Hypokalemia is associated frequently with
High-Yield Explanation
Insulin, b2-adrenergic activity, thyroid hormone, and alkalosis promote Na+/K+-ATPase-mediated cellular uptake of K+, leading to hypokalemia. Causes of Hypokalemia I. Decreased intake A. Starvation B. Clay ingestion II. Redistribution into cells A. Acid-base 1. Metabolic alkalosis B. Hormonal 1. Insulin 2. Increased b2-adrenergic sympathetic activity: post-myocardial infarction, head injury 3. b2-Adrenergic agonists - bronchodilators, tocolytics 4. a-Adrenergic antagonists 5. Thyrotoxic periodic paralysis 6. Downstream stimulation of Na+/K+-ATPase: theophylline, caffeine C. Anabolic state 1. Vitamin B12 or folic acid administration (red blood cell production) 2. Granulocyte-macrophage colony-stimulating factor (white blood cell production) 3. Total parenteral nutrition D. Other 1. Pseudohyperkalemia 2. Hypothermia 3. Familial hypokalemic periodic paralysis 4. Barium toxicity: systemic inhibition of "leak" K+ channels III. Increased loss A. Nonrenal 1. Gastrointestinal loss (diarrhea) 2. Integumentary loss (sweat) B. Renal 1. Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt-wasting nephropathies 2. Increased secretion of potassium a. Mineralocoicoid excess b. Apparent mineralocoicoid excess c. Distal delivery of nonreabsorbed anions 3. Magnesium deficiency Ref: Harrison 19e pg: 305