Local anesthesia
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Local anesthesia works by reversibly blocking nerve conduction in a localized area of the body. There are several theories that aim to explain its mechanisms of action and effects on nerve fibers. It is classified according to its biological site of action and chemical properties. Commonly used local anesthetics like lidocaine are thought to work by displacing calcium ions inside nerves, which controls sodium channels and nerve impulse transmission. Local anesthetics are formulated with additional ingredients like vasoconstrictors and preservatives for clinical applications like nerve blocks and infiltration anesthesia.
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Synaptic transmission types I Steps of chemical neurotransmission I Nervous S...
Synaptic transmission between neurons occurs either electrically or chemically. In electrical transmission, gap junctions allow ions to pass directly between neurons. In chemical transmission, neurotransmitters are released from vesicles in the presynaptic neuron and bind to receptors in the postsynaptic neuron. The process involves neurotransmitter synthesis, storage in vesicles, calcium-triggered release, binding to receptors, and termination of signaling via reuptake or enzymatic degradation. Chemical transmission is slower but allows for signal modulation, in contrast to electrical transmission.
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(1) Synaptic transmission occurs via either electrical or chemical synapses. (2) At chemical synapses, neurotransmitters are released from presynaptic terminals and bind to receptors on the postsynaptic cell, eliciting electrical responses. (3) The summation of excitatory and inhibitory postsynaptic potentials determines whether an action potential is generated in the postsynaptic neuron.
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A synapse is the junction between neurons that allows electrical or chemical signals to pass from one cell to another. At a chemical synapse, an action potential in the presynaptic neuron causes neurotransmitters to be released into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic cell, causing ion channels to open and potentially triggering an action potential in that cell. Precise transmission of signals across synapses is crucial for normal nervous system function.
Synapses
A synapse transmits nerve impulses between neurons. During transmission: 1) an electrical impulse travels along an axon, 2) neurotransmitters are released, and 3) these chemicals bind to receptors on the next neuron, stimulating it. Neurotransmitters like serotonin and dopamine relay signals between neurons and control functions like mood, sleep, and movement. Drugs like ecstasy and cocaine affect synapses by preventing neurotransmitter reabsorption, increasing their levels in the synapse. Nobel Prizes have been awarded for discoveries relating to neurotransmitters, synaptic transmission, and their roles in conditions like Parkinson's and memory formation.
Synaptic transmission
This document discusses synaptic transmission between neurons. It defines a synapse as the junction that allows signals to pass between neurons. There are three main types of synapses: chemical, electrical, and conjoint. The process of synaptic transmission involves neurotransmitters being synthesized, stored, transported to the axon terminal, released into the synapse upon neuronal firing, binding to receptors on the post-synaptic neuron, activating those receptors, and then being degraded or reuptaken. Neurotransmitters can have stimulatory or inhibitory effects depending on the receptor subtypes activated. The synaptic signal is terminated through reuptake, enzymatic degradation, or diffusion of the neurotransmitters.
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this ppt shares what synapses are and how information of one neuron is transmitted to other through the synapses. it also includes the properties and plasticity of synaptic transmission
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Synaptic transmission between neurons occurs either electrically or chemically. In electrical transmission, gap junctions allow ions to pass directly between neurons. In chemical transmission, neurotransmitters are released from vesicles in the presynaptic neuron and bind to receptors in the postsynaptic neuron. The process involves neurotransmitter synthesis, storage in vesicles, calcium-triggered release, binding to receptors, and termination of signaling via reuptake or enzymatic degradation. Chemical transmission is slower but allows for signal modulation, in contrast to electrical transmission.
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A synapse transmits nerve impulses between neurons. During transmission: 1) an electrical impulse travels along an axon, 2) neurotransmitters are released, and 3) these chemicals bind to receptors on the next neuron, stimulating it. Neurotransmitters like serotonin and dopamine relay signals between neurons and control functions like mood, sleep, and movement. Drugs like ecstasy and cocaine affect synapses by preventing neurotransmitter reabsorption, increasing their levels in the synapse. Nobel Prizes have been awarded for discoveries relating to neurotransmitters, synaptic transmission, and their roles in conditions like Parkinson's and memory formation.
