Dental Courses by 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
Local anaesthetis /certified fixed orthodontic courses by Indian dental academy 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 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.
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and preventing pain sensation. Lidocaine was the first modern local anesthetic introduced in 1940. Local anesthetics are either esters or amides, with amides like lidocaine causing less allergic reactions. The onset and duration of local anesthetics is influenced by their lipid solubility, pH, presence of vasoconstrictors, and peak circulation levels to avoid toxicity.
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.
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.
Unconventional modes of anaesthetic administrationSelva Kumar
This document discusses unconventional modes of anesthetic drug administration. It begins by explaining why inhalational anesthesia became conventional, due to ease of administration and reversibility. It then explores potential benefits of unconventional methods like improved patient compliance and bioavailability. Several unconventional routes are described, including transdermal, transmucosal, intranasal, rectal, intra-articular, interpleural, perineural, and intratracheal administration. Specific techniques like transdermal fentanyl patches, EMLA cream, intranasal medications, oral and sublingual opioids, ketamine premedication, and interpleural analgesia are outlined. The conclusion is that unconventional methods increase
This document summarizes neurotoxicity caused by snake venom. It discusses the main neurotoxic snakes found in India, including cobras, kraits and vipers. The venom contains various proteins like neurotoxins that interfere with neuromuscular transmission. Two main types of neurotoxins are alpha-neurotoxins and beta-neurotoxins. Alpha-neurotoxins bind competitively to nicotinic acetylcholine receptors at the post-synaptic membrane in a reversible manner. Beta-neurotoxins irreversibly bind to the pre-synaptic membrane, depleting synaptic vesicles and impairing neurotransmitter release. Neurotoxicity can cause flaccid paralysis and is a major cause of snakebite mortality
Local anesthetics reversibly block nerve impulse conduction. They are classified based on chemical structure into amide and ester types, with varying durations of action. Common local anesthetics include lidocaine, bupivacaine, and prilocaine. Local anesthetics work by blocking voltage-gated sodium channels, preventing nerve depolarization. Their effects depend on factors like pH, concentration, and addition of vasoconstrictors. Adverse effects can involve the central nervous system or cardiovascular system in cases of overdose. Proper technique and drug selection are important for safe and effective local anesthesia.
Local anaesthetis /certified fixed orthodontic courses by Indian dental academy 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 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.
Local anesthetics work by blocking sodium channels in nerves, limiting the propagation of action potentials and preventing pain sensation. Lidocaine was the first modern local anesthetic introduced in 1940. Local anesthetics are either esters or amides, with amides like lidocaine causing less allergic reactions. The onset and duration of local anesthetics is influenced by their lipid solubility, pH, presence of vasoconstrictors, and peak circulation levels to avoid toxicity.
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.
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.
Unconventional modes of anaesthetic administrationSelva Kumar
This document discusses unconventional modes of anesthetic drug administration. It begins by explaining why inhalational anesthesia became conventional, due to ease of administration and reversibility. It then explores potential benefits of unconventional methods like improved patient compliance and bioavailability. Several unconventional routes are described, including transdermal, transmucosal, intranasal, rectal, intra-articular, interpleural, perineural, and intratracheal administration. Specific techniques like transdermal fentanyl patches, EMLA cream, intranasal medications, oral and sublingual opioids, ketamine premedication, and interpleural analgesia are outlined. The conclusion is that unconventional methods increase
This document summarizes neurotoxicity caused by snake venom. It discusses the main neurotoxic snakes found in India, including cobras, kraits and vipers. The venom contains various proteins like neurotoxins that interfere with neuromuscular transmission. Two main types of neurotoxins are alpha-neurotoxins and beta-neurotoxins. Alpha-neurotoxins bind competitively to nicotinic acetylcholine receptors at the post-synaptic membrane in a reversible manner. Beta-neurotoxins irreversibly bind to the pre-synaptic membrane, depleting synaptic vesicles and impairing neurotransmitter release. Neurotoxicity can cause flaccid paralysis and is a major cause of snakebite mortality
Local anesthetics reversibly block nerve impulse conduction. They are classified based on chemical structure into amide and ester types, with varying durations of action. Common local anesthetics include lidocaine, bupivacaine, and prilocaine. Local anesthetics work by blocking voltage-gated sodium channels, preventing nerve depolarization. Their effects depend on factors like pH, concentration, and addition of vasoconstrictors. Adverse effects can involve the central nervous system or cardiovascular system in cases of overdose. Proper technique and drug selection are important for safe and effective local anesthesia.
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.
The document discusses molecular aspects of drug action, focusing on receptors, ion channels, enzymes, and carrier molecules. It describes how receptors mediate communication between cells and coordinate body functions. Many drugs act as agonists or antagonists on receptors for endogenous mediators. Receptors have been isolated from fish tissues and venom toxins, cloned, and had subtypes identified. Ion channels are also drug targets and can be ligand-gated or voltage-gated. Enzymes are reversible or irreversible drug targets. Carrier molecules transport ions and molecules across cell membranes using carrier proteins.
This document discusses molecular aspects of drug action, focusing on receptors and how drugs can interact with them. It describes different types of receptors like ligand-gated ion channels and G-protein coupled receptors. It explains how receptors mediate communication between cells and how drugs can act as agonists or antagonists on receptors for endogenous mediators to produce effects. Messenger molecules like hormones and neurotransmitters activate receptors to trigger downstream cellular responses.
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.
This document provides a review of local anesthetics and anxiolytics used in dental practice. It discusses the history of local anesthetics from early use of whiskey and nitrous oxide to modern drugs like lidocaine and bupivacaine. The pharmacology of local anesthetics is covered, including how they work by blocking sodium ion channels. Factors that influence the effects of local anesthetics like pH, drug properties and injection technique are reviewed. Common local anesthetic drugs, their durations of action, adverse effects and appropriate uses are summarized. Monitoring parameters and special considerations for patient populations are also addressed.
