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Local anaesthetics work by inhibiting the conduction of electrical impulses in peripheral nerves. They do this by preventing the entry of sodium ions needed to produce the depolarization stage of the action potential. There are two theories for how this is accomplished - the non-specific membrane expansion theory, where the local anaesthetic attaches to and swells the cell membrane to block sodium channels, and the specific receptor theory, where the local anaesthetic binds to specific sodium channel receptors to prevent ion flow. Common local anaesthetics include lidocaine, prilocaine, articaine, and bupivacaine, which each have varying properties in terms of onset time, duration of effect, formulations, and maximum safe dosages.
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Local anesthesia
Local anesthesia is the reversible loss of sensation in a body area caused by inhibiting nerve conduction. This document discusses the introduction, composition, mechanism of action, and dose calculation of local anesthesia. It covers topics like nerve physiology, electrophysiology of nerve conduction, impulse propagation, and the site and mode of action of local anesthetics. The document provides details on how local anesthetics work by blocking sodium channels and raising the firing threshold of nerves.
Use dependent & voltage dependent
This document discusses sodium channels, the generation of action potentials, local anesthetics, and their mechanisms of action. It contains the following key points:
1) Sodium channels have two gates, h-gates and m-gates, that open and close during an action potential.
2) Local anesthetics reversibly block sodium channels, preventing the generation of action potentials and nerve conduction.
3) Local anesthetics act in a use-dependent and voltage-dependent manner, blocking more sodium channels when they are open or activated.
Salah
Local anesthetics work by preventing the generation and conduction of nerve impulses. They do this by altering the nerve membrane's threshold potential, slowing the rate of depolarization so the membrane potential does not reach the firing level needed to produce an action potential. The primary site of action is the nerve membrane, where local anesthetics decrease the rate of depolarization during nerve excitation, preventing a propagated impulse from developing and interpretation of sensation by the brain.
Local anaesthesia
Local anaesthesia involves blocking nerve transmission through injection of local anaesthetic drugs near nerve endings or trunks. The document discusses various local anaesthetics including esters like cocaine and procaine, and amides like lidocaine, bupivacaine and prilocaine. It describes how local anaesthetics work by inhibiting sodium channels and preventing nerve impulse conduction. The ideal properties, structures, mechanisms of action, and uses of different local anaesthetics are summarized.
Physiology of local anasthesia
This document discusses the physiology of local anesthesia. It begins by describing nerve anatomy, with peripheral nerves composed of axons bundled together. The nerve membrane is selectively permeable and maintains ion concentration gradients. Local anesthetics work by blocking sodium channels and preventing nerve impulse generation and conduction. Factors like pH, lipid solubility, and protein binding affect how long local anesthesia lasts. Common local anesthetics are classified as ester or amide types. Vasoconstrictors are often added to local anesthetics to prolong their duration and reduce toxicity. Adrenaline is a commonly used vasoconstrictor that acts on alpha and beta receptors.
Local anaesthesia
Local anesthetics work by preventing the entry of sodium ions into neurons, inhibiting the propagation of action potentials and conduction in peripheral nerves. There are two theories for how this occurs - the non-specific membrane expansion theory where the anesthetic attaches to and swells the cell membrane blocking sodium channels, and the specific receptor theory where it binds to receptors on sodium gates. Common local anesthetics discussed include lidocaine, prilocaine, articaine, and bupivacaine, each with different properties in terms of onset, duration, and maximum dosage.
Local anesthesia 2
This document provides an overview of local anesthesia. It discusses the historical background of local anesthetics beginning with cocaine in the 1860s. It defines local anesthesia and describes the mechanisms of action, desirable properties, and theories regarding how local anesthetics work. The document outlines the classification, mode of action, descriptions, and administration techniques of various local anesthetic agents. It also discusses complications and special patient groups.
La seminar
This document provides an overview of local anesthesia in dentistry. It begins with definitions and a brief history of local anesthesia. It then discusses the classification, properties, and mechanisms of action of local anesthetics. Specific local anesthetics like lidocaine, bupivacaine and articaine are described. The document outlines maximum recommended doses and durations of different local anesthetics. It also discusses potential complications and undesired effects. Finally, it reviews common local anesthesia techniques like infiltration, field block, and topical administration.
