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