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| *reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities. | | *reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities. |
| *increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities. | | *increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities. |
| + | Potassium is largely an intracellular ion. Plasma potassium levels are not always a good indicator of intracellular levels; in acidosis the exchange of H+ and K+ ions leads to the depletion of intracellular potassium and elevated plasma potassium. The converse occurs in alkalosis. Aldosterone secretion promotes sodium retention and potassium excretion. Clinical features of potassium depletion include muscle weakness, ileus and cardiac arrhythmias, rhabdomyolysis and renal dysfunction. Hypokalaemia is of particular significance in the cat and is usually associated with CRF. In most cases, hyperkalaemia arises due to a diminished ability to excrete potassium. Potassium excess is therefore associated with hypoadrenocorticism and some forms of renal disease (especially post renal azotaemia). Marked hyperkalaemia is potentially life threatening causing bradycardia and cardiac arrest. Refrences: [[NationWide Laboratories]] |
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| ==Sources of Potassium== | | ==Sources of Potassium== |
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| * The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron | | * The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron |
| 2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone. | | 2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone. |
| + | |
| + | == Causes of Hyperkalaemia == |
| + | |
| + | === Small Animals === |
| + | |
| + | * Acute renal failure |
| + | * Hypoadrenocorticism |
| + | * Post renal azotaemia (urethral obstruction, urinary tract trauma) |
| + | * Pseudohyperkalaemia: |
| + | |
| + | EDTA contamination of serum |
| + | |
| + | Thrombocytosis |
| + | |
| + | Leucocytosis (leakage from cells) |
| + | |
| + | Haemolysis (Akitas and Shibas) |
| + | |
| + | * Massive tissue damage |
| + | * Metabolic acidosis (renal failure, certain types of diarrhoea) |
| + | * Peritoneal effusions |
| + | |
| + | === Equine === |
| + | Potassium levels in the extracellular fluid are influenced most by renal function and do not always reflect potassium levels in the intracellular compartment. Potassium distribution depends on the acid-base status as it is exchanged for hydrogen ions across the cell membrane. Hyperkalaemia is a potential emergency due to induction of cardiac dysrhythmias. |
| + | |
| + | * Reduced extracellular fluid volume, hypovolaemia with renal shut down |
| + | * Metabolic acidosis |
| + | * Polyuric renal disease |
| + | * Post renal obstruction in foals |
| + | * Pseudohyperkalaemia |
| + | |
| + | In vitro haemolysis |
| + | |
| + | Prolonged storage |
| + | |
| + | * Muscle damage |
| + | |
| + | ==== Rare causes of hyperkalaemia in equine ==== |
| + | |
| + | * Anuric renal failure |
| + | * Urinary tract disruption |
| + | * Tissue necrosis |
| + | * Inherited hyperkalaemic periodic paralysis |
| + | |
| + | == Causes of Hypokalaemia == |
| + | |
| + | === Small Animals === |
| + | |
| + | * Chronic renal failure (particularly cats) |
| + | * Diuretic therapy |
| + | * Vomiting and diarrhoea |
| + | * Hypokalaemic myopathy (hypokalaemic periodic paralysis) of Burmese kittens |
| + | * Insulin therapy |
| + | * Administration of potassium depleted fluids |
| + | * Excessive mineralocorticoid therapy |
| + | * Metabolic alkalosis for example gastric vomiting |
| + | |
| + | === Equine === |
| + | |
| + | * Prolonged anorexia |
| + | * Dietary deficiencies |
| + | * Gastrointestinal tract loss (lower bowel obstruction), diarrhoea |
| + | * Enterocolitis |
| + | * Profuse sweating |
| + | * Peritonitis |
| + | |
| + | ==== Rare causes of hypokalaemia in equines ==== |
| + | |
| + | * Metabolic alkalosis |
| + | * Renal tubular acidosis |
| + | * Iatrogenic (diuretics, bicarbonate or insulin administration) |
| + | |
| + | == Complementary tests == |
| + | In small animals a Na:K ratio is an aid to the diagnosis of hypoadrenocorticism; a ratio <25:1 is supportive but an ACTH stimulation test is required for confirmation if the clinical signs are suggestive of Addison’s disease. The ratio can also be reduced by other factors increasing plasma potassium including renal disease. |
| + | |
| + | In Equine urine clearance ratios will assist interpretation of serum electrolyte and mineral levels see fractional electrolyte excretion (FE) values (%). |
| + | |
| + | Please visit www.nwlabs.co.uk or see our current price list for more information |
| + | |
| + | == References == |
| + | Text referenced 'Nationwide Laboratories': [[NationWide Laboratories]] |
| + | |
| + | Causes of Hyperkalaemia: [[NationWide Laboratories]] |
| + | |
| + | Causes of Hypokalaemia: [[NationWide Laboratories]] |
| + | |
| + | Complementary tests: [[NationWide Laboratories]] |
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| [[Category:Electrolytes]] | | [[Category:Electrolytes]] |
| [[Category:Minerals]] | | [[Category:Minerals]] |