Recommended
Local anesthesia
Local anesthesia is the reversible loss of sensation in a body area caused by inhibiting nerve conduction. This document discusses the introduction, composition, mechanism of action, and dose calculation of local anesthesia. It covers topics like nerve physiology, electrophysiology of nerve conduction, impulse propagation, and the site and mode of action of local anesthetics. The document provides details on how local anesthetics work by blocking sodium channels and raising the firing threshold of nerves.
Use dependent & voltage dependent
This document discusses sodium channels, the generation of action potentials, local anesthetics, and their mechanisms of action. It contains the following key points:
1) Sodium channels have two gates, h-gates and m-gates, that open and close during an action potential.
2) Local anesthetics reversibly block sodium channels, preventing the generation of action potentials and nerve conduction.
3) Local anesthetics act in a use-dependent and voltage-dependent manner, blocking more sodium channels when they are open or activated.
Salah
Local anesthetics work by preventing the generation and conduction of nerve impulses. They do this by altering the nerve membrane's threshold potential, slowing the rate of depolarization so the membrane potential does not reach the firing level needed to produce an action potential. The primary site of action is the nerve membrane, where local anesthetics decrease the rate of depolarization during nerve excitation, preventing a propagated impulse from developing and interpretation of sensation by the brain.
Local anaesthesia
Local anaesthesia involves blocking nerve transmission through injection of local anaesthetic drugs near nerve endings or trunks. The document discusses various local anaesthetics including esters like cocaine and procaine, and amides like lidocaine, bupivacaine and prilocaine. It describes how local anaesthetics work by inhibiting sodium channels and preventing nerve impulse conduction. The ideal properties, structures, mechanisms of action, and uses of different local anaesthetics are summarized.
Physiology of local anasthesia
This document discusses the physiology of local anesthesia. It begins by describing nerve anatomy, with peripheral nerves composed of axons bundled together. The nerve membrane is selectively permeable and maintains ion concentration gradients. Local anesthetics work by blocking sodium channels and preventing nerve impulse generation and conduction. Factors like pH, lipid solubility, and protein binding affect how long local anesthesia lasts. Common local anesthetics are classified as ester or amide types. Vasoconstrictors are often added to local anesthetics to prolong their duration and reduce toxicity. Adrenaline is a commonly used vasoconstrictor that acts on alpha and beta receptors.
Local anaesthesia
Local anesthetics work by preventing the entry of sodium ions into neurons, inhibiting the propagation of action potentials and conduction in peripheral nerves. There are two theories for how this occurs - the non-specific membrane expansion theory where the anesthetic attaches to and swells the cell membrane blocking sodium channels, and the specific receptor theory where it binds to receptors on sodium gates. Common local anesthetics discussed include lidocaine, prilocaine, articaine, and bupivacaine, each with different properties in terms of onset, duration, and maximum dosage.
Local anesthesia 2
This document provides an overview of local anesthesia. It discusses the historical background of local anesthetics beginning with cocaine in the 1860s. It defines local anesthesia and describes the mechanisms of action, desirable properties, and theories regarding how local anesthetics work. The document outlines the classification, mode of action, descriptions, and administration techniques of various local anesthetic agents. It also discusses complications and special patient groups.
La seminar
This document provides an overview of local anesthesia in dentistry. It begins with definitions and a brief history of local anesthesia. It then discusses the classification, properties, and mechanisms of action of local anesthetics. Specific local anesthetics like lidocaine, bupivacaine and articaine are described. The document outlines maximum recommended doses and durations of different local anesthetics. It also discusses potential complications and undesired effects. Finally, it reviews common local anesthesia techniques like infiltration, field block, and topical administration.
Local anasthesia
The document discusses local anesthesia, including definitions, classifications, mechanisms of action, and pharmacology. It defines local anesthesia as a transient reversible loss of sensation caused by depression of nerve endings or inhibition of nerve conduction. It classifies local anesthetics into esters, amides, quinolines, and combinations. The mechanisms of action include non-specific membrane expansion and specific receptor binding. Key aspects of the pharmacology discussed are kinetics of onset and duration, the effects of pH on drug form, and factors influencing induction time.
Local Anaesthetics
The document summarizes key aspects of local anesthetics including:
1. It discusses the history and development of various local anesthetic compounds.
2. It describes the anatomy and physiology of nerve conduction and how local anesthetics work by blocking sodium channels.
