THERABLOC Atenolol 25mg Tablet 1's
RXDRUG-DR-XY14835-1pc
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Features
Brand
Therabloc
Full Details
Dosage Strength
25mg
Drug Ingredients
- Atenolol
Drug Packaging
Tablet 1's
Generic Name
Atenolol
Dosage Form
Tablet
Registration Number
DR-XY14835
Drug Classification
Prescription Drug (RX)
Description
Indications/Uses
Long-term management of angina pectoris due to coronary atherosclerosis.
Management of hypertension; may be used alone or in combination with other antihypertensive drugs particularly with a thiazide-type diuretic.
Acute myocardial infarction.
Management of hypertension; may be used alone or in combination with other antihypertensive drugs particularly with a thiazide-type diuretic.
Acute myocardial infarction.
Dosage/Direction for Use
Adult Dose: Initially, 50 mg orally once daily. Maintenance dose varies from 25-100 mg daily.
Hypertension: Most patients respond to 50-100 mg orally daily. The effect will be fully established after 1-2 weeks. A further reduction in blood pressure may be achieved by combining therapy with other antihypertensive agents.
Angina Pectoris: Effective oral dose to most patients is 100 mg daily as a single or divided dose. Some patients require a dosage of 200 mg once a day for optimal effect. It is unlikely that an additional benefit will be gained by increasing the dose.
A dose of 25 mg is useful in patients with hypertension or angina who are overly sensitive to the negative chronotropic effect of higher doses (50-100 mg) of atenolol. A 25-mg dose may keep the heart rate within normal levels particularly at night and still produce the desired antihypertensive and antianginal action alone or in combination with other drugs.
Myocardial Infarction: 5 mg by slow IV injection (1 mg/min), should be given to a patient within 12 hrs of the onset of chest pain, followed by another 5 mg IV 10 min later. In patients who tolerate the full IV dose (10 mg), atenolol 50 mg should be initiated 10 min after the last IV dose followed by another 50-mg oral dose 12 hrs later. Thereafter, atenolol can be given orally either 100 mg once daily or 50 mg twice daily for a further 6-9 days or until discharge from the hospital. If bradycardia or hypotension requiring treatment or any untoward effects occur, atenolol therapy should be discontinued. An oral dose of 100 mg daily is recommended for long-term prophylaxis.
Hypertension: Most patients respond to 50-100 mg orally daily. The effect will be fully established after 1-2 weeks. A further reduction in blood pressure may be achieved by combining therapy with other antihypertensive agents.
Angina Pectoris: Effective oral dose to most patients is 100 mg daily as a single or divided dose. Some patients require a dosage of 200 mg once a day for optimal effect. It is unlikely that an additional benefit will be gained by increasing the dose.
A dose of 25 mg is useful in patients with hypertension or angina who are overly sensitive to the negative chronotropic effect of higher doses (50-100 mg) of atenolol. A 25-mg dose may keep the heart rate within normal levels particularly at night and still produce the desired antihypertensive and antianginal action alone or in combination with other drugs.
Myocardial Infarction: 5 mg by slow IV injection (1 mg/min), should be given to a patient within 12 hrs of the onset of chest pain, followed by another 5 mg IV 10 min later. In patients who tolerate the full IV dose (10 mg), atenolol 50 mg should be initiated 10 min after the last IV dose followed by another 50-mg oral dose 12 hrs later. Thereafter, atenolol can be given orally either 100 mg once daily or 50 mg twice daily for a further 6-9 days or until discharge from the hospital. If bradycardia or hypotension requiring treatment or any untoward effects occur, atenolol therapy should be discontinued. An oral dose of 100 mg daily is recommended for long-term prophylaxis.
Administration
May be taken with or without food.
Contraindications
Sinus bradycardia, heart block greater than 1st-degree, cardiogenic shock and acute unstable cardiac failure.
Warnings
Cardiac Failure: Sympathetic stimulation is necessary in supporting circulatory function in congestive heart failure, and β-blockade carries the potential hazard of depressing myocardial contractility and precipitating more severe failure. In patients who have congestive heart failure controlled by digitalis and/or diuretics, atenolol should be cautiously administered, since both digitalis and atenolol slow AV conduction.
