Local Anaesthesia
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Local anesthetics can interfere with nerve excitation in several ways such as altering the resting or threshold potential of the nerve membrane or decreasing the rate of depolarization. The proposed mechanisms of action include displacement of calcium ions from nerve receptor sites and blockade of sodium channels, decreasing sodium conductance and preventing the development of an action potential. Local anesthetics are absorbed into the bloodstream and distributed to tissues, with highly perfused organs receiving higher levels. They are metabolized primarily in the liver or plasma and excreted mainly through the kidneys, with esters being hydrolyzed more completely than amides before excretion.
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Local Anesthetics
Local anesthetics work by blocking voltage-dependent sodium channels in nerves, preventing the conduction of action potentials. They are classified as esters or amides. Esters are metabolized rapidly via plasma esterases, while amides are metabolized more slowly, some via hepatic cytochrome P450 enzymes. Local anesthetics are used clinically for analgesia via various routes of administration depending on the specific agent. Toxicity can cause central nervous system effects like seizures as well as cardiovascular issues. Treatment focuses on supportive care and controlling symptoms.
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local anesthetics
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.
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Local anesthetics work by reversibly blocking voltage-gated sodium channels in nerve cell membranes, inhibiting the influx of sodium ions needed to initiate the action potential for nerve impulse conduction. This document discusses the pharmacology of common local anesthetics like lidocaine, bupivacaine and procaine. It describes their classification, mechanisms of action, indications, dosages, onset times, durations of action and adverse effects.
Local anaesthesia
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the rapid influx of sodium ions needed to generate nerve impulses. They bind preferentially to activated sodium channels, inhibiting nerve conduction and establishing a localized loss of sensation. The mechanism of action involves inhibiting nerve depolarization and propagation of impulses by reducing sodium ion influx, thereby preventing transmission of sensations like pain.
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Local Anesthetics
Local anesthetics work by blocking voltage-dependent sodium channels in nerves, preventing the conduction of action potentials. They are classified as esters or amides. Esters are metabolized rapidly via plasma esterases, while amides are metabolized more slowly, some via hepatic cytochrome P450 enzymes. Local anesthetics are used clinically for analgesia via various routes of administration depending on the specific agent. Toxicity can cause central nervous system effects like seizures as well as cardiovascular issues. Treatment focuses on supportive care and controlling symptoms.
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local anesthetics
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.
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Local anesthetics work by reversibly blocking voltage-gated sodium channels in nerve cell membranes, inhibiting the influx of sodium ions needed to initiate the action potential for nerve impulse conduction. This document discusses the pharmacology of common local anesthetics like lidocaine, bupivacaine and procaine. It describes their classification, mechanisms of action, indications, dosages, onset times, durations of action and adverse effects.
Local anaesthesia
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the rapid influx of sodium ions needed to generate nerve impulses. They bind preferentially to activated sodium channels, inhibiting nerve conduction and establishing a localized loss of sensation. The mechanism of action involves inhibiting nerve depolarization and propagation of impulses by reducing sodium ion influx, thereby preventing transmission of sensations like pain.
LOCAL ANAESTHETIC 1.pptx
Local anesthetics (LAs) produce reversible nerve blockade and sensory anesthesia without loss of consciousness. They work by blocking voltage-gated sodium channels, preventing nerve impulse generation. LAs have both hydrophilic and lipophilic components. Absorption and effects depend on site of injection, drug properties, and use of vasoconstrictors. Toxicities include allergic reactions, systemic toxicity from high plasma levels, and rare neurotoxicity. Proper administration and monitoring can minimize risks from these important medications.
Local anaesthetics
1) The document discusses local anesthetics, providing their history, uses, mechanisms of action, classifications, and factors influencing their effects.
2) It describes the pharmacokinetics of local anesthetics including absorption, distribution, metabolism and excretion of ester and amide-linked drugs.
3) Guidelines are provided for managing severe local anesthetic toxicity, including airway management, treating seizures and arrhythmias, and considering lipid emulsion therapy.
