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.
Local Anesthetics are used to induce reversible loss of sensation in a localized area without loss of consciousness. They work by blocking voltage-gated sodium channels and preventing the generation and conduction of nerve impulses. The first local anesthetic used in surgery was ether in 1846. Cocaine was later used for its numbing properties but was replaced by procaine and later lignocaine due to toxicities. Local anesthetics can be ester-linked like cocaine and procaine, or amide-linked like lignocaine. Amide-linked ones are safer as they are metabolized by the liver rather than plasma esterases. Local anesthetics are often mixed with vasoconstrictors like epinephrine
1) The document discusses local anesthetics, providing their history, uses, mechanisms of action, classifications, and factors influencing their effects.
2) It describes the pharmacokinetics of local anesthetics including absorption, distribution, metabolism and excretion of ester and amide-linked drugs.
3) Guidelines are provided for managing severe local anesthetic toxicity, including airway management, treating seizures and arrhythmias, and considering lipid emulsion therapy.
Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a localized area of the body without damaging neurons. They work by blocking the generation and conduction of nerve impulses at the site of action, which is the axonal membrane. The order of block is pain, temperature, touch, pressure, and then motor function. Common local anesthetics include lidocaine, bupivacaine, tetracaine, and prilocaine. They provide analgesia for minor procedures but can also be used for major surgery via regional techniques like epidurals.
Local anesthetics work by blocking sodium channels in nerve fibers, preventing the generation of action potentials and conduction of nerve impulses. They typically contain a hydrophilic amine group, hydrophobic aromatic moiety, and intermediate ester or amide linkage. Esters are metabolized rapidly by plasma esterases while amides are metabolized more slowly by the liver. Common uses of local anesthetics include minor surgery, dental procedures, nerve blocks, epidurals and caudals. Adverse effects can include central nervous system toxicity, cardiac issues like arrhythmias or hypotension, and allergic reactions. Chloroprocaine and lidocaine are examples of commonly used local anesthetic agents.
Local anesthetics work by reversibly blocking sodium channels, preventing nerve impulse conduction. This summary will discuss the key points about local anesthetics:
1. Local anesthetics come in different classes based on their chemical structure and duration of action. They are used to numb specific body regions without loss of consciousness.
2. The effectiveness of local anesthetics depends on factors like pH, lipophilicity, and concentration. Adding epinephrine prolongs the numbing effect and reduces systemic absorption.
3. Overdose of local anesthetics can cause seizures, cardiac issues, and other toxic effects. The dose must be carefully controlled to safely numb nerves without systemic side effects.
The document discusses local anesthetics, including their definition, history, ideal criteria, classification based on duration of action and chemical structure, examples used, pharmacokinetics, indications, adverse effects, contraindications, drug interactions, and routes of administration such as topical, nerve block, infiltration, spinal, and epidural. It also covers their mechanism of action in blocking voltage-gated sodium channels, factors affecting their reaction like lipid solubility and pH, and use of vasoconstrictors to prolong duration.
Local anesthetics work by reversibly blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and sensation. They are useful for minor procedures as they cause loss of sensation in a localized area without loss of consciousness. Common local anesthetics include lidocaine, bupivacaine, and procaine. Factors like lipid solubility and pH influence their onset and duration of action. While generally safe, local anesthetics can potentially cause adverse effects like numbness, seizures, or cardiac issues depending on the drug and dosage. Proper technique and patient health assessment are important considerations for safe use of local anesthesia.
Local anesthesia works by reversibly inhibiting sensory nerve impulse conduction, preventing pain sensation from being transmitted to the central nervous system. The effectiveness of local anesthetics depends on their potency, onset of action, and duration of effect, which are determined by the drug's physiochemical properties like lipid solubility and protein binding. Common local anesthetics include lidocaine, bupivacaine, ropivacaine, and levobupivacaine. While generally safe when used properly, local anesthetics can cause toxicity issues if too much enters the bloodstream, potentially leading to central nervous system or cardiovascular side effects.
Local Anesthetics are used to induce reversible loss of sensation in a localized area without loss of consciousness. They work by blocking voltage-gated sodium channels and preventing the generation and conduction of nerve impulses. The first local anesthetic used in surgery was ether in 1846. Cocaine was later used for its numbing properties but was replaced by procaine and later lignocaine due to toxicities. Local anesthetics can be ester-linked like cocaine and procaine, or amide-linked like lignocaine. Amide-linked ones are safer as they are metabolized by the liver rather than plasma esterases. Local anesthetics are often mixed with vasoconstrictors like epinephrine
1) The document discusses local anesthetics, providing their history, uses, mechanisms of action, classifications, and factors influencing their effects.
2) It describes the pharmacokinetics of local anesthetics including absorption, distribution, metabolism and excretion of ester and amide-linked drugs.
3) Guidelines are provided for managing severe local anesthetic toxicity, including airway management, treating seizures and arrhythmias, and considering lipid emulsion therapy.
Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a localized area of the body without damaging neurons. They work by blocking the generation and conduction of nerve impulses at the site of action, which is the axonal membrane. The order of block is pain, temperature, touch, pressure, and then motor function. Common local anesthetics include lidocaine, bupivacaine, tetracaine, and prilocaine. They provide analgesia for minor procedures but can also be used for major surgery via regional techniques like epidurals.
