The document provides information on the history and properties of local anesthesia. It discusses how cocaine was the first local anesthetic isolated in 1860 and procaine was the first widely used synthetic agent in 1905. Key events include the discovery of lidocaine in 1948 and its clinical introduction in 1949. Local anesthesia works by reversibly blocking nerve conduction, producing loss of sensation while maintaining consciousness. The mechanisms of action and properties of various local anesthetic agents are explained.
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.
This document discusses various techniques for achieving local anesthesia in dental procedures. It describes common methods such as local infiltration, field block, nerve block, intraligamentary injection, intraseptal injection, intrapulpal injection, intraosseous injection, jet injection, computer-controlled local anesthetic delivery systems, and electronic dental anesthesia. It also discusses topical anesthesia and provides details on the principles, indications, contraindications, advantages and disadvantages of each technique. The goal is to outline options for effectively achieving anesthesia for different dental treatments and patient situations.
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.
Dr. Shalini Singh's document discusses local anesthetics. It provides definitions, classifications, mechanisms of action, properties and examples of specific local anesthetics. It also covers the history of local anesthetics from early discoveries like cocaine to modern drugs like lidocaine. Complications from both local and systemic effects are discussed.
Local anesthesia in dentistry : RECENT ADVANCESPooja Jayan
This document provides an overview of local anesthesia. It begins with definitions of local anesthesia and discusses its history from the isolation of cocaine in 1859 to the development of modern local anesthetics like lidocaine. It describes the ideal properties, theories of action, classification, composition, maximum doses, armamentarium, techniques for maxillary and mandibular injections, and potential complications. The key information is that local anesthesia temporarily interrupts nerve conduction to produce loss of sensation in a circumscribed area, allowing for painless dental procedures.
This document provides information on various techniques for local anesthesia in dentistry. It discusses the mechanism of action, classifications, and maximum recommended doses of local anesthetics. It also describes in detail techniques for maxillary injections including inferior alveolar nerve block, Gow Gates, and Vazirani Akinosi techniques for mandibular anesthesia. Complications and contraindications of local anesthesia are mentioned.
Local anesthesia is used to induce temporary loss of sensation in a specific area of the body without loss of consciousness. It works by blocking sodium channels and preventing nerve impulse propagation. Common local anesthetics used in dentistry include lidocaine and articaine. They are administered via injection using various needle sizes and lengths. The onset and duration of anesthesia is influenced by factors like pH, lipid solubility, and presence of vasoconstrictors. Local anesthetics provide a safe alternative to general anesthesia for minor dental procedures by restricting effects to localized areas.
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.
This document discusses various techniques for achieving local anesthesia in dental procedures. It describes common methods such as local infiltration, field block, nerve block, intraligamentary injection, intraseptal injection, intrapulpal injection, intraosseous injection, jet injection, computer-controlled local anesthetic delivery systems, and electronic dental anesthesia. It also discusses topical anesthesia and provides details on the principles, indications, contraindications, advantages and disadvantages of each technique. The goal is to outline options for effectively achieving anesthesia for different dental treatments and patient situations.
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.
Dr. Shalini Singh's document discusses local anesthetics. It provides definitions, classifications, mechanisms of action, properties and examples of specific local anesthetics. It also covers the history of local anesthetics from early discoveries like cocaine to modern drugs like lidocaine. Complications from both local and systemic effects are discussed.
Local anesthesia in dentistry : RECENT ADVANCESPooja Jayan
This document provides an overview of local anesthesia. It begins with definitions of local anesthesia and discusses its history from the isolation of cocaine in 1859 to the development of modern local anesthetics like lidocaine. It describes the ideal properties, theories of action, classification, composition, maximum doses, armamentarium, techniques for maxillary and mandibular injections, and potential complications. The key information is that local anesthesia temporarily interrupts nerve conduction to produce loss of sensation in a circumscribed area, allowing for painless dental procedures.
This document provides information on various techniques for local anesthesia in dentistry. It discusses the mechanism of action, classifications, and maximum recommended doses of local anesthetics. It also describes in detail techniques for maxillary injections including inferior alveolar nerve block, Gow Gates, and Vazirani Akinosi techniques for mandibular anesthesia. Complications and contraindications of local anesthesia are mentioned.
Local anesthesia is used to induce temporary loss of sensation in a specific area of the body without loss of consciousness. It works by blocking sodium channels and preventing nerve impulse propagation. Common local anesthetics used in dentistry include lidocaine and articaine. They are administered via injection using various needle sizes and lengths. The onset and duration of anesthesia is influenced by factors like pH, lipid solubility, and presence of vasoconstrictors. Local anesthetics provide a safe alternative to general anesthesia for minor dental procedures by restricting effects to localized areas.
Local anesthesia is defined as a transient reversible loss of sensation caused by blocking nerve conduction in a localized area. There are two types of local anesthetics: amides and esters. Amides such as lidocaine are preferred due to their longer duration of action and lower risk of allergic reactions. Local anesthetic solutions also contain vasoconstrictors to prolong the effects and buffering agents. The document discusses the mechanisms, uses, contraindications and toxicity of local anesthesia in detail. It provides classifications based on duration and vasoconstrictor types used. Potential adverse effects on the central nervous system, cardiovascular system and risks of methemoglobinemia are outlined.
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.
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 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.
The document provides information on local anesthetics including their history, mechanism of action, properties of ideal anesthetics, constituents, and vasoconstrictors. It discusses how local anesthetics work by blocking sodium channels and preventing nerve impulse propagation. Ideal anesthetics should have rapid onset and sufficient duration while being non-toxic, stable, and sterile. Vasoconstrictors are added to local anesthetics to prolong their duration by decreasing absorption and increasing the amount that remains near the nerve.
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
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.
The document provides an overview of local anesthetics. It defines local anesthesia as the loss of sensation in a circumscribed area caused by depression of nerve endings or inhibition of nerve conduction. Local anesthetics reversibly block action potentials in excitable membranes. They are classified based on their chemical structure and duration of action. Properties, composition, indications, contraindications and mechanisms of action are described. The calcium displacement theory and specific receptor theory are discussed in relation to the mechanism by which local anesthetics block nerve conduction.
