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Aspirin: Mechanisms of Action, Absorption and Elimination

Paper Type: Free Essay Subject: Biology
Wordcount: 2080 words Published: 1st Jun 2018

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Today, there are many medicines used to treat human diseases and one of the medicines is called Bayer aspirin. Aspirin (acetylsalicylic acid) is a white or colourless crystalline powder. Anthony (2002). It is used to treat mainly minor pains, but has their benefits like lowering fever, inflammation, and reduces blood from clotting. The trade name of aspirin is Bayer and the chemical name is acetylsalicylic acid. The manufacture name is time cap laboratories Inc that produces aspirin. Bayer aspirin contains both active and inactive ingredients. In each tablet the active ingredient is acetylsalicylic acid. Other than the active ingredients other components are the inactive ingredient. Now I will be mentioning the absorption, mode of administration, mechanism of action and the elimination of aspirin.

Both carboxylic acid and ester doesn’t reacts with phenol. Aspirin has the chemical formula of C9H8O4.


A drug wouldn’t be effective if the human body doesn’t breakdown and absorb the drug easily. When the aspirin enters the stomach some of it absorbs within the stomach as the aspirin is acetylsalicylic acid and the stomach contains acid. Anthony (2002). In the stomach (pH 2) the hydrolysis rate is lower than at pH 9-11 that is found in the upper G.I tract as the rate goes up significantly. Not all aspirin is absorbed in the stomach as it is a weak acid, but most of the absorption occurs in the upper part of the small intestine by passive diffusion. Aschenbrenner and Samantha (2009). The reason that less absorption occurs in the stomach is due to the surface area of the mucosa in the stomach and the coating layer that is on the tablet. Rainsford (2004). In the stomach about 24% of aspirin is ionised. About 10 minutes and after in the stomach the mass of the aspirin roughly about 12% is absorbed from a solution that is un-buffered. Cooke and Hunt. (1970). If the pH of gastric has risen up to pH 6 there would be a decrease about 1% of the area of absorption as the majority of aspirin would then be in a less permeable ionised form. Slower gastric absorption which is due to increased pH isn’t reflected in the overall slower absorption. This is because the solution that is buffered is rapidly removed into the upper part of the gastrointestinal tract and here the rate of absorption is fast. Dotevall and Ekenved (1976). The rate of absorption of aspirin salts is quick in a man on an empty stomach having a half life of absorption about 5-16 minutes. Rowland et al. (1972).

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In the small intestine the aspirin solubility is improved, where the lower down you go through the small intestine the higher or increased the pH will be and by having a large surface area the absorption of aspirin would be increased. Karsten (2009). About 70% of the unchanged aspirin is absorbed in both stomach and in the upper intestine with 30% of salicylate. Quinn (2008). Also the skin can absorb aspirin, but it would be a slow process, but can be beneficial when treating herpeszoster. Rougier et al. (1987). Normally about 30 minutes he absorption of aspirin takes places, but there are many factors that can affect the absorption of aspirin like pH of gastrointestinal (GI) lumens, time of intestinal transit, the time of, taken with food and gastric emptying. Ling et al. (2001) and Aschenbrenner and Samantha (2009). There are also factors that can reduce gastric empting like having a meal that has high fat and having drinks that are acid. To maximize the absorption rate aspirin should be taken on an empty stomach with enough cold water. Williams and Schleader (2003). However it is not recommended to take aspirin with alcohol as it will increase the effect of alcohol. Caffeine increases the pain relief effect of aspirin.


After the uptake of aspirin from the G.I tract it goes into the portal venous system that enters the first pass, which is the liver, where drug metabolism occurs. Part of the aspirin is hydrolyzed into saclicylate by action of carboxylesterases. Rainsford (2004). Aspirin is distributed throughout the body, which may last about 15 to 20 min. Quinn (2008). Aspirin has a molecular weight of 180.15, which is low. Rainsford (2004). This makes aspirin easier to leave the bloodstream and enter the capillaries. Page et al. (2006). The lipid solubility of a drug can effect the diffusion that will occur across the membrane. Aspirin is quite lipid soluble having a log P value, which is 1.19. Salicyclic acid on the other hand is more soluble in lipid and will have a quite high distribution It has a log P value of 2.26. Drayton (1990). Also it is non-ionized, so it can pass through the lipid membrane of the cell. King and Mary (2009). Aspirin bounds to a plasma protein like albumin through reversibly and irreversible. Rainsford (2004). 50% of aspirin is bounded to plasma protein. Anthony (2002). An acetyl group is joined to the plasma protein when binding irreversible. Acetylsalicylic acid has an half life of 15 minutes, but it is longer for salicylate that has a half life of 2 hours. Aschenbrenner and Samantha (2009).

Mode of administration

Drugs are available in different forms. Before aspirin tablets were available the first aspirin was in the form of a power. In 1915 aspirin was no longer in powder form, but now produced in tablet form that was white in appearance and round shaped. Ament (2007). At that time prescription weren’t needed if someone wanted aspirin. Later in 1952 a chewable aspirin was now available making it easier for children to take the drug or haven’t learnt to swallow yet. Ament (2007). There are other advantages like it can be taken with water, the stability is better and portability and palatability. The mode of administration was taken further as toleraid was added to aspirin. This is a thin coating of aspirin tablets or to granules that makes the tablet easier to consume. Rainsford (2004). Today Bayer aspirin are in the form of tablets that are taken orally.