However, latest clinical trials using other β-blockers, metoprolol, bisoprolol and carvedilol have been shown to improve symptoms and to decrease long-term cardiac morbidity and mortality among patients with chronic stable heart failure. However, initial doses used are small and titration to full dose is achieved after several weeks.
Patients with a History of Cardiac Failure: Continued depression of the myocardium with β-blocking agents over a period of time can, in some cases, lead to cardiac failure. At the first sign or symptom of impending cardiac failure, patients should be fully digitalized and/or be given a diuretic and the response observed closely. If cardiac failure continues despite adequate digitalization and diuresis, atenolol should be withdrawn.
Cessation of Therapy with Atenolol: Patients with coronary artery disease, who are being treated with atenolol, should be advised against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction and ventricular arrhythmias have been reported in angina patients following abrupt discontinuation of therapy with β-blockers. As with other β-blockers, when abrupt discontinuation of atenolol is planned, the patients should be carefully observed and advised to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol therapy abruptly even in patients treated only for hypertension.
Use in pregnancy: Atenolol can cause fetal harm when administered to a pregnant woman. Atenolol crosses the placental barrier. Administration of atenolol, starting in the 2nd trimester of pregnancy, has been associated with birth of infants who are small for gestational age. Atenolol has been shown to cause a dose-related increase in embryonal and fetal resorptions in rats when given at dosages at ≥25 times the maximum human dosage, similar effects were not observed in rabbits receiving atenolol dosages up to 12.5 times the maximum human dosage. If the drug is used during pregnancy or if the patient becomes pregnant while taking atenolol, the patient should be appraised of the potential hazard to the fetus.
However, latest clinical trials using other β-blockers, metoprolol, bisoprolol and carvedilol have been shown to improve symptoms and to decrease long-term cardiac morbidity and mortality among patients with chronic stable heart failure. However, initial doses used are small and titration to full dose is achieved after several weeks.
Patients with a History of Cardiac Failure: Continued depression of the myocardium with β-blocking agents over a period of time can, in some cases, lead to cardiac failure. At the first sign or symptom of impending cardiac failure, patients should be fully digitalized and/or be given a diuretic and the response observed closely. If cardiac failure continues despite adequate digitalization and diuresis, atenolol should be withdrawn.
Cessation of Therapy with Atenolol: Patients with coronary artery disease, who are being treated with atenolol, should be advised against abrupt discontinuation of therapy. Severe exacerbation of angina and the occurrence of myocardial infarction and ventricular arrhythmias have been reported in angina patients following abrupt discontinuation of therapy with β-blockers. As with other β-blockers, when abrupt discontinuation of atenolol is planned, the patients should be carefully observed and advised to limit physical activity to a minimum. If the angina worsens or acute coronary insufficiency develops, it is recommended that atenolol be promptly reinstituted, at least temporarily. Because coronary artery disease is common and may be unrecognized, it may be prudent not to discontinue atenolol therapy abruptly even in patients treated only for hypertension.
Use in pregnancy: Atenolol can cause fetal harm when administered to a pregnant woman. Atenolol crosses the placental barrier. Administration of atenolol, starting in the 2nd trimester of pregnancy, has been associated with birth of infants who are small for gestational age. Atenolol has been shown to cause a dose-related increase in embryonal and fetal resorptions in rats when given at dosages at ≥25 times the maximum human dosage, similar effects were not observed in rabbits receiving atenolol dosages up to 12.5 times the maximum human dosage. If the drug is used during pregnancy or if the patient becomes pregnant while taking atenolol, the patient should be appraised of the potential hazard to the fetus.
