Atenolol Tablets Bp 25mg
Out of date information, search anotherSUMMARY OF PRODUCT CHARACTERISTICS
1 NAME OF THE MEDICINAL PRODUCT
Atenolol Tablets BP 25 mg
2. QUALITATIVE AND QUANTITATIVE COMPOSITION
Atenolol EP 25 mg
3. PHARMACEUTICAL FORM
Tablet
4 CLINICAL PARTICULARS
4.1. Therapeutic Indications
i) management of hyp erten sion
ii) management of angina pectoris
iii) management of cardiac dysrhythmias
iv) myocardial infarction: early intervention in the acute phase
4.2. Posology and Method of Administration
Adults: Hypertension: Most patients respond to 100 mg daily given orally as a single dose. Some patients, however, will respond to 50 mg given as a single dose. The effect will be fully established after one to two weeks. A further reduction in blood pressure may be achieved by combining atenolol with other anti-hypertensive agents. For example, co-administration of atenolol with a diuretic, provides a highly effective and convenient antihypertensive therapy.
Angina: Most patients with angina pectoris will respond to 100 mg given orally once daily or 50 mg given twice daily. It is unlikely that additional benefit will be gained by increasing the dose.
Dysrhythmias: A suitable initial dose of atenolol is 2.5 mg (5 ml) injected intravenously over a 2.5 minute period (ie 1 mg/minute). This may be repeated at five minute intervals until a response is observed up to a maximum dosage of 10 mg. If atenolol is given by infusion, 0.15 mg/kg body weight may be administered over a 20 minute period. If required, the injection or infusion may be repeated every 12 hours. Having controlled the disrhythmias with intravenous atenolol, a suitable oral maintenance dosage is 50-100 mg daily, given as a single dose.
Myocardial infarction: For patients suitable for treatment with intra-venous beta-blockade and presenting within 12 hours of the onset of the chest pain, atenolol 5-10 mg should be given by slow intravenous injection (1 mg/minute) followed by atenolol 50 mg orally about 15 minutes later provided no untoward effects occur from the intravenous dose. This should be followed by a further 50 mg orally 12 hours after the intravenous dose and then 12 hours later by 100 mg orally to be given once daily. If bradycardia and/or hypotension requiring treatment, or any other untoward effects occur, atenolol should be discontinued.
Elderly patients: dosage requirements may be reduced, especially in patients with impaired renal function.
Children: there is no paediatric experience with atenolol and for this reason it is not recommended for use in children.
Renal failure: since atenolol is excreted via the kidneys dosage should be adjusted in case of severe impairment of renal function. No significant accumulation of atenolol occurs in patients who have a creatinine clearance greater than 35ml/min/1.73m (normal range is 100-150 ml/min/1.73m , equivalent to serum creatinine of 300-600mcmol/litre), the oral dose should be 50 mg daily and the intravenous dose should be 10 mg once every two days. For patients with a creatinine clearance of <15ml/min/1.73m (equivalent to serum creatinine of >600mcmol/litre) the oral dose should be 25 mg daily or 50 mg on alternate days and the intravenous dose should be given 50 mg orally after each dialysis; this should be done under hospital supervision as marked falls in blood pressure can occur.
4.3 Contra-Indications
hypersensitivity to atenolol in patients with second or third degree heart block in patients with cardiogenic shock uncontrolled heart failure
sick sinus syndrome (unless a pacemaker is in situ) hypotension
untreated phaeochromocytoma
severe peripheral circulatory disturbances
bradycardia (<45-50bpm)
after prolonged fasting
in metabolic acidosis (eg in some diabetics)
4.4. Special warnings and precautions for use
Special care should be taken with patients whose cardiac reserve is poor. Beta-adrenoceptor blockers should be avoided in overt heart failure.
However, they may be used in patients whose signs of failure have been controlled.
One of the pharmacological actions of atenolol is to reduce heart rate. In the rare instances when symptoms may be attributable to the slow heart rate, the dose may be reduced.
Due to its negative effect on conduction time, caution must be exercised if given to patients with first degree heart block.
Atenolol modifies the tachycardia of hypoglycaemia.
In patients with phaeochromocytoma, a beta-blocker should only be given with an alpha-blocker.
While cardioselective beta-blockers such as atenolol may have less effect on pulmonary function than non-selective ones, they should be avoided in patients with reversible obstructive airways disease, bronchospasm or a history of asthma unless absolutely necessary. When administration is required, the use of a beta2-bronchodilator such as terbutaline may be advisable in some cases.
In patients suffering from ischaemic heart disease, as with other beta-blocking agents, treatment should not be discontinued abruptly.
Caution should be exercised when transferring patients from clonidine to beta-adrenoceptor blocking drugs. If beta-adrenoceptor blocking drugs and clonidine are given concurrently, clonidine should not be discontinued until several days after the withdrawal of the beta-adrenoceptor blocking drug.
