This document discusses various chemical mediators involved in inflammation and disease. It describes autacoids like histamine, serotonin, angiotensin, and prostanoids. It discusses their receptors, synthesis, actions, and clinical uses of agonists and antagonists. The document also covers eicosanoids like prostaglandins and leukotrienes, as well as chemokines, cytokines, and analgesics/anti-inflammatory drugs.
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.
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
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.
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 provides information on various non-steroidal anti-inflammatory drugs (NSAIDs) including their classification, mechanisms of action, pharmacokinetics, uses, and side effects. It discusses the history of NSAID development from willow bark to current drugs. NSAIDs are classified based on their structures and selectivities for COX-1 and COX-2 enzymes. Common NSAID mechanisms of action, properties, and side effects related to prostaglandin synthesis inhibition are also summarized. The document reviews individual NSAID drugs like aspirin, ibuprofen, ketorolac, and acetaminophen in detail. It proposes flexible prescription plans for using analgesics after endodontic procedures.
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.
NSAIDs can be categorized into four groups based on their selectivity for inhibiting COX-1 and COX-2 enzymes. Selective COX-2 inhibitors were developed to reduce gastrointestinal side effects, but were later found to increase cardiovascular risks. NSAIDs can affect several body systems including the gastrointestinal, hepatic, renal and cardiovascular systems. Common side effects include ulcers, bleeding, elevated liver enzymes, acute kidney injury and increased risk of heart attack or stroke. The document discusses the mechanisms of these side effects and considerations for prescribing NSAIDs.
- NSAIDs are the most commonly prescribed drugs for chronic pain but can have serious side effects.
- While effective for pain relief and inflammation, all NSAIDs inhibit the COX enzyme and can increase risks of gastrointestinal bleeding, kidney damage, and cardiovascular events.
- Newer COX-2 inhibitors were found to have lower risk of gastrointestinal side effects but similar or higher risk of cardiovascular events compared to other NSAIDs.
- Due to their risks and side effects, NSAIDs should generally only be used at the lowest effective dose for the shortest necessary time period. Non-drug alternatives and treatments should also be considered.
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.
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
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.
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 provides information on various non-steroidal anti-inflammatory drugs (NSAIDs) including their classification, mechanisms of action, pharmacokinetics, uses, and side effects. It discusses the history of NSAID development from willow bark to current drugs. NSAIDs are classified based on their structures and selectivities for COX-1 and COX-2 enzymes. Common NSAID mechanisms of action, properties, and side effects related to prostaglandin synthesis inhibition are also summarized. The document reviews individual NSAID drugs like aspirin, ibuprofen, ketorolac, and acetaminophen in detail. It proposes flexible prescription plans for using analgesics after endodontic procedures.
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.
NSAIDs can be categorized into four groups based on their selectivity for inhibiting COX-1 and COX-2 enzymes. Selective COX-2 inhibitors were developed to reduce gastrointestinal side effects, but were later found to increase cardiovascular risks. NSAIDs can affect several body systems including the gastrointestinal, hepatic, renal and cardiovascular systems. Common side effects include ulcers, bleeding, elevated liver enzymes, acute kidney injury and increased risk of heart attack or stroke. The document discusses the mechanisms of these side effects and considerations for prescribing NSAIDs.
- NSAIDs are the most commonly prescribed drugs for chronic pain but can have serious side effects.
- While effective for pain relief and inflammation, all NSAIDs inhibit the COX enzyme and can increase risks of gastrointestinal bleeding, kidney damage, and cardiovascular events.
- Newer COX-2 inhibitors were found to have lower risk of gastrointestinal side effects but similar or higher risk of cardiovascular events compared to other NSAIDs.
- Due to their risks and side effects, NSAIDs should generally only be used at the lowest effective dose for the shortest necessary time period. Non-drug alternatives and treatments should also be considered.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs) and their effect on renal function. It defines NSAIDs, describes the two main categories, and explains how they work by inhibiting prostaglandin synthesis from arachidonic acid through the COX pathway. The renal effects of prostaglandin inhibition are a decrease in reabsorption in the proximal tubule and vasoconstriction, which can reduce glomerular filtration rate and potentially cause acute renal failure in at-risk patients with long-term use.
