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.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production. This reduces pain, fever, and inflammation. NSAIDs inhibit both COX-1 and COX-2, with COX-1 inhibition causing side effects like gastric ulceration, while selective COX-2 inhibitors have fewer side effects but higher costs. The mechanisms of analgesia, antipyresis, and anti-inflammation by NSAIDs are through inhibition of prostaglandin biosynthesis in both the central and peripheral nervous systems.
NSAIDs are a group of drugs that relieve pain, fever, and inflammation by inhibiting prostaglandin synthesis. They can be classified based on their action on COX enzymes or their chemical structure. Their mechanism of action involves blocking COX pathways to prevent the formation of prostaglandins. Common adverse effects include gastric irritation and impaired healing. NSAIDs should be used cautiously in patients with conditions like peptic ulcer or impaired kidney function.
NSAIDs are a chemically diverse group of drugs that are grouped together because they have common analgesic, antipyretic, and anti-inflammatory effects. They work by inhibiting cyclooxygenase (COX) enzymes and reducing the production of prostaglandins. NSAIDs are generally weaker analgesics than opioids except for inflammatory pain conditions. Common adverse effects include gastrointestinal irritation and potential kidney toxicity. Newer selective COX-2 inhibitors were developed to reduce gastrointestinal side effects.
Dr. Jannatul Ferdoush discusses pain and its components, including perception of pain and emotional response. She then covers the central and peripheral regulation of pain, including the roles of substances like bradykinin, prostaglandins, opioids, and the descending inhibitory pathway. Finally, she classifies analgesics as either peripherally or centrally acting and discusses factors to consider when choosing an analgesic, such as the origin and severity of pain.
NSAIDs are a class of drugs that relieve pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. There are various types of NSAIDs classified by their chemical structure. All NSAIDs work by blocking prostaglandin production, but they differ in their selectivity for COX-1 vs COX-2 enzymes. Common adverse effects include gastrointestinal irritation and bleeding, as well as renal impairment. NSAIDs are commonly used to treat pain, fever, and inflammatory conditions like arthritis.
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.
Anti histamine.First generation, second generation,Antagonism of histamine ...FarsanaM
This document discusses antihistamines and their mechanisms of action. It describes the four main histamine receptors (H1, H2, H3, H4) and how antihistamines work by competitively binding to H1 receptors. Antihistamines are classified as first or second generation. First generation antihistamines are more sedating due to other receptor interactions, while second generation antihistamines are more selective for H1 receptors with less sedation side effects. Antihistamines are used to treat allergic conditions by blocking the effects of histamine at H1 receptors and relieving symptoms like itching, hives, and swelling.
This document provides an overview of analgesics, with a focus on non-steroidal anti-inflammatory drugs (NSAIDs). It defines pain and discusses the classification, mechanism of action, and history of analgesics. NSAIDs are introduced as a class of drugs that relieve pain and inflammation by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. The document outlines the role of prostaglandins in inflammation and bone resorption, as well as the beneficial and harmful actions of NSAIDs through COX inhibition. Host modulation is discussed as a treatment concept in periodontics where NSAIDs may reduce tissue destruction by modulating the host inflammatory response.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production. This reduces pain, fever, and inflammation. NSAIDs inhibit both COX-1 and COX-2, with COX-1 inhibition causing side effects like gastric ulceration, while selective COX-2 inhibitors have fewer side effects but higher costs. The mechanisms of analgesia, antipyresis, and anti-inflammation by NSAIDs are through inhibition of prostaglandin biosynthesis in both the central and peripheral nervous systems.
NSAIDs are a group of drugs that relieve pain, fever, and inflammation by inhibiting prostaglandin synthesis. They can be classified based on their action on COX enzymes or their chemical structure. Their mechanism of action involves blocking COX pathways to prevent the formation of prostaglandins. Common adverse effects include gastric irritation and impaired healing. NSAIDs should be used cautiously in patients with conditions like peptic ulcer or impaired kidney function.
NSAIDs are a chemically diverse group of drugs that are grouped together because they have common analgesic, antipyretic, and anti-inflammatory effects. They work by inhibiting cyclooxygenase (COX) enzymes and reducing the production of prostaglandins. NSAIDs are generally weaker analgesics than opioids except for inflammatory pain conditions. Common adverse effects include gastrointestinal irritation and potential kidney toxicity. Newer selective COX-2 inhibitors were developed to reduce gastrointestinal side effects.
Dr. Jannatul Ferdoush discusses pain and its components, including perception of pain and emotional response. She then covers the central and peripheral regulation of pain, including the roles of substances like bradykinin, prostaglandins, opioids, and the descending inhibitory pathway. Finally, she classifies analgesics as either peripherally or centrally acting and discusses factors to consider when choosing an analgesic, such as the origin and severity of pain.
NSAIDs are a class of drugs that relieve pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. There are various types of NSAIDs classified by their chemical structure. All NSAIDs work by blocking prostaglandin production, but they differ in their selectivity for COX-1 vs COX-2 enzymes. Common adverse effects include gastrointestinal irritation and bleeding, as well as renal impairment. NSAIDs are commonly used to treat pain, fever, and inflammatory conditions like arthritis.
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.
Anti histamine.First generation, second generation,Antagonism of histamine ...FarsanaM
This document discusses antihistamines and their mechanisms of action. It describes the four main histamine receptors (H1, H2, H3, H4) and how antihistamines work by competitively binding to H1 receptors. Antihistamines are classified as first or second generation. First generation antihistamines are more sedating due to other receptor interactions, while second generation antihistamines are more selective for H1 receptors with less sedation side effects. Antihistamines are used to treat allergic conditions by blocking the effects of histamine at H1 receptors and relieving symptoms like itching, hives, and swelling.
This document provides an overview of analgesics, with a focus on non-steroidal anti-inflammatory drugs (NSAIDs). It defines pain and discusses the classification, mechanism of action, and history of analgesics. NSAIDs are introduced as a class of drugs that relieve pain and inflammation by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. The document outlines the role of prostaglandins in inflammation and bone resorption, as well as the beneficial and harmful actions of NSAIDs through COX inhibition. Host modulation is discussed as a treatment concept in periodontics where NSAIDs may reduce tissue destruction by modulating the host inflammatory response.
