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AI-Generated response:

How do NSAID pain relievers work?

Answer generated on June 4, 2024

The AI-generated responses are for illustration purposes only and should not be used for medical purposes.

Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which are involved in the synthesis of prostaglandins, mediators of inflammation and pain.[1-7]

  • NSAIDs block the conversion of arachidonic acid to prostaglandin G2 (PGG2), the initial step in prostaglandin synthesis, reducing inflammation, pain, and fever.[1-4]

  • COX-1 is expressed in most tissues and is involved in maintaining gastric mucosal integrity, renal function, and hemostasis, while COX-2 is inducible and primarily involved in inflammation.[1-4]

  • Selective COX-2 inhibitors may preserve COX-1 mediated synthesis of gastroprotective prostaglandins, potentially reducing gastrointestinal side effects compared to non-selective NSAIDs.[3]

  • The inhibition of COX enzymes by NSAIDs does not affect the peroxidase reaction or leukotriene synthesis by lipoxygenase pathways.[1-2][4]

  • While effective for pain relief and inflammation reduction, NSAIDs can cause gastrointestinal irritation, cardiovascular risks, and renal impairment, particularly with long-term use.[3][8]

Additional info

It is important for the prescribing physician to consider the patient's overall health status, including any pre-existing conditions such as cardiovascular disease or gastrointestinal issues, when choosing an NSAID for treatment. The balance between efficacy in reducing pain and inflammation and the potential for adverse effects is a critical consideration. For instance, while selective COX-2 inhibitors might offer a lower risk of gastrointestinal complications, they may not be suitable for patients with certain cardiovascular risks. Additionally, the physician should monitor for signs of gastrointestinal bleeding, renal impairment, and any cardiovascular symptoms during NSAID therapy, especially in patients using these drugs long-term or in higher doses. This careful management is essential to maximize therapeutic benefits while minimizing risks.

References

Reference 1

1.

Elsevier ClinicalKey Drug Monograph

Content last updated: April 1, 2024.

Mechanism Of Action **Mechanism of Action:** All Day Pain Relief competitively inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. The enzymes COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses. COX isoenzymes are also responsible for a peroxidase reaction, which is not affected by NSAIDs. In addition, NSAIDs do not suppress leukotriene synthesis by lipoxygenase pathways. COX-1 is constitutively expressed in almost all tissues, while COX-2 appears to only be constitutively expressed in the brain, kidney, bones, reproductive organs, and some neoplasms (e.g., colon and prostate cancers). COX-1 is responsible for prostaglandin synthesis in response to stimulation by circulating hormones, as well as maintenance of normal renal function, gastric mucosal integrity, and hemostasis. However, COX-2 is inducible in many cells in response to certain mediators of inflammation (e.g., interleukin-1, tumor necrosis factor, lipopolysaccharide, mitogens, and reactive oxygen intermediates). ** •Anti-inflammatory Activity:** The anti-inflammatory mechanism of all day pain relief is due to decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to inhibition of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation.

Reference 2

2.

Elsevier ClinicalKey Drug Monograph

Content last updated: March 4, 2024.

Mechanism Of Action Aspercreme Arthritis Pain Reliever competitively inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. The enzymes COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses. COX isoenzymes are also responsible for a peroxidase reaction, which is not affected by NSAIDs. In addition, NSAIDs do not suppress leukotriene synthesis by lipoxygenase pathways. COX-1 is constitutively expressed in almost all tissues, while COX-2 appears to only be constitutively expressed in the brain, kidney, bones, reproductive organs, and some neoplasms (e.g., colon and prostate cancers). COX-1 is responsible for prostaglandin synthesis in response to stimulation by circulating hormones, as well as maintenance of normal renal function, gastric mucosal integrity, and hemostasis. However, COX-2 is inducible in many cells in response to certain mediators of inflammation (e.g., interleukin-1, tumor necrosis factor, lipopolysaccharide, mitogens, and reactive oxygen intermediates). ** •Anti-inflammatory Activity:** The anti-inflammatory mechanism of aspercreme arthritis pain reliever is due to decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to inhibition of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation.

Mechanism Of Action Zipsor competitively inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. The enzymes COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses. COX isoenzymes are also responsible for a peroxidase reaction, which is not affected by NSAIDs. In addition, NSAIDs do not suppress leukotriene synthesis by lipoxygenase pathways. COX-1 is constitutively expressed in almost all tissues, while COX-2 appears to only be constitutively expressed in the brain, kidney, bones, reproductive organs, and some neoplasms (e.g., colon and prostate cancers). COX-1 is responsible for prostaglandin synthesis in response to stimulation by circulating hormones, as well as maintenance of normal renal function, gastric mucosal integrity, and hemostasis. However, COX-2 is inducible in many cells in response to certain mediators of inflammation (e.g., interleukin-1, tumor necrosis factor, lipopolysaccharide, mitogens, and reactive oxygen intermediates). ** •Anti-inflammatory Activity:** The anti-inflammatory mechanism of zipsor is due to decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to inhibition of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation. COX-1 is expressed in the joints of rheumatoid arthritis or osteoarthritis patients, especially the synovial lining, and it is the primary enzyme of prostaglandin synthesis in human bursitis.

