This document discusses disorders of sodium and potassium metabolism, including abnormalities of potassium and sodium balance. It outlines the major mediators that regulate sodium and water balance, including the renin-angiotensin-aldosterone axis and antidiuretic hormone. It then reviews the etiologies and pathophysiology of hyperkalemia, hypokalemia, hyponatremia, and hypernatremia. Finally, it presents four case studies as examples.

1. Disorders of Sodium and Potassium Metabolism Electrolyte disbalance

4. Renin-Angiotensin-Aldosterone Axis Angiotensin II  1. Stimulates production of aldosterone 2. Acts directly on arterioles to cause vasoconstriction 3. Stimulates Na + /H + exchange in the proximal tubule Aldosterone  1. Stimulates reabsorption of Na + and excretion of K + in the late distal tubule 2. Stimulates activity of H + ATPase pumps in the late distal tubule

8. Overview of Biochemical Homeostasis

9. Overview of Potassium Balance

10. Etiologies of Hyperkalemia Excessive Dietary Intake Decreased Urinary Excretion Decreased GFR Aldosterone deficiency Adrenal insufficiency ACE inhibitors Hyporeninemic hypoaldosteronism Diabetic nephropathy Aldosterone resistance Potassium sparing diuretics Internal Redistribution Transmembrane Shift Acidosis Exercise Cell Lysis Rhabdomyolysis Tumor lysis syndrome

11. Etiologies of Hypokalemia Poor Intake Increased Urinary Excretion Decreased reabsorption in loop of Henle Furosemide Increased excretion in the late distal tubule Increased delivery of Na + to the late distal tubule Furosemide, thiazides, and acetazolamide Proximal RTA Reduced function of the K + /H + ATPase Distal RTA Hyperaldosteronism Primary hyperaldosteronism Adrenal adenoma Adrenal hyperplasia Secondary hyperaldosteronism Renovascular hypertension Renin-secreting tumor Increased GI Losses Diarrhea Laxative abuse Vomiting / NG drainage Increased Transcutaneous Losses Copious sweating Transmembrane Shift Alkalosis Insulin treatment for DKA High catecholamine states

12. Overview of Sodium Balance

13. Etiologies of Hyponatremia Poor Intake of Sodium Increased Urinary Loss of Sodium Diuretics Proximal RTA Aldosterone deficiency/resistance Increased GI Loss of Sodium (Fluid loss must be followed by repletion with free water). Vomitting Diarrhea Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water). Excessive Intake of Water (1 ° polydipsia) Psychosis Decreased Urinary Excretion of Water Decreased GFR Increased ADH Decreased effective circulating volume True volume depletion (any cause) Apparent volume depletion Heart failure Cirrhosis SIADH Reset osmostat Transmembrane Shift of Water Hyperglycemia Primary Sodium Loss Primary Water Excess

14. Etiologies of Hypernatremia Primary Sodium Excess Excess Intake of Sodium Decreased Urinary Excretion of Sodium Hyperaldosteronism Primary Water Loss Poor Intake of Water Impaired access to water (i.e. infants, elderly patients with dementia or whom are bedbound) Impaired thirst sensation Hypothalamic lesions Increased Urinary Loss of Water ADH deficiency (Central DI) ADH resistance (Nephrogenic DI) Increased GI Loss of Water Increased Transcutaneous Loss of Water Transmembrane Shift of Water (most often due to rapid production of intracellular lactate)