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This document discusses polytherapy, or the use of multiple antiepileptic drugs (AEDs), for the treatment of epilepsy. It notes that while polytherapy was discouraged in the past due to drug interactions and side effects, newer AEDs may have lower interaction potential and side effects when combined. The document then examines the mechanisms of various AEDs including sodium channel blockers, calcium channel blockers, GABAergic drugs, and others. It provides guidelines on choosing AEDs based on epilepsy syndrome and seizure type. Factors like comorbidities, side effect profiles, and pharmacokinetic interactions are considered in selecting appropriate drug combinations for polytherapy.
slide consist of cholinergic system, neuronal transmission, receptors of cholinergic system, anti cholinergic drugs its classification, Mechanism of action and organophosphate poisoning and treatment approaches
This document summarizes 5 major categories of transducer mechanisms:
1) G-protein coupled receptors which activate downstream effectors like adenylyl cyclase or phospholipase C.
2) Ion channel receptors which directly open or close ion channels.
3) Transmembrane enzyme-linked receptors which activate intracellular protein kinases.
4) Transmembrane JAK-STAT binding receptors which activate the JAK/STAT signaling pathway.
5) Receptors regulating gene expression which bind intracellularly to directly regulate gene transcription.
This document discusses catecholamines and adrenergic receptors. It describes the steps of catecholamine biosynthesis and metabolism. It explains the distribution of alpha and beta adrenergic receptors in the body and their functions. The document outlines various adrenergic agonists and their uses, including endogenous catecholamines like epinephrine and norepinephrine, and synthetic agonists like isoproterenol. It provides details on receptor selectivity and mechanisms of compounds that affect catecholamine storage, release, and breakdown in the body.
This document discusses catecholamines and non-catecholamines used as autonomic drugs. It describes the classifications of autonomic drugs and their mechanisms of action. Specific catecholamines discussed include norepinephrine, epinephrine, isoproterenol, and dopamine. Non-catecholamines discussed include ephedrine, pseudoephedrine, amphetamine, methylphenidate, phenylpropanolamine, and oxymetazoline. Their pharmacological effects, clinical uses, and dosages are summarized for various conditions and species. The document provides an overview of important adrenergic drugs and their mechanisms and applications in veterinary medicine.
Phenytoin is metabolized into reactive intermediates like arene oxide and catechol that can bind to proteins and trigger immune responses. These metabolites are deactivated by enzymes like epoxide hydrolase and glutathione transferase. Phenytoin strongly induces several CYP450 isozymes and drug metabolizing enzymes. Carbamazepine is metabolized by CYP3A4 into an epoxide metabolite suspected of causing idiosyncratic reactions. Gabapentin and pregabalin modulate calcium influx and stimulate GABA biosynthesis without being metabolized. Felbamate undergoes hydroxylation and hydrolysis to form a toxic metabolite, 2-phenylpropanal. Future anticonvulsants
This document discusses the adrenergic system. It describes the origins and divisions of the autonomic nervous system, including the sympathetic and parasympathetic systems. It then focuses on the adrenergic system, summarizing the neurotransmitters involved, including norepinephrine, epinephrine, and dopamine. It outlines the steps in catecholamine synthesis, storage, release, reuptake, and metabolism. It also describes the different types of adrenergic receptors, including alpha and beta receptors, and provides examples of agonists and antagonists for each. Finally, it categorizes different types of adrenergic drugs.
This document discusses polytherapy, or the use of multiple antiepileptic drugs (AEDs), for the treatment of epilepsy. It notes that while polytherapy was discouraged in the past due to drug interactions and side effects, newer AEDs may have lower interaction potential and side effects when combined. The document then examines the mechanisms of various AEDs including sodium channel blockers, calcium channel blockers, GABAergic drugs, and others. It provides guidelines on choosing AEDs based on epilepsy syndrome and seizure type. Factors like comorbidities, side effect profiles, and pharmacokinetic interactions are considered in selecting appropriate drug combinations for polytherapy.
slide consist of cholinergic system, neuronal transmission, receptors of cholinergic system, anti cholinergic drugs its classification, Mechanism of action and organophosphate poisoning and treatment approaches
This document summarizes 5 major categories of transducer mechanisms:
1) G-protein coupled receptors which activate downstream effectors like adenylyl cyclase or phospholipase C.
2) Ion channel receptors which directly open or close ion channels.
3) Transmembrane enzyme-linked receptors which activate intracellular protein kinases.
4) Transmembrane JAK-STAT binding receptors which activate the JAK/STAT signaling pathway.
5) Receptors regulating gene expression which bind intracellularly to directly regulate gene transcription.
This document discusses catecholamines and adrenergic receptors. It describes the steps of catecholamine biosynthesis and metabolism. It explains the distribution of alpha and beta adrenergic receptors in the body and their functions. The document outlines various adrenergic agonists and their uses, including endogenous catecholamines like epinephrine and norepinephrine, and synthetic agonists like isoproterenol. It provides details on receptor selectivity and mechanisms of compounds that affect catecholamine storage, release, and breakdown in the body.
This document discusses catecholamines and non-catecholamines used as autonomic drugs. It describes the classifications of autonomic drugs and their mechanisms of action. Specific catecholamines discussed include norepinephrine, epinephrine, isoproterenol, and dopamine. Non-catecholamines discussed include ephedrine, pseudoephedrine, amphetamine, methylphenidate, phenylpropanolamine, and oxymetazoline. Their pharmacological effects, clinical uses, and dosages are summarized for various conditions and species. The document provides an overview of important adrenergic drugs and their mechanisms and applications in veterinary medicine.