Local anesthetics work by blocking sodium channels in nerve fibers, preventing the generation of action potentials and conduction of nerve impulses. They typically contain a hydrophilic amine group, hydrophobic aromatic moiety, and intermediate ester or amide linkage. Esters are metabolized rapidly by plasma esterases while amides are metabolized more slowly by the liver. Common uses of local anesthetics include minor surgery, dental procedures, nerve blocks, epidurals and caudals. Adverse effects can include central nervous system toxicity, cardiac issues like arrhythmias or hypotension, and allergic reactions. Chloroprocaine and lidocaine are examples of commonly used local anesthetic agents.
Local anesthetics work by reversibly blocking sodium channels, preventing nerve impulse conduction. This summary will discuss the key points about local anesthetics:
1. Local anesthetics come in different classes based on their chemical structure and duration of action. They are used to numb specific body regions without loss of consciousness.
2. The effectiveness of local anesthetics depends on factors like pH, lipophilicity, and concentration. Adding epinephrine prolongs the numbing effect and reduces systemic absorption.
3. Overdose of local anesthetics can cause seizures, cardiac issues, and other toxic effects. The dose must be carefully controlled to safely numb nerves without systemic side effects.
The document discusses local anesthetics, including their definition, history, ideal criteria, classification based on duration of action and chemical structure, examples used, pharmacokinetics, indications, adverse effects, contraindications, drug interactions, and routes of administration such as topical, nerve block, infiltration, spinal, and epidural. It also covers their mechanism of action in blocking voltage-gated sodium channels, factors affecting their reaction like lipid solubility and pH, and use of vasoconstrictors to prolong duration.
Local anesthetics work by reversibly blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and sensation. They are useful for minor procedures as they cause loss of sensation in a localized area without loss of consciousness. Common local anesthetics include lidocaine, bupivacaine, and procaine. Factors like lipid solubility and pH influence their onset and duration of action. While generally safe, local anesthetics can potentially cause adverse effects like numbness, seizures, or cardiac issues depending on the drug and dosage. Proper technique and patient health assessment are important considerations for safe use of local anesthesia.
Local anesthesia works by reversibly inhibiting sensory nerve impulse conduction, preventing pain sensation from being transmitted to the central nervous system. The effectiveness of local anesthetics depends on their potency, onset of action, and duration of effect, which are determined by the drug's physiochemical properties like lipid solubility and protein binding. Common local anesthetics include lidocaine, bupivacaine, ropivacaine, and levobupivacaine. While generally safe when used properly, local anesthetics can cause toxicity issues if too much enters the bloodstream, potentially leading to central nervous system or cardiovascular side effects.
This document provides information on local anesthesia. It begins by defining local anesthesia and classifying local anesthetics. It then discusses the pharmacokinetics and mechanisms of action of local anesthetics. Factors that affect the efficacy of local anesthetics like pH, inflammation, dosage, and vasoconstrictors are covered. Potential adverse effects and allergic reactions are described. Guidelines for administering local anesthesia to special patient populations like children, handicapped patients, and those on anticoagulants are provided. The document concludes by discussing dosing considerations and choices of local anesthetic for different procedures.
This document provides an overview of local anaesthesia. It discusses the history of local anaesthetics from cocaine to lidocaine. It describes the properties, theories of action, classifications, composition, and pharmacology of local anaesthetics. The key modes of action are blocking sodium channels to prevent nerve impulse conduction. Local anaesthetics reversibly bind to specific receptor sites on sodium channels to inhibit sodium influx and nerve depolarization. Complications can include both local tissue toxicity and systemic effects.
This document provides an overview of local anaesthesia including:
- A definition and historical background of local anaesthetics such as cocaine and procaine.
- Desirable properties and classifications of local anaesthetics.
- Details on common local anaesthetics like lidocaine including mechanism of action, dosage, and comparisons to other agents.
- Factors to consider in selecting a local anaesthetic for a patient and important information to obtain from the patient.
- Techniques for administering local anaesthesia and managing complications.
Local anesthesia works by reversibly inhibiting the propagation of nerve signals in a specific body area. The first local anesthetic was cocaine, discovered in 1860. Local anesthetics are classified as esters or amides based on their chemical structure and method of metabolism. They work by blocking the influx of sodium ions through nerve cell membranes, preventing nerve depolarization. Factors like pH, lipophilicity, and vasoconstrictors affect their potency and duration of action. Common techniques for administering local anesthesia include infiltration, nerve blocks, epidurals, and spinal anesthesia. Potential side effects include both local and systemic toxicity.
This document defines local anesthetics and describes their properties and mechanisms of action. It discusses various local anesthetics including lidocaine, prilocaine, bupivacaine, ropivacaine, dibucaine, benzocaine, butamben, and oxethazaine. It covers their uses for surface anesthesia, infiltration, nerve blocks, epidurals, and other techniques. Complications are also summarized.
This document provides information on local anesthetics used in plastic surgery. It defines local anesthesia and classifies local anesthetics as esters or amides. It describes the pharmacology of different local anesthetics including onset, maximum dose, and duration. It discusses the ideal properties of a local anesthetic and the benefits of adding a vasoconstrictor like epinephrine. The document also covers different techniques for local anesthesia including topical, infiltration, nerve blocks, and tumescent anesthesia. It provides details on administering local anesthetics safely and effectively for plastic surgery procedures.
