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Acidosis

Definition

Acidosis is a condition characterized by excessive acid in the body fluids.

Causes

The acid/base status of the body (pH) is regulated by the kidneys and the lungs. Acidosis is caused by an accumulation of acid or a significant loss of bicarbonate. The major categories of acidosis are respiratory acidosis and metabolic acidosis.

The human body is programmed to correct for either respiratory or metabolic acidosis to maintain normal pH. For example, if the acidosis was caused by excessive carbon dioxide (which is an acid) the body will correct the pH by retaining bicarbonate (a base).

Respiratory acidosis develops when there are excessive amounts of carbon dioxide in the body, primarily caused by decreased breathing. Other names for this include hypercapnic acidosis and carbon dioxide acidosis.

There are several types of metabolic acidosis. Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when ketone bodies accumulate during uncontrolled diabetes.

Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body, as in severe diarrhea, for example.

Lactic acidosis is an accumulation of lactic acid. This can be caused by many conditions, including prolonged lack of oxygen (from, for example, shock, heart failure, or severe anemia), prolonged exercise, seizures, hypoglycemia (low blood sugar), alcohol, liver failure, malignancy, or certain medications like salicylates.

Other causes of metabolic acidosis include severe dehydration -- resulting in decreased tissue perfusion (decreased blood flow), kidney disease (see distal renal tubular acidosis and proximal renal tubular acidosis), and other metabolic diseases.


Review Date: 1/16/2004
Reviewed By: Jacqueline A. Hart, M.D., Department of Internal Medicine, Newton-Wellesley Hospital, Newton, Ma., and Senior Medical Editor, A.D.A.M., Inc. Previously reviewed by Andrew Koren, M.D., Department of Nephrology, NYU-Mount Sinai Medical Center, New York, NY. Review provided by VeriMed Healthcare Network (1/19/2002).
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