- Aspirin is also known as acetylsalicylic acid in the Non-Steroidal Anti-inflammatory Drug (NSAID) class of drugs. It is a non-opioid analgesic which also has significant anti-inflammatory, antipyretic actions and inhibits platelet aggregation, decreasing the risk of thrombus (blood clot) formation.
- It inhibits the enzyme cyclooxygenase (COX) which lead to the formation of prostaglandins that cause inflammation, swelling, pain and fever. Aspirin also inhibits the production of prostaglandins which aggregate platelets when required.
Pain
- Acetylsalicylic acid (ASA) disrupts the production of prostaglandins throughout the body by targeting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) . Prostaglandins are potent, irritating substances that have been shown to cause headaches and pain. This occurs as they increase the sensitivity of pain receptors and substances such as histamine and bradykinin. Through the disruption of the production and prevention of release of prostaglandins in inflammation, Aspirin my stop their action at pain receptor sites, preventing symptoms of pain.
Antipyretic
- Acetylsalicylic acid is considered an antipyretic agent because of its ability to interfere with the production of brain prostaglandin E1. This is known to be an extremely powerful fever-inducing agent
Platelet Aggregation
- The inhibition of platelet aggregation by ASA occurs because of its interference with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke.
- Acetylsalicylic acid (ASA) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes. Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation. Platelet aggregation can result in clots and harmful venous and arterial thromboembolism, leading to conditions such as pulmonary embolism and stroke.
- GI upset: pH of salicylic acis is 2.4 and stomach has a low pH. When aspirin is consumed on an empty stomach the aspirin hydrolysis and salicylic acid decreases the pH of the stomach. This can result in GI symptoms
- Gastric and duodenal inhibits COX-1 activity in gastric mucosa by supressing the synthesis of protective prostaglandins. This creates a state of propensity for the development of aspirin-associated gastrointestinal ulcers and ulcer complications
- Salicylism: salicylates are weak acids that cross the cell membrane easily; thus they have increased toxicity when the blood pH is decreased. Dehydration, hyperthermia and chronic ingestion increase salicylate toxicity because they result in greater distribution of salicylate to the tissues. Some signs and symptoms include: vomiting, headache, tinnitus, dizziness
- Haemophilia: Aspirin alters platelet function causing imparement of small vessel hemostasia and prolongation of bleeding time
- Gout: affects pain and inflammation associated with gout due to its bimodal effect on renal handling of uric acid
- Warfarin: results in the increased chance of bleeding when oral anticoagulation is combined with antiplatelet therapy
- Phenytoin: leads to a decrease in total phenytoin level. This can mislead clinicians to increase the dose of phenytoin to bring it back to a normal therapeutic level. This can lead to clinical toxicity
- Probenecid: decreases the effect by anionic drug competition for renal tubular clearance. It decreases uricosuric action of probenecid
- <150mg/kg: Minimal symptoms
- 150-300mg/kg: Mild to moderate intoxication. Salicylism with hyperpnoea, tinnitus and vomiting
- >300mg/kg: Severe intoxication, metabolic acidosis, altered mental state and seizures
- >500mg/kg: Potentially lethal
Pharmacokinetics
- Rapid absorption initially through the oral mucosa when chewed
- Weak acid which promotes rapid absorption from the stomach and upper small intestine
- Salicylate is distributed throughout most body tissues and fluids, including synovial fluid and cerebrospinal fluid, and is 50-90% bound to plasma proteins
- Rapid hydrolysis to acetic acid and salicylate by esterases in tissue and blood
- Salicylate is non-linearly bound to albumin
- Saturable metabolism and excretion with increasing dose
- Renal- pH dependent
- Urinary alkalinisation increases excretion of free salicylate and its water-soluble conjugates
Pharmacodynamics
- Irreversible non-selective COX inhibitor
- In platelets, irreversible of COX-1 results in reduction of thromboxane A2 and inhibition of platelet aggregation for life of platelet (10 days)
- In tissues, inhibits COX-2 resulting in anti-inflammatory, antipyretic and analgesic effects
- Peak serum levels where of acetylsalicylic acid where platelets cannot generate new COX are reached within 20-40 minutes after oral administration
- Peak plasma levels within 2-4 hours
- Effects of Aspirin last for duration of platelet (10 days)
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