NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which prevents the formation of prostaglandins. They can be classified based on their selectivity for the COX-1 or COX-2 isoforms. Aspirin is a nonselective, irreversible inhibitor of both COX-1 and COX-2. It has analgesic, antipyretic and anti-inflammatory effects. While generally well tolerated, aspirin can cause gastrointestinal irritation and bleeding and increase bleeding time by inhibiting platelet aggregation. Its use is not recommended in children due to the risk of Reye's Syndrome.
Nonsteroidal anti inflammatory drugs (NSAIDS)abdul waheed
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which prevents the formation of prostaglandins. Aspirin is a nonselective COX inhibitor that irreversibly acetylates both COX-1 and COX-2. It has analgesic, antipyretic and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation and bleeding. Aspirin is metabolized to salicylic acid and excreted by the kidneys. It is used to treat fever, pain, and inflammatory conditions like rheumatoid arthritis, but carries risks in children and those with asthma or prior gastrointestinal issues.
Nonsteroidal anti-inflammatory drug (nsaids)ManoharKumar81
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes that produce prostaglandins. Aspirin irreversibly inhibits both COX-1 and COX-2, while other NSAIDs generally reversibly inhibit the enzymes. This inhibition of prostaglandin production provides the drugs' analgesic, antipyretic, and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation and bleeding. NSAIDs may also interact with other drugs like diuretics, beta-blockers, and anticoagulants.
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which reduces the production of prostaglandins. They are classified based on their selectivity for the COX-1 and COX-2 isoenzymes. Aspirin irreversibly inhibits both COX-1 and COX-2, while some NSAIDs like ibuprofen and naproxen are nonselective. Newer NSAIDs like celecoxib selectively inhibit COX-2. NSAIDs have analgesic, antipyretic, and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation, but hypersensitivity reactions also occur.
NSAIDS -Unit III CHEMISTRY ,COLOGY,NOTESAffrin Shaik
This document discusses different classifications of NSAIDs including traditional nonselective COX inhibitors like aspirin and propionic acid derivatives like ibuprofen. It provides details on the pharmacological actions, pharmacokinetics, uses and adverse effects of aspirin and ibuprofen. Aspirin is a prototype traditional NSAID that is commonly used and irreversibly inhibits COX, while ibuprofen is a propionic acid derivative that is better tolerated than aspirin but still carries risks of gastric irritation and bleeding.
NSAIDs have analgesic, antipyretic and anti-inflammatory properties. They work by inhibiting cyclooxygenase (COX) enzymes and reducing prostaglandin production. NSAIDs are classified as nonselective COX inhibitors like aspirin, preferential COX-2 inhibitors like nimesulide, or selective COX-2 inhibitors like celecoxib. Common adverse effects include gastrointestinal irritation. NSAIDs are used to treat pain, fever, and inflammation conditions like arthritis.
This document provides information on non-narcotic analgesics (NSAIDs) that have analgesic, antipyretic, and anti-inflammatory properties. It discusses the inflammatory process and pain pathway, how NSAIDs work by inhibiting prostaglandin synthesis via inhibition of cyclooxygenase enzymes, and the classification of various NSAIDs including aspirin, ibuprofen, naproxen, indomethacin, and others. It covers the pharmacological actions, pharmacokinetics, uses, and adverse effects of different NSAID classes.
This document summarizes key information about aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses aspirin's mechanism of action as an irreversible inhibitor of cyclooxygenase, leading to reduced prostaglandin production and its analgesic, antipyretic and anti-inflammatory effects. It also outlines aspirin's effects on platelets and potential interactions, as well as its therapeutic uses including cardiovascular applications. The document details aspirin's absorption, distribution, metabolism and excretion, along with its adverse effects and drug interactions.
This document summarizes NSAIDs (non-steroidal anti-inflammatory drugs) including aspirin, ibuprofen, and acetaminophen. It discusses their mechanisms of action, pharmacokinetics, uses for analgesia, fever reduction and anti-inflammation, adverse effects like gastrointestinal irritation, and toxicity from overdose. Paracetamol is noted to have weak anti-inflammatory effects but comparable analgesic and antipyretic actions to low doses of aspirin through central prostaglandin inhibition. Toxicity from paracetamol overdose can cause liver damage by exceeding glutathione stores.
Nonsteroidal anti inflammatory drugs (NSAIDS)abdul waheed
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which prevents the formation of prostaglandins. Aspirin is a nonselective COX inhibitor that irreversibly acetylates both COX-1 and COX-2. It has analgesic, antipyretic and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation and bleeding. Aspirin is metabolized to salicylic acid and excreted by the kidneys. It is used to treat fever, pain, and inflammatory conditions like rheumatoid arthritis, but carries risks in children and those with asthma or prior gastrointestinal issues.
Nonsteroidal anti-inflammatory drug (nsaids)ManoharKumar81
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes that produce prostaglandins. Aspirin irreversibly inhibits both COX-1 and COX-2, while other NSAIDs generally reversibly inhibit the enzymes. This inhibition of prostaglandin production provides the drugs' analgesic, antipyretic, and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation and bleeding. NSAIDs may also interact with other drugs like diuretics, beta-blockers, and anticoagulants.
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which reduces the production of prostaglandins. They are classified based on their selectivity for the COX-1 and COX-2 isoenzymes. Aspirin irreversibly inhibits both COX-1 and COX-2, while some NSAIDs like ibuprofen and naproxen are nonselective. Newer NSAIDs like celecoxib selectively inhibit COX-2. NSAIDs have analgesic, antipyretic, and anti-inflammatory effects. Common adverse effects include gastrointestinal irritation, but hypersensitivity reactions also occur.