3. It compares the mechanisms of action, pharmacokinetics, and differences between amide and ester local anesthetics.
Local anesthetic agents by Dr. Deepesh
This document provides an overview of local anesthetic agents and techniques used in dentistry. It discusses the history and desired properties of local anesthetics. It covers the electrophysiology of nerve conduction and various theories of how local anesthetics produce nerve blockade. The document examines the structure, classification, pharmacology, and clinical actions of specific local anesthetic agents. It also addresses complications from local anesthetics and techniques for their administration.
Local anesthesis
This document discusses local anesthesia, including how it works and its properties. It begins by defining local anesthesia as a loss of sensation caused by depressing nerve endings or inhibiting nerve conduction. It then discusses various methods of inducing local anesthesia and desirable properties like reversibility and lack of toxicity. The bulk of the document focuses on neurophysiology, explaining how nerves generate and transmit impulses through changes in electrolyte permeability and membrane potential. It discusses several theories for how local anesthetics specifically block nerve conduction, settling on the theory that they displace calcium from sodium channels, blocking sodium conductance and preventing action potentials. It notes local anesthesia is less effective in inflamed areas due to changes in pH. The document concludes by providing an example dose calculation
Local anesthesia
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Pharmacology of local anaesthetics
1. Local anesthetics work by reversibly blocking sodium channels in nerves, preventing the transmission of nerve impulses and causing numbness.
2. Cocaine was the first local anesthetic used clinically in the 1880s, but its addictive properties led to the development of safer synthetic options like procaine and lidocaine.
3. Local anesthetics are administered topically, via infiltration of tissues, or through peripheral nerve blocks to temporarily numb areas of the body for procedures. Their effects are reversible and they do not damage nerves when used properly.
L a agents
This document provides information on local anesthetic agents including their definition, history, chemistry, mechanism of action, and clinical pharmacology. It defines local anesthetics as drugs that reversibly block nerve impulse generation and conduction. The first effective local anesthetic was procaine, introduced in 1905. Local anesthetics work by inhibiting the passage of sodium ions through voltage-gated sodium channels in nerve membranes. Their onset, duration, and potency depend on factors like protein binding, dose, and site of administration. Local anesthetics are classified based on their relative potency, onset, minimum concentration for conduction blockade, and duration of action.
Local anesthetic agents
The document outlines local anesthetic agents used in surgery. It discusses the definition of local anesthetics, the ideal properties, and brief history. It then covers classification based on biological sites/mechanism of action and chemical structure. The document outlines the anatomy and physiology of neurons involved in nerve conduction and the mechanism of action of local anesthetics in blocking nerve conduction. It discusses pharmacokinetics including uptake, distribution, metabolism and excretion. It also covers factors affecting drug action and applications of local anesthetics in different surgical procedures.
Pharmacology 2
Local anesthesia works by temporarily blocking nerve impulses in a specific area without loss of consciousness. It involves local anesthetic drugs diffusing through tissues and binding to sodium channels in nerve cell membranes, preventing the conduction of nerve impulses and sensation in the anesthetized area. The proportion of charged and uncharged drug molecules depends on properties like the drug's pKa and tissue pH, with more uncharged molecules able to diffuse through membranes and induce anesthesia faster.
Local anaesthesia
Local anesthetics work by blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and conduction of sensations. This document discusses the classification, composition, mechanisms of action, and examples of commonly used local anesthetic drugs and vasoconstrictors. It also covers the techniques for maxillary nerve blocks and factors that influence the onset and duration of local anesthesia.
Local anaesthetics
This document provides an overview of regional anaesthetics. It begins by defining regional anaesthesia as anaesthesia of a segment of the body through peripheral or neuraxial interruption of nerve transmission without loss of consciousness. The document then discusses the history of local anaesthetics from cocaine in the 1860s to modern agents like lidocaine and bupivacaine. It also covers the classification, mechanisms of action, pharmacological properties and therapeutic uses of various local anaesthetic agents.
local anesthesia by d. zakaria k.mansour
The document discusses local anesthetics, including their definitions, classifications, mechanisms of action, routes of administration, and pharmacokinetics. Local anesthetics work by blocking sodium channels and preventing the generation and conduction of nerve impulses. There are two main classes - amides like lidocaine, which are metabolized in the liver, and esters like procaine, which can cause allergic reactions and are metabolized in plasma. Factors like lipid solubility, pH, and vasodilation influence the onset and duration of action of local anesthetics.
