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Compare And Contrast Paracetamol And Aspirin

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Compare and contrast the mechanism of action and therapeutic uses of aspirin and paracetamol

Aspirin, also known as acetylsalicylic acid, was among the earliest drugs to be synthesized and is still commonly used worldwide today. Aspirin is useful as an anti pyretic, anti platelet, analgesic, as well as, anti-inflammatory drugs. Its main clinical importance now is in the treatment of cardiovascular disease. It can be orally administered and is rapidly absorbed as the liver metabolizes 75%, but can’t be given to human beings under the age of 16. The elimination of aspirins metabolite, salicylate, follows first-order kinetics at low doses, but at high doses, it follows saturation kinetics. (Rang et al., 2012).

Paracetamol, also known as acetaminophen,
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It does this by diffusing from the inner membrane space acting as a protein carrier and back into the mitochondrial matrix, when aspirin ionizes again and it releases proteins. Therefore in this mechanism, aspirin is used as a buffer and transports protons.
If high doses of aspirin is administered, this administration can cause a fever, due to the heat release from the electron transport chain, compared to the antipyretic effect of aspirin at lower doses.
When aspirin is broken down to salicylic acid, which has antipyretic and analgesic effects, it was found that salicylic acid, activated AMP-activated protein kinase, which can be suggested as a possible explanation of both salicylic acid and aspirin. The acetyl portion of aspirin have its own targets and acetylation of the cellular proteins can be used as a theory for the regulation of protein function at a post-translational level. These acetylation reactions may be used to explain many of the hitherto unexplained effects of
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By inhibiting the COX enzyme it controls pain by controlling the signals before they reach the brain.
The analgesic mechanism of paracetamol has been suggested that the metabolites of paracetamol such as NAPQI, which act on TRPA1-receptors in the spinal cord, suppress the signal transduction from the superficial layers of the dorsal horn, therefore alleviating pain.
The exact mechanisms by which COX is inhibited in various circumstances are still being discussed and this is because of the differences in activity of aspirin, paracetamol and other NSAIDs. With these differences it has been proposed that further COX enzymes may exist. A theory of how paracetamol may work is by the inhibition of the COX-3 isoform (a COX-1 splice variant). COX-3 has been expressed in dogs and it shows that this enzyme shares similarities to other COX enzymes, while producing pro-inflammatory chemicals and is selectively inhibited by paracetamol. But research has continued and in humans the COX-3 enzyme doesn’t show inflammatory action and paracetamols blockage of it is not significant in its functioning in
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