Phenytoin is metabolized into reactive intermediates like arene oxide and catechol that can bind to proteins and trigger immune responses. These metabolites are deactivated by enzymes like epoxide hydrolase and glutathione transferase. Phenytoin strongly induces several CYP450 isozymes and drug metabolizing enzymes. Carbamazepine is metabolized by CYP3A4 into an epoxide metabolite suspected of causing idiosyncratic reactions. Gabapentin and pregabalin modulate calcium influx and stimulate GABA biosynthesis without being metabolized. Felbamate undergoes hydroxylation and hydrolysis to form a toxic metabolite, 2-phenylpropanal. Future anticonvulsants
This document discusses the adrenergic system. It describes the origins and divisions of the autonomic nervous system, including the sympathetic and parasympathetic systems. It then focuses on the adrenergic system, summarizing the neurotransmitters involved, including norepinephrine, epinephrine, and dopamine. It outlines the steps in catecholamine synthesis, storage, release, reuptake, and metabolism. It also describes the different types of adrenergic receptors, including alpha and beta receptors, and provides examples of agonists and antagonists for each. Finally, it categorizes different types of adrenergic drugs.
(1) The document discusses the history of the discovery of neurotransmitters and the role of Ramón y Cajal and Otto Loewi in determining neurons communicate via chemical messengers rather than electrical signals.
(2) It provides definitions of neurotransmitter and criteria that must be met for a substance to be classified as a neurotransmitter.
(3) Glutamate is described as the major excitatory neurotransmitter in the brain, present at high concentrations in presynaptic terminals and involved in many key pathways.
Neurotransmitters are chemical messengers that transmit signals between neurons. They include acetylcholine, dopamine, serotonin, glutamate, GABA, and others. Neurotransmitters are synthesized and stored in neurons then released into the synaptic cleft in response to an action potential. They bind to receptors on the postsynaptic neuron and are then inactivated by reuptake or degradation to terminate their effects. Common neurological disorders involve imbalances in neurotransmitters, such as Parkinson's disease being linked to low dopamine levels and Myasthenia gravis involving antibodies against acetylcholine receptors.
Benzodiazepines are a class of drugs with a core chemical structure consisting of a benzene ring attached to a diazepine ring. Different benzodiazepines are variations on this core structure due to chemical substitutions at two positions. The duration of action of individual benzodiazepines depends on their half-life and metabolic fate.
This document provides information on the biochemistry of neurotransmitters. It discusses the structure and function of neurons and the nervous system. It explains the role of neurotransmitters in neurotransmission and classifies them as either inhibitory or excitatory. The document describes the synthesis, storage, release and degradation of several important neurotransmitters including acetylcholine, catecholamines like dopamine and norepinephrine, and serotonin. It also discusses how imbalances in these neurotransmitters can lead to conditions like Parkinson's disease, schizophrenia and depression.
Neurohumoral Transmission in central nervous systemSONALPANDE5
Neurohumoral transmission in the central nervous system involves four main processes:
1) Neurotransmitters transmit signals across synapses. 2) Neuromodulators produce slower pre- or post-synaptic responses. 3) Neuromediators play a role in eliciting post-synaptic responses. 4) Neurotropic factors regulate neuronal growth and morphology.
Dopamine is a key neurotransmitter in the central nervous system. It is synthesized from tyrosine and functions in motor control, reward, and other behaviors. Dopamine receptors are G-protein coupled and include D1-like and D2-like families. Dopamine pathways project from midbrain regions to other areas and are involved in motor control and reward
The document discusses adrenergic drugs and the adrenergic nervous system. It defines the adrenergic nervous system as a group of organs and nerves that release neurotransmitters like adrenaline and noradrenaline. It describes adrenergic drugs as those that produce effects similar to the sympathetic nervous system, known as sympathomimetic drugs. These drugs can affect three main types of adrenergic receptors: alpha, beta, and dopamine receptors. The document also classifies adrenergic drugs according to their mode of action, receptor selectivity, chemical nature, and therapeutic effects. Finally, it outlines some of the pharmacological actions and clinical indications of adrenergic drugs.
This document discusses the biosynthesis, mechanisms of action, receptors, and pharmacological uses of catecholamines and adrenergic drugs. It describes the steps of catecholamine biosynthesis and metabolism. It explains that adrenergic receptors are G protein-coupled receptors that bind endogenous ligands like epinephrine and norepinephrine. The document categorizes adrenergic drugs as agonists that mimic sympathetic effects or antagonists that block sympathetic effects. It provides examples of specific adrenergic drugs and their uses and mechanisms of action.
The Effect of Curcumin on AMPA Receptors PharmacokineticsHasan Arafat
This document outlines a study examining the effect of curcumin derivatives on AMPA receptor kinetics. The objectives are to identify potent and selective curcumin derivatives that inhibit AMPA receptors and characterize their effects. HEK293 cells will be transfected with GluA2 receptors to study the effects of curcumin derivative A on whole cell current, desensitization, and deactivation. Preliminary results show that derivative A decreases peak current, increases desensitization rate and extent, and increases deactivation rate, indicating it inhibits AMPA receptors. The study aims to better understand how curcumin derivatives modify AMPA receptor properties to develop new natural drugs without side effects.
The content starts from brief introduction to nervous system. Introduction to adrenergic nervous system and cholinergic nervous system, classification, mechanism of action, receptors, classification including agonists and antagonists, structure activity relationships, therapeutic uses. This content is prepared by using various books and internet sources.
This document discusses cholinergic transmission in the autonomic and somatic nervous systems. It notes that acetylcholine is the main neurotransmitter and describes the cholinergic fibers involved in the peripheral and central nervous systems. These include preganglionic autonomic fibers, somatic motor fibers to skeletal muscles, and some postganglionic fibers. The document also summarizes the synthesis, storage, release, and termination of acetylcholine, as well as the two main types of cholinergic receptors: muscarinic and nicotinic receptors.
