Spurious hypokalemia: high number of metabolically active cells present in blood absorb the ECF potassium.
Decreased net intake
GI or renal losses
Shift into cells
Alkalemia
Insulin
Catecholamines
Hypokalemic periodic paralysis
Increased net loss
Nonrenal loss:
Lower GI tract losses.
Hypokalemia from vomiting is due to renal K secretion from secondary hyperaldosteronism. Diaphoresis
Renal loss: Accounts for most cases of chronic hypokalemia.
Augmented distal urine flow rate: diuretic use and osmotic diuresis (glucosuria). Bartter's and Gitelman's syndromes mimic diuretic use.
Disorder that promote K+ loss by increasing the lumen-negative gradient, which drives K+ secretion. This can be achieved with reabsorption of a cation (Na+) or presence of a nonreabsorbed anion (HCO3 - metabolic alkalosis or type 2 RTA, ketones, and hippurate from toulene intoxication or glue sniffing).
Distal Na+ reabsorption is influences by mineralocorticoid activity.
Primary mineralocorticoid excess seen in primary hyperaldosteronism due to an adenoma or adrenocortical hyperplasia.
Cushing's syndrome (excess cortisol)
Secondary hyperaldosteronism can be seen in any situation with a decreased effective circulating volume
Liddle's synd.