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.
Anti inflammatory drugs
Non steroidal anti inflammatory drugs
steroids
mechanism of action of anti inflammatory drugs
adverse effects of drugs
contraindications of anti inflammatory agents
uses of anti inflammatory drugs
dose rates of anti inflammatory agents
list of anti inflammatory drugs
NSAIDs are non-steroidal anti-inflammatory drugs that address fever, pain, and swelling by inhibiting the enzyme COX and thereby reducing the production of prostaglandins. There are two types - nonselective COX inhibitors like aspirin that inhibit both COX-1 and COX-2, and selective COX-2 inhibitors like celecoxib. Common NSAIDs include aspirin, ibuprofen, indomethacin, and piroxicam. While effective for pain, fever, and inflammation, NSAIDs can cause adverse effects like GI bleeding, ulcers, renal toxicity, and interference with platelet function. Precautions are needed in patients with liver or kidney disease.
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.
The document summarizes non-steroidal anti-inflammatory drugs (NSAIDs). It discusses their mechanism of action by inhibiting cyclooxygenase enzymes and reducing prostaglandin formation, leading to analgesic, anti-inflammatory, and antipyretic effects. NSAIDs are classified based on selectivity for COX-1 and COX-2. Common NSAIDs and their uses for pain relief are described. Adverse effects include gastric irritation and bleeding. Dental considerations advise avoiding NSAIDs if allergic and not using aspirin before and after surgery due to bleeding risk.
NSAIDs are a large group of drugs that have analgesic, anti-inflammatory, and antipyretic properties. They work by inhibiting the arachidonic acid pathway and prostaglandins, which reduces pain, fever, and inflammation. Common side effects include gastrointestinal issues like ulcers, as well as renal and cardiovascular problems. Nurses monitor patients taking NSAIDs for therapeutic effects and side effects.
This document discusses NSAIDs and antipyretic drugs. It defines NSAIDs as drugs used for pain relief, especially in inflammatory conditions. Antipyretic drugs are those that reduce fever by lowering body temperature. The document discusses the pharmacokinetics, mechanisms of action, examples of drugs, adverse effects, and management of toxicity for these drug classes. It provides dosing instructions for various NSAIDs and antipyretic drugs including aspirin, paracetamol, and paracetamol suppositories.
The document discusses various antipyretic drugs, including their mechanisms of action, pharmacological effects, clinical uses, and side effects. It provides details on common antipyretic drugs like paracetamol, aspirin, meloxicam, and piroxicam. The drugs are used to reduce fever and inflammation, and help relieve pain, with their effects stemming from inhibition of prostaglandin synthesis.
Drugs used in musculoskeletal disorders iPravin Prasad
This document discusses drugs used to treat musculoskeletal disorders, focusing on non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin and paracetamol. It classifies NSAIDs, explains their mechanisms of action in inhibiting cyclooxygenase enzymes and decreasing prostaglandin formation, and details their indications, adverse effects, contraindications, and overdose management for aspirin and paracetamol. The document ends with sample test questions on appropriate aspirin dosing, risks of giving aspirin to a child with chickenpox, and treatment for paracetamol overdose.
Anti inflammatory drugs
Non steroidal anti inflammatory drugs
steroids
mechanism of action of anti inflammatory drugs
adverse effects of drugs
contraindications of anti inflammatory agents
uses of anti inflammatory drugs
dose rates of anti inflammatory agents
list of anti inflammatory drugs
NSAIDs are non-steroidal anti-inflammatory drugs that address fever, pain, and swelling by inhibiting the enzyme COX and thereby reducing the production of prostaglandins. There are two types - nonselective COX inhibitors like aspirin that inhibit both COX-1 and COX-2, and selective COX-2 inhibitors like celecoxib. Common NSAIDs include aspirin, ibuprofen, indomethacin, and piroxicam. While effective for pain, fever, and inflammation, NSAIDs can cause adverse effects like GI bleeding, ulcers, renal toxicity, and interference with platelet function. Precautions are needed in patients with liver or kidney disease.
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.
The document summarizes non-steroidal anti-inflammatory drugs (NSAIDs). It discusses their mechanism of action by inhibiting cyclooxygenase enzymes and reducing prostaglandin formation, leading to analgesic, anti-inflammatory, and antipyretic effects. NSAIDs are classified based on selectivity for COX-1 and COX-2. Common NSAIDs and their uses for pain relief are described. Adverse effects include gastric irritation and bleeding. Dental considerations advise avoiding NSAIDs if allergic and not using aspirin before and after surgery due to bleeding risk.
NSAIDs are a large group of drugs that have analgesic, anti-inflammatory, and antipyretic properties. They work by inhibiting the arachidonic acid pathway and prostaglandins, which reduces pain, fever, and inflammation. Common side effects include gastrointestinal issues like ulcers, as well as renal and cardiovascular problems. Nurses monitor patients taking NSAIDs for therapeutic effects and side effects.
This document discusses NSAIDs and antipyretic drugs. It defines NSAIDs as drugs used for pain relief, especially in inflammatory conditions. Antipyretic drugs are those that reduce fever by lowering body temperature. The document discusses the pharmacokinetics, mechanisms of action, examples of drugs, adverse effects, and management of toxicity for these drug classes. It provides dosing instructions for various NSAIDs and antipyretic drugs including aspirin, paracetamol, and paracetamol suppositories.
The document discusses various antipyretic drugs, including their mechanisms of action, pharmacological effects, clinical uses, and side effects. It provides details on common antipyretic drugs like paracetamol, aspirin, meloxicam, and piroxicam. The drugs are used to reduce fever and inflammation, and help relieve pain, with their effects stemming from inhibition of prostaglandin synthesis.
Drugs used in musculoskeletal disorders iPravin Prasad
This document discusses drugs used to treat musculoskeletal disorders, focusing on non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin and paracetamol. It classifies NSAIDs, explains their mechanisms of action in inhibiting cyclooxygenase enzymes and decreasing prostaglandin formation, and details their indications, adverse effects, contraindications, and overdose management for aspirin and paracetamol. The document ends with sample test questions on appropriate aspirin dosing, risks of giving aspirin to a child with chickenpox, and treatment for paracetamol overdose.
Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits the cyclooxygenase enzymes COX1 and COX2, preventing the formation of prostaglandins and leading to analgesic, antipyretic, and anti-inflammatory effects. It is rapidly absorbed orally and highly protein bound, undergoing extensive hepatic metabolism primarily by CYP2C9 and excreted in urine as metabolites. While generally safe, it can cause gastrointestinal adverse effects and interacts with other drugs like aspirin and warfarin by inhibiting platelet aggregation.
Inflammation is the body's response to tissue injury and involves the release of chemical mediators that cause vascular responses and recruit fluids and cells to the injured site. Anti-inflammatory drugs work by inhibiting the biosynthesis of prostaglandins, chemical mediators involved in inflammation. There are several classes of nonsteroidal anti-inflammatory drugs (NSAIDs) that do this, including aspirin, indomethacin, ibuprofen, and celecoxib. Corticosteroids are also commonly used as potent anti-inflammatory agents for systemic inflammatory disorders.
This document provides information on paracetamol and various nonsteroidal anti-inflammatory drugs (NSAIDs). It describes paracetamol's mechanism of action, pharmacokinetics, uses, advantages over aspirin, and toxicity in overdose. It then discusses several classes of NSAIDs including propionic acid derivatives like ibuprofen and naproxen, fenamate derivatives like mefenamic acid, acetic acid derivatives like indomethacin, selective COX-2 inhibitors like celecoxib and meloxicam, and their mechanisms, pharmacokinetics, uses, and adverse effects. Clinical indications and formulations of specific NSAIDs are also mentioned.
1. NSAIDs work by inhibiting prostaglandin synthesis via blocking cyclooxygenase (COX) enzymes. They are classified based on selectivity for COX-1 vs COX-2.
2. Aspirin is a non-selective, irreversible COX inhibitor. It provides analgesic, antipyretic and anti-inflammatory effects. Common adverse effects include gastric irritation and bleeding risks.