A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
The document discusses the cholinergic system and neuromuscular blocking drugs. It begins by outlining the objectives and intended learning outcomes, which are to understand the locations of acetylcholine receptors, the synthesis and fate of acetylcholine, and the classifications and effects of various cholinergic drugs. It then describes the autonomic nervous system, including its parts, locations of ganglia, innervations of organs, and neurotransmitters. Next, it explains the synthesis, storage, release, binding, termination and recycling of acetylcholine. It also classifies cholinergic receptors and their locations and mechanisms. Finally, it discusses the classifications, actions, uses and effects of cholinergic drugs that directly activate receptors
The document discusses the glycine receptor, a ligand-gated chloride channel protein that is the major inhibitory neurotransmitter in the adult central nervous system. It exists as a pentameric protein composed of alpha and beta subunits that surround a central pore. Glycine binding activates the receptor, allowing chloride ion influx that hyperpolarizes the neuron. Disorders involving glycine receptor mutations can cause startle disease or non-ketotic hyperglycinemia. The receptor has many ligands but is antagonized primarily by strychnine.
This document discusses neurotransmitters, including their classification and the synthesis of dopamine. Neurotransmitters transmit signals between neurons through synapses. They are classified into amino acids, peptides, amines, and others based on their chemical structure. Dopamine is an amine neurotransmitter that is synthesized through specific pathways in the brain. Dopamine deficiency is associated with Parkinson's disease, where there is degeneration of an area of the brain called the substantia nigra resulting in decreased dopamine production and characteristic motor symptoms.
This document discusses adrenergic neurotransmission and the catecholamine neurotransmitters adrenaline and noradrenaline. It describes the biosynthesis, storage, release, reuptake, and metabolism of catecholamines. It discusses the different types of adrenergic receptors (alpha and beta), their subtypes, molecular effects, and clinical impacts. It also covers Dale's phenomenon, the actions of adrenaline as a prototype catecholamine, and the adverse effects of catecholamines.
The document discusses receptor desensitization, which is the decrease in response of cells to agonists after continuous stimulation. It can occur via two types: homologous, mediated by the same receptor; or heterologous, mediated by a different receptor. Factors that can cause desensitization include changes to receptors, loss of receptors, exhaustion of mediators, increased drug metabolism, and physiological adaptation. The mechanism involves phosphorylation of receptors and binding of arrestins, which uncouple the receptor from G proteins and promote internalization. β-arrestins play a key role in desensitization and can also translocate to the nucleus to influence transcription.
Barbiturates are a group of drugs that have calming effects on the body ranging from mild relaxation to loss of consciousness. They act as sedatives, hypnotics, and anticonvulsants. Barbiturates potentiate the effects of GABA at GABAA receptors and also block AMPA and kainate glutamate receptors. The core structure is barbituric acid, which is substituted at various positions to produce different effects. Substitution of alkyl groups at R1 and R2 affects lipid solubility and duration of action. Increasing the chain length at R3 and R4 enhances potency while branched chains decrease duration. Carbonyl groups are essential for activity. Common bar
Basics of anatomy of endocrine glands and functions of their hormones with disorders as per the Pharmacy Council of India curriculum.
Only for educational purpose for undergraduate B pharmacy students.
This document provides information on cholinergic drugs and the autonomic nervous system. It discusses:
1) How acetylcholine is synthesized and stored in neurons.
2) The spectrum of action of direct-acting cholinergic drugs like acetylcholine and indirect-acting drugs that inhibit acetylcholinesterase.
3) The pharmacological effects of cholinergics like vasodilation, negative chronotropy, and negative inotropy.
This document discusses cholinomimetic drugs and acetylcholine (ACh) signaling in the nervous system. It begins by describing the autonomic and somatic divisions of the nervous system. It then discusses how ACh acts as a neurotransmitter at cholinergic synapses in both divisions. Cholinomimetic drugs can be direct agonists that mimic ACh or indirect inhibitors of acetylcholinesterase (AChE) to prolong the actions of endogenous ACh. Examples of direct agonists include pilocarpine and nicotine. Indirect agonists like galantamine and donepezil inhibit AChE. The document provides detailed information on the mechanisms and clinical uses of various cholinomime
The document discusses ways to save water in the home. It defines volume as the amount of three-dimensional space an object occupies and is usually measured in cubic meters, liters or milliliters. Capacity refers to the amount of liquid or number of objects a container can hold. The document provides examples of how much water different daily activities like showering, teeth brushing, and hand washing use and offers ways to reduce this usage to conserve water.
Ropivacane: A new break through in regional and neuraxial BlockadeProf. Mridul Panditrao
No significant changes in vitals. Minimal bradycardia and fall in BP observed in a few patients.
No significant events like Nausea, Vomiting, Shivering,
Pruritus, Sedation, Respiratory distress etc.
No need for rescue analgesia in 30 patients (75%)
Rescue analgesia given in 10 patients (25%)
(1) The document discusses the history of the discovery of neurotransmitters and the role of Ramón y Cajal and Otto Loewi in determining neurons communicate via chemical messengers rather than electrical signals.
(2) It provides definitions of neurotransmitter and criteria that must be met for a substance to be classified as a neurotransmitter.
(3) Glutamate is described as the major excitatory neurotransmitter in the brain, present at high concentrations in presynaptic terminals and involved in many key pathways.
Neurotransmitters are chemical messengers that transmit signals between neurons. They include acetylcholine, dopamine, serotonin, glutamate, GABA, and others. Neurotransmitters are synthesized and stored in neurons then released into the synaptic cleft in response to an action potential. They bind to receptors on the postsynaptic neuron and are then inactivated by reuptake or degradation to terminate their effects. Common neurological disorders involve imbalances in neurotransmitters, such as Parkinson's disease being linked to low dopamine levels and Myasthenia gravis involving antibodies against acetylcholine receptors.
Benzodiazepines are a class of drugs with a core chemical structure consisting of a benzene ring attached to a diazepine ring. Different benzodiazepines are variations on this core structure due to chemical substitutions at two positions. The duration of action of individual benzodiazepines depends on their half-life and metabolic fate.
This document provides information on the biochemistry of neurotransmitters. It discusses the structure and function of neurons and the nervous system. It explains the role of neurotransmitters in neurotransmission and classifies them as either inhibitory or excitatory. The document describes the synthesis, storage, release and degradation of several important neurotransmitters including acetylcholine, catecholamines like dopamine and norepinephrine, and serotonin. It also discusses how imbalances in these neurotransmitters can lead to conditions like Parkinson's disease, schizophrenia and depression.