NSAIDS -Unit III CHEMISTRY ,COLOGY,NOTESAffrin Shaik
This document discusses different classifications of NSAIDs including traditional nonselective COX inhibitors like aspirin and propionic acid derivatives like ibuprofen. It provides details on the pharmacological actions, pharmacokinetics, uses and adverse effects of aspirin and ibuprofen. Aspirin is a prototype traditional NSAID that is commonly used and irreversibly inhibits COX, while ibuprofen is a propionic acid derivative that is better tolerated than aspirin but still carries risks of gastric irritation and bleeding.
NSAIDs have analgesic, antipyretic and anti-inflammatory properties. They work by inhibiting cyclooxygenase (COX) enzymes and reducing prostaglandin production. NSAIDs are classified as nonselective COX inhibitors like aspirin, preferential COX-2 inhibitors like nimesulide, or selective COX-2 inhibitors like celecoxib. Common adverse effects include gastrointestinal irritation. NSAIDs are used to treat pain, fever, and inflammation conditions like arthritis.
This document provides information on non-narcotic analgesics (NSAIDs) that have analgesic, antipyretic, and anti-inflammatory properties. It discusses the inflammatory process and pain pathway, how NSAIDs work by inhibiting prostaglandin synthesis via inhibition of cyclooxygenase enzymes, and the classification of various NSAIDs including aspirin, ibuprofen, naproxen, indomethacin, and others. It covers the pharmacological actions, pharmacokinetics, uses, and adverse effects of different NSAID classes.
This document summarizes key information about aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses aspirin's mechanism of action as an irreversible inhibitor of cyclooxygenase, leading to reduced prostaglandin production and its analgesic, antipyretic and anti-inflammatory effects. It also outlines aspirin's effects on platelets and potential interactions, as well as its therapeutic uses including cardiovascular applications. The document details aspirin's absorption, distribution, metabolism and excretion, along with its adverse effects and drug interactions.
This document summarizes NSAIDs (non-steroidal anti-inflammatory drugs) including aspirin, ibuprofen, and acetaminophen. It discusses their mechanisms of action, pharmacokinetics, uses for analgesia, fever reduction and anti-inflammation, adverse effects like gastrointestinal irritation, and toxicity from overdose. Paracetamol is noted to have weak anti-inflammatory effects but comparable analgesic and antipyretic actions to low doses of aspirin through central prostaglandin inhibition. Toxicity from paracetamol overdose can cause liver damage by exceeding glutathione stores.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) which provide analgesic, antipyretic, and anti-inflammatory effects. It classifies NSAIDs based on their selectivity for inhibiting cyclooxygenase-1 and cyclooxygenase-2 enzymes. Traditional NSAIDs nonselectively inhibit both enzymes, while newer selective COX-2 inhibitors like celecoxib only target COX-2. The document also covers the mechanisms of pain and how NSAIDs work to reduce inflammation by blocking prostaglandin synthesis. Specific details are provided about aspirin's pharmacological actions, adverse effects, and common uses.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, uses, and examples like aspirin and ibuprofen. NSAIDs are analgesics that reduce pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. They are classified as non-selective, preferential, or selective inhibitors of COX-1 and COX-2. Common side effects include stomach ulcers, kidney problems, and platelet dysfunction. Aspirin and ibuprofen are two widely used NSAIDs; they work by blocking prostaglandin production and have analgesic, antipyretic, and anti-inflammatory properties.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) and their mechanisms of action. It describes how NSAIDs work by inhibiting cyclooxygenase enzymes (COX-1 and COX-2) and thereby blocking the production of prostaglandins. NSAIDs are classified based on their selectivity for COX-1 vs COX-2. Aspirin is highlighted as a nonselective NSAID. Its mechanisms of analgesic, antipyretic and anti-inflammatory effects are explained. Adverse effects of aspirin including gastrointestinal irritation and bleeding are also summarized.
This document provides an overview of nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses their classification, mechanism of action involving inhibition of prostaglandin synthesis, beneficial effects, toxicities, and individual drug profiles. NSAIDs are a chemically diverse class of drugs that reduce pain, fever, and inflammation by blocking cyclooxygenase (COX) enzymes and subsequent prostaglandin production. While effective analgesics, NSAIDs can cause adverse effects like gastric irritation, bleeding risks, and interference with other drugs due to competition for protein binding sites.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs) and their role in periodontal disease treatment. It covers the definition of NSAIDs, their history of use, classification, mechanisms of action including inhibition of prostaglandin synthesis, and various types including salicylates, propionic acid derivatives, and selective COX-2 inhibitors. NSAIDs are proposed to have host modulatory properties for periodontal disease by suppressing inflammation and bone resorption mediated by prostaglandins. However, risks of adverse gastrointestinal effects must be weighed against potential benefits for periodontitis.
This whole slide is all about the NSAIDs in detail
it contents - 1. Inflammation 2. NSAIDs 3. Salicylate (Aspirin)
4. Propionic Acid Derivatives (Ibuprofen) 5. Anthranilic Acid Derivatives[Fenamate] (Mephenamic Acid)
Related questions about above topics
Non-steroidal anti-inflammatory drugs is a class of analgesic medication that reduces pain, fever and inflammation. Since most episodes of back pain involve inflammation, NSAIDs such as ibuprofen and naproxen are often an effective treatment option.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the prostaglandin synthase enzymes, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Traditional NSAIDs nonselectively inhibit both COX-1 and COX-2, whereas some newer NSAIDs preferentially or selectively inhibit COX-2. NSAIDs are used to reduce inflammation, fever, and pain in conditions like arthritis but can cause adverse gastrointestinal, renal, and cardiovascular effects. Aspirin irreversibly inhibits COX-1 and COX-2 and is used at low doses as an antiplatelet drug to reduce the risk of cardiovascular
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, examples of different drug classes, and pharmacological effects. It focuses on aspirin as the prototype NSAID, describing its absorption, metabolism, uses, adverse effects, and interactions. Selective COX-2 inhibitors like celecoxib and rofecoxib are also introduced as NSAIDs with reduced gastric irritation.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the COX enzymes responsible for prostaglandin biosynthesis. NSAIDs are classified as non-selective or selective COX-2 inhibitors. Non-selective NSAIDs like aspirin and ibuprofen inhibit both COX-1 and COX-2, which can cause side effects like gastrointestinal irritation. NSAIDs provide analgesic, antipyretic, and anti-inflammatory effects through inhibition of prostaglandin production. While effective for relieving pain and inflammation, long-term NSAID use increases risk of ulcers and gastrointestinal bleeding.
