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Drug Monograph of Aspirin

Info: 4892 words (20 pages) Nursing Essay
Published: 11th Feb 2020

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Mechanism of Action of the Drug……………………………………..03



Therapeutic Use and Efficacy……………………………………………06



Distribution in the Body…………………………………………………..09



Adverse Drug Reactions…………………………………………………..11

Drug Interactions…………………………………………………………….12





Figure 1: Chemical Structure of Aspirin1

Carboxylic Acid Group


Ester Functional Group


Figure 1: The chemical composition of Aspirin – no chiral centre present. Two functional groups that can form hydrogen bonds with water.

Table 1: Chemical Properties of Aspirin1

Table 1: A table showing the chemical properties of Aspirin.

Systematic Name

Acetylsalicylic Acid

Molecular Formula


Molecular Weight


Solubility (in Water)


Boiling Point


Melting Point


Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) which is predominantly used as an analgesic, antipyretic or anti-inflammatory drug. The identification of salicylates as the active ingredient for the anti-inflammatory effects of willow bark led to the synthesis of aspirin. Aspirin was first synthesized in 1897 by Felix Hoffmann at the Bayer laboratories2. The therapeutic effects of aspirin originate from its ability to inhibit cyclooxygenases (COXs). The identification of COX isoforms led to the characterization of aspirin as a nonselective inhibitor. Aspirin is normally administered by either an enteric-coated or buffered tablet1.

Mechanism of Action

Aspirin is an irreversible inhibitor that inhibits the synthesis of thromboxane A2 (TXA2) and prostaglandins (PGs)3. Aspirin binds to cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is usually found in platelets, interstitial cells and blood vessels whilst COX-2 is usually found in parenchymal cells4.

As shown in figure 2, TXA2 is synthesised in the COX-1 pathway. Firstly, Arachidonic acid is converted to a biological intermediate known as Prostaglandin H2 (PGH2). This reaction is catalysed by PGH2 synthase. PGH2 is then converted into TXA2, which is catalysed by thromboxane synthase5.

Figure 2: Synthesis of TXA2 and PGs5

Figure 2: The physiological pathway in which PGs and TXa2 are formed.

TXA2 releases ADP which causes a platelet to undergo a morphological change of shape. The change in shape is essential for the activation of platelets, especially for its role in an inflammatory response5. This physiological pathway is activated when tissue cells are damaged by either harmful substances or foreign invaders6.

Figure 3: Inhibition of COX-17

Figure 3: A diagram showing the COX-1 pathway and how aspirin inhibits it.


As shown in figure 3, COX-1 is inhibited by aspirin. This occurs by an irreversible acetylation at the serine 529 residues of COX-1. This prevents Arachidonic Acid, from entering the catalytic site which prevents the synthesis of TXA2. As the synthesis of TXA2 decreases, there is a reduced aggregation of platelets. This reduced aggregation is sustained across the whole lifespan of a platelet which causes a significant decrease in the number of activated platelets8.

Figure 4: Platelet Aggregation9

Figure 4: A graph showing how the aggregation of platelet is significantly reduced when under therapeutic effects of aspirin.


Figure 5: Inhibition of COX-210

Figure 5: A diagram showing how COX-2 is inhibited by Aspirin.



As shown in figure 5, COX-2 is inhibited by aspirin. COX-2 is irreversibly acetylated at the serine 516 residues, which prevents the synthesis of PGs. Therefore, the catalytic activity of the pathway changes, leading to the synthesis of Lipoxins. Lipoxins are high-affinity receptors that play an essential role in the resolution of an inflammatory response. As the concentration of Lipoxins increase, there is a greater stimulation to stop the inflammatory response and initiate the repair process11. Aspirin has a significantly greater affinity of inhibition for COX-1 in comparison to COX-2. This allows smaller dosages of aspirin to be used for its antithrombotic effect whilst high dosages of aspirin can be used for its anti-inflammatory effect6.

Figure 6: Inhibition of TXA2 and PGs12

Figure 6: A graph showing that there is a decrease of Prostaglandin E (PGE) and Thromboxane B2 (TXB2 – A metabolite of TXA2) as the dosage of aspirin increases.

Therapeutic Use and Efficacy

Uses of Aspirin

Aspirin can be administered intravenously by a drip or enterally in the form of a tablet. This tablet can either be buffered, buccal or enteric-coated. A buffered tablet shortens the half-life of aspirin. A buccal tablet enables aspirin to bypass phase one metabolism. An enteric-coated tablet enables aspirin to be resistant to the stomach juices1.