Neurohumoral Transmission in central nervous systemSONALPANDE5
Neurohumoral transmission in the central nervous system involves four main processes:
1) Neurotransmitters transmit signals across synapses. 2) Neuromodulators produce slower pre- or post-synaptic responses. 3) Neuromediators play a role in eliciting post-synaptic responses. 4) Neurotropic factors regulate neuronal growth and morphology.
Dopamine is a key neurotransmitter in the central nervous system. It is synthesized from tyrosine and functions in motor control, reward, and other behaviors. Dopamine receptors are G-protein coupled and include D1-like and D2-like families. Dopamine pathways project from midbrain regions to other areas and are involved in motor control and reward
The document discusses adrenergic drugs and the adrenergic nervous system. It defines the adrenergic nervous system as a group of organs and nerves that release neurotransmitters like adrenaline and noradrenaline. It describes adrenergic drugs as those that produce effects similar to the sympathetic nervous system, known as sympathomimetic drugs. These drugs can affect three main types of adrenergic receptors: alpha, beta, and dopamine receptors. The document also classifies adrenergic drugs according to their mode of action, receptor selectivity, chemical nature, and therapeutic effects. Finally, it outlines some of the pharmacological actions and clinical indications of adrenergic drugs.
This document discusses the biosynthesis, mechanisms of action, receptors, and pharmacological uses of catecholamines and adrenergic drugs. It describes the steps of catecholamine biosynthesis and metabolism. It explains that adrenergic receptors are G protein-coupled receptors that bind endogenous ligands like epinephrine and norepinephrine. The document categorizes adrenergic drugs as agonists that mimic sympathetic effects or antagonists that block sympathetic effects. It provides examples of specific adrenergic drugs and their uses and mechanisms of action.
The Effect of Curcumin on AMPA Receptors PharmacokineticsHasan Arafat
This document outlines a study examining the effect of curcumin derivatives on AMPA receptor kinetics. The objectives are to identify potent and selective curcumin derivatives that inhibit AMPA receptors and characterize their effects. HEK293 cells will be transfected with GluA2 receptors to study the effects of curcumin derivative A on whole cell current, desensitization, and deactivation. Preliminary results show that derivative A decreases peak current, increases desensitization rate and extent, and increases deactivation rate, indicating it inhibits AMPA receptors. The study aims to better understand how curcumin derivatives modify AMPA receptor properties to develop new natural drugs without side effects.
The content starts from brief introduction to nervous system. Introduction to adrenergic nervous system and cholinergic nervous system, classification, mechanism of action, receptors, classification including agonists and antagonists, structure activity relationships, therapeutic uses. This content is prepared by using various books and internet sources.
This document discusses cholinergic transmission in the autonomic and somatic nervous systems. It notes that acetylcholine is the main neurotransmitter and describes the cholinergic fibers involved in the peripheral and central nervous systems. These include preganglionic autonomic fibers, somatic motor fibers to skeletal muscles, and some postganglionic fibers. The document also summarizes the synthesis, storage, release, and termination of acetylcholine, as well as the two main types of cholinergic receptors: muscarinic and nicotinic receptors.
A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
The document discusses the cholinergic system and neuromuscular blocking drugs. It begins by outlining the objectives and intended learning outcomes, which are to understand the locations of acetylcholine receptors, the synthesis and fate of acetylcholine, and the classifications and effects of various cholinergic drugs. It then describes the autonomic nervous system, including its parts, locations of ganglia, innervations of organs, and neurotransmitters. Next, it explains the synthesis, storage, release, binding, termination and recycling of acetylcholine. It also classifies cholinergic receptors and their locations and mechanisms. Finally, it discusses the classifications, actions, uses and effects of cholinergic drugs that directly activate receptors
The document discusses the glycine receptor, a ligand-gated chloride channel protein that is the major inhibitory neurotransmitter in the adult central nervous system. It exists as a pentameric protein composed of alpha and beta subunits that surround a central pore. Glycine binding activates the receptor, allowing chloride ion influx that hyperpolarizes the neuron. Disorders involving glycine receptor mutations can cause startle disease or non-ketotic hyperglycinemia. The receptor has many ligands but is antagonized primarily by strychnine.
This document discusses neurotransmitters, including their classification and the synthesis of dopamine. Neurotransmitters transmit signals between neurons through synapses. They are classified into amino acids, peptides, amines, and others based on their chemical structure. Dopamine is an amine neurotransmitter that is synthesized through specific pathways in the brain. Dopamine deficiency is associated with Parkinson's disease, where there is degeneration of an area of the brain called the substantia nigra resulting in decreased dopamine production and characteristic motor symptoms.
This document discusses adrenergic neurotransmission and the catecholamine neurotransmitters adrenaline and noradrenaline. It describes the biosynthesis, storage, release, reuptake, and metabolism of catecholamines. It discusses the different types of adrenergic receptors (alpha and beta), their subtypes, molecular effects, and clinical impacts. It also covers Dale's phenomenon, the actions of adrenaline as a prototype catecholamine, and the adverse effects of catecholamines.
The document discusses receptor desensitization, which is the decrease in response of cells to agonists after continuous stimulation. It can occur via two types: homologous, mediated by the same receptor; or heterologous, mediated by a different receptor. Factors that can cause desensitization include changes to receptors, loss of receptors, exhaustion of mediators, increased drug metabolism, and physiological adaptation. The mechanism involves phosphorylation of receptors and binding of arrestins, which uncouple the receptor from G proteins and promote internalization. β-arrestins play a key role in desensitization and can also translocate to the nucleus to influence transcription.