This document discusses pain management strategies and non-steroidal anti-inflammatory drugs (NSAIDs). It begins with an introduction on the importance of pain management and the three main categories of pain control medication: narcotics, aspirin and other NSAIDs, and acetaminophen. The document then provides a history of the development of NSAIDs from willow bark to modern drugs. It classifies NSAIDs and discusses their mechanisms of action, beneficial effects, toxicities, properties, and examples like aspirin and salicylates. The document covers the pharmacological actions, pharmacokinetics, adverse effects, precautions, interactions, and uses of aspirin and salicylates.
This document summarizes different classes of nonsteroidal anti-inflammatory drugs (NSAIDs), including their mechanisms of action, pharmacokinetics, uses, and adverse effects. It discusses aspirin and other NSAIDs such as ibuprofen, mephenamic acid, diclofenac, piroxicam, and ketorolac. All NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and decreasing prostaglandin production, providing analgesic, antipyretic and anti-inflammatory effects. However, they can also cause gastrointestinal, renal, hepatic, and bleeding side effects due to this mechanism of action.
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes COX-1 and COX-2, which decreases the production of prostaglandins and leads to their anti-inflammatory, analgesic, and antipyretic effects. Aspirin irreversibly inhibits COX-1 and COX-2, while other NSAIDs reversibly inhibit the enzymes. NSAIDs are used to treat pain, fever, and inflammation conditions but can cause gastrointestinal adverse effects by reducing protective prostaglandins in the stomach. Their antiplatelet effect from COX-1 inhibition also increases bleeding risk. Acetaminophen is an effective antipyretic that is preferred in pregnancy due to safety.
This document discusses antipyretic analgesic drugs including salicylates like aspirin and paracetamol, as well as nonsteroidal anti-inflammatory drugs. It provides details on the mechanism of action, pharmacological properties, therapeutic uses and side effects of various salicylates and NSAIDs. These include the absorption, distribution, metabolism and excretion of drugs like aspirin, mechanisms of analgesic and anti-inflammatory effects, dose-dependent effects of salicylates, and uses of NSAIDs to treat conditions like arthritis, gout and rheumatoid arthritis.
The document discusses different types of NSAIDs and acetaminophen, their mechanisms of action, and adverse effects. It describes how aspirin and nonselective NSAIDs like ibuprofen inhibit both COX-1 and COX-2 isoforms, decreasing prostaglandin synthesis throughout the body. More recent COX-2 selective inhibitors like celecoxib were developed to reduce gastrointestinal toxicity. Acetaminophen is only a weak inhibitor of COX-1 and COX-2 and may inhibit COX-3 in the CNS. While NSAIDs can cause gastrointestinal ulceration and renal damage, acetaminophen is generally safe at therapeutic doses but overdose can cause hepatotoxicity.
This document summarizes guidelines for prescribing various classes of analgesics, including non-opioids like acetaminophen and NSAIDs, opioid analgesics of varying efficacy, and drugs for neuropathic pain and migraines. It provides details on mechanisms of action, dosing, adverse effects, and contraindications for common prescription and over-the-counter pain relievers.
NON STEROIDAL ANTI INFLAMMTORY DRUGS ( NSAID'S)Suvarta Maru
NSAIDs are a heterogeneous group of drugs that have analgesic, antipyretic, and anti-inflammatory properties. They work by inhibiting the enzyme cyclooxygenase (COX) and the synthesis of prostaglandins. NSAIDs can be classified as non-selective COX inhibitors, preferential COX-2 inhibitors, or selective COX-2 inhibitors. Common NSAIDs like aspirin, ibuprofen, and naproxen are available over the counter, while others require a prescription. Celecoxib is a selective COX-2 inhibitor used to treat pain and inflammation.
The document discusses inflammation and the mechanisms by which nonsteroidal anti-inflammatory drugs (NSAIDs) work to reduce inflammation. It describes how NSAIDs inhibit the cyclooxygenase (COX) enzymes that produce prostaglandins, leading to their analgesic, antipyretic, and anti-inflammatory effects. However, it also notes that NSAID inhibition of prostaglandin production can cause gastric mucosal damage and bleeding risks as side effects. The document provides details on the classification and mechanisms of different types of NSAIDs including selective and non-selective COX inhibitors.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) which provide analgesic, antipyretic, and anti-inflammatory effects. It classifies NSAIDs based on their selectivity for inhibiting cyclooxygenase-1 and cyclooxygenase-2 enzymes. Traditional NSAIDs nonselectively inhibit both enzymes, while newer selective COX-2 inhibitors like celecoxib only target COX-2. The document also covers the mechanisms of pain and how NSAIDs work to reduce inflammation by blocking prostaglandin synthesis. Specific details are provided about aspirin's pharmacological actions, adverse effects, and common uses.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, uses, and examples like aspirin and ibuprofen. NSAIDs are analgesics that reduce pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. They are classified as non-selective, preferential, or selective inhibitors of COX-1 and COX-2. Common side effects include stomach ulcers, kidney problems, and platelet dysfunction. Aspirin and ibuprofen are two widely used NSAIDs; they work by blocking prostaglandin production and have analgesic, antipyretic, and anti-inflammatory properties.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) and their mechanisms of action. It describes how NSAIDs work by inhibiting cyclooxygenase enzymes (COX-1 and COX-2) and thereby blocking the production of prostaglandins. NSAIDs are classified based on their selectivity for COX-1 vs COX-2. Aspirin is highlighted as a nonselective NSAID. Its mechanisms of analgesic, antipyretic and anti-inflammatory effects are explained. Adverse effects of aspirin including gastrointestinal irritation and bleeding are also summarized.