Cocaine was the first local anesthetic discovered and is derived from coca plants. Other synthetic local anesthetics were later developed, including procaine and lidocaine. Local anesthetics work by reversibly binding sodium channels and inhibiting nerve conduction. There are two classes - amino amides like lidocaine and amino esters like cocaine. Proper administration of local anesthetics involves considering the patient, dose, presence of epinephrine, speed of injection, tissue vascularity, and injection technique. Dilution, addition of epinephrine, and slow administration can allow for safer use of local anesthetics.
Local anesthetics work by reversibly blocking nerve conduction without damaging neurons. They are commonly used in ophthalmic procedures to block sensation in the treated area. The two main types are esters and amides. Local anesthetics work by blocking voltage-gated sodium channels, preventing the generation of action potentials. Commonly used ophthalmic local anesthetics include lidocaine, bupivacaine, and proparacaine. Side effects can include cardiovascular and central nervous system issues. Local anesthetics are applied topically, via infiltration, nerve blocks, or other regional methods.
The document discusses local anesthetics, including their definition, requirements, mechanisms of action, classifications, and biotransformation. It notes that local anesthetics work by inhibiting sodium influx through voltage-gated sodium channels in neuronal cells, blocking nerve conduction. Local anesthetics are classified based on duration of action, chemical nature, and origin. Common examples are discussed and appropriate uses along with potential complications and contraindications are outlined.
This document provides an overview of local anesthetics (LAs) including:
1. Definitions and classifications of LAs including injectable and surface types.
2. The chemistry, structure, and structure-activity relationships that determine potency and duration.
3. The mechanism of action in which LAs block voltage-gated sodium channels.
4. The pharmacological properties including local effects, actions on the cardiovascular and central nervous systems.
5. Pharmacokinetics, uses, techniques, adverse effects, and factors affecting LA activity and selection for patients.
Pharmacology of local aesthetics and its mechanism of action, adverse effects and uses of local aesthetics with a note on the techniques of local aesthetics
This document summarizes information about local anesthetics used in central neuraxial blocks and their toxicity. It discusses how local anesthetics work, the drugs and doses used in epidural and spinal anesthesia, risks of local anesthetic systemic toxicity, prevention methods, and treatment of toxicity. Signs and symptoms of toxicity are outlined for the central nervous and cardiovascular systems. Risk factors, complications like methemoglobinemia, and neural toxicity are also reviewed.
This document provides information on local anesthesia. It defines local anesthesia and classifies local anesthetic agents into esters and amides. It describes the mechanism of action of local anesthetics in blocking nerve conduction and lists some commonly used local anesthetic agents like lidocaine, bupivacaine, and procaine. It also discusses vasoconstrictors that are often added to local anesthetics to prolong their duration of action and the composition, effects, administration and side effects of local anesthetic solutions.
Local anesthetics work by blocking sodium channels and interrupting nerve conduction. They are classified based on their chemical structure as esters or amides. Amides like lidocaine and bupivacaine are metabolized in the liver and have a lower risk of allergic reactions compared to esters. The potency, onset, and duration of local anesthetics depends on factors like lipid solubility, dose, pH, and addition of vasoconstrictors. Toxicity from local anesthetics is related to the dose administered and rate of absorption. Early symptoms of toxicity involve the central nervous system like agitation and seizures. Later, cardiovascular symptoms like arrhythmias and hypotension can occur. Treatment involves stopping administration, managing
This document summarizes key information about local anesthesia. It discusses how local anesthetics work by diffusing through nerve sheaths and binding to ion channels. It describes the differences between ester and amide anesthetics and lists common local anesthetics. Factors like pH, lipid solubility, and protein binding determine onset and duration. Vasoconstrictors like epinephrine are often added to prolong the effects. Proper use and storage of local anesthesia cartridges is also outlined.
Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a restricted area of the body by blocking the generation and conduction of nerve impulses where the drugs come into contact with neurons. Local anesthetics work by prolonging the inactive state of voltage-gated sodium channels, preventing the influx of sodium ions and blocking the generation and conduction of action potentials. The mechanism, potency, and duration of action varies between different classes of local anesthetics, with amides generally having more intense and longer lasting effects than esters. Local anesthetics can be administered through various methods like surface application, infiltration, nerve blocks, and regional techniques like epidurals and spinal anesthesia to temporarily numb sensation in a targeted area.
Lidocaine is a local anesthetic that has several indications and mechanisms of action. It can be used as a local anesthetic for procedures or to treat arrhythmias when given intravenously. Intravenous lidocaine may provide pain relief for postoperative, neuropathic, and chronic pain by blocking sodium channels. Studies have shown intravenous lidocaine can reduce postoperative pain and opioid use when given perioperatively, leading to benefits like shorter hospital stays. Lidocaine may be more effective than placebo for treating neuropathic pain, though epidural administration provides better pain relief than intravenous lidocaine for some surgeries. Adverse effects are typically minor when given at therapeutic doses by trained medical professionals.