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
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.
This document discusses various techniques for local anesthesia in the maxilla. It begins by defining local infiltration, field block, and nerve block injections. It then describes specific maxillary injections including supraperiosteal, intraligamentary, intrapulpal, intraosseous, intraseptal, and various nerve blocks of the anterior superior alveolar, middle superior alveolar, and greater palatine nerves. For each technique, it provides indications, contraindications, anatomy anesthetized, complications and failure causes. The anterior superior alveolar nerve block is described in detail as the most common and effective maxillary nerve block.
This document provides an introduction to local anesthesia. It discusses the anatomy and neurohistology of neurons, including the different types of neurons and their functions. It also describes the pathway of pain from the site of injury to the brain. Specifically, it outlines how pain signals travel from first order neurons at the injury site to second order neurons in the spinal cord to third order neurons in the thalamus and somatosensory cortex. Finally, it discusses theories of how local anesthetic agents work to block the propagation of pain impulses, such as by preventing the influx of sodium ions through neuronal gates.
Cocaine
1) Cocaine was the first local anesthetic but has been replaced due to its addictive properties and toxicity.
2) Local anesthetics work by blocking sodium channels and inhibiting nerve impulse conduction, with a faster onset and recovery on small diameter myelinated fibers.
3) Important factors determining a drug's potency and duration include its chemical structure (aromatic, amide/ester, lipophilicity), binding affinity, and rate of metabolism.
Local anesthetics work by blocking sodium channels in nerves, preventing impulse transmission and sensation. The document traces the history of local anesthetics from ancient use of coca leaves to modern drugs like lidocaine. It discusses the development of cocaine as the first local anesthetic and its replacement by safer amide-based drugs like procaine and lidocaine due to cocaine's high toxicity and potential for addiction. The mechanisms of action, factors affecting onset and duration, and properties of common dental anesthetics are also outlined.
The document provides an overview of local anesthesia. It begins with the historical background of local anesthetics starting with cocaine in 1860. It defines local anesthesia and discusses the ideal properties, electrophysiology of nerve conduction, and theories of the mechanism of action. It classifies local anesthetics and discusses their types, biokinetics, metabolism, and armamentarium. It also outlines various local anesthesia injection techniques and potential complications. The document contains a comprehensive but concise review of the fundamentals of local anesthesia.
This document discusses newer advances in local anesthesia (LA) for dental procedures. It summarizes that while LA remains important for pain control, research continues to develop safer methods of administration and new drugs. Specifically, it outlines that adding sodium bicarbonate or CO2 to LA can increase effectiveness by raising pH levels and enhancing diffusion. Newer LA drugs discussed include articaine and centbucridine, and alternative painless methods like EDA and C-CLAD are presented.
Local anesthesia in dentistry /certified fixed orthodontic courses by Indian...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 provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
0091-9248678078
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 provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
00919248678078
This document summarizes recent advances in local anesthesia for dentistry. It discusses newer local anesthetic drugs like articaine and centbucridine that are equally or more effective than lignocaine. It also describes new delivery systems for local anesthesia like computer-controlled local anesthesia delivery systems, jet injectors, and iontophoresis that reduce injection pain and improve patient comfort. Devices like CCLADs allow controlled infusion of anesthetic for more precise needle insertion and placement.
This document discusses complications of local anesthesia. It begins by defining local anesthesia and providing a brief history. It then discusses various local complications that can occur, such as needle breakage, prolonged anesthesia, facial nerve paralysis, and soft tissue injury. Causes of these local complications include needle trauma to nerves, intraneural injection, and hematoma formation around nerves. The document also discusses systemic complications like toxicity and allergic reactions. Prevention strategies aim to avoid nerve trauma during injection and proper use and handling of local anesthetic materials. Most local complications resolve on their own, but persistent cases may require reassurance and follow-up.
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 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.
This document discusses the pharmacology of local anesthesia. It defines local anesthesia as drug-induced reversible blockade of nerve conduction in a specific part of the body without altering consciousness. It describes the ideal properties of local anesthetics and classifies them based on their chemical structure as esters or amides. The document discusses the mechanism of action of local anesthetics in blocking nerve conduction and their pharmacokinetics of absorption, distribution, metabolism and excretion. It also covers the systemic effects, interactions, contraindications and proper use of local anesthetics.
Local anesthesia is defined as a transient reversible loss of sensation caused by blocking nerve conduction in a localized area. There are two types of local anesthetics: amides and esters. Amides such as lidocaine are preferred due to their longer duration of action and lower risk of allergic reactions. Local anesthetic solutions also contain vasoconstrictors to prolong the effects and buffering agents. The document discusses the mechanisms, uses, contraindications and toxicity of local anesthesia in detail. It provides classifications based on duration and vasoconstrictor types used. Potential adverse effects on the central nervous system, cardiovascular system and risks of methemoglobinemia are outlined.
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.
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 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.
The document provides information on local anesthetics including their history, mechanism of action, properties of ideal anesthetics, constituents, and vasoconstrictors. It discusses how local anesthetics work by blocking sodium channels and preventing nerve impulse propagation. Ideal anesthetics should have rapid onset and sufficient duration while being non-toxic, stable, and sterile. Vasoconstrictors are added to local anesthetics to prolong their duration by decreasing absorption and increasing the amount that remains near the nerve.
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
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.
The document provides an overview of local anesthetics. It defines local anesthesia as the loss of sensation in a circumscribed area caused by depression of nerve endings or inhibition of nerve conduction. Local anesthetics reversibly block action potentials in excitable membranes. They are classified based on their chemical structure and duration of action. Properties, composition, indications, contraindications and mechanisms of action are described. The calcium displacement theory and specific receptor theory are discussed in relation to the mechanism by which local anesthetics block nerve conduction.
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
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.