This presentation deals with the various non-steroidal antiinflammatory drugs used in day-to-day practice enumerating their mechanism of action, uses, adverse effects, etc.
This document discusses anti-inflammatory drugs and their mechanisms and uses. It focuses on aspirin and other salicylates. It explains that inflammation is a normal response to injury but can become inappropriate, and anti-inflammatory drugs work by blocking prostaglandin synthesis. Aspirin and other NSAIDs are commonly used to treat conditions involving pain, fever and inflammation like arthritis. While effective, these drugs can cause adverse effects like GI issues, bleeding risks and interactions with other medications if not taken carefully.
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 various types of non-narcotic analgesics and muscle relaxants used to treat pain associated with arthritis. It covers disease-modifying antirheumatic drugs and biological DMARDs for rheumatoid arthritis, corticosteroids and their adverse effects, treatments for osteoarthritis and gout, and the traditional stepped care approach to pain management. Specific drugs mentioned include baclofen, carisoprodol, chlorzoxazone, cyclobenzaprine, diazepam, methocarbamol, orphenadrine, azathioprine, cyclophosphamide, hydroxychloroquine, leflunomide, methotrexate, penicillamine, gold salts,
NSAIDs are a class of drugs that provide analgesic, antipyretic, and anti-inflammatory effects by inhibiting the COX enzyme and subsequent prostaglandin production. Aspirin is a prototypical NSAID that is non-selective and irreversibly inhibits both COX-1 and COX-2 isoforms. It is well absorbed but has a short half-life due to rapid metabolism. While effective at reducing pain, fever and inflammation, high doses of aspirin can cause adverse effects like gastric irritation, salicylism, and Reye's syndrome in children. Overdose of aspirin leads to serious toxicity that requires supportive care and dialysis.
The document discusses nonsteroidal anti-inflammatory drugs (NSAIDs). It describes how NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and thereby reducing the production of prostaglandins involved in inflammation, pain, and fever. NSAIDs are commonly used to treat inflammation and pain conditions like arthritis as well as fever. Common NSAIDs include aspirin, ibuprofen, and naproxen. The document outlines their mechanisms of action, therapeutic uses, and potential adverse effects like gastrointestinal irritation and hypersensitivity reactions.
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 summarizes anti-inflammatory drugs. It discusses the inflammatory process and mediators like histamine, prostaglandins, leukotrienes and thromboxane A2. It describes the three phases of inflammation and signs like redness, heat, swelling and pain. Two major classes of anti-inflammatory drugs are discussed: steroidal anti-inflammatory drugs (SAIDs) like cortisone and hydrocortisone, and non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin, ibuprofen and naproxen. The mechanisms, common uses and potential side effects of various NSAIDs are outlined.
The document discusses autacoids and inflammation. It describes how within 5 minutes of being stung by a bee, a boy develops a swollen, red lesion at the site of injury. The predominant finding in tissue from the lesion would be neutrophilic migration (D). Autacoids like eicosanoids and histamine are involved in the inflammatory response and produce effects like vasodilation, pain, swelling and fever. Prostaglandins, thromboxanes and leukotrienes derived from arachidonic acid mediate inflammation.
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 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.
hey why we fall ill... wat is that causes fever.... to kws this in a very simple way please have a look..... next time instead of cursing fever you will thnk your immune system.
Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat pain and inflammation. They work by inhibiting the enzyme cyclooxygenase (Cox) and subsequent prostaglandin production. NSAIDs can be non-selective Cox inhibitors or selective Cox-2 inhibitors. Common side effects include gastrointestinal upset, which can be reduced by selective Cox-2 inhibitors or gastroprotectants. Ibuprofen is often preferred due to its relatively mild side effect profile. Proper patient selection and risk minimization strategies are important due to the side effect risks of long-term NSAID use.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by blocking cyclooxygenase (COX) enzymes, which reduces prostaglandin production and consequently decreases inflammation, pain, and fever. NSAIDs are used to treat conditions like arthritis, gout, and postoperative pain but can cause side effects like gastrointestinal ulceration and bleeding by inhibiting protective prostaglandins in the stomach. They may also increase risks of cardiovascular and renal issues. Care must be taken with NSAID combinations or when used with other drugs that impact renal function.
