Nutricom

Nutricom Uses, Dosage, Side Effects, Food Interaction and all others data.

Pantothenic acid, also called pantothenate or vitamin B5 (a B vitamin), is a water-soluble vitamin discovered by Roger J. Williams in 1919. For many animals, pantothenic acid is an essential nutrient as it is required to synthesize coenzyme-A (CoA), as well as to synthesize and metabolize proteins, carbohydrates, and fats. Pantothenic acid is the amide between pantoic acid and β-alanine and commonly found as its alcohol analog, the provitamin panthenol, and as calcium pantothenate. Small quantities of pantothenic acid are found in nearly every food, with high amounts in whole-grain cereals, legumes, eggs, meat, royal jelly, avocado, and yogurt. Pantothenic acid is an ingredient in some hair and skin care products. Only the dextrorotatory (D) isomer of pantothenic acid possesses biological activity. while the levorotatory (L) form may antagonize the effects of the dextrorotatory isomer.

Pantothenic acid is used in the synthesis of coenzyme A (CoA). CoA is thought to act as a carrier molecule, allowing the entry of acyl groups into cells. This is of critical importance as these acyl groups are used as substrates in the tricarboxylic acid cycle to generate energy and in the synthesis of fatty acids, cholesterol, and acetylcholine. Additionally, CoA is part of acyl carrier protein (ACP), which is required in the synthesis of fatty acids in addition to CoAs use as a substrate.

Pantothenic acid in the form of CoA is also required for acylation and acetylation, which, for example, are involved in signal transduction and enzyme activation and deactivation, respectively.

Potassium chloride is a major cation of the intracellular fluid. It plays an active role in the conduction of nerve impulses in the heart, brain and skeletal muscle; contraction of cardiac skeletal and smooth muscles; maintenance of normal renal function, acid-base balance, carbohydrate metabolism and gastric secretion.

The potassium ion is in the principle intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle, and the maintenance of normal renal function. The intracellular concentration of potassium is approximately 150 to 160 mEq per liter. The normal adult plasma concentration is 3.5 to 5 mEq per liter. An active ion transport system maintains this gradient across the plasma membrane. Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops as a consequence of therapy with diuretics, primarily or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients, potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate.

Nutricom
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Nutricom
Generic	Pantothenic Acid + Phosphorus + Potassium Chloride + Sod
Type	Syrup
Therapeutic Class
Manufacturer	Panjon Pharma Ltd
Available Country	India
Last Updated:	September 19, 2023 at 7:00 am

Uses

Pantothenic acid is a vitamin B5 found in various nutritional supplements.

Studied for the treatment of many uses such as treatment of testicular torsion, diabetic ulceration, wound healing, acne, obesity, diabetic peripheral polyneuropathy. It has also been investigated for its hypolipidemic effects and as cholesterol lowering agent.

Phosphorus is a medication indicated in the treatment of hypophosphatemia.

Potassium chloride is used for drug induced hypokalemia, liver cirrhosis, nausea, vomiting, cholera, diarrhoea, muscular weakness, paralysis, cardiac and congestive heart failure, diabetic ketoacidosis, ulcerative colitis, weakness, anorexia, drowsiness, Cushing's syndrome, pyloric stenosis, low blood pressure etc.

Nutricom is also used to associated treatment for these conditions: Nutritional supplementationBone Loss, Nutritional supplementationDehydration, Dry Mouth, Hypokalemia, Hypotonic Dehydration, Hypovolaemia, Isotonic Dehydration, Markedly Reduced Food Intake, Metabolic Acidosis, Hypodermoclysis, Mild Metabolic acidosis, Mild, moderate Metabolic Acidosis, Ocular edema, Acid-Base Balance, Bowel preparation therapy, Electrolyte replacement, Fluid replacement therapy, Hemodialysis Treatment, Hemofiltration, Parenteral Nutrition, Parenteral rehydration therapy, Plasma Volume Replacement, Urine alkalinization therapy, Fluid and electrolyte maintenance therapy

How Nutricom works

Pantothenic acid is incorporated into COENZYME A and protects cells against peroxidative damage by increasing the level of GLUTATHIONE.

Supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels.

Dosage

Nutricom dosage

Oral:Dosage must be adjusted to the individual needs of each patient.

Adults: In severe deficiencies 3-6 tablets or 4-8 teaspoonful or 25-50 mmol per day orally in divided doses for some days with fruit juice, sweet or plain water.
Children: ½-1 teaspoonful twice daily or 1-3 mmol/kg body weight a day in several divided doses.

Patient should take Potassium chloride with meals.

Intravenous:

Severe acute hypokalaemia:

Adult: If serum potassium level >2.5 mEq/L, give at a rate not exceeding 10 mEq/hr in a concentration of up to 40 mEq/L. Max dose: 200 mEq/24 hr. If serum potassium level <2 mEq/L, may infuse at a rate of up to 40 mEq/hr. Continuous cardiac monitoring is essential. Max dose: 400 mEq/24 hr.

75 mg KCl equivalent to 1 mmol K+

Side Effects

GI ulceration (sometimes with haemorrhage and perforation or with late formation of strictures) following the use of enteric-coated K chloride preparation; hyperkalaemia. Oral: Nausea, vomiting, diarrhoea and abdominal cramps. IV: Pain or phloebitis; cardiac toxicity.

Toxicity

No Tolerable Upper Level Intake (UL) has been established for the vitamin.

The administration of oral potassium salts to persons with normal excretory mechanisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are impaired, of if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result. It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic changes (peaking of T-waves, loss of P-wave, depression of S-T segment, and prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).

Precaution

Renal or adrenocortical insufficiency; cardiac disease; acute dehydration; extensive tissue destruction. Pregnancy. Ensure adequate urine output; monitor plasma-potassium and other electrolyte concentrations. Discontinue treatment if severe nausea, vomiting or abdominal distress develops. Accumulation of potassium may occur in renal impairment.

Interaction

Potassium-sparing diuretics, ACE inhibitors, ciclosporin and potassium-containing drugs. Antimuscarinics delay gastric emptying time consequently increasing risk of GI adverse effects esp of solid oral dosage forms.

Elimination Route

Dietary pantothenic acid is primarily in the form of CoA or ACP and must be converted into free pantothenic acid for absorption. CoA and ACP are hydrolyzed into 4'-phosphopantetheine which is then dephosphorylated into pantetheine and subsequently hydrolyzed again to free pantothenic acid by Pantetheinase in the intestinal lumen. Free pantothenic acid is absorbed into intestinal cells via a saturable, sodium-dependent active transport system with passive diffusion acting as a secondary pathway. As intake increases up to 10-fold absorption rate can decrease to as low as 10% due to transporter saturation.

Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine.

Elimination Route

Potassium is a normal dietary constituent and, under steady-state conditions, the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake.

Pregnancy & Breastfeeding use

Category C: Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the foetus.