Table 2: Dosage of Aspirin13

Table 2: A table showing the clinical uses of aspirin and their corresponding dosages. In addition to that, it shows the dosage of aspirin that is considered to be toxic.



A low dose of aspirin is used for its antithrombotic effect. Aspirin prevents the formation of TXA2, which causes a reduction in platelet aggregation. As the number of activated platelets decreases, there is a reduced chance for the formation of a blood clot. A high dose of aspirin is used for its analgesic and antipyretic effect. As shown in table 2, the dosage of aspirin used is dependent on the health problem. This is due to aspirin having a significantly greater affinity of inhibition to COX-1 than COX-2. Aspirin is normally given to adults and not children. The only exception for a child to be given aspirin is when they have undergone heart surgery or have the Kawasaki disease14.

Table 3: Health Problems treated by Aspirin14

Table 3: The most common health problem treated by aspirin.



COX-2 has an important role in the inhibition of apoptosis, tumour promotion and the carcinogenesis in several cancers. As shown in table 4, there is supporting data that suggests aspirin can be used as a chemopreventive drug in several cancers.The combination of aspirin and chemopreventive compounds would potentiate aspirin’s therapeutic effects. In particular the chance to inhibit the proliferation of neoplastic cells and induce apoptosis15.

Table 4: Types of Cancers15

Table 4: A table showing the use of aspirin in treating cancer cell lines.



Efficacy of Aspirin

Table 5: Dose-Dependent Acetylation16

Table 5: A table showing how the inactivation of cox varies with the dosage of aspirin.


The efficacy of aspirin is independent of free salicylate because the mechanism of action is only dependent on the acetylation of aspirin. As shown in table 5, as the dosage of aspirin increases, there is a greater degree of inhibition of COX16.

Table 6: Efficacy Studies15

Table 6: A table showing studies on the efficacy of aspirin in the use of primary and secondary prevention of cardiovascular events.

Distribution in the body

Absorption and Distribution

Figure 7: Bioavailability of Aspirin1

Figure 7: A diagram showing the bioavailability of Aspirin – once ingested. Bioavailability is the percentage of the aspirin that reaches the systemic circulation.



Table 7: Pharmacokinetic Profile of Aspirin17

Table 7: A table showing the pharmacokinetic parameters of aspirin.



Aspirin can be taken by an individual intravenously, enterally or through buccal administration. The tablet is taken into the body through oral ingestion and travels down the oesophagus and into the stomach. The percentage of aspirin absorbed in the stomach is usually around 10%, by passive diffusion. Aspirin will then travel through the epithelium and cilia via the bloodstream18.

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Blood consists of two main components, blood plasma and red blood cells. Within the blood plasma, there are specialised proteins that are made in the liver called Albumins. Albumin forms a complex with aspirin by binding to aspirin via the phenolic hydroxyl group19. This complex can be filtered out by the liver. The remaining aspirin molecules will have a therapeutic effect on the body. These aspirin molecules will travel into the liver by the hepatic portal vein and undergo phase one metabolism18.

Metabolism and Excretion

Figure 8: Hydrolysis of Aspirin20-22

Figure 8: A diagram showing the hydrolysis of Aspirin.



Table 8: Aspirin Half-Life23

Table 8: A table showing the hydrolysis half-life of aspirin in different body fluids.



The metabolism of aspirin occurs in the liver and can be split into two phases, phase one and phase two. As shown in figure 8, the ethanoic acid group of aspirin is broken off, which converts aspirin into the metabolite salicylic acid. This process is carried out by the enzymes PAFAH1b2 and Butyrylcholinesterase (BChE). As shown in table 8, the time taken for aspirin to be hydrolysed depends on what bodily fluid it is in. The importance of this reaction is that salicylic acid has a low solubility, therefore it’s unlikely to be excreted in urine24.

In the second phase of metabolism, an ionized group is added to the salicylic acid group forming a metabolite called Glucuronide. Glucuronide is soluble in water which means that it can be excreted in urine. The remaining particles of aspirin will travel to the site of injury and have an effect. An individual that is administered aspirin intravenously or through a buccal tablet will have the maximum bioavailability for the body as it bypasses the liver18.