Synaptic transmission
This document discusses synaptic transmission between neurons. It defines a synapse as the junction that allows signals to pass between neurons. There are three main types of synapses: chemical, electrical, and conjoint. The process of synaptic transmission involves neurotransmitters being synthesized, stored, transported to the axon terminal, released into the synapse upon neuronal firing, binding to receptors on the post-synaptic neuron, activating those receptors, and then being degraded or reuptaken. Neurotransmitters can have stimulatory or inhibitory effects depending on the receptor subtypes activated. The synaptic signal is terminated through reuptake, enzymatic degradation, or diffusion of the neurotransmitters.
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Graded potentials are local changes in membrane potential that vary in strength depending on the stimulus. They spread through passive diffusion but decay over short distances. Action potentials occur when the membrane reaches threshold potential, causing voltage-gated sodium and potassium channels to open and reverse the membrane potential before restoring it. They travel along axons through contiguous conduction. At synapses, neurotransmitters released from presynaptic neurons can excite or inhibit postsynaptic neurons through temporal and spatial summation of EPSPs and IPSPs. Presynaptic inputs determine postsynaptic responses through facilitation or inhibition of neurotransmitter release.
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EPSP is an excitatory postsynaptic potential that occurs when a neurotransmitter like glutamate binds to receptors on the postsynaptic neuron, making its membrane permeable to sodium ions and depolarizing the neuron. IPSP is an inhibitory postsynaptic potential that occurs when GABA binds to receptors, making the membrane permeable to chloride ions and hyperpolarizing the neuron. EPSPs can summate and cause the neuron to generate an action potential, while IPSPs make action potential generation less likely. Together, the balance of EPSPs and IPSPs control whether a neuron will fire an action potential.
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The document discusses several key properties and features of nerve fibers:
- Nerve fibers are excitable, conductive, and do not fatigue easily. They conduct all-or-none action potentials and exhibit phenomena like summation and accommodation.
- Nerve fibers have different conduction velocities depending on their type and diameter. Myelination allows for faster conduction.
- When injured, nerve fibers undergo Wallerian degeneration where the distal segment degrades over weeks and the soma attempts repair through axonal sprouting.
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Here are the key types of mechanoreceptors and their properties:
- Cutaneous mechanoreceptors:
- Meissner's corpuscles - detect light touch and pressure on fingertips and lips. Found in dermal papillae.
- Merkel's discs - detect sustained light touch. Found just below the epidermis.
- Pacinian corpuscles - detect deep pressure and vibration. Found in dermis and connective tissue.
- Ruffini endings - detect skin stretch and joint movement. Found in dermis and connective tissue.
- Free nerve endings - detect pain. Found throughout the dermis and epidermis.
- Proprioceptors:
- Muscle spind
Neurotransmission
Neurotransmission involves the release of neurotransmitters from the axon terminal of one neuron that bind to and react with receptors on another neuron. Nerve signals travel as electrical nerve impulses along neurons. A neuron consists of a cell body, dendrites that receive signals, and an axon that transmits signals. When a neuron is stimulated, sodium ions enter the cell causing an action potential to propagate along the axon. At synaptic junctions, neurotransmitters are released from vesicles and bind to receptors, causing excitation or inhibition of the downstream neuron. Neurotransmitters are then removed from the synapse to terminate signaling.
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Neuromuscular junction
This document provides an overview of the neuromuscular junction. It defines the neuromuscular junction as the junction between the terminal branch of a nerve fiber and a muscle fiber. It describes the structure of the neuromuscular junction including the presynaptic and postsynaptic membranes separated by a synaptic cleft. It explains the process of neuromuscular transmission from the release of acetylcholine to the destruction of acetylcholine and the development of end plate potentials. It discusses neuromuscular blockers and stimulators and their uses. It also covers motor units, recruitment of motor units, and some applied physiology concepts like myasthenia gravis and Eaton-Lambert syndrome.