Barbiturates are a group of drugs that have calming effects on the body ranging from mild relaxation to loss of consciousness. They act as sedatives, hypnotics, and anticonvulsants. Barbiturates potentiate the effects of GABA at GABAA receptors and also block AMPA and kainate glutamate receptors. The core structure is barbituric acid, which is substituted at various positions to produce different effects. Substitution of alkyl groups at R1 and R2 affects lipid solubility and duration of action. Increasing the chain length at R3 and R4 enhances potency while branched chains decrease duration. Carbonyl groups are essential for activity. Common bar
Basics of anatomy of endocrine glands and functions of their hormones with disorders as per the Pharmacy Council of India curriculum.
Only for educational purpose for undergraduate B pharmacy students.
This document provides information on cholinergic drugs and the autonomic nervous system. It discusses:
1) How acetylcholine is synthesized and stored in neurons.
2) The spectrum of action of direct-acting cholinergic drugs like acetylcholine and indirect-acting drugs that inhibit acetylcholinesterase.
3) The pharmacological effects of cholinergics like vasodilation, negative chronotropy, and negative inotropy.
This document discusses cholinomimetic drugs and acetylcholine (ACh) signaling in the nervous system. It begins by describing the autonomic and somatic divisions of the nervous system. It then discusses how ACh acts as a neurotransmitter at cholinergic synapses in both divisions. Cholinomimetic drugs can be direct agonists that mimic ACh or indirect inhibitors of acetylcholinesterase (AChE) to prolong the actions of endogenous ACh. Examples of direct agonists include pilocarpine and nicotine. Indirect agonists like galantamine and donepezil inhibit AChE. The document provides detailed information on the mechanisms and clinical uses of various cholinomime
The document discusses ways to save water in the home. It defines volume as the amount of three-dimensional space an object occupies and is usually measured in cubic meters, liters or milliliters. Capacity refers to the amount of liquid or number of objects a container can hold. The document provides examples of how much water different daily activities like showering, teeth brushing, and hand washing use and offers ways to reduce this usage to conserve water.
Ropivacane: A new break through in regional and neuraxial BlockadeProf. Mridul Panditrao
No significant changes in vitals. Minimal bradycardia and fall in BP observed in a few patients.
No significant events like Nausea, Vomiting, Shivering,
Pruritus, Sedation, Respiratory distress etc.
No need for rescue analgesia in 30 patients (75%)
Rescue analgesia given in 10 patients (25%)
Ropivacaine is a long-acting local anesthetic similar to bupivacaine that provides both anesthesia and analgesia. It has decreased cardiotoxicity compared to bupivacaine. Ropivacaine is metabolized in the liver and excreted renally. It works by reversibly blocking sodium ion influx in nerve fibers, inhibiting impulse conduction. It can be used for epidural, spinal, infiltration, and peripheral nerve blocks for surgical anesthesia, C-sections, and postoperative or chronic pain management. Side effects include central nervous system and cardiovascular toxicity at high doses.
The document summarizes key aspects of local anesthetics including:
1. It discusses the history and development of various local anesthetic compounds.
2. It describes the anatomy and physiology of nerve conduction and how local anesthetics work by blocking sodium channels.
3. It compares the mechanisms of action, pharmacokinetics, and differences between amide and ester local anesthetics.
Ropivacaine is a long-acting local anesthetic similar to bupivacaine but with less cardiotoxicity due to its stereospecificity as a pure S-enantiomer. Studies have shown ropivacaine to have approximately half the potency of bupivacaine in depressing the heart while providing comparable surgical anesthesia. Ropivacaine may be better suited than bupivacaine for epidural analgesia due to its ability to differentiate sensory and motor block at low concentrations and its toxicity not increasing in pregnancy.
This document provides an overview of local anesthetics including their ideal properties, commercial preparations, structure-activity relationships, mechanisms of action, pharmacokinetics, side effects, and individual local anesthetics. It discusses topics such as how local anesthetics work by producing reversible conduction blockade along nerves, their absorption, distribution, metabolism and excretion from the body, and potential adverse effects including neurological, cardiovascular and respiratory side effects.
Local anesthetics work by blocking sodium channels in nerve cell membranes, preventing the propagation of action potentials and conduction of sensations. This document discusses the classification, composition, mechanisms of action, and examples of commonly used local anesthetic drugs and vasoconstrictors. It also covers the techniques for maxillary nerve blocks and factors that influence the onset and duration of local anesthesia.
LOCAL ANAESTHETICS.pptbshsjsjsjsjsjsjjsjsDakaneMaalim
Local anaesthetics are drugs that cause reversible loss of sensation in a specific body region without loss of consciousness. They are classified based on their structure and potency. Local anaesthetics work by blocking sodium channels to prevent nerve impulse propagation. Factors like lipid solubility, protein binding, and pKa determine a drug's potency, duration of action, and onset. Local anaesthetics are widely used for infiltration, nerve blocks, epidurals, and other regional techniques to provide anaesthesia or post-operative analgesia. Toxicity can occur if local anaesthetics enter the systemic circulation in high amounts. Proper dosing and technique help prevent local anaesthetic systemic toxicity.
1. Local anesthetics work by reversibly blocking sodium channels in nerves, preventing the transmission of nerve impulses and causing numbness.
2. Cocaine was the first local anesthetic used clinically in the 1880s, but its addictive properties led to the development of safer synthetic options like procaine and lidocaine.
3. Local anesthetics are administered topically, via infiltration of tissues, or through peripheral nerve blocks to temporarily numb areas of the body for procedures. Their effects are reversible and they do not damage nerves when used properly.
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 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.
Everything you need to know about Local Anesthetics. Dose, mechanism of action, toxicity, management. How to use, where to use. It also contains receptors which are involved. Which factors prolongs and makes the drug work quicker.
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 anesthesia: Uses, Types, Side effects and SafetyPrachiRathi40
This document provides an overview of local anesthesia. It begins with definitions and an introduction. It then covers the historical background, classifications, components, mechanisms of action, techniques, and complications of local anesthesia. The classifications section divides local anesthetics based on their pharmacology, route of administration, biologic site and mode of action, and duration of action. Key local anesthetic agents like lidocaine, mepivacaine, articaine, bupivacaine, and topical anesthetics are also summarized. Maximum recommended doses and specific nerve block techniques for the maxillary nerve are outlined. In conclusion, the document reviews local anesthesia in detail.