Pharmacology of local anesthesia
This document provides an overview of pharmacology topics related to local anesthetics. It begins with a brief history of local anesthetics and discusses the chemistry, including the differences between ester and amide local anesthetics. It covers stereoisomerism, structure-activity relationships, and peripheral nerve anatomy. Mechanisms of action are explained, including the roles of lipophilicity, pKa, and ionized vs. non-ionized forms. Pharmacokinetics, systemic absorption, and toxicity risks are also summarized. The document aims to inform on the essential science underlying local anesthetic use and effects.
Local anaesthetics 1
This document provides an overview of local anesthetics for medical students. It defines pain and the pathways involved, then classifies local anesthetics as injectables or surface types. The mechanism of action is described as reversible blockade of voltage-gated sodium channels. Factors influencing sensitivity are discussed. Systemic effects include potential central nervous system stimulation or depression and cardiovascular effects like hypotension. Metabolism and adverse reactions are also summarized. The document aims to review the physiology of pain and mechanisms of local anesthetics.
Local anesthesia /certified fixed orthodontic courses by Indian dental academy
Local anesthesia /certified fixed orthodontic courses by Indian dental academy Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
State of the art comprehensive training-Faculty of world wide repute &Very affordableLocal anaesthetics
A teaching slide set describing the mechanisms of action and clinical use of local anaesthetics. This session is a basic introduction to the pharmacodynamics and pharmacokinetics of local anaesthetics. It is aimed at preclinical medical or dental students, or students in the early years of a pharmacology degree.
local anesthetics pharmacology
1. The seminar discussed the pharmacology of local anesthetics, covering their history, mechanisms of action, and clinical uses.
2. Local anesthetics work by binding to sodium channels in nerve cell membranes and preventing sodium influx, which inhibits nerve impulse conduction.
3. The potency, onset, and duration of local anesthetics depends on factors like their pKa, lipid solubility, and degree of protein binding. This determines their rate of diffusion to nerve fibers and length of action.
Local Anesthesia in Dentistry
The document provides information on local anesthesia, including:
1) It discusses the historical background of local anesthesia, from the isolation of cocaine in 1860 to the development of procaine and lidocaine.
2) It defines local anesthesia as the loss of sensation in a specific body area caused by inhibiting nerve conduction without loss of consciousness.
3) It describes the mechanisms of action of local anesthetics, including that they work by binding to specific receptor sites on sodium channels in nerves to inhibit sodium conduction and excitation.
4) It provides classifications of local anesthetics according to their biological site and mode of action, including examples like lidocaine that work through both receptor-dependent and independent mechanisms.
Neurophysiology of LA
Local anesthesia causes loss of sensation in a specific body area by depressing nerve excitation or inhibiting nerve conduction without loss of consciousness. Local anesthetics work by altering the nerve membrane's resting potential, threshold potential, rate of depolarization, or rate of repolarization. They may act at receptor sites on the membrane surfaces or through physicochemical mechanisms. Anesthetics first block sensation in mantle nerve bundles near the surface before reaching deeper core bundles, potentially explaining inadequate pulpal anesthesia with profound soft tissue effects. Reinjection can provide immediate profound anesthesia but risks tachyphylaxis.
Local anaesthesia
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the rapid influx of sodium ions needed to generate nerve impulses. They bind preferentially to activated sodium channels, inhibiting nerve conduction and establishing a localized loss of sensation. The mechanism of action involves inhibiting nerve depolarization and propagation of impulses by reducing sodium ion influx, thereby preventing transmission of sensations like pain.
Local Anaesthetics
- Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a localized area of the body when applied topically or injected locally. They block the generation and conduction of nerve impulses at the site of contact without damaging neurons.
- Common uses include dentistry, excision procedures, dermatology, and spinal or regional anesthesia. Local anesthetics work by inhibiting sodium influx through voltage-gated sodium channels in neurons, interrupting action potential generation and signal conduction.
- Examples of side effects include central nervous system stimulation or depression in high doses, cardiovascular effects like arrhythmias and hypotension, and hypersensitivity reactions.
Local Anaesthetics
Local Anaesthesia CME presentation by Gareth Wahl discusses local anaesthetics used at SCGH. It covers the physiology of local anaesthetics including the differences between amide and ester types. Commonly used local anaesthetics at SCGH are discussed such as lignocaine, ropivacaine, bupivacaine and prilocaine. The presentation also addresses local anaesthetic toxicology and the treatment options for toxicity including sodium bicarbonate, hyperventilation, and intravenous lipid emulsion therapy. Pearls for local anaesthetic use are also briefly mentioned.