Table 9: Excretion of Metabolites25

Table 9: A table showing an average percentage of the composition of patients’ urine who’ve taken aspirin



The excretion of aspirin mainly occurs as either salicylic acids or salicylic acid metabolites. The excretion of salicylic acids or its metabolites through urine is promoted by the alkalinisation of urine. This causes acids in the body to be dissociated which increases the amount of excretion by 5-10 times1.

As shown in table 9, the most common metabolite for excretion is Salicyluric acid. The formation of Salicyluric acid is limited by capacity and cannot be altered by an increase in the dosage of aspirin. It is formed from the bonding of glycine and salicylic acid. The most uncommon metabolite that is excreted in urine is Gentisic acid. Gentisic acid is formed from the hydroxylation of salicylic acid25.

Adverse Drug Reactions

Aspirin has a range of therapeutic uses, but there are undesirable side effects. This can include mucosal injury to the small intestine and the colon. As shown in table 10, in rare cases there is a chance of bleeding to occur in the brain26.

Table 10: Side Effects of Aspirin26

Table 10: A table showing the incidence of each side effects and their rarity.



Side Effect


Gastric Intolerance

1% – 10%


0.1% – 1%


0.01% – 0.1%


0.01% – 0.1%


Incidence not known

Asthma Attack

Incidence not known

Allergic Reaction

Incidence not known

Bleeding in the Brain

Incidence not known


As shown in table 10, the side effect with the greatest incidence is gastric intolerances. Gastric intolerances can occur in patients taking either a low or high dose of aspirin. The most common symptoms of gastric intolerances are pyrosis, nausea and dyspepsia26.

Figure 9: Relative Risk27

Figure 9: A graph showing how the relative risk of developing a gastric ulcer increases with the number of aspirin tablets taken in a week.



Figure 10: Bleeding Time28

Figure 10: A chart showing how the bleeding time increases, as the dose of aspirin increases. Sodium salicylate is used as a control to ensure that the only independent variable is Aspirin



As shown in figure 10, there is a positive correlation between the bleeding time and the dosage of aspirin. There is still ongoing research into the physiological mechanism of the prolonged bleeding. Currently, it is believed to be linked with the inhibition of TXA2 which prevents the formation of thrombin. This is clinically important because a patient that has taken aspirin within a week of their surgery is at an increased risk of 50% of being subject to periprocedural bleeding29.

Drug Interactions

A drug interaction is defined as the therapeutic effects of a drug being altered by the presence of food, drink or another drug. Aspirin has over 250 unique drug interactions, however; a significant proportion of these interactions are not clinically significant30.

The absorption of aspirin is delayed when taken with food because the digestive system needs to deal with the food and aspirin at the same time. A study was carried out in which 25 healthy individuals in which some were fasting, which meant that they took aspirin with no food. The remaining people took a 600mg dose of aspirin with their food. The results showed that the serum salicylate levels were halved in the individuals that had aspirin with food30.

There is a slight increase in the loss of gastrointestinal blood when aspirin is taken with alcohol. A study was carried out on 17 healthy individuals, in which they took aspirin alongside 180ml of whisky. The initial mean of blood loss was 3.1ml. This increased to 5.3ml when each individual started to take a 2.1g dose of aspirin30.

Table 11: Drug Interactions of Aspirin30

Table 11: A table showing the most clinically relevant interactions between aspirin and other drugs.



Aspirin should not be given to an individual that has an increased risk of internal bleeding, especially for those that have active peptic ulceration. The stronger the dosage and longer the time period in which an individual takes aspirin, the increased chance of bleeding within the stomach.


Aspirin is a prodrug that is currently being used in the treatment of individuals experiencing prolonged inflammation, a fever or pain relief. Aspirin is an NSAID that acts an irreversible inhibitor to COX-1 and COX-2. This prevents the formation of TXA2 and PGs, which causes a reduction of platelet aggregation. Therefore, there is a reduced inflammatory response, which causes aspirin’s therapeutic effects. However, there are side effects associated with the use of aspirin for example, prolonged bleed or gastric intolerances.

The potential implications of aspirin being used as a chemopreventive agent are very significant. The inexpensive cost and easy accessibility to aspirin warrants ongoing research into aspirins potential uses in cancer. The knowledge gained from these ongoing studies could lead to the development of new treatment plans or a better understanding of how to use novel therapies to combat cancer.


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