SEARCH RESULTS FOR: Hypokalemia-Physiology

Hypokalemia Physiology

Hypokalemia: Physiology Authors: Samin Dolatabadi, Ran (Marissa) Zhang, Mannat Dhillon Reviewers: Meena Assad, Yan Yu*, Juliya Hemmett* Beta-2 receptor stimulation (e.g. Salbutamol) ↑ Red blood cell production ↑ Na+/K+ ATPase activity in skeletal muscle cells (moves K+ into the cell & Na+ out of cell) ↑ K+ entry into skeletal muscle cells * MD at time of publication Abbreviations: • EABV – Effective Arterial Blood Volume • ENaC – Epithelial Sodium Channel • HCL – Hydrochloric acid • HCO3- –Bicarbonate ion ↑ K+ uptake by new red blood cells ↑ Intracellular shift of K+ into cells Refeeding Syndrome Exogenous insulin ↓ K+ dietary intake (rare cause in isolation) ↑ Insulin in response to carbohydrate load ↑ Na+/K+ ATPase activity in skeletal muscle & hepatic cells ↑ K+ entry into skeletal muscle & hepatic cells ↓ K+ availability for gastrointestinal absorption Hypokalemia (Serum [K+] < 3.5 mmol/L) ↑ Renal K+ secretion K+ follows the electrical gradient into tubular lumen ↑ Electronegativity of tubular lumen ↑ Na+ reabsorptionin principal cellsà Cl- left behind in tubular lumen of kidneys Gastric acid depletionà ↓HCl Loss of H+àShift in bicarbonate buffer system to ↑ plasma HCO3- Plasma HCO3- above reabsorptive capacity of the proximal tubule ↑ HCO3- in the distal tubular lumen of kidneys Vomiting Diarrhea Laxatives Renin secreting tumour Hyperaldosteronism Renal artery stenosis Loop and Thiazide diuretics Bartter’s and Gittelman’s syndrome Liddle syndrome Extracellular fluid volume depletion ↓ EABV ↑ Renin secretion ↓ Afferent arteriole pressure perfusing kidneys Renin-Angiotensin- Aldosterone System (RAAS) activationà ↑ Aldosterone release from the adrenal cortex ↑ Expression of ENaC (Na+ reabsorption) in principal cells of the cortical collectingduct) + ↑Na & water excretion in kidneys ↓ EABV Genetic condition leading to inability to degrade ENaC channels in principal cells of the cortical collecting duct Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published March 6, 2019, updated Jan 23, 2022 on www.thecalgaryguide.com Hypokalemia: Physiology Authors: Samin Dolatabadi Reviewers: Meena Assad Dr. Juliya Hemmett* * MD at time of publication TTKG > 4 with N/↑ EABV in hypokalemia is inappropriate and a principal cell problem. β2 Stimulation (e.g., Salbutamol) ↑ Na+/K+ ATPase activity ↑ K+ entry into cell ↑ RBC Production ↑ Cell production ↑ K+ uptake by new cells ↓ Extracellular ↑ Insulin in response to H+ carbohydrate load ↑ Na+/H+ antiporter activity (movement of H+ out of cell and Na+ into cell) ↑ Intracellular Na+ ↑ Na+/K+ ATPase activity ↑ K+ entry into cell ↑ Intracellular Shift of K+ Notes: Refeeding Syndrome Insulin Alkalemia • Abbreviations: • CCD – Cortical Collecting Duct • EABV – Effective Arterial Blood Volume • RAAS – Renin-Angiotensin-Aldosterone System • TTKG – Trans-tubular Potassium Gradient • ENaC – Epithelial Sodium Channel ↓ K+ Intake (Rare cause in isolation) ↓ K+ availability Diarrhea, Vomiting, Laxatives ↑ Gastrointestinal loss of K+ Polyuria ↑ Renal loss of K+ (TTKG < 4 as principal cell is working appropriately but small amount of K+ is lost per urination) Hypokalemia (Serum [K+] < 3.5 mmol/L) Liddle Syndrome Hyperaldosteronism Renin Secreting Tumour Renal artery stenosis Loop and Thiazide Diuretics Bartter’s and Gittelman’s Syndrome Genetic condition leading to inability to degrade ENaC channels ↑ Renin ↑ Renal K+ secretion K+ follows the electrical gradient Electronegative lumen ↓ Pressure perfusing the kidney RAAS activation RAAS activation ↑ Aldosterone ↑ Na+ and water excretion ↓ EABV ↑ Expression of ENaC in principal cells of CCD ↑ Na+ reabsorption Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published March 6, 2019 on www.thecalgaryguide.com

Hypokalemia Physiology