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Local anasthesia
The document discusses local anesthesia, including definitions, classifications, mechanisms of action, and pharmacology. It defines local anesthesia as a transient reversible loss of sensation caused by depression of nerve endings or inhibition of nerve conduction. It classifies local anesthetics into esters, amides, quinolines, and combinations. The mechanisms of action include non-specific membrane expansion and specific receptor binding. Key aspects of the pharmacology discussed are kinetics of onset and duration, the effects of pH on drug form, and factors influencing induction time.
Local Anaesthetics
The document summarizes key aspects of local anesthetics including:
1. It discusses the history and development of various local anesthetic compounds.
2. It describes the anatomy and physiology of nerve conduction and how local anesthetics work by blocking sodium channels.
3. It compares the mechanisms of action, pharmacokinetics, and differences between amide and ester local anesthetics.
Local anesthetic agents by Dr. Deepesh
This document provides an overview of local anesthetic agents and techniques used in dentistry. It discusses the history and desired properties of local anesthetics. It covers the electrophysiology of nerve conduction and various theories of how local anesthetics produce nerve blockade. The document examines the structure, classification, pharmacology, and clinical actions of specific local anesthetic agents. It also addresses complications from local anesthetics and techniques for their administration.
Local anesthesis
This document discusses local anesthesia, including how it works and its properties. It begins by defining local anesthesia as a loss of sensation caused by depressing nerve endings or inhibiting nerve conduction. It then discusses various methods of inducing local anesthesia and desirable properties like reversibility and lack of toxicity. The bulk of the document focuses on neurophysiology, explaining how nerves generate and transmit impulses through changes in electrolyte permeability and membrane potential. It discusses several theories for how local anesthetics specifically block nerve conduction, settling on the theory that they displace calcium from sodium channels, blocking sodium conductance and preventing action potentials. It notes local anesthesia is less effective in inflamed areas due to changes in pH. The document concludes by providing an example dose calculation
Local anesthesia
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Pharmacology of local anaesthetics
1. Local anesthetics work by reversibly blocking sodium channels in nerves, preventing the transmission of nerve impulses and causing numbness.
2. Cocaine was the first local anesthetic used clinically in the 1880s, but its addictive properties led to the development of safer synthetic options like procaine and lidocaine.
3. Local anesthetics are administered topically, via infiltration of tissues, or through peripheral nerve blocks to temporarily numb areas of the body for procedures. Their effects are reversible and they do not damage nerves when used properly.
L a agents
This document provides information on local anesthetic agents including their definition, history, chemistry, mechanism of action, and clinical pharmacology. It defines local anesthetics as drugs that reversibly block nerve impulse generation and conduction. The first effective local anesthetic was procaine, introduced in 1905. Local anesthetics work by inhibiting the passage of sodium ions through voltage-gated sodium channels in nerve membranes. Their onset, duration, and potency depend on factors like protein binding, dose, and site of administration. Local anesthetics are classified based on their relative potency, onset, minimum concentration for conduction blockade, and duration of action.
Local anesthetic agents
The document outlines local anesthetic agents used in surgery. It discusses the definition of local anesthetics, the ideal properties, and brief history. It then covers classification based on biological sites/mechanism of action and chemical structure. The document outlines the anatomy and physiology of neurons involved in nerve conduction and the mechanism of action of local anesthetics in blocking nerve conduction. It discusses pharmacokinetics including uptake, distribution, metabolism and excretion. It also covers factors affecting drug action and applications of local anesthetics in different surgical procedures.
Pharmacology 2
Local anesthesia works by temporarily blocking nerve impulses in a specific area without loss of consciousness. It involves local anesthetic drugs diffusing through tissues and binding to sodium channels in nerve cell membranes, preventing the conduction of nerve impulses and sensation in the anesthetized area. The proportion of charged and uncharged drug molecules depends on properties like the drug's pKa and tissue pH, with more uncharged molecules able to diffuse through membranes and induce anesthesia faster.
Local anaesthesia
Local anesthetics work by blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and conduction of sensations. This document discusses the classification, composition, mechanisms of action, and examples of commonly used local anesthetic drugs and vasoconstrictors. It also covers the techniques for maxillary nerve blocks and factors that influence the onset and duration of local anesthesia.