This document discusses various techniques for local anesthesia in the maxilla. It begins by defining local infiltration, field block, and nerve block injections. It then describes specific maxillary injections including supraperiosteal, intraligamentary, intrapulpal, intraosseous, intraseptal, and various nerve blocks of the anterior superior alveolar, middle superior alveolar, and greater palatine nerves. For each technique, it provides indications, contraindications, anatomy anesthetized, complications and failure causes. The anterior superior alveolar nerve block is described in detail as the most common and effective maxillary nerve block.
This document provides an introduction to local anesthesia. It discusses the anatomy and neurohistology of neurons, including the different types of neurons and their functions. It also describes the pathway of pain from the site of injury to the brain. Specifically, it outlines how pain signals travel from first order neurons at the injury site to second order neurons in the spinal cord to third order neurons in the thalamus and somatosensory cortex. Finally, it discusses theories of how local anesthetic agents work to block the propagation of pain impulses, such as by preventing the influx of sodium ions through neuronal gates.
Cocaine
1) Cocaine was the first local anesthetic but has been replaced due to its addictive properties and toxicity.
2) Local anesthetics work by blocking sodium channels and inhibiting nerve impulse conduction, with a faster onset and recovery on small diameter myelinated fibers.
3) Important factors determining a drug's potency and duration include its chemical structure (aromatic, amide/ester, lipophilicity), binding affinity, and rate of metabolism.
Local anesthetics work by blocking sodium channels in nerves, preventing impulse transmission and sensation. The document traces the history of local anesthetics from ancient use of coca leaves to modern drugs like lidocaine. It discusses the development of cocaine as the first local anesthetic and its replacement by safer amide-based drugs like procaine and lidocaine due to cocaine's high toxicity and potential for addiction. The mechanisms of action, factors affecting onset and duration, and properties of common dental anesthetics are also outlined.
The document provides an overview of local anesthesia. It begins with the historical background of local anesthetics starting with cocaine in 1860. It defines local anesthesia and discusses the ideal properties, electrophysiology of nerve conduction, and theories of the mechanism of action. It classifies local anesthetics and discusses their types, biokinetics, metabolism, and armamentarium. It also outlines various local anesthesia injection techniques and potential complications. The document contains a comprehensive but concise review of the fundamentals of local anesthesia.
This document discusses newer advances in local anesthesia (LA) for dental procedures. It summarizes that while LA remains important for pain control, research continues to develop safer methods of administration and new drugs. Specifically, it outlines that adding sodium bicarbonate or CO2 to LA can increase effectiveness by raising pH levels and enhancing diffusion. Newer LA drugs discussed include articaine and centbucridine, and alternative painless methods like EDA and C-CLAD are presented.
Local anesthesia in dentistry /certified fixed orthodontic courses by Indian...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 provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
0091-9248678078
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 provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
00919248678078
This document summarizes recent advances in local anesthesia for dentistry. It discusses newer local anesthetic drugs like articaine and centbucridine that are equally or more effective than lignocaine. It also describes new delivery systems for local anesthesia like computer-controlled local anesthesia delivery systems, jet injectors, and iontophoresis that reduce injection pain and improve patient comfort. Devices like CCLADs allow controlled infusion of anesthetic for more precise needle insertion and placement.
This document discusses complications of local anesthesia. It begins by defining local anesthesia and providing a brief history. It then discusses various local complications that can occur, such as needle breakage, prolonged anesthesia, facial nerve paralysis, and soft tissue injury. Causes of these local complications include needle trauma to nerves, intraneural injection, and hematoma formation around nerves. The document also discusses systemic complications like toxicity and allergic reactions. Prevention strategies aim to avoid nerve trauma during injection and proper use and handling of local anesthetic materials. Most local complications resolve on their own, but persistent cases may require reassurance and follow-up.
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 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.
This document discusses the pharmacology of local anesthesia. It defines local anesthesia as drug-induced reversible blockade of nerve conduction in a specific part of the body without altering consciousness. It describes the ideal properties of local anesthetics and classifies them based on their chemical structure as esters or amides. The document discusses the mechanism of action of local anesthetics in blocking nerve conduction and their pharmacokinetics of absorption, distribution, metabolism and excretion. It also covers the systemic effects, interactions, contraindications and proper use of local anesthetics.
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.
The document provides an overview of local anesthesia including its background, definition, properties, mechanism of action, theories, classification, and complications. It discusses how local anesthetics work by interfering with nerve conduction and blocking sodium channels. The two major types are esters and amides, which are metabolized differently. Proper technique and protocols can help prevent complications like needle breakage, prolonged anesthesia, and nerve injury.
A overview of local anesthesia and various advancement in its modern day approach. A post graduate periodontology approach to application of local anesthesia in day to day dental surgeries and various other dental and maxillofacial treatment procedures.
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 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.
The document defines local anesthesia and classifies local anesthetics. It discusses the mechanism of action, including the non-specific membrane expansion and specific receptor theories. It also covers the electrophysiology of nerve conduction, pharmacology of local anesthetics including onset, duration, and maximum recommended doses. Factors affecting the kinetics like concentration, pH, pKa, lipid solubility and protein binding are explained.
The document discusses local anesthetics (LA), including:
- Their mechanism of action in blocking sodium channels to inhibit nerve conduction and sensation of pain.
- Types include infiltration, nerve block, spinal, epidural, and caudal anesthesia.
- Common LA drugs are procaine, lidocaine, tetracaine, and bupivacaine. Cocaine was the first LA discovered.
- LA chemistry aims to balance lipid solubility for potency versus ionization for reduced toxicity.
1. Local anesthetics work by preventing the generation and conduction of nerve impulses through chemical blockade between the source of impulse and the brain.
2. They act on nerve membranes by decreasing permeability to sodium ions, inhibiting the transmission of action potentials.
3. Doses are presented in milligrams per kilogram of body weight, with a maximum dose between 70-500mg depending on the drug and presence of vasoconstrictors. The dose is reduced for children.
This document provides an overview of local anesthesia in pediatric dentistry. It defines local anesthesia and discusses the history, classification, composition, properties, and mechanisms of local anesthetic agents. It also covers the metabolism, excretion, and systemic effects of local anesthetics. Maximum recommended doses and types of injection procedures for different regions are mentioned. Complications and recent advances in local anesthesia techniques are briefly discussed.