Synapse
The majority of the content is physiology-based, but it's also built-in an anatomical perspective.i've also included disorder of synapses
Instagram @Rajamd_
Local Anesthesia
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
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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6. cns 2
Graded potentials are local changes in membrane potential that vary in strength depending on the stimulus. They spread through passive diffusion but decay over short distances. Action potentials occur when the membrane reaches threshold potential, causing voltage-gated sodium and potassium channels to open and reverse the membrane potential before restoring it. They travel along axons through contiguous conduction. At synapses, neurotransmitters released from presynaptic neurons can excite or inhibit postsynaptic neurons through temporal and spatial summation of EPSPs and IPSPs. Presynaptic inputs determine postsynaptic responses through facilitation or inhibition of neurotransmitter release.
Synaptic integration, Types of synapses, EPSP and IPSP
A brief overview of Synaptic integration, Types of Synapses and Excitatory and inhibitory post synaptic potentials.
EPSP and IPSP
EPSP is an excitatory postsynaptic potential that occurs when a neurotransmitter like glutamate binds to receptors on the postsynaptic neuron, making its membrane permeable to sodium ions and depolarizing the neuron. IPSP is an inhibitory postsynaptic potential that occurs when GABA binds to receptors, making the membrane permeable to chloride ions and hyperpolarizing the neuron. EPSPs can summate and cause the neuron to generate an action potential, while IPSPs make action potential generation less likely. Together, the balance of EPSPs and IPSPs control whether a neuron will fire an action potential.
SLEEP AND EEG
The document discusses sleep and the electroencephalogram (EEG). It describes the different stages of sleep including non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. NREM sleep has 4 stages that progress from light to deep sleep as shown by changes in EEG patterns and waves like alpha, beta, theta, and delta waves. REM sleep is characterized by low amplitude, high frequency EEG similar to wakefulness along with physiological changes like eye movements and muscle paralysis. The neural and chemical bases of wakefulness and factors regulating the sleep-wake cycle are also covered.
Nerve signal processing
This document summarizes key concepts in nerve signal processing including the discovery of neurons, types of neurons, bioelectricity, ion distribution across cell membranes, transport of solutes across neuronal membranes, resting membrane potential, action potentials, propagation of action potentials, synaptic transmission, types of synapses, neurotransmitter release and receptors, excitatory and inhibitory postsynaptic potentials, inhibition, reflexes, organization of neurons, convergence and divergence, reverberatory circuits, major neurotransmitter systems including acetylcholine, serotonin, dopamine, norepinephrine, glutamate, and GABA, and the role of second messengers.
Physiology of Cortex
The document summarizes key information about the structure and function of the human cerebral cortex. It discusses the layers of the cortex, methods used to study cortical functions including stimulation and electrophysiological procedures like EEG. Specific topics covered include sensory and motor areas of the cortex, sleep centers and stages of sleep, and the influence of the reticular formation on cortical activity.
Chapter 03: Synaptic Communications
The document discusses the concept of the synapse between neurons. It describes how synapses allow neurons to communicate via neurotransmitters. Neurotransmitters are released from the presynaptic neuron and bind to receptors on the postsynaptic neuron, which can excite or inhibit the postsynaptic neuron. The document outlines different types of neurotransmitters and how they work, including their synthesis, transport, release, effects, and inactivation methods like reuptake. It also discusses how drugs can influence synaptic activity and neurotransmitters. Finally, it suggests synapses may be important for personality traits and behaviors.
Nerve transmission
Neurons communicate with each other via electrical and chemical signals. At the synapse, an electrical signal in the presynaptic neuron causes it to release neurotransmitters like acetylcholine or glutamate. These chemicals bind to and open ion channels in the postsynaptic neuron, generating an electrical signal there. This transmission allows neurons to form complex communication networks and coordinate the functions of the nervous system.