This document provides an overview of nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses their classification, mechanism of action involving inhibition of prostaglandin synthesis, beneficial effects, toxicities, and individual drug profiles. NSAIDs are a chemically diverse class of drugs that reduce pain, fever, and inflammation by blocking cyclooxygenase (COX) enzymes and subsequent prostaglandin production. While effective analgesics, NSAIDs can cause adverse effects like gastric irritation, bleeding risks, and interference with other drugs due to competition for protein binding sites.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs) and their role in periodontal disease treatment. It covers the definition of NSAIDs, their history of use, classification, mechanisms of action including inhibition of prostaglandin synthesis, and various types including salicylates, propionic acid derivatives, and selective COX-2 inhibitors. NSAIDs are proposed to have host modulatory properties for periodontal disease by suppressing inflammation and bone resorption mediated by prostaglandins. However, risks of adverse gastrointestinal effects must be weighed against potential benefits for periodontitis.
This whole slide is all about the NSAIDs in detail
it contents - 1. Inflammation 2. NSAIDs 3. Salicylate (Aspirin)
4. Propionic Acid Derivatives (Ibuprofen) 5. Anthranilic Acid Derivatives[Fenamate] (Mephenamic Acid)
Related questions about above topics
Non-steroidal anti-inflammatory drugs is a class of analgesic medication that reduces pain, fever and inflammation. Since most episodes of back pain involve inflammation, NSAIDs such as ibuprofen and naproxen are often an effective treatment option.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the prostaglandin synthase enzymes, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Traditional NSAIDs nonselectively inhibit both COX-1 and COX-2, whereas some newer NSAIDs preferentially or selectively inhibit COX-2. NSAIDs are used to reduce inflammation, fever, and pain in conditions like arthritis but can cause adverse gastrointestinal, renal, and cardiovascular effects. Aspirin irreversibly inhibits COX-1 and COX-2 and is used at low doses as an antiplatelet drug to reduce the risk of cardiovascular
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, examples of different drug classes, and pharmacological effects. It focuses on aspirin as the prototype NSAID, describing its absorption, metabolism, uses, adverse effects, and interactions. Selective COX-2 inhibitors like celecoxib and rofecoxib are also introduced as NSAIDs with reduced gastric irritation.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the COX enzymes responsible for prostaglandin biosynthesis. NSAIDs are classified as non-selective or selective COX-2 inhibitors. Non-selective NSAIDs like aspirin and ibuprofen inhibit both COX-1 and COX-2, which can cause side effects like gastrointestinal irritation. NSAIDs provide analgesic, antipyretic, and anti-inflammatory effects through inhibition of prostaglandin production. While effective for relieving pain and inflammation, long-term NSAID use increases risk of ulcers and gastrointestinal bleeding.
This document discusses pain management strategies and non-steroidal anti-inflammatory drugs (NSAIDs). It begins with an introduction on the importance of pain management and the three main categories of pain control medication: narcotics, aspirin and other NSAIDs, and acetaminophen. The document then provides a history of the development of NSAIDs from willow bark to modern drugs. It classifies NSAIDs and discusses their mechanisms of action, beneficial effects, toxicities, properties, and examples like aspirin and salicylates. The document covers the pharmacological actions, pharmacokinetics, adverse effects, precautions, interactions, and uses of aspirin and salicylates.
This document summarizes different classes of nonsteroidal anti-inflammatory drugs (NSAIDs), including their mechanisms of action, pharmacokinetics, uses, and adverse effects. It discusses aspirin and other NSAIDs such as ibuprofen, mephenamic acid, diclofenac, piroxicam, and ketorolac. All NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and decreasing prostaglandin production, providing analgesic, antipyretic and anti-inflammatory effects. However, they can also cause gastrointestinal, renal, hepatic, and bleeding side effects due to this mechanism of action.
NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes COX-1 and COX-2, which decreases the production of prostaglandins and leads to their anti-inflammatory, analgesic, and antipyretic effects. Aspirin irreversibly inhibits COX-1 and COX-2, while other NSAIDs reversibly inhibit the enzymes. NSAIDs are used to treat pain, fever, and inflammation conditions but can cause gastrointestinal adverse effects by reducing protective prostaglandins in the stomach. Their antiplatelet effect from COX-1 inhibition also increases bleeding risk. Acetaminophen is an effective antipyretic that is preferred in pregnancy due to safety.
This document discusses antipyretic analgesic drugs including salicylates like aspirin and paracetamol, as well as nonsteroidal anti-inflammatory drugs. It provides details on the mechanism of action, pharmacological properties, therapeutic uses and side effects of various salicylates and NSAIDs. These include the absorption, distribution, metabolism and excretion of drugs like aspirin, mechanisms of analgesic and anti-inflammatory effects, dose-dependent effects of salicylates, and uses of NSAIDs to treat conditions like arthritis, gout and rheumatoid arthritis.
The document discusses different types of NSAIDs and acetaminophen, their mechanisms of action, and adverse effects. It describes how aspirin and nonselective NSAIDs like ibuprofen inhibit both COX-1 and COX-2 isoforms, decreasing prostaglandin synthesis throughout the body. More recent COX-2 selective inhibitors like celecoxib were developed to reduce gastrointestinal toxicity. Acetaminophen is only a weak inhibitor of COX-1 and COX-2 and may inhibit COX-3 in the CNS. While NSAIDs can cause gastrointestinal ulceration and renal damage, acetaminophen is generally safe at therapeutic doses but overdose can cause hepatotoxicity.
This document summarizes guidelines for prescribing various classes of analgesics, including non-opioids like acetaminophen and NSAIDs, opioid analgesics of varying efficacy, and drugs for neuropathic pain and migraines. It provides details on mechanisms of action, dosing, adverse effects, and contraindications for common prescription and over-the-counter pain relievers.