Local anaesthetics
This document provides an overview of regional anaesthetics. It begins by defining regional anaesthesia as anaesthesia of a segment of the body through peripheral or neuraxial interruption of nerve transmission without loss of consciousness. The document then discusses the history of local anaesthetics from cocaine in the 1860s to modern agents like lidocaine and bupivacaine. It also covers the classification, mechanisms of action, pharmacological properties and therapeutic uses of various local anaesthetic agents.
local anesthesia by d. zakaria k.mansour
The document discusses local anesthetics, including their definitions, classifications, mechanisms of action, routes of administration, and pharmacokinetics. Local anesthetics work by blocking sodium channels and preventing the generation and conduction of nerve impulses. There are two main classes - amides like lidocaine, which are metabolized in the liver, and esters like procaine, which can cause allergic reactions and are metabolized in plasma. Factors like lipid solubility, pH, and vasodilation influence the onset and duration of action of local anesthetics.
Pharmacology of local anesthesia
This document provides an overview of pharmacology topics related to local anesthetics. It begins with a brief history of local anesthetics and discusses the chemistry, including the differences between ester and amide local anesthetics. It covers stereoisomerism, structure-activity relationships, and peripheral nerve anatomy. Mechanisms of action are explained, including the roles of lipophilicity, pKa, and ionized vs. non-ionized forms. Pharmacokinetics, systemic absorption, and toxicity risks are also summarized. The document aims to inform on the essential science underlying local anesthetic use and effects.
Local anaesthetics 1
This document provides an overview of local anesthetics for medical students. It defines pain and the pathways involved, then classifies local anesthetics as injectables or surface types. The mechanism of action is described as reversible blockade of voltage-gated sodium channels. Factors influencing sensitivity are discussed. Systemic effects include potential central nervous system stimulation or depression and cardiovascular effects like hypotension. Metabolism and adverse reactions are also summarized. The document aims to review the physiology of pain and mechanisms of local anesthetics.
Local anesthesia /certified fixed orthodontic courses by Indian dental academy
Local anesthesia /certified fixed orthodontic courses by Indian dental academy Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
State of the art comprehensive training-Faculty of world wide repute &Very affordableLocal anaesthetics
A teaching slide set describing the mechanisms of action and clinical use of local anaesthetics. This session is a basic introduction to the pharmacodynamics and pharmacokinetics of local anaesthetics. It is aimed at preclinical medical or dental students, or students in the early years of a pharmacology degree.
local anesthetics pharmacology
1. The seminar discussed the pharmacology of local anesthetics, covering their history, mechanisms of action, and clinical uses.
2. Local anesthetics work by binding to sodium channels in nerve cell membranes and preventing sodium influx, which inhibits nerve impulse conduction.
3. The potency, onset, and duration of local anesthetics depends on factors like their pKa, lipid solubility, and degree of protein binding. This determines their rate of diffusion to nerve fibers and length of action.
Local Anesthesia in Dentistry
The document provides information on local anesthesia, including:
1) It discusses the historical background of local anesthesia, from the isolation of cocaine in 1860 to the development of procaine and lidocaine.
2) It defines local anesthesia as the loss of sensation in a specific body area caused by inhibiting nerve conduction without loss of consciousness.
3) It describes the mechanisms of action of local anesthetics, including that they work by binding to specific receptor sites on sodium channels in nerves to inhibit sodium conduction and excitation.
4) It provides classifications of local anesthetics according to their biological site and mode of action, including examples like lidocaine that work through both receptor-dependent and independent mechanisms.
Neurophysiology of LA
Local anesthesia causes loss of sensation in a specific body area by depressing nerve excitation or inhibiting nerve conduction without loss of consciousness. Local anesthetics work by altering the nerve membrane's resting potential, threshold potential, rate of depolarization, or rate of repolarization. They may act at receptor sites on the membrane surfaces or through physicochemical mechanisms. Anesthetics first block sensation in mantle nerve bundles near the surface before reaching deeper core bundles, potentially explaining inadequate pulpal anesthesia with profound soft tissue effects. Reinjection can provide immediate profound anesthesia but risks tachyphylaxis.
Local anaesthesia
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the rapid influx of sodium ions needed to generate nerve impulses. They bind preferentially to activated sodium channels, inhibiting nerve conduction and establishing a localized loss of sensation. The mechanism of action involves inhibiting nerve depolarization and propagation of impulses by reducing sodium ion influx, thereby preventing transmission of sensations like pain.