3. Paracetamol is considered a COX-3 inhibitor. It has analgesic properties but does not cause gastric irritation or bleeding like other NSAIDs. Acute overdose can cause liver damage.
This document provides an overview of nonsteroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, examples of drug classes, and key properties. NSAIDs are widely used analgesic, antipyretic and anti-inflammatory drugs. They work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. The document describes both non-selective COX inhibitors like aspirin, ibuprofen, and naproxen, as well as selective COX-2 inhibitors. Common adverse effects and clinical uses are summarized for different NSAID classes.
The document summarizes non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin, ibuprofen, naproxen, celecoxib, and acetaminophen. It discusses their mechanisms of action, therapeutic uses, and adverse effects. It also covers the treatment of gout with NSAIDs, colchicine, allopurinol, and uricosuric agents like probenecid and sulfinpyrazone.
This document summarizes information about nonsteroidal anti-inflammatory drugs (NSAIDs), including their mechanism of action, types, effects, uses, and side effects. NSAIDs work by inhibiting cyclooxygenase enzymes, reducing prostaglandin production and thus pain, fever, and inflammation. Common NSAIDs include aspirin, ibuprofen, and naproxen. While effective for conditions like arthritis, NSAIDs can cause gastrointestinal, renal, and cardiovascular side effects.
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 discusses the use of steroidal and non-steroidal anti-inflammatory drugs in oral and maxillofacial surgery patients. It begins by defining inflammation and outlining the fundamental events and major mediators of the inflammatory process. It then describes how non-steroidal anti-inflammatory drugs (NSAIDs) work by interfering with the cyclooxygenase pathway. The document goes on to classify and discuss individual NSAIDs, including aspirin, ibuprofen, celecoxib, and valdecoxib. It covers their mechanisms of action, clinical uses, dosages, and adverse effects. Selective cyclooxygenase-2 inhibitors like celecoxib and rofecoxib are emphasized as
The document discusses various aspects of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs). It defines NSAIDs and describes their analgesic, antipyretic and anti-inflammatory effects. It classifies different types of NSAIDs based on their selectivity for COX-1 and COX-2 enzymes. It also discusses the mechanisms of action, pharmacological properties, uses, doses and adverse effects of several common NSAIDs like aspirin, ibuprofen, ketorolac, diclofenac, celecoxib, paracetamol and nabumetone.
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.
This document discusses the mechanisms and uses of non-steroidal anti-inflammatory drugs (NSAIDs). It begins by explaining that NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production, providing analgesic, antipyretic, and anti-inflammatory effects. The document then classifies and provides examples of different types of NSAIDs, and discusses their pharmacological actions, mechanisms of action, indications, adverse effects, and drug interactions. Key NSAIDs discussed in more depth include aspirin, acetaminophen, ibuprofen, indomethacin, and diclofenac.
This document discusses Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). It defines NSAIDs as a class of non-narcotic analgesic drugs that are not steroids and do not have steroid side effects. NSAIDs have anti-inflammatory, analgesic, and antipyretic properties by inhibiting prostaglandin production. Common NSAID drugs mentioned include diclofenac, ibuprofen, indomethacin, ketoprofen, mefenamic acid, naproxen, and piroxicam. NSAIDs are indicated for relief of symptoms of arthritis, musculoskeletal disorders, and mild to moderate pain. Potential side effects include gastrointestinal, renal, hepatic, cardiovascular and hematologic effects
Antirheumatic drugs & anti gout drugs PHARMACOLOGY REVISION NOTES TONY SCARIA
This document summarizes various drugs used to treat rheumatoid arthritis and gout. It describes disease-modifying antirheumatic drugs (DMARDs) like methotrexate, hydroxychloroquine, leflunomide, d-penicillamine, gold salts, and biological response modifiers that target TNF-α, IL-1, IL-6, and T cells. It also discusses corticosteroids, NSAIDs, and drugs for acute and chronic gout including colchicine, allopurinol, febuxostat, probenecid, and drugs that increase uric acid metabolism like rasburicase and pegloticase.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers their classification, mechanisms of action, uses, and adverse effects. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin production. They are effective for pain, fever, and inflammation but can cause gastrointestinal, renal, hepatic, and bleeding side effects. The document focuses on specific NSAIDs including aspirin, ibuprofen, indomethacin, and mephenamic acid, outlining their pharmacology, dosing, and indications.
This document provides an overview of anti-diabetic drugs presented by Sadia Unnisa. It begins with an introduction to diabetes mellitus and classifications of anti-diabetic drugs. The main types discussed are insulin, sulfonylureas, biguanides, thiazolidinediones, meglitinides, alpha-glucosidase inhibitors, and dipeptidyl peptidase inhibitors. For each drug class, the document covers mechanisms of action, pharmacokinetics, uses, interactions and adverse effects. Storage and delivery methods of insulin are also reviewed.
NSAIDs such as aspirin and ibuprofen are used as analgesics, antipyretics, and anti-inflammatories by inhibiting the enzyme COX and subsequent prostaglandin production. They relieve pain and reduce inflammation but can cause gastrointestinal irritation or bleeding. Paracetamol is also an analgesic and antipyretic that acts in the central nervous system, but has less anti-inflammatory effects and gastrointestinal side effects than NSAIDs. Both NSAIDs and paracetamol in overdose can cause liver toxicity and require specific treatments. Selective COX-2 inhibitors have fewer gastrointestinal side effects than non-selective NSAIDs but lack cardioprotective effects.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers the classification of NSAIDs, their general mechanism of action involving inhibition of cyclooxygenase (COX) enzymes, and their beneficial and risk factors. Specific NSAIDs discussed include aspirin, diflunisal, piroxicam, indomethacin, ibuprofen, ketorolac, mephenamic acid, diclofenac, and selective COX-2 inhibitors. The roles of NSAIDs in periodontics and controlling disease progression are examined. Current recommendations and the role of NSAIDs in the future are also mentioned.
This document provides an overview of non-steroidal anti-inflammatory drugs (NSAIDs). It discusses inflammation and the pathways involved, including the cyclooxygenase and lipoxygenase pathways. It describes the physiological effects of prostaglandins including their roles in pain, fever, and inflammation. It then summarizes the mechanisms of action, uses, and side effects of various NSAIDs such as aspirin, with a focus on their inhibition of prostaglandin synthesis.
This document discusses the pathophysiology, treatment, and pharmacology of gout. It covers the following key points:
1) Gout is caused by the buildup of uric acid crystals in the joints due to high levels of uric acid in the blood. It discusses the biochemical pathway involved in uric acid production.
2) Treatment involves managing acute gout attacks with NSAIDs or colchicine, and lowering uric acid levels long-term with xanthine oxidase inhibitors like allopurinol and febuxostat, or uricosuric drugs like probenecid.
3) Colchicine provides rapid relief of gout attacks but has gastrointestinal side
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.
Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) that inhibits the cyclooxygenase enzymes COX1 and COX2, preventing the formation of prostaglandins and leading to analgesic, antipyretic, and anti-inflammatory effects. It is rapidly absorbed orally and highly protein bound, undergoing extensive hepatic metabolism primarily by CYP2C9 and excreted in urine as metabolites. While generally safe, it can cause gastrointestinal adverse effects and interacts with other drugs like aspirin and warfarin by inhibiting platelet aggregation.
Inflammation is the body's response to tissue injury and involves the release of chemical mediators that cause vascular responses and recruit fluids and cells to the injured site. Anti-inflammatory drugs work by inhibiting the biosynthesis of prostaglandins, chemical mediators involved in inflammation. There are several classes of nonsteroidal anti-inflammatory drugs (NSAIDs) that do this, including aspirin, indomethacin, ibuprofen, and celecoxib. Corticosteroids are also commonly used as potent anti-inflammatory agents for systemic inflammatory disorders.
