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Potassium Bicarbonate
Overview
What is K-Vescent?
An oral potassium supplement. Each effervescent tablet in solution provides 25 mEq of potassium as supplied by 2.4g potassium bicarbonate with 1.4g Citric Acid, FD and C Yellow #6 Dye, FD and C Yellow #6 Lake, Natural Orange Flavor, Polyethylene Glycol, Saccharin, Sodium Benzoate, and Sorbitol.
What does K-Vescent look like?
What are the available doses of K-Vescent?
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What should I talk to my health care provider before I take K-Vescent?
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How should I use K-Vescent?
1. For therapeutic use in patients with hypokalemia with or without metabolic alkalosis; in digitalis intoxication and in patients with hypokalemic familial periodic paralysis.
2. For prevention of potassium depletion when the dietary intake of potassium is inadequate in the following conditions; patients receiving digitalis and diuretics for congestive heart failure; hepatic cirrhosis with ascites; states of aldosterone excess with normal renal function; potassium-losing nephropathy, and certain diarrheal states.
3. The use of potassium salts in patients receiving diuretics for uncomplicated essential hypertension is often unnecessary when such patients have a normal dietary pattern. Serum potassium should be checked periodically, however, and, if hypokalemia occurs, dietary supplementation with potassium-containing foods may be adequate to control milder cases. In more severe cases supplementation with potassium salts may be indicated.
Adults - One effervescent tablet (25 mEq potassium) completely dissolved in three to four ounces or more of cold water and taken two to four times daily, or as directed by physician. It is suggested this potassium solution be taken with meals and sipped slowly over a five to ten minute period. Do not open foil pouch until time of use.
What interacts with K-Vescent?
Potassium supplements are contraindicated for patients having hyperkalemia, since a further increase in serum potassium level in these patients can results in cardiac arrest. Hyperkalemia may complicate any of the following conditions;chronic renal failure; systemic acidosis, such as diabetic acidosis, acute dehydration; extensive tissue breakdown, as in severe burns; adrenal insufficiency. Hypokalemia should not be treated by the simultaneous use of potassium salts and a potassium sparing diuretic, such as spironolactone or triamterene, since the concomitant use of these medications can result in severe hyperkalmia.
What are the warnings of K-Vescent?
Because buspirone hydrochloride tablets have no established antipsychotic activity, it should not be employed in lieu of appropriate antipsychotic treatment.
What are the precautions of K-Vescent?
General Precautions - The diagnosis of potassium depletion is ordinarily made by demonstrating hypokalemia in a patient with a clinical history suggesting a cause for potassium depletion. When interpreting the serum potassium concentration, the physician should be aware that acute alkalosis can cause hypokalemia without showing a deficit in total body potassium. Acute acidosis can increase the serum potassium level to normal even with a reduced total body potassium.. Thus close attention to acid-base balance, serum electrolytes, the clinical status of the patient, and the ECG is required in the treatment of potassium depletion.
Information for Patients
Laboratory Tests
Drug Interactions
Usage in Pregnancy
Nursing Mothers
Pediatric Use
What are the side effects of K-Vescent?
Abdominal discomfort, diarrhea, vomiting, and nausea are the most common adverse reactions to oral potassium supplements. These adverse reactions occur most frequently when the preparation is not taken with food, is not properly diluted, or not completely dissolved.
Hyperkalemia occurs infrequently in patients with normal renal function who receive oral potassium supplements. The following are symptoms of hyperkalemia: mental confusion, unexplained anxiety, cardiac arrhythmias, numbness or tingling in lips, feet, or hands, difficult breathing or shortness of breath, weakness or heaviness of legs, and unusual fatigue or weakness. (See Contraindications, Warnings, and Overdosage).
What should I look out for while using K-Vescent?