Inflammation is the body's natural response to injury or infection and involves increased blood flow, immune cell activity, and pain. Nonsteroidal anti-inflammatory drugs (NSAsIDs) like aspirin work by inhibiting the cyclooxygenase enzymes, decreasing the production of prostaglandins which mediate inflammation. Aspirin is unique in that it irreversibly inhibits cyclooxygenase. At normal doses, aspirin is hydrolyzed to salicylate which has analgesic, antipyretic, and anti-inflammatory effects. However, NSAIDs can cause adverse gastrointestinal, platelet, renal, and respiratory effects that require consideration of risks and benefits of long-term use.
This document provides an overview of anticholinergic drugs, including:
- Their classification into natural alkaloids, semisynthetic derivatives, and synthetic compounds.
- Their mechanisms of action as muscarinic receptor antagonists and effects on various organ systems like the CNS, eyes, cardiovascular, respiratory, gastrointestinal, and urinary systems.
- Examples of individual drugs from each class and their therapeutic uses for conditions like Parkinson's disease, peptic ulcers, overactive bladder, respiratory diseases, and more.
- Information on pharmacokinetics, pharmacology, interactions, contraindications, and belladonna poisoning from anticholinergic overdose.
The document summarizes key aspects of the nervous system, including the central nervous system (brain and spinal cord), peripheral nervous system, and autonomic nervous system. It describes the sympathetic and parasympathetic divisions of the autonomic nervous system which provide involuntary control of organs. It also outlines the basic structure and function of neurons, neurotransmission, and the roles of key neurotransmitters like acetylcholine and norepinephrine.
Pharmacology of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs (Dr. Sohail Ahmad)Sohail Ahmad
NSAIDs work by inhibiting the biosynthesis of prostanoids like prostaglandins and thromboxane by blocking the cyclooxygenase (COX) enzyme. Aspirin is a non-selective NSAID that irreversibly inhibits both COX-1 and COX-2 isoforms, reducing inflammation and pain. It is used for conditions like arthritis but can cause gastrointestinal adverse effects. Newer selective COX-2 inhibitors have fewer gastrointestinal side effects.
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 provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
This document discusses alpha blockers, which are drugs that inhibit the interaction of hormones like norepinephrine with alpha receptors. It describes their classification as selective or non-selective, their functions in relaxing smooth muscle and reducing vasoconstriction, and individual drugs like prazosin, terazosin, and doxazosin. These drugs are important in managing conditions like pheochromocytoma, benign prostatic hyperplasia, hypertension, and peripheral vascular disease, but can cause adverse effects like postural hypotension and reflex tachycardia.
1. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, mainly COX-1 and COX-2, which decreases prostaglandin synthesis and produces their pharmacological effects. Selective COX-2 inhibitors have fewer side effects than non-selective NSAIDs.
2. NSAIDs have analgesic, antipyretic, and anti-inflammatory effects. Common side effects include gastric irritation, ulcers, renal impairment, and platelet dysfunction.
3. Aspirin has antiplatelet effects useful for cardiovascular protection. Indomethacin is potent but non-selective. Paracetamol is safer for those with bleeding risks but less effective at inflammation. COX-
This document discusses different classes of skeletal muscle relaxants, including neuromuscular blockers and spasmolytic drugs. It describes their mechanisms of action, pharmacokinetics, and adverse effects. Neuromuscular blockers are classified as depolarizing (like succinylcholine) or non-depolarizing (like tubocurarine and rocuronium) and work by preventing acetylcholine from acting at the neuromuscular junction. Spasmolytic drugs used for chronic muscle spasms include baclofen, diazepam, and tizanidine which act in the central nervous system, and dantrolene which acts directly on muscle.
This document summarizes a seminar on hypertension and antihypertensive drugs presented by Debam Chakrabarty. It defines hypertension and blood pressure, describes symptoms of hypertension. It also explains what antihypertensive drugs are, how they work, and examples of different classes of antihypertensive drugs. The document lists side effects of various antihypertensive drugs and natural ways to treat hypertension. It also discusses the structure and synthesis of some antihypertensive drugs and provides updates on new antihypertensive drugs under development.
This document discusses analgesics and anti-inflammatory agents. It begins by defining pain and inflammation, then discusses how analgesics work by selectively relieving pain without altering consciousness. It classifies different types of analgesics and anti-inflammatory agents like salicylates, propionic acid derivatives, aryl-acetic acid derivatives, and preferential/selective COX-2 inhibitors. For each drug class, it provides examples of drugs, discusses mechanisms of action, pharmacokinetics, uses, and adverse drug reactions. The document concludes by summarizing the mechanism of action of NSAIDs in inhibiting cyclooxygenase and thereby decreasing prostaglandin formation and pain/inflammation.
This document summarizes analgesics used to treat pain. It describes how analgesics work on the central and peripheral nervous system. It discusses opioid analgesics like morphine which work on mu receptors in the spinal cord. It also discusses non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, aspirin and paracetamol which inhibit cyclooxygenase enzymes. The document outlines the mechanisms, effects, uses and side effects of various classes of analgesics as well as combination analgesic therapies for treating dental pain.
This is an lecture presentation for MBBS Semester 1 students. Here we discuss cholinergic agonists and anticholinesterase drugs. We end up discussing about OP poisoning in brief.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
This document discusses autonomic neurotransmission and cholinergic drugs. It begins by describing the anatomy and components of the autonomic nervous system, including the sympathetic, parasympathetic, and enteric divisions. It then focuses on cholinergic neurotransmission, outlining the steps of impulse conduction, transmitter release, transmitter action on post-junctional membranes, post-junctional activity, and termination of transmitter action. Finally, it discusses cholinergic drugs that act as direct parasympathomimetics like choline esters or alkaloids, as well as indirect anticholinesterases that inhibit the termination of cholinergic transmission.