The document discusses antiepileptic drugs and their mechanisms and uses. It notes that common antiepileptic drugs work by enhancing GABA inhibition, blocking sodium channels, or blocking calcium channels. The main drug classes discussed are barbiturates like phenobarbital, hydantoins like phenytoin, benzodiazepines, carbamazepine, ethosuximide, and valproates. Each drug has distinct mechanisms and indications for treating different seizure types with varying adverse effect profiles. Newer drugs like topiramate and lamotrigine are also discussed.
Ketamine is a dissociative anesthetic agent that was first used in humans in 1965. It acts as an NMDA receptor antagonist and also interacts with voltage gated sodium channels. Ketamine produces dissociative anesthesia and profound analgesia by inhibiting the cortex and thalamus while stimulating the limbic system. It has a rapid onset of action of 30-60 seconds and is metabolized primarily in the liver before being excreted by the kidneys. Common side effects include increased heart rate and blood pressure as well as emergence reactions like hallucinations. Ketamine can interact with other drugs to increase the risk of seizures or potentiate muscle relaxants and depress the heart.
Ketamine is a dissociative anesthetic that was first used in humans in 1965. It acts as an NMDA receptor antagonist and also interacts with voltage gated sodium channels. Ketamine produces dissociative anesthesia and profound analgesia by inhibiting the cortex and thalamus while stimulating the limbic system. It has a rapid onset of action of 30-60 seconds and is metabolized primarily in the liver before being excreted by the kidneys. Common side effects include increased heart rate and blood pressure as well as emergence reactions like hallucinations. Ketamine can interact with other drugs to increase risks of seizures or potentiate muscle relaxants.
Local anesthetics are drugs that numb pain in specific body regions without loss of consciousness. They work by blocking sodium channels and preventing the transmission of nerve impulses. The document discusses the classification, mechanisms of action, structure-activity relationships, and individual profiles of various local anesthetic drugs. It focuses on ester-type anesthetics like cocaine, procaine, chloroprocaine, benzocaine, and tetracaine as well as amide-type drugs like lidocaine. Key differences between esters and amides are also highlighted.
General anesthetics cause reversible loss of consciousness and perception during surgery by depressing the central nervous system. They provide analgesia, amnesia, muscle relaxation and unconsciousness. Common inhalational anesthetics include halothane, isoflurane and sevoflurane. Pre-anesthetic medications are often administered to relieve anxiety, provide amnesia and reduce anesthetic requirements. Inhalational anesthetics are delivered via open or closed systems and their effects are determined by factors like potency, solubility and metabolism. Their mechanism of action involves actions on ion channels and receptors in the brain.
Drugs affecting the cns psychopharmacology by pharmacologist l mweetwaLarry Mweetwa
This document contains information from L. Mweetwa-Pharmacologist from the University of Zambia's School of Medicine Pharmacy Faculty on central nervous system pharmacology. It discusses neurotransmitters such as acetylcholine, dopamine, GABA, glutamate, serotonin, and neuropeptides. It describes the structure and function of synapses, how neurotransmitters are synthesized, stored, released, and removed from synapses. It also discusses the differences between neurotransmitters and neuromodulators.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking acetylcholine receptors at the neuromuscular junction, causing paralysis. There are two main types - competitive antagonists that compete with acetylcholine for receptor sites, and depolarizing agents like succinylcholine that cause sustained depolarization. Proper anesthesia is required when using these drugs to ensure patient comfort and safety during paralysis.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking neuromuscular transmission either through competition with acetylcholine or by depolarizing the motor end plate. Competitive blockers such as atracurium and cisatracurium are antagonized with anticholinesterases while succinylcholine is a depolarizing blocker that causes initial fasciculation before paralysis. Proper anesthesia is required when using neuromuscular blockers to ensure patient comfort and safety during paralysis.
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.
This document discusses sodium channel modulators. It begins by explaining ion channels and their role in establishing concentration gradients across cell membranes. It then focuses on sodium channels, describing the main types which include voltage-gated sodium channels. Voltage-gated sodium channels are responsible for generating action potentials in neurons and other excitable cells. The document explains the structure and gating of voltage-gated sodium channels, and how they play a role in the stages of the action potential. It discusses various drugs that can act as activators or blockers of sodium channels, including local anesthetics and class I antiarrhythmic agents. Finally, it briefly covers ligand-gated sodium channels such as nicotinic acetylcholine receptors
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.
Drugs affecting the cns psychopharmacology by pharmacologist l mweetwaLarry Mweetwa
This document contains information about L. Mweetwa-Pharmacologist from the University of Zambia School of Medicine, Pharmacy Faculty. It provides their name, title, and affiliation multiple times. The rest of the document discusses topics related to central nervous system pharmacology including neurotransmitters, synapses, and synaptic transmission.
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
You can complete the whole process in 3-4 months.Salary range for DH/DT is around 2500-3500 Pounds per month.
Eligibility / requirements-
1. An International English Language Testing System (IELTS) certificate
at the appropriate level.(Within 2 yrs of application date )
2: A recent primary dental qualification that has been taught and examined in English..(Within 2 yrs of application date )
3: A recent pass in a language test for registration with a regulatory authority in a country where the first language is English.
If you are interested Please contact us for more details.
1ST, 2ND AND 3RD ORDER BENDS IN STANDARD EDGEWISE APPLIANCE SYSTEM /Fixed ort...Indian dental academy
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.
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.
The document discusses molecular aspects of drug action, focusing on receptors, ion channels, enzymes, and carrier molecules. It describes how receptors mediate communication between cells and coordinate body functions. Many drugs act as agonists or antagonists on receptors for endogenous mediators. Receptors have been isolated from fish tissues and venom toxins, cloned, and had subtypes identified. Ion channels are also drug targets and can be ligand-gated or voltage-gated. Enzymes are reversible or irreversible drug targets. Carrier molecules transport ions and molecules across cell membranes using carrier proteins.
This document discusses molecular aspects of drug action, focusing on receptors and how drugs can interact with them. It describes different types of receptors like ligand-gated ion channels and G-protein coupled receptors. It explains how receptors mediate communication between cells and how drugs can act as agonists or antagonists on receptors for endogenous mediators to produce effects. Messenger molecules like hormones and neurotransmitters activate receptors to trigger downstream cellular responses.
