Specific electrolyte imbalnces
Sodium /font>
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Approximately 1/2 of the total body concentration of sodium is found in ECF.
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The quantity of sodium in the body is controlled by dietary intake and loss.
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The most important route for sodium excretion is through the kidney. Most sodium presented to renal tubules is reabsorbed in a process controlled by aldosterone.
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Renal reabsorption of sodium requires an equivalent passage of hydrogen or potassium ions in the opposite direction.
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Sodium is also lost in sweat and in digestive tract secretions.
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In carnivores and most herbivores, sodium is reabsorbed in the lower intestinal tract.
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In herbivores with large quantities of fluid in the feces, such as the cow and the horse, there may be considerable fecal loss of sodium.
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A decrease in plasma sodium concentration (hyponatremia) occurs most frequently because of excessive sodium loss.
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from the gastrointestinal tract through diarrhea or vomition
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in renal disease in which the sodium conservation mechanism is operating deficiently because of tubular damage
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Hyponatremia may occur with hyperglycemia due to increased sodium excretion to prevent hyperosmolarity.
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An increase in plasma sodium concentration (hypernatremia) is rare and can occur when there is restricted water intake with excessive sodium intake, in advanced chronic renal failure with a low glomerular filtration rate, and with primary hyperaldosteronism.
Potassium /font>
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Potassium concentration is low in ECF and high in most cells of the body.
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Most potassium is excreted by the kidneys through glomerular filtration and tubular secretion.
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Aldosterone facilitates excretion of potassium since it causes increased sodium reabsorption by promoting the exchange of sodium in tubular fluid for potassium in the tubular cell.
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Potassium excretion by the kidneys is also controlled by competition between potassium and hydrogen ions for reabsorption.
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Alterations in serum potassium levels occur when there is a disturbance in the equilibrium between potassium in the ICF and potassium in the ECF.
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In alkalosis, potassium moves into the cell in exchange for hydrogen ions and may cause hypokalemia.
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In acidosis, potassium moves out of the cell in exchange for hydrogen ions and may cause hyperkalemia.
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Plasma potassium increases about 0.6 mEq/L for each 0.1 unit decrease in blood pH. Therefore, if an acidotic animal has a normal plasma potassium level, it should be considered hypokalemic and corrective therapy should be initiated.
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In addition to its role in maintaining the tonicity of the ICF, potassium is of great importance in the mechanism of neuromuscular transmission.
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Low concentrations of K+ in the ECF result in profound muscular weakness and ECG abnormalities.
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High concentration of K+ in the ECF (10-12 mEq/L) result in severe myocardial disturbances and death due to cardiac arrest.
Chloride /font>
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Chloride concentration is low in ICF and high in ECF.
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Excretion, absorption and distribution of chloride are passive processes in association with active sodium transport.
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Unusual reduction in chloride concentration in the absence of comparable change in sodium, usually reflects sequestration of gastric juice in the stomach or vomiting.
Bicarbonate /font>
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Bicarbonate is mostly of endogenous origin in that it comes from the hydration of carbon dioxide to carbonic acid which then dissociates to bicarbonate and hydrogen ions.
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Bicarbonate is lost through secretions to the digestive tract and in the urine.
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Bicarbonate levels are regulated by respiratory and metabolic (kidney) processes.
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Last modified: Wednesday, 22 February 2012, 4:49 AM