ACIDOSIS (DECREASED pH)
ACIDOSIS (DECREASED pH): Excerpt from Differential Diagnosis in Primary Care
Developing a list of possible causes of acidosis is also best
approached by using the physiologic model of production, transport,
excretion, or degradation.
Production
Acids are produced as the end products of
metabolism, thus sugar is broken down to water and carbon dioxide (CO2)
(carbolic acid), fats are broken down to keto acids, and protein is broken
down to sulfur-containing amino acids. In pathophysiologic states, there may
be increased production of these acids. This should call to mind
diabetic acidosis, lactic acidosis, and starvation as diagnostic
possibilities when one is faced with a patient in acidosis.
Transport
If there is inadequate transport of acid to
the kidney for excretion (as occurs in various forms of shock
[prerenal azotemia]), acidosis may develop.
Excretion
Finally, these acids must be excreted by the
lungs and the kidney. Thus, CO2 retention occurs in pulmonary emphysema
leading to pulmonary acidosis, while retention of sulfates and phosphates
occurs in uremia causing uremic acidosis. Primary diseases of the kidney
that may cause uremia acidosis are glomerulonephritis, collagen disease,
toxic nephritis from various drugs, and end-stage renal disease from a host
of causes. Chronic obstructive uropathy from renal stones, bladder neck
obstruction, and congenital anomalies may also lead to uremic acidosis.
Acidosis is also produced by a decrease in production of bicarbonate
by the kidney or an increased excretion of bicarbonate in the intestinal
tract. Consequently, one must add to the differential list renal tubular
acidosis and Fanconi syndrome, which are associated with decreased
production of bicarbonate while not producing uremia at the same time. In
addition, diarrhea of many causes must be added to the list because it is
associated with increased excretion of bicarbonate. Finally, the mechanism
of regulation of bicarbonate production should bring to mind
conditions with acidosis related to decreased production of bicarbonate. In
Addison disease, there is little or no aldosterone hormone to induce the
kidneys to produce bicarbonate; lack of this hormone leads to acidosis. Drugs such as acetazolamide diuretic also
interfere with the kidney’s ability to produce bicarbonate, causing
acidosis.
Approach to the Diagnosis
The laboratory will be of greatest assistance in determining the cause
of acidosis. An elevated blood sugar and serum acetone level will help
diagnose diabetic acidosis. An elevated blood urea nitrogen (BUN) level
would point to uremia acidosis. Arterial blood gases may show an increased
CO2, isolating pulmonary emphysema as the cause.
Other Useful Tests
-
CBC (shock, septicemia, lactic acidosis)
-
Urinalysis (renal tubular acidosis, uremia)
-
Chemistry panel (diabetes, uremia, Addison disease)
-
Serial electrolytes (diabetic acidosis, renal disease, Addison
disease)
-
Lactic acid (shock, lactic acidosis)
-
Pulmonary function tests (pulmonary emphysema)
-
ECG (CHF)
-
Pulmonology consult
-
Nephrology consult
Pictures
Book Source Details
- Book Title: Differential Diagnosis in Primary Care
- Author(s): R. Douglas Collins MD, FACP
- Year of Publication: 2007
- Copyright Details: Differential Diagnosis in Primary Care, Copyright © 2007 Lippincott Williams & Wilkins.
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