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Hypochloremia (or Hypochloraemia) is an electrolyte disturbance in which there is an abnormally low level of the chloride ion in the blood. The normal serum range for chloride is 97 to 107 mEq/L. [ citation needed ]
Hypochloremia, or low chloride levels, are commonly associated with gastrointestinal (e.g., vomiting) and kidney (e.g., diuretics) losses. [20] Greater water or sodium intake relative to chloride also can contribute to hypochloremia. [20]
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.
The causes are divided into benign or malignant. Benign Peptic ulcer disease; Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.; A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret syndrome" or "Bouveret's syndrome".
Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and an increase in plasma chloride concentration [1] (see anion gap for a fuller explanation).
The most common causes of high anion gap metabolic acidosis are: ketoacidosis, lactic acidosis, kidney failure, and toxic ingestions. [3]Ketoacidosis can occur as a complication of diabetes mellitus (diabetic ketoacidosis), but can occur due to other disorders, such as chronic alcoholism and malnutrition.
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.
Proximal renal tubular acidosis (pRTA) or type 2 renal tubular acidosis (RTA) is a type of RTA caused by a failure of the proximal tubular cells to reabsorb filtered bicarbonate from the urine, leading to urinary bicarbonate wasting and subsequent acidemia.