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.
This document provides a review of local anesthetics and anxiolytics used in dental practice. It discusses the history of local anesthetics from early use of whiskey and nitrous oxide to modern drugs like lidocaine and bupivacaine. The pharmacology of local anesthetics is covered, including how they work by blocking sodium ion channels. Factors that influence the effects of local anesthetics like pH, drug properties and injection technique are reviewed. Common local anesthetic drugs, their durations of action, adverse effects and appropriate uses are summarized. Monitoring parameters and special considerations for patient populations are also addressed.
The document discusses antiepileptic drugs and their mechanisms and uses. It notes that common antiepileptic drugs work by enhancing GABA inhibition, blocking sodium channels, or blocking calcium channels. The main drug classes discussed are barbiturates like phenobarbital, hydantoins like phenytoin, benzodiazepines, carbamazepine, ethosuximide, and valproates. Each drug has distinct mechanisms and indications for treating different seizure types with varying adverse effect profiles. Newer drugs like topiramate and lamotrigine are also discussed.
Ketamine is a dissociative anesthetic agent that was first used in humans in 1965. It acts as an NMDA receptor antagonist and also interacts with voltage gated sodium channels. Ketamine produces dissociative anesthesia and profound analgesia by inhibiting the cortex and thalamus while stimulating the limbic system. It has a rapid onset of action of 30-60 seconds and is metabolized primarily in the liver before being excreted by the kidneys. Common side effects include increased heart rate and blood pressure as well as emergence reactions like hallucinations. Ketamine can interact with other drugs to increase the risk of seizures or potentiate muscle relaxants and depress the heart.
Ketamine is a dissociative anesthetic that was first used in humans in 1965. It acts as an NMDA receptor antagonist and also interacts with voltage gated sodium channels. Ketamine produces dissociative anesthesia and profound analgesia by inhibiting the cortex and thalamus while stimulating the limbic system. It has a rapid onset of action of 30-60 seconds and is metabolized primarily in the liver before being excreted by the kidneys. Common side effects include increased heart rate and blood pressure as well as emergence reactions like hallucinations. Ketamine can interact with other drugs to increase risks of seizures or potentiate muscle relaxants.
Local anesthetics are drugs that numb pain in specific body regions without loss of consciousness. They work by blocking sodium channels and preventing the transmission of nerve impulses. The document discusses the classification, mechanisms of action, structure-activity relationships, and individual profiles of various local anesthetic drugs. It focuses on ester-type anesthetics like cocaine, procaine, chloroprocaine, benzocaine, and tetracaine as well as amide-type drugs like lidocaine. Key differences between esters and amides are also highlighted.
General anesthetics cause reversible loss of consciousness and perception during surgery by depressing the central nervous system. They provide analgesia, amnesia, muscle relaxation and unconsciousness. Common inhalational anesthetics include halothane, isoflurane and sevoflurane. Pre-anesthetic medications are often administered to relieve anxiety, provide amnesia and reduce anesthetic requirements. Inhalational anesthetics are delivered via open or closed systems and their effects are determined by factors like potency, solubility and metabolism. Their mechanism of action involves actions on ion channels and receptors in the brain.
Drugs affecting the cns psychopharmacology by pharmacologist l mweetwaLarry Mweetwa
This document contains information from L. Mweetwa-Pharmacologist from the University of Zambia's School of Medicine Pharmacy Faculty on central nervous system pharmacology. It discusses neurotransmitters such as acetylcholine, dopamine, GABA, glutamate, serotonin, and neuropeptides. It describes the structure and function of synapses, how neurotransmitters are synthesized, stored, released, and removed from synapses. It also discusses the differences between neurotransmitters and neuromodulators.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking acetylcholine receptors at the neuromuscular junction, causing paralysis. There are two main types - competitive antagonists that compete with acetylcholine for receptor sites, and depolarizing agents like succinylcholine that cause sustained depolarization. Proper anesthesia is required when using these drugs to ensure patient comfort and safety during paralysis.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking neuromuscular transmission either through competition with acetylcholine or by depolarizing the motor end plate. Competitive blockers such as atracurium and cisatracurium are antagonized with anticholinesterases while succinylcholine is a depolarizing blocker that causes initial fasciculation before paralysis. Proper anesthesia is required when using neuromuscular blockers to ensure patient comfort and safety during paralysis.
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.
This document discusses sodium channel modulators. It begins by explaining ion channels and their role in establishing concentration gradients across cell membranes. It then focuses on sodium channels, describing the main types which include voltage-gated sodium channels. Voltage-gated sodium channels are responsible for generating action potentials in neurons and other excitable cells. The document explains the structure and gating of voltage-gated sodium channels, and how they play a role in the stages of the action potential. It discusses various drugs that can act as activators or blockers of sodium channels, including local anesthetics and class I antiarrhythmic agents. Finally, it briefly covers ligand-gated sodium channels such as nicotinic acetylcholine receptors
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.
Drugs affecting the cns psychopharmacology by pharmacologist l mweetwaLarry Mweetwa
This document contains information about L. Mweetwa-Pharmacologist from the University of Zambia School of Medicine, Pharmacy Faculty. It provides their name, title, and affiliation multiple times. The rest of the document discusses topics related to central nervous system pharmacology including neurotransmitters, synapses, and synaptic transmission.
Opportunity for Dentists (BDS/MDS )to relocate to United kingdom -Register as a DENTAL HYGIENIST/ DENTAL THERAPIST without Board exams and after approval you can register in GDC as a DH/DT and start working as a DH/DT Immediately and get paid.
You can complete the whole process in 3-4 months.Salary range for DH/DT is around 2500-3500 Pounds per month.
Eligibility / requirements-
1. An International English Language Testing System (IELTS) certificate
at the appropriate level.(Within 2 yrs of application date )
2: A recent primary dental qualification that has been taught and examined in English..(Within 2 yrs of application date )
3: A recent pass in a language test for registration with a regulatory authority in a country where the first language is English.
If you are interested Please contact us for more details.