Neurotransmitters and receptor
This document discusses neurotransmitters and receptors in the nervous system. It defines neurotransmitters as chemical substances that transmit nerve impulses between neurons through synapses. Neurotransmitters are synthesized in the presynaptic neuron, packaged into vesicles, released into the synaptic cleft when calcium enters during an action potential, bind to receptors, and are then inactivated. The document also defines receptors as proteins that receive chemical signals and cause a cellular response. Receptors are classified as exteroceptors, which respond to external stimuli, or interoceptors, which respond to internal stimuli. Common neurotransmitters and receptor types are also listed.
Properties of nerve fibre
The document discusses several key properties and features of nerve fibers:
- Nerve fibers are excitable, conductive, and do not fatigue easily. They conduct all-or-none action potentials and exhibit phenomena like summation and accommodation.
- Nerve fibers have different conduction velocities depending on their type and diameter. Myelination allows for faster conduction.
- When injured, nerve fibers undergo Wallerian degeneration where the distal segment degrades over weeks and the soma attempts repair through axonal sprouting.
11h learning
Memory involves encoding, storing, and retrieving information. Encoding involves assembling information from the senses. Consolidation converts encoded information into a permanent form stored in the hippocampus and surrounding areas. Retrieval allows accessing stored memories. Learning refers to long-lasting behavior changes from practice or repetition and includes non-associative learning like habituation and associative learning like classical and operant conditioning. Classical conditioning associates a stimulus with a response while operant conditioning uses rewards and punishments to modify behaviors. Studies in Aplysia show how sensitization and habituation produce long-term changes in synaptic connections related to learning. Long-term potentiation in the hippocampus involves strengthening synapses and is important for spatial memory.
Neurohumoral transmission in body action
The document discusses neurohumoral transmission, which is how nerves transmit messages through the release of chemical signals called neurotransmitters across synapses. There are five key steps in the process: 1) impulse conduction along nerve fibers, 2) transmitter release from nerve endings when an action potential occurs, 3) the transmitter binding and activating receptors on the postjunctional cell, 4) a response in the postjunctional cell such as muscle contraction, and 5) termination of the transmitter action through reuptake. The most common neurotransmitters are acetylcholine and norepinephrine. Neurohumoral transmission is important for autonomic drug actions and functions like muscle contraction.
Neurotransmitter ppt
Neurotransmitters are chemical messengers that transmit signals between neurons. The document discusses the history and criteria for classifying a substance as a neurotransmitter. Neurotransmitters are classified based on their chemical nature as amino acids, amines, or others. They are also classified based on their function as either excitatory or inhibitory. The document describes examples from each group and where they are secreted in the body. It further explains the processes of transport, release, inactivation, and reuptake of neurotransmitters at the synapse.
Nervous Syst
The autonomic nervous system functions below consciousness to control visceral functions like the heart and digestive system. It transmits messages via neurohumoral transmission where nerves release chemical messengers called neurotransmitters at synapses. The steps involve nerve impulse conduction, transmitter release from synaptic vesicles into the synaptic cleft upon calcium ion influx, transmitter binding to post-synaptic receptors to cause excitation or inhibition, and termination of transmitter action via degradation or reuptake.
Synapse
Here are the key types of mechanoreceptors and their properties:
- Cutaneous mechanoreceptors:
- Meissner's corpuscles - detect light touch and pressure on fingertips and lips. Found in dermal papillae.
- Merkel's discs - detect sustained light touch. Found just below the epidermis.
- Pacinian corpuscles - detect deep pressure and vibration. Found in dermis and connective tissue.
- Ruffini endings - detect skin stretch and joint movement. Found in dermis and connective tissue.
- Free nerve endings - detect pain. Found throughout the dermis and epidermis.
- Proprioceptors:
- Muscle spind
Neurotransmission
Neurotransmission involves the release of neurotransmitters from the axon terminal of one neuron that bind to and react with receptors on another neuron. Nerve signals travel as electrical nerve impulses along neurons. A neuron consists of a cell body, dendrites that receive signals, and an axon that transmits signals. When a neuron is stimulated, sodium ions enter the cell causing an action potential to propagate along the axon. At synaptic junctions, neurotransmitters are released from vesicles and bind to receptors, causing excitation or inhibition of the downstream neuron. Neurotransmitters are then removed from the synapse to terminate signaling.