NSAIDs work by inhibiting the enzyme cyclooxygenase (COX), which reduces the production of prostaglandins. This inhibition decreases pain, fever, and inflammation. NSAIDs are weak analgesics that provide anti-inflammatory, antipyretic, and antiplatelet effects to varying degrees without depressing the central nervous system. They act by blocking the production of prostaglandins, which are mediators of pain, fever, and inflammation. The document discusses the mechanisms of pain, fever, and inflammation along with the roles of prostaglandins and how NSAIDs work to reduce these conditions by inhibiting prostaglandin synthesis.
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 summarizes information about NSAIDs (non-steroidal anti-inflammatory drugs) and COX-2 inhibitors for pain management. It defines pain and classifications of pain such as acute vs chronic pain. It describes the mechanisms of COX-1 and COX-2 enzymes and how different NSAIDs and COX-2 inhibitors work. It discusses the use of NSAIDs and COX-2 inhibitors for various types of pain and their potential adverse effects.
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.
The document discusses several autacoids including histamine, bradykinin, 5-hydroxytryptamine (5HT), eicosanoids, and platelet activating factor (PAF). It describes their synthesis, mechanisms of action, functions, and pharmacological properties. Histamine is involved in allergic responses and acts on H1 and H2 receptors. Bradykinin causes pain and vasodilation. 5HT is involved in platelet aggregation and gastrointestinal motility. Eicosanoids like prostaglandins are lipid-derived autacoids formed from arachidonic acid. PAF causes potent vasodilation and increases vascular permeability.
This document discusses non-steroidal anti-inflammatory drugs (NSAIDs) and their effect on renal function. It defines NSAIDs, describes the two main categories, and explains how they work by inhibiting prostaglandin synthesis from arachidonic acid through the COX pathway. The renal effects of prostaglandin inhibition are a decrease in reabsorption in the proximal tubule and vasoconstriction, which can reduce glomerular filtration rate and potentially cause acute renal failure in at-risk patients with long-term use.
This presentation deals with the various non-steroidal antiinflammatory drugs used in day-to-day practice enumerating their mechanism of action, uses, adverse effects, etc.
This document discusses anti-inflammatory drugs and their mechanisms and uses. It focuses on aspirin and other salicylates. It explains that inflammation is a normal response to injury but can become inappropriate, and anti-inflammatory drugs work by blocking prostaglandin synthesis. Aspirin and other NSAIDs are commonly used to treat conditions involving pain, fever and inflammation like arthritis. While effective, these drugs can cause adverse effects like GI issues, bleeding risks and interactions with other medications if not taken carefully.
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 various types of non-narcotic analgesics and muscle relaxants used to treat pain associated with arthritis. It covers disease-modifying antirheumatic drugs and biological DMARDs for rheumatoid arthritis, corticosteroids and their adverse effects, treatments for osteoarthritis and gout, and the traditional stepped care approach to pain management. Specific drugs mentioned include baclofen, carisoprodol, chlorzoxazone, cyclobenzaprine, diazepam, methocarbamol, orphenadrine, azathioprine, cyclophosphamide, hydroxychloroquine, leflunomide, methotrexate, penicillamine, gold salts,
NSAIDs are a class of drugs that provide analgesic, antipyretic, and anti-inflammatory effects by inhibiting the COX enzyme and subsequent prostaglandin production. Aspirin is a prototypical NSAID that is non-selective and irreversibly inhibits both COX-1 and COX-2 isoforms. It is well absorbed but has a short half-life due to rapid metabolism. While effective at reducing pain, fever and inflammation, high doses of aspirin can cause adverse effects like gastric irritation, salicylism, and Reye's syndrome in children. Overdose of aspirin leads to serious toxicity that requires supportive care and dialysis.
The document discusses nonsteroidal anti-inflammatory drugs (NSAIDs). It describes how NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and thereby reducing the production of prostaglandins involved in inflammation, pain, and fever. NSAIDs are commonly used to treat inflammation and pain conditions like arthritis as well as fever. Common NSAIDs include aspirin, ibuprofen, and naproxen. The document outlines their mechanisms of action, therapeutic uses, and potential adverse effects like gastrointestinal irritation and hypersensitivity reactions.
