Potassium gluconate

234.25

234.014191

206-074-2

12H3K5QKN9

DTXSID7029617

YELLOWISH-WHITE CRYSTALS

A - Alimentary tract and metabolism

29181600

141

-4.82780

White to off-white Crystalline Powder

1.73 g/cm3

106 °C (decomp)

673.6°C at 760 mmHg

375.2ºC

soluble in water. (50 mg/ml).

room temp

LD50 oral in rat: 10380mg/kg

ODORLESS

MILD, SLIGHTLY SALINE TASTE

Between 7,0 and 8,3 (10 % solution)

DECOMP @ 180 °C

NONH for all modes of transport

1

36/37/38

24/25

LZ5230000

STABLE IN AIR.

P264, P270, P301+P312, P330, P501

H302

Acute oral toxicity (LD50): 9100 mg/kg in the mouse [MSDS] Toxicity from overdose is rare but may result from intentional ingestion of potassium. Iatrogenic overdoses may occur. Local irritation after ingestion causes GI upset. Severe hyperkalemia after large IV or oral overdoses causes muscular dysfunction including weakness, paralysis, cardiac dysrhythmias, and rarely death. **Mild to moderate toxicity** Nausea, vomiting, diarrhea, paresthesias, and muscle cramps are common. Rarely, gastrointestinal bleed may occur. **Severe toxicity** In severe toxicity, muscular weakness progressing to paralysis may occur. Cardiac arrhythmia often occur at concentrations greater than 8 mEq/L and death from cardiac arrest at concentrations of 9 to 12 mEq/L or higher. Characteristic ECG findings occur in the following order: peaked T waves, QRS complex blends into the T wave, PR interval prolongation, P wave is lost and ST segments depress, merging S and T waves, and finally, sine waves. The presence of the sine wave is a near terminal event, signaling that hemodynamic collapse and cardiac arrest are near. As serum hyperkalemia is corrected towards normal concentrations, the ECG changes resolve in reverse order.

Because of potassium’s wide-ranging roles in the body, low intakes can increase the risk of illness. Potassium supplements are indicated to prevent hypokalemia in patients who would be at particular risk if hypokalemia were to develop (e.g., digitalis treated patients with significant cardiac arrhythmias). Potassium deficiency occurs when the rate of loss through renal excretion and/or loss from the gastrointestinal tract is higher than the rate of potassium intake. In addition to serving as a preventative supplement, potassium gluconate also serves as a treatment for decreased potassium levels,,.

IRRESPECTIVE OF THE SALT USED, POTASSIUM IS COMPLETELY DISSOCIABLE & HENCE IS UNAFFECTED IN ITS IRRITANT ACTIONS & ABSORPTION BY THE ANION IN THE COMPD. /POTASSIUM SALTS/|A SOURCE OF POTASSIUM FOR MGMNT OF HYPOKALEMIC STATES, SUCH AS OCCUR CONSEQUENT TO ADRENOCORTICOID THERAPY OR USE OF THIAZIDE DIURETICS, OR FOR DELIBERATE PRODN OF HYPERKALEMIA, AS FOR TREATMENT OF DIGITALIS INTOXICATION.|...USED TO TREAT HYPOKALEMIA ASSOC WITH HYPERCHLOREMIA (EG RENAL TUBULAR ACIDOSIS, HYPOKALEMIA ASSOC WITH ACIDOSIS). IF...USED IN PT WITH HYPOKALEMIC HYPOCHLOREMIC ALKALOSIS, A SOURCE OF CHLORIDE ION (EG, AMMONIUM CHLORIDE, LYSINE MONOHYDROCHLORIDE) SHOULD BE PROVIDED. /POTASSIUM PREPN/