Beta-blockers should be used with great caution in patients with peripheral circulatory disorders (Raynaud’s disease/syndrome, intermittant claudication) as they may aggravate these disorders.
Atenolol may increase the number and duration of angina attacks in patients with Prinzmetals angina. Caution must be exercised when considering using atenolol with a Prinzmetals angina patient.
Caution should be exercised when using anaesthetic agents with atenolol as there is an increased risk of hypotension and reflex tachycardia. Anaesthetics which cause myocardial depression should be avoided.
Renal failure: since atenolol is excreted via the kidneys, dosage should be adjusted in cases of severe impairment of renal function. No significant accumulation of atenolol occurs at a GFR greater than 35 ml/min/1.73m2 (normal range is 100-150 ml/min/1.73m ). For patients with a creatinine clearance of 15-35 ml/min/1.73m2 (equivalent to serum creatinine of 300-600 mcmol/litre) the oral dose should be 50 mg daily and the intravenous dose should be 10 mg once every two days. For patients with a creatinine clearance of <15 ml/min/1.73m2 (equivalent to serum creatinine of >600 mcmol/litre) the oral dose should be 25 mg daily or 50 mg on alternate days and the intravenous dose should be 10 mg once every four days.
Atenolol may cause a more serious reaction to a variety of allergens, when given to patients with a history of anaphylactic reaction to such allergens.
Such patients may be unresponsive to the usual doses of adrenaline used to treat the allergic reactions.
Patients with known psoriasis should take beta-blockers only after careful consideration.
The label will state ‘this product should not be taken if there is an history of wheezing or asthma’.
Patients on haemodialysis should be given 50 mg orally after each dialysis; this should be done under hospital supervision as marked falls in blood pressure can occur.
If a beta-blocker is withdrawn before surgery therapy, it should be discontinued for at least 24 hours.
In hypertensive patients, there is evidence that beta-blockers, including atenolol, may affect glucose metabolism and may be associated with the development of diabetes.
4.5. Interactions with other Medicinal Products and other Forms of Interaction
Other anti-hypertensive agents will potentiate the hypotensive action of atenolol.
Parenteral administration of preparations containing adrenaline to patients taking beta adrenoceptor blocking drugs may, in rare cases, result in vasoconstriction, hypertension and bradycardia.
Beta-adrenoreceptor blocking drugs may enhance the negative inotropic and chronotropic actions of Verapamil. Therefore, concurrent use requires great care. The negative inotropic effects of class I anti-dysrhythmic agents such as disopyramide and certain anaesthetics may also be enhanced by beta-blocking drugs.
Beta-adrenoceptor blocking drugs can exacerbate the rebound hypertension associated with sudden withdrawal of clonidine.
Beta blockers may enhance hypoglycaemic effects of anti-diabetic agents and mask the warning signs of hypoglycaemia such as tremor and tachycardia.
Co-administration with an NSAID such as indomethacin or ibuprofen may lead to a decrease in the hypotensive effect of atenolol.
Concurrent administration with a cardiac glycoside may lead to an increase in atrio-ventricular conduction time.
Combined use of beta-blocking drugs and calcium channel blockers with negative inotropic effects eg Verapamil, Diltiazem can lead to an exaggeration of these effects, particularly in patients with impaired ventricular function and/or sino-atrial or atrio-ventricular conduction abnormalities. Coadministration of beta-blockers with Cimetidine or Hydralazine can increase the effect of beta-blockers.
Concurrent use of beta-blockers and alcohol can decrease the effect of beta-blockers.
4.6. Pregnancy and Lactation
The safety of atenolol in pregnancy has not been established and its use should be avoided unless the potential benefits are likely to outweigh the possible risk to the foetus.
Atenolol crosses the placental barrier and appears in cord blood. There have been isolated reports of intra-uterine growth retardation in association with the use of beta-blockers. Beta-blockers may cause neonatal hypoglycaemia and bradycardia.
Beta-blocking drugs reduce placental perfusion which may result in intrauterine foetal death, immature and premature deliveries.
Atenolol is excreted in breast milk with accumulation occurring at concentrations significantly greater than corresponding plasma levels. Nursing infants must be closely monitored for bradycardia and other signs and symptoms of beta-blockade if the mother is receiving atenolol, although breast feeding is not recommended.
4.7. Effects on Ability to Drive and Use Machines
Although symptoms such as dizziness and fatigue have occasionally been reported in association with the use of beta-blockers, the ability to drive and use machines is usually unaffected by atenolol therapy.
4.8. Undesirable Effects
In clinical studies, the side effects reported are usually attributable to its pharmacological actions and include coldness of the extremities, muscular fatigue and, in isolated cases, bradycardia. Bradycardia and hypotension are usually a sign of overdosage, but may rarely be due to intolerance of the drug. Sleep disturbances of the type noted with other beta-blockers.