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 summarizes anti-inflammatory drugs. It discusses the inflammatory process and mediators like histamine, prostaglandins, leukotrienes and thromboxane A2. It describes the three phases of inflammation and signs like redness, heat, swelling and pain. Two major classes of anti-inflammatory drugs are discussed: steroidal anti-inflammatory drugs (SAIDs) like cortisone and hydrocortisone, and non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin, ibuprofen and naproxen. The mechanisms, common uses and potential side effects of various NSAIDs are outlined.
The document discusses autacoids and inflammation. It describes how within 5 minutes of being stung by a bee, a boy develops a swollen, red lesion at the site of injury. The predominant finding in tissue from the lesion would be neutrophilic migration (D). Autacoids like eicosanoids and histamine are involved in the inflammatory response and produce effects like vasodilation, pain, swelling and fever. Prostaglandins, thromboxanes and leukotrienes derived from arachidonic acid mediate inflammation.
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 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.
hey why we fall ill... wat is that causes fever.... to kws this in a very simple way please have a look..... next time instead of cursing fever you will thnk your immune system.
Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat pain and inflammation. They work by inhibiting the enzyme cyclooxygenase (Cox) and subsequent prostaglandin production. NSAIDs can be non-selective Cox inhibitors or selective Cox-2 inhibitors. Common side effects include gastrointestinal upset, which can be reduced by selective Cox-2 inhibitors or gastroprotectants. Ibuprofen is often preferred due to its relatively mild side effect profile. Proper patient selection and risk minimization strategies are important due to the side effect risks of long-term NSAID use.
Nonsteroidal anti-inflammatory drugs (NSAIDs) work by blocking cyclooxygenase (COX) enzymes, which reduces prostaglandin production and consequently decreases inflammation, pain, and fever. NSAIDs are used to treat conditions like arthritis, gout, and postoperative pain but can cause side effects like gastrointestinal ulceration and bleeding by inhibiting protective prostaglandins in the stomach. They may also increase risks of cardiovascular and renal issues. Care must be taken with NSAID combinations or when used with other drugs that impact renal function.
NSAIDs work by inhibiting the enzyme cyclooxygenase (COX), which reduces the production of prostaglandins. This inhibition decreases pain, fever, and inflammation. NSAIDs are weak analgesics that provide anti-inflammatory, antipyretic, and antiplatelet effects to varying degrees without depressing the central nervous system. They act by blocking the production of prostaglandins, which are mediators of pain, fever, and inflammation. The document discusses the mechanisms of pain, fever, and inflammation along with the roles of prostaglandins and how NSAIDs work to reduce these conditions by inhibiting prostaglandin synthesis.
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 summarizes information about NSAIDs (non-steroidal anti-inflammatory drugs) and COX-2 inhibitors for pain management. It defines pain and classifications of pain such as acute vs chronic pain. It describes the mechanisms of COX-1 and COX-2 enzymes and how different NSAIDs and COX-2 inhibitors work. It discusses the use of NSAIDs and COX-2 inhibitors for various types of pain and their potential adverse effects.
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.
The document discusses several autacoids including histamine, bradykinin, 5-hydroxytryptamine (5HT), eicosanoids, and platelet activating factor (PAF). It describes their synthesis, mechanisms of action, functions, and pharmacological properties. Histamine is involved in allergic responses and acts on H1 and H2 receptors. Bradykinin causes pain and vasodilation. 5HT is involved in platelet aggregation and gastrointestinal motility. Eicosanoids like prostaglandins are lipid-derived autacoids formed from arachidonic acid. PAF causes potent vasodilation and increases vascular permeability.
This document summarizes the medical history and examination of a 49-year-old female patient presenting with increasing lower back, hip, and knee pain. The patient has a history of diabetes, deep vein thrombosis, and hypercholesterolemia. A physical examination revealed pain on motion of the hips and right knee crepitus. X-rays showed degenerative changes consistent with osteoarthritis in the lumbar spine, hips, and right knee. Laboratory tests showed elevated blood glucose, HbA1c, and cholesterol levels. The provisional diagnosis is osteoarthritis with diabetes and hypercholesterolemia.