Introduction to Opioid analgesis, Terms, History, Classification, Morphine, Opioid receptors, Mechanism of action, Pharmacological actions of morphine, Pharmacokinetics, Adverse effects, Contraindications, Therapeutic uses
Presented by
B . Kranthi Kumar
Department of Pharmacology
Non-steroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the enzyme cyclooxygenase (COX) and subsequent prostaglandin synthesis. They are classified based on selectivity for COX-1 vs COX-2. Common side effects include gastric irritation, while selective COX-2 inhibitors were developed to reduce this but increase cardiovascular risk. NSAIDs are used for analgesic, antipyretic and anti-inflammatory effects in conditions like arthritis, but choice depends on safety profile and potency needed.
Inflammation is the body's natural response to injury or infection and involves increased blood flow, immune cell activity, and pain. Nonsteroidal anti-inflammatory drugs (NSAsIDs) like aspirin work by inhibiting the cyclooxygenase enzymes, decreasing the production of prostaglandins which mediate inflammation. Aspirin is unique in that it irreversibly inhibits cyclooxygenase. At normal doses, aspirin is hydrolyzed to salicylate which has analgesic, antipyretic, and anti-inflammatory effects. However, NSAIDs can cause adverse gastrointestinal, platelet, renal, and respiratory effects that require consideration of risks and benefits of long-term use.
This document provides an overview of anticholinergic drugs, including:
- Their classification into natural alkaloids, semisynthetic derivatives, and synthetic compounds.
- Their mechanisms of action as muscarinic receptor antagonists and effects on various organ systems like the CNS, eyes, cardiovascular, respiratory, gastrointestinal, and urinary systems.
- Examples of individual drugs from each class and their therapeutic uses for conditions like Parkinson's disease, peptic ulcers, overactive bladder, respiratory diseases, and more.
- Information on pharmacokinetics, pharmacology, interactions, contraindications, and belladonna poisoning from anticholinergic overdose.
The document summarizes key aspects of the nervous system, including the central nervous system (brain and spinal cord), peripheral nervous system, and autonomic nervous system. It describes the sympathetic and parasympathetic divisions of the autonomic nervous system which provide involuntary control of organs. It also outlines the basic structure and function of neurons, neurotransmission, and the roles of key neurotransmitters like acetylcholine and norepinephrine.
Pharmacology of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs (Dr. Sohail Ahmad)Sohail Ahmad
NSAIDs work by inhibiting the biosynthesis of prostanoids like prostaglandins and thromboxane by blocking the cyclooxygenase (COX) enzyme. Aspirin is a non-selective NSAID that irreversibly inhibits both COX-1 and COX-2 isoforms, reducing inflammation and pain. It is used for conditions like arthritis but can cause gastrointestinal adverse effects. Newer selective COX-2 inhibitors have fewer gastrointestinal side effects.
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 provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
This document discusses alpha blockers, which are drugs that inhibit the interaction of hormones like norepinephrine with alpha receptors. It describes their classification as selective or non-selective, their functions in relaxing smooth muscle and reducing vasoconstriction, and individual drugs like prazosin, terazosin, and doxazosin. These drugs are important in managing conditions like pheochromocytoma, benign prostatic hyperplasia, hypertension, and peripheral vascular disease, but can cause adverse effects like postural hypotension and reflex tachycardia.
1. NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, mainly COX-1 and COX-2, which decreases prostaglandin synthesis and produces their pharmacological effects. Selective COX-2 inhibitors have fewer side effects than non-selective NSAIDs.
2. NSAIDs have analgesic, antipyretic, and anti-inflammatory effects. Common side effects include gastric irritation, ulcers, renal impairment, and platelet dysfunction.
3. Aspirin has antiplatelet effects useful for cardiovascular protection. Indomethacin is potent but non-selective. Paracetamol is safer for those with bleeding risks but less effective at inflammation. COX-
This document discusses different classes of skeletal muscle relaxants, including neuromuscular blockers and spasmolytic drugs. It describes their mechanisms of action, pharmacokinetics, and adverse effects. Neuromuscular blockers are classified as depolarizing (like succinylcholine) or non-depolarizing (like tubocurarine and rocuronium) and work by preventing acetylcholine from acting at the neuromuscular junction. Spasmolytic drugs used for chronic muscle spasms include baclofen, diazepam, and tizanidine which act in the central nervous system, and dantrolene which acts directly on muscle.
This document summarizes a seminar on hypertension and antihypertensive drugs presented by Debam Chakrabarty. It defines hypertension and blood pressure, describes symptoms of hypertension. It also explains what antihypertensive drugs are, how they work, and examples of different classes of antihypertensive drugs. The document lists side effects of various antihypertensive drugs and natural ways to treat hypertension. It also discusses the structure and synthesis of some antihypertensive drugs and provides updates on new antihypertensive drugs under development.
This document discusses analgesics and anti-inflammatory agents. It begins by defining pain and inflammation, then discusses how analgesics work by selectively relieving pain without altering consciousness. It classifies different types of analgesics and anti-inflammatory agents like salicylates, propionic acid derivatives, aryl-acetic acid derivatives, and preferential/selective COX-2 inhibitors. For each drug class, it provides examples of drugs, discusses mechanisms of action, pharmacokinetics, uses, and adverse drug reactions. The document concludes by summarizing the mechanism of action of NSAIDs in inhibiting cyclooxygenase and thereby decreasing prostaglandin formation and pain/inflammation.
This document summarizes analgesics used to treat pain. It describes how analgesics work on the central and peripheral nervous system. It discusses opioid analgesics like morphine which work on mu receptors in the spinal cord. It also discusses non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, aspirin and paracetamol which inhibit cyclooxygenase enzymes. The document outlines the mechanisms, effects, uses and side effects of various classes of analgesics as well as combination analgesic therapies for treating dental pain.
