- Decreased intake
- Redistribution into cells
- Acid-base
- Metabolic alkalosis
- Hormonal
- Insulin
- Increased β2-adrenergic sympathetic activity: post-myocardial infarction, head injury, theophylline
- β2-Adrenergic agonists: bronchodilators, tocolytics
- α-Adrenergic antagonists
- Thyrotoxic periodic paralysis
- Downstream stimulation of Na+ /K+ -ATPase: theophylline, caffeine
- Anabolic state
- Vitamin B12 or folic acid administration (red blood cell production)
- Granulocyte-macrophage colony-stimulating factor (white blood cell production)
- Total parenteral nutrition
- Other
- Pseudohypokalemia
- Hypothermia
- Familial hypokalemic periodic paralysis
- Barium toxicity: systemic inhibition of leak K+ channels
- Increased loss
- Nonrenal
- Gastrointestinal loss (diarrhea)
- Integumentary loss (sweat)
- Renal
- Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt-wasting nephropathies
- Increased secretion of potassium
- Mineralocorticoid excess: primary hyperaldosteronism (APAs), PAH or UAH, IHA due to bilateral adrenal hyperplasia and adrenal carcinoma, familial hyperaldosteronism (FH-I, FH-II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome
- Apparent mineralocorticoid excess: genetic deficiency of 11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice, food products, drugs), Liddle's syndrome (genetic activation of ENaC)
- Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin)
- Magnesium deficiency, amphotericin B, Liddle's syndrome
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