Lidocaine is a rapid-acting local anesthetic first synthesized in 1943 that was approved by the FDA in 1948. It is widely used for local anesthesia and pain management. Lidocaine works by blocking sodium channels in neurons, preventing action potentials and nerve conduction. It has a short half-life of 1.6 hours and is metabolized in the liver. Lidocaine is commonly administered via local injection but is also available in topical forms and as an intravenous antiarrhythmic. When combined with a vasoconstrictor like epinephrine, lidocaine has an increased duration of anesthesia. Lidocaine remains the gold standard for local anesthesia due to its fast onset and short duration of action.
This document provides a historical overview of local anesthesia techniques from the 18th century introduction of chemical compounds to modern developments. It discusses key events and discoveries such as the first use of nitrous oxide and ether for dental procedures. The era of inhalation anesthesia gave way to injection techniques using hypodermic syringes and localized drugs like cocaine and procaine. Modern techniques for mandibular nerve blocks and vasoconstrictors that prolong anesthesia are also covered. The document concludes with sections on interactions, side effects, contraindications and toxicity of local anesthetic drugs and recommended maximum dosing.
the topic contain nonsteroidal antiinflammatory drugs which include, mediatorsof inflammation, cox-1 and cox-2, classification of drugs, its pharmacological effect and adverse reaction of drug.
This document provides information on NSAIDs (non-steroidal anti-inflammatory drugs). It discusses their history, mechanisms of action, classifications, common features, individual drugs, and screening methods. NSAIDs work mainly by inhibiting prostaglandin synthesis. They are effective for mild to moderate pain and have anti-inflammatory and antipyretic effects. Common NSAIDs include aspirin, ibuprofen, and naproxen. While effective analgesics, NSAIDs can cause gastrointestinal irritation and bleeding with long-term use.
This document provides information on local anesthesia. It begins by defining local anesthesia and classifying local anesthetics. It then discusses the pharmacokinetics and mechanisms of action of local anesthetics. Factors that affect the efficacy of local anesthetics like pH, inflammation, dosage, and vasoconstrictors are covered. Potential adverse effects and allergic reactions are described. Guidelines for administering local anesthesia to special patient populations like children, handicapped patients, and those on anticoagulants are provided. The document concludes by discussing dosing considerations and choices of local anesthetic for different procedures.
This document provides an overview of local anaesthesia. It discusses the history of local anaesthetics from cocaine to lidocaine. It describes the properties, theories of action, classifications, composition, and pharmacology of local anaesthetics. The key modes of action are blocking sodium channels to prevent nerve impulse conduction. Local anaesthetics reversibly bind to specific receptor sites on sodium channels to inhibit sodium influx and nerve depolarization. Complications can include both local tissue toxicity and systemic effects.
This document provides an overview of local anaesthesia including:
- A definition and historical background of local anaesthetics such as cocaine and procaine.
- Desirable properties and classifications of local anaesthetics.
- Details on common local anaesthetics like lidocaine including mechanism of action, dosage, and comparisons to other agents.
- Factors to consider in selecting a local anaesthetic for a patient and important information to obtain from the patient.
- Techniques for administering local anaesthesia and managing complications.
Local anesthesia works by reversibly inhibiting the propagation of nerve signals in a specific body area. The first local anesthetic was cocaine, discovered in 1860. Local anesthetics are classified as esters or amides based on their chemical structure and method of metabolism. They work by blocking the influx of sodium ions through nerve cell membranes, preventing nerve depolarization. Factors like pH, lipophilicity, and vasoconstrictors affect their potency and duration of action. Common techniques for administering local anesthesia include infiltration, nerve blocks, epidurals, and spinal anesthesia. Potential side effects include both local and systemic toxicity.
This document defines local anesthetics and describes their properties and mechanisms of action. It discusses various local anesthetics including lidocaine, prilocaine, bupivacaine, ropivacaine, dibucaine, benzocaine, butamben, and oxethazaine. It covers their uses for surface anesthesia, infiltration, nerve blocks, epidurals, and other techniques. Complications are also summarized.
This document provides information on local anesthetics used in plastic surgery. It defines local anesthesia and classifies local anesthetics as esters or amides. It describes the pharmacology of different local anesthetics including onset, maximum dose, and duration. It discusses the ideal properties of a local anesthetic and the benefits of adding a vasoconstrictor like epinephrine. The document also covers different techniques for local anesthesia including topical, infiltration, nerve blocks, and tumescent anesthesia. It provides details on administering local anesthetics safely and effectively for plastic surgery procedures.
Cocaine was the first local anesthetic discovered and is derived from coca plants. Other synthetic local anesthetics were later developed, including procaine and lidocaine. Local anesthetics work by reversibly binding sodium channels and inhibiting nerve conduction. There are two classes - amino amides like lidocaine and amino esters like cocaine. Proper administration of local anesthetics involves considering the patient, dose, presence of epinephrine, speed of injection, tissue vascularity, and injection technique. Dilution, addition of epinephrine, and slow administration can allow for safer use of local anesthetics.
Local anesthetics work by reversibly blocking nerve conduction without damaging neurons. They are commonly used in ophthalmic procedures to block sensation in the treated area. The two main types are esters and amides. Local anesthetics work by blocking voltage-gated sodium channels, preventing the generation of action potentials. Commonly used ophthalmic local anesthetics include lidocaine, bupivacaine, and proparacaine. Side effects can include cardiovascular and central nervous system issues. Local anesthetics are applied topically, via infiltration, nerve blocks, or other regional methods.