Potassium supplements are contraindicated for patients having hyperkalemia, since a further increase in serum potassium level in these patients can results in cardiac arrest. Hyperkalemia may complicate any of the following conditions;chronic renal failure; systemic acidosis, such as diabetic acidosis, acute dehydration; extensive tissue breakdown, as in severe burns; adrenal insufficiency. Hypokalemia should not be treated by the simultaneous use of potassium salts and a potassium sparing diuretic, such as spironolactone or triamterene, since the concomitant use of these medications can result in severe hyperkalmia.
The administration of potassium salts can produce hyperkalemia and cardiac arrest in patients with impaired mechanisms for potassium excretion. These reactions most commonly occur in patients receiving potassium intravenously, but may also occur in patients receiving oral potassium. Potentially fatal hyperkalemia can develop quickly and be asymptomatic. Patients using potassium salts with chronic renal disease, or any other condition which impairs the excretion of potassium, require especially careful monitoring of serum potassium concentration and appropriate adjustment of dosage.
What might happen if I take too much K-Vescent?
The use of oral potassium salts by persons with normal renal functions rarely results in serious hyperkalemia. However, if excretory mechanisms are impaired or if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result (See Contraindications and Warnings). The earliest clinical signs of hyperkalemia may be only increased serum potassium concentrations and characteristic ECG changes, such as depression of S-T segment, prolongation of the QT interval, peaking of T-waves and the loss of P-wave. The above mentioned changes in the ECG most frequently occur when the serum potassium level gets to 7 or 8 mEq per liter. At a level of 9 to 10 mEq per liter, other clinical manifestations may occur, such as muscle paralysis and death due to cardiac arrest.
The focus of the treatment of severe hyperkalemia should be on the reduction of the serum potassium level by furthering the transfer of potassium from the extracellular to the intracellular space. The treatment may include the following: a) intravenous administration of 1 liter of a 10 percent glucose solution which contains 30 to 40 units of insulin; b) in the acidolic patient, 150 mEq to 300 mEq of sodium bicarbonate administered intravenously. Other actions should include the discontinuing of potassium-sparing diuretics and potassium-containing drugs and often the oral use of a cations exchange resin (such as sodium polystyrene sulfonate) in order to eliminate gastrointestinal potassium. To make sure that the resin moves rapidly through the gastrointestinal tract, a nonabsorbable polyhydric alcohol such as sorbitol should be administered in sufficient amounts to cause a soft to semiliquid bowel movement to occur every few hours.
Hemodialysis can also be used as an effective alternative means to remove excess potassium.
How should I store and handle K-Vescent?
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Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
Potassium ion is the principal intracellular cation of most body tissues. Potassium ions participate in many essential physiological processes, such as the maintenance of intracellular tonicity, nerve impulse transmission, enzymatic reactions in intermediary metabolism, cardiac, skeletal and smooth muscle function, and the maintenance of normal renal function.
Potassium depletion may occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Potassium depletion usually develops slowly as a result of lengthy therapy with oral diuretics, primary or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion is additionally associated with severe diarrhea, accompanied by vomiting. Potassium depletion due to these causes is usually accompanied by a concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may result in fatigue, weakness, nausea, drowsiness, loss of appetite, edema, oliguria and chronic ileus with distention. Potassium deficiency may be manifested by shallow breathing, lowered blood pressure, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, or other ECG changes, such as lengthened Q-T interval, depressed S-T segment, and depressed or inverted T-wave. In advanced cases of potassium deficiency, flaccid paralysis and/or impaired ability to concentrate urine may be evident.
Non-Clinical Toxicology
Potassium supplements are contraindicated for patients having hyperkalemia, since a further increase in serum potassium level in these patients can results in cardiac arrest. Hyperkalemia may complicate any of the following conditions;chronic renal failure; systemic acidosis, such as diabetic acidosis, acute dehydration; extensive tissue breakdown, as in severe burns; adrenal insufficiency. Hypokalemia should not be treated by the simultaneous use of potassium salts and a potassium sparing diuretic, such as spironolactone or triamterene, since the concomitant use of these medications can result in severe hyperkalmia.The administration of potassium salts can produce hyperkalemia and cardiac arrest in patients with impaired mechanisms for potassium excretion. These reactions most commonly occur in patients receiving potassium intravenously, but may also occur in patients receiving oral potassium. Potentially fatal hyperkalemia can develop quickly and be asymptomatic. Patients using potassium salts with chronic renal disease, or any other condition which impairs the excretion of potassium, require especially careful monitoring of serum potassium concentration and appropriate adjustment of dosage.
