causes of hypokalemia(3)

1. I. decreased intake

1.1. starvation

1.2. clay ingestion

2. II. redistribution into cells

2.1. A. acid base

2.1.1. metabolic alkalosis

2.2. B. hormonal (6)

2.2.1. 1. insulin

2.2.2. 2. Increased β2-adrenergic sympathetic activity: post–myocardial infarction, head injury

2.2.3. 3. β2-Adrenergic agonists—bronchodilators, tocolytics

2.2.4. 4. α-Adrenergic antagonists

2.2.5. Thyrotoxic periodic paralysis

2.2.6. downstream stimulation of Na+/K+-ATPase: theophylline, caffeine C. Anabolic state

2.3. C. anabolic state (3)

2.4. 1. Vitamin B12 or folic acid administration (red blood cell production)

2.5. 2. Granulocyte-macrophage colony-stimulating factor (white blood cell production)

2.6. 3. Total parenteral nutrition

2.7. D. Other (4)

2.8. 1. Pseudohypokalemia

2.9. 2. Hypothermia

2.10. 3. Familial hypokalemic periodic paralysis

2.11. 4. Barium toxicity: systemic inhibition of “leak” K+ channels

3. increased loss(2)

3.1. non renal (2)

3.2. 1. Gastrointestinal loss (diarrhea)

3.3. 2. Integumentary loss (sweat)

3.4. renal (3)

3.5. 1. Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt-wasting nephropathies

3.6. 2. Increased secretion of potassium (3)

3.7. . Mineralocorticoid excess: primary hyperaldosteronism (aldosterone-producing adenomas, primary or unilateral adrenal hyperplasia, idiopathic hyperaldosteronism due to bilateral adrenal hyperplasia, and adrenal carcinoma), genetic hyperaldosteronism (familial hyperaldosteronism types I/II/III, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), Cushing’s syndrome, Bartter’s syndrome, Gitelman’s syndrome

3.8. 2. 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 epithelial Na+ channels)

3.9. 3. 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)

3.10. 3. 3. Magnesium deficiency