Local anaesthetics
Local anesthetics work by reversibly blocking sodium channels in neural membranes, preventing action potentials. The first local anesthetic was cocaine in the 1860s. Local anesthetics are now classified as esters or amides and commonly used in infiltration, nerve blocks, and regional techniques. Factors like lipid solubility, dose, and pH influence their duration and potency. Toxicity can affect the central nervous system, heart, and lungs. Severe toxicity requires securing the airway, oxygen, benzodiazepines or propofol for seizures, and IV lipid emulsion along with standard cardiac life support protocols.
Local anaesthetics
Local anesthetics work by reversibly blocking sodium channels in neural membranes, preventing action potentials. The first local anesthetic was cocaine in the 1860s. Local anesthetics are now classified as esters or amides and commonly used in infiltration, nerve blocks, and regional techniques. Factors like lipid solubility, dose, and site of injection influence onset and duration of their effects. Toxicity can involve the central nervous system, heart, or lungs. Treatment of severe toxicity includes securing the airway, oxygen, benzodiazepines or propofol for seizures, lipid emulsion therapy, and CPR if needed.
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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.
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Local anesthetics work by blocking sodium channels and preventing the influx of sodium ions needed for nerve impulse conduction. Early pioneers discovered cocaine's local anesthetic properties in the 1880s, leading to other developments like procaine and lidocaine. Local anesthetics are weak bases containing an aromatic ring, amine, and ester or amide linkage. They vary in potency, duration of action, and lipid solubility. The specific receptor theory states they reversibly bind sodium channels intracellularly to block conduction.
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Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
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ANESTESICOS LOCALES
Local anesthetics block nerve conduction by reversibly binding to voltage-gated sodium channels and preventing the influx of sodium ions needed to generate action potentials. They are used to provide localized pain relief and are delivered through various techniques including infiltration, nerve blocks, and epidurals. The choice of local anesthetic depends on factors like duration of action, with esters having a shorter duration than amides. Additives like epinephrine prolong the effect by reducing absorption. While effective for analgesia, local anesthetics must be carefully administered to avoid toxicity from high systemic levels that can cause seizures or cardiac issues.
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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.
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Local anesthetics work by reversibly blocking voltage-gated sodium channels, inhibiting nerve impulse transmission. Their potency, onset, and duration of action depend on factors like lipid solubility, pKa, and protein binding. They exist in both charged and uncharged forms, and increasing the proportion of uncharged forms through alkalization can speed onset. Amide local anesthetics generally have a longer duration than esters.
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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.
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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.
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This document provides an overview of local anesthetics. It discusses their mechanism of action, which involves inhibiting sodium channel function and preventing nerve impulse propagation. It describes the basic chemical structure of local anesthetic molecules and how modifications impact properties like potency and duration. Factors influencing local anesthetic action and their pharmacokinetics, including absorption, distribution, metabolism and excretion, are summarized. Specific local anesthetics and details of their metabolism are also outlined.
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Local anesthetics 2
Local anesthetics work by blocking sodium channels in nerve fibers, preventing the generation of action potentials and conduction of nerve impulses. They typically contain a hydrophilic amine group, hydrophobic aromatic moiety, and intermediate ester or amide linkage. Esters are metabolized rapidly by plasma esterases while amides are metabolized more slowly by the liver. Common uses of local anesthetics include minor surgery, dental procedures, nerve blocks, epidurals and caudals. Adverse effects can include central nervous system toxicity, cardiac issues like arrhythmias or hypotension, and allergic reactions. Chloroprocaine and lidocaine are examples of commonly used local anesthetic agents.
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Local anesthetics work by reversibly blocking sodium channels in neural membranes, preventing action potentials. The first local anesthetic was cocaine in the 1860s. Local anesthetics are now classified as esters or amides and commonly used in infiltration, nerve blocks, and regional techniques. Factors like lipid solubility, dose, and pH influence their duration and potency. Toxicity can affect the central nervous system, heart, and lungs. Severe toxicity requires securing the airway, oxygen, benzodiazepines or propofol for seizures, and IV lipid emulsion along with standard cardiac life support protocols.
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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.
