Brands Of Propranolol in Kenya
Carderal , Pharma Life Science Limited
Hipertol , Laboratory & Allied Ltd
Propranolol , Cosmos Limited
MODE OF ACTION
Propranolol is a competitive antagonist at both the beta1- and beta2 adrenoceptors. It has no agonist activity at the beta adrenoceptor, but has membrane stabilising activity at concentrations exceeding 1 to 3 mg/litre, though such concentrations are rarely achieved during oral therapy.
- Angina pectoris.
- Long-term prophylaxis against myocardial reinfarction after recovery from acute myocardial infarction
- Hypertrophic obstructive cardiomyopathy.
- Essential tremor.
- Supraventricular cardiac arrhythmia.
- Ventricular cardiac arrythmias.
- Hyperthyroidism and thyrotoxicosis
- Phaeochromocytoma (with an alpha-blocker).
- Prophylaxis of upper gastrointestinal bleeding in patients with portal hypertension and oesophageal varices.
DOSAGE AND ADMINISTRATION
Initially 40 mg two or three times daily, which may be increased by 80 mg per day at weekly intervals according to response. The usual dose range is 160 to 320 mg per day. With concurrent diuretic or other antihypertensive drugs a further reduction of blood pressure is obtained.
Angina, migraine and essential tremor
The starting dose is 40 mg two to three times daily, increasing by the same amount at weekly intervals according to the patient response. An adequate response in migraine is usually seen in the range 80 to 160 mg/day and in angina and essential tremor in the range 120 to 240 mg/day.
Arrhythmias, , hypertrophic obstructive cardiomyopathy and thyrotoxicosis
A dosage range of 10 to 40 mg three or four times a day usually achieves the required response.
Post myocardial infarction:
Treatment should start between days 5 and 21 after myocardial infarction, with an initial dose of 40mg four times a day for two or three days. In order to improve compliance, the total daily dosage may thereafter be given as 80mg twice a day.
The dose is adjusted according to clinical response
Dosage should be titrated to achieve approximately 25% reduction in heart rate at rest. Dosing should begin with 40mg twice daily, increasing to 80mg twice daily depending on heart rate response. If necessary, the dose may be increased incrementally to a maximum of 160mg twice daily.
(Used only with an alpha-receptor blocking drug).
Pre-operative: 60 mg daily for 3 days is recommended. Non-operable malignant cases: 30 mg daily.
Hypersensitivity to the active substance(s) or to any of the excipients.
Cardiac decompensation which is not adequately treated.
Sick sinus syndrome/SA-block.
History of bronchospasm or bronchial asthma, chronic obstructive pulmonary disease.
Second and third-degree heart block.
Patients prone to hypoglycaemia, e.g. due to prolonged fasting or restricted counter regulatory reserve.
Severe peripheral arterial disturbances
Combination not recommended:
Beta-agonist bronchodilators :
Non-cardioselective beta-blockers oppose the bronchodilator effects of beta-agonist bronchodilators, propranolol is contraindicated in patients with asthma .
Potentiation of bradycardia effects with possible fatal outcomes. Treatment with Fingolimod should not be initiated in patients receiving beta blockers. In case of combination, appropriate monitoring for treatment initiation, at least overnight monitoring is recommended.
The plasma levels and the effects of beta-blockers are reduced by the barbiturates. Barbiturates are potent liver enzyme inducers which may increase the metabolism of propranolol.
Plasma propranolol levels can be raised up to 100% by propafenone. This probably was because propranolol is partially metabolized by the same enzyme like propafenone (CYP2D6). This combination is also not advisable because propafenone has negative inotropic effects.
Propranolol may cause a reduction in clearance and an increase in plasma concentrations of warfarin.
Concomitant use of MAO inhibitors (except MAO-B inhibitors) with antihypertensive agents may diminish the antihypertensive effect and lead to hypertensive reactions.
Digitalis glycosides, in association with beta-blockers, may increase atrio-ventricular conduction time.
Combination to be used with caution, dose adjustment may be required
A few case reports suggest that patients treated with amiodarone can have severe sinus bradycardia when treated concomitantly with propranolol. Amiodarone has an extremely long half-life (about 50 days), which means that interactions may occur long after discontinuation of therapy.
Class I antiarrhythmic drugs (disopyramide, quinidine):
Class I antiarrhythmic drugs and beta-blockers have additive negative inotropic effects which may result in hypotension and severe hemodynamic side effects in patients with impaired left ventricular function.
Non-steroidal anti-inflammatory / anti-rheumatic drugs (NSAIDs):
Anti-inflammatory drugs of NSAID-type counter the antihypertensive effect of beta-blockers. It has been studied mainly in indomethacin. In a study on diclofenac no such interaction could be detected. Data for COX-2 inhibitors are missing.
Cimetidine increases levels of propranolol in plasma, probably by inhibiting its first pass metabolism. There may be a risk of eg bradycardia with oral dosing.
Concomitant use of alcohol may increase the plasma levels of propranolol.
Concomitant use of beta-adrenergic antagonists and anaesthetics may attenuate reflex tachycardia and increase the risk of hypotension (see section 4.4). As a general rule, avoid sudden withdrawal of beta-blocker treatment. The anaesthesiologist should be informed when the patient is receiving beta-adrenergic antagonists. Anaesthetic agents causing myocardial depression are best avoided.
A number of reports are available for severe hypertension and bradycardia in patients treated with propranolol and epinephrine. These clinical observations have been confirmed by studies in healthy volunteers. It has also been suggested that the intravascular administration of epinephrine may trigger these reactions.
Fluvoxamine inhibits oxidative metabolism and increases plasma concentrations of propranolol. This may result in severe bradycardia.