This is an lecture presentation for MBBS Semester 1 students. Here we discuss cholinergic agonists and anticholinesterase drugs. We end up discussing about OP poisoning in brief.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
This document discusses autonomic neurotransmission and cholinergic drugs. It begins by describing the anatomy and components of the autonomic nervous system, including the sympathetic, parasympathetic, and enteric divisions. It then focuses on cholinergic neurotransmission, outlining the steps of impulse conduction, transmitter release, transmitter action on post-junctional membranes, post-junctional activity, and termination of transmitter action. Finally, it discusses cholinergic drugs that act as direct parasympathomimetics like choline esters or alkaloids, as well as indirect anticholinesterases that inhibit the termination of cholinergic transmission.
Introduction to Opioid analgesis, Terms, History, Classification, Morphine, Opioid receptors, Mechanism of action, Pharmacological actions of morphine, Pharmacokinetics, Adverse effects, Contraindications, Therapeutic uses
Presented by
B . Kranthi Kumar
Department of Pharmacology
Non-steroidal anti-inflammatory drugs (NSAIDs) work by inhibiting the enzyme cyclooxygenase (COX) and subsequent prostaglandin synthesis. They are classified based on selectivity for COX-1 vs COX-2. Common side effects include gastric irritation, while selective COX-2 inhibitors were developed to reduce this but increase cardiovascular risk. NSAIDs are used for analgesic, antipyretic and anti-inflammatory effects in conditions like arthritis, but choice depends on safety profile and potency needed.
This document provides an overview of analgesic drugs including definitions of pain, classifications of analgesics, and details on specific drugs. It discusses:
1) Definitions of pain and classifications as acute vs chronic and by severity. Analgesics are classified as non-opioid (e.g. NSAIDs, paracetamol) or opioid.
2) Mechanisms of action for different classes of drugs including NSAIDs inhibiting COX enzymes and paracetamol inhibiting prostaglandin synthesis in the CNS.
3) Specific drugs like aspirin, ibuprofen, naproxen, and details on indications, mechanisms of action, and adverse effects. Selective COX-2 inhibitors and
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.
This document provides information about NSAIDs (non-steroidal anti-inflammatory drugs). It defines NSAIDs as non-narcotic analgesics that have anti-inflammatory, antipyretic, and uricosuric properties. The document discusses the mechanisms of action of NSAIDs, including their inhibition of the cyclooxygenase enzyme which reduces prostaglandin synthesis. Various classes of NSAIDs are described based on their selectivity for the COX-1 and COX-2 isoenzymes. The therapeutic uses, pharmacokinetics, and adverse effects of common NSAIDs like aspirin, ibuprofen, indomethacin, and ketorolac are summarized.
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 summarizes nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses how NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and thereby decreasing production of prostaglandins involved in pain, fever and inflammation. NSAIDs are classified based on selectivity for COX-1 versus COX-2. Key points covered include the physiological roles of prostaglandins, properties and side effects of common NSAIDs like aspirin, ibuprofen, naproxen, and COX-2 inhibitors, as well as their various clinical uses and precautions.
This document discusses NSAIDs (non-steroidal anti-inflammatory drugs), their mechanisms of action, and effects. NSAIDs work by inhibiting the COX enzymes COX-1 and COX-2, which produce prostaglandins involved in inflammation, fever, and pain. Common NSAIDs like aspirin are effective for relieving mild to moderate pain and reducing fever and inflammation, but can have adverse effects on the gastrointestinal tract and kidneys. The document outlines the specific actions and uses of aspirin and paracetamol, as well as their mechanisms of toxicity.
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.
Analgesic is a drug that relieves pain by acting on the CNS or on the peripheral pain mechanism without altering consciousness
Opioid analgesics
Non Opioid analgesics (NSAIDs)
NSAIDs are non-steroidal anti-inflammatory drugs. These are not only pain killers but also are anti-inflammatory drugs that are widely used in dentistry. These are weaker analgesics, also called nonnarcotic or aspirin-like or antipyretic analgesics. They do not depress CNS, do not produce physical dependence, and have no abuse liability. They act primarily on peripheral pain mechanisms.
Inflammation is the body's protective response to injury or infection that can lead to tissue damage. Inappropriate activation of the immune system can cause inflammation and lead to autoimmune diseases like rheumatoid arthritis (RA). In RA, white blood cells attack the synovium, stimulating T lymphocytes and macrophages to secrete pro-inflammatory cytokines that cause further inflammation and joint damage. Nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs) are used to treat RA by reducing inflammation and slowing disease progression. NSAIDs work by inhibiting cyclooxygenase enzymes and reducing prostaglandin production, while DMARDs target specific inflammatory cytokines involved in RA pathogenesis.
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.
The document discusses pain and analgesics like NSAIDs and paracetamol. It describes how NSAIDs work by inhibiting the cyclooxygenase enzymes COX-1 and COX-2, which are responsible for prostaglandin synthesis. NSAIDs are classified as non-selective or selective COX inhibitors. Aspirin is a prototype non-selective NSAID that is used for analgesia, antipyresis and inflammation. Its mechanism of action, pharmacokinetics, therapeutic uses and side effects are detailed. Paracetamol is discussed as a non-NSAID analgesic-antipyretic that is metabolized in the liver and can cause toxicity in overdose through its reactive metabolite NAP
5) NON STEROIDAL ANTI INFLAMMATORY DRUGS.pptVarshaPatel72
NSAIDs work by inhibiting the enzyme cyclooxygenase, which prevents the formation of prostaglandins responsible for pain and inflammation. They have analgesic, antipyretic, and anti-inflammatory effects. Common NSAIDs include aspirin, ibuprofen, naproxen, and celecoxib. While effective at reducing pain and inflammation, NSAIDs can cause gastrointestinal irritation and bleeding. Due to their safety risks, use should be discussed with a medical provider.
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.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin. It provides details on their mechanism of action as cyclooxygenase inhibitors, reducing prostaglandin synthesis and inflammation. Common uses include analgesia, antipyresis, and reducing the risk of cardiovascular events like heart attacks. Adverse effects include gastrointestinal irritation and bleeding. Aspirin is prototypical and its pharmacology and therapeutic uses are discussed in depth.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs), including their uses for pain, fever, and inflammation. It classifies NSAIDs based on their chemistry and half-lives. The mechanisms of NSAID action and their therapeutic effects such as analgesia, antipyresis, and anti-inflammation are described. Adverse effects involving the gastrointestinal tract and kidneys are also summarized. Specific NSAIDs like aspirin, diclofenac, ketorolac, and tolmetin are highlighted regarding their pharmacology, administration, and indications.