Special Precautions
Patients with bronchospastic disease should, in general, not receive β-blockers. Because of its relative β1-selectivity, however, atenolol may be used with caution in patients with bronchospastic disease who do not respond to, or cannot tolerate other antihypertensive treatment. Since β1-selectivity is not absolute, the lowest possible dose of atenolol should be used with therapy initiated at 50 mg and β2-stimulating agent should be made available. Atenolol should be used with caution in patients with diabetes mellitus. The drug may mask the tachycardia but usually not the dizziness and sweating seen with insulin-induced hypoglycemia. β-Blocking agents, especially the nonselective ones, may potentially precipitate severe acute hyperglycemia.
Atenolol should be used with caution in patients undergoing major surgery involving general anesthesia. It is not advisable to withdraw β-adrenoreceptor-blocking drugs prior to surgery in the majority of patients. However, care should be exercised when using anesthetic agents eg, those which may depress the myocardium.
Atenolol should be used with caution and in reduced dosage in patients with impaired renal function, especially when creatinine clearance is <35 mL/min/1.73 m2. It is recommended that patients receiving atenolol after hemodialysis be administered with Therabloc under close supervision in a hospital setting, since marked hypotension may occur.
Use in children: There is no pediatric experience with atenolol and for this reason, it is not recommended for pediatric use. Safety and efficacy of atenolol in children have not been established.
Atenolol should be used with caution in patients undergoing major surgery involving general anesthesia. It is not advisable to withdraw β-adrenoreceptor-blocking drugs prior to surgery in the majority of patients. However, care should be exercised when using anesthetic agents eg, those which may depress the myocardium.
Atenolol should be used with caution and in reduced dosage in patients with impaired renal function, especially when creatinine clearance is <35 mL/min/1.73 m2. It is recommended that patients receiving atenolol after hemodialysis be administered with Therabloc under close supervision in a hospital setting, since marked hypotension may occur.
Use in children: There is no pediatric experience with atenolol and for this reason, it is not recommended for pediatric use. Safety and efficacy of atenolol in children have not been established.
Adverse Reactions
Cardiovascular System: Potentially serious adverse cardiovascular effects of atenolol include bradycardia, profound hypotension, 2nd- or 3rd-degree atrioventricular (AV) block and precipitation of severe congestive heart failure (CHF).
Central Nervous System: Reversible mental depression progressing to catatonia (an acute reversible syndrome characterized by disorientation of time and place), short-term memory loss, emotional lability with slightly clouded sensorium and decreased performance on neuropsychometrics.
Gastrointestinal: Mesenteric arterial thrombosis and ischemic colitis.
Hematologic: Agranulocytosis.
Allergic: Fever, with aching and sore throat, laryngospasm and respiratory distress.
Others: Wheezing and dyspnea have occurred in patients receiving atenolol and are likely to occur when dosage of the drug exceeds 100 mg daily. Skin rashes and drying of the eyes have also been reported.
The possibility that other adverse effects associated with other β-adrenergic-blocking agents may occur during atenolol therapy should be considered. These include hematologic reactions (ie, agranulocytosis, thrombocytopenic purpura); elevation of cholesterol, plasma total triglycerides and decrease in high-density cholesterol; reversible alopecia; Peyronie's disease; Raynaud's phenomenon; erythematous rash; and impotence.
Central Nervous System: Reversible mental depression progressing to catatonia (an acute reversible syndrome characterized by disorientation of time and place), short-term memory loss, emotional lability with slightly clouded sensorium and decreased performance on neuropsychometrics.
Gastrointestinal: Mesenteric arterial thrombosis and ischemic colitis.
Hematologic: Agranulocytosis.
Allergic: Fever, with aching and sore throat, laryngospasm and respiratory distress.
Others: Wheezing and dyspnea have occurred in patients receiving atenolol and are likely to occur when dosage of the drug exceeds 100 mg daily. Skin rashes and drying of the eyes have also been reported.
The possibility that other adverse effects associated with other β-adrenergic-blocking agents may occur during atenolol therapy should be considered. These include hematologic reactions (ie, agranulocytosis, thrombocytopenic purpura); elevation of cholesterol, plasma total triglycerides and decrease in high-density cholesterol; reversible alopecia; Peyronie's disease; Raynaud's phenomenon; erythematous rash; and impotence.
