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metabolic-alkalosis-pathogenesis

Metabolic Alkalosis: Pathogenesis Authors: Wazaira Khan Reviewers: Jessica Krahn, Emily Wildman, Austin Laing, Huneza Nadeem, Ran (Marissa) Zhang, Adam Bass* * MD at time of publication Primary hyperaldosteronism E.g., aldosterone- secreting mass, adrenal hyperplasia Secondary hyperaldosteronism E.g., renin-secreting mass, renal artery stenosis Pseudo- hypoaldosteronism E.g., Liddle’s Syndrome Unregulated aldosterone production in adrenal cortex Excess aldosterone suppresses renin production Unregulated renin production by juxtaglomerular cells Sustained ↑ in mineralocorticoid (aldosterone) activity Insertion of epithelial sodium channels on principal cells in collecting duct ↑ Water retention by the kidney ↑ Na+ reabsorption by principal cells ↑ EABV • ↑ Jugular venous pressure • Hypertension • Urine Na+ > 40 mEq/L Low renin, high aldosterone state Activation of renin- angiotensin-aldosterone system (RAAS) Release of aldosterone from adrenal cortex High renin, high aldosterone state ↑ Negative charge in collecting duct lumen K+ leaks into collecting duct lumen by principal cell to maintain electroneutrality Hypokalemia Intracellular K+ leaks out of any cell in the body to compensate for low serum K+ levels Extracellular H+ enters cell to maintain electroneutrality Intracellular acidosis Activation of compensatory acid secreting mechanisms in kidney Impaired tubular function E.g., loop/thiazide diuretics, Bartter’s/ Gitelman’s Syndrome Upper GI Loss E.g., vomiting, nasogastric suction Unregulated epithelial sodium channel activity in collecting duct mimicking aldosterone function ↑ in Na+ and water retention à RAAS inhibition ↓ Na+ and Cl- reabsorption in thick ascending limb or distal convoluted tubule Low renin, low aldosterone state ↑ Na+, Cl- and water secretion through kidney RAAS activation See “Physiology of RAAS” slide ↓ EABV • • • Temporary ↑ in mineralocorticoid (aldosterone) activity ↓ Jugular venous pressure Orthostatic hypotension Dry mucous membranes Urine Na+ < 20 mEq/L • Loss of fluid through GI tract ↓ HCl delivery to small intestine ↑ NH + secretion and 4 ↑ HCO3- reabsorption in proximal tubule ↑ H+ secretion in cortical collecting duct Loss of gastric contents, including HCl ↓ HCO3- secretion by pancreas, liver and intestines to neutralize HCl Loss of intrinsic acid to neutralize HCO3- ↑ Plasma [HCO3-] Metabolic Alkalosis Arterial blood gas pH > 7.40 Plasma [HCO3-] > 24 mEq/L Effective Arterial Blood Volume (EABV): component of arterial blood volume that is effectively perfusing organs Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published May 31, 2022 on www.thecalgaryguide.com