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 discusses ocular NSAIDs and steroids, their uses, and indications. It begins with an introduction to inflammation and the inflammatory response. It then discusses the mechanisms of action of NSAIDs, including their inhibition of prostaglandin synthesis. Various topical ocular NSAIDs are presented, along with their indications for use in preoperative miosis prevention, postoperative inflammation, cystoid macular edema, conjunctivitis, corneal pain, and other conditions. Dosing regimens are provided for common NSAID medications.
Similar to Non Steroidal Anti Inflammatory Drugs (20)
The external carotid artery arises from the common carotid artery and supplies structures in the head and neck. It gives off several branches in the neck including the superior thyroid artery and lingual artery. The lingual artery travels deep to the hyoglossus muscle in three parts before terminating on the undersurface of the tongue. The facial artery arises from the external carotid and has both cervical and facial parts to its course where it supplies structures in the face such as the lips and nose. It gives off branches like the ascending palatine and tonsillar arteries in the neck.
Trigeminal neuralgia is a disorder causing severe facial pain. It affects branches of the trigeminal nerve, the largest cranial nerve. The pain is usually sudden, severe, and described as electric shock-like. It is commonly triggered by trivial stimuli like talking or brushing teeth. Treatment options include medications like carbamazepine or surgery to decompress the trigeminal nerve if medications do not provide relief from pain.
This document provides an overview of the various types of instruments used in exodontia (tooth extraction). It begins with a brief introduction and objectives. It then covers the history of dental instruments and moves into sections on diagnostic instruments, instruments for attaining asepsis, anesthetic tools, instruments for gaining surgical access and retracting tissues, extraction forceps for different types and locations of teeth, elevators, suturing instruments, and miscellaneous tools. In summary, it provides a comprehensive review of the armamentarium, or complete set of instruments, used in tooth extraction and related procedures.
The document provides information about blood transfusion including:
- It discusses the components of blood including plasma, red blood cells, white blood cells and platelets.
- The history of blood transfusion is summarized beginning in the 17th century and developments through the 20th century including the discovery of blood groups.
- Important blood groups discussed are ABO, Rh, and other groups like MN, Kidd, Duffy and Bombay.
- Indications for blood transfusion include external and internal bleeding, anemia, and blood disorders.
- The document outlines donor selection processes including testing, history screening, blood typing and cross matching.
- Common blood products are discussed such as packed red
Access osteotomies in oral & cranio-maxillofacial surgeryDr Rayan Malick
This document discusses various surgical approaches and osteotomies for accessing lesions in the skull base and deep neck spaces. It begins with an introduction and history of access osteotomy. It then discusses the indications, classifications, advantages/disadvantages of different approaches like Lefort I/II osteotomies, zygomatic osteotomies, and transpalatal approaches. Specific approaches like fronto-orbitozygomatic and transnaso-orbitomaxillary are also summarized. The goal of these osteotomies is to provide direct surgical access while minimizing trauma.
This document discusses oroantral fistula, which is a pathological communication between the oral cavity and maxillary sinus. It can develop after maxillary tooth extractions or other surgical procedures if the communication is not properly closed. The document covers the anatomy of the maxillary sinus, causes of oroantral fistula, clinical signs and symptoms, diagnostic tests, and various surgical treatment options like buccal flaps and palatal rotational flaps to close the communication. Autogenous tissue flaps are often used to close openings under 4mm, while larger defects require excision and closure with flaps to prevent complications like sinus infection or food entering the sinus.
This document provides an overview of temporomandibular joint ankylosis. It begins with definitions and historical perspectives on the condition. It then discusses the etiology, pathogenesis, classifications, anatomy, and treatment approaches for TMJ ankylosis. Key points include that ankylosis involves pathologic changes that limit jaw movement, common causes are trauma, infection, inflammation, and it can be classified as true/false, complete/partial, and bony/fibrous. The document provides detailed anatomy of the TMJ and surrounding structures to inform surgical treatment approaches.
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share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
5. All drugs grouped in this class have three main actions in different
measures:
ANALGESIC
ANTIINFLAMMATORY
ANTIPYRETIC
They are also called
“Nonnarcotic ,Nonopioid ,or Aspirin like analgesics”
Definition:
NSAIDs are chemically diverse class of drugs(>70 NSAIDs in use) that
have antiinflammatory , analgesic, and antipyretic properties.
8. NSAIDs and Prostaglandins
Prostaglandins, Prostacyclins,Thromboxane A2 are produced from
arachidonic acid by the enzyme cyclooxygenase
Cyclooxygenase exists in two forms. They are:
1.Cox-1-Constitutive
(House keeper)
Mucus secretion, Haemostasis, renal functions
2. Cox-2 Inducible-
Inflammatory response
Sites-brain, JG cells (constitutive)
9. Normal Tissue Inflammation Site
Physiolgical
Prostaglandin
Production
Pathological
Prostaglandin
Production
COX-1
Constitutive
COX-2
Inducible
Arachidonic Acid
Normal Functions Inflammation, pain, fever
NSAIDs
COX-2
Inhibitors
Cytokines
Growth factors
ILs,TNF
+
11. Mechanism of action
When a tissue is injured, from any cause, prostaglandin synthesis in
that tissue increases.
PGs have TWO major actions:
They are mediators of inflammation
They also sensitize pain receptors at the nerve endings,
lowering their threshold of response to stimuli and allowing
the other mediators of inflammation
12. Naturally, a drug that prevents the synthesis of PGs is likely to be
effective in relieving pain due to inflammation of any kind
In 1971 Vane and coworkers made the landmark observation that
aspirin and some NSAIDs blocked PG generation.