This document provides information on paracetamol and various nonsteroidal anti-inflammatory drugs (NSAIDs). It describes paracetamol's mechanism of action, pharmacokinetics, uses, advantages over aspirin, and toxicity in overdose. It then discusses several classes of NSAIDs including propionic acid derivatives like ibuprofen and naproxen, fenamate derivatives like mefenamic acid, acetic acid derivatives like indomethacin, selective COX-2 inhibitors like celecoxib and meloxicam, and their mechanisms, pharmacokinetics, uses, and adverse effects. Clinical indications and formulations of specific NSAIDs are also mentioned.
1. NSAIDs work by inhibiting prostaglandin synthesis via blocking cyclooxygenase (COX) enzymes. They are classified based on selectivity for COX-1 vs COX-2.
2. Aspirin is a non-selective, irreversible COX inhibitor. It provides analgesic, antipyretic and anti-inflammatory effects. Common adverse effects include gastric irritation and bleeding risks.
3. Paracetamol is considered a COX-3 inhibitor. It has analgesic properties but does not cause gastric irritation or bleeding like other NSAIDs. Acute overdose can cause liver damage.
This document provides an overview of nonsteroidal anti-inflammatory drugs (NSAIDs), including their classification, mechanisms of action, examples of drug classes, and key properties. NSAIDs are widely used analgesic, antipyretic and anti-inflammatory drugs. They work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. The document describes both non-selective COX inhibitors like aspirin, ibuprofen, and naproxen, as well as selective COX-2 inhibitors. Common adverse effects and clinical uses are summarized for different NSAID classes.
The document summarizes non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin, ibuprofen, naproxen, celecoxib, and acetaminophen. It discusses their mechanisms of action, therapeutic uses, and adverse effects. It also covers the treatment of gout with NSAIDs, colchicine, allopurinol, and uricosuric agents like probenecid and sulfinpyrazone.
This document summarizes information about nonsteroidal anti-inflammatory drugs (NSAIDs), including their mechanism of action, types, effects, uses, and side effects. NSAIDs work by inhibiting cyclooxygenase enzymes, reducing prostaglandin production and thus pain, fever, and inflammation. Common NSAIDs include aspirin, ibuprofen, and naproxen. While effective for conditions like arthritis, NSAIDs can cause gastrointestinal, renal, and cardiovascular side effects.
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 discusses the use of steroidal and non-steroidal anti-inflammatory drugs in oral and maxillofacial surgery patients. It begins by defining inflammation and outlining the fundamental events and major mediators of the inflammatory process. It then describes how non-steroidal anti-inflammatory drugs (NSAIDs) work by interfering with the cyclooxygenase pathway. The document goes on to classify and discuss individual NSAIDs, including aspirin, ibuprofen, celecoxib, and valdecoxib. It covers their mechanisms of action, clinical uses, dosages, and adverse effects. Selective cyclooxygenase-2 inhibitors like celecoxib and rofecoxib are emphasized as
The document discusses various aspects of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs). It defines NSAIDs and describes their analgesic, antipyretic and anti-inflammatory effects. It classifies different types of NSAIDs based on their selectivity for COX-1 and COX-2 enzymes. It also discusses the mechanisms of action, pharmacological properties, uses, doses and adverse effects of several common NSAIDs like aspirin, ibuprofen, ketorolac, diclofenac, celecoxib, paracetamol and nabumetone.
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.
This document discusses the mechanisms and uses of non-steroidal anti-inflammatory drugs (NSAIDs). It begins by explaining that NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production, providing analgesic, antipyretic, and anti-inflammatory effects. The document then classifies and provides examples of different types of NSAIDs, and discusses their pharmacological actions, mechanisms of action, indications, adverse effects, and drug interactions. Key NSAIDs discussed in more depth include aspirin, acetaminophen, ibuprofen, indomethacin, and diclofenac.
This document discusses Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). It defines NSAIDs as a class of non-narcotic analgesic drugs that are not steroids and do not have steroid side effects. NSAIDs have anti-inflammatory, analgesic, and antipyretic properties by inhibiting prostaglandin production. Common NSAID drugs mentioned include diclofenac, ibuprofen, indomethacin, ketoprofen, mefenamic acid, naproxen, and piroxicam. NSAIDs are indicated for relief of symptoms of arthritis, musculoskeletal disorders, and mild to moderate pain. Potential side effects include gastrointestinal, renal, hepatic, cardiovascular and hematologic effects
Antirheumatic drugs & anti gout drugs PHARMACOLOGY REVISION NOTES TONY SCARIA
This document summarizes various drugs used to treat rheumatoid arthritis and gout. It describes disease-modifying antirheumatic drugs (DMARDs) like methotrexate, hydroxychloroquine, leflunomide, d-penicillamine, gold salts, and biological response modifiers that target TNF-α, IL-1, IL-6, and T cells. It also discusses corticosteroids, NSAIDs, and drugs for acute and chronic gout including colchicine, allopurinol, febuxostat, probenecid, and drugs that increase uric acid metabolism like rasburicase and pegloticase.
The document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers their classification, mechanisms of action, uses, and adverse effects. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes and subsequent prostaglandin production. They are effective for pain, fever, and inflammation but can cause gastrointestinal, renal, hepatic, and bleeding side effects. The document focuses on specific NSAIDs including aspirin, ibuprofen, indomethacin, and mephenamic acid, outlining their pharmacology, dosing, and indications.
This document provides an overview of anti-diabetic drugs presented by Sadia Unnisa. It begins with an introduction to diabetes mellitus and classifications of anti-diabetic drugs. The main types discussed are insulin, sulfonylureas, biguanides, thiazolidinediones, meglitinides, alpha-glucosidase inhibitors, and dipeptidyl peptidase inhibitors. For each drug class, the document covers mechanisms of action, pharmacokinetics, uses, interactions and adverse effects. Storage and delivery methods of insulin are also reviewed.
NSAIDs such as aspirin and ibuprofen are used as analgesics, antipyretics, and anti-inflammatories by inhibiting the enzyme COX and subsequent prostaglandin production. They relieve pain and reduce inflammation but can cause gastrointestinal irritation or bleeding. Paracetamol is also an analgesic and antipyretic that acts in the central nervous system, but has less anti-inflammatory effects and gastrointestinal side effects than NSAIDs. Both NSAIDs and paracetamol in overdose can cause liver toxicity and require specific treatments. Selective COX-2 inhibitors have fewer gastrointestinal side effects than non-selective NSAIDs but lack cardioprotective effects.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs). It covers the classification of NSAIDs, their general mechanism of action involving inhibition of cyclooxygenase (COX) enzymes, and their beneficial and risk factors. Specific NSAIDs discussed include aspirin, diflunisal, piroxicam, indomethacin, ibuprofen, ketorolac, mephenamic acid, diclofenac, and selective COX-2 inhibitors. The roles of NSAIDs in periodontics and controlling disease progression are examined. Current recommendations and the role of NSAIDs in the future are also mentioned.
This document provides an overview of non-steroidal anti-inflammatory drugs (NSAIDs). It discusses inflammation and the pathways involved, including the cyclooxygenase and lipoxygenase pathways. It describes the physiological effects of prostaglandins including their roles in pain, fever, and inflammation. It then summarizes the mechanisms of action, uses, and side effects of various NSAIDs such as aspirin, with a focus on their inhibition of prostaglandin synthesis.
This document discusses the pathophysiology, treatment, and pharmacology of gout. It covers the following key points:
1) Gout is caused by the buildup of uric acid crystals in the joints due to high levels of uric acid in the blood. It discusses the biochemical pathway involved in uric acid production.
2) Treatment involves managing acute gout attacks with NSAIDs or colchicine, and lowering uric acid levels long-term with xanthine oxidase inhibitors like allopurinol and febuxostat, or uricosuric drugs like probenecid.
3) Colchicine provides rapid relief of gout attacks but has gastrointestinal side
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.