Drug Interactions
Because of reserpine's catecholamine-depleting activity, concomitant administration of atenolol with reserpine may increase the incidence of hypotension and bradycardia compared to atenolol alone.
Atenolol has a synergistic blood pressure-lowering effect when given in combination with dihydropyridine calcium-channel blockers (ie, nifedipine). However, its combination with nondihydropyridine calcium-channel blockers (ie, verapamil, diltiazem) is not advisable because such a combination may excessively depress heart rate and cardiac function.
β-Blockers may exacerbate the rebound hypertension that may follow after withdrawal from clonidine. If the 2 drugs are concomitantly administered, the β-blocker should be withdrawn several days before the gradual withdrawal of clonidine. In replacing clonidine with β-blocker therapy, the introduction of β-blockers should be delayed for several days after clonidine administration has stopped.
Atenolol has a synergistic blood pressure-lowering effect when given in combination with dihydropyridine calcium-channel blockers (ie, nifedipine). However, its combination with nondihydropyridine calcium-channel blockers (ie, verapamil, diltiazem) is not advisable because such a combination may excessively depress heart rate and cardiac function.
β-Blockers may exacerbate the rebound hypertension that may follow after withdrawal from clonidine. If the 2 drugs are concomitantly administered, the β-blocker should be withdrawn several days before the gradual withdrawal of clonidine. In replacing clonidine with β-blocker therapy, the introduction of β-blockers should be delayed for several days after clonidine administration has stopped.
Storage
Store at temperatures not exceeding 30°C. Protect from light.
Action
Cardioselective β-blocker.
Pharmacology: Atenolol is a β1-selective adrenergic-blocking agent. It competitively blocks adrenergic stimulation of β1-adrenergic receptors within the myocardium and vascular smooth muscle. Low doses of atenolol selectively inhibit cardiac and lipolytic β1-receptors but with little effect on the β2-adrenergic receptors of bronchial and vascular smooth muscle. At high doses (ie, >100 mg daily), this selectivity of atenolol for β1-adrenergic receptors may diminish and the drug may competitively block β1- and β2-adrenergic receptors. Atenolol does not exhibit any intrinsic sympathomimetic activity nor any membrane-stabilizing activity.
By inhibiting myocardial β1-adrenergic receptors, atenolol produces negative-chronotropic and negative-inotropic effects. The negative-chronotropic action of atenolol on the sinoatrial (SA) node results in a decrease in the rate of SA node discharge and an increase in recovery time, thereby decreasing resting and exercise-stimulated heart rate and reflex orthostatic node. Therefore, high doses of atenolol may produce sinus arrest or AV block especially in patients with sick-sinus syndrome. Although stroke index may be increased moderately by about 10%, atenolol usually reduces cardiac output by about 20%, probably secondary to its effect on heart rate. The decrease in myocardial contractility and heart rate, as well as the reduction in myocardial oxygen consumption accounts for the effectiveness of the drug in chronic stable angina pectoris. However, in cardiac failure, atenolol can increase oxygen requirements by increasing left ventricular fiber length and end-diastolic pressure.
Pharmacokinetics: Absorption: Atenolol is rapidly but incompletely absorbed from the gastrointestinal tract. Approximately 50-60% of an oral dose is absorbed. In healthy adults, peak plasma concentrations of 1-2 mcg/mL are achieved after oral administration of a single 200-mg dose of atenolol. An approximately 4-fold interindividual variation in plasma concentrations attained has been reported with a specific oral dose of atenolol. The effect of atenolol on heart rate usually has an onset of 1 hr, peaks 2-4 hrs and persists for 24 hrs. The antihypertensive effect of a single oral dose usually persists for 24 hrs. Atenolol's effect on heart rate, but not on blood pressure, correlates linearly with plasma atenolol concentrations of 0.02-200 mcg/mL.
Distribution: In animals, atenolol is well distributed into most tissues and fluids except brain and CSF. Unlike propranolol, only a small amount of atenolol is distributed into the CNS.
Approximately 6-16% of atenolol is bound to plasma protein.
