Electrolytes play a vital role in maintaining homeostasis within the body. They help to regulate myocardial and neurological function, fluid balance, oxygen delivery, acid-base balance and much more. Electrolyte imbalances can develop by the following mechanisms: excessive ingestion; diminished elimination of an electrolyte; diminished ingestion or excessive elimination of an electrolyte. The most common cause of electrolyte disturbances is renal failure.
The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium, and/or calcium. Other electrolyte imbalances are less common, and often occur in conjunction with major electrolyte changes. Chronic laxative abuse or severe diarrhea or vomiting can lead to electrolyte disturbances along with dehydration. People suffering from bulimia or anorexia are at especially high risk for an electrolyte imbalance.
Additional recommended knowledge
Nomenclature
There is a standard nomenclature for electrolyte disorders:
- The name starts with a prefix denoting whether the electrolyte is abnormally elevated ("hyper-") or depleted ("hypo-").
- The word stem then gives the name of the electrolyte in Latin. If no Latin equivalent exists, then the corresponding term in English is used.
- The name ends with the suffix "-emia," meaning "in the blood." (Note, this doesn't mean that the disturbance is only in the blood; usually, electrolyte disturbance is systemic. However, since the disturbance is usually detected from blood testing, the convention has developed.)
For instance, elevated potassium in the blood is called "hyperkalemia" from the Latin term for potassium, "kalium".
Table of common electrolyte disturbances
General Function
Electrolytes are important because they are what your cells (especially nerve, heart, muscle) use to maintain voltages across their cell membranes and to carry electrical impulses (nerve impulses, muscle contractions) across themselves and to other cells. Your kidneys work to keep the electrolyte concentrations in your blood constant despite changes in your body. For example, when you exercise heavily, you lose electrolytes in your sweat, particularly sodium and potassium. These electrolytes must be replaced to keep the electrolyte concentrations of your body fluids constant.
Electrolyte Abnormalities and ECG Changes
The most notable feature of hyperkalemia is the "tent shaped" or "peaked" T wave. Delayed ventricular depolarization leads to a widened QRS complex and the P wave becomes wider and flatter. When hyperkalemia becomes severe, the ECG resembles a sine wave as the P wave disappears from view. In contrast, hypokalemia is associated with flattenting of the T wave and the appearance of a U wave. When untreated, hypokalemia may lead to severe arrhythmias.
The fast ventricular depolarization and repolarization associated with hypercalcemia lead to a characteristic shortening of the QT interval. Hypocalcemia has the opposite effect, lengthening the QT interval.
See also
Metabolic pathology / Inborn error of metabolism (E70-90, 270-279) |
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Amino acid | Aromatic (Phenylketonuria, Alkaptonuria, Ochronosis, Tyrosinemia, Albinism, Histidinemia) - Organic acidemias (Maple syrup urine disease, Propionic acidemia, Methylmalonic acidemia, Isovaleric acidemia, 3-Methylcrotonyl-CoA carboxylase deficiency) - Transport (Cystinuria, Cystinosis, Hartnup disease, Fanconi syndrome, Oculocerebrorenal syndrome) - Sulfur (Homocystinuria, Cystathioninuria) - Urea cycle disorder (N-Acetylglutamate synthase deficiency, Carbamoyl phosphate synthetase I deficiency, Ornithine transcarbamylase deficiency, Citrullinemia, Argininosuccinic aciduria, Hyperammonemia) - Glutaric acidemia type 1 - Hyperprolinemia - Sarcosinemia |
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Carbohydrate | Lactose intolerance - Glycogen storage disease (type I, type II, type III, type IV, type V, type VI, type VII) - fructose metabolism (Fructose intolerance, Fructose bisphosphatase deficiency, Essential fructosuria) - galactose metabolism (Galactosemia, Galactose-1-phosphate uridylyltransferase galactosemia, Galactokinase deficiency) - other intestinal carbohydrate absorption (Glucose-galactose malabsorption, Sucrose intolerance) - pyruvate metabolism and gluconeogenesis (PCD, PDHA) -
Pentosuria - Renal glycosuria |
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Lipid storage | Sphingolipidoses/Gangliosidoses: GM2 gangliosidoses (Sandhoff disease, Tay-Sachs disease) - GM1 gangliosidoses - Mucolipidosis type IV - Gaucher's disease - Niemann-Pick disease - Farber disease - Fabry's disease - Metachromatic leukodystrophy - Krabbe disease
Neuronal ceroid lipofuscinosis (Batten disease) - Cerebrotendineous xanthomatosis - Cholesteryl ester storage disease (Wolman disease) |
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Fatty acid metabolism | Lipoprotein/lipidemias: Hyperlipidemia - Hypercholesterolemia - Familial hypercholesterolemia - Xanthoma - Combined hyperlipidemia - Lecithin cholesterol acyltransferase deficiency - Tangier disease - Abetalipoproteinemia
Fatty acid: Adrenoleukodystrophy - Acyl-coA dehydrogenase (Short-chain, Medium-chain, Long-chain 3-hydroxy, Very long-chain) - Carnitine (Primary, I, II) |
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Mineral | Cu Wilson's disease/Menkes disease - Fe Haemochromatosis - Zn Acrodermatitis enteropathica - PO43�' Hypophosphatemia/Hypophosphatasia - Mg2+ Hypermagnesemia/Hypomagnesemia - Ca2+ Hypercalcaemia/Hypocalcaemia/Disorders of calcium metabolism |
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Fluid, electrolyte and acid-base balance | Electrolyte disturbance - Na+ Hypernatremia/Hyponatremia - Acidosis (Metabolic, Respiratory, Lactic) - Alkalosis (Metabolic, Respiratory) - Mixed disorder of acid-base balance - H2O Dehydration/Hypervolemia - K+ Hypokalemia/Hyperkalemia - Cl�' Hyperchloremia/Hypochloremia |
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Purine and pyrimidine | Hyperuricemia - Lesch-Nyhan syndrome - Xanthinuria |
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Porphyrin | Acute intermittent, Gunther's, Cutanea tarda, Erythropoietic, Hepatoerythropoietic, Hereditary copro-, Variegate |
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Bilirubin | Unconjugated (Lucey-Driscoll syndrome, Gilbert's syndrome, Crigler-Najjar syndrome) - Conjugated (Dubin-Johnson syndrome, Rotor syndrome) |
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Glycosaminoglycan | Mucopolysaccharidosis - 1:Hurler/Hunter - 3:Sanfilippo - 4:Morquio - 6:Maroteaux-Lamy - 7:Sly |
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Glycoprotein | Mucolipidosis - I-cell disease - Pseudo-Hurler polydystrophy - Aspartylglucosaminuria - Fucosidosis - Alpha-mannosidosis - Sialidosis |
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Other | Alpha 1-antitrypsin deficiency - Cystic fibrosis - Amyloidosis (Familial Mediterranean fever) - Acatalasia |
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