Nonopioid analgesics can be used alone or in combination with opioids for pain management. They provide advantages like improved recovery and reduced nausea. Classes of nonopioids include paracetamol, NSAIDs, aspirin, alpha-2 agonists, NMDA receptor antagonists, anticonvulsants, membrane stabilizers, nitrous oxide, and nerve blocks. Each drug has different mechanisms of action, efficacy, dosing considerations, and potential adverse effects. The American Society of Anesthesiologists recommends a multimodal approach using combinations of these nonopioid classes along with regional anesthesia techniques and opioids to optimize pain relief and reduce side effects.
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
The document provides information on managing acute poisoning in adults. It discusses how poisoning is common in emergency departments, accounting for 3-5% of attendances with 900 deaths per year in Egypt. The summary outlines general management principles of assessing airway, breathing, circulation, disability and glucose (ABCDG). It then discusses specific management of paracetamol, opiate, salicylate and tricyclic antidepressant overdoses, including use of N-acetylcysteine, naloxone, sodium bicarbonate, haemodialysis, activated charcoal and gastric lavage to treat different poisonings. The key message is that the initial focus is on supportive care while considering ways to decrease drug absorption or increase
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 discusses drugs used to treat peptic ulcers and gastroesophageal reflux disease (GERD). It begins by defining peptic ulcers and their causes, including an imbalance between aggressive and defensive factors in the gastrointestinal tract. It then covers the different types of ulcers and regulators of gastric acid secretion. The document categorizes and describes the mechanisms and uses of several classes of drugs: H2 antagonists like cimetidine and ranitidine; proton pump inhibitors like omeprazole; prostaglandin analogues like misoprostol; antacids; and anti-H. pylori drugs. It discusses the interactions, adverse effects, and treatment of peptic ulcers, G
This document discusses drugs that modulate the acetylcholinesterase enzyme. It begins by describing acetylcholine and how it is synthesized and degraded by acetylcholinesterase. It then discusses anticholinesterases, which are drugs that inhibit acetylcholinesterase, increasing acetylcholine levels. The main classes described are reversible inhibitors like carbamates and tacrine, and irreversible inhibitors like organophosphates. It provides details on the mechanisms, pharmacology, individual drug properties, uses and treatment of organophosphate poisoning with atropine and pralidoxime.
The all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
This document provides information on nonsteroidal anti-inflammatory drugs (NSAIDs) and antipyretic-analgesics. It discusses the classes of NSAIDs including mechanisms of action, therapeutic uses, examples of drugs, and side effects. NSAIDs work by inhibiting cyclooxygenase enzymes and thereby reducing production of prostaglandins involved in inflammation, pain, and fever. The document also reviews antirheumatic drugs for conditions like rheumatoid arthritis, as well as drugs for treating gout such as allopurinol, probenecid, and corticosteroids.
This document discusses various classes of nonsteroidal anti-inflammatory drugs (NSAIDs) including their mechanisms of action, classifications, and individual drug properties. Key points include: NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and reducing prostaglandin production, providing analgesic, antipyretic, and anti-inflammatory effects. Common NSAID classes described are salicylates, propionic acid derivatives, fenamates, enolic acid derivatives, acetic acid derivatives, and pyrazolones. Individual drugs like aspirin, ibuprofen, ketoprofen, indomethacin, and metamizol are highlighted with details on their pharmacokinetics, uses
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.
Action of anticholinergics on Genito-urinary SystemJasleenrait
It describes the action of Anticholinergics on the genitourinary system. Detailed description of each anticholinergic drug is given .
they can be given in urinary incontinence.
This document discusses drugs used for pain management, including analgesics, anti-inflammatory drugs, and adjunctive medications. It covers the pathways of pain and inflammation, describing how nociceptive and neuropathic pain arise. It details the mechanisms of common drug classes like opioids, NSAIDs, anticonvulsants, and muscle relaxants. Key topics include the arachidonic acid cascade, prostaglandin functions, COX enzyme inhibition, and the differences between non-selective and COX-2 selective NSAIDs. Adverse effects, drug interactions, and considerations for specific pain types are also addressed.
The document compares the cholinergic and adrenergic systems. Some key differences include:
- Cholinergic preganglionic fibers are longer while adrenergic fibers are shorter.
- Cholinergic ganglia are farther from organs and closer to the spinal cord, while adrenergic ganglia are nearer to organs and farther from the spinal cord.
- The cholinergic system is generally stimulatory except in the heart and blood vessels, while the adrenergic system is generally inhibitory except in the heart and blood vessels.
Antigout pharmacology. Medicine use in goutPawan Maharjan
This document discusses drug use in the treatment of gout. It begins by describing gout as a disorder of purine metabolism that causes high uric acid levels and the precipitation of urate crystals in joints. It then covers the types and pathogenesis of gout. The main drug classes used for treatment are nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids for acute attacks. For chronic management, uricosuric agents like probenecid increase uric acid excretion, while allopurinol and febuxostat inhibit uric acid synthesis by blocking xanthine oxidase. The document provides details on the mechanisms of action, pharmacokinetics
Poisoning is commonly accidental or suicidal and occurs through substances in homes or workplaces. Acetaminophen is a common oral analgesic and antipyretic that is generally safe in proper doses but can cause liver toxicity and failure in overdose due to formation of a toxic metabolite. Clinical features progress from nausea and vomiting to liver damage and failure over 72-96 hours. Treatment involves assessing for toxicity using acetaminophen levels and the Rumack-Matthew nomogram to determine if N-acetylcysteine is needed. Organophosphates inhibit acetylcholinesterase, accumulating acetylcholine and causing nicotinic and muscarinic effects like increased secretions, nausea, weakness and seizures. Salicy
Non steroidal anti inflamatory drugs final presetation.pptxshivanshverma55
This document provides an overview of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). It discusses the history and classification of NSAIDs, including non-selective COX inhibitors, preferential COX-2 inhibitors, and selective COX-2 inhibitors. Specific NSAIDs are described in more detail, including aspirin, paracetamol, diclofenac, indomethacin, ketorolac, etodolac, naproxen, ibuprofen, piroxicam, meloxicam, celecoxib, and etoricoxib. Their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects are summarized for each. The document aims
The document discusses drugs used for pain and inflammation management. It begins by defining inflammation, analgesics, NSAIDs, and antipyretics. NSAIDs like aspirin, ibuprofen, and paracetamol are described in more detail, including their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects. Specific concerns for NSAID use in pregnancy and risks of overdose like Reye's syndrome and hepatitis are also summarized. The document provides an overview of pharmacotherapy options for pain and fever treatment.
Similar to anti inflammatory drugs by Yatendra Singh (20)
Tissues are groups of cells that work together to perform specific functions. There are four primary tissue types found in animals: epithelial, connective, muscular, and nervous tissue. Epithelial tissues cover and protect surfaces, connective tissue binds tissues together and provides support, muscular tissue enables movement, and nervous tissue transmits signals throughout the body to coordinate functions. Each tissue type has different cell structures and locations according to their specialized roles.
This document summarizes and compares general anesthesia and local anesthesia. General anesthesia involves drugs that produce reversible loss of consciousness and sensations throughout the body, allowing for major surgery. It carries more risks than local anesthesia, which uses drugs to reversibly block nerve conduction and sensation in a restricted area only, making it safer but only suitable for minor procedures. The document outlines the classification, mechanisms of action, therapeutic uses and potential complications of both general and local anesthetics.
Joints connect bones and allow movement. There are 230 joints in the body which are classified structurally as fibrous, cartilaginous, or synovial joints depending on how the bones connect, and functionally as synarthrosis, amphiarthrosis, or diarthrosis based on movement. Common joint disorders include sprains, dislocations, bursitis, tendonitis, and various forms of arthritis such as osteoarthritis and rheumatoid arthritis.
The skeletal system is composed of bones, cartilage, joints, and ligaments. It supports the body, protects organs, allows for movement, stores minerals, and produces blood cells. The skeleton is divided into the axial skeleton and appendicular skeleton. The axial skeleton includes the skull, vertebral column, thoracic cage, and sternum, and protects the brain, spinal cord, and thoracic organs. It is composed of numerous bones that connect to form the cranium, face, vertebrae, ribs, and sternum. The skeletal system provides structure, movement, and protection for the human body.
