Atenolol/chlorthalidone Disease Interactions
There are 24 disease interactions with atenolol/chlorthalidone:
Atenolol (Includes Atenolol/chlorthalidone) ↔ Hemodialysis
Severe Potential Hazard, High plausibility
Applies to: hemodialysis
Atenolol is moderately removed by conventional hemodialysis. Patients on hemodialysis should receive a dose of atenolol following each dialysis session when they are hemodynamically stable to avoid marked falls in blood pressure. The hemodynamic status should be closely monitored before and after the dose.
Atenolol (Includes Atenolol/chlorthalidone) ↔ Renal Dysfunction
Severe Potential Hazard, High plausibility
Applies to: Renal Dysfunction
Atenolol is eliminated by the kidney. Significant accumulation of the drug occurs in patients with a creatinine clearance below 35 mL/min/1.73 m2. Dosage adjustments are recommended for these patients.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Asthma/Copd
Severe Potential Hazard, Moderate plausibility
Applies to: Asthma, Chronic Obstructive Pulmonary Disease
In general, beta-adrenergic receptor blocking agents (i.e., beta-blockers) should not be used in patients with bronchospastic diseases. Beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Bradyarrhythmia/Av Block
Severe Potential Hazard, High plausibility
Applies to: Heart Block, Sinus Node Dysfunction
The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Cardiogenic Shock/Hypotension
Severe Potential Hazard, High plausibility
Applies to: Cardiogenic Shock, Hypotension
The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Diabetes
Severe Potential Hazard, High plausibility
Applies to: Diabetes Mellitus
Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Hypersensitivity
Severe Potential Hazard, High plausibility
Applies to: Allergies
The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Pvd
Severe Potential Hazard, High plausibility
Applies to: Peripheral Arterial Disease, Cerebrovascular Insufficiency
Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Anuria
Severe Potential Hazard, High plausibility
Applies to: Anuria
The use of thiazide diuretics is contraindicated in patients with anuria.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Electrolyte Losses
Severe Potential Hazard, High plausibility
Applies to: Hypokalemia, Diarrhea, Electrolyte Abnormalities, Hyperaldosteronism, Hyponatremia, Magnesium Imbalance, Malnourished, Vomiting, Ventricular Arrhythmia, Dehydration
The use of thiazide diuretics is commonly associated with loss of electrolytes, most significantly potassium but also sodium, chloride, bicarbonate, and magnesium. The loss of other electrolytes such as phosphate, bromide and iodide is usually slight. Potassium and magnesium depletion may lead to cardiac arrhythmias and cardiac arrest. Other electrolyte-related complications include metabolic alkalosis and hyponatremia, which are rarely life-threatening. Therapy with thiazide diuretics should be administered cautiously in patients with or predisposed to fluid and electrolyte depletion, including patients with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; and those with poor nutritional status. Fluid and electrolyte abnormalities should be corrected prior to initiating therapy, and blood pressure as well as serum electrolyte concentrations monitored periodically and maintained at normal ranges during therapy. Patients should be advised to immediately report signs and symptoms of fluid or electrolyte imbalance, including dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Digitalized patients and patients with a history of ventricular arrhythmias should be monitored carefully, since development of hypokalemia may be particularly dangerous in these patients. The risk of hypokalemia may be minimized by slow diuresis, a lower thiazide dosage, potassium supplementation, or combined use with a potassium-sparing diuretic.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Liver Disease
Severe Potential Hazard, High plausibility
Applies to: Liver Disease
Patients with severe liver disease or cirrhosis are very susceptible to thiazide-induced hypokalemic hypochloremic alkalosis. Blood ammonia concentrations may be further increased in patients with previously elevated concentrations. Hepatic encephalopathy and death have occurred secondary to the electrolyte alterations accompanying diuretic use. Therapy with thiazide diuretics should be administered cautiously in patients with impaired hepatic function or progressive liver disease, and discontinued promptly if signs of impending hepatic coma appear (e.g., tremors, confusion, and increased jaundice).