Psychotropic Agents:
The use of monoamine oxidase inhibitors (MAOIs) intended to treat depression with buspirone or within 14 days of stopping treatment with buspirone is contraindicated because of an increased risk of serotonin syndrome and/or elevated blood pressure. The use of buspirone within 14 days of stopping an MAOI intended to treat depression is also contraindicated.
Starting buspirone in a patient who is being treated with reversible MAOIs such as linezolid or intravenous methylene blue is also contraindicated because of an increased risk of serotonin syndrome. (see , and )
After addition of buspirone to the amitriptyline dose regimen, no statistically significant differences in the steady-state pharmacokinetic parameters (C, AUC, and C) of amitriptyline or its metabolite nortriptyline were observed.
After addition of buspirone to the diazepam dose regimen, no statistically significant differences in the steady-state pharmacokinetic parameters (C, AUC, and C) were observed for diazepam, but increases of about 15% were seen for nordiazepam, and minor adverse clinical effects (dizziness, headache, and nausea) were observed.
In a study in normal volunteers, concomitant administration of buspirone and haloperidol resulted in increased serum haloperidol concentrations. The clinical significance of this finding is not clear.
[see ].
There is one report suggesting that the concomitant use of Desyrel (trazodone hydrochloride) and buspirone may have caused 3- to 6-fold elevations on SGPT (ALT) in a few patients. In a similar study attempting to replicate this finding, no interactive effect on hepatic transaminases was identified.
Coadministration of buspirone with either triazolam or flurazepam did not appear to prolong or intensify the sedative effects of either benzodiazepine.
Other Psychotropics:
Because the effects of concomitant administration of buspirone with most other psychotropic drugs have not been studied, the concomitant use of buspirone with other CNS-active drugs should be approached with caution.
Buspirone has been shown to be metabolized by CYP3A4. This finding is consistent with the interactions observed between buspirone and the following:
In a study of nine healthy volunteers, coadministration of buspirone (10 mg as a single dose) with verapamil (80 mg t.i.d.) or diltiazem (60 mg t.i.d.) increased plasma buspirone concentrations (verapamil increased AUC and Cof buspirone 3.4-fold while diltiazem increased AUC and C 5.5-fold and 4-fold, respectively.) Adverse events attributable to buspirone may be more likely during concomitant administration with either diltiazem or verapamil. Subsequent dose adjustment may be necessary and should be based on clinical assessment.
In a study in healthy volunteers, coadministration of buspirone (10 mg as a single dose) with erythromycin (1.5 g/day for 4 days) increased plasma buspirone concentrations (5-fold increase in C and 6-fold increase in AUC). These pharmacokinetic interactions were accompanied by an increased incidence of side effects attributable to buspirone. If the two drugs are to be used in combination, a low dose of buspirone (e.g., 2.5 mg b.i.d.) is recommended. Subsequent dose adjustment of either drug should be based on clinical assessment.
In a study in healthy volunteers, coadministration of buspirone (10 mg as a single dose) with grapefruit juice (200 mL double-strength t.i.d. for 2 days) increased plasma buspirone concentrations (4.3-fold increase in C; 9.2-fold increase in AUC). Patients receiving buspirone should be advised to avoid drinking such large amounts of grapefruit juice.
In a study in healthy volunteers, coadministration of buspirone (10 mg as a single dose) with itraconazole (200 mg/day for 4 days) increased plasma buspirone concentrations (13-fold increase in C and 19-fold increase in AUC). These pharmacokinetic interactions were accompanied by an increased incidence of side effects attributable to buspirone. If the two drugs are to be used in combination, a low dose of buspirone (e.g., 2.5 mg q.d.) is recommended. Subsequent dose adjustment of either drug should be based on clinical assessment.
