Effects Mechanisms Side Effects Naids Cardiovascular Benefits Aspirin Biology Essay


History of aspirin in briefly. Aspirin is the acetylated form of salicylic acid. Salicylate is a common constituent of numerous medicinal plants which have been used for thousands of years to treat an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant (blood-thinning) effect and is used in long-term low-doses to prevent heart attacks. Ancient Egyptians used the leaves of the Myrtle tree to treat rheumatic pain and Hippocrates treated eye infections with extracts from poplar trees and used extracts from willow bark in treating the pain and fever associated with childbirth.

Salicylate was first chemically synthesized in 1859 and it entered into widespread use as an anti-inflammatory in 1876. Salicylate has an extremely bitter taste and causes gastric irritation so researchers set out to develop analogs that would have the same pharmacological benefits but be easier to tolerate upon ingestion.


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How Aspirin and NSAIDs Works.

Prostaglandins are potent mediators of inflammation. The first and committed step in the production of prostaglandins from arachidonic acid is the bis-oxygenation of arachindonate to prostaglandin PGG2. This is followed by reduction to PGH2 in a peroxidase reaction. Both these reactions are catalyzed by cyclooxygenase, also known as PGH syntheses.

Cyclooxygenase (COX), an enzyme that participates in the production of prostaglandins and thromboxanes, is irreversibly inhibited when aspirin acetylates it. This makes aspirin different from other non-steroidal anti-inflammatory drugs or NSAIDs. Aspirin, ibuprofen, flurbiprofen and acetaminophen (trade name Tylenol) are all NSAIDs.

Prostaglandins are local hormones (paracrine) produced in the body and have diverse effects in the body, including but not limited to transmission of pain information to the brain, modulation of the hypothalamic thermostat, and inflammation. Thromboxanes are responsible for the aggregation of platelets that form blood clots.

There are two isoforms of COX in animals: COX-1, which carries out normal, physiological production of prostaglandins, and COX-2, which is induced by cytokines, mitogens and endotoxins in inflammatory cells, and which is responsible for the production of prostaglandins in inflammation. One of the best known aromatic acetates is acetylsalicylic acid, or aspirin, which is prepared by the esterification of the phenolic hydroxyl group of salicylic acid.

Approved and Common Usage of Aspirin

Aspirin has several different approved uses.

Strokes: Aspirin use recommended in both men and women to treat mini-strokes (transient ischemic attack --TIA) or ischemic stroke to prevent subsequent cardiovascular events or death.


Heart Attacks: Blood clots are formed by platelets grouping together.  Aspirin interferes with this process by making the platelets less "sticky" and therefore less successful in grouping together by inhibiting the manufacture of prostaglandins.  This same blood "thinning" action that makes aspirin effective in reducing a person's risk for heart disease is also the reason that some people are unable to take the drug

reduces the risk of death in patients with suspected acute heart attacks (myocardial infarctions)

prevents recurrent heart attacks and

Reduces the risk of heart attacks or sudden death in patients with unstable and chronic stable angina pectoris (chest pain).

Other coronary conditions: Aspirin can be used to treat patients who have had certain revascularization procedures such as angioplasty, and coronary bypass operations -- if they have a vascular condition for which aspirin is already indicated.

Rheumatologic diseases: Aspirin is indicated for relief of the signs and symptoms of rheumatoid arthritis, juvenile rheumatoid arthritis, osteoarthritis, spondylarthropathies, and arthritis and pleurisy associated with systemic lupus erythematosus.

Pain relief: Aspirin is indicated for the temporary relief of minor aches and pains.

Aspirin has potential risks as well as benefits, like any drug.

Some of the Side effects that are associated with aspirin are.

High doses can cause hearing loss or tinnitus ringing in the ears. Usually occurs with large doses as prescribed in rheumatologic diseases and is rare in treatment with low doses used for cardiovascular purposes.

Aspirin has some potentially serious side effects on the stomach and cause nausea; it can aggravate gastric ulcers; and cause internal bleeding.  It may increase the risk for stroke due to bleeding.  Those who are allergic to aspirin can go into shock.  And, aspirin is the trigger to a rare and sometimes fatal childhood disease, Reyes Syndrome, when taken following certain viral infections.

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Non-steroidal anti inflammatory drugs (NSAIDs) widely prescribed drugs in the treatment of inflammation and pain act by inhibition of the enzyme cyclooxygenase (Cox). But, these beneficial effects with the cost of various side effects such as ulcers and other serious gastrointestinal (GI). These side effects are due to the non-specific inhibition of the two isoforms Cox-1 and Cox-2 that are the constitutive and inducible forms of the enzyme, prostaglandin synthase (PG synthesis). Cox-2 is responsible for inflammation whereas Cox-1 is required for normal homeostasis.

