
How does ibuprofen affect prostaglandins?
Answer
543.9k+ views
Hint: Ibuprofen is a known non-steroidal anti-inflammatory drug or NSAID. Other examples of drugs in NSAIDs include aspirin and diclofenac. These are all pain killers that are used in the management of mild to moderate pain, inflammation and fever. These symptoms arise when the body releases such chemicals called prostaglandins.
Complete answer:
Ibuprofen is a non-selective inhibitor of an enzyme called cyclooxygenase (COX), required for the synthesis of prostaglandins via the arachidonic acid pathway. COX is required to convert arachidonic acid to prostaglandin $H_2$ ($PGH_2$) in the body. This $PGH_2$ is then converted to those prostaglandins. The inhibition of COX by ibuprofen then lowers down the level of prostaglandins made by the body.
Most prostaglandins formed from $PGH_2$ are important mediators of sensations such as pain and processes such as fever and inflammation. antipyretic effects might occur as a result of action on the hypothalamus leading to vasodilation, an increased peripheral blood flow and subsequent heat dissipation.
Anticoagulant effects are also mediated through inhibition of COX, which converts arachidonic acid into thromboxane $A_2$, a vital component in platelet aggregation that leads to the formation of blood clots.
Note: The initial effect of ibuprofen is a reduction in pain. The anti-inflammatory actions somehow may fail to take effect for up to two to three weeks. Just like other NSAIDs, ibuprofen is associated with unwanted side effects, due to the quantity of roles prostaglandins play in the body, such as protecting the gut lining and contributing to coagulation. The use of ibuprofen can irritate the gut, as well as increasing the likelihood of bleeding.
Complete answer:
Ibuprofen is a non-selective inhibitor of an enzyme called cyclooxygenase (COX), required for the synthesis of prostaglandins via the arachidonic acid pathway. COX is required to convert arachidonic acid to prostaglandin $H_2$ ($PGH_2$) in the body. This $PGH_2$ is then converted to those prostaglandins. The inhibition of COX by ibuprofen then lowers down the level of prostaglandins made by the body.
Most prostaglandins formed from $PGH_2$ are important mediators of sensations such as pain and processes such as fever and inflammation. antipyretic effects might occur as a result of action on the hypothalamus leading to vasodilation, an increased peripheral blood flow and subsequent heat dissipation.
Anticoagulant effects are also mediated through inhibition of COX, which converts arachidonic acid into thromboxane $A_2$, a vital component in platelet aggregation that leads to the formation of blood clots.
Note: The initial effect of ibuprofen is a reduction in pain. The anti-inflammatory actions somehow may fail to take effect for up to two to three weeks. Just like other NSAIDs, ibuprofen is associated with unwanted side effects, due to the quantity of roles prostaglandins play in the body, such as protecting the gut lining and contributing to coagulation. The use of ibuprofen can irritate the gut, as well as increasing the likelihood of bleeding.
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