Can you take Liquihistine DM with Potassium chloride?

Potassium chloride has a major potential interaction with Acidosis.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride has a moderate potential interaction with Acidosis.

Hypokalemia in patients with metabolic acidosis should be treated with an alkalinizing potassium salt (i.e. acetate, bicarbonate, citrate, or gluconate) rather than potassium chloride, since alkali therapy helps to promote cellular uptake of potassium. Close monitoring of acid-base balance, serum electrolytes, electrocardiogram, and clinical status is recommended.

Potassium chloride has a major potential interaction with Adrenal Insufficiency.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Asthma.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

The phenylpropanolamine in Liquihistine DM has a moderate potential interaction with Benign Prostatic Hyperplasia.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Potassium chloride has a major potential interaction with Burns, External.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The phenylpropanolamine in Liquihistine DM 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 brompheniramine in Liquihistine DM has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The phenylpropanolamine in Liquihistine DM has a major potential interaction with Cerebrovascular Insufficiency.

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 brompheniramine in Liquihistine DM has a moderate potential interaction with COPD.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Potassium chloride has a major potential interaction with Dehydration.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride has a major potential interaction with Dehydration.

Potassium chloride liquid suspension contains the stool softener, docusate sodium, as a dispersing agent. Clinical studies with potassium chloride liquid suspension indicate that minor changes in stool consistency may be common though usually well tolerated. However, patients may rarely experience diarrhea or cramping abdominal pain. Patients with severe or chronic diarrhea or who are dehydrated ordinarily should not be prescribed potassium chloride liquid suspension.

Potassium chloride has a major potential interaction with Diabetes Mellitus.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The phenylpropanolamine in Liquihistine DM 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.

Potassium chloride has a major potential interaction with Diarrhea.

Administration of potassium salts in severe dehydration may predispose to renal impairment. Therapy with potassium salts should be administered cautiously in patients with acute dehydration (e.g., due to severe or prolonged diarrhea or heat stress). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride has a major potential interaction with Diarrhea.

Potassium chloride liquid suspension contains the stool softener, docusate sodium, as a dispersing agent. Clinical studies with potassium chloride liquid suspension indicate that minor changes in stool consistency may be common though usually well tolerated. However, patients may rarely experience diarrhea or cramping abdominal pain. Patients with severe or chronic diarrhea or who are dehydrated ordinarily should not be prescribed potassium chloride liquid suspension.

Potassium chloride has a major potential interaction with Esophageal Disease.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Potassium chloride has a major potential interaction with Familial Periodic Paralysis.

Administration of potassium salts may precipitate attacks in familial hyperkalemic periodic paralysis or paramyotonia congenita. Therapy with potassium preparations should be administered cautiously in patients with these conditions.

Potassium chloride has a major potential interaction with Gastritis/Duodenitis.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Potassium chloride has a major potential interaction with Gastrointestinal Hemorrhage.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Potassium chloride has a major potential interaction with Gastrointestinal Obstruction.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Gastrointestinal Obstruction.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Potassium chloride has a major potential interaction with Gastrointestinal Perforation.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

The phenylpropanolamine in Liquihistine DM has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

Potassium chloride has a major potential interaction with Hemolytic Anemia.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

Potassium chloride has a major potential interaction with History, Peptic Ulcer.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

Potassium chloride has a major potential interaction with Hyperkalemia.

The use of potassium salts is contraindicated in patients with hyperkalemia, since a further increase in serum potassium concentration in such patients can lead to cardiac arrhythmias or arrest. Potassium therapy should be administered cautiously in patients with conditions predisposing to hyperkalemia, such as chronic renal failure, systemic acidosis, acute dehydration, hypoaldosteronism (e.g., due to primary adrenal insufficiency or congenital adrenal enzyme deficiency), uncontrolled diabetes mellitus, and extensive tissue breakdown (e.g., due to severe burns, intravascular hemolysis, tumor lysis syndrome, or rhabdomyolysis). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The phenylpropanolamine in Liquihistine DM 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.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Hyperthyroidism.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Hypotension.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Liver Disease.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Potassium chloride has a major potential interaction with Peptic Ulcer.

The use of all solid oral formulations of potassium is contraindicated in patients with arrested or delayed gastrointestinal (GI) transit, whether due to structural, pathological, or pharmacological causes. Potassium is irritating to the GI mucosa and may cause ulcerative and/or stenotic lesions during prolonged physical contact. Based on spontaneous adverse reaction reports, the frequency of small bowel lesions associated with enteric-coated preparations of potassium chloride is 40 to 50 per 100,000 patient-years, while that for wax matrix controlled-release formulations is less than one per 100,000 patient years. Esophageal ulceration has also been reported following administration of controlled-release formulations of potassium chloride in cardiac patients with esophageal compression due to enlarged left atrium. Potassium supplementation should be administered as a liquid preparation or as an aqueous suspension in patients with esophageal obstruction and/or delayed gastrointestinal transit time.

Because of ulcerogenic effects, oral potassium should be administered cautiously in patients with peptic ulcers or other upper gastrointestinal diseases associated with inflammation, bleeding, or perforation. Patients should be advised not to crush, chew, or break potassium tablets or capsules, and to take them with meals and a full glass of water or other liquid. Potassium liquids should be diluted prior to consumption.

The phenylpropanolamine in Liquihistine DM has a moderate potential interaction with Prostate Tumor, Benign.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

The phenylpropanolamine in Liquihistine DM has a moderate potential interaction with Psychiatric Disorders.

Phenylpropanolamine may precipitate or exacerbate psychotic symptoms, particularly at high dosages. Therapy with phenylpropanolamine should be administered cautiously in patients with a history of psychiatric disorders.

The phenylpropanolamine in Liquihistine DM has a moderate potential interaction with Psychosis.

Phenylpropanolamine may precipitate or exacerbate psychotic symptoms, particularly at high dosages. Therapy with phenylpropanolamine should be administered cautiously in patients with a history of psychiatric disorders.

Potassium chloride has a major potential interaction with Renal Dysfunction.

The use of potassium salts is contraindicated in patients with severe renal impairment characterized by oliguria, anuria, or azotemia. Since potassium is excreted by the kidney, the administration of potassium salts in such patients, particularly by the intravenous route, may produce hyperkalemia and cardiac arrhythmias or arrest. Therapy with potassium salts should be administered cautiously in patients with diminished renal function or other conditions which impairs potassium excretion (e.g. adrenal insufficiency). Close monitoring of serum potassium concentrations is recommended, as potentially fatal hyperkalemia can develop rapidly and is often asymptomatic, manifested only by an increased potassium level (6.5 to 8 mEq/L) and characteristic electrocardiographic changes (peaking of T waves, loss of P waves, depression of ST segment, prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9 to 12 mEq/L). Continuous or serial electrocardiography may be appropriate in some patients during replacement therapy, particularly if given intravenously.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Renal Dysfunction.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

The brompheniramine in Liquihistine DM has a moderate potential interaction with Urinary Retention.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.