Thiazides (Includes Atenolol/chlorthalidone) ↔ Lupus Erythematosus
Severe Potential Hazard, Low plausibility
Applies to: Lupus Erythematosus
The use of thiazide diuretics has been reported to possibly exacerbate or activate systemic lupus erythematosus. Reported cases have generally been associated with chlorothiazide and hydrochlorothiazide. Therapy with thiazide diuretics should be administered cautiously in patients with a history or risk of SLE.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Renal Function Disorders
Severe Potential Hazard, High plausibility
Applies to: Renal Dysfunction
Thiazide diuretics may be ineffective when the glomerular filtration rate is low (GFR < 25 mL/min) because they are not expected to be filtered into the renal tubule, their site of action. In addition, thiazide diuretics decrease the GFR and may precipitate azotemia in renal disease. Cumulative effects may also develop because most of these drugs are excreted unchanged in the urine by glomerular filtration and active tubular secretion. Therapy with thiazide diuretics should be administered cautiously at reduced dosages in patients with renal impairment. If renal function becomes progressively worse, as indicated by rising BUN or serum creatinine levels, an interruption or discontinuation of thiazide therapy should be considered.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Chf
Moderate Potential Hazard, High plausibility
Applies to: Congestive Heart Failure
Beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with overt congestive heart failure (CHF). Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. However, therapy with beta-blockers may be beneficial and can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Carvedilol, specifically, is indicated for use with these agents in the treatment of mild to severe heart failure of ischemic or cardiomyopathic origin. There is also increasing evidence that the addition of a beta-blocker to standard therapy can improve morbidity and mortality in patients with advanced heart failure, although it is uncertain whether effectiveness varies significantly with the different agents. Data from one meta-analysis study suggest a greater reduction of mortality risk for nonselective beta-blockers than for beta-1 selective agents.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Hyperlipidemia
Moderate Potential Hazard, Moderate plausibility
Applies to: Hyperlipidemia
Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Hyperthyroidism
Moderate Potential Hazard, High plausibility
Applies to: Hyperthyroidism
When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Iop
Moderate Potential Hazard, Moderate plausibility
Applies to: Glaucoma/Intraocular Hypertension
Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Ischemic Heart Disease
Moderate Potential Hazard, High plausibility
Applies to: Ischemic Heart Disease
Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.
Beta-Blockers (Includes Atenolol/chlorthalidone) ↔ Myasthenia Gravis
Moderate Potential Hazard, Low plausibility
Applies to: Myoneural Disorder
Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Diabetes
Moderate Potential Hazard, Moderate plausibility
Applies to: Diabetes Mellitus, Abnormal Glucose Tolerance
Thiazide diuretics may cause hyperglycemia and glycosuria in patients with diabetes. They may also precipitate diabetes in prediabetic patients. These effects are usually reversible following discontinuation of the drugs. Therapy with thiazide diuretics should be administered cautiously in patients with diabetes mellitus, glucose intolerance, or a predisposition to hyperglycemia. Patients with diabetes mellitus should be monitored more closely during thiazide therapy, and their antidiabetic regimen adjusted accordingly.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Hyperlipidemia
Moderate Potential Hazard, Moderate plausibility
Applies to: Hyperlipidemia
Thiazide diuretics may increase serum triglyceride and cholesterol levels, primarily LDL and VLDL. Whether these effects are dose-related and sustained during chronic therapy are unknown. Patients with preexisting hyperlipidemia may require closer monitoring during thiazide therapy, and adjustments made accordingly in their lipid-lowering regimen
Thiazides (Includes Atenolol/chlorthalidone) ↔ Hyperparathyroidism
Moderate Potential Hazard, Moderate plausibility
Applies to: Hyperparathyroidism
Urinary calcium excretion is decreased by thiazide diuretics during chronic administration. Pathologic changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been reported during prolonged therapy. However, the common complications of hyperparathyroidism such as renal lithiasis, bone resorption, and peptic ulceration have not been seen. Clinicians should be cognizant of these effects when prescribing or administering thiazide therapy to patients with hyperparathyroidism. These drugs should be discontinued before carrying out tests for parathyroid function.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Hyperuricemia
Moderate Potential Hazard, High plausibility
Applies to: Gout
Thiazide diuretics decrease the rate of uric acid excretion. Hyperuricemia occurs frequently but is usually asymptomatic and rarely leads to clinical gout except in patients with a history of gout or chronic renal failure. Therapy with thiazide diuretics should be administered cautiously in such patients.
Thiazides (Includes Atenolol/chlorthalidone) ↔ Thyroid Function Tests
Moderate Potential Hazard, Moderate plausibility
Applies to: Thyroid Disease
Thiazide diuretics may decrease serum PBI (protein-bound iodine) levels without associated thyroid disturbance. Clinicians should be cognizant of this effect when prescribing or administering thiazide therapy to patients with thyroid disorders.
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See also...
Drug Interaction Classification
The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.
| Major | Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit. |
| Moderate | Moderately clinically significant. Usually avoid combinations; use it only under special circumstances. |
| Minor | Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan. |
Do not stop taking any medications without consulting your healthcare provider.
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