generate barcode in asp.net using c# THE METABOLIC AND TOXIC MYOPATHIES in Microsoft Office

Generating QR Code 2d barcode in Microsoft Office THE METABOLIC AND TOXIC MYOPATHIES

THE METABOLIC AND TOXIC MYOPATHIES
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The administration of thyroxine corrects the muscle disturbance Pathogenesis of the Thyroid Myopathies How thyroid hormone affects the muscle ber is still a matter of conjecture Clinical data indicate that thyroxine in uences the contractile process in some manner but does not interfere with the transmission of impulses in the peripheral nerve across the myoneural junction or along the sarcolemma In hyperthyroidism this functional disorder enhances the speed of the contractile process and reduces its duration, the net effect being fatigability, weakness, and loss of endurance of muscle action In hypothyroidism, muscle contraction is slowed, as is relaxation, and its duration is prolonged The speed of the contractile process is related to the quantity of myosin adenosinetriphosphatase (ATPase), which is increased in hyperthyroid muscle and decreased in hypothyroid muscle The speed of relaxation depends on the rate of release and reaccumulation of calcium in the endoplasmic reticulum This is slowed in hypothyroidism and increased in hyperthyroidism (Ianuzzo et al) The myopathic effects of hypothyroidism need to be distinguished from those of a neuropathy, which may rarely complicate hypothyroidism (page 1151)
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surable decrease in the uptake of amino acids and protein synthesis by muscle cells Acute Steroid Myopathy (Critical Illness Myopathy; Acute Quadriplegic Myopathy) In addition to the well-known proximal myopathy induced by the long-term use of steroids, an acute and severe myopathy has been recognized in critically ill patients It was described initially in patients with severe asthma who were exposed to high doses of steroids Subsequently this acute myopathy has been recognized with numerous critical systemic diseases and organ failures, again, in the context of treatment with high doses of corticosteroids and, in a few cases, with sepsis and shock alone The use of neuromuscular blocking agents appears to play an important complementary role in the genesis of the myopathy, being a factor in over 80 percent of reported cases, but it is uncertain whether these agents alone can produce a similar process (see reviews by Gorson and Ropper, Lacomis et al, and Barohn et al) Patients who acquire this problem have generally been exposed to high doses of corticosteroids, sometimes for only brief periods Exceptional instances have been reported in which the myopathy was induced by doses as low as 60 mg prednisone administered for 5 days, but we have not encountered such a case The degree and type of simultaneous exposure to neuromuscular blocking agents has varied, but the doses have generally been quite high, falling in the range of a total dose of 500 to 4000 mg of pancuronium or its equivalent over several days The severe muscle weakness usually becomes evident when the systemic illness subsides, as attempts are made to wean the patient from the ventilator The tendon re exes are normal or diminished and there may be confounding features of a polyneuropathy, which is also known to be induced by critical illness and sepsis (page 1128) Most of our patients with acute myopathy have recovered over a period of many weeks after the corticosteroid agent has been withdrawn, but a few have remained weak for as long as a year Serum CK is elevated, at least early in the process The EMG discloses the characteristic features of a myopathy; often there are brillations as well, theorized to be due to separation of the motor end-plate region from intact segments of muscle bers Polyneuropathy and residual effects of neuromuscular blockade can be excluded by appropriate electrophysiologic studies Muscle biopsy shows varying degrees of necrosis and vacuolation affecting mainly type 2 bers The most characteristic feature is a striking loss of thick (myosin) laments Severe degrees of muscle necrosis have been accompanied by massively elevated CK levels and by myoglobinuria and renal failure Several experimental observations may explain the apparent additive effect on muscle of corticosteroids and neuromuscular blocking agents Animals exposed to high doses of steroids soon after muscle denervation display a selective loss of myosin, the characteristic nding of acute steroid myopathy This depletion of myosin is reversed by reinnervation but not by withdrawal of the corticosteroids Furthermore, denervation of muscle has been found to induce an increase in glucocorticoid receptors on the surface of the muscle Dubois and Almon have postulated that exposure to neuromuscular blocking agents creates a functional denervation, rendering the muscle ber vulnerable to the damaging effects of steroids It is curious that this myopathy has not been seen after high-dose corticosteroid administration for neurologic diseases such as multiple sclerosis, but the observation of Panegyres and colleagues of a patient with myasthenia who developed a severe,
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