Gastric ulceration and bleeding

Local irritation, back diffusion of H+, acid secretion.

Bleeding causes iron-deficiency.

prostaglandin used to GI inflammation with salicylates of NSAIDS; Overused and expensive- causes nausea and severe diarrhea

Aspirin Hypersensitivity

Caused by formation of leukotrienes; Not true antigen/antibody reaction but resembles hypersensitivity reaction.

Very low overall incidence


Susceptible to dose dependent hepatotoxicity.

Reye's syndrome

Sudden loss of consciousness, cerebral edema, fatty liver and renal tubules, and brain damage upon recovery


May prolong labour, bleeding and birth weight

Drug interactions

Oral anticoagulants: prothrombin, platelet aggregation, GI bleeding, displaces anticoagulants from plasma binding sites.

Displaces other drugs: oral hypoglycemics, NSAIDS, sulfonamides, methotrexate, phenytoin.

Alcohol (GI bleeding), antacids.

Acute dose uncouples oxidative phosphorylation, affects CHO, amino acid and fat metabolism resulting in CO2 production, organic acids such as lactate and b-hydroxybutyrate.

Central nervous system hyperventilation (medulla), tinnitis, hearing difficulty, confusion and convulsions.

Bleeding, nausea and vomiting, dehydration.

Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). It is used for relief of symptoms of arthritis, primary dysmenorrhoea, fever, and as an analgesic, especially where there is an inflammatory component. Ibuprofen, have analgesic, anti-inflammatory and antipyretic properties. In single doses NSAIDs have analgesic activity comparable to that of paracetamol. In regular full dosage, they have a lasting analgesic and anti-inflammatory effect, which makes them useful for continuous or regular pain due to inflammation. Differences in anti-inflammatory activity between different NSAIDs are small but there is considerable variation in individual patient response and in the incidence and type of adverse effects. Ibuprofen has fewer adverse effects than other NSAIDs but its anti-inflammatory properties are weaker.

Ibuprofen works through inhibition of cyclooxygenase (COX), thus inhibiting prostaglandin synthesis. Ibuprofen inhibits both COX-1 and COX-2. It appears that it's analgesic, antipyretic, and anti-inflammatory activities are achieved principally through COX-2 inhibition; whereas COX-1 inhibition is responsible for its unwanted effects on platelet aggregation and the GI mucosa. Where as Paracetamol is a common analgesic and antipyretic drug that is used for the relief of fever, headaches, and other minor aches and pains. Paracetamol is also useful in managing more severe pain, allowing lower dosages of additional NSAID.

Paracetamol, unlike other common analgesics such as aspirin and ibuprofen, has no anti-inflammatory properties, and so it is not a member of the class of drugs known as non-steroidal anti-inflammatory drugs (NSAIDs). In recommended doses, paracetamol does not irritate the lining of the stomach, affect blood coagulation as much as NSAIDs, or affect function of the kidneys.

Paracetamol has similar mechanism of action to aspirin because of the similarity in structure. That is, it has been assumed that paracetamol acts by reducing production of prostaglandins, which are involved in the pain and fever processes, by inhibiting the cyclooxygenase (COX) enzyme.

However, there are important differences between the effects of aspirin and those of paracetamol. Prostaglandins participate in the inflammatory response which is why it has been known to trigger symptoms in asthmatics, but paracetamol has no appreciable anti-inflammatory action and hence does not have this side effect. Furthermore, COX also produces thromboxanes, which aid in blood clotting aspirin reduces blood clotting, but paracetamol does not. Finally, aspirin and the other NSAIDs commonly have detrimental effects on the stomach lining, where prostaglandins serve a protective role, but paracetamol is safe.

Aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, paracetamol indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This is why paracetamol is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides.

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Recently discovered

Aspirin has two additional modes of actions, contributing to its strong analgesic, antipyretic and anti-inflammatory properties: It uncouples oxidative phosphorylation in cartilaginous (and hepatic) mitochondria. It induces the formation of NO-radicals in the body that enables the white blood cells to fight infections more effectively.

This has been found recently by Dr. Derek W. Gilroy, winning Bayer's International Aspirin Award 2005.

Source of information:




Pharmacology by H. P. Rang. Published 2003, page: 104, 245, 250-1, 323-4, 326