This they do by inhibiting cyclo –oxygenase (COX) enzyme in the
pathway for PGs synthesis
13. Beneficial actions due to PG synthesis inhibition
Analgesia
Antipyresis
Antiinflammatory
Antithrombotic
Closure of ductus arteriosus
Dysmenorrohea
14. Analgesia
PGs---induce hyperalgesia by increasing sensitivity of afferent nerve
endings to chemical and mechanical stimuli and thus amplify action
of other algesics-bradykinins, histamine, TNF-alpha, ILs.
NSAIDS block this pain sensitizing mechanism induced by these
algesics, therefore effective against inflammation associated pain.
15. Antipyresis
Fever in infection is produced by pyrogens, TNF, ILs, interferon-
induce production of PGs in hypothalamus-raise its temprature set
point.
NASIDs block the action of pyrogens(cox-2).
16. Anti-inflammatory
Inhibition of PG synthesis at the site of injury.
Anti-inflammatory action of each drug corresponds with their
potency to inhibit COX.
17. Antiplatelet
Inhibit synthesis of TXA2 by acetylating platelet COX irreversibly.
By inhibiting platelet aggregation lowers the incidence of
reinfarction.
18. Ductus arteriosus closure
PGE2, responsible for maintaining patency in foetal circulation.
At birth ductus closes
19. Dysmenorrhea
Involvement of PG’s in dysmenorrhea is demonstrated by
Increase levels of PGs in menstrual blood flow
Endometrial biopsies
PGF2 metabolite in circulation are raised in dysmenorrhoeic
women
Myometrial ischemia –menstrual cramps.
NSAIDs-lowers uterine PGs--relief
20. Renal effects
Conditions like hypovolaemia, decrease renal perfusion, and Na+
loss- induce renal PG synthesis –leading to vasodilatation, inhibition
of cl, Na, water reabsorption and opposing Antidiuretic action.
NSAIDs produce renal effects by-
1. Cox-1 dependent impairment of renal blood flow and reduction in
gfr- can worsen renal insufficiency.
2. JG Cox 2 dependent Na and water retention.
3. Rare ability to cause papillary necrosis on habitual intake.
Renal effects more marked in patients of
CHF, hypovolemia, hepatic cirrhosis, renal disease and patients on
diuretics and antihypertensives----edema can occur
21. Parturition
Sudden increase in PG synthesis by uterus triggers labour and
facilitate progression.
NSAIDs –delay and retard labour
22. Shared toxicities due to PG synthesis
inhibition
Gastric mucosal damage
Bleeding
Limitation of renal blood flow/Na+ & water retention
Delay/prolongation of labour
Asthma and anaphylactoid reactions in susceptible individuals
23. Gastric mucosal damage
Inhibition of synthesis of gastro protective PGS (E2,I2)- decrease in
mucus,HCO3,increases acid secretion, may promote mucosal
ischemia.
24. Bleeding
Inhibition of platelet function
Bleeding time is prolonged
Risk of surgical bleeding is increased
26. Salicylates-Aspirin
Aspirin is acetyl salicylic acid converted in body to salicylic acid.
Mechanism of action - aspirin inhibits COX irreversibly by
acetylating one of its serine residue.
27. Pharmacological actions
1.Analgesic- Relives pain related to inflammation, tissue injury,
MOA: -Obtunding peripheral receptors
-Prevents PGs mediated nerve ending sensitization.
-Raises threshold for pain perception in central sub cortical regions.
2.Antipyretic- Resets the hypothalamic thermostat and reduces fever by
promoting heat loss.
28. 3.Antiinflammatory-
Signs of inflammation like pain, tenderness, swelling, vasodilatation and
leukocyte infiltration are suppressed.
4.Metabolic effects-
At anti-inflammatory doses there is:
-Increased cellular metabolism
-Increased heat production
-decrease blood sugar level(especially in diabetics)
But in toxic doses hyperglycemia is often seen.
29. 5. Respiration:
-At anti-inflammatory doses – respiration is stimulated
-In salicylate poisoning- hyperventilation is prominent
-Further rise in salicylate level causes respiratory depression
6. Acid – base and electrolyte balance:
-Initially increased Co2 production and its washout causes respiratory alkalosis.
-Later Co2 retention causes respiratory acidosis (high doses)
-Followed by metabolic acidosis.
-Dehydration occurs in poisoning.
30. 7. CVS:
-In therapeutic doses – no direct effect
-At toxic doses –depresses vasomotor centre – BP may fall
-CHF may be precipitated
8. GIT:
-Causes epigastric distress, nausea and vomiting
-Focal necrosis of mucosal cells and capillaries- acute ulcers, erosive
gastritis, congestion and microscopic hemorrhages
31. 9. Urate excretion: Dose related effect:
< 2g/day - urate retention and antagonism of all other uricosuric drugs.
2-5g/day – often no change
>5g/day – increased urate excretion
10.Blood:
-TXA2 synthesis inhibition
-Interferes with platelet aggregation
-Bleeding time is prolonged
32. Pharmacokinetics
Absorbed from stomach and small intestine
Poor water solubility is the limiting factor
Solubility is more at higher pH
Rapidly deacetylated in the gut wall, liver, plasma and other tissues
to salicylic acid
80% bound to proteins
Volume of distribution=0.17L/kg
Slowly enters the brain but freely crosses placenta
33. Conjugated in the liver by glycine and glucuronic acid
Excreted by glomerular filtration as well as tubular secretion
t1/2 of aspirin as such is 15-20min
Taken together with that of released salicylic acid is 3-5hrs
Metabolic processes get saturated over therapeutic range
t1/2 of antiinflammatory doses may be 8-12hrs
While that during poisoning may be upto 30hrs
Thus elimination is dose dependant
34. Adverse effects
a) Gastrointestinal:
Most common
Epigastric distress, Nausea, Vomiting
Increased occult blood loss in stools
Gastric mucosal damage and peptic ulcer
b) Rey’s syndrome:
Occurs in infants and children
Occurs when aspirin given during viral infections
Characterized by liver damage and encephalopathy
Replaced by acetaminophen in such condition to reduce fever
35. c) Hypersensitivity:
Though infrequent, these can be serious
Reactions include; rashes, urticaria, angioedema, rhinorrhoea,
asthma and anaphylactoid shock
d) Salicylism:
High doses(at antiinflammatory doses) or chronic use of aspirin
may induce a syndrome characterised by tinnitus, hearing defects,
blurring of vision, dizziness, headache and mental confusion
Effects are reversible
36. e) Acute salicylate poisoning:
More common in children
Fatal dose in adults estimated to be 15-30gm, but considerably low
in children
Serious toxicities seen at serum levels >50mg/dl
Manifestations are:
-vomiting, dehydration, electrolyte imbalance, acidotic breathing,
hyper/hypoglycemia, petecheal hemorrhages, restlessness, delirium,
hallucinations, hyperpyrexia, convulsions, coma and death due to
respiratory and cardiovascular failure
37. Treatment:
Symptomatic and supportive
Gastric lavage
i.v. infusion of Na+, K+, HCO3 and glucose(dextrose-5%)
Vitamin K 10mg i.v.