The document summarizes the key components and functions of the human digestive system. It describes the major organs including the mouth, esophagus, stomach, small intestine and large intestine. It also discusses accessory organs like the liver, gallbladder and pancreas. The digestive system breaks down food, reduces it to smaller molecules, and absorbs nutrients for the body. Each organ plays an important role through mechanical and chemical digestion as well as nutrient absorption.
The respiratory system allows oxygen to enter the body and carbon dioxide to exit through a series of organs. Air enters through the nose and mouth, then travels through the pharynx, larynx, trachea, and bronchi into the lungs. In the lungs, oxygen passes into blood in the alveoli and carbon dioxide passes out of the blood into the alveoli to be exhaled. Breathing is facilitated by the contraction and relaxation of the diaphragm and rib cage, which decreases and increases the volume of the chest cavity to inhale and exhale air.
Apoptosis is a genetically controlled and energy-dependent process where single cells undergo programmed cell death. During apoptosis, a cell shrinks, detaches from neighboring cells, and its nuclear material is condensed and fragmented into apoptotic bodies which are then phagocytosed by surrounding cells. Apoptosis occurs through two main pathways: the extrinsic death receptor pathway and the intrinsic mitochondrial pathway. In both pathways, initiator caspases activate executioner caspases that degrade cellular proteins and lead to cell death. Dysregulation of apoptosis can contribute to diseases like cancer, autoimmune disorders, and neurodegenerative conditions.
G protien coupled receptor by yatendra singhYatendra Singh
This document discusses G protein-coupled receptors (GPCRs), which are a large family of cell membrane receptors linked to intracellular effector systems through G proteins. GPCRs have seven transmembrane domains and interact with a wide range of ligands like neurotransmitters, hormones, and light-sensitive compounds. They function by activating heterotrimeric G proteins composed of α, β, and γ subunits, which then activate various intracellular effector pathways like adenylyl cyclase and phospholipase C. GPCRs are important drug targets, comprising about 40% of modern medicines.
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
Travis Hills' Endeavors in Minnesota: Fostering Environmental and Economic Pr...Travis Hills MN
Travis Hills of Minnesota developed a method to convert waste into high-value dry fertilizer, significantly enriching soil quality. By providing farmers with a valuable resource derived from waste, Travis Hills helps enhance farm profitability while promoting environmental stewardship. Travis Hills' sustainable practices lead to cost savings and increased revenue for farmers by improving resource efficiency and reducing waste.
Current Ms word generated power point presentation covers major details about the micronuclei test. It's significance and assays to conduct it. It is used to detect the micronuclei formation inside the cells of nearly every multicellular organism. It's formation takes place during chromosomal sepration at metaphase.
EWOCS-I: The catalog of X-ray sources in Westerlund 1 from the Extended Weste...Sérgio Sacani
Context. With a mass exceeding several 104 M⊙ and a rich and dense population of massive stars, supermassive young star clusters
represent the most massive star-forming environment that is dominated by the feedback from massive stars and gravitational interactions
among stars.
Aims. In this paper we present the Extended Westerlund 1 and 2 Open Clusters Survey (EWOCS) project, which aims to investigate
the influence of the starburst environment on the formation of stars and planets, and on the evolution of both low and high mass stars.
The primary targets of this project are Westerlund 1 and 2, the closest supermassive star clusters to the Sun.
Methods. The project is based primarily on recent observations conducted with the Chandra and JWST observatories. Specifically,
the Chandra survey of Westerlund 1 consists of 36 new ACIS-I observations, nearly co-pointed, for a total exposure time of 1 Msec.
Additionally, we included 8 archival Chandra/ACIS-S observations. This paper presents the resulting catalog of X-ray sources within
and around Westerlund 1. Sources were detected by combining various existing methods, and photon extraction and source validation
were carried out using the ACIS-Extract software.
Results. The EWOCS X-ray catalog comprises 5963 validated sources out of the 9420 initially provided to ACIS-Extract, reaching a
photon flux threshold of approximately 2 × 10−8 photons cm−2
s
−1
. The X-ray sources exhibit a highly concentrated spatial distribution,
with 1075 sources located within the central 1 arcmin. We have successfully detected X-ray emissions from 126 out of the 166 known
massive stars of the cluster, and we have collected over 71 000 photons from the magnetar CXO J164710.20-455217.
Or: Beyond linear.
Abstract: Equivariant neural networks are neural networks that incorporate symmetries. The nonlinear activation functions in these networks result in interesting nonlinear equivariant maps between simple representations, and motivate the key player of this talk: piecewise linear representation theory.
Disclaimer: No one is perfect, so please mind that there might be mistakes and typos.
dtubbenhauer@gmail.com
Corrected slides: dtubbenhauer.com/talks.html
The technology uses reclaimed CO₂ as the dyeing medium in a closed loop process. When pressurized, CO₂ becomes supercritical (SC-CO₂). In this state CO₂ has a very high solvent power, allowing the dye to dissolve easily.
ESR spectroscopy in liquid food and beverages.pptxPRIYANKA PATEL
With increasing population, people need to rely on packaged food stuffs. Packaging of food materials requires the preservation of food. There are various methods for the treatment of food to preserve them and irradiation treatment of food is one of them. It is the most common and the most harmless method for the food preservation as it does not alter the necessary micronutrients of food materials. Although irradiated food doesn’t cause any harm to the human health but still the quality assessment of food is required to provide consumers with necessary information about the food. ESR spectroscopy is the most sophisticated way to investigate the quality of the food and the free radicals induced during the processing of the food. ESR spin trapping technique is useful for the detection of highly unstable radicals in the food. The antioxidant capability of liquid food and beverages in mainly performed by spin trapping technique.
ESPP presentation to EU Waste Water Network, 4th June 2024 “EU policies driving nutrient removal and recycling
and the revised UWWTD (Urban Waste Water Treatment Directive)”
Authoring a personal GPT for your research and practice: How we created the Q...Leonel Morgado
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
The use of Nauplii and metanauplii artemia in aquaculture (brine shrimp).pptxMAGOTI ERNEST
Although Artemia has been known to man for centuries, its use as a food for the culture of larval organisms apparently began only in the 1930s, when several investigators found that it made an excellent food for newly hatched fish larvae (Litvinenko et al., 2023). As aquaculture developed in the 1960s and ‘70s, the use of Artemia also became more widespread, due both to its convenience and to its nutritional value for larval organisms (Arenas-Pardo et al., 2024). The fact that Artemia dormant cysts can be stored for long periods in cans, and then used as an off-the-shelf food requiring only 24 h of incubation makes them the most convenient, least labor-intensive, live food available for aquaculture (Sorgeloos & Roubach, 2021). The nutritional value of Artemia, especially for marine organisms, is not constant, but varies both geographically and temporally. During the last decade, however, both the causes of Artemia nutritional variability and methods to improve poorquality Artemia have been identified (Loufi et al., 2024).
Brine shrimp (Artemia spp.) are used in marine aquaculture worldwide. Annually, more than 2,000 metric tons of dry cysts are used for cultivation of fish, crustacean, and shellfish larva. Brine shrimp are important to aquaculture because newly hatched brine shrimp nauplii (larvae) provide a food source for many fish fry (Mozanzadeh et al., 2021). Culture and harvesting of brine shrimp eggs represents another aspect of the aquaculture industry. Nauplii and metanauplii of Artemia, commonly known as brine shrimp, play a crucial role in aquaculture due to their nutritional value and suitability as live feed for many aquatic species, particularly in larval stages (Sorgeloos & Roubach, 2021).
