The mechanisms actions of non-steroidal anti-inflammatory drugs (NSAIDs) To summarise, non-steroidal anti-inflammatory drugs are drugs which have anti-inflammatory, analgesic and antipyretic properties due to their mechanism and enzymes involved COX-1 and COX-2. However as well as being beneficial NSAIDs have many unwanted side effects such as diarrhoea, nausea, vomiting, and constipation. In frequent high doses can be fatal and cause kidney and liver failure. Non-steroidal anti-inflammatory drugs (NSAIDs) are therapeutic agents. They can be prescribed for ‘rheumatic’ musculoskeletal problems but are frequently taken without prescription for minor aches and pains. The expression ‘non-steroidal’ is used to tell the difference between corticosteroids (a class of steroid hormone) which also reduce inflammation but by a different method. NSAIDs have three main therapeutic effects: anti-inflammatory, analgesic and antipyretic.  NSAIDS generally work by inhibiting the fatty acid cyclooxygenase (COX) enzyme and therefore inhibit the production of prostaglandins and thromboxanes. There are three isomers of the COX enzyme: COX-1, COX-2 and COX-3. COX-3 enzyme has not been proven to have a functional use in humans and is not discussed in this essay. COX-1 is a constitutive enzyme involved in tissue homeostasis and is responsible for the production of prostaglandins, while COX-2 is induced in inflammatory cells and is responsible for the production of the prostanoid mediators of inflammation. COX first oxidises arachidonic acid to prostaglandin G2 (PGG2) through a cyclooxygenase process and then peroxidises PGG2 to PGH2. NSAIDs inhibit the cyclooxygenases thus reducing the change of arachidonic acid to prostaglandins. 
Aspirin has three main therapeutic effects in the body: the antipyretic effect, the analgesic effect and the anti-inflammatory effect. This is due to the decreased production of prostaglandins and thromboxanes by the irreversible inactivation of the cyclooxygenase enzyme. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. This makes Aspirin different to other NSAIDS whereby they are reversible inhibitors and aspirin is not. The side effects are caused by the inhibition of COX-1 enzyme, which synthesises prostaglandin that serve essential physiological functions such as causing appropriate platelet aggregation, protection of the gastric mucosa, inhibition of thrombogenesis and maintenance of renal function. The therapeutic effects of NSAIDs are due to inhibition of COX-2, an enzyme induced by various factors released by bacteria, the vascular endothelium or other cells involved in the inflammatory response.  Anti-inflammatory effects reduce inflammation. Inflammation occurs due to the release of histamine. Histamine causes vasodilation, increased vascular permeability and cell accumulation around damaged tissue. Non-steroidal anti-inflammatory drugs reduce the inflammatory results produced by COX-2. This includes pain signals sent to the brain as well as vasodilation and vascular permeability.  Antipyretic effects lower body temperature when this is raised in disease. Normal body temperature is regulated by hypothalamus in the brain which balances the heat lost and the production of heat made in the body. A raised body temperature occurs when there is a disturbance in the hypothalamus. Antipyretic effect is exerted by the inhibition of the prostaglandin in the hypothalamus.  Analgesic effects reduce certain type of pain. Non-steroidal anti-inflammatory drugs inhibit the production of prostaglandins which stimulate receptors that cause pain. This means that NSAIDs are effective in pain of muscular and vascular origin, dysmenorrhoea (period pain), toothache and arthritis. They also relieve headaches due to stopping the dilation of cerebral vasculature caused by prostaglandins.
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