Macitentan is a novel dual endothelin receptor antagonist approved for the treatment of pulmonary arterial hypertension. It works by preventing the binding of endothelin-1 to endothelin receptors in pulmonary arterial smooth muscle cells, which are upregulated in PAH and contribute to pathological changes. In clinical trials, macitentan demonstrated efficacy in improving exercise capacity and other clinical outcomes in PAH patients when taken as a 10 mg oral dose once daily. Adverse effects were generally mild. Macitentan is also under investigation for other pulmonary and non-pulmonary indications involving the endothelin system.
Excellent for medical students, pharmacology students, nursing students, and university or college students. Use it to aid in your studying for semester and board exams!
This document provides an overview of nonsteroidal anti-inflammatory drugs (NSAIDs). It discusses their classification, mechanism of action involving inhibition of prostaglandin synthesis, beneficial effects, toxicities, and individual drug profiles. NSAIDs are a chemically diverse class of drugs that reduce pain, fever, and inflammation by blocking cyclooxygenase (COX) enzymes and subsequent prostaglandin production. While effective analgesics, NSAIDs can cause adverse effects like gastric irritation, bleeding risks, and interference with other drugs due to competition for protein binding sites.
The document discusses prostaglandin-endoperoxide synthase (PTGS), also known as cyclooxygenase (COX), which is responsible for the formation of prostanoids like prostaglandins. It has two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed and regulates normal physiological functions, while COX-2 is induced during inflammation. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit these enzymes to reduce inflammation. Several NSAIDs are described, including their mechanisms of action, medical uses, and potential adverse effects.
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.
The document discusses the body's inflammatory response to injury and how it aims to restore tissue function while fighting invading microorganisms. It can lead to multi-organ failure if overwhelming. Clinical signs of systemic inflammatory response syndrome (SIRS) are also outlined. Various hormones and signaling molecules involved in the response are then reviewed, including their effects on metabolism, immune function, and organ systems.
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 prostaglandin synthase enzymes, namely cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). Traditional NSAIDs nonselectively inhibit both COX-1 and COX-2, whereas some newer NSAIDs preferentially or selectively inhibit COX-2. NSAIDs are used to reduce inflammation, fever, and pain in conditions like arthritis but can cause adverse gastrointestinal, renal, and cardiovascular effects. Aspirin irreversibly inhibits COX-1 and COX-2 and is used at low doses as an antiplatelet drug to reduce the risk of cardiovascular
Prostaglandins and leukotrienes are lipid-derived autacoids that play important roles in various physiological processes and in mediating inflammation. Prostaglandins were first identified in seminal fluid and named after the prostate gland. They are synthesized from arachidonic acid. Leukotrienes were initially identified as the "slow reacting substance of anaphylaxis". Prostaglandins and leukotrienes act through G-protein coupled receptors and are involved in cardiovascular, pulmonary, gastrointestinal, renal and ocular functions. They also mediate fertility, labor and abortion. Drugs targeting prostaglandin and leukotriene pathways are used to treat conditions like asthma, glaucoma and inflammation.
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.
The document discusses endocrine issues in critical illness, including the stress response and its effects on glucose levels and insulin resistance. It presents evidence that tight glycemic control with intensive insulin therapy reduces mortality in critically ill patients. The text also examines glucocorticoid physiology and biosynthesis, noting that adrenal insufficiency is common in sepsis and ICU patients. Studies demonstrate improved outcomes with hydrocortisone replacement in patients with septic shock or adrenal insufficiency.
This document provides an overview of corticosteroids, including their history, biosynthesis, classification, mechanisms of action, therapeutic uses, and adverse effects. Corticosteroids are steroid hormones produced in the adrenal cortex from cholesterol. They have important roles in carbohydrate, protein, and fat metabolism, electrolyte balance, and anti-inflammatory responses. Common therapeutic uses include replacement therapy for adrenal insufficiency, and treatment of conditions like arthritis, asthma, skin diseases, and organ transplantation. Adverse effects can include fluid retention, altered electrolyte levels, infections, delayed wound healing, and osteoporosis. Inhaled corticosteroids are commonly used as first-line therapy for chronic asthma.
This document summarizes a presentation on statins and their pleiotropic effects. It begins with an overview and introduction on statins. It then discusses cholesterol synthesis and statins' mechanism of action in inhibiting HMG-CoA reductase to lower cholesterol. The document outlines various pleiotropic effects of statins including improving endothelial function, providing plaque stability, anti-inflammatory effects, and effects on other organs. It summarizes several research articles on topics like statins' effect on CRP and the association between statins and vitamin D.