This document summarizes guidelines for prescribing various classes of analgesics, including non-opioids like acetaminophen and NSAIDs, opioid analgesics of varying efficacy, and drugs for neuropathic pain and migraines. It provides details on mechanisms of action, dosing, adverse effects, and contraindications for common prescription and over-the-counter pain relievers.
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.
Local anesthetics are drugs that cause reversible loss of sensation, especially pain, in a localized area of the body without damaging neurons. They work by blocking the generation and conduction of nerve impulses at the site of action, which is the axonal membrane. The order of block is pain, temperature, touch, pressure, and then motor function. Common local anesthetics include lidocaine, bupivacaine, tetracaine, and prilocaine. They provide analgesia for minor procedures but can also be used for major surgery via regional techniques like epidurals.
This document discusses local anesthesia, including how it works and its properties. It begins by defining local anesthesia as a loss of sensation caused by depressing nerve endings or inhibiting nerve conduction. It then discusses various methods of inducing local anesthesia and desirable properties like reversibility and lack of toxicity. The bulk of the document focuses on neurophysiology, explaining how nerves generate and transmit impulses through changes in electrolyte permeability and membrane potential. It discusses several theories for how local anesthetics specifically block nerve conduction, settling on the theory that they displace calcium from sodium channels, blocking sodium conductance and preventing action potentials. It notes local anesthesia is less effective in inflamed areas due to changes in pH. The document concludes by providing an example dose calculation
This document provides an overview of local anesthetics, including their physicochemical properties, mechanisms of action, classifications, toxicity risks, and clinical applications. It discusses how local anesthetics reversibly block sodium channels, preventing nerve impulse generation. The summary properties like lipid solubility, ionization, and protein binding determine onset and duration. Local anesthetics are classified as amide and ester types, with differences in stability and allergic potential. Toxicity can impact the central nervous system or cardiovascular system. Additives like epinephrine or bicarbonate alter anesthetic properties. Common amide and ester local anesthetics like lidocaine, bupivacaine, and cocaine are compared in terms of metabolism and indications.
Thiopentone is an ultra short-acting barbiturate used for induction of anesthesia. It works by enhancing the effect of the inhibitory neurotransmitter GABA at GABAA receptors in the brain, causing sedation, hypnosis and general anesthesia. It has a rapid onset of 10-20 seconds when given intravenously and is redistributed and metabolized quickly, typically causing awakening within 5-15 minutes. Common uses include induction of anesthesia and treatment of increased intracranial pressure. Side effects are generally mild and related to its cardiovascular and respiratory depressant effects.
This document discusses the pharmacology of local anesthetics. It defines local anesthetics as drugs that reversibly prevent nerve impulse transmission in the applied region without affecting consciousness. It describes the ideal properties of local anesthetics and compares local versus general anesthesia. It discusses the molecular structures, classifications, mechanisms of action, and structure-activity relationships of various local anesthetics. Specific local anesthetics like cocaine, procaine, lidocaine, bupivacaine and their properties are also summarized.
Barbiturates are a class of drugs that act as central nervous system depressants and were one of the first intravenous anesthetic agents used clinically, with thiopental and methohexital being two examples that are ultra short-acting and can be used for anesthetic induction. Barbiturates work by enhancing the effects of the inhibitory neurotransmitter GABA in the brain and have a variety of clinical uses but also potential adverse effects like respiratory depression if overdosed.
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.
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.
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2. Introduction.
LA are drugs that produce reversible
depression of nerve impulse and
conduction when applied to nerve fibres
The ester group of LA were first used in
1884 – cocaine for topical use in
opthalmology
Amino amide LA were manufactured in
1943 – lidnocaine, since then many newer
safer LA has been produced
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3. IDEAL PROPERTIES
Physiochemical properties
Easy to produce and economical
Stability during storage
Easy aaccessibility; appropriate packaging and
labelling
Formulation (where possible, additive free)
Soluble in water
Sterilisable by heat without decomposition
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4. IDEAL PROPERTIES cont.
Pharmacokinetics
Ease of administration
Rapid onset
Duration appropriate to use
Clearance independent of hepatic and renal
function
No active or toxic metabolites
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5. IDEAL PROPERTIES cont.
Pharmacodynamics
High therapeutics ratio
No hypersensitivity reaction
Absence of toxicity on : local tissue, liver, brain and other
tissue
Nervous depression, especially of sensory fibres
Administration should be effective by topical application,
injection near a nerve trunk or infiltration
Specificity – only nerve tissue should be affected
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6. Chemistry and Structure Activity
Relationship
All typical LA contain h.philic and h.phobic
domain that are separated by intermediate alkyl
chain
The h.philic grp usually tertiary amine
The h.phobic grp usually an aromatic residue
Intermediate bond is either of the ester or amide
type – determines many of the properties of the
agent
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8. Cont.
Intermediate chain = either ester or amide
Determines many of the properties of the agent
Classification of LA
Changes to any part of the molecule lead to
alteration in activity and tocxicity
Increase length of intermed. Alkyl group will
increase potency up to critical length increase
further will increase toxicity
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9. Cont.
Length of two terminal group are also
equally important
Eg. Add butyl group to mepivacain
bupivacain
Inc. lipid solubility
Greater potency
Longer duration of action
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10. Mode of action
All has similar MOA
Most LA bind to Na channels in the inactivated state,
preventing subsequent channel activation and the large
transient Na influx associated with mb depn.
Marked depression of rate of depn
Failed to reach TP no propogation of AP neural
blockage
LA act in their cationic form but most reach their site of
action by penetrating the nerve sheath and axonal mb as
unionized species
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11. Cont.
