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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] It rarely occurs in the absence of other abnormalities. It is sometimes associated with hypoventilation. [1]
The levels of chloride in the blood can help determine if there are underlying metabolic disorders. [20] Generally, chloride has an inverse relationship with bicarbonate, an electrolyte that indicates acid-base status. [20] Overall, treatment of chloride imbalances involve addressing the underlying cause rather than supplementing or avoiding ...
Calcium chloride (CaCl 2) is a salt that is marketed in pellet form for removing dampness from rooms. Calcium chloride is also used for maintaining unpaved roads and for fortifying roadbases for new construction. In addition, calcium chloride is widely used as a de-icer, since it is effective in lowering the melting point when applied to ice. [23]
Chloride, sodium, potassium, zinc and/or iodine deficiency, as these elements are needed to produce adequate levels of stomach acid (HCl). Sjögren's syndrome , an autoimmune disorder that destroys many of the body's moisture-producing enzymes.
Isolated hyperchlorhidrosis (Carbonic anhydrase XII deficiency), a rare genetic disorder which results in a lifelong tendency to lose excessive amounts of sodium by sweating. Pancreatitis [12] Prolonged exercise and sweating, combined with drinking water without electrolytes is the cause of exercise-associated hyponatremia (EAH).
Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. [5] The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), while levels less than 2.1 mmol/L are defined as hypocalcemic.
He found that a unilateral lesion in the reticular substance at the floor of the fourth ventricle produced a diuresis of chloride, but not glucose. Bernard reproduced this syndrome through renal denervation. [15] Through medullary lesioning in animals, Jungmann and Meyer from Germany induced polyuria and increased urinary salt excretion in 1913.
All responded to sodium chloride administration but administering aldosterone precursor 11-deoxycorticosterone did not reverse renal sodium loss. The authors felt neither pituitary nor adrenal insufficiency was involved, but that direct neural control of renal proximal tubular reabsorption of sodium was disrupted. [ 25 ]