Non-opioid analgesics provide analgesic, anti-inflammatory, and antipyretic effects through inhibiting prostaglandin production via binding to the cyclooxygenase (COX) enzyme. They have weaker analgesic effects than opioids, do not cause central nervous system depression, and have no abuse or dependence potential. Common non-opioid analgesics include aspirin, ibuprofen, and naproxen which are non-selective COX inhibitors, and celecoxib which selectively inhibits COX-2 with fewer gastrointestinal side effects but increased cardiovascular risk. Non-opioid analgesics are used for mild to moderate pain and inflammatory conditions like arthritis but have potential adverse effects including gastrointestinal bleeding, hypersensitivity reactions, and salicylate
The document discusses renal anatomy, physiology, and urine formation. It describes the two regions of the kidney - the cortex and medulla, and the functional unit of the kidney - the nephron. It explains the three steps in urine formation: glomerular filtration, tubular reabsorption, and tubular secretion. Glomerular filtration filters blood in the kidneys and produces an ultrafiltrate. Most of this filtrate is then reabsorbed back into blood in the tubules, while some substances are actively secreted into the tubular fluid for excretion.
Microscopy is a tool used in biological sciences to produce enlarged images of objects. There are two main types of microscopes - light microscopes and electron microscopes. Light microscopes use visible light and magnification ranging from 1000x, while electron microscopes use electron beams and have much higher magnifications up to 200,000x. Different types of light microscopes such as brightfield, darkfield, phase contrast, and fluorescence microscopes are used to view samples in various ways depending on factors like sample staining, structure, and fluorescent properties.
This document discusses safety hazards in clinical laboratories. It outlines biological, sharp, chemical, radioactive, electrical, fire/explosive, and physical hazards. For biological hazards, it discusses sources like specimens and patients and infections from bacteria, fungi, viruses, and parasites. It also discusses universal precautions, body substance isolation, and standard precautions for handling potential biological hazards. For other hazards, it provides brief descriptions of sources and possible injuries. Throughout, it provides guidelines for proper handling and disposal of hazardous materials.
1. The document discusses principles of quality assurance in laboratory testing. It defines quality assurance as the overall program that ensures correct test results are delivered to the right person on time.
2. Quality control refers to measures taken during each test to ensure results are accurate and precise. This includes analyzing controls to verify the test is working properly.
3. Quality assessment involves external evaluation of a laboratory's performance through proficiency testing, allowing assessment of the effectiveness of the quality assurance and quality control programs.
This document outlines the course details for Clinical Microscopy/UBF, a 2nd semester course. It will cover the macroscopic, chemical and microscopic study of various non-blood body fluids and byproducts, including urine, feces, cerebral spinal fluid, and others. Students will learn about specimen collection, handling, processing, and the clinical significance of test results. The course requirements include laboratory activities, case reports, lectures, and exams. Safety protocols for handling biological and chemical hazards are also covered.
This document provides an overview of urinalysis, including its history, rationale, urine composition, collection techniques, specimen types, and preservation methods. It discusses how urinalysis can provide information about the body's major metabolic functions in a non-invasive way using a readily available specimen. The document outlines factors that can affect urine composition and volume, such as diet, activity level, endocrine functions, and body position. It also describes various urine collection techniques and issues related to specimen handling and preservation.
This document provides an introduction to the field of pharmacology. It defines key terms like pharmacy, pharmacology, drugs, medicines, and drug interactions. It describes how drugs are classified based on origin, chemical structure, means of procurement, body system affected, and mechanism of action. The stages of drug discovery, development and clinical trials are outlined. Philippine laws regarding drug use like the Generics Act and those establishing the Philippine National Drug Formulary are mentioned. Community drug outlets called Botika ng Barangay aimed at improving access to essential medicines are also introduced.
This document summarizes key aspects of drug excretion from the body. It discusses excretion through the kidneys including glomerular filtration and tubular secretion. It also covers biliary excretion through the liver and factors that influence the various orders of excretion such as zero-order and first-order kinetics. The concepts of half-life, clearance, volume of distribution, bioavailability and achieving steady-state concentrations with repetitive dosing are defined. Considerations for dosing adjustments in renal disease are provided.
