Aspirin: Clinical use, Adverse effects, Contraindications of aspirin, Why aspirin is not used in pregnancy?

Clinical use / Indication of aspirin:

1. Relieve mild to moderate pain:

·         Headache(non-visceral pain)

·         Myalgia (non-visceral pain)·        
Arthalgia (non-visceral pain)

How does aspirin reduce fever? Anti-pyretic action of aspirin:

There are 3 ways aspirin combats fever

1. The function of prostaglandin E2 (PG E2) is to elevate the hypothalamic set point of temperature, which means it causes an increase in body temperatue and thus fever.

Aspirin is an NSAID (Non-steroidal anti-inflammatory drug). All NSAIDs inhibits the cycloxygenase (COX-1 and COX-2) enzyme (by irreversible non-competetive inhibition) which is required for the synthesis of prostaglandin E2.

So, since no prostaglandin, particularly prostaglandin E2 in this case, is produced the temperature point in hypothalamus goes back to normal and thus the body temperature becomes normal again.

How does aspirin prevent thromboembolism / heart attack? Antiplatelete action of aspirin:

A thrombus is formed due to platelete aggregation. And platelete aggragation is mediated by a prostaglandin called thromboxane A2 (TX A2). As aspirin inhibits prostaglandin systhesis by inhibiting the COX enzyme, no thromboxane is produced.

So since there is no TX A2, there is no platelete aggragation and no thrombus or embolus formation.

This is particularly important in heart patients suffering from myocardial infarction. They have to take 75 mg of aspirin for life long to prevent myocardial infarction.

How does aspirin prevent pain? Analgesic action of aspirin:

There are two mechanism by which aspirin combats pain:

1. Centrally aspirin acts at subcortical sites like thalamus and inhibits the pain stimuli, thus causing analgesia.

How aspirin prevents inflammation?

How does aspirin prevent inflammation? Anti-inflammatory action of aspirin

There are two ways aspirin combat inflammation:

1. Prostaglandin is the main mediator of inflammation. Aspirin inhibits the synthesis of this prostaglandin by inhibiting the cycloxygenase (COX) enzyme. See the diagram below.

Aspirin: Basic Mechanism of action of aspirin

Aspirin is a non-selective, non-competetive irrversible cycloxygenase (COX) enzyme inhibitor. Even so it is about 160 times more specific to COX 1 than COX 2. 

The COX enzymes are responsible for the systhesis of prostaglandins (PG) which are the mediators of inflammation, pain, fever, platelet aggregation. 

So aspirin acts by inhibiting the prostaglandin synthesis.

Aspirin: Introduction to asprin and its actions

Introduction to aspirin – an essential medicine:

Aspirin is a weak organic acid – acetylsalicylic acid. It is obtained naturally from the Willow bark which contains Salicin. It can also be produced synthetically.

It is mainly a non-opioid analgesic and non steroidal anti-inflammatory drug and is the initial choice of drug in the treatment of articular (arthritis) and musculoskeletal disorders.

Chief pharmacological actions of aspirin:

1. Anti-inflammatory action (Peripheral nervous system effect)

2. Analgesic action (pain-killer) (Both Central and Peripheral nervous system effect)

3. Anti-pyretic action (reduces fever) (Both Central and Peripheral nervous system effect)

4. Anti-platelet action (prevents platelet aggregation) ( Peripheral nervous system effect)

Other effects of aspirin:

Respiratory system	1. Stimulates respiratory center so increases the repiration rate 2. Uncoupling of oxidative phosphorylation
Liver	1. Mild reversible hepatic damage 2. Increase SGPT and SGOT level 3. Reye’s syndrome
Endocrine system	1. Increase steroid synthesis 2. Thyroid suppression by decreasing iodine uptake 3. Prolongs the labor period
Haematological effect	Large dose (>5g/day) cause inhibition of prothrombin synthesis in the liver.
Gastrointestinal tract	1. Gastric irritation                                                                Ulcer formation Bleeding leading to iron deficiency anaemia 2. Nausea and vomiting by stimulation of chemoreceptor trigger zone (CTZ) 3. Reduces the cytoprotective role of PG PG E2 and PG I2 ie decreases mucous production and increases the hydrochloric acid secretion
Renal system	Decreases the renal blood flow leading to renal salt and water retention leading to renal damage.

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