NON STEROIDAL ANTI INFLAMMTORY DRUGS ( NSAID'S)Suvarta Maru
NSAIDs are a heterogeneous group of drugs that have analgesic, antipyretic, and anti-inflammatory properties. They work by inhibiting the enzyme cyclooxygenase (COX) and the synthesis of prostaglandins. NSAIDs can be classified as non-selective COX inhibitors, preferential COX-2 inhibitors, or selective COX-2 inhibitors. Common NSAIDs like aspirin, ibuprofen, and naproxen are available over the counter, while others require a prescription. Celecoxib is a selective COX-2 inhibitor used to treat pain and inflammation.
The document discusses inflammation and the mechanisms by which nonsteroidal anti-inflammatory drugs (NSAIDs) work to reduce inflammation. It describes how NSAIDs inhibit the cyclooxygenase (COX) enzymes that produce prostaglandins, leading to their analgesic, antipyretic, and anti-inflammatory effects. However, it also notes that NSAID inhibition of prostaglandin production can cause gastric mucosal damage and bleeding risks as side effects. The document provides details on the classification and mechanisms of different types of NSAIDs including selective and non-selective COX inhibitors.
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4. B. Preferential COX-2 inhibitors
Nimesulide, Meloxicam, Nabumeton.
C. Selective COX-2 inhibitors
Celecoxib, Etoricoxib, Parecoxib.
D. Analgesic-antipyratics with poor antiinflammatory action
1. para aminophenol derivatives: Paracetamol
2. Pyrazolone derivative: Metamizol, Propiphenazone.
3. Benzoxazocine derivative: Nefopam
4
5. hanism of action o IDs
1. Antiinflammatory effect
due to the inhibition of the enzymes that produce
prostaglandin H synthase (cyclooxygenase, or COX),
which converts arachidonic acid to prostaglandins,
and to TXA2 and prostacyclin.
5
6. Aspirin irreversibly inactivates COX-1 and COX-2 by
acetylation of a specific serine residue.
This distinguishes it from other NSAIDs, which reversibly
inhibit COX-1 and COX-2.
6
7. 2. Analgesic effect
A. The analgesic effect of NSAIDs is thought to be
related to:
the peripheral inhibition of prostaglandin
production
may also be due to the inhibition of pain stimuli at
a subcortical site.
B. NSAIDs prevent the potentiating action of
prostaglandins on endogenous mediators of peripheral
nerve stimulation (e.g., bradykinin).
7
8. 3. Antipyretic effect
The antipyretic effect of NSAIDs is believed to be
related to:
inhibition of production of prostaglandins induced by
interleukin-1 (IL-1) and interleukin-6 (IL-6) in the
hypothalamus
the “resetting” of the thermoregulatory system,
leading to vasodilatation and increased heat loss.
8
9. d r tagl ( G)
synthesis inhibition
NSAIDs blocked PG generation.
Prostaglandins, prostacyclin (PGI2), and thromboxane
A2(TXA2) are produced from arachidonic acid by the enzyme
cyclooxygenase.
Cyclooxygenase (COX) exists in COX-1 and COX-2 isoforms.
COX -3 has recently been identified
9
10. Cyclooxygenase (COX) is found bound to the endoplasmatic
reticulum. It exists in 3 isoforms:
• COX-1 (constitutive) acts in physiological conditions.
• COX-2 (inducible) is induced in inflammatory cells by
pathological stimulus.
• COX-3 (in brain).
10
12. GC S
1. Analgesic, antipyretic, antiinflammatory actions:
Aspirin is a weaker analgesic than morphine type drugs.
Aspirin 600 mg < Codeine 60 mg < 6 mg Morphine
it effectively relieves inflammation, tissue injury, connective tissue and
integumental pain, but is relatively ineffective in severe visceral and
ischaemic pain.
The analgesic action is mainly due to obtunding of peripheral pain receptors
and prevention of PG-mediated sensitization of nerve endings.
No sedation, subjective effects, tolerance or physical dependence is
produced.
Aspirin resets the hypothalamic thermostat and rapidly reduces fever by
promoting heat loss, but does not decrease heat production.
Antiinflammatory action is exerted at high doses (3-6 g/ day or 100 mg/kg/
day)
12
13. 2. Metabolic effects:
significant only at antiinflammatory doses
Cellular metabolism is increased, especially in skeletal
muscles, due to uncoupling of oxidative phosphorylation
increased heat production.
There is increased utilization of glucose blood sugar may
decrease (especially in diabetics) and liver glycogen is
depleted.
Chronic use of large doses cause negative N2 balance by
increased conversion of protein to carbohydrate. Plasma free
fatty acid and cholesterol levels are reduced.
13
14. 3. Respiration:
Effects are dose dependent.
At antiinflammatory doses, respiration is stimulated by
peripheral (increased C02 production) and central (increased
sensitivity of respiratory centre to C02) actions.
Hyperventilation is prominent in salicylate poisoning. Further
rise in salicylate level causes respiratory depression; death is
due to respiratory failure.
14
15. 4. Acid-base and electrolyte balance:
Antiinflammatory doses produce significant changes in the
acid-base and electrolyte composition of body fluids.
Initially, respiratory stimulation predominates and tends to
wash out C02 despite increased production ….respiratory
alkalosis, which is compensated by increased renal
excretion of HCO3; (with accompanying Na+, K+ and
water).
Still higher doses cause respiratory depression with C02
retention, while excess C02 production continues….
respiratory acidosis .
15
16. 5. CVS:
Aspirin has no direct effect in therapeutic doses.
Larger doses increase cardiac output to meet increased
peripheral O2 demand and causes direct vasodilatation.
Toxic doses depress , vasomotor centre: BP may fall. Because
of increased cardiac work as well as Na+ and water retention,
CHF may be precipitated in patients with low cardiac reserve.
