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Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate (HCO − 3), or alternatively a direct result of increased bicarbonate concentrations.
Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher).
Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.
Common symptoms include hypertension, hypokalemia, metabolic alkalosis, and low plasma renin activity. [1] DOC excess syndrome is an excessive secretion of 21-hydroxyprogesterone also called 11-Deoxycorticosterone from adrenal glands and may cause mineralocorticoid hypertension. [4] [5] [6]
The clinical findings characteristic of Bartter syndrome is hypokalemia, metabolic alkalosis, and normal to low blood pressure. These findings may also be caused by other conditions, which may cause confusion. When diagnosing a Bartter's syndrome, the following conditions must be ruled out as possible causes of the symptomatology: [citation needed]
Low potassium is caused by increased excretion of potassium, decreased consumption of potassium rich foods, movement of potassium into the cells, or certain endocrine diseases. [3] Excretion is the most common cause of hypokalemia and can be caused by diuretic use, metabolic acidosis , diabetic ketoacidosis , hyperaldosteronism , and renal ...
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In summary, hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis. [ 13 ] Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells , increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron , possibly due to widespread ...