Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two trials were conducted to evaluate the effect of dietary replacement of .30% sodium chloride (NaCl) with a sodium-equivalent amount of sodium bicarbonate (NaHCO3) on leg weakness in swine. Three lines of Duroc swine established by six generations of divergent selection for front leg structure were used. In the first trial, a total of 80 low-line (increased leg weakness), 75 high-line (decreased leg weakness), 80 control-line (intermediate leg weakness) and 80 high x low pigs were used. Pigs were assigned within litter to an experimental or control diet and tested from approximately 37 to 104 kg live weight. The experimental diet contained .43% NaHCO3, replacing .30% NaCl in the control diet. Pigs had ad libitum access to feed. In the second trial, 48 high- and 48 low-line pigs were fed the same diets from 29 to 104 kg. At the completion of each trial, pigs were scored for various leg traits. The model used for statistical analyses included the effects of replicate, genetic line, dietary treatment and the dietary treatment x genetic line interaction. Trials were analyzed separately. Results indicated that there was no significant improvement in clinical signs of leg weakness due to dietary supplementation with NaHCO3 for front leg structure and movement, rear leg movement or rear toe size. Rear hock angle was improved in Trial 1 (P less than .05) but was reduced in Trial 2 (P less than .10).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary sodium bicarbonate on leg structure in Duroc swine that differ genetically for leg weakness. 217 Mar 18

The effect of replacing dietary sodium chloride by sodium bicarbonate on leg weakness, osteochondrosis and growth in young fattening pigs was studied in two experiments using 104 and 126 animals. The experimental pigs were fed 0.43% dietary sodium bicarbonate, which replaced the sodium chloride (0.30%), was present in the diets of the control groups. It was found that the clinical symptoms of leg weakness could be improved significantly in the experimental group which received bicarbonate. No positive effects on osteochondrosis, however, could be shown. The treated animals even tended to have more severe osteochondral lesions. Reasons for the negative tendency are discussed. Daily weight gain and food conversion were not influenced by the experimental bicarbonate diet excluding a chloride deficiency. Differences in carcass grading were not significant, although barrows fed the NaHCO3-containing diet tended to score better, while the carcass quality of the experimental gilts was slightly less in comparison to the control animals.
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PMID:The effect of replacement of 0.30% sodium chloride by 0.43% sodium bicarbonate in rations of fattening pigs on leg weakness, osteochondrosis and growth. 301 10

Hypernatremia (sodium chloride intoxication) is described in two calves due to presumed mixing errors of oral electrolyte solutions while undergoing therapy for neonatal diarrhea. The experimental induction of hypernatremia in two clinically normal calves is also reported. Physical findings in diarrheic calves included depression, weakness, dehydration, and diarrhea. Serum sodium concentrations were found to be 171.6 mEq/l and 208.0 mEq/l, respectively. Treatment with intravenous fluids was attempted in both cases, but one calf died after 6 hours and the other calf died after 2 days and exhibited periodic convulsions before death. Experimental induction with oral administration of 1 l of electrolyte concentrate, which contained approximately 2750 mEq sodium revealed that the normal calves would willingly consume the solution as mixed with milk and develop clinical signs of hypernatremia within 6 hours of administration. Serum sodium concentrations of 176.0 and 179.8 were found in the experimental calves and coincided with the onset of overt depression and weakness, at which time they were euthanatized. Cerebrospinal fluid electrolyte analysis paralleled the serum electrolyte alterations.
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PMID:Hypernatremia in calves. 322 59

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49

Salt poisoning developed in captive sandhill cranes (Grus canadensis) when sea salt was added to normal drinking water to produce a sodium chloride concentration of 1%. Two of 18 cranes died and 2 were euthanatized when moribund. Muscle weakness, paresis, dyspnea, and depression were observed. Brain and serum sodium, serum uric acid, and plasma osmolality values were abnormally high. Lesions were those of visceral gout, renal tubular necrosis, nephrosis, and skeletal muscle necrosis.
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PMID:Iatrogenic salt poisoning in captive sandhill cranes. 732 5

In 4 cases of metabolic alkalosis with paradoxic aciduria in cattle, generalized muscle weakness was the predominant feature. In 3 of the 4 cases, prolonged anorexia preceded development of muscle weakness and aciduria. Plasma electrolyte concentrations varied but, in 3 of 4 cases, a transient decrease in plasma potassium concentration was detected. In the 3 cases in which prolonged therapy with sodium chloride, potassium chloride, and dextrose was offered, resolution of aciduria was rapid, followed by correction of metabolic alkalosis and return of muscle strength.
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PMID:Metabolic alkalosis with paradoxic aciduria in cattle. 744 Mar 50

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

Broiler chicks in different groups were fed furazolidone (0, 400 and 800 mg/kg feed) and sodium chloride (500 and 1510 mg/kg feed) separately and concurrently from 1 to 30 days of age. Furazolidone (Fz) induced ascites, leg weakness, convulsions, depression and mortality was exacerbated by concurrent feeding of 1510 mg NaCl. Hemorrhages in the liver, swollen kidneys, pallor of the kidneys and cystic testes were present in all birds fed furazolidone either alone or in combination with NaCl. However, at microscopic level, necrotic changes were observed in the liver and kidneys of birds fed NaCl only. Fz-induced cardiac ventricular dilatation and thinning of walls were more severe when 400 mg Fz was fed concurrently with 1510 mg NaCl but feeding of 800 mg Fz with the same level of NaCl resulted in partial amelioration of cardiac changes. It is suggested that high dietary NaCl may exacerbate and alter the clinical and morphological picture of Fz toxicosis.
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PMID:Effect of concurrent feeding of furazolidone and sodium chloride upon some clinical, pathological and cardiac morphometric parameters in broiler chicks. 859 92

Gitelman's syndrome is an autosomal recessive disorder caused by various mutations of the thiazide- sensitive sodium chloride cotransporter gene. Hypokalaemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria are major clinical features of the syndrome. The onset of the disease is in early adulthood with a mild muscle weakness complaint or incidentally diagnosed hypokalaemia by blood test. However, it has a significant impact on quality of life of patients. Rarely, patients with Gitelman's syndrome may present with hypokalaemic paralysis. Profound hypokalaemia is uncommon in Gitelman's syndrome. Here we report a case of Gitelman's syndrome, who presented with hypokalaemic paralysis and extreme hypokalaemia. To the best of our knowledge, after a Medline search, this is the most severe hypokalaemia described in a patient with Gitelman's syndrome.
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PMID:A case of Gitelman's syndrome presenting with extreme hypokalaemia and paralysis. 1852 31


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