Electrolytes/Electrolyte Disorders


Electrolytes are essential for basic life functioning.



Electrolytes maintain electrical neutrality in cells, generating and conducting action potentials in the nerves and muscles. 



The significant electrolytes include: sodium, potassium, and chloride along with magnesium, calcium, phosphate, and bicarbonates. 



Electrolytes are derived  from food and fluids. 



Electrolyte imbalance can lead to either high or low levels, disrupting normal bodily functions, which can lead to even life-threatening complications. 



((Sodium)) is an osmotically active anion, and one of the most important electrolytes in the extracellular fluid. 



Sodium is responsible for maintaining the extracellular fluid volume, and for regulation of the membrane potential of cells. 



Sodium is exchanged along with potassium across cell membranes as part of active transport. 



Sodium regulation occurs in the kidneys. 



The proximal tubule is where the majority of the sodium reabsorption takes place, and  at the distal convoluted tubule, sodium undergoes reabsorption.  



Sodium transport takes place by sodium-chloride symporters, by aldosterone hormone.



Hyponatremia is the most frequent electrolyte disorder.



Diagnosis is when the serum sodium level less than 135 mmol/L. 



Hyponatremia has neurological manifestations: headache, confusion, nausea, deliriums. 



Hypernatremia presents when the serum sodium levels greater than145 mmol/L. 



Symptoms of hypernatremia: include tachypnea, sleeping difficulty, and feeling restless. 



Rapid sodium corrections can have serious consequences like cerebral edema and osmotic demyelination syndrome. 



((Potassium)) is a mainly intracellular ion. 



The sodium-potassium adenosine triphosphatase pump primarily regulates the homeostasis between sodium and potassium.



The sodium-potassium adenosine triphosphatase pump, pumps out sodium in exchange for potassium, which moves into the cells. 



In the kidneys, the filtration of potassium takes place at the glomerulus. 



The reabsorption of potassium takes place at the proximal convoluted tubule and thick ascending loop of Henle.



Potassium secretion occurs at the distal convoluted tubule. 



((Aldosterone)) increases potassium secretion.



Potassium disorders are related to cardiac arrhythmias. 



((Hypokalemia)) occurs when serum potassium levels under 3.6 mmol/L—weakness, fatigue, and muscle twitching present in hypokalemia. 



Administration of intravenous insulin is associated with a spurious decrease in potassium levels as insulin shifts potassium intracellularly.



((Hyperkalemia)) occurs when the serum potassium levels above 5.5 mmol/L, which can result in arrhythmias. 



Muscle cramps, muscle weakness, rhabdomyolysis, myoglobinuria are presenting signs and symptoms in hyperkalemia.



((Calcium)) is involved in skeletal mineralization, contraction of muscles, the transmission of nerve impulse, blood clotting, and secretion of hormones. 



Calcium is mostly present in the extracellular fluid. 



Diet is the predominant source of calcium. 



Absorption of calcium in the intestine is primarily under the control of the hormonally active form of vitamin D, which is 1,25-dihydroxy vitamin D3. 



Parathyroid hormone also regulates calcium secretion in the distal tubule of kidneys.



Calcitonin acts on bone cells to increase the calcium levels in the blood.



((Hypocalcemia)) diagnosis occurs when the corrected serum total calcium levels are less than 8.8 mg/dl, as in vitamin D deficiency or hypoparathyroidism. 



Most calcium remains bound to proteins, out of which albumin-bound calcium comprises about 80%: a patient with hypoalbuminemia, as seen in liver 


cirrhosis, the nephrotic syndrome will demonstrate low calcium levels vs. the actual values.



((Hypercalcemia)) occurs when corrected serum total calcium levels exceed 10.7 mg/dl, as seen with primary hyperparathyroidism. 



Humoral hypercalcemia presents in malignancy, primarily due to PTHrP secretion.



((Bicarbonate)) drives the acid-base status of the blood.



The kidneys predominantly regulate bicarbonate concentration.



The kidneys are responsible for maintaining the acid-base balance. 



Kidneys reabsorb the filtered bicarbonate and also generate new bicarbonate by net acid excretion, which occurs by excretion of both titrable acid and ammonia. 



Diarrhea usually results in loss of bicarbonate.



((Magnesium)) is an intracellular cation,


mainly involved in ATP metabolism, contraction and relaxation of muscles, proper neurological functioning, and neurotransmitter release. 



In muscle contraction, calcium re-uptake by the calcium-activated ATPase of the sarcoplasmic reticulum is brought about by magnesium.



Hypomagnesemia occurs when the serum magnesium levels are less under 1.46 mg/dl. 



Hypomagnesemia is seen with alcohol use disorder and gastrointestinal and renal losses.



Ventricular arrhythmias, which include torsades de pointes can be seen with hypomagnesemia. 



Hypomagnesemia can lead to hypocalcemia as it interferes with the action of parathormone. 