1ST, 2ND AND 3RD ORDER BENDS IN STANDARD EDGEWISE APPLIANCE SYSTEM /Fixed ort...Indian dental academy
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.
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.
I –Aligners are made with FDA approved transparent thermoplastic materials using 3D scanning, 3D Printing and finally Trays with Pressure vacuum formers.
Dear Doctor,
Indian Dental Academy Now offers comprehensive online Orthodontics course.
Course includes:
1.whiteboard lecture presentations
2.Case Discussions
3.with hundreds of pictures.
4.Demo on Models
5.Demo on Patients
6. subtitles in your own language
12 months unlimited access and support @350 USD only.
For Demo please visit :www.idalectures.com/preview/
For more details visit: www.idalectures.com
Please contact us for any clarifications:
idalectures@gmail.com
indiandentalacademy@gmail.com
Thanks & Regards
Indian Dental Academy
--
Indian Dental Academy
Leader in continuing dental education
www.indiandentalacademy.com
skype:indiandentalacademy
+919248678078
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
Cytotoxicity of silicone materials used in maxillofacial prosthesis / dental ...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.for more details please visit
www.indiandentalacademy.com
Diagnosis and treatment planning in completely endntulous arches/dental coursesIndian 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.for more details please visit
www.indiandentalacademy.com
Properties of Denture base materials /rotary endodontic coursesIndian 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.for more details please visit
www.indiandentalacademy.com
Use of modified tooth forms in complete denture occlusion / dental implant...Indian dental academy
This document discusses dental occlusion concepts and philosophies for complete dentures. It introduces key terms like physiologic occlusion and defines different occlusion schemes like balanced articulation and monoplane articulation. The document discusses advantages and disadvantages of using anatomic versus non-anatomic teeth for complete dentures. It also outlines requirements for maintaining denture stability, such as balanced occlusal contacts and control of horizontal forces. The goal of occlusion for complete dentures is to re-establish the homeostasis of the masticatory system disrupted by edentulism.
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
This document discusses dental casting investment materials. It describes the three main types of investments - gypsum bonded, phosphate bonded, and ethyl silicate bonded investments. For gypsum bonded investments specifically, it details their classification, composition including the roles of gypsum, silica, and modifiers, setting time, normal and hygroscopic setting expansion, and thermal expansion. It provides information on how the properties of gypsum bonded investments are affected by their composition. The document serves as a comprehensive overview of dental casting investment materials.
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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.for more details please visit
www.indiandentalacademy.com
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
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2. Introduction.Introduction.
LA are drugs that produce reversibleLA are drugs that produce reversible
depression of nerve impulse anddepression of nerve impulse and
conduction when applied to nerve fibresconduction when applied to nerve fibres
The ester group of LA were first used inThe ester group of LA were first used in
1884 – cocaine for topical use in1884 – cocaine for topical use in
opthalmologyopthalmology
Amino amide LA were manufactured inAmino amide LA were manufactured in
1943 – lidnocaine, since then many newer1943 – lidnocaine, since then many newer
safer LA has been producedsafer LA has been produced
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3. IDEAL PROPERTIESIDEAL PROPERTIES
Physiochemical propertiesPhysiochemical properties
Easy to produce and economicalEasy to produce and economical
Stability during storageStability during storage
Easy aaccessibility; appropriate packaging andEasy aaccessibility; appropriate packaging and
labellinglabelling
Formulation (where possible, additive free)Formulation (where possible, additive free)
Soluble in waterSoluble in water
Sterilisable by heat without decompositionSterilisable by heat without decomposition
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4. IDEAL PROPERTIES cont.IDEAL PROPERTIES cont.
PharmacokineticsPharmacokinetics
Ease of administrationEase of administration
Rapid onsetRapid onset
Duration appropriate to useDuration appropriate to use
Clearance independent of hepatic and renalClearance independent of hepatic and renal
functionfunction
No active or toxic metabolitesNo active or toxic metabolites
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5. IDEAL PROPERTIES cont.IDEAL PROPERTIES cont.
PharmacodynamicsPharmacodynamics
High therapeutics ratioHigh therapeutics ratio
No hypersensitivity reactionNo hypersensitivity reaction
Absence of toxicity on : local tissue, liver, brain and otherAbsence of toxicity on : local tissue, liver, brain and other
tissuetissue
Nervous depression, especially of sensory fibresNervous depression, especially of sensory fibres
Administration should be effective by topical application,Administration should be effective by topical application,
injection near a nerve trunk or infiltrationinjection near a nerve trunk or infiltration
Specificity – only nerve tissue should be affectedSpecificity – only nerve tissue should be affected
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6. Chemistry and Structure ActivityChemistry and Structure Activity
RelationshipRelationship
All typical LA contain h.philic and h.phobicAll typical LA contain h.philic and h.phobic
domain that are separated by intermediate alkyldomain that are separated by intermediate alkyl
chainchain
The h.philic grp usually tertiary amineThe h.philic grp usually tertiary amine
The h.phobic grp usually an aromatic residueThe h.phobic grp usually an aromatic residue
Intermediate bond is either of the ester or amideIntermediate bond is either of the ester or amide
type – determines many of the properties of thetype – determines many of the properties of the
agentagent
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8. Cont.Cont.
Intermediate chain = either ester or amideIntermediate chain = either ester or amide
Determines many of the properties of the agentDetermines many of the properties of the agent
Classification of LAClassification of LA
Changes to any part of the molecule lead toChanges to any part of the molecule lead to
alteration in activity and tocxicityalteration in activity and tocxicity
Increase length of intermed. Alkyl group willIncrease length of intermed. Alkyl group will
increase potency up to critical lengthincrease potency up to critical length increaseincrease
further will increase toxicityfurther will increase toxicity
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9. Cont.Cont.
Length of two terminal group are alsoLength of two terminal group are also
equally importantequally important
Eg. Add butyl group to mepivacainEg. Add butyl group to mepivacain
bupivacainbupivacain
Inc. lipid solubilityInc. lipid solubility
Greater potencyGreater potency
Longer duration of actionLonger duration of action
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10. Mode of actionMode of action
All has similar MOAAll has similar MOA
Most LA bind to Na channels in the inactivated state,Most LA bind to Na channels in the inactivated state,
preventing subsequent channel activation and the largepreventing subsequent channel activation and the large
transient Na influx associated with mb depn.transient Na influx associated with mb depn.