Haemodialysis
38.
39. Interactions
Aspirin displaces warfarin, naproxen, phenytoin from its binding sites-
toxicity of these agents.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to interact with
the oral anticoagulant warfarin and can cause a serious bleeding
complication. NSAIDs can affect the pharmacologic action of warfarin
through their direct interaction. High protein binding and the cytochrome
P450 (CYP)-dependent clearance mechanisms of NSAIDs can affect the
serum levels of warfarin
Choi KH et al. Risk Factors of Drug Interaction between Warfarin and Nonsteroidal Anti-Inflammatory Drugs in Practical
Setting.
Journal of Korean Medical Science. 2010;25(3):337-341
40. Sequential administration of naproxen and low-dose aspirin interferes with
the irreversible inhibition of platelet cyclooxygenase 1 afforded by aspirin.
Salicylates displace phenytoin from plasma binding sites, thus raising its
level in plasma and producing anticonvulsant effect
Anzellotti P et al, Low-dose naproxen interferes with the antiplatelet effects of aspirin in healthy subjects: recommendations
to minimize the functional consequences;Arthritis Rheum. 2011 Mar;63(3):850-9
41. Precautions and contraindications
Peptic ulcer
Sensitive patients
Children suffering from influenza, chickenpox
Chronic liver diseases
Diabetics
CHF, lower cardiac reserve
Pregnancy
Delayed or prolonged labor, more postpartum blood loss, premature closure of
ductus arteriosus
G6PD deficiency
Before elective surgery
Breastfeeding mothers
42. Interactions
Aspirin displaces warfarin, naproxen, sulfonylureas, phenytoin from
its plasma proteins binding sites-toxicity of these agents.
Inhibits tubular secretion of uric acid and antagonizes action of
uricosuric agents.
Blunts action of diuretics
43. Uses:
1. As analgesic-
Aspirin 300mg-600mg 6-8.hlly
2. As antipyretic
3. Acute rheumatic fever 4-5 g/day
4. Rheumatoid arthritis 3-5 g/day
5. Osteoarthitiis
6. Post myocardial infraction & post stroke patients
Aspirin 60-100mg/day
7. Other-
pregnancy induced hypertension
preeclampsia
to delay labour
to close patent ductus arteriosus
45. Propionic acid Derivatives
These are:
Ibuprofen, naproxen, flurbiprofen and ketoprofen
Analgesic, antipyretic and anti-inflammatory efficacy is lower
than high dose of aspirin.
All inhibit PG synthesis
47. Pharmacokinetics
Well absorbed orally
Highly bound to plasma proteins
Can cross placenta
Metabolised in liver by hydroxylation
Excreted in urine as well as bile
50. Anthranilic acid derivatives-
Mephenamic acid
Analgesic, antipyretic, anti-inflammatory
Inhibits COX
Antagonizes certain actions of PGs
Exerts peripheral as well as central analgesic action
Adverse effects:
diarrhea,
epigastric distress,
skin rashes, dizziness
haemolytic anaemia
51. Pharmacokinetics:
Oral absorption is slow but complete
Highly bound to plasma proteins.
Excreted in urine as well as bile.
Plasma t1/2 is 2-4 hours
Uses- analgesic,
effective in dysmenorrhea
Dose- 250-500mg TDS
Trade name:
MEDOL(250, 500mg cap), MEFTAL(250,500mg tab)
52. Aryl - acetic acid derivative-
Diclofenac sodium, Aceclofenac
Analgesic, antipyretic, anti-inflammatory
Similar in efficacy to naproxen
Inhibits PG synthesis and is somewhat cox-2 selective
Anti inflammatory action- reduces neutrophil chemotaxis and
superoxide production at the inflammatory site
53. Pharmacokinetics
Well absorbed orally
99% protein bound
Metabolised and excreted both in urine and bile
Plasma t1/2 is 2 hours
Has good tissue penetrability and concentration in synovial fluid is
maintained for 3 times longer than in plasma
56. Para-amino phenol Derivatives
Paracetamol:(acetaminophen)
Deethylated active metabolite of phenacetin
Mechanism of action:
Poor inhibitor of PG synthesis in peripheral tissues
More active on cox in brain
So, poor peripheral antiinflammatory component , more potent as
analgesic and antipyretic
57. Pharmacokinetics:
Well absorbed orally
25% plasma protein bound
Metabolism occurs mainly by conjugation with glucuronic acid and
sulfate
Excreted rapidly in urine
T1/2 is 2-3 hours
Adverse effects:
In isolated antipyretic doses paracetamol is safe and well tolerated
Rashes and nausea occur occasionally
58. Analgesic nephropathy:
• Occurs after years of heavy ingestion
• Papillary necrosis, tubular atrophy, renal fibrosis occurs
• Urine concentrating ability is lost
• Kidneys shrink
Acute paracetmol poisoning:
• Occurs in small children having low hepatic glucuronide conjugating
ability
• If a large doses is taken (>150mg/kg or >10 gm in an adult)
59. Manifestations:
Nausea, vomiting, abdominal pain, liver tenderness
After 12-18 hours centrilobular hepatic necrosis
Hypoglycaemia may progress to coma
Treatment:
Vomiting should be induced
Gastric lavage
Activated charcoal is given
N-acetylcysteine(MUCOMIX, ANTIFEN 2OOmg/ml inj)
60. Uses:
As analgesic for headache, mild migraine, musculoskeletal pain
Dysmenorrhoea
Osteoarthritis
As antipyretic
Dose:
0.5-1gm TDS
Trade name:
CROCIN(0.5,1gm tab), CALPOL(500mg tab)
61. Oxicam derivatives- Piroxicam
Long acting potent NSAID with anti inflammatory potency similar
to Indomethacin
Good analgesic and antipyretic action
Reversible inhibitor of cox
In addition it decreases the production of IgM rheumatoid factor and
leucocyte chemotaxis
62. Pharmacokinetics
Rapidly and completely absorbed
99% plasma protein bound
Metabolised in liver by hydroxylation and glucuronide conjugation
Excreted in urine and bile
Plasma t1/2 is 2 days
Adverse effects:
• Gastrointestinal side effects are more than ibuprofen, but it is better tolerated and
less ulcerogenic than indomethacin.