Some LA act by
Penetrating the mb, causing mb expansion and
channel distortion (analogous to the critical
volume hypothesis)
Partial penetration by LA of the axonal mb could
increase the transmembrane potential and inhibit
depn. (surface charge theory)
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12. Differential sensitivity of nerve fibre
class
Aα
Aβ
Aχ
Aδ
B
C
mylination
Functions
diamete
r
Conductio
n
heavy
12-20
velocity
70-120
Moderate
5-12
30-70
Touch and pressure
Moderately
3-6
15-30
Motor to muscle spindle
lightly
2-5
12-30
Pain, temperature, touch
lightly
1-3
3-15
Preganglionic autonomic
None
0.4-1.2
0.7-1.3
none
0.3-1.3
0.7-1.3
Pain & reflex response
Motor and propioception
Postganglionic sympathetics
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13. Factors influence
potency,speed of onset and
duration of action
POTENCY
1. Lipophilic nature = lipid solubility
Inc. lipid solubility = inc potency
(penetrare mb more easily)
less molecule required for nerve blockage
Inc alkyl substitution to aromatic ring and
amine inc lipophilic nature
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14. Cont.
2. Partition coefficient /
vasodilatation
? Lidocaine > potent than mepivicaine in
vitro
vasodilatation
Bupivacaine > Etidocaine in vivo
inc fat uptake
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15.
2. SPEED OF ONSET
1. Unionized fraction / pKa & pH
Weak bases tend to be relatively ionized at high
concentration H+
The uncharged form diffuse more readily across
nerve mb determine the onset of LA
Mechanism of ion trapping?
Onset of blockage ∝ pKa
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17. Cont.
3. Lipid solubility
Its effect on onset is poorly understood
?high lipid solubility inc rate of diff and
shorten onset time BUT it also inc
solubility in the surrounding tissue
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18. Cont.
4. Barrier eg. Nerve root
Epineurium
Perineurium
Endoneurium
! Subarachnoid block rapid onset because
nerve rootlets are almost completely bare
of fibrous
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19. Cont.
Sensitivity ∝ 1/size
Autonomic > sensory >
Small, unmyelinated
medium, < myelin
Order of blockage :
motor
large, myelinated
B – C, Ad – Ag – Ab - Aa
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20. Cont.
Duration of blockage
Protein binding regulate the duration of
anaesthetic activity
Due to protein binding of LA to protein receptor
in the Na channel of nerve mb
Highly protein bound will remain for a long time
Procain 6% protein bound
Ropi, bupi, etidocaine 94-96% prot. bound
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21. Factors affecting anaesthetic activity
∀
Dosage
↑ mass injected (vol x conc.)
Red onset time
Inc duration
Inc depth
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25. Absorption of LA
Site of injection ( intercostal > caudal >
brachial plexus etc )
Dosage (blood level of LA related to total
dose of drug rather than spesific volume
or concentration of solution
Addition of vasoconstrictor
Disease process
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26. Systemic disposition kinetics
•
Ultimate plasma conc. Of LA is determined by
rate of tissue distribution and rate of clearance
(metabolism and excretion ) of the drug
Distribution depends on
Tissue perfusion ( alpha and beta phase)
Tissue/blood partision coefficient
Tissue mass
Lung extract significant amount of LA
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27. Cont.
Placental transfer
Protein binding ( lidocaine > bupivacaine X
placental )
Acidosis in fetus ( ion trapping )
Ester LA – rapid hydrolysis not available to cross
placental in significant amount
Clearance
Mainly hepatic metabolism
Minimal renal excretion
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28. Metabolism of LA
A. ESTERS
Rapid hydrolysis by plasma cholinesterase
Water soluble metabolites excreted in the urine
(p-aminobenzoic, diethylaminoethanol
Abnormal pseudocholinesterase inc risk of
toxic side effect
CSF lack of esterase enzyme
Exception Cocain - partially metabolized in liver
and partially excreted in urine unchanged
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29. Cont.
B. AMIDE
Enzymatic degradation in liver by microsomal
enzymes (prilocaine > lidnocaine > mepivacaine
> bupivacaine and etidocaine )
Much slower than ester hydrolysis
N-dealkylation, aromatic and amide hydrolysis
Decrease hepatic function or hepatic blood flow
reduce metabolic rate pred systemic toxicity
Very little drug excreted unchanged by kidney
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30. Cont.
Metabolite of prilocaine (o-toluidine ) which
accumulate after large dose (>10mg/kg) convert
hemoglobin to methemoglobin
Prilocaine epidural labour
Benzocaine also may cause
methemoglobinemia
Tx iv methylene blue @ 1-2 mg/kg of 1% over 5
minutes reduce methemoglobin ( Fe3+ ) to
hemoglobin ( Fe2+ )
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31. cont
Renal
Poor water solubility of LA – limit renal
excretion of unchange drug to < 5% of
injected dose (except cocain 10-12%
urine)
Water soluble metabolites paraaminobenzoic acid readily excreted in the
urine
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32. Side effects
Toxicity often directly proportionate to its
potency
Mixture of LA roughly give additive toxic
effect
In addition to blocking transmission in the
nerve axon, LA affect all tissue where
conduction of impulse occur, therefore in
The CNS
Autonomic ganglia
The NMJ
All form of muscle fibre, esp cardiac
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33. CVS
Affect both myocardium and peripheral
vascular smooth muscle
Primary site is myocardium once absorbed
Effects : ↓conduction, contractility and
excitability
CVS effect are seen at ↑ dose, when CNS
effects are already evident
Inadvertent iv adm may lead to suddent
death
!VF, it is more likely if soln contain
adrenalin
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34. Cont.