In a study of steady-state pharmacokinetics in healthy volunteers, coadministration of buspirone (2.5 or 5 mg b.i.d.) with nefazodone (250 mg b.i.d.) resulted in marked increases in plasma buspirone concentrations (increases up to 20-fold in C and up to 50-fold in AUC) and statistically significant decreases (about 50%) in plasma concentrations of the buspirone metabolite 1-PP. With 5 mg b.i.d. doses of buspirone, slight increases in AUC were observed for nefazodone (23%) and its metabolites hydroxynefazodone (HO-NEF) (17%) and meta-chlorophenylpiperazine (9%). Slight increases in C were observed for nefazodone (8%) and its metabolite HO-NEF (11%).
Subjects receiving buspirone 5 mg b.i.d. and nefazodone 250 mg b.i.d experienced lightheadedness, asthenia, dizziness, and somnolence, adverse events also observed with either drug alone. If the two drugs are to be used in combination, a low dose of buspirone (e.g., 2.5 mg q.d.) is recommended. Subsequent dose adjustment of either drug should be based on clinical assessment.
In a study in healthy volunteers, coadministration of buspirone (30 mg as a single dose) with rifampin (600 mg/day for 5 days) decreased the plasma concentrations (83.7% decrease in C; 89.6% decrease in AUC) and pharmacodynamic effects of buspirone. If the two drugs are to be used in combination, the dosage of buspirone may need adjusting to maintain anxiolytic effect.
Other Inhibitors and Inducers of CYP3A4:
Substances that inhibit CYP3A4, such as ketoconazole or ritonavir, may inhibit buspirone metabolism and increase plasma concentrations of buspirone while substances that induce CYP3A4, such as dexamethasone, or certain anticonvulsants (phenytoin, phenobarbital, carbamazepine), may increase the rate of buspirone metabolism. If a patient has been titrated to a stable dosage on buspirone, a dose adjustment of buspirone may be necessary to avoid adverse events attributable to buspirone or diminished anxiolytic activity. Consequently, when administered with a potent inhibitor of CYP3A4, a low dose of buspirone used cautiously is recommended. When used in combination with a potent inducer of CYP3A4 the dosage of buspirone may need adjusting to maintain anxiolytic effect.
Other Drugs:
Coadministration of buspirone with cimetidine was found to increase C (40%) and T (2–fold), but had minimal effects on the AUC of buspirone.
Protein Binding:
Therapeutic levels of aspirin, desipramine, diazepam, flurazepam, ibuprofen, propranolol, thioridazine, and tolbutamide had only a limited effect on the extent of binding of buspirone to plasma proteins (see ).
General Precautions - The diagnosis of potassium depletion is ordinarily made by demonstrating hypokalemia in a patient with a clinical history suggesting a cause for potassium depletion. When interpreting the serum potassium concentration, the physician should be aware that acute alkalosis can cause hypokalemia without showing a deficit in total body potassium. Acute acidosis can increase the serum potassium level to normal even with a reduced total body potassium.. Thus close attention to acid-base balance, serum electrolytes, the clinical status of the patient, and the ECG is required in the treatment of potassium depletion.
Information for Patients
Laboratory Tests
Drug Interactions
Usage in Pregnancy
Nursing Mothers
Pediatric Use
Abdominal discomfort, diarrhea, vomiting, and nausea are the most common adverse reactions to oral potassium supplements. These adverse reactions occur most frequently when the preparation is not taken with food, is not properly diluted, or not completely dissolved. Hyperkalemia occurs infrequently in patients with normal renal function who receive oral potassium supplements. The following are symptoms of hyperkalemia: mental confusion, unexplained anxiety, cardiac arrhythmias, numbness or tingling in lips, feet, or hands, difficult breathing or shortness of breath, weakness or heaviness of legs, and unusual fatigue or weakness. (See Contraindications, Warnings, and Overdosage).
Reference
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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