16
17. 6. GIT:
Aspirin and released salicylic acid irritate gastric mucosa,
cause epigastric distress, nausea and vomiting.
It also stimulates CTZ.
7. Urate excretion:
Aspirin in high dose reduces renal tubular excretion of
urate
17
18. 8. Blood:
Aspirin, even in small doses, irreversibly inhibits TXA2
synthesis by platelets. Thus, it interferes with platelet
aggregation and bleeding time is prolonged to nearly twice the
normal value.
long-term intake of large dose decreases synthesis of clotting
factors in liver and predisposes to bleeding; can be prevented
by prophylactic vit K therapy.
18
19. Pharmacokinetics
Aspirin is absorbed from the stomach and small intestines.
Its poor water solubility is the limiting factor in absorption:
microfining the drug particles and inclusion of an alkali
(solubility is more at higher pH) enhances absorption.
Aspirin is rapidly deacetylated in the gut wall, liver, plasma
and other tissues to release salicylic acid which is the major
circulating and active form.
It slowly enters brain but freely crosses placenta.
The metabolites are excreted by glomerular filtration as well as
tubular secretion.
19
20. s of Aspirin
As analgesic (300 to 600 mg during 6 to 8 h) for headache,
backache, pulled muscle, toothache, neuralgias.
As antipyretic in fever of any origin in the same doses as for
analglesia. However, paracetamol and metamizole are safer,
and generally preferred.
Acute rheumatic fever. Aspirin is the first drug of choice. Other
drugs substitute Aspirin only when it fails or in severe cases.
Antirheumatic doses are 75 to 100 mg/kg/24 h (resp. 4-6 g
daily) in the first weeks.
Rheumatoid arthritis. Aspirin a dose of 3 to 5 g/24 h after meal
is effective in most cases. Since large doses of Aspirin are
poorly tolerated for a long time, the new NSAIDs (diclofenac,
ibuprofen, etc.) in depot form are preferred.
20
21. Aspirin therapy in children with rheumatoid arthritis has been
found to raise serum concentration transaminases, indicating
liver damage. Most cases are asymptomatic but it is potentially
dangerous.
An association between salicylate therapy and “Reye’s
syndrome”, a rare form of hepatic encephalopathy seen in
children, having viral infection (varicella, influenza), has been
noted.
Aspirin should not be given to children under 15years unless
specifically indicated, e.g. for juvenile arthritis (paracetamol is
preferred).
Postmyocardial infarction and poststroke patients: By
inhibiting platelet aggregation in low doses (100 mg daily)
Aspirin decreases the incidence of reinfarction.
21
22. Adverse effects
1. Gastrointestinal effects
most common adverse effects of high-dose aspirin use
(70% of patients):
nausea
vomiting
diarrhea or constipation
dyspepsia (impaired digestion)
epigastric pain
bleeding, and ulceration (primarily gastric).
23
23. These gastrointestinal effects are thought to be due to:
1. direct chemical effect on gastric cells or
2. decrease in the production and cytoprotective activity of
prostaglandins, which leads to gastric tissue susceptibility to
damage by hydrochloric acid.
24
24. The gastrointestinal effects may contraindicate aspirin use
in patients with an active ulcer.
Aspirin may be taken with prostaglandins to reduce gastric
damage.
Decrease gastric irritation by:
Substitution of enteric-coated or timed-release preparations, or
the use of nonacetylated salicylates, may decrease gastric
irritation.
25
25. 2. Hypersensitivity (intolerance)
Hypersensitivity is relatively uncommon with the use of aspirin
(0.3% of patients); hypersensitivity results in:
rash
bronchospasm
rhinitis
Edema, or
an anaphylactic reaction with shock, which may be life
threatening.
The incidence of intolerance is highest in patients with asthma,
nasal polyps, recurrent rhinitis, or urticaria.
Aspirin should be avoided in such patients.
26
26. Cross-hypersensitivity may exist:
to other NSAIDs
to the yellow dye tartrazine, which is used in many
pharmaceutical preparations.
Hypersensitivity is not associated with:
sodium salicylate or
magnesium salicylate.
27
27. The use of aspirin and other salicylates to control fever during
viral infections (influenza and chickenpox) in children and
adolescents is associated with an increased incidence of Reye's
syndrome, an illness characterized by vomiting, hepatic
disturbances, and encephalopathy that has a 35% mortality rate.
Acetaminophen is recommended as a substitute for children
with fever of unknown etiology.
28
28. M l n o ad n
contraindications
May decrease the glomerular filtration rate, particularly in
patients with renal insufficiency.
Occasionally produce mild hepatitis
Prolong bleeding time.
Aspirin irreversibly inhibits platelet COX-1 and COX-2 and,
thereby, TXA2 production, suppressing platelet adhesion and
aggregation.
The use of salicylates is contraindicated in patients with
bleeding disorders
Salicylates are not recommended during pregnancy; they may
induce:
postpartum hemorrhage
premature closure of the fetal ductus arteriosus. 29
29. r interactions
Drugs Result
Diuretics Decrease diuresis
Beta-blockers Decrease antihypertensive effect
ACE inhibitors Decrease antihypertensive effect
Anticoagulants Increase of GI bleeding
Sulfonylurea Increase hypoglycemic risk
Cyclosporine Increase nephrotoxicity
GCS Increase of GI bleeding
Alcohol Increase of GI bleeding
30
30. PROPIONIC ACID DERIVATIVES
Ibuprofen was the first member
The analgesic, antipyretic and antiinflammatory efficacy is
rated somewhat lower than high dose of aspirin.
All inhibit PG synthesis, naproxen being the most potent; but
their in vitro potency tor this action does not closely parallel in
vitro antiinflammatory potency.
Inhibition of platelet aggregation is short-lasting with
ibuprofen, but longer lasting with naproxen.