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Local anesthesia /certified fixed orthodontic courses by Indian dental academy
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Local Anaesthetics
- Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a localized area of the body when applied topically or injected locally. They block the generation and conduction of nerve impulses at the site of contact without damaging neurons.
- Common uses include dentistry, excision procedures, dermatology, and spinal or regional anesthesia. Local anesthetics work by inhibiting sodium influx through voltage-gated sodium channels in neurons, interrupting action potential generation and signal conduction.
- Examples of side effects include central nervous system stimulation or depression in high doses, cardiovascular effects like arrhythmias and hypotension, and hypersensitivity reactions.
Local Anaesthetics
Local Anaesthesia CME presentation by Gareth Wahl discusses local anaesthetics used at SCGH. It covers the physiology of local anaesthetics including the differences between amide and ester types. Commonly used local anaesthetics at SCGH are discussed such as lignocaine, ropivacaine, bupivacaine and prilocaine. The presentation also addresses local anaesthetic toxicology and the treatment options for toxicity including sodium bicarbonate, hyperventilation, and intravenous lipid emulsion therapy. Pearls for local anaesthetic use are also briefly mentioned.
Ropivacane: A new break through in regional and neuraxial Blockade
No significant changes in vitals. Minimal bradycardia and fall in BP observed in a few patients.
No significant events like Nausea, Vomiting, Shivering,
Pruritus, Sedation, Respiratory distress etc.
No need for rescue analgesia in 30 patients (75%)
Rescue analgesia given in 10 patients (25%)
Pharmacology of local anesthetics
Local anaesthetics work by reversibly depressing nerve conduction in peripheral nerves, which causes loss of sensation in a localized area. They are administered via various routes including orally, topically, and via injection. After administration, local anaesthetics are distributed throughout the body via blood circulation but only cause numbness in targeted areas by selectively altering the functioning of certain nerve cells. High doses can depress the central nervous system and cause seizures, respiratory arrest, and death by lowering seizure thresholds and depressing brain activity and respiration.
Ropivacaine
Ropivacaine is a long-acting local anesthetic similar to bupivacaine that provides both anesthesia and analgesia. It has decreased cardiotoxicity compared to bupivacaine. Ropivacaine is metabolized in the liver and excreted renally. It works by reversibly blocking sodium ion influx in nerve fibers, inhibiting impulse conduction. It can be used for epidural, spinal, infiltration, and peripheral nerve blocks for surgical anesthesia, C-sections, and postoperative or chronic pain management. Side effects include central nervous system and cardiovascular toxicity at high doses.
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Local anaesthetics pharmacology
Local anesthetics work by reversibly blocking voltage-gated sodium channels, inhibiting nerve impulse transmission. Their potency, onset, and duration of action depend on factors like lipid solubility, pKa, and protein binding. They exist in both charged and uncharged forms, and increasing the proportion of uncharged forms through alkalization can speed onset. Amide local anesthetics generally have a longer duration than esters.
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The document discusses brachial plexus block techniques and reviews relevant anatomy, history, approaches, and complications. It provides an overview of the brachial plexus anatomy and different block techniques like interscalene, supraclavicular, infraclavicular, and axillary blocks. Complications discussed include nerve injuries from mechanical trauma, ischemia, or chemical toxicity from local anesthetics. Proper technique and drug administration are important to minimize risks.
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Local anesthetics work by blocking sodium channels in nerve cell membranes. They exist in both ionized and unionized forms, and a higher pKa means slower onset of action as the drug is less likely to be in the unionized form needed to pass through membranes. Factors like lipid solubility and protein binding determine a drug's potency and duration. Ropivacaine has a sensory blockade similar to bupivacaine but shorter motor blockade, and its duration can be increased through alkalinization. Local anesthetic toxicity is treated by recognizing the symptoms and providing immediate care, treatment, and follow-up which may include Intralipid infusion which is thought to work by sequestering lipophilic drugs.
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Local anesthetics work by blocking sodium channels and preventing the influx of sodium ions needed for nerve impulse conduction. Early pioneers discovered cocaine's local anesthetic properties in the 1880s, leading to other developments like procaine and lidocaine. Local anesthetics are weak bases containing an aromatic ring, amine, and ester or amide linkage. They vary in potency, duration of action, and lipid solubility. The specific receptor theory states they reversibly bind sodium channels intracellularly to block conduction.