3. COX1
Constitutive always present
in cell
Serve as house keeping
function e.g. Gastro
protection
COX2
Inducible (Synthesis
stimulated by endotoxin and
other inflammatory mediator
Participate in inflammation
Constitutive in Brain ,
endothelium and Kidney
COX3
Recently isolated from
cerebral cortex
Not involve in inflammation
Paracetamol target COX 3
4. NSAIDs
Shared Toxicities Due to PG synthesis
Inhibition
1. Gastric mucosal damage .
2. Bleeding: inhibition of platelet
function
3. Limitation of renal blood flow : Na+
and water retention
4. Delay/prolongation of labour
5. Asthma and anaphylactoid reactions
in susceptible individuals
Adverse Effect of NSAIDs
Gastrointestinal
Gastric irritation, erosions, peptic
ulceration,gastric bleeding.
Renal
Na+ and water retention, chronic renal
failure, interstitial nephritis, papillary
necrosis (rare).
Hepatic
Raised transaminases,hepatic failure (rare).
CNS
Headache, mental confusion, behavioural
disturbances.
Haematological
Bleeding, thrombocytopenia, haemolytic
anaemia, agranulocytosis
Others
Asthma exacerbation, nasal polyposis,skin
rashes, pruritus, angioedema
Beneficial Action Due to PG Synthesis
Inhibition
1. Analgesia
2. antipyretics
3. Anti-inflammatory
4. Closure of ductus arteriosus in newborn
5. Dysmenorrhoea- intermittent ischemia
of myometrium probaly responsible for
menstrual cramp.
6. Parturition- Sudden spurt of PG synthesis by
uterus probably triggers labour and facilitate
its progression.
6. Aspirin
PHAFMACOLOGIC AL ACTIONS
1. Analgesic, antipyretic and anti-inflammatory.
2. Metabolic effect- These are significant only at anti-inflammatory doses.
I. Cellular metabolism is increased, especially in skeletal muscles, due to uncoupling of oxidative
phosphorylation
II. increased heat production.
III. There is increased utilization of glucose --> blood sugar may decrease (especially in diabetics)
hyperglycamia is often seen at toxic doses: this is due to central sympathetic stimulation,
Chronic use of large doses cause negative N2 balance by increased conversion of protein to
carbohydrate
3. Respiration
The effect are dose dependent
At anti-inflammatory doses, respiration is stimulated by peripheral (increased CO2 production)
and central (increased sensitivity of respiratory centre to CO2) actions.
Hyperventilation is prominent in salicylate poisoning.
Further rise in salicylate level causes respiratory depression; death is due to respiratory failure
7. Aspirin
CVS-
• Aspirin has no direct effect in therapeutic doses.
• Larger doses increase cardiac output to meet increased peripheral O2 demand.
• Toxic doses depress vasomotor centre: BP may fall.
GIT- Aspirin and released salicylic acid irrigatate gastric mucosa- cause epigastric distress, nausea
and vomiting
• Aspirin (pKa 3.5) remains unionized and diffusible in the acid gastric juice, but on entering the
mucosal cell (pH 7.1) it ionizes and becomes indiffusible. This 'ion trapping' in the gastric mucosal
cell enhances gastric toxicity.
• Further aspirin particle coming in contact with gastric mucosa promotes local back diffusion of
acids focal necrosis of mucosal cells and capillaries- acute ulcers, erosive gastritis, congestion
and
• The occult blood loss in stools is increased by even a single tablet of aspirin.
URATE Excretion - Dose-related effect is seen:
• <2 g/day-urate retention and antagonism of all other uricosuric drugs.
• 2-5 g/ day-variable effects, often no change.
• >5 g/day-increased urate excretion.
8. Aspirin
Pharmacokinetics
• absorbed from the stomach and small intestine.
• its poor water solubility is the limiting factor in absorption: micro fining the drug particles
and inclusion of an alkali 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 is -80% bound to plasma proteins and has volume of distribution -0.17 L / kg. It slowly
enters brain but freely crosses placenta. Both
• only 1/10th is excreted as free salicylic acid.
ADVERSE EFFECTS –
1. Side effects that occur at analgesic dose (0.3-1.5 g/ day) are nausea, vomiting, epigastric
distress, increased occult blood loss in stools.
The most important adverse effect of aspirin is gastric mucosal damage and peptic
ulceration.
2) Hypersensitivity and idiosyncrasy
9. Aspirin
ADVERSE EFFECTS –
3) anti-inflammatory dose- (3-5 g/day)
• Produce the syndrome called salicylism- its characteristics is
1. Dizziness,
2. Tinnitus,
3. vertigo
4. Reversible impairment of hearing and vision.
5. excitement and mental confusion,
• Aspirin therapy in children with rheumatoid arthritis has been found to raise serum transaminases,
indicating liver damage.
• In adults also, long-term therapy can cause insidious onset hepatic injury.
4) Asute salicylate poisoning
• It is more common in children.
• Fatal dose in adults is estimated to be 15-30 g, but is considerably lower in children. Serious toxicity
is seen at serum salicylate levels > 50 mg/dl.
• Manifestations are: Vomiting, dehydration, electrolyte imbalance,acidotic breathing,
hyper/hypoglycaemia,petechial haemorrhages, restlessness, delirium, hallucinations,
hyperpyrexia, convulsions, coma and death due to respiratory failure.
10. 2- Propionic Acid Derivative
Ibuprofen is 1st member of this class.
Adverse effect- ibuprofen and all its congeners are better tolerated than aspirin.
• Gastric discomfort, nausea and vomiting, though less than aspirin
• Gastric erosion and occult in blood loss are rare.
• CNS side effect include headache, dizziness, blurring of vision, tinnitus and depression
• Rashes , itching and other hypersensitivity phenomena are infrequent.
Pharmacokinetic-
• All well absorb orally, high bound to plasma protein(90-99%).
• Propionic acid derivative inter brain, synovial fluid and cross placenta.
• Metabolize in liver
• Excreted in urine as well as bile.
Uses-
• 1- analgesic and antipyretic
• 2-dysmenorrhorea
• 3- Ibuprofen and its congeners are widely used in arthritis, osteoarthritis ,and other musculosleton
disorder.
11. 3- Anthranilic acid derivative
Mephenamic Acid
• An analgesic ,antipyretic ,and anti-inflammatory drugs which inhibit COX as well as antagonize
certain actions of PGs.
Pharmacokinetics –
• Oral absorption is slow but almost complete.
• It is highly bound to plasma proteins.
• Partly metabolized and excreted in urine as well as bile.
• Plasma t1/2is 24 hours.
Adverse effect-
• 1-Diarrhoea is most important dose related side effect.
• 2-Epigastric distress complained, but gut bleeding is not significant.
• 3- Skin rashes, dizziness and other CNS manifestations have occurred.
Uses –
• joint and soft tissue pain where strong anti-inflammatory action is not needed.
• In dysmenorrhoea.
• In some cases of rheumatoid and osteoarthritis.
12. 4- ARYL-ACETIC ACID DERIVATIVES
Diclofenac sodium
• An analgesic ,Antipyretic ,anti-inflammatory drug.
• The antiplatelet action is short lasting.
Pharmacokinetics-
• It is well absorbed orally,99 % protein bound.
• metabolized and excreted both in urine and bile.
• The plasma t1/2 2hours.
• However, it has good tissue penetrability and concentration in synovial fluid is maintained for 3
times longer period than in plasma, exerting extended therapeutic action in joints.
Adverse effects
• epigastric pain, nausea, headache, dizziness, rashes.
• Gastric ulceration and bleeding are less common.
• kidney damage is rare.
Uses-
• Diclofenac is among the most extensively used NSAID;
• employed in rheumatoid and osteoarthritis,
• Ankylosing spondylitis, toothache, dysmenorrhoea, post-traumatic and postoperative
inflammatory conditions-affords quick relief of pain and wound edema.
Aceclefenac -A somewhat COX-2 selective of diclofenac having similar properties.
13. 5- OXICAM DERIVATIVES
Piroxicam
• It is a long-acting potent NSAID with antiinflammatory potency and good analgesic-antipyretic
action.
Pharmacokinetics
• It is rapidly and completely absorbed. 99% plasma protein bound.
• largely metabolized in liver .
• excreted in urine and bile.
• Plasma t1/2 is long nearly 2 days.
Adverse effects
1. The g.i. side effects are more than ibuprofen.
2. causes less faecal blood loss than Aspirin.