Atenolol is generally well tolerated. Other side effects include nausea, vomiting, dry mouth, diarrhoea, postural hypotension, confusion, dizziness, nightmares and lassitude. Headache, mood changes, psychoses, hallucinations and deterioration in heart failure may occur occasionally. Rarely thrombocytopenia, alopecia, purpura, psoriasiform skin reactions and exacerbation of psoriasis.
Precipitation of heart block, intermittent claudication and Raynaud’s phenomenon in susceptible patients have been reported.
Other side effects include paraesthesia and eyesight changes. Bronchospasm may occur in patients with bronchial asthma or a history of allergic disease.
May mask the signs of thyrotoxicosis.
An increase in ANA (anti nuclear antibodies) has been observed, however the clinical relevance of this is not clear.
There have been reports of skin rashes and/or dry eyes associated with the use of beta-adrenergic blocking drugs. The reported incidence is small and in most cases the symptoms have cleared when treatment was withdrawn. Discontinuance of the drug should be considered if any such reaction is not otherwise explicable. Cessation of therapy with a beta-blocker should be gradual.
4.9. Overdose
Clinical features of overdosage may include bradycardia, hypotension, bronchospasm, hypoglycaemia, delirium and unconsciousness. Following recent overdosage, the stomach should be emptied by gastric aspiration and lavage.
Severe bradycardia may respond to Atropine 1 to 2 mg intravenously. If necessary, this may be followed by a bolus dose of Glucagon 5 to 10 mg intravenously, followed if necessary by an intravenous infusion of Glucagon 1 to 5 mg per hour or more according to response. If there is no response to Glucagon, or if Glucagon is unavailable, a beta-adrenoceptor stimulant such as Dobutamine 2.5-10 mcg/kg/minute by intravenous infusion or Isoprenaline 1025 mcg given as an infusion at a rate not exceeding 5 mcg/minute may be given. Occasionally a temporary pacing wire may be required. Atenolol is dialysable.
5 PHARMACOLOGICAL PROPERTIES
5.1. Pharmacodynamic Properties
Principally atenolol acts by competitive inhibition of the effects of catecholamines on the beta1 (cardiac) adrenoreceptors and has less effect on the beta2 (bronchial) adrenoreceptors. However, it is not cardiospecific. It does not possess membrane stabilising activity or intrinsic sympathomimetic action (I.S.A.).
A reduction in cardiac activity is obtained by diminishing or preventing beta-adrenoreceptor stimulation. The response of the heart to stress and exercise is reduced as a consequence of the reduction in the rate and force of contraction of the heart and the decrease in the rate of conduction of impulses through the conducting system.
Such effects are useful in the treatment of angina to reduce oxygen consumption and increase the exercise tolerance of the heart. These effects are also exploited in the treatment of cardiac arrhythmias to block beta-adrenergic stimulation of cardiac pacemaker potentials.
Atenolol is useful in the long-term treatment of hypertension but its mode of action is not fully understood.
A reduction in the size of infarct and morbidity can be obtained by initiating early treatment with atenolol in acute myocardial infarction. Studies have shown that atenolol can cause a reduction in the recurrence rate of myocardial infarction.
5.2. Pharmacokinetic Properties
Atenolol seems to be completely absorbed from the gastro-intestinal tract and is not significantly metabolised. It is excreted in the urine and its biological half-life is longer than would be anticipated from its plasma half life of about 6 hours. Atenolol diffuses across the placenta and is excreted in breast milk.
Only small amounts are reported to cross the blood brain barrier, and it is only about 5% bound to plasma proteins.
5.3. Pre-clinical Safety Data
There are no additional data of relevance to the prescriber.
There are no additional data of relevance to the prescr
6 PHARMACEUTICAL PARTICULARS
6.1. List of Excipients
Calcium Hydrogen Phosphate (anhydrous) EP
Heavy Magnesium Carbonate EP
Sodium Starch Glycollate EP
Maize Starch EP
Collodial Anhydrous Silica EP
Magnesium Stearate EP
Film Coat
Opadry white 7-1-7000 HSE
Purified water EP
Carnauba Wax BP
6.2. Incompatibilities
None known
6.3. Shelf Life
3 years
6.4. Special Precautions for Storage
Protect from light, store in a dry place below 25°C.
Nature and Content of Container
6.5.
Polypropylene pots with polyethylene caps with optional use of a polyethylene filler (securitainer), and PVDC/Aluminium foil blister packs.
Pack sizes for both containers: 28, 30, 50, 56, 60, 100, 250 & 500
6.6. Instructions for Use, Handling and Disposal
No special requirements.
7 MARKETING AUTHORISATION HOLDER
Generics [UK] Limited T/A Mylan Station Close Potters Bar Hertfordshire EN6 1TL
8. MARKETING AUTHORISATION NUMBER
PL 04569/0243
9. DATE OF FIRST AUTHORISATION/RENEWAL OF AUTHORISATION
11th June 1992 / 23rd April 1998
10 DATE OF REVISION OF THE TEXT
27/01/2010