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Local anesthetics work by blocking sodium channels in nerve cell membranes, preventing the transmission of electrical signals and therefore sensation. They can access the binding site within the sodium channel when the channel opens briefly, binding tightly and preventing sodium influx. This stops pain signal transmission without affecting signal transmission in non-sensory nerves. The potency of local anesthetics is related to their chemical structure, with aromatic rings and longer linker chains between functional groups generally increasing potency.
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This document discusses the pharmacodynamics and mechanisms of action of local anesthetics. It explains that local anesthetics work by reversibly blocking nerve conduction through either membrane expansion in the lipid cell membrane or specific binding to sodium channels. It then summarizes various local anesthetic drugs, including ester types like cocaine and procaine that are rapidly metabolized, and amide types like lidocaine, prilocaine, and bupivacaine that are metabolized in the liver. It provides details on the dosages, onsets of action, durations of action, and metabolism of several common local anesthetic drugs used in dentistry.
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Local anesthetics work by blocking voltage-gated sodium channels in nerve membranes, preventing the transmission of nerve impulses. They are classified as esters or amides and have varying potencies, onset times, and durations of action. Common uses include local infiltration, peripheral nerve blocks, and epidural or spinal anesthesia. Toxic reactions can involve the central nervous system or cardiovascular system and are treated by supporting vital functions. Proper dosing and addition of vasoconstrictors can limit systemic absorption and toxicity risks.
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Local anaesthesia final_copy_to_put_on_slideshare[1]
- 2. Local Anaesthetics produce loss of pain sensation in a circumscribed area of the body by inhibiting the conduction process in the peripheral nerves.
- 3. In order for us to understand how local anaesthetics work, we first have to look at how electrical impulses are generated and take you back to first year physiology!!
- 5. This picture shows how membrane potential changes with an action potential.
- 6. As we have learnt, nerve impulses are conducted by a wave of action potentials. When a stimulus is great enough to reach the threshold potential of -55mV, sodium ions flow into the neurone. It does so via sodium gates to produce depolarisation.
- 7. When depolarised, the membrane potential is reversed to +40 mV from -70mV. At the same time, there is passive outward diffusion of potassium ions to bring about repolarisation and the membrane potential is again restored to -70mV.
- 8. Local anaesthetics work by preventing the entry of sodium ions to inhibit the propagation of action potentials.
- 9. There are two theories on the subject of how sodium channels are blocked: 1. Non-specific membrane expansion theory 2. Specific receptor theory
- 10. Non-specific membrane expansion theory: The lipophilic part of the local anaesthetic attaches to the cell membrane to cause swelling. This then reduces the size of the sodium channel to obstruct the flow of sodium ions.
- 11. Specific receptor theory: The hydrophilic charged amino terminal binds to specific receptors of the sodium gates to block the passage of sodium ions.
- 12. Lignocaine(Xylocaine) Prilocaine(Citanest) Articaine(Septocaine) Bupivacaine(Marcaine)
- 13. First found by Nils Lofgren in 1943, and has been in clinical use since 1948 used as 2% plain or 2% with 1: 80000 adrenaline Short onset of 2-3 minutes Duration of action for ~ 2hrs Each 2.2ml cartridge contains 44mg of lidocaine Max dose with vasoconstrictor is 7mg/Kg
- 14. Less toxic and metabolises quicker than lignocaine. Used as 4% plain or 3% with IU/ml Felypressin; Felypressin is an analogue of Oxytocin. Oxytocin induces labour hence its use should be avoided in pregnant women. Slower onset of 4 minutes. Max dose is 6mg/Kg. A metabolite of prilocaine can very rarely oxidise heme to cause methemoglobinemia. This of course, reduces the oxygen carrying capacity of haemoglobin. Consequently the patient becomes hypoxic.
- 15. The molecular structure of articaine is different from other local anaesthetics due to the presence of a thiophene ring. It also contains an additional ester group which is metabolized by estearases found in the blood and tissues. For this reason. Articaine is hydrolysed quicker than other anaesthetics. -used as 4% solution with 1:100000 or 1:200000 adrenaline. More rapid onset. Anaesthesia is more profound. Maximum dose 7mg/kg.
- 16. used as 0.25% or 5% solution with 1: 200000adrenaline. Onset of 5 minutes. Can last for ~8 hours. Used for longer duration surgery, post- operative pain control and pain control for intractable facial pain. Maximum dose 1.3mg/kg.
- 17. THIS IS THE END OF THE SLIDE SHOW ON LOCAL ANAESTHETICS