31
31. Ibuprofen:
In doses of 2.4 g daily it is equivalent to 4 g of Aspirin in anti-
inflammatory effect.
Oral ibuprofen is often prescribed in lower doses (< 2.4 g/d), at
which it has analgesic but not antiinflammatory efficacy. It is
available in low dose forms under several trade names (e. g.
Nurofen® - film-tabl. 400 mg).
A topical cream preparation is absorbed into fascia and muscle.
A liquid gel preparation of ibuprofen provides prompt relief in
postsurgical dental pain.
In comparison with indometacin, ibuprofen decreases urine
output less and also causes less fluid retention.
It is effective in closing ductus arteriosus in preterm infants,
with much the same efficacy as indometacin.
32
32. Flurbiprofen:
Its (S)(-) enantiomer inhibits COX nonselectively, but it has
been shown in rat tissue to also affect TNF-α and NO
synthesis.
Hepatic metabolism is extensive. It does demonstrate
enterohepatic circulation.
The efficacy of flurbiprofen at dosages of 200-400 mg/d is
comparable to that of Aspirin and other NSAIDs for patients
with rheumatoid arthritis, gout, and osteoarthritis.
Flurbiprofen i.v. is effective for perioperative analgesia in
minor ear, neck, and nose surgery and in lozenge form for sore
throat.
33
33. Adverse effect
Ibuprofen and all its congeners are better tolerated than aspirin.
Side effects are milder and their incidence is lower.
Gastric discomfort, nausea and vomiting, though less than
aspirin or indomethacin, are still the most common side effects.
Gastric erosion and occult blood loss are rare.
CNS side effects include headache, dizziness, blurring of
vision, tinnitus and depression.
Rashes, itching and other hypersensitivity phenomena are
infrequent.
They are not to be prescribed to pregnant woman and should be
avoided in peptic ulcer patient.
34
34. Pharmacokinetic and interactions
Well absorbed orally.
Highly bounded to the plasma protein (90-99%).
Because they inhibit platelet function, use with anticoagulants
should, nevertheless, be avoided.
Similar to other NSAIDs, they are likely to decrease diuretic
and antihypertensive action of thiazides, furosemide and β
blockers.
All propionic acid derivatives enter brain, synovial fluid and
cross placenta. They are largely metabolized in liver by
hydroxylation and glucuronide conjugation and excreted in
urine as well as bile.
35
35. Uses
Ibuprofen is used as a simple analgesic, and antipyretic in the
same way as low dose of aspirin. It is particularly effective in
dysmenorrhoea. In which the action is clearly due to PG
synthesis inhibition.
It is available as an over-the-court drug.
Ibuprofen and its congeners are widely used in rheumatoid
arthritis, osteoarthritis and other musculoskeletal disorders.
They are indicated in soft tissue injuries, vasectomy, tooth
extraction, postpartum and postoperatively: suppress swelling
and inflammation.
36
36. Anthranilic acid derivative
Mephenamic acid:
An analgesic, antipyretic and weaker antiinflammatory drug,
which inhibits COX as well as antagonises certain actions of
PGs.
Mephenamic acid exerts peripheral as well central analgesic
action.
37
37. Adverse effects:
Diarrhoea is the most important dose-related side effect. Epigastric distress
is complained, but gut bleeding is not significant.
Skin rashes, dizziness and other CNS manifestations have occurred.
Haemolytic anaemia is a rare but serious complication.
Pharmacokinetics:
Oral absorption is slow but almost complete. It is highly bound to plasma
proteins-displacement interactions can occur; partly metabolized and
excreted in urine as well as bile. Plasma t1/2 is 2-4 hours.
Uses:
Mephenamic acid is indicated primarily as analgesic in muscle, joint and
soft tissue pain where strong antiinflammatory action is not needed. It is
quite effective in dysmenorrhoea. It may be useful in some cases of
rheumatoid and osteoarthritis but has no distinct advantage.
38
38. ryl-acetic acid derivatives
Diclofenac:
An analgesic-antipyretic antiinflammatory drug, similar in efficacy to
naproxen. It inhibits PG synthesis and is somewhatCOX-2 selective. The
antiplatelet action is short lasting. Neutrophil chemotaxis and superoxide
production at the inflammatory site are reduced.
Adverse effects of diclofenac are generally mild epigastric pain, nausea,
headache, dizziness, rashes. Gastric ulceration and bleeding are less
common. Reversible elevation of serum aminotransferases has been
reported more commonly; kidney damage is rare.
A preparation combining diclofenac and misoprostol (PGE1) decreases
upper GI ulceration but may result in diarrhoea.
Diclofenac is among the most extensively used NSAID; employed in
rheumatoid and osteoarthritis, bursitis, ankylosing spondylitis, toothache,
dysmenorrhoea, post-traumatic and postoperative inflammatory conditions-
affords quick relief of pain and wound edema.
39
39. Aceclofenac:
A somewhat COX-2 selective congener of diclofenac having
similar properties. Enhancement of glycosaminoglycan
synthesis may confer chondroprotective property.
40
40. Oxicam derivatives
Piroxicam:
It is a long-acting potent NSAID with antiinflammatory
potency similar to indomethacin and good analgesic-
antipyretic action.
It is a reversible inhibitor of COX; lowers PG concentration in
synovial fluid and inhibits platelet aggregation-prolonging
bleeding time.
In addition, it decreases the production of IgM rheumatoid
factor and leucocyte chemotaxis.
41
41. Pharmacokinetics:
It is rapidly and completely absorbed
99% plasma protein bound;
Largely metabolized in liver by hydroxylation and glucuronide
conjugation;
Excreted in urine and bile;
Plasma t1/2 is long nearly 2 days.
Adverse effects:
The g.i. side effects are more than ibuprofen, but it is better
tolerated and less ulcerogenic than indomethacin or
phenylbutazone; causes less faecal blood loss than aspirin.