The document discusses local anesthetics, including their definition, requirements, mechanisms of action, classifications, and biotransformation. It notes that local anesthetics work by inhibiting sodium influx through voltage-gated sodium channels in neuronal cells, blocking nerve conduction. Local anesthetics are classified based on duration of action, chemical nature, and origin. Common examples are discussed and appropriate uses along with potential complications and contraindications are outlined.
This document provides an overview of local anesthetics (LAs) including:
1. Definitions and classifications of LAs including injectable and surface types.
2. The chemistry, structure, and structure-activity relationships that determine potency and duration.
3. The mechanism of action in which LAs block voltage-gated sodium channels.
4. The pharmacological properties including local effects, actions on the cardiovascular and central nervous systems.
5. Pharmacokinetics, uses, techniques, adverse effects, and factors affecting LA activity and selection for patients.
Pharmacology of local aesthetics and its mechanism of action, adverse effects and uses of local aesthetics with a note on the techniques of local aesthetics
This document summarizes information about local anesthetics used in central neuraxial blocks and their toxicity. It discusses how local anesthetics work, the drugs and doses used in epidural and spinal anesthesia, risks of local anesthetic systemic toxicity, prevention methods, and treatment of toxicity. Signs and symptoms of toxicity are outlined for the central nervous and cardiovascular systems. Risk factors, complications like methemoglobinemia, and neural toxicity are also reviewed.
This document provides information on local anesthesia. It defines local anesthesia and classifies local anesthetic agents into esters and amides. It describes the mechanism of action of local anesthetics in blocking nerve conduction and lists some commonly used local anesthetic agents like lidocaine, bupivacaine, and procaine. It also discusses vasoconstrictors that are often added to local anesthetics to prolong their duration of action and the composition, effects, administration and side effects of local anesthetic solutions.
Local anesthetics work by blocking sodium channels and interrupting nerve conduction. They are classified based on their chemical structure as esters or amides. Amides like lidocaine and bupivacaine are metabolized in the liver and have a lower risk of allergic reactions compared to esters. The potency, onset, and duration of local anesthetics depends on factors like lipid solubility, dose, pH, and addition of vasoconstrictors. Toxicity from local anesthetics is related to the dose administered and rate of absorption. Early symptoms of toxicity involve the central nervous system like agitation and seizures. Later, cardiovascular symptoms like arrhythmias and hypotension can occur. Treatment involves stopping administration, managing
This document summarizes key information about local anesthesia. It discusses how local anesthetics work by diffusing through nerve sheaths and binding to ion channels. It describes the differences between ester and amide anesthetics and lists common local anesthetics. Factors like pH, lipid solubility, and protein binding determine onset and duration. Vasoconstrictors like epinephrine are often added to prolong the effects. Proper use and storage of local anesthesia cartridges is also outlined.
Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a restricted area of the body by blocking the generation and conduction of nerve impulses where the drugs come into contact with neurons. Local anesthetics work by prolonging the inactive state of voltage-gated sodium channels, preventing the influx of sodium ions and blocking the generation and conduction of action potentials. The mechanism, potency, and duration of action varies between different classes of local anesthetics, with amides generally having more intense and longer lasting effects than esters. Local anesthetics can be administered through various methods like surface application, infiltration, nerve blocks, and regional techniques like epidurals and spinal anesthesia to temporarily numb sensation in a targeted area.
Lidocaine is a local anesthetic that has several indications and mechanisms of action. It can be used as a local anesthetic for procedures or to treat arrhythmias when given intravenously. Intravenous lidocaine may provide pain relief for postoperative, neuropathic, and chronic pain by blocking sodium channels. Studies have shown intravenous lidocaine can reduce postoperative pain and opioid use when given perioperatively, leading to benefits like shorter hospital stays. Lidocaine may be more effective than placebo for treating neuropathic pain, though epidural administration provides better pain relief than intravenous lidocaine for some surgeries. Adverse effects are typically minor when given at therapeutic doses by trained medical professionals.
Lidocaine is a rapid-acting local anesthetic first synthesized in 1943 that was approved by the FDA in 1948. It is widely used for local anesthesia and pain management. Lidocaine works by blocking sodium channels in neurons, preventing action potentials and nerve conduction. It has a short half-life of 1.6 hours and is metabolized in the liver. Lidocaine is commonly administered via local injection but is also available in topical forms and as an intravenous antiarrhythmic. When combined with a vasoconstrictor like epinephrine, lidocaine has an increased duration of anesthesia. Lidocaine remains the gold standard for local anesthesia due to its fast onset and short duration of action.
This document provides a historical overview of local anesthesia techniques from the 18th century introduction of chemical compounds to modern developments. It discusses key events and discoveries such as the first use of nitrous oxide and ether for dental procedures. The era of inhalation anesthesia gave way to injection techniques using hypodermic syringes and localized drugs like cocaine and procaine. Modern techniques for mandibular nerve blocks and vasoconstrictors that prolong anesthesia are also covered. The document concludes with sections on interactions, side effects, contraindications and toxicity of local anesthetic drugs and recommended maximum dosing.
the topic contain nonsteroidal antiinflammatory drugs which include, mediatorsof inflammation, cox-1 and cox-2, classification of drugs, its pharmacological effect and adverse reaction of drug.