Sleep and anesthesia
This document provides an overview of sleep, its stages, circadian rhythms, and relationship to anesthesia. It defines sleep and describes its typical stages: non-rapid eye movement (NREM) sleep including stages 1-3, and rapid eye movement (REM) sleep. NREM sleep involves slow brain waves and restoration, while REM involves dreaming and autonomic instability. Circadian rhythms regulate daily cycles of activity and rest and are generated by biological clocks in cells. Perioperative sleep deprivation and sleep disorders like sleep apnea can impact patient outcomes, making sleep important for anesthesia.
Functions of Diencephalon & Subcortical Ganglia
The document discusses the integrative functions of the diencephalon and subcortical ganglia. It describes the nuclei and functions of the thalamus and hypothalamus. The thalamus is divided into specific relay nuclei, motor nuclei, and associative nuclei that integrate sensory information and regulate movements and behaviors. The hypothalamus receives internal and external signals to regulate homeostasis, emotions, and motivations through connections with the limbic system, somatic and vegetative nervous systems, and endocrine system. The basal ganglia, consisting of the striatum and globus pallidus, integrate motor and associative cortical functions and facilitate complex movements through connections with the motor thalamus and brainstem. Dys
Neuromuscular junction
This document provides an overview of the neuromuscular junction. It defines the neuromuscular junction as the junction between the terminal branch of a nerve fiber and a muscle fiber. It describes the structure of the neuromuscular junction including the presynaptic and postsynaptic membranes separated by a synaptic cleft. It explains the process of neuromuscular transmission from the release of acetylcholine to the destruction of acetylcholine and the development of end plate potentials. It discusses neuromuscular blockers and stimulators and their uses. It also covers motor units, recruitment of motor units, and some applied physiology concepts like myasthenia gravis and Eaton-Lambert syndrome.
Synapse
The majority of the content is physiology-based, but it's also built-in an anatomical perspective.i've also included disorder of synapses
Instagram @Rajamd_
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Synaptic integration, Types of synapses, EPSP and IPSP
Synaptic integration, Types of synapses, EPSP and IPSP
Similar to Local anesthesia
Local Anesthesia
Local anesthesia, all in one place with all the references and all the important points.
It contains some videos and animations, for which feel free to contact. As such animations are not compatible with Slideshare. Enjoy and please hit the like button if you liked the presentation.
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.
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.
Local anesthetics drm
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.
Local anasthesia
A overview of local anesthesia and various advancement in its modern day approach. A post graduate periodontology approach to application of local anesthesia in day to day dental surgeries and various other dental and maxillofacial treatment procedures.
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The document summarizes an experiment testing the effects of neuromuscular blocking agents on an isolated rat diaphragm preparation. It describes how tubocurarine, succinylcholine, and edrophonium act on nicotinic acetylcholine receptors and outlines the methods used. An isolated rat diaphragm was stimulated via its phrenic nerve and different drugs were administered to observe their effects, including paralysis from tubocurarine and succinylcholine or reversal of paralysis from edrophonium. The experiment aimed to study the mechanisms of these neuromuscular blocking agents.
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This document discusses parasympathomimetic drugs, which mimic the effects of the parasympathetic nervous system. It describes how these drugs activate parasympathetic receptors, especially muscarinic and nicotinic acetylcholine receptors. It provides details on the mechanisms of different parasympathomimetic drugs, including how they stimulate receptors to produce various effects in the body. Specific drugs discussed include acetylcholine, carbachol, and their therapeutic uses and side effects.
Anesthetics.pptx
Local anesthetics work by reversibly blocking sodium channels in nerve fibers, inhibiting pain signal conduction. They can provide local anesthesia through infiltration of tissues or regional anesthesia through epidural administration. The two main types are esters and amides, with amides being safer and more commonly used. Potential adverse effects include allergy, toxicity from high doses, and methemoglobinemia. Proper administration techniques and monitoring can help prevent complications.
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.