Local anaesthesia is defined as a reversible loss of sensation in a circumscribed area caused by depressing nerve excitation or inhibiting peripheral nerve conduction. It can be induced by low temperature, trauma, anoxia, neurolytic agents like alcohol and phenol, or chemical agents like local anaesthetics. Local anaesthetics work by altering the nerve membrane's resting potential, threshold potential, rate of depolarization, or rate of repolarization. They are available as salts and can exist as uncharged molecules or positively charged ions depending on pH. Local anaesthetics contain the active agent, a vasoconstrictor to decrease absorption, a reducing agent for stability, a preservative, and a vehicle for isotonicity. They are classified based
This document provides an overview of local anesthesia. It begins with the historical background, then defines local anesthesia and discusses relevant anatomy. It explores the physiologic considerations of nerve conduction and impulse propagation. Modes and sites of action for local anesthetics are examined, along with their mechanism of action and pharmacology. Various classifications of local anesthetics are presented based on chemical structure, biological site/mode of action, application method, potency, and duration. Factors influencing local anesthetic action and pharmacokinetics are also summarized.
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 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 anesthetics work by altering the membrane potential of nerve cells and blocking sodium channels, which prevents the propagation of action potentials and results in loss of sensation. Early local anesthetics like cocaine were derived from coca leaves and provided pain relief for surgery. Later developments included procaine, lidocaine, and other synthetic amide and ester local anesthetics. The pharmacokinetics and effects of local anesthetics depend on factors like lipid solubility, pH, vasoconstriction, and metabolism. Toxicity can occur if maximum dosage levels are exceeded.
This document provides an overview of neurophysiology and local anesthetics. It discusses the structure of neurons, nerve conduction, definitions of local anesthesia, and theories of local anesthesia mechanisms. It describes the properties, composition, classification, pharmacokinetics and complications of local anesthetics. Specific local anesthetic drugs like lidocaine, prilocaine and bupivacaine are also discussed. Factors affecting local anesthetic action and contraindications are summarized. Topical local anesthetics like benzocaine and lidocaine are also reviewed.
This document provides an overview of local anesthesia and local anesthetic agents. It begins with definitions of local anesthesia and discusses the desirable properties of local anesthetics. It then covers the history of local anesthesia from early uses of coca leaves to the development of procaine and lidocaine. The rest of the document discusses modes of action, classifications, compositions, examples of local anesthetic agents, and considerations for their safe use.
Or: Beyond linear.
Abstract: Equivariant neural networks are neural networks that incorporate symmetries. The nonlinear activation functions in these networks result in interesting nonlinear equivariant maps between simple representations, and motivate the key player of this talk: piecewise linear representation theory.
Disclaimer: No one is perfect, so please mind that there might be mistakes and typos.
dtubbenhauer@gmail.com
Corrected slides: dtubbenhauer.com/talks.html
Remote Sensing and Computational, Evolutionary, Supercomputing, and Intellige...University of Maribor
Slides from talk:
Aleš Zamuda: Remote Sensing and Computational, Evolutionary, Supercomputing, and Intelligent Systems.
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Inter-Society Networking Panel GRSS/MTT-S/CIS Panel Session: Promoting Connection and Cooperation
https://www.etran.rs/2024/en/home-english/
Phenomics assisted breeding in crop improvementIshaGoswami9
As the population is increasing and will reach about 9 billion upto 2050. Also due to climate change, it is difficult to meet the food requirement of such a large population. Facing the challenges presented by resource shortages, climate
change, and increasing global population, crop yield and quality need to be improved in a sustainable way over the coming decades. Genetic improvement by breeding is the best way to increase crop productivity. With the rapid progression of functional
genomics, an increasing number of crop genomes have been sequenced and dozens of genes influencing key agronomic traits have been identified. However, current genome sequence information has not been adequately exploited for understanding
the complex characteristics of multiple gene, owing to a lack of crop phenotypic data. Efficient, automatic, and accurate technologies and platforms that can capture phenotypic data that can
be linked to genomics information for crop improvement at all growth stages have become as important as genotyping. Thus,
high-throughput phenotyping has become the major bottleneck restricting crop breeding. Plant phenomics has been defined as the high-throughput, accurate acquisition and analysis of multi-dimensional phenotypes
during crop growing stages at the organism level, including the cell, tissue, organ, individual plant, plot, and field levels. With the rapid development of novel sensors, imaging technology,
and analysis methods, numerous infrastructure platforms have been developed for phenotyping.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...AbdullaAlAsif1
The pygmy halfbeak Dermogenys colletei, is known for its viviparous nature, this presents an intriguing case of relatively low fecundity, raising questions about potential compensatory reproductive strategies employed by this species. Our study delves into the examination of fecundity and the Gonadosomatic Index (GSI) in the Pygmy Halfbeak, D. colletei (Meisner, 2001), an intriguing viviparous fish indigenous to Sarawak, Borneo. We hypothesize that the Pygmy halfbeak, D. colletei, may exhibit unique reproductive adaptations to offset its low fecundity, thus enhancing its survival and fitness. To address this, we conducted a comprehensive study utilizing 28 mature female specimens of D. colletei, carefully measuring fecundity and GSI to shed light on the reproductive adaptations of this species. Our findings reveal that D. colletei indeed exhibits low fecundity, with a mean of 16.76 ± 2.01, and a mean GSI of 12.83 ± 1.27, providing crucial insights into the reproductive mechanisms at play in this species. These results underscore the existence of unique reproductive strategies in D. colletei, enabling its adaptation and persistence in Borneo's diverse aquatic ecosystems, and call for further ecological research to elucidate these mechanisms. This study lends to a better understanding of viviparous fish in Borneo and contributes to the broader field of aquatic ecology, enhancing our knowledge of species adaptations to unique ecological challenges.
The ability to recreate computational results with minimal effort and actionable metrics provides a solid foundation for scientific research and software development. When people can replicate an analysis at the touch of a button using open-source software, open data, and methods to assess and compare proposals, it significantly eases verification of results, engagement with a diverse range of contributors, and progress. However, we have yet to fully achieve this; there are still many sociotechnical frictions.