This document provides information on NSAIDs (non-steroidal anti-inflammatory drugs). It discusses their history, mechanisms of action, classifications, common features, individual drugs, and screening methods. NSAIDs work mainly by inhibiting prostaglandin synthesis. They are effective for mild to moderate pain and have anti-inflammatory and antipyretic effects. Common NSAIDs include aspirin, ibuprofen, and naproxen. While effective analgesics, NSAIDs can cause gastrointestinal irritation and bleeding with long-term use.
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 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.
This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs) and their mechanisms of action. It describes how NSAIDs work by inhibiting cyclooxygenase enzymes (COX-1 and COX-2) and thereby blocking the production of prostaglandins. NSAIDs are classified based on their selectivity for COX-1 vs COX-2. Aspirin is highlighted as a nonselective NSAID. Its mechanisms of analgesic, antipyretic and anti-inflammatory effects are explained. Adverse effects of aspirin including gastrointestinal irritation and bleeding are also summarized.
The document discusses various antipyretic drugs, including their mechanisms of action, pharmacological effects, clinical uses, and side effects. It provides details on common antipyretic drugs like paracetamol, aspirin, meloxicam, and piroxicam. The drugs are used to reduce fever and inflammation, and help relieve pain, with their effects stemming from inhibition of prostaglandin synthesis.
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 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 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.
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.
1. The document discusses various drugs used in musculoskeletal system including prostaglandins, NSAIDs, and paracetamol.
2. Prostaglandins are lipid compounds derived from arachidonic acid that have hormone-like effects. NSAIDs like aspirin, ibuprofen, and diclofenac work by inhibiting prostaglandin synthesis.
3. The document describes the mechanisms of action, uses, doses, side effects and toxicity of common NSAIDs and paracetamol. NSAIDs are used for their anti-inflammatory, analgesic and antipyretic effects while paracetamol is primarily used for its analgesic and antipyretic properties.
Lecture 13- Non Steroidal Anti- Inflammatory Drugs.pptxAmrDuski1
NSAIDs are a widely used class of drugs that work by inhibiting the COX enzymes responsible for prostaglandin synthesis. They provide analgesic, anti-inflammatory, and antipyretic effects. While COX-2 inhibition is responsible for their therapeutic effects, COX-1 inhibition can cause adverse effects like gastric irritation. NSAIDs vary in their selectivity for COX-1 vs COX-2. Paracetamol is considered unique among NSAIDs for having little anti-inflammatory action but good analgesic properties at therapeutic doses.
The document provides information on non-steroidal anti-inflammatory drugs (NSAIDs) including their classification, mechanisms of action, and major effects. NSAIDs are chemically diverse drugs that reduce pain, fever, and inflammation by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. They are classified based on their selectivity for COX-1 versus COX-2 isoenzymes. The major effects of inhibiting prostaglandin synthesis include analgesia, antipyresis, anti-inflammatory action, antiplatelet aggregation, and closure of the ductus arteriosus in newborns. NSAIDs produce gastric mucosal damage by inhibiting protective prostaglandins in
This document discusses the mechanisms and uses of non-steroidal anti-inflammatory drugs (NSAIDs). It begins by explaining that NSAIDs work by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin production, providing analgesic, antipyretic, and anti-inflammatory effects. The document then classifies and provides examples of different types of NSAIDs, and discusses their pharmacological actions, mechanisms of action, indications, adverse effects, and drug interactions. Key NSAIDs discussed in more depth include aspirin, acetaminophen, ibuprofen, indomethacin, and diclofenac.
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.
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
Nonsteroidal anti-inflammatory drugs (usually abbreviated to NSAIDs /ˈɛnsɛd/ en-sed), also called nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs), are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.
This document summarizes anti-inflammatory drugs and NSAIDs. It describes the inflammatory process and key mediators like prostaglandins. NSAIDs work by inhibiting cyclooxygenase enzymes, decreasing prostaglandin production and thus reducing inflammation, pain, and fever. Common NSAIDs like aspirin do this through reversible or irreversible inhibition of COX-1 and COX-2. The document outlines their mechanisms of action, therapeutic uses, and potential adverse effects like gastrointestinal irritation and bleeding.
Similar to Non Steroidal Anti Inflammatory Drugs (20)
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
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TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
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2. Inflammation
• Reaction to injury of the living microcirculation and related tissues
CARDINAL SIGNS :
• Redness (Rubor),
• Swelling (Tumour),
• Heat (Calor),
• Pain (Dolor),
• Loss of function
3. NSAIDS
• Non steroidal anti-inflammatory drugs
• One of the most commonly prescribed drugs
• Mostly used for:
• Anti pyretic
• Anti inflammatory
• Analgesic action
4.
5.
6. COX-1 and COX-2
• Cycloxygenase-1 ( COX-1)
• Present in most of the cells
• Mediates normal physiological function
• Cycloxygenase-2 (COX-2)
• Induced during inflammation by cytokines, growth factors, etc.
• Not present in all cells at all times
• Activated by Interleukin-1 and TNF-α
7. • Majority of tissues synthesize all PGH intermediates but the
predominant PG in a tissue depends on the enzyme present and their
amount
• Example:
• Lungs and spleen- all PGs
• Platelets- Thromboxane synthase
• Blood vessels ( vascular endothelium)- Prostacyclin synthase
8.