Atenolol readily crosses the placenta and during continuous administration, fetal serum concentrations of the drug are probably equivalent to those in maternal serum. Atenolol is distributed into milk. The extent of distribution of atenolol into milk has not been clearly determined, but the amount of drug a nursing infant would ingest is believed to be too small to be clinically significant.
Elimination: In patients with normal renal function, atenolol has a plasma t½ of 6-7 hrs. Plasma t½ of the drug increases to 16-27 hrs in patients with creatinine clearances of 15-35 mL/min/1.73 m2 and exceeds 27 hrs with progressive renal impairment. Little or no metabolism of atenolol occurs in the liver. Approximately 40-50% of an oral dose of the drug is excreted unchanged in urine. The remainder is excreted unchanged in feces, principally as unabsorbed drug.
Pharmacology: Atenolol is a β1-selective adrenergic-blocking agent. It competitively blocks adrenergic stimulation of β1-adrenergic receptors within the myocardium and vascular smooth muscle. Low doses of atenolol selectively inhibit cardiac and lipolytic β1-receptors but with little effect on the β2-adrenergic receptors of bronchial and vascular smooth muscle. At high doses (ie, >100 mg daily), this selectivity of atenolol for β1-adrenergic receptors may diminish and the drug may competitively block β1- and β2-adrenergic receptors. Atenolol does not exhibit any intrinsic sympathomimetic activity nor any membrane-stabilizing activity.
By inhibiting myocardial β1-adrenergic receptors, atenolol produces negative-chronotropic and negative-inotropic effects. The negative-chronotropic action of atenolol on the sinoatrial (SA) node results in a decrease in the rate of SA node discharge and an increase in recovery time, thereby decreasing resting and exercise-stimulated heart rate and reflex orthostatic node. Therefore, high doses of atenolol may produce sinus arrest or AV block especially in patients with sick-sinus syndrome. Although stroke index may be increased moderately by about 10%, atenolol usually reduces cardiac output by about 20%, probably secondary to its effect on heart rate. The decrease in myocardial contractility and heart rate, as well as the reduction in myocardial oxygen consumption accounts for the effectiveness of the drug in chronic stable angina pectoris. However, in cardiac failure, atenolol can increase oxygen requirements by increasing left ventricular fiber length and end-diastolic pressure.
Pharmacokinetics: Absorption: Atenolol is rapidly but incompletely absorbed from the gastrointestinal tract. Approximately 50-60% of an oral dose is absorbed. In healthy adults, peak plasma concentrations of 1-2 mcg/mL are achieved after oral administration of a single 200-mg dose of atenolol. An approximately 4-fold interindividual variation in plasma concentrations attained has been reported with a specific oral dose of atenolol. The effect of atenolol on heart rate usually has an onset of 1 hr, peaks 2-4 hrs and persists for 24 hrs. The antihypertensive effect of a single oral dose usually persists for 24 hrs. Atenolol's effect on heart rate, but not on blood pressure, correlates linearly with plasma atenolol concentrations of 0.02-200 mcg/mL.
Distribution: In animals, atenolol is well distributed into most tissues and fluids except brain and CSF. Unlike propranolol, only a small amount of atenolol is distributed into the CNS.
Approximately 6-16% of atenolol is bound to plasma protein.
Atenolol readily crosses the placenta and during continuous administration, fetal serum concentrations of the drug are probably equivalent to those in maternal serum. Atenolol is distributed into milk. The extent of distribution of atenolol into milk has not been clearly determined, but the amount of drug a nursing infant would ingest is believed to be too small to be clinically significant.
Elimination: In patients with normal renal function, atenolol has a plasma t½ of 6-7 hrs. Plasma t½ of the drug increases to 16-27 hrs in patients with creatinine clearances of 15-35 mL/min/1.73 m2 and exceeds 27 hrs with progressive renal impairment. Little or no metabolism of atenolol occurs in the liver. Approximately 40-50% of an oral dose of the drug is excreted unchanged in urine. The remainder is excreted unchanged in feces, principally as unabsorbed drug.
MedsGo Class
Beta-Blockers
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