Inspired by David Donoho's vision, this talk aims to revisit the three crucial pillars of frictionless reproducibility (data sharing, code sharing, and competitive challenges) with the perspective of deep software variability.
Our observation is that multiple layers — hardware, operating systems, third-party libraries, software versions, input data, compile-time options, and parameters — are subject to variability that exacerbates frictions but is also essential for achieving robust, generalizable results and fostering innovation. I will first review the literature, providing evidence of how the complex variability interactions across these layers affect qualitative and quantitative software properties, thereby complicating the reproduction and replication of scientific studies in various fields.
I will then present some software engineering and AI techniques that can support the strategic exploration of variability spaces. These include the use of abstractions and models (e.g., feature models), sampling strategies (e.g., uniform, random), cost-effective measurements (e.g., incremental build of software configurations), and dimensionality reduction methods (e.g., transfer learning, feature selection, software debloating).
I will finally argue that deep variability is both the problem and solution of frictionless reproducibility, calling the software science community to develop new methods and tools to manage variability and foster reproducibility in software systems.
Exposé invité Journées Nationales du GDR GPL 2024
hematic appreciation test is a psychological assessment tool used to measure an individual's appreciation and understanding of specific themes or topics. This test helps to evaluate an individual's ability to connect different ideas and concepts within a given theme, as well as their overall comprehension and interpretation skills. The results of the test can provide valuable insights into an individual's cognitive abilities, creativity, and critical thinking skills
When I was asked to give a companion lecture in support of ‘The Philosophy of Science’ (https://shorturl.at/4pUXz) I decided not to walk through the detail of the many methodologies in order of use. Instead, I chose to employ a long standing, and ongoing, scientific development as an exemplar. And so, I chose the ever evolving story of Thermodynamics as a scientific investigation at its best.
Conducted over a period of >200 years, Thermodynamics R&D, and application, benefitted from the highest levels of professionalism, collaboration, and technical thoroughness. New layers of application, methodology, and practice were made possible by the progressive advance of technology. In turn, this has seen measurement and modelling accuracy continually improved at a micro and macro level.
Perhaps most importantly, Thermodynamics rapidly became a primary tool in the advance of applied science/engineering/technology, spanning micro-tech, to aerospace and cosmology. I can think of no better a story to illustrate the breadth of scientific methodologies and applications at their best.
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
2. Cocaine- first local anesthetic agent isolated by NIEMAN-
1860 from the leaves of the coca tree.
Its anesthetic action was demonstrated by KARL KOLLER In
1884.
First effective and widely used synthetic local anesthetic-
PROCAINE-produced by EINHORN in 1905 from benzoic acid
and diethyl amino ethanol.
Its anesthetic properties were identified by BIBERFIELD and
the agent was introduced into clinical practice by BRAUN.
HISTORY
3. LIDOCAINE-LOFGREN in 1948.
The discovery of its anesthetic properties was followed in
1949 by its clinical use by T.GORDH.
4. Local anesthesia is defined as a loss of sensation in a
circumscribed area of the body caused by depression of
excitation in nerve endings or an inhibition of the conduction
process in peripheral nerves. STANLEY F. MALAMED
LOSS OF SENSATION WITHOUT LOSS OF CONSCIOUSNESS…
DEFINITION
An important feature of local anesthesia is that it
produces:
5. PROPERTIES OF LOCAL ANESTHESIA
I==It should not be irritating to tissue to which it is applied
N==It should not cause any permanent alteration of nerve
structure
S==Its systemic toxicity should be low
T==Time of onset of anesthesia should be short
E== It should be effective regardless of whether it is injected
into the tissue or applied locally to mucous membranes
D==The duration of action should be long enough to permit
the completion of procedure
6. It should have the potency sufficient to give complete
anesthesia with out the use of harmful concentration
solutions
It should be free from producing allergic reactions
It should be free in solution and relatively undergo
biotransformation in the body
It should be either sterile or be capable of being sterilized by
heat with out deterioration.
8. STEP 1:
A stimulus excites the nerve, leading to following sequence of
events:
A. An initial phase of slow depolarization.The electrical
potential within nerve become lightly less negative
B. When the falling electrical potential reaches a critical level,
an extremely rapid phase of depolarization results. This is
termed threshold potential or firing threshold.
C. This phase of rapid depolarization results in a reversal of the
electrical potential across the nerve membrane.The interior of
the nerve is now electrically positive in relation to the exterior.
An electrical potential of +40 mV exists on the interior of the
nerve cell.
9. STEP 2: -
After these steps of depolarization,
repolarization occurs. The electrical
potential gradually becomes more
negative inside the nerve cell relative to
outside until the original resting potential
of -70 mV again achieved.
10.
11.
12. MODE AND SITE OF ACTION OF LOCAL
ANESTHETICS
Local anesthetic agent interferes with excitation process in a
nerve membrane in one of the following ways:
Altering the basic resting potential of nerve membrane
Altering the threshold potential
Decreasing the rate of depolarization
Prolonging the rate of repolarization
13. Many theories have been promulgated over the years to explain
the mechanism of action of local anesthetics.
ACETYLECHOLINE THEORY: Stated that acetylcholine was
involved in nerve conduction in addition to its role as a
neurotransmitter at nerve synapses. There is no evidence that
acetylcholine is involved in neural transmission.
WHERE DO LOCAL ANESTHETIC WORKS?
14. CALCIUM DISPLACEMENT THEORY:
States that local anesthetic nerve block was produced by
displacement of calcium from some membrane site that
controlled permeability of sodium. Evidence that varying the
concentration of calcium ions bathing a nerve does not affect
local anesthetic has diminished the credibility of those theory
15. SURFACE CHARGE (REPULSION) THEORY:
Proposed that local anesthetic acted by binding to nerve
membrane and changing the electrical potential at the
membrane surface. Cationic drug molecule were aligned at the
membrane water interface, and since some of the local
anesthetic molecule carried a net positive charge, they made
the electrical potential at the membrane surface more positive,
thus decreasing the excitability of nerve by increasing the
threshold potential. Current evidence indicate that resting
potential of nerve membrane is unaltered by local anesthetic.