9. Natural Prostaglandins
1. PGE2- many receptors, many functions
• Bronchodilation
• Vasodilation
• Increase mucus secretion in stomach
• Patency of ductus arteriosus
2. PGD2 – vasodilation, inhibition of platelet aggregation
3. PGF2α – contracts smooth muscles of uterus, facilitates parturition
10. 4. PGI2 or Prostacyclin- vasodilation, inhibition of platelet
aggregation, prevents platelets adherence to healthy blood vessels
wall
5. TXA2- vasoconstriction, platelet aggregation
11. Anti- inflammatory effects of NSAIDs
A. Reduce those components of inflammatory response in which PGs
play a role:
1. Vasodilation
2. Oedema
3. Pain
B. Suppress pain, swelling and increased blood flow due to
inflammation but have little action on the actual progress of the
underlying chronic disease itself.
C. No effect on other aspects of inflammation- leucocyte migration,
lysosomal enzyme release and toxic oxygen radical production that
contribute to tissue damage in chronic inflammatory conditions
12. Fever
• Disturbance of hypothalamic thermostat leads to raised setpoint of
body temperature
• Normal temperature in humans not affected by NSAIDs
• Bacterial endotoxins cause release of IL-1, which stimulates the
generation of PGE, that elevate the temperature setpoint
14. Analgesic effect
• Effective against mild or moderate pain from tissue damage or
inflammation
• Decrease the production of Prostaglandins that sensitize nociceptors
to inflammatory mediators such as bradykinin. Hence effective in
arthritis, muscular/vascular pain, toothache, dysmenorrhea – all
conditions associated with increased local prostaglandin synthesis
• Combined with opioids, they decrease postoperative pain
• Ability to relieve headache maybe due to stopping of vasodilator
effect of prostaglandins on the cerebral vasculature
15. Clinical Implications of PGs and NSAIDs
1. Patent Ductus Arteriosus- Ductus Arteriosus is kept open by PGE2
and PGI2 in foetal life. Aspirin and Indomethacin are given in high
doses to close ductus arteriosus if closure does not occur in usual
time.
2. Platelet aggregation- Aspirin in low doses inhibits synthesis of TXA2
and produces antiplatelet action
3. PGE2 and PGF2α are used in induction of labour as they contract
uterus, and NSAIDs used to delay the labour. NSAIDS not used for
the purpose for the fear of early closure of ductus arteriosus.
16. 4. PGF2α constricts the sphincter muscle of iris causing miosis,
increasing uveoscleral and trabecular outflow, decreasing
intraocular pressure. Latanoprost, a synthetic PGF2α has been
developed for treatment of open angle glaucoma.
5. PGE2 analogue (Misoprostol) is used in peptic ulcer to increase
gastric mucus secretion( gastro-protective effect).
6. TXA2, PGF2α both cause bronchoconstriction. In asthma, LTs are
considered to be causative. Hence, NSAIDs might direct all
production of AA to LTs increasing the severity of asthma.
17. 7. PGE2 and PGI2 are vasodilators, increase renal blood flow due to
direct action on renal tubules, causing natriuresis, diuresis and
kaliuresis. NSAIDs, hence, cause retention of sodium and water and
may block the effect of diuretics.
18.
19. Common adverse effects of NSAIDs
1. Effect on gastric mucosa: PGs like PGE2 and PGI2 protect gastric
mucosa by inhibiting gastric acid secretion, increasing mucus, and
increasing the gastric blood flow. Loss of these actions damages
gastric mucosa causing ulcers.
20. 2. Renal toxicity: In hypovolemia or decreased renal perfusion, PGs
synthesized in the kidneys maintain perfusion by vasodilation,
antagonizing action of ADH and other mechanisms. NSAIDs block
this mechanism and give rise to analgesic nephropathy – a slow
developing renal failure. Avoid by
• short course or after gap of few weeks
• Only one NSAID at a time
21. 3. Cardiovascular adverse effects:
a) Inhibition of PG production in the kidney may retain sodium and
water. NSAIDs are therefore associated with risk of hypervolemia-
hence worsening heart failure, especially if controlled by diuretics
b) Risk of increase in BP.
c) Increased stroke and Myocardial infarction due to inhibition of
prostacyclins
24. Aspirin (Acetyl Salicylic Acid)
• Derived from Willow bark, which used for centuries
• Prototype drug with a range of actions
• Used for
1. Pain- sp. Tension headache
2. Fever
3. Acute Rheumatic Fever
4. Post myocardial infarction and
post stroke patients
25. Actions
1. Pain, fever, inflammation
• Inflammatory, connective tissue related pain
• Peripheral pain receptors desensitized, PG- mediated sensitization of
nerve endings prevented. Also, pain threshold increases.
• Resets hypothalamic thermostat, rapidly reduces fever by promoting
sweating, cutaneous vasodilation
• Inhibits PG synthesis, suppress signs and symptoms of inflammation
but do NOT affect the progression of the disease
26. 2. Antiplatelet effect:
• In lower doses( 50-325 mg) Irreversibly inhibits platelet TXA2
synthesis producing antiplatelet effect, which lasts for 8-10 days, i.e.
the lifetime of platelets.
• In high doses (2-3 g/day) inhibits both PGI2 and TXA2 synthesis,
hence beneficial effect of PGI2 is lost.