Marked depression of rate of depnMarked depression of rate of depn
Failed to reach TPFailed to reach TP no propogation of APno propogation of AP neuralneural
blockageblockage
LA act in their cationic form but most reach their site ofLA act in their cationic form but most reach their site of
action by penetrating the nerve sheath and axonal mb asaction by penetrating the nerve sheath and axonal mb as
unionized speciesunionized species
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11. Cont.Cont.
Some LA act bySome LA act by
Penetrating the mb, causing mb expansion andPenetrating the mb, causing mb expansion and
channel distortion (analogous to the criticalchannel distortion (analogous to the critical
volume hypothesis)volume hypothesis)
Partial penetration by LA of the axonal mb couldPartial penetration by LA of the axonal mb could
increase the transmembrane potential and inhibitincrease the transmembrane potential and inhibit
depn. (surface charge theory)depn. (surface charge theory)
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12. Differential sensitivity of nerve fibreDifferential sensitivity of nerve fibre
classclass mylinationmylination diametediamete
rr
ConductioConductio
nn
velocityvelocity
FunctionsFunctions
AAαα
heavyheavy 12-2012-20 70-12070-120
Motor and propioceptionMotor and propioception
AAββ
ModerateModerate 5-125-12 30-7030-70
Touch and pressureTouch and pressure
AAχχ
ModeratelyModerately 3-63-6 15-3015-30
Motor to muscle spindleMotor to muscle spindle
AAδδ
lightlylightly 2-52-5 12-3012-30
Pain, temperature, touchPain, temperature, touch
BB
lightlylightly 1-31-3 3-153-15
Preganglionic autonomicPreganglionic autonomic
CC
NoneNone
nonenone
0.4-1.20.4-1.2
0.3-1.30.3-1.3
0.7-1.30.7-1.3
0.7-1.30.7-1.3
Pain & reflex responsePain & reflex response
Postganglionic sympatheticsPostganglionic sympathetics
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13. Factors influenceFactors influence
potency,speed of onset andpotency,speed of onset and
duration of actionduration of action POTENCYPOTENCY
1.1. Lipophilic natureLipophilic nature = lipid solubility= lipid solubility
Inc. lipid solubility = inc potencyInc. lipid solubility = inc potency
(penetrare mb more easily)(penetrare mb more easily)
less molecule required for nerve blockageless molecule required for nerve blockage
Inc alkyl substitution to aromatic ring andInc alkyl substitution to aromatic ring and
amineamine inc lipophilic natureinc lipophilic nature
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14. Cont.Cont.
2. Partition coefficient /2. Partition coefficient /
vasodilatationvasodilatation
? Lidocaine > potent than mepivicaine in? Lidocaine > potent than mepivicaine in
vitrovitro
vasodilatationvasodilatation
Bupivacaine > Etidocaine in vivoBupivacaine > Etidocaine in vivo
inc fat uptakeinc fat uptake
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15. 2. SPEED OF ONSET2. SPEED OF ONSET
1. Unionized fraction / pKa & pH1. Unionized fraction / pKa & pH
Weak bases tend to be relatively ionized at highWeak bases tend to be relatively ionized at high
concentration H+concentration H+
The uncharged form diffuse more readily acrossThe uncharged form diffuse more readily across
nerve mbnerve mb determine the onset of LAdetermine the onset of LA
Mechanism of ion trapping?Mechanism of ion trapping?
Onset of blockageOnset of blockage ∝∝ pKapKa
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16. Cont.Cont.
2. Fick’s Law of diffusion2. Fick’s Law of diffusion
DD ∝∝ A.Pc.(P1-P2)A.Pc.(P1-P2)
/MW.T/MW.T
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17. Cont.Cont.
3. Lipid solubility3. Lipid solubility
Its effect on onset is poorly understoodIts effect on onset is poorly understood
?high lipid solubility?high lipid solubility inc rate of diff andinc rate of diff and
shorten onset time BUT it also incshorten onset time BUT it also inc
solubility in the surrounding tissuesolubility in the surrounding tissue
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18. Cont.Cont.
4. Barrier eg. Nerve root4. Barrier eg. Nerve root
EpineuriumEpineurium
PerineuriumPerineurium
EndoneuriumEndoneurium
! Subarachnoid block rapid onset because! Subarachnoid block rapid onset because
nerve rootlets are almost completely barenerve rootlets are almost completely bare
of fibrousof fibrous
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19. Cont.Cont.
SensitivitySensitivity ∝∝ 1/size1/size
Autonomic > sensory > motorAutonomic > sensory > motor
SmallSmall,, unmyelinatedunmyelinated medium, < myelinmedium, < myelin large, myelinatedlarge, myelinated
Order of blockage : B – C, Ad – Ag – Ab - AaOrder of blockage : B – C, Ad – Ag – Ab - Aa
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20. Cont.Cont.
Duration of blockageDuration of blockage
Protein binding regulate the duration ofProtein binding regulate the duration of
anaesthetic activityanaesthetic activity
Due to protein binding of LA to protein receptorDue to protein binding of LA to protein receptor
in the Na channel of nerve mbin the Na channel of nerve mb
Highly protein bound will remain for a long timeHighly protein bound will remain for a long time
ProcainProcain 6% protein bound6% protein bound
Ropi, bupi, etidocaineRopi, bupi, etidocaine 94-96% prot. bound94-96% prot. bound
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21. Factors affecting anaesthetic activityFactors affecting anaesthetic activity
DosageDosage
∀ ↑↑ mass injected (vol x conc.)mass injected (vol x conc.)
Red onset timeRed onset time
Inc durationInc duration
Inc depthInc depth
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22. Cont.Cont.