Centrally-acting antihypertensives (clonidine, moxonidine, methyldopa):
Concomitant use of centrally acting antihypertensive drugs may worsen heart failure by a decrease in the central sympathetic tonus (reduction of heart rate and cardiac output, vasodilation). Abrupt withdrawal, particularly if prior to beta-blocker discontinuation, may increase risk of “rebound hypertension”.
If the two drugs are co administered, the beta-blocker should be withdrawn several days before discontinuing clonidine. If replacing clonidine by beta blocker therapy, the introduction of beta-blockers should be delayed for several days after clonidine administration has stopped.
The metabolism of propranolol may be increased by potent liver enzyme inducer rifampicin.
Concomittant use with alpha blockers increases the risk of hypotension, especially orthostatic hypotension, and tachycardia and palpitations.
Dihydropyridine calcium channel blockers: e.g nifedipine:
Concomitant use may increase the risk of hypotension, and cardiac failure may occur with latent cardiac insufficiency.
The concurrent use of chlorpromazine with propranolol can result in a marked rise in plasma levels of both drugs, and thereby enhance its effects on heart rate and blood pressure as well as an enhanced antipsychotic effect for chlorpramazine and an increased antihypertensive effect for propranolol.
Administration of propranolol during infusion of lidocaine may increase the plasma concentration of lidocaine by approximately 30%. Patients already receiving propranolol tend to have higher lidocaine levels than controls. The combination should be avoided.
During concomitant treatment with propranolol it inhibited the first-pass metabolism of rizatriptan whose AUC increases by 70-80%. A dose of 5 mg of rizatriptan is recommended for combination therapy. Ergotamine with propranolol has resulted in reports of vasospastic reactions in some patients.
Propranolol reduces the metabolic clearance of theophylline by about 30% at a dosage of 120 mg / day and 50% at doses of 720 mg / day.
Insulin and oral antidiabetic drugs:
Concomitant use may mask certain symptoms of hypoglycaemia (palpitations, tachycardia). Propranolol may prolong the hypoglycaemic response to insulin.
Tobacco smoking can reduce the beneficial effects of the beta-blockers on heart rate and blood pressure.
Interference with laboratory tests – Propranolol has been reported to interfere with the estimation of serum bilirubin by the diazo method and with the determination of catecholamines by methods using fluorescence.
Blood and lymphatic system disorders
Immune system disorders
Metabolism and nutrition disorders
Hypoglycaemia in neonates, infants, children, elderly patients, patients on haemodialysis, patients on concomitant antidiabetic therapy, patients with prolonged fasting and patients with chronic liver disease has been reported.
Changes in lipid metabolism(changes in blood concentrations of triglycerides and cholesterol). Severe hypoglycemia may rarely lead to seizures or coma.
Sleep disturbances, nightmares
Hallucinations, psychoses, mood changes
Nervous system disorders
Confusion, memory loss, paraesthesia, dizziness
Isolated reports of myasthenia gravis like syndrome or exacerbation of myasthenia gravis have been reported
Headache, seizure linked to hypoglycaemia
Dry eyes, visual disturbances
Bradycardia, cold extremities
Heart failure deterioration, precipitation of heart block, postural hypotension, which may be associated with syncope
Worsening of attacks of angina pectoris
Exacerbation of intermittent claudication
Respiratory, thoracic and mediastinal disorders
Bronchospasm may occur in patients with bronchial asthma or a history of asthmatic complaints, sometimes with fatal outcome
Gastrointestinal disturbance, such as nausea, vomiting, diarrhoea
Constipation, dry mouth
Skin and subcutaneous tissue disorders
Purpura, alopecia, psoriasiform skin reactions, exacerbation of psoriasis, skin rashes
Isolated cases of hyperhidrosis has been reported
Musculoskeletal and connective tissue disorders
Renal and urinary disorders
Reduced renal blood flow and GFR
Reproductive system and breast disorders
General disorders and administration site conditions
Fatigue and/or lassitude (often transient)
An increase in ANA (Antinuclear Antibodies) has been observed, however the clinical relevance of this is not clear
Reporting of suspected adverse reactions:
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Reporting suspected adverse reactions after authorization of the medicinal product are important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals/ Patients are encouraged to report any suspected adverse reactions via Pharmacovigilance Yellow Form, firstname.lastname@example.org or clicking below button:
Propranolol in Kenya
Propranolol in Kenya
Propranolol in Kenya
Propranolol in Kenya
Propranolol in Kenya
Propranolol in Kenya
Clinical | Pharmacokinetic data
Pregnancy Category: C
Routes of Administration: By mouth, rectal, intravenous
Protein Binding: 90%
Metabolosim: Liver (extensive) 1A2, 2D6; minor: 2C19, 3A4
Onset of Action: Not Available
Elimination Half life: 4-5 Hours
Excretion: Kidney (
Legal Status | Dosage forms & Strengths
Prescription only Medicine (POM) , ℞-only
Narcotic Drugs and Psychotropic Substances (Control ) Act Schedule:
This drug is not a controlled substance under Narcotic Drugs and Psychotropic Substances (Control ) Act
Dosage Forms | Strengths:
|CompTox Dashboard (EPA)|
- Léauté-Labrèze, Christine, et al. “Propranolol for severe hemangiomas of infancy.” New England Journal of Medicine 358.24 (2008): 2649-2651.
- Prichard, B. N. C., and P. M. S. Gillam. “Treatment of hypertension with propranolol.” Br Med J 1.5635 (1969): 7-16.
- Stephen, Stewart A. “Unwanted effects of propranolol.” American Journal of Cardiology 18.3 (1966): 463-472.
- Routledge, P. A., and D. G. Shand. “Clinical pharmacokinetics of propranolol.” Clinical Pharmacokinetics 4.2 (1979): 73.