The differential diagnosis of<unk>  is relatively short (when compared to the differential diagnosis of acidosis): * Hyperalimentation (e.g. from TPN containing ammonium chloride) * Acetazolamide and other carbonic anhydrase inhibitors * Renal tubular acidosis * Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a<unk><unk> <unk> , or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl−; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl−, results in a decrease in the plasma Na+ concentration relative to the Cl−concentration. This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of<unk>  saline to replace GI losses. * Ureteroenteric fistula – an abnormal connection (fistula) between a ureter and the gastrointestinal tract * Pancreaticoduodenal fistula – an abnormal connection between the pancreas and duodenum * Spironolactone * High ostomy output * Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a<unk><unk> <unk>  metabolic acidosis. Patients with hyperparathyroidism may have a lower than<unk>  pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a<unk><unk> <unk> . As opposed to high<unk> <unk>  acidosis (which involves increased organic acid production),<unk>  involves either increased production of chloride (hyperchloremic acidosis) or increased excretion of bicarbonate.
Normal anion gap acidosis
Metabolic alkalosis
Metabolic acidosis
High anion gap metabolic acidosis
Respiratory acidosis
Contraction alkalosis
Acidosis
Respiratory alkalosis