Mechanism Of Action Vopac Mds competitively inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. The enzymes COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses. COX isoenzymes are also responsible for a peroxidase reaction, which is not affected by NSAIDs. In addition, NSAIDs do not suppress leukotriene synthesis by lipoxygenase pathways. COX-1 is constitutively expressed in almost all tissues, while COX-2 appears to only be constitutively expressed in the brain, kidney, bones, reproductive organs, and some neoplasms (e.g., colon and prostate cancers). COX-1 is responsible for prostaglandin synthesis in response to stimulation by circulating hormones, as well as maintenance of normal renal function, gastric mucosal integrity, and hemostasis. However, COX-2 is inducible in many cells in response to certain mediators of inflammation (e.g., interleukin-1, tumor necrosis factor, lipopolysaccharide, mitogens, and reactive oxygen intermediates). ** •Anti-inflammatory Activity:** The anti-inflammatory mechanism of vopac mds is due to decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to inhibition of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation.

Reference 3

3.

Nonsteroidal Antiinflammatory Drugs (NSAIDs), Elsevier ClinicalKey Drug Class Overview

Content last updated: August 5, 2022.

NSAIDs have analgesic, anti-inflammatory, and antipyretic pharmacologic effects mediated by inhibition of prostaglandin synthesis by inhibition of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) enzymes. Prostaglandins are mediators of inflammation, sensitize afferent nerves, and potentiate the action of bradykinin in inducing pain[32122]. [56268][68341] COX-2 inhibitors selectively inhibit COX-2, which may preserve the synthesis of prostaglandins with gastric cytoprotective effects that occurs through the COX-1 enzyme; inhibition of platelet aggregation does not occur due to selective COX-2 inhibitory activity[56268]. [68321]

Reference 4

4.

Elsevier ClinicalKey Drug Monograph

Content last updated: April 1, 2024.

Mechanism Of Action **Mechanism of Action:** Ponstel inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. The enzymes COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses. COX isoenzymes are also responsible for a peroxidase reaction, which is not affected by NSAIDs. In addition, NSAIDs do not suppress leukotriene synthesis by lipoxygenase pathways. COX-1 is constitutively expressed in almost all tissues, while COX-2 appears to only be constitutively expressed in the brain, kidney, bones, reproductive organs, and some neoplasms (e.g., colon and prostate cancers). COX-1 is responsible for prostaglandin synthesis in response to stimulation by circulating hormones, as well as maintenance of normal renal function, gastric mucosal integrity, and hemostasis. However, COX-2 is inducible in many cells in response to certain mediators of inflammation (e.g., interleukin-1, tumor necrosis factor, lipopolysaccharide, mitogens, and reactive oxygen intermediates). **•Anti-inflammatory Activity:** The anti-inflammatory mechanism of ponstel is decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to inhibition of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation. COX-1 is expressed in the joints of rheumatoid arthritis or osteoarthritis patients, especially the synovial lining, and it is the primary enzyme of prostaglandin synthesis in human bursitis. These drugs are considered non-selective NSAIDs, affecting COX-1 and COX-2 to a similar degree.

Reference 5

5.

Food and Drug Administration (DailyMed).

Publish date: March 4, 2023.

Mechanism Of Action 12.1 Mechanism of Action Analgesia Combogesic (acetaminophen and ibuprofen) contains Combogesic (acetaminophen and ibuprofen). Acetaminophen is a non-opiate, non-salicylate analgesic. The precise mechanism of the analgesic properties of acetaminophen is not established but is thought to primarily involve central actions. Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID). Its mechanism of action for analgesia, like that of other NSAIDs, is not completely understood, but involves inhibition of cyclooxygenase (COX-1 and COX-2). Ibuprofen is a potent inhibitor of prostaglandin synthesis in vitro. Prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain in animal models. Prostaglandins are mediators of inflammation. Because ibuprofen is an inhibitor of prostaglandin synthesis, its mode of action may be due to a decrease of prostaglandins in peripheral tissues.

Reference 6

6.

Food and Drug Administration (DailyMed).

Publish date: January 5, 2021.

Mechanism Of Action 12.1 Mechanism of Action The mechanism of action of diclofenac is similar to that of other non-steroidal anti-inflammatory drugs. Diclofenac inhibits the enzyme, cyclooxygenase (COX), an early component of the arachidonic acid cascade, resulting in the reduced formation of prostaglandins, thromboxanes and prostacylin. It is not completely understood how reduced synthesis of these compounds results in therapeutic efficacy.

Reference 7

7.

Food and Drug Administration (DailyMed).

Publish date: April 5, 2024.

Mechanism Of Action 12.1 Mechanism of Action ACULAR LS (ketorolac tromethamine) is a nonsteroidal anti-inflammatory drug which, when administered systemically, has demonstrated analgesic, anti-inflammatory, and anti-pyretic activity. The mechanism of its action is thought to be due to its ability to inhibit prostaglandin biosynthesis.

Reference 8

8.

Trasolini NA, Yanke AB, Verma NN, Cole BJ. The Journal of the American Academy of Orthopaedic Surgeons. 2022;30(12):535-542. doi:10.5435/JAAOS-D-21-01228.

Publish date: June 3, 2022.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for multimodal pain control after surgery. These medications work by selective or nonselective inhibition of cyclooxygenase, which has downstream effects on thromboxanes, prostaglandins, and prostacyclins. Clinical studies have shown beneficial effects for alleviating pain and reducing opioid consumption after surgery. Within hip arthroscopy, there is evidence that postoperative NSAIDs can also reduce the risk of symptomatic heterotopic bone formation. However, preclinical and animal studies have raised concern over the effect of NSAIDs on bone and soft-tissue healing. In addition, selective and nonselective cyclooxygenase 2 inhibitors may have different safety profiles regarding postoperative soft-tissue healing. The purpose of this review was to outline the mechanisms of action, efficacy, and effect on soft-tissue healing of postoperative NSAIDs and to provide evidence-based recommendations for appropriate use.

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