Tablets contain drugs that are mixed with excipients, which are inactive substance that carrier the active ingredients of the drug. Enteric coating is added to Bayer aspirin as this will hold the aspirin together when it in the stomach, but dissolves when it reaches the intestine. King and Mary (2009). This reduces stomach irritation and prevents the enzymes and acid in the stomach to reduce the effectiveness of the drug. Rainsford (2004). This is why aspirin tablets aren’t scored meaning that there isn’t a thin line in the middle of the tablet, so it can be halved. It should also not be crushed or chewed, but the whole of the tablet should be swallowed with water. Enteric coating doesn’t break down at low pH, but will dissolve at higher pH that is found in the intestine. Due to this it would take longer for the aspirin to be absorbed. Tablets are relatively slow compared to liquid and powder forms of drug and take about 1-3 hours delay before effect can take place. Also the drug hasn’t got an unpleasant taste making it easier for people to get it. There are also micro fined aspirin that is absorbed ever more quickly.

When taking the aspirin e.g. aspirin regimen Bayer it is recommended for adults and children over the age of 12 to take 1-2 caplets every 4 hours with full glass of water. Also 3 caplets can be taken, but for every 6 hours. During the 24 hours an individual shouldn’t take more than 12 caplets. A doctor should be consulted before giving aspirin to children under the age of 12, pregnant or breast-feeding. The carton should be kept, so directions and warnings of aspirin can be known and should be store at room temperature.

Mechanism of action

One of the benefits of aspirin is that it can reduce the risk of having cardiovascular diseases. When aspirin is in the body it targets the enzyme cyclooxygenase, where it irreversibly prevents the inactivating platelet cyclo-oxygenase. There are two types of cyclooxygenase; COX-1 and COX-2. COX-1 is found in many cells and COX-2 is in places of inflammation. Anthony (2002). Platelets in the human body give out COX-1 and not COX-2. Platelets are found in the blood and are involved it blood clot. When aspirin is present it stops arachidonic acid being converted to prostaglandin H2 and reduces TXA2 from being produced. Anthony (2002). The aspirin effect last for 5 to 7 days, which is the life of the platelets. King and Mary (2009). Platelets can still stimulate through ADP, thrombin and epinephrine. Page et al. (2006). In endothelial cell the platelets inhibitor PGI2 is also block by aspirin.

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When there isn’t aspirin in the body this makes the enzyme cyclooxygenase easier to convent arachidonic acid to thromboxane A2. This diffuses across the platelet membrane that then binds to the receptor onto another platelet. King and Mary (2009). This cause the platelets to stick together in the wall of the artery and as they slowly build up in the artery of the heart or the brain, therefore increasing the risk of arterial thrombotic disorders.

Mechanism of action. Platelet cyclooxygenase is inhibited by aspirin, therefore less production of TXA2. Activation and aggregation of platelets occurs when thromboxane A2 starts reactions. Acetylsalicylic acid works as a strong anti-platelet agent and the aspirin effects lasts the life of the platelets, which is about 5 to 7 days.


Metabolism and excretion are the process that takes place to eliminate drug. Page et al. (2006). Aspirin forms polar metabolites in the liver as it is quickly glucuronidated. Anthony (2002). Part of the aspirin is hydrolyzed into saclicylate by action of carboxylesterases in the liver. Rainsford (2004). Before aspirin is converted to salicylate it goes through enzymatic and spontaneous hydrolysis. However, in the body the spontaneous hydrolysis has little or no importance as this can be seen by the half life of 15.5 hours in buffered saline. Rowland et al., (1972). There should be a slight different in the half life in any point inside 1.2-8.0 Ph range. (Edwards 1952). In tissue like the G.I tract, kidney, liver, blood and hind limbs the enzymatic hydrolysis of acetylsalicylic acid happens. (Cossum et al., 1986) and (gaspari et al., 1989). In human plasma the cholinesterases, which is a main enzymes may hydrolyses acetylsalicylic acid. Rainsford et al., (1980). In proteins especially albumin an acety group is introduced by aspirin and therefore let go of salicylate. Rainsford et al., (1980). The thermal breakdown of acetylsalicylic acid will form acetyl-salicylsalicylic acid, salicylsalicylic acid and cyclic polymers of the salicylic acid as well as salicylic and acetic acids. Rainsford (2004).

Acetylsalicylic acid is excreted by the body in the kidney in the form of urine. Renal excretion of aspirin involves filtration that happens in glomerulus of the kidney, reabsorption and secretion along the nephron. Page et al. (2006). Passive diffusion and carrier mediated of un-ionised species takes place in the proximal tube There will be small quantity of unaffected aspirin in urine due to quick hydrolysis, but >98% happens fully as salicylic acid and its metabolites. The metabolites are gentritic acid, which is about 10%, salicylic acid (10%) and 5-10% of salicylic acid glucuronides. Rainsford (2004). There are factors that control the elimination of salicylate like urinary pH, corticosteroids, circadian pattern and age. However, one factor that may affect the elimination of aspirin is sex. Once aspirin has been in the body for some time there has been lower plasma concentration of the unaffected aspirin in males. Rainsford (2004).


As we came to know more about aspirin over the years we understand what happens to aspirin when it enters in human body and how it is removed. There is clear advantage of the use of excipients and when aiding the absorption rate certain factors should be avoided. There is still more to explore from aspirin. Since aspirin is absorbed from the skin aspirin patch preparation may be produced in the future that could be placed on the skin. This may help to ease the pain of shingles. Also aspirin could help individual who have Alzheimer’s disease, but further trials are being performed. WF et al. (1997).


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