16. MEMBRANE EXPANSION THEORY
It states that local anesthetic molecule diffuse to hydrophobic
regions of excitable membranes,producing a general
disturbance of bulk membrane structure, expanding membrane,
and thus preventing an increase in permeability to sodium ions.
Lipid soluble LA can easily penetrate the lipid portion of cell
membrane changing the configuration of lipoprotein matrix of
nerve membrane. This results in decreased diameter of sodium
channel, which leads to inhibition of sodium conduction and
neural excitation.
17.
18. SPECIFIC RECEPTOR THEORY:
The most favored today, proposed that local anesthetics
act by binding to specific receptors on sodium
channel the action of the drug is direct, not mediated
by some change in general properties of cell
membrane. Biochemical and electrophysiological
studies have indicated that specific receptor sites for
local anesthetic agents exists in sodium channel
either on its external surface or on internal
axoplasmic surface. Once the LA has gained access
to receptors, permeability to sodium ion is decreased
or eliminated and nerve conduction is interrupted.
19. DISSOCIATION OF LOCAL ANESTHETICS
• Local anesthetics are available as salts (usually
hydrochlorides) for clinical use.
• The salts, both water soluble and stable, is dissolved in either
sterile water or saline.
• In this solution it exists simultaneously as
unchanged molecule (RN), also called base and
positively charged molecules (RNH+) called cations.
RNH+ ==== RN+ H+
20. The relative concentration of each ionic form in the solution
varies in the pH of the solution or surrounding tissue.
In the presence of high concentration of hydrogen ion (low
pH) the equilibrium shifts to left and most of the anesthetic
solution exists in cationic form.
RNH+ > RN + H+
As hydrogen ion concentration decreases (higher pH) the
equilibrium shifts towards the free base form.
RNH+ < RN + H+
21. • The relative proportion of ionic form also depends on pKa or
DISSOCIATION CONSTANT, of the specific local anesthetic.
• The pKa is a measure of molecules affinity for H+ ions.
• When the pH of the solution has the same value as pKa of the
local anesthetic, exactly half the drug will exists in the RNH+
form and exactly half in RN form.
• The percentage of drug existing in either form can be
determined by Henderson Hasselbalch equation
22. • Henderson hasselbach equation
Determines how much of a local anesthetic will be in a non-
ionized vs ionized form . Based on tissue pH and anesthetic Pka
.
• Injectable local anesthetics are weak bases (pka=7.5-9.5)
When a local anesthetic is injected into tissue it is neutralized
and part of the ionized form is converted to non-ionized
The non-ionized base is what diffuses into the nerve.
23. • Hence if the tissue is infected, the pH is lower (more acidic) and
according to the HH equation; there
will be less of the non-ionized form of the drug to cross into the
nerve (rendering the LA less effective)
• Once some of the drug does cross; the pH in the nerve will be
normal and therefore the LA re-equilibrates to both the ionized and
non-ionized forms; but there are fewer cations which may cause
incomplete anesthesia.
24. MECHANISM OF ACTION OF LOCAL ANESTHETICS
The following sequence is proposed mechanism of action of LA:
Displacement of calcium ions from the sodium channel
receptor site
Binding of local anesthetic molecule to this receptor site
Blockade of sodium channel
25. Decrease in sodium conductance
Depression of rate of electrical depolarization
Failure to achieve the threshold potential level
Lack of development of propagated action potential
Conduction blockade…
27. COMERCIALLY PREPARED LOCAL ANESTHESIA CONSISTS OF:
Local anesthetic agent : lignocaineHCL 2%(20mg/ml)
Vasoconstrictor -adrenaline 1:80,000)
Reducing agent -sodium metabisulphite
Preservative -methylparaben,capryl hydrocuprienotoxin
Fungicide -thymol
Diluting agent: Distillded water
Isotonic solution: NaCl or Ringers solution-6mg
Nitogen bubble: 1-2 mm in diameter and is present to
prevent oxygen from being trapped in the cartridge and
potentially destroying the vasopressor.
28. LOCAL ANESTHETIC AGENT
The local anesthetics used in dentistry are divided into two
groups:
ESTER GROUP
AMIDE GROUP
29. ESTER GROUP:
It is composed of the following
An aromatic lipophilic group
An intermediate chain containing an ester linkage
A hydrophilic secondary or tertiary amino group
AMIDE GROUP:
It is composed of the following
An aromatic, lipophilic group
An intermediate chain containing amide linkage
A hydrophilic secondary or tertiary amino group
30.
31. CLASSIFICATION OF LOCAL ANESTHETICS ESTERS
Esters of benzoic acid
Butacaine
Cocaine
Benzocaine
Hexylcaine
Piperocaine
Tetracaine
Esters of Para-amino
benzoic acid
Chloroprocain
Procaine
Propoxycaine
33. CLASSIFICATION OF LOCAL
ANESTHETIC SUBSTANCES
ACCORDING TO BIOLOGICAL SITE
AND MODE OF ACTION
CLASS A: Agents acting at receptor site on external
surface of nerve membrane
Biotoxins (e.g., tetrodotoxin and saxitoxin)
CLASS B: Agents acting on receptor sites on internal
surface of nerve membrane.
Quaternary ammonium analogues of lidocaine, scorpion venom
34. CLASS C: Agents acting by receptor independent of physiochemical
mechanism
Chemical substance: Benzocaine.
CLASS D: Agents acting by combination of receptors and receptor
independent mechanisms
Chemical substance: most clinically useful
anesthetic agents.(e.g. lidocaine, mepivacaine, prilocaine)
35. PHARMACOKINETICS OF LOCAL ANESTHETICS
UPTAKE:
When injected into soft tissue most local anesthetics produce
dilation of vascular bed.
Cocaine is the only local anesthetic that produces
vasoconstriction, initially it produces vasodilation which is
followed by prolonged vasoconstriction.
Vasodilation is due to increase in the rate of absorption of the
local anesthetic into the blood, thus decreasing the duration of
pain control while increasing the anesthetic blood level and
potential for over dose.