This document summarizes key concepts in pharmacodynamics including:
- Mechanisms of drug action including receptor interactions, dose effects, and therapeutic/toxic effects
- Definitions of terms like agonist, antagonist, affinity, potency, efficacy
- Mechanisms of signal transduction between drug binding and intracellular effects
- Types of drug targets including receptors, ion channels, enzymes, and carriers
- Concepts of drug-receptor binding and interactions, dose-response curves, and agonists vs antagonists
- Factors influencing drug properties like safety, interactions, adverse effects, toxicity, idiosyncrasies, and tolerance
This document provides an introduction to the field of pharmacology. It defines key terms like pharmacy, pharmacology, drugs, medicines, and drug interactions. It describes how drugs are classified based on origin, chemical structure, means of procurement, body system affected, and mechanism of action. The stages of drug discovery, development and clinical trials are outlined. Philippine laws regarding drug use like the Generics Act and those establishing the Philippine National Drug Formulary are mentioned. Community drug outlets called Botika ng Barangay aimed at improving access to essential medicines are also introduced.
Toxicology is the study of the adverse effects of chemicals on living things. Common causes of poisoning in 1964 included barbiturates, carbon monoxide, and alcohols. Antidotes work by decreasing absorption, neutralizing the poison, enhancing elimination, or intervening pharmacodynamically. Toxicity screening evaluates acute and chronic effects of substances and their potential to cause mutations, cancer, or birth defects.
The document discusses drug prescriptions and dosages. It defines the key contents of a prescription as the name, amount, route, frequency of administration, and prescribing physician's information. It then provides examples of common dosage abbreviations and explanations, such as q.d. for every day. The document also covers drug dosage calculations for both oral and parenteral medications, including formulas for intravenous drip rates. Finally, it discusses pediatric dosage calculations based on either body surface area or body weight.
This document discusses drug formulations and routes of administration. It begins with general considerations of pharmaceutics and how formulations are designed for easy delivery and desired therapeutic effects. It then describes various oral preparations like tablets, capsules, liquids and sustained release formulations. Topical preparations like creams, ointments and patches are also outlined. The document concludes by explaining different parenteral and specialized routes of administration like intravenous, intramuscular, intrathecal and others.
The document defines drugs of abuse and classifies them into different categories based on their mechanisms and effects. It describes opioids like morphine, heroin and synthetic opioids; stimulants like cocaine, amphetamines and nicotine; depressants like alcohol, barbiturates and benzodiazepines; hallucinogens; and cannabis. It discusses the acute and chronic effects of these substances, as well as tolerance, dependence and withdrawal. The legal classification of drugs from Schedule I to V is also outlined based on abuse potential and medical utility.
This document discusses the processes involved in pharmacokinetics, including absorption, distribution, metabolism, and excretion of drugs in the body. It describes the key components of each process and influencing factors. Absorption involves passive diffusion and active transport of drugs into systemic circulation. Distribution is influenced by factors like protein binding, lipid solubility, and tissue permeability. Metabolism occurs mainly in the liver and involves oxidative, reductive, and hydrolytic reactions to make drugs more polar and excretable. Excretion eliminates drugs from the body through renal and biliary routes.
This document summarizes key aspects of drug excretion from the body. It discusses excretion through the kidneys including glomerular filtration and tubular secretion. It also covers biliary excretion through the liver and factors that influence the various orders of excretion such as zero-order and first-order kinetics. The concepts of half-life, clearance, volume of distribution, bioavailability and achieving steady-state concentrations with repetitive dosing are defined. Considerations for dosing adjustments in renal disease are provided.
This document discusses chemical and drug injuries, adverse drug reactions, and various therapeutic agents that can cause injuries. It notes that all chemicals and drugs are capable of causing injury or death through accidental exposure, overdose, or unintended effects. Adverse drug reactions are classified as predictable side effects or unpredictable idiosyncratic reactions. Several classes of therapeutic agents like analgesics, antimicrobials, and anti-neoplastics are described in detail, noting their therapeutic doses, toxic doses, known side effects and potential adverse reactions affecting different body systems.
