Symptom Finder - Hypokalemia
HYPOKALEMIA
The physiologic model of intake, absorption, regulation, and excretion serves well to help recall the diagnostic possibilities in a case of hypokalemia.
Intake: Potassium enters the body through the GI tract. It follows that starvation and anything else that interferes with the intake of potassium (such as vomiting or diarrhea) will cause depletion of body potassium.
In addition, potassium is secreted in the GI tract in the digestive juices. This mechanism contributes to the depletion of potassium in pyloric obstruction, intestinal obstruction, and diarrhea of many causes.
Absorption: The poor absorption of water and salts in malabsorption syndrome leads to hypokalemia.
Regulation: The hormone aldosterone activates the kidney to reabsorb large amounts of sodium in exchange for potassium and hydrogen ion. Consequently, when the adrenal cortex secretes large amounts of this hormone, as in primary aldosteronism, there is associated hypokalemia. Hypokalemia is also associated with secondary aldosteronism as occurs in malignant hypertension, renal artery stenosis, and Bartter syndrome.
Excretion: In chronic renal failure of many causes, there is damage to the distal tubules of the kidney so that reabsorption of potassium is impaired; therefore, hypokalemia results. Diuretics such as hydrochlorothiazide may inhibit the distal tubular reabsorption of potassium, causing hypokalemia. Hypokalemia develops in renal tubular acidosis because of a renal tubular defect causing more sodium to be absorbed in exchange for potassium, which creates a potassium deficit. Metabolic alkalosis also enhances the secretion of potassium in exchange for sodium to conserve hydrogen ion, causing hypokalemia.
Approach to the Diagnosis
A history of vomiting, diarrhea, or use of diuretics will be helpful in determining the cause of hypokalemia. However, serial electrolytes, chemistry panel, and a 24-hour urine potassium level will be most useful.
Other Useful Tests
1. CBC (infection, septicemia)
2. Urinalysis (chronic nephritis)
3. Plasma renin level (aldosteronism)
4. 24-hour urine aldosterone level (primary aldosteronism)
5. Plasma cortisol level (Cushing syndrome)
6. d-xylose absorption test (malabsorption syndrome)
7. Endocrinology consult
8. Nephrology consult
The physiologic model of intake, absorption, regulation, and excretion serves well to help recall the diagnostic possibilities in a case of hypokalemia.
Intake: Potassium enters the body through the GI tract. It follows that starvation and anything else that interferes with the intake of potassium (such as vomiting or diarrhea) will cause depletion of body potassium.
In addition, potassium is secreted in the GI tract in the digestive juices. This mechanism contributes to the depletion of potassium in pyloric obstruction, intestinal obstruction, and diarrhea of many causes.
Absorption: The poor absorption of water and salts in malabsorption syndrome leads to hypokalemia.
Regulation: The hormone aldosterone activates the kidney to reabsorb large amounts of sodium in exchange for potassium and hydrogen ion. Consequently, when the adrenal cortex secretes large amounts of this hormone, as in primary aldosteronism, there is associated hypokalemia. Hypokalemia is also associated with secondary aldosteronism as occurs in malignant hypertension, renal artery stenosis, and Bartter syndrome.
Excretion: In chronic renal failure of many causes, there is damage to the distal tubules of the kidney so that reabsorption of potassium is impaired; therefore, hypokalemia results. Diuretics such as hydrochlorothiazide may inhibit the distal tubular reabsorption of potassium, causing hypokalemia. Hypokalemia develops in renal tubular acidosis because of a renal tubular defect causing more sodium to be absorbed in exchange for potassium, which creates a potassium deficit. Metabolic alkalosis also enhances the secretion of potassium in exchange for sodium to conserve hydrogen ion, causing hypokalemia.
Approach to the Diagnosis
A history of vomiting, diarrhea, or use of diuretics will be helpful in determining the cause of hypokalemia. However, serial electrolytes, chemistry panel, and a 24-hour urine potassium level will be most useful.
Other Useful Tests
1. CBC (infection, septicemia)
2. Urinalysis (chronic nephritis)
3. Plasma renin level (aldosteronism)
4. 24-hour urine aldosterone level (primary aldosteronism)
5. Plasma cortisol level (Cushing syndrome)
6. d-xylose absorption test (malabsorption syndrome)
7. Endocrinology consult
8. Nephrology consult