36. ORAL ROUTE:
Except cocaine, local anesthetics are poorly absorbed from
GIT
Most local anesthetics undergo hepatic first-pass effect
following oral administration.
72% of dose is biotransformed into inactive metabolites
TOCAINIDE HYDROCHLORIDE an analogue of lidocaine is
effective orally
37. TOPICAL ROUTE:
Local anesthetics are absorbed at different rates after
application to mucous membranes, in the tracheal mucosa
uptake is as rapid as with intravenous administration.
In pharyngeal mucosa uptake is slow
In bladder mucosa uptake is even slower
Eutectic mixture of local anesthesia (EMLA) has been
developed to provide surface anesthesia for intact skin.
38. INJECTION:
The rate of uptake of local anesthetics after injection is
related to both the vascularity of the injection site and the
vasoactivity of the drug.
IV administration of local anesthetics provide the most rapid
elevation of blood levels and is used for primary treatment of
ventricular dysrhythmias.
39. DISTRIBUTION
Once absorbed in the blood stream local anesthetics are
distributed through out the body to all tissues.
Highly perfused organs such as brain, head, liver, kidney,
lungs have higher blood levels of anesthetic than do less
higher perfused organs.
40. The blood level is influenced by the following factors:
Rate of absorption into the blood stream.
Rate of distribution of the agent from the vascular
compartment to the tissues.
Elimination of drug through metabolic and/or excretory
pathways.
All local anesthetic agents readily cross the blood-brain
barrier, they also readily cross the placenta.
41. METABOLISM (BIOTRANSFORMATION)
ESTER LOCAL ANESTHETICS:
Ester local anesthetics are hydrolyzed in the plasma by the
enzyme pseudocholinesterase.
Chloroprocaine the most rapidly hydrolyzed, is the least toxic.
Tertracaine hydrolyzed 16 times more slowly than
Chloroprocaine ,hence it has the greatest potential toxicity.
42. AMIDE LOCAL ANESTHETICS
The metabolism of amide local anesthetics is more
complicated then esters. The primary site of
biotransformation of amide drugs is liver.
Entire metabolic process occurs in the liver for lidocaine,
articaine, etidocaine, and bupivacaine.
Prilocaine undergoes more rapid biotransformation then the
other amides.
43. EXCREATION
Kidneys are the primary excretory organs for both the local
anesthetic and its metabolites
A percentage of given dose of local anesthetic drug is
excreted unchanged in the urine.
Esters appear in only very small concentration as the parent
compound in urine.
Procaine appears in the urine as PABA (90%) and 2%
unchanged.
10% of cocaine dose is found in the urine unchanged.
Amides are present in the urine as a parent compound in a
greater percentage then are esters.
44. VASOCONSTRICTORS
Constrict vessels and decrease blood flow to the site of
injection.
Absorption of LA into bloodstream is slowed, producing
lower levels in the blood.
Lower blood levels lead to decreased risk of overdose (toxic)
reaction.
Higher LA concentration remains around the nerve
increasing the LA's duration of action.
45. Minimize bleeding at the site of administration.
Naturally Occurring Vasoconstrictors:
- Epinephrine
- Norepinephrine
Vasoconstrictors should be included unless contraindicated.
Mode of Action - Attach to and directly stimulate adrenergic
receptors . Act indirectly by provoking the release of
endogenous catecholamine from intraneuronal storage sites.
46. Concentrations of Vasoconstrictor in Local Anesthetics -
1:50,000, 1:80,000, 1:100,000,
1:200,000 - 0.020mg/ml, 0.012mg/ml, 0.010mg/ml, 0.005
mg/ml
Calculation 1:50,000= 1gram/50,000ml=1000mg/50,000ml=
1mg/50ml= 0.02mg/ml
Levonordefrin - One fifth as active as epinephrine
Vasoconstrictors - Unstable in Solution
49. OTHER COMMON NAMES- Tuberosity block, zygomatic block.
NERVE ANESTHETIZED- Posterior superior alveolar nerve and
branches.
AREA ANESTHETIZED-
1.Pulps of the maxillary third, second, and first molars (entire
tooth=72%; mesiobuccal root of the maxillary first molar not
anesthetized=28%)
2.Buccal periodontium and bone overlying these teeth.
INDICATION
1.When treatment involves two or more maxillary molars.
50. 1. A 27- gauge short needle recommended
2. Area of insertion: height of the mucobuccal fold above the
maxillary second molar
3. Target area: PSA nerve- posterior, superior, and medial to
the posterior border of the maxilla
4. LANDMARKS :
a. Mucobuccal fold
b. Maxillary tuberocity
c. Zygomatic process of maxilla
TECHNIQUE
51.
52. 5.Procedure:
a. Assume the correct position
1)For a left PSA nerve block, a right handed administrater should
sit at the 10 o’ clock position facing the patient.
2)For a right PSA block, a right handed administrater should sit at
the 8 ‘ clock position .
b. Prepare the tissues at the height of the mucobuccal fold for
penetration.
c. Orient the bevel of the needle toward bone.
d. Partially open the patients mouth, pulling the mandible to the side
of injection.
e.Insert the needle into height of mucobuccal fold over second molar
f.Advance the needle slowly in an upward, inward, and backward
direction in one movement.
g.Advanc the needle to the desired depth ( in an adult of normal
size, needle penetration depth is 16 mm)
h. Aspirate in two plane, if both aspirations are negative , deposi
0.9 to 1.8 ml of anesthetic solution slowly over 30 to 60 seconds.
54. Provides pulpal anaesthesia to the maxillary premolars and
the mesiobuccal root of the maxillary first molar,and
supporting buccal soft and hard tissues.
Recommended needle-27 gauge short.
MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK
55. INICATIONS:
1.Where the ASA nerve block fails to provide pupal anesthesia
distal to the maxillary canine
2.Dental procedures involving both maxillary premolars only.
TECHNIQUE:
-Area of insertion: height of mucobuccal fold above the
maxillary second premolar
-Assume the correct position
-Insert the needle into height the height of mucobuccal fold
above second premolar with the bevel directed toward bone
-Penetrate the mucous membrane slowly advance the needle
until its tip is located well above the apex of second premolar.