• Less faecal blood loss than aspirin
63. Uses:
Rheumatoid and osteoarthritis
ankylosing spondylitis,
toothache, dysmenorrhea
acute gout
Dose:
20 mg bd for two days followed by 20 mg od
Trade name:
DOLONEX, PIROX(10,20 mg cap)
64. Pyrrolo-pyrrole derivative-Ketorolac
Acetic acid derivative
Potent analgesic and modest anti inflammatory activity.
In post operative pain it has equaled efficacy of morphine but do
not have morphine like side effects.
It inhibits PG synthesis
65. PHARMACOKINETICS:
Rapidly absorbed after oral and IM administration
Highly plasma protein bound
Excreted in urine
Plasma t1/2 is 5-7 hours
Adverse effects:
Nausea, abdominal pain,
dyspepsia, ulceration,
ulceration, loose stools
drowsiness, pain at injection site
66. Uses:
1. Post operative pain
2. Acute musculoskeletal pain
3. Renal colic
4. Migraine
5. Pain due to metastasis
6. Dental pain
Dose:
15-30mg i.m. or i.v. every 4-6 hours(max. 90mg/day)
Orally 10-20 mg 6 hourly for not more than 5 days
Trade name:
KETOROL, KETANOV(10mg tab)
67. Indole derivatives- Indomethacin
• Potent anti-inflammatory with prompt antipyretic action
• Inhibits PG synthesis
• Suppresses the neutrophil motility
PHARMACOKINETICS:
Well absorbed orally, rectal absorption is slow
Highly plasma protein bound
Metabolised in liver
Excreted in urine
Plasma t1/2 is 2-5 hours
68. Adverse effects:
• High incidence of GIT and CNS side effects
Gastric irritation, nausea, anorexia
gastric bleeding, diarrhea
frontal headache, dizziness
mental confusion, psychosis
Uses:
Because of prominent adverse effects indomethacin is used as a reserve
drug in conditions requiring potent anti-inflammatory action like:
Ankylosing spondylitis,
acute exacerbation of destructive arthropathies,
psoriatic arthritis,
acute gout
69. Other uses:
Malignancy associated fever
Bartter’s syndrome
For closure of patent ductus arteriosus
Dose:
25-50mg bd orally
Three 12 hourly doses of 0.1-0.2 mg/kg for closure of ductus
arteriosus
Trade name:
INDOFLAM(25, 75 mg cap), IDICIN(25,27 mg cap)
70. Pyrazolone Derivatives
Aminopyrine and antipyrine:
Introduced in 1884
Associated with agranulocytosis, are banned in many countries
including India.
Phenylbutazone and oxyphenbutazone:
Introduced in 1949
Potent anti-inflammatory drugs
Gastric toxicity is high
Edema and CNS side effects are seen
Hence now it is rarely used
71. Metamizol:
Derivative of amidopyrine
Potent analgesic and antipyretic
Gastric irritation and pain at injection site occurs
Few cases agranulocytosis were reported
Rarely used now a days
Dose: 0.5-1.5 gm oral/i.m./i.v
Trade name: ANALGIN, NOVALGIN(0.5 gm tab)
72. Preferential COX-2 inhibitors
Nimesulide:
Newer NSAID which is relatively weak inhibitor of PG synthesis
Mechanism of action:
Preferential COX-2 inhibitor
Antiinflammatory action may be exerted by other mechanisms also
such as:
-Reduced generation of superoxide by neutrophils
-Inhibition of TNF-alpha release
73. Pharmacokinetics:
Well absorbed orally
99% plasma protein bound
Excreted mainly in urine
T1/2 2-5 hours
Adverse effects:
Gastrointestinal- epigastralgia, heart burn, nausea, loose motions
Dermatological- rash, pruritus
CNS- dizziness
Liver- hepatic faliure
Renal- haematuria in children
74. Uses:
Used mainly for short-lasting painful conditions-
sport injuries, sinusitis, ear nose disorders,
dental surgery, bursitis, low backache,
dysmenorrhoea, post operative pain,
osteoarthritis
Dose:
100mg bd
Trade name:
NIMULID, NIMEGESIC, NIMODOL(100mg tab)
75. Selective COX-2 Inhibitors
Selectively block COX-2 activity more than COX-1 activity
This group includes:
Celecoxib, Rofecoxib and Valdecoxib
Celecoxib is available in india
Rofecoxib and Valdecoxib have been withdrawn for increasing
cardiovascular risk
76. Celecoxib:
It exerts anti-inflammatory, analgesic, antipyretic action with low
ulcerogenic potential
Pharmacokinetics:
Slowly absorbed, 97% plasma protein bound
Metabolised primarily by CYP2C9
T1/2 is 10 hours
78. REFERENCES
- Goodman and Gilman’s: The pharmacological basis of Therapeutics
12th edition
- Essentials of medical pharmacology, KD Tripathi
- Pharmacology and pharmacotherapeutics, R.S.Satoskar,
S.D.Bhandarkar, 19th edition