3. Rashes and pruritus are seen in < 1% patients.
4. Short term analgesic as well as long-term anti-inflammatory drugs.
5. Rheumatoid and osteo-arthritis, and, acute gout, musculoskeleton injuries, dentistry,
6. Episiotomy, dysmenorrhea
Tenoxicam- Similar properties and uses
14. 6- PYROLO-PYROLE DERIVATIVE
Ketorolac- A novel NSAID with potent analgesic and modest anti-inflammatory activity.
Pharmakokinetcs
• Ketorolac is rapidly absorbed after oral and i.m. administration.
• It is highly plasma protein bound and 60% excreted unchanged in urine.
• plasma t1/2 is 5-7 hours.
Adverse effects
1. Nausea
2. Abdominal pain
3. Dyspepsia
4. Ulceration
5. loose stools
6. drowsiness.
Uses
• Ketorolac is frequently used in postoperative dental and acute musculoskeletal pain
• It may also be used for renal colic, migraine and pain due to bony metastasis.
15. 7- Indole Derivative
Indomethacin
• It is a potent anti-inflammatory drugs with prompt antipyretic action. Indomethacin relives only
inflammatory or tissue injury related to pain . It is a highly potent inhibitor of PG synthesis
Pharmacokinetis
well absorb orally .90% bound to plasma proteins,
Partly Metabolise in liver to inactive products and Excreted by kidney. Plasma t ½ 2-5 hours.
Advese Effect
A high incidence (up to 50%) of gastrointestinal and CNS side effects is produced.
gastric irritation, nausea/ anorexia, gastric bleeding .
diarrhoea are prominent.
frontal headache (very common), dizziness, mental confusion, hallucination, depression
Use
As a reserve drugs in conditions requiring potent anti-inflammatory action like ankylosing
spondylitis,
acute exacerbations of destructive arthropathies,
psoriatic arthritis acute gout that are not responding to better tolerated NSAIDs.
16. 8- Pyrazolones
Metamizole (Dipyrone)
In contrast to phenylbutazone,this derivative of amidopyrine is a potent and promptly acting
analgesic and antipyretic but poor anti-inflammatory and not uricosuric.
It can be given orally, i.m. as well as i.v, but gastric irritation, pain at injection site occurs.
Occasionally, i.v. injection produces precipitous fall in BP.
Few cases of agranulocytosis were reported and metamizol is banned in the USA and some
European countries. Extensively used in India.
Propiphenazone
similar in properties to metamizol.
Agranulocytosis has not been reported.
17. B. PREFERENTIAL COX-2 INHIBITORS
NIMESULIDE
This newer NSAID is a relatively weak inhibitor of PG synthesis and there is some evidence to
indicate relative COX-2 selectivity.
Anti-inflammatory action may be exerted by other mechanisms as well, e.g. reduced generation of
superoxide by neutrophils, inhibition of PAF synthesis and TNFᾀ release.
Pharmacokinetics
Nimesulide is almost completely absorbed orally, 99% plasma protein bound excreted mainly in
urine with at1/2 of 2-5 hours.
The analgesic, antipyretic and anti-inflammatory activity of nimesulide has been rated comparable
to other NSAIDs.
Uses
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.
18. B. PREFERENTIAL COX-2 INHIBITORS
Adverse effects :
• gastrointestinal (epigastralgia, heart burn, nausea, loose motions), dermatological (rash,
pruritus)
• hematuria is reported in few children.
19. B. PREFERENTIAL COX-2 INHIBITORS
Meloxicam
• This newer congener piroxicam has a COX-2 / COX-I selectivity ratio of about of 10.
• Since measurable inhibition of platelet TXA2 production (a COX-1 function) occurs at therapeutic
doses of meloxicam.
• It has been labelled preferential COX-2 inhibitor. Efficacy of meloxicam in osteo- and rheumatoid
arthritis is comparable to piroxicam.
• Gastric Side effects of meloxicam are milder.
• but ulcer complications (bleeding, perforation) have been reported on long-term use.
Nabumetone
• It is a prodrug generates activemetabolite(6 -MNA)
• is a relatively morer potent COX-2 than COX-1 inhibitor.
• It possesses analgesic, antipyretic and anti-inflammatory activities.
• Effective in the treatment of rheumatoid and osteoarthritis as well as soft tissue injury.
• Nabumetone has caused a lower incidence of gastric erosions, ulcers and bleeding
20. C. SELECTIVE COX-2 INHIBITORS
(Coxibs)
Celecoxib
The COX-2 selectivity of celecoxib is modest (6-20 fold). It exerts anti-inflammatory, 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.
Side effect- Though tolerability of celecoxib is better than traditional NSAIDs,
abdominal pain, dyspepsia and mild diarrhoea are the common side effects. Rashes, edema and a
small rise in BP have also been noted.
Pharmacokinetics- Celecoxib is slowly absorbed, 97% plasma protein
T1/2 of ~10 hours.
Use It is approved for use in osteo- and rheumatoid arthritis.
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.
21. D. PARA AMINO PHENOL DERIVATIVE
Paracetamol(acetaminophen) the deethylated activemetabolite of phenacetin, was also introduced
in the last century but has come into common use only since 1950.
The central analgesic action of paracetamol is like aspirin, i.e. it raises pain threshold, but has weak
peripheral anti-inflammatory component. Analgesic action of aspirin and paracetamol is additive.
Paracetamol is a good and promptly acting antipyretic.
Paracetamol has negligible anti-inflammatory action.
• The ability of paracetamol to inhibit COX-3 could also account for its analgesic-antipyretic action.
Pharmacokinetics
• well absorbed orally, only about 1/4th portion is absorbed from plasma and it is uniformly
distributed in the body.
• excreted rapidly in urine. Plasma t1/2 is 2-3hrs.
• Effects after an oral dose last for 3-5 hours.
Adverse Effect
• In isolated antipyretic doses paracetamol is safe and well tolerated.
• Nausea and rashes occur occasionally.
• leukopenia is rare.
22. E. BENZOXAZOCINE DERIVATIVE
Nefopam
• It is a non opioid analgesic which does not inhibit PG synthesis and acts rapidly in traumatic
and postoperative pain
• Favourable results have been obtained in short-lasting musculoskeletal pain.
• Nefopam produces anticholinergic (dry mouth, urinary retention, blurred vision) and
sympathomimetic (tachycardia, nervousness) side effects.
• and nausea is often dose limiting It is contraindicated in epileptics.
25. Immnosuppressants
Methotrexate-
• This dihydrofolate reductase inhibitor has prominent immunosuppressant and anti-inflammatory
property.
• Beneficial effects in RA are probably related to inhibition of cytokine production, chemotaxis and
cell-mediatede immune reaction.
• Induction of oral low-dose(7.5-15 mg) weekly Mtx regimen has improved acceptability of this drug
in RA.
• Onset of symptom relief is relatively rapid (4-6 weeks), therefore preferred for initial treatment.
• Mtx is now the DMARD of first choice and the standard Treatment for most patients, including
cases of Juvenile RA Response is more predictable and sustained overer long-term.
Pharmacokinetics
• Oral bioavailability of Mtx is variable and may be effected by food .
• Its excretion is hindered in renal disease not recommended for patients.
• probenecid and aspirin increase Mtx levels and Toxicity
• Trimethoprim can add to inhibition of dihydrofolate reductase and depress bone marrow
26. Immnosuppressants
Methotrexate-
• Side effect
• nodulosis, oral ulceration and g.i. upset are major side effects of low dose Mtx regimen.
• With prolonged therapy, dose dependent progressive liver damage leading to cirrhosis occurs in
some patient.(this is not seen with short courses used in cancer).
• Mtx is contraindicated in pregnancy ,breast feeding , liver disease, active infection , leucopenia and
peptic ulcer.
27. Immnosuppressants
Azathioprine
• This purine antimetabolite acts after getting converted to 6-mercaptopurine by Enzyme thiopurine
methyl transferase
• It is potent suppressant of cell-mediated immunity, appears to selectively affect differentiation and
function of T-cells and natural killer cells.