Addition of vasoconstictorAddition of vasoconstictor
Red LA absorptionRed LA absorption
inc depthinc depth
inc durationinc duration
red toxicityred toxicity
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23. contcont
Site of injectionSite of injection
CarbonationCarbonation
Mixture of LAMixture of LA
Chloroprocaine & bupivacaineChloroprocaine & bupivacaine
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25. Absorption of LAAbsorption of LA
Site of injection ( intercostal > caudal >Site of injection ( intercostal > caudal >
brachial plexus etc )brachial plexus etc )
Dosage (blood level of LA related to totalDosage (blood level of LA related to total
dose of drug rather than spesific volumedose of drug rather than spesific volume
or concentration of solutionor concentration of solution
Addition of vasoconstrictorAddition of vasoconstrictor
Disease processDisease process
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26. Systemic disposition kineticsSystemic disposition kinetics
Ultimate plasma conc. Of LA is determined byUltimate plasma conc. Of LA is determined by
rate of tissue distribution and rate of clearancerate of tissue distribution and rate of clearance
(metabolism and excretion ) of the drug(metabolism and excretion ) of the drug
Distribution depends onDistribution depends on
Tissue perfusion ( alpha and beta phase)Tissue perfusion ( alpha and beta phase)
Tissue/blood partision coefficientTissue/blood partision coefficient
Tissue massTissue mass
• Lung extract significant amount of LALung extract significant amount of LA
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27. Cont.Cont.
Placental transferPlacental transfer
Protein binding ( lidocaine > bupivacaine XProtein binding ( lidocaine > bupivacaine X
placental )placental )
Acidosis in fetus ( ion trapping )Acidosis in fetus ( ion trapping )
Ester LA – rapid hydrolysis not available to crossEster LA – rapid hydrolysis not available to cross
placental in significant amountplacental in significant amount
ClearanceClearance
Mainly hepatic metabolismMainly hepatic metabolism
Minimal renal excretionMinimal renal excretion
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28. Metabolism of LAMetabolism of LA
A. ESTERSA. ESTERS
Rapid hydrolysis by plasma cholinesteraseRapid hydrolysis by plasma cholinesterase
Water soluble metabolites excreted in the urineWater soluble metabolites excreted in the urine
(p-aminobenzoic, diethylaminoethanol(p-aminobenzoic, diethylaminoethanol
Abnormal pseudocholinesteraseAbnormal pseudocholinesterase inc risk ofinc risk of
toxic side effecttoxic side effect
CSF lack of esterase enzymeCSF lack of esterase enzyme
Exception Cocain - partially metabolized in liverException Cocain - partially metabolized in liver
and partially excreted in urine unchangedand partially excreted in urine unchanged
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29. Cont.Cont.
B. AMIDEB. AMIDE
Enzymatic degradation in liver by microsomalEnzymatic degradation in liver by microsomal
enzymes (prilocaine > lidnocaine > mepivacaineenzymes (prilocaine > lidnocaine > mepivacaine
> bupivacaine and etidocaine )> bupivacaine and etidocaine )
Much slower than ester hydrolysisMuch slower than ester hydrolysis
N-dealkylation, aromatic and amide hydrolysisN-dealkylation, aromatic and amide hydrolysis
Decrease hepatic function or hepatic blood flowDecrease hepatic function or hepatic blood flow
reduce metabolic ratereduce metabolic rate pred systemic toxicitypred systemic toxicity
Very little drug excreted unchanged by kidneyVery little drug excreted unchanged by kidney
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30. Cont.Cont.
Metabolite of prilocaine (o-toluidine ) whichMetabolite of prilocaine (o-toluidine ) which
accumulate after large dose (>10mg/kg) convertaccumulate after large dose (>10mg/kg) convert
hemoglobin to methemoglobinhemoglobin to methemoglobin
Prilocaine epidural labourPrilocaine epidural labour
Benzocaine also may causeBenzocaine also may cause
methemoglobinemiamethemoglobinemia
Tx iv methylene blue @ 1-2 mg/kg of 1% over 5Tx iv methylene blue @ 1-2 mg/kg of 1% over 5
minutesminutes reduce methemoglobin ( Fe3+ ) toreduce methemoglobin ( Fe3+ ) to
hemoglobin ( Fe2+ )hemoglobin ( Fe2+ )
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31. contcont
RenalRenal
Poor water solubility of LA – limit renalPoor water solubility of LA – limit renal
excretion of unchange drug to < 5% ofexcretion of unchange drug to < 5% of
injected dose (except cocain 10-12%injected dose (except cocain 10-12%
urine)urine)
Water soluble metabolites para-Water soluble metabolites para-
aminobenzoic acid readily excreted in theaminobenzoic acid readily excreted in the
urineurine
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32. Side effectsSide effects
Toxicity often directly proportionate to itsToxicity often directly proportionate to its
potencypotency
Mixture of LA roughly give additive toxicMixture of LA roughly give additive toxic
effecteffect
In addition to blocking transmission in theIn addition to blocking transmission in the
nerve axon, LA affect all tissue wherenerve axon, LA affect all tissue where
conduction of impulse occur, therefore inconduction of impulse occur, therefore in
The CNSThe CNS
Autonomic gangliaAutonomic ganglia
The NMJThe NMJ
All form of muscle fibre, esp cardiacAll form of muscle fibre, esp cardiac
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33. CVSCVS
Affect both myocardium and peripheralAffect both myocardium and peripheral
vascular smooth musclevascular smooth muscle
Primary site is myocardium once absorbedPrimary site is myocardium once absorbed
Effects :Effects : ↓↓conduction, contractility andconduction, contractility and
excitabilityexcitability
CVS effect are seen atCVS effect are seen at ↑↑ dose, when CNSdose, when CNS
effects are already evidenteffects are already evident
Inadvertent iv adm may lead to suddentInadvertent iv adm may lead to suddent
death !VF, it is more likely if soln containdeath !VF, it is more likely if soln contain
adrenalinadrenalin
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34. Cont.Cont.