((Chloride)) is an anion found predominantly in the extracellular fluid. 



The kidneys predominantly regulate serum chloride levels. 



Chloride, which is filtered by the glomerulus, is reabsorbed by both proximal and distal tubules.



It is mainly reabsorbed  by proximal the tubule by both active and passive transport.



Hyperchloremia can occur due to gastrointestinal bicarbonate loss. 



Hypochloremia presents in gastrointestinal losses like vomiting or excess water gain like congestive 


heart failure. 



((Phosphorus)) is an extracellular fluid cation. 



Eighty-five percent of the total body phosphorus is in the bones and teeth in the form of hydroxyapatite.



 Phosphate plays a crucial role in metabolic pathways, and component of many metabolic intermediates and, most importantly of adenosine triphosphate(ATPs) and nucleotides. 



Phosphorus imbalance results  from three processes: dietary intake, gastrointestinal disorders, and excretion by the kidneys.



In-patients and ICU patients, the monitoring of serum electrolytes often occurs daily or more frequently as they can be affected by the medications, fluid therapy, diet changes, and illnesses.



Illness that can cause electrolyte derangement include: malnutrition, gastrointestinal disorders, cardiac disorders, kidney dysfunction, endocrine disorders, circulatory disorders, lung disorders, acid-base imbalance


arrhythmias, cardiac arrest, and the usee of diuretics or any medications that can interfere with fluid and electrolyte homeostasis



Laboratory Values: 



Serum Sodium: 



Normal Range: 135 to 145 mmol/L  



Mild-moderate Hyponatremia: 125 to 135 mmol/L, Severe: less than 125 mmol/L



Hypernatremia: Mild-moderate: 145 to 160 mmol/L, Severe: over 160 mmol/L



Serum Potassium:



Normal Range: 3.6 to 5.5 mmol/L 



Hypokalemia: Mild Hypokalemia under 3.6 mmol/L, Moderate: 2.5 mmol/L, Severe : greater than 2.5 mmol/L



Hyperkalemia: Mild hyperkalemia: 5 to 5.5 mmol/L, Moderate- 5.5 to 6.5, Severe: 6.5 to 7 mmol/L



Serum Calcium: 



Normal Range: 8.8 to 10.7 mg/dl



Hypercalcemia: greater than 10.7 mg/dl , Severe: over 11.5 mg/dl 



Hypocalcemia: less than 8.8 mg/dl



Serum Magnesium: 



Normal Range: 1.46 to 2.68 mg/dl 



Hypomagnesemia: under 1.46 mg/dl



Hypermagenesemia: over 2.68






Normal Range: 23 to 30 mmol/L



It increases or decreases depending on the acid-base status.






Normal Range: 3.4 to 4.5 mg/dl 



Hypophosphatemia: less than 2.5 mg/dl



Hyperphosphatemia: greater than 4.5 mg/dl



Complications of electrolyte disorders: 



Both hyponatremia and hypernatremia, as well as hypomagnesemia, can lead to neurological consequences such as seizure disorders. 



Hypokalemia and hyperkalemia, as well as hypocalcemia, are more responsible for arrhythmias. 



Bicarbonate imbalance can lead to metabolic acidosis or alkalosis.



Some of the common electrolyte disorders and their causes: 



Hyponatremia: low dietary sodium intake, primary polydipsia, SIADH, congestive, heart failure, hepatic cirrhosis, failure of adrenal glands, hyperglycemia, dyslipidemia.



Hypernatremia: unreplaced fluid loss through the skin and gastrointestinal tract, osmotic diuresis, hypertonic saline administration



Hypokalemia: hyperaldosteronism, loop diuretics 



Hyperkalemia: metabolic acidosis, insulin deficiency, beta-blocker or decreased potassium excretion as in acute or chronic kidney disease, aldosterone deficiency or resistance, ACE inhibitors.



Hypercalcemia: malignancy, hyperparathyroidism, chronic granulomatous disease



Hypocalcemia: acute pancreatitis, parathyroid hormone deficiency after thyroidectomy, neck dissection, resistance to parathormone, hypomagnesemia, sepsis.



Hypermagnesemia: increase oral magnesium intake



Hypomagnesemia: renal losses as in diuretics, alcohol use disorder or GI losses as in diarrhea



Bicarbonate level: increases in primary metabolic alkalosis or compensation to primary respiratory acidosis – decreases in primary metabolic acidosis or compensation to primary respiratory alkalosis.



Hyperchloremia: normal saline infusion



Hypochloremia: GI loss as in diarrhea, renal losses with diuretics



Hypophosphatemia: refeeding syndrome, vitamin D deficiency, hyperparathyroidism



Hyperphosphatemia: hypoparathyroidism, chronic kidney disease


Management of such abnormalities is inappropriate in greater than 31% of patients during hospitalizations.


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