Can you take Acetohexamide with Flavalta?

The EPINEPHrine in Flavalta has a moderate potential interaction with Acidosis.

Acidosis, hypoxia, and hypercapnia may reduce the effectiveness of sympathomimetic amines in raising blood pressure. These conditions should be corrected before initiating therapy with sympathomimetic amines, if possible. Monitoring the patients acid-base balance, carbon dioxide levels, and oxygen saturation is recommended.

acetoHEXAMIDE has a major potential interaction with Adrenal Insufficiency.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

acetoHEXAMIDE has a major potential interaction with Anorexia/Feeding Problems.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

acetoHEXAMIDE has a major potential interaction with Autonomic Neuropathy.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

acetoHEXAMIDE has a major potential interaction with Cardiovascular Conditions and Disorders.

The use of oral hypoglycemic agents may be associated with an increased risk of cardiovascular mortality compared to treatment with diet alone or diet with insulin. This warning is based on the University Group Diabetes Program (UGDP) study, a long-term prospective clinical trial designed to evaluate the effectiveness of glucose-lowering drugs in preventing or delaying vascular complications in patients with non-insulin-dependent diabetes. Patients treated with diet plus a fixed dosage of either tolbutamide (a sulfonylurea) or phenformin (a biguanide) for 5 to 8 years had a cardiovascular mortality rate approximately 2.5 times that of patients treated with diet alone, resulting in discontinuation of both these treatments in the study. Despite controversy regarding interpretation of these results, clinicians and patients should be aware of the potential risk when making treatment decisions for diabetes, particularly in the presence of underlying cardiovascular disease. Data are not available for other sulfonylureas or biguanides, nor for hypoglycemic agents belonging to other classes. However, given the similarities in chemical structure and/or mode of action, the same caution should be applied.

The EPINEPHrine in Flavalta has a major potential interaction with Cardiovascular Conditions and Disorders.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

The EPINEPHrine in Flavalta has a major potential interaction with Dehydration.

The use of sympathomimetic amines has been infrequently associated with significant hypotension especially in dehydrated patients secondary to the drug's beta-2 mediated vasodilation. Hypovolemia should be corrected, if possible, before administering sympathomimetic amines. Blood pressure and ECG should be monitored at regular intervals. Monitoring of cardiac output and pulmonary wedge pressure may also be desired.

acetoHEXAMIDE has a moderate potential interaction with Dehydration.

Treatment with sulfonylureas may cause hyponatremia, in patients who are on other medications or have medical conditions known to cause hyponatremia or increase release of antidiuretic hormone. The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has been reported with certain sulfonylureas and these drugs may augment the peripheral (antidiuretic) action of ADH and/or increase release of ADH. Caution should be used when treating patients with hyponatremia or at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted.

The EPINEPHrine in Flavalta has a moderate potential interaction with Diabetes Mellitus.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

acetoHEXAMIDE has a moderate potential interaction with G-6-PD Deficiency.

Sulfonylureas can cause hemolytic anemia in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency. Therapy with these agents should be used with caution in patients with G6PD deficiency and consider the use of a non-sulfonylurea alternative. There have been postmarketing reports of hemolytic anemia in patients receiving these drugs who did not have known G6PD deficiency.

The lidocaine in Flavalta has a major potential interaction with Heart Block.

The use of lidocaine is contraindicated in patients with Stokes-Adam syndrome, Wolff-Parkinson White syndrome, or second- or third-degree AV block in the absence of a functional artificial pacemaker, or congenital QT prolongation.

The lidocaine in Flavalta has a major potential interaction with Heart Failure.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

The lidocaine in Flavalta has a moderate potential interaction with Hyperkalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The EPINEPHrine in Flavalta has a major potential interaction with Hyperthyroidism.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

acetoHEXAMIDE has a major potential interaction with Hypoglycemia.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

The lidocaine in Flavalta has a moderate potential interaction with Hypokalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

acetoHEXAMIDE has a moderate potential interaction with Hyponatremia.

Treatment with sulfonylureas may cause hyponatremia, in patients who are on other medications or have medical conditions known to cause hyponatremia or increase release of antidiuretic hormone. The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has been reported with certain sulfonylureas and these drugs may augment the peripheral (antidiuretic) action of ADH and/or increase release of ADH. Caution should be used when treating patients with hyponatremia or at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted.

The lidocaine in Flavalta has a major potential interaction with Hypotension.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

acetoHEXAMIDE has a major potential interaction with Liver Disease.

Sulfonylureas are metabolized in the liver, and their metabolites (some with pharmacologic activity) are excreted in the urine and feces. Patients with impaired liver and/or renal function treated with sulfonylureas may be exposed to higher serum drug concentrations, which can increase the potential for severe hypoglycemic episodes induced by these agents. In the presence of hepatic impairment, gluconeogenic capacity may also be diminished, further compounding the risk. Therapy with sulfonylureas should be administered cautiously in patients with liver and/or renal disease. Reduced dosages and longer intervals between dosage adjustments may be required. Hypoglycemia, if it occurs during treatment, may be prolonged in these patients because of slowed metabolism and/or excretion of the drugs.