At Tx conc lidocaine cause no ECG changeAt Tx conc lidocaine cause no ECG change
↑↑ to toxic level, prolonged conductionto toxic level, prolonged conduction ↑↑PRPR
and QRS intervaland QRS interval
VeryVery ↑↑suppress SANsuppress SAN sinus brady/arrestsinus brady/arrest
and alsoand also ↓↓AVNAVN AV blockAV block ± dissociation± dissociation
Cardiac toxicity of bupivacaine ppt VFCardiac toxicity of bupivacaine ppt VF
Bupivacaine markedly depress dV/dtBupivacaine markedly depress dV/dt
Slow rate of recoverySlow rate of recovery arrhytmiasarrhytmias
Produce direct pulm vasoconstrictive effectProduce direct pulm vasoconstrictive effect
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35. ContCont
Most LA cause biphasic peripheralMost LA cause biphasic peripheral
arteriolar response, with initialarteriolar response, with initial
vasoconstriction then vasodilatationvasoconstriction then vasodilatation
As doseAs dose ↑↑ action change to inhibition/Vdilaction change to inhibition/Vdil
Cocaine produce vasoconstriction at mostCocaine produce vasoconstriction at most
doses, inhibit noradrenalin uptake bydoses, inhibit noradrenalin uptake by
tissue binding sitetissue binding site
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36. RESPIRATORYRESPIRATORY
Depress hypoxic driveDepress hypoxic drive
Apnoea can result from phrenic and IC nerveApnoea can result from phrenic and IC nerve
paralysis or depression of medulla RCparalysis or depression of medulla RC
LA relax bronchial smooth muscleLA relax bronchial smooth muscle
Iv lidocaine 1.5 g/kg red reflex b/constrictionIv lidocaine 1.5 g/kg red reflex b/constriction
upon intubationupon intubation
Occationally direct LA aerosolOccationally direct LA aerosol b/spasmb/spasm
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37. NEUROLOGICALNEUROLOGICAL
Earliest signs are circumoral and tongue numbness,Earliest signs are circumoral and tongue numbness,
tinnitus, nystagmus and dizzinesstinnitus, nystagmus and dizziness
Following absorption, all nitrogenous LA cause CNSFollowing absorption, all nitrogenous LA cause CNS
excitationexcitation
Restlessness, tremor, eventually tonic-clonic fitsRestlessness, tremor, eventually tonic-clonic fits
CNS stimulation then followed by depressionCNS stimulation then followed by depression
Death usually d/t subsequent respiratory depressionDeath usually d/t subsequent respiratory depression
Both stimulation and depression are thought to be d/tBoth stimulation and depression are thought to be d/t
neuronal depressionneuronal depression
↓↓ in inhibitory p/w in ARAS being responsible for thein inhibitory p/w in ARAS being responsible for the
excitatory effectsexcitatory effects
Ventilatory support may be req. laterVentilatory support may be req. later
Convultion can be controlled by barbiturate egConvultion can be controlled by barbiturate eg
diazepamdiazepam
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38. Cont.Cont.
Factors affecting the occurance ofFactors affecting the occurance of
CNS toxicity:CNS toxicity:
Relative toxicityRelative toxicity approx LA potencyapprox LA potency
Rate of injectionRate of injection r[plasma] achievedr[plasma] achieved
pCO2pCO2 inversely related to fit thresholdinversely related to fit threshold
pHpH ↓↓pHpH ↓↓fit thresholdfit threshold
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39. IMMUNOLOGICALIMMUNOLOGICAL
True allergy to LA are uncommonTrue allergy to LA are uncommon
Ester are more likely – ester derivativeEster are more likely – ester derivative
para aminobenzoic acid is a knownpara aminobenzoic acid is a known
allergenallergen
Amide often contain methylparaben asAmide often contain methylparaben as
additive – structure similar to PABAadditive – structure similar to PABA
LA may inhibit neutrophil fx andLA may inhibit neutrophil fx and
theoritically may retard wound healingtheoritically may retard wound healing
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40. MUSCULOSKELETALMUSCULOSKELETAL
Direct inj into skeletal muscleDirect inj into skeletal muscle LA areLA are
myotoxicmyotoxic
Histopathologically cause myofibrilHistopathologically cause myofibril
hypercontractionhypercontraction lytic degenerationlytic degeneration
oedemaoedema necrosisnecrosis
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41. HEMATOLOGICALHEMATOLOGICAL
Lidocaine demonstrate redn coagulationLidocaine demonstrate redn coagulation
(prevent thrombosis and platelet(prevent thrombosis and platelet
aggregation) and enhance fibrinolysisaggregation) and enhance fibrinolysis
Lower incident of embolic event in patientLower incident of embolic event in patient
receiving epidural anaesthesiareceiving epidural anaesthesia
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43. Drug interactionDrug interaction
Non depolarising muscle relaxant blockade isNon depolarising muscle relaxant blockade is
potentiated by LApotentiated by LA
Concurrent administration of succinylcholine andConcurrent administration of succinylcholine and
an ester LA may potentiate the effect of bothan ester LA may potentiate the effect of both
drugs (pseudocholinesterase dependant)drugs (pseudocholinesterase dependant)
Dibucaine inhibit pseudocholinesteraseDibucaine inhibit pseudocholinesterase
Cimetidine and propanolol red liver blood flowCimetidine and propanolol red liver blood flow
and lidocaine clearanceand lidocaine clearance
Opiods andOpiods and aa2 agonist potentiate LA pain relief2 agonist potentiate LA pain relief
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44. ContraindicationContraindication
Allergy/hypersensitivity to LA / sol. AdditivesAllergy/hypersensitivity to LA / sol. Additives
Adrenalin is contraindicated forAdrenalin is contraindicated for
Tachycardia! (thyrotoxicosis,CCF,IHD)Tachycardia! (thyrotoxicosis,CCF,IHD)
Anesthesia around end arteriesAnesthesia around end arteries
Iv regional anaesthesiaIv regional anaesthesia