-Aspirate
56. Slowly deposit 0.9 to 1.2 ml of solution( approx. in 30 to 40
seconds)
60. AREA ANESTHETIZED:
1.Pulps of the maxillary central incisor to the canine on
injected side
2.In about 72% of patients, pulps of the maxillary premolars
and mesiobuccal root of the first molar
3. Buccal periodontium and bone of these same teeth
4. Lower eyelid ,lateral aspect of nose, upper lip
61. AREA OF INSERTION: height of mucobuccal fold directly over first premolar
TARGET AREA: infraorbital foramen
LANDMARKS:
Mucobuccal fold
infraorbital notch
infraorbital foramen
PROCEDURE
-Assume the correct position
-prepare the tissue at the injection site
-Locate the infraorbital foramen
-Maintain finger on the foramen or mark the skin at the site
-Insert the needle into the height o mucobuccal fold over the first premolar with
the bevel facing bone
-Orient syringe toward the infraorbital foramen
-The needle should be hel parellel with the long axis of the tooth as it is
advanced, to avoid premature contact with bone
-Advance the needle slowly until bone is gently contacted.
-Aspirate in two planes
-Slowly deposit 0.9 to 1.2 ml solution.
TECHNIQUE
63. AREA ANESTHETIZED:
Provides anesthesia to the posterior portion of the hard
palate and its overlying soft tissues extending anteriorly as
far as the first premolar and medially to the midline
64. TARGET AREA: greater palatine nerve as it passes anteriorly between
soft tissues and bone of the hard palate
LANDMARK:greater palatine foramen and junction of maxillary
alveolar process and palatine bone
AREA OF INSERTION: soft tissue slightly anterior to greater palatine
foramen
PATH OF INSRTION: advance the syringe from opposite side of the
mouth at a right angle to the target area
PROCEURE
-Assume the correct position
-Locate greater palatine foramen
-Direct the syringe into the mouth from opposite side with the needle
approching the injection site at right angle
Place the bevel of needle gently against the previously blanched soft
tissue at the injection site
-Slowly advance the needle until palatine bone is gently contacted.
Aspirate , slowly deposite 0.45 to 6ml of LA solution
TECHNIQUE
66. Provides anaesthesia to the anterior portion of the hard
palate,affecting both soft and hard tissues,from the mesial of
the right first premolar to the mesial of the left first premolar.
AREA ANESTHETIZED
67. AREA OF INSERTION: palatal mucosa just lateral to the incisive papilla(
located in the midline behind the central incisor)
TARGET AREA: incisive foramen beneath the incisive papilla
LANDMARK: Central incisor and incisive papilla
PATH OF INSERTION: approach the injection site at a 45 degree angle
toward incisive papilla.
PROCEDURE:
-Assume the correct position
-prepare the tissue just lateral to the incisive papilla
-Place the bevel against the ischemic soft tissues at the injection site
-Straighten the needle and permit the bevel to penetrate the mucosa.
-Slowly advance the needle toward incisive foramen until bone is gently
contacted
-Withdraw the needle 1 mm to prevent subperiosteal injection
-Aspirate
-Slowly deposit 0.45 ml of local anesthetic solution
70. Mandibular teeth to the midline
Body of the mandible, inferior portion of the ramus
Buccal mucoperiosteum, mucous membrane anterior to the
mental foramen
Anterior two third of the tongue and floor of the oral cavity
Lingual soft tissues and periosteum
AREA ANESTHETIZED
71. A long dental needle is recommended for the adult patient.
A 25-gauge long needle is preferred
LANDMARKS:
-Coronoid notch( greatest concavity on the anterior border of
ramus)
-Pterygomandibular raphe
-Occlusal plane of mandibular posterior teeth
TARGET AREA: Inferior alveolar nerve as it passes downward
toward the mandibular foramen
AREA OF INSERTION: Mucous membrane on the medial side of
mandibular ramus
TECHNIQUE
72. PROCEDURE
-locate the needle penetration site
three parameters must be considered during administration of
IANB:
1)The height of injection
2)The antero-posterior placement of needle
3)The depth of penetration
-Place the syringe barrel in the corner of the mouth on the
contralateral side
-Insert the needle: when bone is contacted, withdraw
approximately 1 mm to prevent subperiosteal injection
-Aspirate in two plan. If negative, slowly deposit 1.5 ml of
anesthetic solution over a minimum of 60 seconds.
-Slowly withdraw the syringe, and when approximately half of its
length remains within tissues, reaspirate. If negative, deposit a
portion of the remaining solution(0.2 ml) to anesthetize the
lingual nerve.
74. AREA ANESTHETIZED: Soft tissue and periostium buccal to
the mandibular molar teeth.
LONG BUCCAL NERVE BLOCK
75.
76. TECHNIQUE:
LANDMARK: Mandibular molars, mucobuccal fold
TARGET AREA: Buccal nerve as it passes over the anterior border of the
ramus
AREA OF INSERTION: Mucous membrane distal and buccal to the most
distal molar tooth in the arch
-Prepare the tissues for penetration distal and buccal to the most
posterior molar.
-Penetrate mucous membrane at the injection site, distal and buccal to
the last molar
-Advance the needle slowly untill mucoperiosteum is gently contacted
-The depth of penetration is seldom more than 2 to 4 mm, and usually
only 1 or 2 mm.
-Aspirate
-If negative, slowly deposit 0.3 ml over 10 seconds.
80. AREA ANESTHETIZED:
Mandibular teeth to the midline
Buccal mucoperiosteum and mucous membranes on the side
of injection
Anterior two third of the tongue and floor of the oral cavity
Lingual soft tissues and periosteum
Body of the mandible, inferior portion of the ramus
Skin over the zygoma, posterior portion of the cheek, and
temporal regions
81.
82. AREA OF INSERTION: Mucous membrane on the mesial of the
mandibular ramus, on a line from the intertragic notch to the
corner of the mouth, just distal to the maxillary second molar