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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is much individual variability in the clinical manifestations of hypocalcemia. The rapidly of the development of hypocalcemia will determine whether or not symptoms will be present. Signs and symptoms of hypocalcemia consisted of tetany (Chvostek's and Trousseau's signs), seizures, diminshed to absent deep tendon reflexes, papilledema, mental changes (weakness, fatigue, irritability, memory loss, confusion, delusion, hallucination), and skin changes. Etiologic factors for hypocalcemia in man include (1) decreased calcium absorption or increased loss from the gastrointestinal tract; (2) parathyroid hormone deficiency; (3) skeletal resistance to parathyroid hormone; (4) ineffective parathyroid hormone; (5) decreased production or increased degradation of 25-hydroxycholecalciferol or 1,25-dihydroxycholecalciferol; (6) increased complex formation with calcium; (7) increased skeletal uptake of calcium; (8) hypomagnesemic state; and (9) direct inhibition of bone resorption. Measurement of total and ionic calcium, magnesium, parathyroid hormone, vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol), and nephrogenous cyclic adenosine monophosphate are especially helpful in the laboratory evaluation of the hypocalcemic patient.
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PMID:Hypocalcemia. Differential diagnosis and mechanisms. 22 22

Power output and blood flow were determined in dogs for four muscles (gastrocnemius, latissimus dorsi, rectus abdominis, and triceps) to determine effects of choice of muscle, tetany or twitch rates, force loading of the muscle, and blood flow on muscle power output. Total power for a 20-Kg dog was greatest for triceps at 0.77 watts (W) and least for rectus at 0.22 W; power per gram was greatest for gastrocnemius at 5.77 mW/g. Muscle perfusion of latissimus and rectus is greatly decreased by overstretching of the muscle. Overstretching also produces severe, persistent, power loss in latissimus and rectus muscles. Gastrocnemius and triceps tolerate stretching much better. We conclude that power can be improved without causing muscle fatigue by choice of muscle, choice of electrical stimulation parameters, linear geometry for contraction of the muscle, and matching the force load to each individual muscle.
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PMID:Comparison of canine skeletal muscle power from twitches and tetanic contractions in untrained muscle: a preliminary report. 183 65

Significant improvement in symptoms of disabling cramps and muscle spasms was obtained in 9 patients with motor neuron diseases, tetany, and myotonic disorders who were treated with tocainide, a lidocaine analog. No significant side effects were observed except for light-headedness and fatigue in 1 patient, who also showed slight prolongation of intraventricular conduction time. Tocainide is useful in treating disabling muscle spasms and cramps associated with conditions characterized by neuromuscular irritability. This effect is probably based on stabilization of the membrane potential at various levels (motor neurons, peripheral nerve, or muscle fiber membrane).
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PMID:Tocainide therapy in muscle cramps and spasms due to neuromuscular disease. 176 57

Total Body Potassium (TBK) was measured by whole body counting of 40K in 3 patients with Bartter's syndrome before, after 3 months and after 1 year of treatment with enalapril. In 2 patients TBK was found to be decreased before treatment, whereas TBK was within the normal range in the 3rd. During treatment serum potassium concentration and TBK increased in each subject and symptoms of fatigue and tetany disappeared. Enalapril is shown to be an effective treatment in Bartter's syndrome as it improves serum potassium, TBK and complaints.
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PMID:Total body potassium in Bartter's syndrome before and during treatment with enalapril. 303 21

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.
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PMID:Endocrine myopathies. 306 2

Dynamic and static stretch responses in muscle spindles were investigated in fatigued muscle to determine if acute adaptations do occur in receptor discharge as has been shown after contractions of short duration. Fatigue to 60-50% maximum tetanic tension was induced in the isolated gastrocnemius muscle in 16 cats by sustained, 7 X threshold electrical stimulation (100 Hz) of the cut L7 ventral root and S1 ventral root. Group Ia and II afferent fiber responses to slow ramp stretches (5 mm X s-1) and vibration (100 Hz) applied to the Achilles tendon were monitored before and immediately after muscle tetany to fatigue. Changes in firing characteristics were similar when results from faster (25-30 mm X s-1) ramp stretches were contrasted. During muscle fatigue, decreases in response latency to displacement and increases in resting discharge, mean frequency during stretch, and frequency of firing to vibration were predominant in both afferent fiber types. Static responses were generally lower, indicating a decrease in position sensitivity. Resting muscle force and passive peak muscle stiffness were consistently higher following contraction. The sum effects of these proprioceptive afferent and mechanical muscle responses would be to increase muscle stiffness and thus resist yield in muscle length to perturbations at lower muscle forces. The magnitude of these adaptations in proprioceptive discharge appears dependent on intrafusal muscle fiber activation.
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PMID:Dynamic and static stretch responses in muscle spindle receptors in fatigued muscle. 316 75

Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
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PMID:Magnesium and inflammatory bowel disease. 329 19

We have observed a high frequency of chronic Candida albicans infection and of allergic sensitization to candida among patients with normocalcemic latent tetany (LT). Among 50 LT patients, 34% suffered from recurrent or chronic candida infection by history, 24% showed evidence of active infection and 48% demonstrated type I hypersensitivity to C. albicans extract on intradermal testing. Treatment with oral antifungal drugs and allergy desensitization to Candida produced complete relief of symptoms in 44% of the patients, with remission occurring for symptoms of depression, irritable bowel syndrome, fatigue, premenstrual tension, headache, anxiety and back pain. The complex relationship between candidiasis and Mg deficit is discussed. Patients with LT, refractory symptoms and a history of prolonged antibiotic exposure or recurrent candida infection should be considered for oral antifungal therapy and candida desensitization.
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PMID:Normocalcemic tetany and candidiasis. 391 83

The classical symptoms of malabsorption syndrome are diarrhea, steatorrhea, weight loss, and fatigue. Tetany, ecchymosis, anorexia, bone pain, pallor, muscle wasting, hyperpigmentation, apathy, digital clubbing, abdominal distention which contrasts in view of the reduced common statement are other signs of malabsorption. Long before the onset of these symptoms there may be a disinterest in regular daily activities often associated with the passage of three soft stools per day and with the remarkable sign of difficulties in flushing bulky stools. Anamnesia, clinical examination in connection with common laboratory findings, small intestinal x-rays and endoscopic investigations associated with biopsies of the small (and large) bowel as well as estimation of stool fat excretion, xylose- and Schilling-test allow the diagnosis in most of the cases.
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PMID:[Clinical aspects and differential diagnosis of malabsorption]. 684 29

An analytic method based on simulation and modeling of long-term 45Ca2+ efflux data was used to estimate Ca2+ contents (nmol Ca2+/g tissue wet wt) and exchange fluxes (nmol Ca2+.min-1.g-1) for extracellular and intracellular compartments in in vitro hamster diaphragm. Three physiological states were studied: control (n = 5), acute fatigue (after repeated tetany; n = 5), and long-lasting fatigue (1-h recovery; n = 5). Experimental muscles were loaded with 45Ca2+ for 1 h, and efflux data were collected for 8 h by use of a flow-through tissue chamber. Induction of acute diaphragm fatigue led to a uniform 200% elevation of the 8-h efflux curve (expressed as dpm.min-1.mg-1) relative to control. Conversely, in long-lasting fatigue the early component of the efflux curve was depressed compared with control, whereas the balance of the curve was restored to baseline. Analysis of control efflux data revealed that the early curve (0-2 h) contained data on two rapidly exchanging extracellular Ca2+ compartments, whereas the late curve (2-8 h) reflected information on two slowly exchanging intracellular compartments. Modeling of acute fatigue efflux data estimated a 239% increase in one extracellular Ca2+ compartment (putative t-tubular membrane) and a 546% increase in one intracellular Ca2+ compartment (putative terminal cisternae). These increase accounted for the model prediction of a twofold rise in total diaphragm Ca2+. The kinetic data were quantitatively consistent with the hypothesis that diaphragm Ca2+ overload in acute fatigue required sarcolemmal Ca2+ permeability to double and Ca2+ diffusion into the t-tubular and terminal cisternal compartments to escalate nearly threefold. Fitting of long-lasting fatigue efflux data was associated with the sole prediction that t-tubular membrane Ca2+ was reduced to less than one-half of the control value.
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PMID:Compartmental analysis of Ca2+ kinetics in long-lasting diaphragm fatigue: loss of t-tubular membrane Ca2+. 880 8


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