Epidural/spinal anaesthesia in the presence ofEpidural/spinal anaesthesia in the presence of
significantsignificant
Hypotention/hypovolaemiaHypotention/hypovolaemia
CoagulopathyCoagulopathy
Presence of local tissue sepsisPresence of local tissue sepsis
Patient refusalPatient refusal
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45. PrecautionsPrecautions
Resuscitation equipment and drugs should be availableResuscitation equipment and drugs should be available
Reliable iv accessReliable iv access
Injection should follow aspiration TRO iv injInjection should follow aspiration TRO iv inj
Lowest effective dose possibleLowest effective dose possible
Careful in pt withCareful in pt with
Pre-existing CNS & cardiac disorderPre-existing CNS & cardiac disorder
Cardiac glycoside toxicityCardiac glycoside toxicity
Hepatic or renal impairmentHepatic or renal impairment
Pred to malignant hyperthermiaPred to malignant hyperthermia
PorphriaPorphria
Fetal bradycardia after Xcess maternal adm with subsequentFetal bradycardia after Xcess maternal adm with subsequent
hypoxia and acidosishypoxia and acidosis
Retrobulbar block have been a/w respiratory areestRetrobulbar block have been a/w respiratory areest
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46. lidocainelidocaine
pKa 7.85pKa 7.85
Plain aq solution 1, 1.5, 2% @ pH 5-7Plain aq solution 1, 1.5, 2% @ pH 5-7
Solution with adrenalin @ pH 3-4.5Solution with adrenalin @ pH 3-4.5
Ralative potency 2Ralative potency 2
T1/2T1/2ß adult 1.8 hr, neonate 2hrß adult 1.8 hr, neonate 2hr
Xtremely stableXtremely stable
Max dose : plain 3mg/kg, adrenalin 7mg/kgMax dose : plain 3mg/kg, adrenalin 7mg/kg
E.A. of 400mg/70kg @ [blood] = 2-4ug/mlE.A. of 400mg/70kg @ [blood] = 2-4ug/ml
Toxicity begin @5 ug/mlToxicity begin @5 ug/ml
Relatively quickly absorbed from GITRelatively quickly absorbed from GIT
Metab in liver (dealkylation)Metab in liver (dealkylation) excreted urineexcreted urine
Toxic dose lead to death by VF or cardiac arrestToxic dose lead to death by VF or cardiac arrest
Suitable for surface, infiltration,nerve block, caudal, epidural and SASuitable for surface, infiltration,nerve block, caudal, epidural and SA
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47. BupivacaineBupivacaine
pKa 8.1pKa 8.1
Plain aq soln .25, .375, .5% @ pH 4.5-6Plain aq soln .25, .375, .5% @ pH 4.5-6
If with adrenalin pH 3.5-5.5If with adrenalin pH 3.5-5.5
Potency 8Potency 8
Protein binding 95%Protein binding 95%
> lipid solubility than lidocaine> lipid solubility than lidocaine
T1/2T1/2ß adult 3.5hr, neonate 8.1-14hrß adult 3.5hr, neonate 8.1-14hr
Amide link LAAmide link LA
Prod prolonged anaesthesia with slower onsetProd prolonged anaesthesia with slower onset
Add adrenalin -Add adrenalin - ↓↓toxicity, h/e no change in durationtoxicity, h/e no change in duration
Post op analgesia : IC 7hr, EA 3-4hrPost op analgesia : IC 7hr, EA 3-4hr
Epid/caudal peak [plasma] 30-45 minEpid/caudal peak [plasma] 30-45 min
Lower foetal/maternal ratio cf lidnocaine (! Protein binding)Lower foetal/maternal ratio cf lidnocaine (! Protein binding)
Max dose : plain/with adrenalin 2 mg/kgMax dose : plain/with adrenalin 2 mg/kg
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48. RopivacaineRopivacaine
Chemical analogue of bupivacaineChemical analogue of bupivacaine
The molecule is designed to modify the spesificThe molecule is designed to modify the spesific
cardiotoxicity associated with bupivacainecardiotoxicity associated with bupivacaine
pKa 8.2 and pH solution 5.5-6.0pKa 8.2 and pH solution 5.5-6.0
Equally potent as bupivacaineEqually potent as bupivacaine
Its quality of clinical block appear to be veryIts quality of clinical block appear to be very
similar in onset, duration and quality that ofsimilar in onset, duration and quality that of
bupivacainebupivacaine
No spesific toxicity has been detectedNo spesific toxicity has been detected
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49. CocaineCocaine
From leaves of erytroxylon coca – is an ester of benzoicFrom leaves of erytroxylon coca – is an ester of benzoic
acidacid
CNS stimulant. At low dose produce euphoria. HigherCNS stimulant. At low dose produce euphoria. Higher
dose cause convulsion, coma, medullary depressant anddose cause convulsion, coma, medullary depressant and
deathdeath
Stimulate vomiting centreStimulate vomiting centre
Block reuptake of catecholamineBlock reuptake of catecholamine enhance SNSenhance SNS
activityactivity
Small dose may cause bradycardia d/t central vagalSmall dose may cause bradycardia d/t central vagal
stimulationstimulation
Larger dose cause tachycardia, inc TPR andLarger dose cause tachycardia, inc TPR and
hypertentionhypertention larger may produce myocardiallarger may produce myocardial
depression, VF and deathdepression, VF and death
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50. contcont
May be used as surface anaesthesiaMay be used as surface anaesthesia
As topical LA in ENT (5%)As topical LA in ENT (5%)
Cocain itself constrict blood vessel and theCocain itself constrict blood vessel and the
use of adrenalin is contraindicated as ituse of adrenalin is contraindicated as it
sensitises the myocardiumsensitises the myocardium
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51. Uses of LAUses of LA
Surface anaesthesiaSurface anaesthesia
Infiltration anaesthesiaInfiltration anaesthesia
Nerve block anaesthesia (peripheral,plexus)Nerve block anaesthesia (peripheral,plexus)
Intravenous regional anaesthesiaIntravenous regional anaesthesia
Spinal/subarachnoid anaesthesiaSpinal/subarachnoid anaesthesia
Other uses (antiarrhytmic, reduction in ICP,Other uses (antiarrhytmic, reduction in ICP,
Blunting of CVS responses to intubation andBlunting of CVS responses to intubation and
extubationextubation
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52. Thank youThank you
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