Potassium, metabolism

In contrast to the typical effects of hypocalcemia, hypokalemia may cause myasthenia and flaccid paralysis of muscle because potassium is a critical activator of intermediary metabolism. Potassium is also critical for vasodilation in muscle during exercise, so hypokalemia may cause exertional rhabdomyolysis. Hypokalemia may be produced by potassium-losing diuretics and secondary to hypomagnesemia (Scola et al. 2007). 

Whereas sodium participates in metabolism mainly by its cationic properties, potassium is more directly involved in metabolism. Potassium stimulates the activity of a specific enzyme— pyruvic kinase—and is required for the phosphorylation of fructose-1-phosphate to fructose-1,6-diphosphate. Similarly, potassium stimulates acetyl kinase activity. Many alterations in the bioenergetic pathways of the cell are accompanied by changes in the intracellular concentration of potassium. After insulin administration, some of the potassium of the extracellular fluid is transferred inside the cells. During oxidative phosphorylation, potassium accumulates inside the mitochondria, and dinitrophenol uncouples the ion penetration and the oxidation. 

Electrolyte metabolism Potassium depleiion Neat to normal... 

Poor Metabolizer Phenotype Population Pharmacokinetics Positron Emission Tomography Post-translational Modification Potassium Channels Potassium Competitive Acid Blockers PP... 

Potassium is contraindicated in patients who are at risk for experiencing hyperkalemia, such as those with renal failure, oliguria, or azotemia (file presence of nitrogen-containing compounds in the blood), anuria, severe hemolytic reactions, untreated Addison s disease (see Chap. 50), acute dehydration, heat cramps, and any form of hyperkalemia Potassium is used cautiously in patients with renal impairment or adrenal insufficiency, heart disease, metabolic acidosis, or prolonged or severe diarrhea. Concurrent use of potassium with... 

Diuretics are often required in addition to the sodium restriction described previously. Spironolactone and jurosemide form the basis of pharmacologic therapy for ascites. Spironolactone is an aldosterone antagonist and counteracts the effects of activation of the renin-angiotensin-aldosterone system. In hepatic disease not only is aldosterone production increased, but its half-life is prolonged because it is hepatically metabolized. Spironolactone acts to conserve the potassium that would be otherwise excreted because of elevated aldosterone levels. 

Advanced stages Increased potassium, phosphorus, and magnesium decreased bicarbonate (metabolic acidosis) calcium levels are generally low in earlier stages of CKD and may be elevated in stage 5 CKD, secondary to the use of calcium-containing phosphate binders. 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. 

Any time an ABG is analyzed it is wise to concurrently inspect the serum chemistry values to calculate the anion gap. The body does not generate an anion gap to compensate for a primary disorder. As such, if the calculated anion gap exceeds 12 mEq/L (mmol/L) there is a primary metabolic acidosis regardless of the pH or the serum HC03 concentration. The anion gap may be artificially lowered by decreased serum albumin, multiple myeloma, lithium intoxication, or a profound increase in the serum potassium, calcium, or magnesium. 

A 70-year-old man presents to the emergency department because of diffuse abdominal pain and nonbloody diarrhea. One day earlier he had been discharged from the hospital, where he had received ceftriaxone and levofloxacin for 7 days for an upper respiratory infection. Soon after going home, he passed numerous liquid brown stools. A few hours later, the patient became disoriented, and an ambulance was called. His medical history is unremarkable. Laboratory values White blood cell count 50,000 cells/mm3, hematocrit 43%, sodium 125 mmol/L, potassium 5.6 mmol/L, C02 14 mmol/L, and metabolic acidosis. An abdominal radiograph series show no evidence of obstruction. The patient was admitted to the hospital. 

Potassium is the second most abundant cation in the body and is found primarily in the intracellular fluid. Potassium has many important physiologic functions, including regulation of cell membrane electrical action potential (especially in the myocardium), muscular function, cellular metabolism, and glycogen and protein synthesis. Potassium in PN can be provided as chloride, acetate, and phosphate salts. One millimole of potassium phosphate provides 1.47 mEq of elemental potassium. Generally, the concentration of potassium in peripheral PN (PPN) admixtures should not exceed 80 mEq/L (80 mmol/L). While it is safer to also stick to the 80 mEq/L (80 mmol/L) limit for administration through a central vein, the maximum recommended potassium concentration for infusion via a central vein is 150 mEq/L (150 mmol/L).14 Patients with abnormal potassium losses (e.g., loop or thiazide diuretic therapy) may have higher requirements, and patients with renal failure may require potassium restriction. 

Basic metabolic panel (i.e., sodium, potassium, chloride, bicarbonate, blood urea nitrogen, creatinine, glucose, and calcium), phosphorus, and magnesium... 

Liver function, including AST, ALT, alkaline phosphatase, lactate dehydrogenase (LDH), total and conjugated bilirubin a comprehensive metabolic panel can be ordered (i.e., sodium, potassium, chloride, bicarbonate, blood urea nitrogen, creatinine, glucose, calcium, AST, ALT, alkaline phosphatase, albumin, and total bilirubin), but phosphorus, magnesium, and fractionated... 

As metabolism increases, oxygen consumption and carbon dioxide production are enhanced. The concentration of hydrogen ions is also enhanced as more carbonic acid (formed from carbon dioxide) and lactic acid are produced by the working tissue. Furthermore, the concentration of potassium ions in the interstitial fluid is increased. The rate of potassium release from the cells due to repeated action potentials exceeds the rate of potassium... 

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