• It also suppresses inflammation. However, remission is induced in smaller percentage of RA
patients and it is less commonly used.
• Given along with corticosteroids, it has a steroid sparing effect, for which it is primarily used now,
especially incases with systemic manifestations.
• It is not combined with Mtx.
28. DMARDs
Sulfasalazine
• It is a compound of sulfapyridine and 5-amino salicylic acid (5-ASA); has anti-inflammatory activity
and is primarily used in ulcerative colitis.
• In addition, it suppresses the disease in significant number of RA patients.
• The mechanism of action is not known.
• Sulfapyridine split off in the colon by bacterial action and absorbed systemically appears to be the
active moiety (contrast ulcerative colitis, in which 5-ASA acting locally in the colon is the active
component).
• Generation of superoxide radicals and cytokine elaboration by inflammatory cells may be
suppressed.
• Efficacy of sulfasalazine in RA is modest and side effects are few, but
neutropenia/thrombocytopenia occurs in about 10% patients and hepatitis is possible.
• It is used as a second line drug for milder cases.
29. DMARDs
Chloroquine and hydroxychloroquine
• These are antimalarial drugs found to induce remission in upto 50% patients of RA, but take 3-6
months.
• Their advantage is relatively low toxicity, but efficacy is also low; bony erosions are not prevented.
• Their mechanism of action is not known.
• however, they have been found to reduce monocyte IL-I, consequently inhibiting B lymphocytes.
• Antigen processing may be interfered with Lysosomal stabilization and free radical scavenging are
the other proposed mechanisms.
Adverse Effect-
• For RA, these drugs have to be given for long periods: accumulate in tissues and produce toxicity,
most disturbing of which is retinal damage and corneal opacity. This is less common and reversible
in case of hydroxychloroquine, which is preferred over chloroquine.
• rashes, graying of hair, irritable bowel syndrome, myopathy and neuropathy.
• Chloroquine /hydroxychloroquine are employed n milder nonerosive disease, especially when only
one or a few joints are involved, or they are combined with Mtx / sulfasalazine.
30. DMARDs
Leflunomide
• This immunomodulator inhibits proliferation of activated lymphocytes in patients with active RA.
• Arthritic symptoms are suppressed and radiological progression of disease is retarded.
• In clinical trials its efficacy has been rated comparable to Mtx and onset of benefit is as fast
(4 weeks).
• Leflunomide is rapidly converted in the body to an active metabolite which inhibits dihydroorotate
dehydrogenase and pyrimidine synthesis in actively dividing cells.
• Antibody production by B-cells may be depressed.
• The active metabolite has a long t1/2 of 2 weeks.
• Adverse effects of leflunomide are diarrhoea, headache, nausea, rashes, loss of hair
thrombocytopenia, leucopenia, increased chances of chest infection and raised hepatic
transaminases.
• It is not to be used in children and pregnant/ lactating women.
• Leflunomide is an alternative to Mtx or can be added to it, but the combination is more
hepatotoxic. Combination with sulfasalazine improves benefit.
31. DMARDs
Auranofin
Main adverse effects
• diarrhoea
• abdominal cramps
• Pruritus
• taste disturbances
• mild anaemia
• Alopecia
D-penicillamine
• It is a copper chelating agent with a gold like action in RA, but less efficacious; bony erosions do not
heal.
• It is not favoured now, because it does not offer any advantage in terms of toxicity, which is similar
to that of gold.
adverse effects Loss of taste, systemic lupus and myasthenia gravis
• Penicillamine increases soluble collagen and is the preferred drug for stage II and III scleroderma
32. Biologic response modifiers
TNFᾀ inhibitors
Etanercept
• it is a recombinant fusion protein of TNFᾀ receptor and Fc portion of human IgG1
administered by s.c. injection 50 mg weekly Pain, redness, itching and swelling occur at
injection site and chest infections may be increased, but immunogenicity is not a clinical
problem.
Infliximab
• It is a chimeral monoclonal antibody which binds and neutralizes TNFᾀ;
• 3-5 mg/kg is infused i.v every weeks
• An acute reaction comprising of fever, chills, urtricaria, bronchospasm, rarely anaphylaxis
may follow the infusion.
• Susceptibility to respiratory infections is increased and worsenings of CHF has been noted
• It is usually combined with Mtx which improves the response and decreases antibody
formation against infliximab.
33. Corticosteroid
• they have potent immunosuppressant and anti-inflammatory activity: can be inducted almost at
stage in RA along with first or second line drugs.
• if potent anti-inflammatory action is required while continuing the NSAID+ DMARD.
• symptomatic relief is prompt, but they do not arrest the rheumatoid process, though joint
destruction may be slowed and bony erosions delayed.
• Long-term use of corticosteroids carries serious disadvantages. Therefore, either low doses (5-10
mg prednisolone or equivalent) are used to supplement NSAIDs.
• or high doses are employed over short periods in cases with severe systemic manifestations.
• In cases with single or few joint involvement with severe symptoms, intraarticular injection of a
soluble glucocorticoid affords relief for several weeks; joint damage may be slowed. However, this
procedure should not be repeated before 4-6 months.
35. Drugs for Acute Gout
NSAIDs
• Strong anti-inflammatory drugs piroxicam naproxen declofenac and etoricoxib.
• Naproxen and piroxicam specifically inhibit chemotactic migration of leucocytes into the inflamed joint.
• After the attack is over, they may be continued at lower doses for 3-4 weeks.
36. Drugs for Acute Gout
Colchicine
• It is an alkaloid from Colchicum autumnale which was used in gout since 1763.
• Colchicine is neither analgesic nor anti-inflammatory, but it especificaly suppresses gouty
inflammation.
Pharmacokinetics
• Colchicine is rapidly absorbed orally.
• Partly metabolize in liver.
• ultimate disposal occurs in urine and faeces over many days.
Adverse Effect-
• high and dose related.
• Nausea, vomiting, watery or bloody diarrhoea and abdominal cramps occur as dose limiting
adverse effects. Accumulation of the drug in intestine .
• ln overdose produces kidney damage, CNS depression, intestinal bleeding; death is due to muscular
paralysis and respiratory failure.
Use;
• Treatment of acute Gout.
• prophylaxis
37. Drugs for Chronic Gout
• When pain and stiffness persist in a joint between attacks , gout has become chronic.
• Feature- hyperuresemia and thophi , Urate stones in kidney
Uricosuric Drugs-
• These are week organic acids.
• Promote renal clearance of uric acid by inhibiting urate anion exchange in proximal tubule that
mediate urate reabsorption
• Ex. Probencid and sulphinpyrazone
Probencid
• Pharmacokinetics-
• Complete absorb orally.
• 90% plasma protein bound
• T1/2 is 8 to 10 hrs.
Adverse effects
• Probenecid is generally well tolerated.
• Dipepsia
Use-
• Chronic Gout.
• For prolong action of Protiene
38. Drugs for Chronic Gout
Sulfinpyrazone
Pharmacokinetics
• Sulfinpyrazone is well absorbed orally;
• 98% plasma protein bound.
• Excretion is fairly rapid, mainly by active secretion in proximal tubule. Uricosuric action of a
single dose lasts for 6-10 hours.
Adverse effects
• Gastric irritation is the most common side effect.
• Contra indicated in patients with peptic ulcer.
• Rashes and other hypersensitivity reactions are uncommon.
Use-
• In Chronic Gout
39. URIC ACID SYNTHESIS INHIBITOR
Allopurinol
Pharmacokinetics
• About 80% of orally administered allopurinol is absorbed.
• not bound to Plasma Protiene
• 1/3rd is exceted Unchange in Urine.
Adverse effect
• These are uncommon.
• Hyper sensitivity reaction consisting of rashes, fever, malaise and muscle pain is the most frquent
• Gastric irritation, headache, nausea and dizziness are infrequent
• do not need withdrawl
• Liver Damage is rare.