The lidocaine in Flavalta has a major potential interaction with Liver Disease.

Lidocaine is rapidly and extensively metabolized by the liver. Less than 10% is eliminated unchanged in the urine. Several inactive and two active forms (MEGX and GX) have been identified. MEGX and GX exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. The pharmacokinetic disposition of lidocaine is altered by changes in hepatic function, including hepatic blood flow. Therapy with lidocaine should be administered cautiously and dosing modifications for repeated or loading and maintenance doses may be necessary. Clinical monitoring of cardiac (continuous ECG) is required and serum metabolite concentrations and monitoring hepatic function are recommended.

The lidocaine in Flavalta has a moderate potential interaction with Magnesium Imbalance.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

acetoHEXAMIDE has a major potential interaction with Malnourishment.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

The EPINEPHrine in Flavalta has a moderate potential interaction with Neurological Disorders.

Epinephrine should be administered with caution to patients with Parkinson's disease as these patients may experience psychomotor agitation or notice a temporary worsening of symptoms.

acetoHEXAMIDE has a major potential interaction with Panhypopituitarism.

The use of insulin is contraindicated during episodes of hypoglycemia. Hypoglycemia may commonly occur during treatment with insulin and/or oral hypoglycemic agents. Care should be taken in patients who may be particularly susceptible to the development of hypoglycemic episodes during the use of these drugs, including but not limited to those who are debilitated or malnourished, those with renal or hepatic impairment, those with defective counterregulatory mechanisms (e.g., autonomic neuropathy and adrenal or pituitary insufficiency), and those with reduced awareness of hypoglycemia. Symptomatic awareness of hypoglycemia may be reduced in patients with longstanding diabetes, diabetic nerve disease, recurrent hypoglycemia, or concomitant medications that block the sympathetic nervous system (e.g., beta-blockers). Changes to any glucose-lowering medications, meal pattern, or physical activity may also increase risk of hypoglycemia. Increased frequency of glucose monitoring is recommended in patients at higher risk for hypoglycemia.

The EPINEPHrine in Flavalta has a moderate potential interaction with Parkinsonism.

Epinephrine should be administered with caution to patients with Parkinson's disease as these patients may experience psychomotor agitation or notice a temporary worsening of symptoms.

The EPINEPHrine in Flavalta has a major potential interaction with Pheochromocytoma.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

acetoHEXAMIDE has a major potential interaction with Renal Dysfunction.

Sulfonylureas are metabolized in the liver, and their metabolites (some with pharmacologic activity) are excreted in the urine and feces. Patients with impaired liver and/or renal function treated with sulfonylureas may be exposed to higher serum drug concentrations, which can increase the potential for severe hypoglycemic episodes induced by these agents. In the presence of hepatic impairment, gluconeogenic capacity may also be diminished, further compounding the risk. Therapy with sulfonylureas should be administered cautiously in patients with liver and/or renal disease. Reduced dosages and longer intervals between dosage adjustments may be required. Hypoglycemia, if it occurs during treatment, may be prolonged in these patients because of slowed metabolism and/or excretion of the drugs.

The lidocaine in Flavalta has a major potential interaction with Renal Dysfunction.

Lidocaine is primarily eliminated by the kidney. Less than 10% is eliminated unchanged in the urine. Two active metabolites (MEGX and GX) have been identified that exhibit antiarrhythmic and convulsant properties. GX accumulates during prolonged intravenous lidocaine infusion. Serum concentrations of lidocaine and the active metabolites are increased and the half-life prolonged in patients with renal impairment. Therapy with lidocaine should be administered cautiously and dosing modified for repeated or maintenance doses in patients with compromised renal function. Clinical monitoring of cardiac function (continual ECG) is required and serum metabolite concentrations and monitoring renal function are recommended.

The lidocaine in Flavalta has a major potential interaction with Seizures.

Seizures have occurred during lidocaine therapy and have been associated with the rapid administration of a large intravenous doses or accumulation of active metabolites with maintenance therapy. Therapy with lidocaine should be administered cautiously to patients with or predisposed to seizure disorders. Clinical monitoring of cardiac (continuous ECG) is required, and serum metabolite concentrations are recommended.

acetoHEXAMIDE has a moderate potential interaction with SIADH.

Treatment with sulfonylureas may cause hyponatremia, in patients who are on other medications or have medical conditions known to cause hyponatremia or increase release of antidiuretic hormone. The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has been reported with certain sulfonylureas and these drugs may augment the peripheral (antidiuretic) action of ADH and/or increase release of ADH. Caution should be used when treating patients with hyponatremia or at greater risk of developing hyponatremia such as elderly patients, patients taking diuretics or those who are volume-depleted.