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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).
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 ...
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]
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.
Hypertension, hypokalemia, metabolic alkalosis, and low plasma renin activity. [ 1 ] Apparent mineralocorticoid excess is an autosomal recessive [ 2 ] disorder causing hypertension (high blood pressure ), hypernatremia (increased blood sodium concentration) and hypokalemia (decreased blood potassium concentration).
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.
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
Blood biochemistry should be monitored regularly until it is stable. Although clinical trials are lacking in patients other than those admitted to intensive care, it is commonly recommended that energy intake should remain lower than that normally required for the first 3–5 days of treatment of refeeding syndrome for all patients.