• Aspirin should be withdrawn 1 week prior to elective surgery because
of this risk of bleeding.
3. At high doses, increased respiration/ hyperventilation is stimulated
by Aspirin. Even higher doses can cause respiratory failure.
27. 3. Acid- base and electrolyte balance:
• At high doses, hyperventilation drives out CO2 causing respiratory
alkalosis, which is compensated by increased renal excretion of HCO3
-.
• Still higher doses- depressed respiration- more CO2 produced in the
body- respiratory acidosis.
• Metabolic acids produced in excess + metabolites of salicylic acid
present, decreased HCO3
- in the body- uncompensated metabolic
acidosis
28. 4. GIT: Ion trapping prominent
• Aspirin is easily absorbed into the gastric mucosal cells as it remains
unionized in the acidic medium of the stomach. But once inside the
gastric cells, most part of it gets ionized and cannot cross the cell
membrane to reach the bloodstream
• Irritates gastric mucosa, causing nausea, v
vomiting and epigastric distress.
• Also stimulates CTZ
29. 5. Urate excretion:
<2 g/day- urate retention, antagonize other uricosuric drugs
2-5g/day- variable effects
>5 g/day- increased urate excretion
6. Metabolic effects: At high doses,
• Uncoupling of oxidative phospholylation
→ increased heat production
• Increased utilization of glucose →
hyperglycemia
30. Pharmacokinetics
• Rapidly absorbed from upper GIT
• Metabolized in liver
• Low dose- 1st order kinetics of elimination
• High doses- 0 order kinetics of elimination, as the metabolizing
enzymes are saturated
31. Adverse effects
1. GIT: Nausea, vomiting, epigastric pain, gastric ulcer and bleeding.
2. Hypersensitivity: Patients with asthma, nasal polyps, recurrent
rhinitis or urticarial
3. Reye’s syndrome: Children with viral infection- Avoid NSAIDs as
they can cause liver damage with fatty infiltration and
encephalopathy
4. Pregnancy: Delay natural contractions of labour, increase chances of
postpartum hemorrhage. Also in the newborn, inhibition of PG
synthesis results in premature closure of ductus arteriosus.
5. Analgesic nephropathy: Renal failure
32. Aspirin poisoning
• Symptoms:
• CNS: headache, tinnitus, vertigo, convulsions, coma
• GIT: nausea, vomiting, diarrhoea
• Sweating and hyperventilation
• Hypo/hyperglycemia
• Hyperpyrexia
• Death by respiratory failure/ Cardiovascular collapse
33. Treatment:
NO ANTIDOTE, Symptomatic treatment
1. Gastric lavage + activated charcoal
2. Fluid and electrolytes, acid-base balance
3. IV sodium bicarbonate to treat metabolic acidosis, also alkalinizes
urine and increases excretion of salicylates
4. External cooling
5. Hemodialysis in severe cases
6. Vitamin K1 and blood transfusion if there is bleeding
35. Paracetamol
• COX-3 is a variant of COX-1, sensitive to Paracetamol
• Weak inhibitor of PG synthesis of COX-1 and COX-2
Adverse effects
1. Rare, occasionally causes skin rashes and nausea
2. Hepatotoxicity
3. Nephrotoxicity Chronic use
36. Paracetamol
1. NO ANTI INFLAMMATORY ACTION: Increases pain threshold;
produces analgesic and antipyretic action due to action in CNS.
Weak inhibitor of cyclooxygenase in presence of high concentration
of cyclic endoperoxides at peripheral inflammatory sites
2. No effect on cardiovascular/ respiratory function
3. No acid base imbalance
4. No gastric irritation/ bleeding
5. No effect on platelets, bleeding time
and uric acid
39. • Alcohol is an inducer of CYP2E1, increases conversion of paracetamol
to NAPQI, increasing paracetamol toxicity
• Fatal dose reduced to 5-6 g in chronic alcoholics
• Overdose occurs when high dose (>8 g/day) is consumed
• Symptoms: Nausea, vomiting, abdominal pain, liver tenderness,
jaundice, unconsciousness
• ANTIDOTE: N-acetylcysteine (NAC)- repletes the glutathione
• Alternatively, methionine can be used- avoid with charcoal as it will
get bound in charcoal particles hence useless
• Supportive measures: Activated charcoal, gastric lavage
41. Ketorolac
• Good for postoperative pain ( analgesic action
equal to morphine)
• Reduces the dose of opioids in severe pain
• Renal toxicity more than other NSAIDs
• Continuous use >5 days orally and >2 days
i.m/i.v. not recommended due to high
incidence of GIT bleeding and bleeding at
surgical site
42. Indomethacin
• Drug of choice for Acute Gout
• Rheumatoid arthritis
• Ankylosing spondylitis
• Antipyretic in Hodgkin’s disease- fever refractory to other antipyretics
• Medical treatment of Patent Ductus Arteriosus
43. Ibuprofen
• Safest among the traditional NSAIDs
• Effective and safe antipyretic as paracetamol
• Well tolerated in patients who
cannot tolerate other NSAIDs
44. Nimesulide
• Partially selective COX-2 inhibitor, less gastric effects
• Serious life threatening toxic effect- hepatic damage and
agranulocytosis
• BANNED IN MANY COUNTRIES