7. clinical use of Anti-histamines
H1 blockers –
anti-allergy,
anti-inflammatory,
anti-motion sickness.
common side effect: sedation
H2 blockers – reduce secretion of
gastric acid.
in peptic ulcer disease
8. Serotonin
sources: vertebrates, molluscs, pineapple,
banana,
nuts, stings, venom; in man – 80% in GI
chromaffin cells, rest in platelets & CNS
functions:
central chemical transmitter for tryptominergic neurons in the
brain;
precursor for melatonin;
regulation of GI motility by increasing tone & peristalsis;
hemostasis – vasospasm & platelet activation/aggregation;
contraction of smooth muscle in the uterus, bronchi
synthesis: Tryptophan (tryptophan 5-
hydroxylase) 5hydroxytryptophan(L-amino-
decarboxylase) 5HydroxyTryptamine (5HT,
Serotonin)
9. 5HT receptor subtypes & effector systems
recepto
r
mechanism effect
5HT1A Adenylyl cyclase
stimulation
direct vasodilatation &
inotropic effect
5HT1A
B
5HT1D
Adenylyl cyclase
inhibition
inhibition of NE release
5HT1C Phospholipase
C activation
indirect vasodilation via
EDRF release
5HT2 Phospholipase
C stimulation
vasoconstriction,
↑intracellular Calcium
5HT3 Calcium channel depolarization of
10. 5HT Antagonists
Ketanserin – blocks 5HT2 receptors –
lowers blood pressure by blocking 5HT-induced contraction of
vascular smooth muscle & platelet aggregation;
minor side effects: sedation, dry mouth, dizziness, nausea;
clinical application: treatment of HTN & vasospastic disorders
Methysergide (1-methy-d-lysergic acid
butanolamide) -
inhibits vasoconstrictor & pressor effects of 5HT on vascular
smooth muscle
clinical use: prophylaxis for migraine & vascular headaches
11. Kinins
synthesis: HMWK & LMWK are acted upon by
plasma & tissue Kallikrein to produce Bradykinin
& Kallidin
metabolism: half-life=15 sec; inactivated by
kininase or converting enzyme
functions:
inflammatory mediators
(also in rhinitis, hereditary angioneurotic edema, gout, endotoxic
shock, DIC);
nociception;
composition/volume of urine;
BP regulation;
fetal to neonatal adjustment
12. Receptors & effector systems
B1 Contraction of arteries &
most veins
pain
B2 Arteriolar vasodilation via
EDRF or H release;
contraction of endothelial
cells in venules
↑Capillary
permeability,
edema
B1 &
B2
Contraction of bronchial
smooth muscle; stimulate
nerve endings
pain
17. Eicosanoids
def. unsaturated fatty acid derivatives
locally synthesized & released as needed,
widely distributed in the body, very short
duration of action, rapidly metabolized to
inactive products
receptors: DP1, DP2 (PGD2); EP1, EP2,
EP3, EP4 (PGE2); FP (PGF2); IP (PGI2);
TP (TXA2)
23. Chemokines & Cytokines
Chemokines – small proteins (90-130 AAs)
containing 4 conserved Cysteines
CC chemokines: 2 consecutive cysteine pairs
CXC chemokines: 2 cysteine pairs separated by other AA
over 50, produced by a wide variety of cell types
major regulators of Leukocyte traffic; chemotactic; bind to
proteoglycans on the endothelial cell surface & within the
extracellular matrix & set up chemokine gradients for the
migrating leukocytes to follow
24. Chemokines & receptors
Examples of Chemokines:
IL8 – interleukin 8
RANTES – regulated upon activation normal T cell expressed &
secreted
MCP – monocyte chemoattractant protein
“serpentine receptors” – polypeptide chain
“snakes through” the cell membrane with 7
transmembrane segments
CCR – bind CC chemokines
CXCR – bind CXC chemokines
25. Cytokines
Soluble factors released by lymphocytes
& monocytes : Interferons & Interleukins
have potent pro-inflammatory properties
IL 1, IL 6, TNF-⍺ : endogenous pyrogens
29. Aspirin
hypersensitivity reactions
anaphylaxis
special precaution: use in children with
viral infection is associated with Reye’s
syndrome – hepatic fatty degeneration &
encephalopathy
overdose: metabolic acidosis;
dehydration; hyperthermia; collapse;
coma; death
Tx of overdose: dialysis