At Tx conc lidocaine cause no ECG change
↑ to toxic level, prolonged conduction ↑PR
and QRS interval
Very ↑suppress SAN sinus brady/arrest
and also ↓AVN AV block ± dissociation
Cardiac toxicity of bupivacaine ppt VF
Bupivacaine markedly depress dV/dt
Slow rate of recovery arrhytmias
Produce direct pulm vasoconstrictive effect
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35. Cont
Most LA cause biphasic peripheral
arteriolar response, with initial
vasoconstriction then vasodilatation
As dose ↑ action change to inhibition/Vdil
Cocaine produce vasoconstriction at most
doses, inhibit noradrenalin uptake by
tissue binding site
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36. RESPIRATORY
Depress hypoxic drive
Apnoea can result from phrenic and IC nerve
paralysis or depression of medulla RC
LA relax bronchial smooth muscle
Iv lidocaine 1.5 g/kg red reflex b/constriction
upon intubation
Occationally direct LA aerosol b/spasm
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37. NEUROLOGICAL
Earliest signs are circumoral and tongue numbness,
tinnitus, nystagmus and dizziness
Following absorption, all nitrogenous LA cause CNS
excitation
Restlessness, tremor, eventually tonic-clonic fits
CNS stimulation then followed by depression
Death usually d/t subsequent respiratory depression
Both stimulation and depression are thought to be d/t
neuronal depression
↓ in inhibitory p/w in ARAS being responsible for the
excitatory effects
Ventilatory support may be req. later
Convultion can be controlled by barbiturate eg
diazepam
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38. Cont.
Factors affecting the occurance of
CNS toxicity:
Relative toxicity approx LA potency
Rate of injection r[plasma] achieved
pCO2 inversely related to fit threshold
pH ↓pH ↓fit threshold
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39. IMMUNOLOGICAL
True allergy to LA are uncommon
Ester are more likely – ester derivative
para aminobenzoic acid is a known
allergen
Amide often contain methylparaben as
additive – structure similar to PABA
LA may inhibit neutrophil fx and
theoritically may retard wound healing
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40. MUSCULOSKELETAL
Direct inj into skeletal muscle LA are
myotoxic
Histopathologically cause myofibril
hypercontraction lytic degeneration
oedema necrosis
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41. HEMATOLOGICAL
Lidocaine demonstrate redn coagulation
(prevent thrombosis and platelet
aggregation) and enhance fibrinolysis
Lower incident of embolic event in patient
receiving epidural anaesthesia
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43. Drug interaction
Non depolarising muscle relaxant blockade is
potentiated by LA
Concurrent administration of succinylcholine and
an ester LA may potentiate the effect of both
drugs (pseudocholinesterase dependant)
Dibucaine inhibit pseudocholinesterase
Cimetidine and propanolol red liver blood flow
and lidocaine clearance
Opiods and a2 agonist potentiate LA pain relief
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44. Contraindication
Allergy/hypersensitivity to LA / sol. Additives
Adrenalin is contraindicated for
Tachycardia! (thyrotoxicosis,CCF,IHD)
Anesthesia around end arteries
Iv regional anaesthesia
Epidural/spinal anaesthesia in the presence of
significant
Hypotention/hypovolaemia
Coagulopathy
Presence of local tissue sepsis
Patient refusal
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45. Precautions
Resuscitation equipment and drugs should be available
Reliable iv access
Injection should follow aspiration TRO iv inj
Lowest effective dose possible
Careful in pt with
Pre-existing CNS & cardiac disorder
Cardiac glycoside toxicity
Hepatic or renal impairment
Pred to malignant hyperthermia
Porphria
Fetal bradycardia after Xcess maternal adm with subsequent
hypoxia and acidosis
Retrobulbar block have been a/w respiratory areest
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46. lidocaine
pKa 7.85
Plain aq solution 1, 1.5, 2% @ pH 5-7
Solution with adrenalin @ pH 3-4.5
Ralative potency 2
T1/2ß adult 1.8 hr, neonate 2hr
Xtremely stable
Max dose : plain 3mg/kg, adrenalin 7mg/kg
E.A. of 400mg/70kg @ [blood] = 2-4ug/ml
Toxicity begin @5 ug/ml
Relatively quickly absorbed from GIT
Metab in liver (dealkylation) excreted urine
Toxic dose lead to death by VF or cardiac arrest
Suitable for surface, infiltration,nerve block, caudal, epidural and SA
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47. Bupivacaine
pKa 8.1
Plain aq soln .25, .375, .5% @ pH 4.5-6
If with adrenalin pH 3.5-5.5
Potency 8
Protein binding 95%
> lipid solubility than lidocaine
T1/2ß adult 3.5hr, neonate 8.1-14hr
Amide link LA
Prod prolonged anaesthesia with slower onset
Add adrenalin - ↓toxicity, h/e no change in duration
Post op analgesia : IC 7hr, EA 3-4hr
Epid/caudal peak [plasma] 30-45 min
Lower foetal/maternal ratio cf lidnocaine (! Protein binding)
Max dose : plain/with adrenalin 2 mg/kg
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48. Ropivacaine
Chemical analogue of bupivacaine
The molecule is designed to modify the spesific
cardiotoxicity associated with bupivacaine
pKa 8.2 and pH solution 5.5-6.0
Equally potent as bupivacaine
Its quality of clinical block appear to be very
similar in onset, duration and quality that of
bupivacaine
No spesific toxicity has been detected
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49. Cocaine
From leaves of erytroxylon coca – is an ester of benzoic
acid
CNS stimulant. At low dose produce euphoria. Higher
dose cause convulsion, coma, medullary depressant and
death
Stimulate vomiting centre
Block reuptake of catecholamine enhance SNS
activity
Small dose may cause bradycardia d/t central vagal
stimulation
Larger dose cause tachycardia, inc TPR and
hypertention larger may produce myocardial
depression, VF and death
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50. cont
May be used as surface anaesthesia
As topical LA in ENT (5%)
Cocain itself constrict blood vessel and the
use of adrenalin is contraindicated as it
sensitises the myocardium
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51. Uses of LA
Surface anaesthesia
Infiltration anaesthesia
Nerve block anaesthesia (peripheral,plexus)
Intravenous regional anaesthesia
Spinal/subarachnoid anaesthesia
Other uses (antiarrhytmic, reduction in ICP,
Blunting of CVS responses to intubation and
extubation
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52. Thank you
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