SUGAR-COATED POTASSIUM GLUCONATE TABLETS DISSOLVE @ HIGHER LEVEL /IN GI TRACT/ THAN DO ENTERIC-COATED TABLETS OF POTASSIUM CHLORIDE BUT, BY THIS VERY FACT, ARE FREE TO CAUSE THE IRRITATION FOR WHICH CHLORIDE TABLET WAS COATED. /THUS/...GLUCONATE HAS NO ADVANTAGE OVER NONENTERIC-COATED POTASSIUM CHLORIDE TABLETS.|A FULL GLASS OF WATER TAKEN WITH /POTASSIUM GLUCONATE/...GREATLY REDUCES THE IRRITANT EFFECTS... HYPOCHLOREMIA IS FREQUENT ACCOMPANIMENT OF HYPOKALEMIA; IN SUCH INSTANCES /POTASSIUM/ CHLORIDE IS DEFINITELY PREFERRED /OVER POTASSIUM GLUCONATE/.|...SINCE GLUCONATE METABOLIZES TO BICARBONATE, IT CONTRIBUTES TO ALKALOSIS, WHICH MAY BE...PRESENT IN HYPOKALEMIA. THUS IT WOULD BE DIFFICULT TO FIND SITUATIONS IN WHICH GLUCONATE WOULD BE SUPERIOR /TO POTASSIUM CHLORIDE/.

Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid, where it plays a key role in maintaining cell function, especially in excitable cells such as skeletal muscles, the heart, and nerves. Increases in interstitial potassium play an important role in eliciting rapid vasodilation, allowing for blood flow to increase in exercising muscle.

Potassium is rapidly and well absorbed. A 2016 dose-response trial found that humans absorb about 94% of potassium gluconate in supplements, and this absorption rate is similar to that of potassium from potatoes.|90% of potassium is eliminated via the kidneys. A small amount is eliminated in feces and sweat.|Distribution is largely intracellular, but it is the intravascular concentration that is primarily responsible for toxicity.|Potassium is freely filtered by the glomerulus in the kidney. The majority of filtered potassium is reabsorbed in the proximal tubule and loop of Henle. Less than 10% of the filtered load reaches the distal nephron. In the proximal tubule of the nephron, potassium absorption is mainly passive and proportional to Na+ and water. K+ reabsorption in the thick ascending limb of Henle occurs through both transcellular and paracellular pathways. The transcellular component is regulated by potassium transport on the apical membrane Na+-K+-2Cl− cotransporter. The secretion of potassium begins in the early distal convoluted tubule of the nephron and progressively increases along the distal nephron into the cortical collecting duct. Most urinary K+ can be accounted for by electrogenic K+ secretion mediated by principal cells in the initial collecting duct and the cortical collecting duct. An electroneutral K+ and Cl− cotransport mechanism is also present on the apical surface of the distal nephron. Under conditions of potassium deficiency, reabsorption of the cation occurs in the collecting duct. This process is regulated by the upregulation in the apically located H+-K+-ATPase on α-intercalated cells.

Potassium is the most abundant cation (approximately 150 to 160 mEq per liter) within human cells. Intracellular sodium content is relatively low. In the extracellular fluid, sodium predominates and the potassium content is low (3.5 to 5 mEq per liter). A membrane-bound enzyme, sodium-potassium–activated adenosinetriphosphatase (Na +K +ATPase), actively transports or pumps sodium out and potassium into cells to maintain the concentration gradients. The intracellular to extracellular potassium gradients are necessary for nerve impulse signaling in such specialized tissues as the heart, brain, and skeletal muscle, and for the maintenance of physiologic renal function and maintenance of acid-base balance. High intracellular potassium concentrations are necessary for numerous cellular metabolic processes. Intracellular K+ serves as a reservoir to limit the fall in extracellular potassium concentrations occurring under pathologic conditions with loss of potassium from the body.

...MAY CAUSE NAUSEA, VOMITING, DIARRHEA, & ABDOMINAL DISCOMFORT... SINCE GLUCONATE METAB TO BICARBONATE, IT CONTRIBUTES TO ALKALOSIS, WHICH MAY ALSO BE PRESENT IN HYPOKALEMIA.

boron gluconate

All other chemical product and preparation manufacturing|D-Gluconic acid, potassium salt (1:1): ACTIVE

EPA Safer Chemical Functional Use Classes -> Skin Conditioning Agents|Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern|Food additives

Food Additives -> ACIDITY_REGULATOR; NUTRIENT_SUPPLEMENT; YEAST_FOOD;