscle contraction.
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