Potassium homeostasis is maintained by a balance between intake, excretion, and cellular uptake and efflux. Ninety per cent of the total body potassium is available for exchange, allowing for major translocations or shifts between body compartments.
Factors stimulating K+ entry into cells
Alkalosis, mainly metabolic;
Hormonal: insulin, beta-adrenergic agonists (catecholamines); High extracellular potassium concentration; Hyperosmolarity of the extracellular fluid.
Factors stimulating exit from cells
Acidosis, mainly respiratory;
Low osmolarity of the extracellular fluid;
Hormonal: glucagon, beta-adrenergic blockade; alpha-adrenergic agonists
(catecholamines); Cell injury.
Renal excretion of potassium
This depends on the net effect following: Reabsorption in the proximal convoluted tubule and in the ascending limb of the loop of Henle.
Secretion, which depends on the basolateral Na+K+ -ATPase, and the luminal S
voltage-gated potassium channels.
Abnormalities in potassium homeostasis 3
Serum potassium is normally maintained between 3.5 and 5.0 mmol/l. A reduction of 1 mmol/l reflects a deficit of 150-400 mmol in total body potassium. Hypokalaemia can be related to the following pathophysiological mechanisms:
* Redistribution due to transcellular shifts: alkalosis, beta 2-adrenergic stimulation, insulin, rapid cell growth in acute anabolic states.
* True hypokalaemia:
Renal losses, associated with urine potassium greater than 20 mmol in 24 hours. This can be produced by diuretics, mineralocorticoids, high dose glucocorticoids, or in states of osmotic diuresis. Gastrointestinal losses: malabsorption; secretory diarrhoea; laxative abuse; cation-binding resins; villous adenoma. Hyperkalaemia can be related to:
* Pseudohyperkalaemia: improper blood collection with haemolysis; marked leukocytosis; marked thrombocytosis.
* True hyperkalaemia:
Transcellular shifts of potassium: acidosis; beta blockers; cell destruction (tumour lysis).
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