Rashes and pruritus are seen in < 1% patients. Edema and
reversible azotaemia have been observed.
Tenoxicam:
A congener of piroxicam with similar properties and uses. 42
42. Pyrrolo-pyrrole derivative
Ketorolac:
A novel NSAID with potent analgesic and modest antiinflammatory
activity.
In postoperative pain it has equalled the efficacy of morphine, but
does not interact with opioid receptors and is free of opioid side
effects.
it inhibits PG synthesis and relieves pain by a peripheral mechanism.
rapidly absorbed after oral and i.m. administration.
It is highly plasma protein bound and 60% excreted unchanged in
urine.
Major metabolic pathway is glucuronidation.
plasma t1/2 is 5-7 hours.
43
43. Adverse effects:
Nausea, abdominal pain, dyspepsia, ulceration, loose stools,
drowsiness, headache, dizziness, nervousness, pruritus, pain at
injection site, rise in serum transaminase and fluid retention
have been noted.
Use:
Ketorolac is frequently used in postoperative, dental and acute
musculoskeletal pain: 15-30 mg i.m. or i.v. every 4-6 hours
(max. 90 mg/day).
It may also be used for renal colic, migraine and pain due to
bony metastasis.
Continuous use for more then 5 days is not recommended.
44
44. Adverse effects:
Nausea, abdominal pain, dyspepsia, ulceration, loose stools,
drowsiness, headache, dizziness, nervousness, pruritus, pain at
injection site, rise in serum transaminase and fluid retention
have been noted.
Use:
Ketorolac is frequently used in postoperative, dental and acute
musculoskeletal pain: 15-30 mg i.m. or i.v. every 4-6 hours
(max. 90 mg/day).
It may also be used for renal colic, migraine and pain due to
bony metastasis.
Continuous use for more then 5 days is not recommended.
44
45. Indole derivative
Indomethacin:
It is a potent antiinflammatory drug with prompt antipyretic action.
Indomethacin relieves only inflammatory or tissue injury related
pain.
It is a highly potent inhibitor of PG synthesis and suppresses
neutrophil motility.
In toxic doses it uncouples oxidative phosphorylation (like aspirin).
Pharmacokinetics:
Indomethacin is well absorbed orally
It is 90% bound to plasma proteins, partly metabolized in liver to
inactive products and excreted by kidney.
Plasma t1/2 is 2-5 hours.
45
46. Adverse effect:
A high incidence (up to 50%) of GI and CNS side effects is
produced: GI bleeding, diarrhoea, frontal headache, mental
confusion, etc.
It is contraindicated in machinery operators,
drivers, psychiatric patients, epileptics, kidney
disease, pregnant women and in children.
46
47. FERENTIAL COX-2 INHIBITORS
Nimesulide:
weak inhibitor of PG synthesis and COX-2 selectivity.
Antiinflammatory action may be exerted by other mechanisms
as well, e.g. reduced generation of superoxide by neutrophils,
inhibition of PAF synthesis and TNFa release, free radical
scavanging, inhibition of metalloproteinase activity in
cartilage.
The analgesic, antipyretic and antiinflammatory activity of
nimesulide has been rated comparable to other NSAIDs.
It has been used primarily for short-lasting painful
inflammatory conditions like sports injuries, sinusitis and other
ear-nose-throat disorders, dental surgery, bursitis, low
backache, dysmenorrhoea, postoperative pain, osteoarthritis
and for fever. 47
48. Nimesulide is almost completely absorbed orally, 99% plasma
protein bound, extensively metabolized and excreted mainly in
urine with a t1/2 of 2-5 hours.
Adverse effects of nimesulide are gastrointestinal
(epigastralgia, heart burn, nausea, loose motions),
dermatological (rash, pruritus) and central (somnolence,
dizziness).
48
49. SELECTIVE COX-2 INHIBITORS
They cause little gastric mucosal damage; occurrence of peptic
ulcer and ulcer bleeds is clearly lower than with traditional
NSAIDs. They do not depress TXA2 Production by platelets
(COX-I dependent); do not inhibit platelet aggregation or
prolong bleeding time but reduce PGI2 production by vascular
endothelium.
It has been concluded that selective COX-2 inhibitors should
be used only in patients at high risk of peptic ulcer, perforation
or bleeds. If selected, they should be administered in the lowest
dose for the shortest period of time. Moreover, they should be
avoided in patients with history of ischaemic heart disease/
hypertension/ cardiac failure/ cerebrovascular disease, who are
predisposed to CV events.
49
50. Celecoxib:
It exerts antiinflammatory, analgesic and antipyretic actions
with low ulcerogenic potential. Comparative trials in
rheumatoid arthritis have found it to be as effective as
naproxen or diclofenac, without affecting COX- 1 activity in
gastroduodenal mucosa . Platelet aggregation in response to
collagen exposure remained intact in celecoxib recipients and
serum TXB2 levels were not reduced. Though tolerability of
celecoxib is better than traditional NSAIDs, still abdominal
pain, dyspepsia and mild diarrhoea are the common side
effects. Rashes, edema and a small rise in BP have also been
noted.
Celecoxib is slowly absorbed, 97% plasma protein bound and
metabolized primarily by CYP2C9 with a t1/2 of 10 hours. It is
approved for use in osteo- and rheumatoid arthritis in a dose of
100-200 mg BD. 50
51. Etoricoxib:
This newer COX-2 inhibitor has the highest COX-2 selectivity.
It is suitable for once-a-day treatment of osteo /rheumatoid /
acute gouty arthritis, dysmenorrhoea, acute dental surgery pain
and similar conditions, without affecting platelet function or
damaging gastric mucosa. The t1/2 is 24 hours. Side effects are
dry mouth, aphthous ulcers, taste disturbance and paresthesias.
Parecoxib:
It is a prodrug of valdecoxib suitable for injection, and to be
used in postoperative or similar short-term pain, with efficacy
similar to ketorolac.
51