- acetylsalicylic acid
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This information is intended for use by health professionals
|Aspirin BPParacetamol Ph EurCaffeine Ph Eur||300 mg/tablet200 mg/tablet45 mg/tablet|
|For excipients see section 6.1|
Aspirin:Other NSAIDS and corticosteroids: Concurrent use of other NSAIDS or corticosteroids may increase the likelihood of GI side effects.Diuretics: Antagonism of the diuretic effect.Anticoagulants: Increased risk of bleeding due to antiplatelet effect.Metoclopramide: Metoclopramide increases the rate of absorption of aspirin. However, concurrent use need not be avoided.Phenytoin : The effect of phenytoin may be enhanced by aspirin. However, no special precautions are needed.Valproate: The effect of valproate may be enhanced by aspirin.Methotrexate: Delayed excretion and increased toxicity of methotrexate.
Paracetamol:Cholestyramine: The speed of absorption of paracetamol is reduced by cholestyramine. Therefore, the cholestyramine should not be taken within one hour if maximal analgesia is required.Metoclopramide and Domperidone : The speed of absorption of paracetamol is increased by metoclopramide and domperidone. However, concurrent use need not be avoided.Warfarin: The anticoagulant effect of warfarin and other coumarins may be enhanced by prolonged regular use of paracetamol with increased risk of bleeding; occasional doses have no significant effect. Chloramphenicol: Increased plasma concentration of chloramphenicol.
|Within the first 24 hours: Pallor Nausea Vomiting Anorexia Abdominal pain After 12-48 hours: Liver damage Abnormalities of glucose metabolism and metabolic acidosis Severe poisoning: Hepatic failure may progress to encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema and death. With or without severe liver damage: Acute renal failure with acute tubular necrosis strongly suggested by loin pain haematuria and proteinuria. Cardiac arrhythmias Pancreatitis||Common: Vomiting, Dehydration, Tinnitus Vertigo, Deafness, Sweating Warm extremities with bounding pulses Increased respiratory rate Hyperventilation Acid base disturbance Mixed respiratory alkalosis and metabolic acidosis with normal or high arterial pH (normal or reduced hydrogen ion concentration) in adults and children aged over 4 years. In children aged 4 years or less, a dominant metabolic acidosis with low arterial pH (raised hydrogen ion concentration) is common. Acidosis can increase salicylate transfer across the blood brain barrier. Uncommon: Haematemesis Hyperpyrexia Hypoglycaemia Hypokalaemia Thrombocytopenia Increased INR/PTR Intravascular coagulation Renal failure Non-cardiac pulmonary oedema Confusion, disorientation, coma and convulsions are more common in children than adults.||Other symptoms of overdosage, associated with the caffeine component, include: CNS stimulation; anxiety, nervousness, restlessness, insomnia, excitement, muscle twitching, confusion, convulsions Cardiac: tachycardia, cardiac arrhythmia Gastric: Abdominal or stomach pains Other: diuresis, facial flushing|
Mechanisms of action/effectSalicylates inhibit the activity of the enzyme cyco-oxygenase to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. Although many of the therapeutic effects may result from inhibition of prostaglandin synthesis (and consequent reduction of prostaglandin activity) in various tissues, other actions may also contribute significantly to the therapeutic effects.
AnalgesicProduces analgesia through a peripheral action by blocking pain impulse generation and via a central action, possibly in the hypothalamus.
Anti-inflammatory (Non-steroidal)Exact mechanisms have not been determined. Salicylates may act peripherally in inflamed tissue probably by inhibiting the synthesis of prostaglandins and possibly by inhibiting the synthesis and/or actions of other mediators of the inflammatory response.
AntipyreticMay produce antipyresis by acting centrally on the hypothalamic heat-regulating centre to produce peripheral vasolidation resulting in increased cutaneous blood flow, sweating and heat loss.
Mechanism of action/effectAnalgesic the mechanism of analgesic action has not been fully determined. Paracetamol may act predominantly by inhibiting prostaglandin synthesis in the central nervous system (CNS) and, to a lesser extent, through a peripheral action by blocking pain-impulse generation.The peripheral action may also be due to inhibition of prostaglandin synthesis or to inhibition of the synthesis or actions of other substances that sensitise pain receptors to mechanical or chemical stimulation.Antipyretic paracetamol probably produces antipyresis by acting centrally on the hypothalamic heat-regulation centre to produce peripheral vasodilation resulting in increased blood flow through the skin, sweating, and heat loss. The central action probably involved inhibition of prostaglandin synthesis in the hypothalamus.
Mechanisms of action/effectCentral nervous system stimulant caffeine stimulates all levels of the CNS, although its cortical effects are milder and of shorter duration than those of amphetamines.
Analgesia adjunctCaffeine constricts cerebral vasculature with an accompanying decrease in the cerebral blood flow and in the oxygen tension of the brain. It is believed that caffeine helps to relieve headache by providing more rapid onset of action and/or enhanced pain relief with lower doses of analgesic. Recent studies with ergotamine indicate that the enhancement of effect by the addition of caffeine may also be due to improved gastrointestinal absorption of ergotamine when administered with caffeine.
AspirinAbsorption and fateAbsorption is generally rapid and complete following oral administration. It is largely hydrolysed in the gastrointestinal tract, liver and blood to salicylate, which is further metabolised primarily in the liver.
ParacetamolAbsorption and fateParacetamol is readily absorbed from the gastro-intestinal tract with peak plasma concentrations occurring about 30 minutes to 2 hours after ingestion. It is metabolised in the liver and excreted in the urine mainly as the glucuronide and sulfate conjugates. Less than 5% is excreted as unchanged paracetamol. The elimination half-life varies from about 1 to 4 hours. Plasma-protein binding is negligible at usual therapeutic concentrations but increases with increasing concentrations.A minor hydroxylated metabolite, which is usually produced in very small amounts by mixed-function oxidases in the liver, and which is usually detoxified by conjugation with liver glutathione may accumulate following paracetamol overdosage and cause liver damage.
CaffeineAbsorption and fateCaffeine is completely and rapidly absorbed after oral administration with peak concentrations occurring between 5 and 90 minutes after dose in fasted subjects. There is no evidence of presystemic metabolism. Elimination is almost entirely by hepatic metabolism in adults.In adults, marked individual variability in the rate of elimination occurs. The mean plasma elimination half-life is 4.9 hours with a range of 1.9 - 12.2 hours. Caffeine distributes into all body fluids. The mean plasma protein binding of caffeine is 35%.Caffeine is metabolised almost completely via oxidation, demethylation, and acetylation, and is excreted in the urine as 1-methyluric acid, 1-methylxanthine, 7-methylxanthine, 1,7-dimethylxanthine (paraxanthine). Minor metabolites include 1-methylacrylic acid and 5-acethylamine-6-formylamine-3-methyluracil (AFMU).
3 years:Blister strip: 4, 6, 8, 12, 16, 24, 32 tablets.
2 years:Paper/Polyethylene strip / laminated strip: 4, 8HDPE tablet container: 10, 24, 32Aluminium containers: 16, 32
Pack ACartons containing blister strips.Pack sizes: 8, 12, 16, 24, 32 tablets.
Pack BThe tablets are packed into tablet containers.Pack sizes: 10, 16, 24 and 32 tablets.
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+44 (0)333 555 2526