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Local anesthetics work by blocking sodium channels and preventing the influx of sodium ions needed for nerve impulse conduction. Early pioneers discovered cocaine's local anesthetic properties in the 1880s, leading to other developments like procaine and lidocaine. Local anesthetics are weak bases containing an aromatic ring, amine, and ester or amide linkage. They vary in potency, duration of action, and lipid solubility. The specific receptor theory states they reversibly bind sodium channels intracellularly to block conduction.
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Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
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Maximum allowable dose
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Local anesthetics block nerve conduction by reversibly binding to voltage-gated sodium channels and preventing the influx of sodium ions needed to generate action potentials. They are used to provide localized pain relief and are delivered through various techniques including infiltration, nerve blocks, and epidurals. The choice of local anesthetic depends on factors like duration of action, with esters having a shorter duration than amides. Additives like epinephrine prolong the effect by reducing absorption. While effective for analgesia, local anesthetics must be carefully administered to avoid toxicity from high systemic levels that can cause seizures or cardiac issues.
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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.
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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.
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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.
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Local Anaesthesia
- 1. AAKRITI ROLL NO. 1 BATCH 2016 LOCAL ANAESTHESIA
- 3. L.A can interfere with the excitation process in a nerve membrane in one or more of the following ways Altering the basic resting potential of the nerve membrane Altering the threshold potential Decreasing the rate of depolarization Prolonging the rate of repolarization MODE OF ACTION
- 8. Current evidence indicates that the resting potential of the nerve membrane is unaltered by la and that conventional la act within the membrane channels rather than at the membrane surface Also the surface charge theory cannot explain the activity of uncharged anesthetic molecules in blocking nerve impulses
- 11. 1. Displacement of calcium ions from nerve receptor site 2. Binding of L.A molecule to this receptor site 3. Blockade of the sodium channel 4. Decrease in sodium conductance 5. Depression of rate of electrical depolarisation 6. Failure to achieve threshold potential level 7. Lack of development of propogated action potential 8. Conduction blockade MECHANISM OF ACTION
- 12. ON THE BASIS OF MODE OF ADMINISTRATION
- 14. Agent acting at external surface of nerve memb. Agent acting at internal surface of nerve memb Agents act by a receptor independent Combination of physiochemical receptors and receptor ind. mechanism
- 16. Distilled water –used as solvent
- 17. PHARMACOKINETICS UPTAKE When injected in soft tissues most la causes vasodilation Cocaine is the only la that produces vasoconstriction (initially vasodilation followed by prolonged vasoconstriction).it is produced by- inhibition of uptake of catecholamines into tissue binding sites Excess of free nor-epinephrine Prolonged vasoconstriction
- 18. The rate at which local anesthetics are absorbed into the blood stream and reach their peak blood level vary according to their route of administration- ROUTE TIME(MINS) INTRAVENOUS 1 TOPICAL 5 INTRAMUSCULAR 5-10 SUBCUTANEOUS 30-90
- 19. Once absorbed in the blood stream local anesthetics are distributed through out the body to all the tissues Highly perfused organs such as brain,head,liver,kidney,lungs have higher blood levels of anesthetic than do less higher perfused organs DISTRIBUTION
- 21. ESTERS- hydrolyzed in the plasma by enzyme pseudocholinesterase • Chloroprocaine most rapidly hydrolised –it is least toxic • Tertracaine hydrolised 16 times more slowlyhence greater potential toxicity AMIDES- primary site of metabolism is liver • Prilocaine –liver +lung • Lidocaine- 70% of the dose injected undergoes metabolism in patients with normal liver function. • If slower metabolism then potential risk of toxicity(hypotension,CHF,liver cirrhosis) METABOLISM
- 22. Kidneys are the primary excretory organs for both la and its metabolites A percentage of given dose of la drug is excreted unchanged in urine ESTERS-appears in very small concentration as parent compound in the urine because they are hydrolysed almost completely by plasma Amides are present in urine as a parent compound in a greater percentage than esters because of their more complex process of metabolism EXCRETION
- 23. LIDOCAINE
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