Local anesthesia in dentistry
Local anesthesia is used to induce temporary loss of sensation in a specific area of the body without loss of consciousness. It works by blocking sodium channels and preventing nerve impulse propagation. Common local anesthetics used in dentistry include lidocaine and articaine. They are administered via injection using various needle sizes and lengths. The onset and duration of anesthesia is influenced by factors like pH, lipid solubility, and presence of vasoconstrictors. Local anesthetics provide a safe alternative to general anesthesia for minor dental procedures by restricting effects to localized areas.
Local anesthesis
This document discusses local anesthesia, including how it works and its properties. It begins by defining local anesthesia as a loss of sensation caused by depressing nerve endings or inhibiting nerve conduction. It then discusses various methods of inducing local anesthesia and desirable properties like reversibility and lack of toxicity. The bulk of the document focuses on neurophysiology, explaining how nerves generate and transmit impulses through changes in electrolyte permeability and membrane potential. It discusses several theories for how local anesthetics specifically block nerve conduction, settling on the theory that they displace calcium from sodium channels, blocking sodium conductance and preventing action potentials. It notes local anesthesia is less effective in inflamed areas due to changes in pH. The document concludes by providing an example dose calculation
Local anesthesia for students
this is a summary of the important points to consider in local anesthesia . most of the information in this jandout are taken from handbook of local anethesia by malamed
Local Anesthesia in Dentistry
The document provides information on local anesthesia, including:
1) It discusses the historical background of local anesthesia, from the isolation of cocaine in 1860 to the development of procaine and lidocaine.
2) It defines local anesthesia as the loss of sensation in a specific body area caused by inhibiting nerve conduction without loss of consciousness.
3) It describes the mechanisms of action of local anesthetics, including that they work by binding to specific receptor sites on sodium channels in nerves to inhibit sodium conduction and excitation.
4) It provides classifications of local anesthetics according to their biological site and mode of action, including examples like lidocaine that work through both receptor-dependent and independent mechanisms.
local anesthetics pharmacology
1. The seminar discussed the pharmacology of local anesthetics, covering their history, mechanisms of action, and clinical uses.
2. Local anesthetics work by binding to sodium channels in nerve cell membranes and preventing sodium influx, which inhibits nerve impulse conduction.
3. The potency, onset, and duration of local anesthetics depends on factors like their pKa, lipid solubility, and degree of protein binding. This determines their rate of diffusion to nerve fibers and length of action.
Sensory systems
The document discusses neuronal pathways and sensory systems, explaining that sensory input travels through a series of connected neurons from sensory organs to the central nervous system. It describes concepts like contralateral representation, sensory transduction, information coding through labeled lines and receptive fields, and how properties like adaptation, threshold, convergence, and acuity contribute to sensory processing. Key sensory examples are provided to illustrate these neuronal and sensory concepts and phenomena.
neurophysiology and drugs of la
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 Anesthetics2
Local anesthetics work by blocking sodium ion channels in nerve cell membranes, preventing the propagation of action potentials and interrupting pain signals. The first local anesthetic was cocaine, discovered in the 1860s. Local anesthetics are classified as esters like cocaine or amides like lidocaine. They take effect by binding to intracellular sodium channels and slowing nerve conduction. The potency of local anesthetics depends on factors like pH, lipophilicity, and protein binding. Different types of nerve fibers vary in their susceptibility to local anesthetic blockade, with small fibers being more easily blocked. Systemic toxicity from overdose can cause central nervous system or cardiovascular effects. Common techniques for local anesthesia include infiltration, topical blocks, nerve blocks, and
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Inferior alveolar nerve block
The inferior alveolar nerve block anesthetizes the inferior alveolar nerve and its branches, providing anesthesia to the mandibular teeth, chin, lower lip, and parts of the tongue. A long needle is inserted into the mucosa on the lingual side of the ramus to anesthetize the inferior alveolar nerve as it passes downward. When bone is contacted, local anesthetic is slowly deposited over 60 seconds while aspirating. Successful anesthesia is confirmed through subjective symptoms like lip tingling and objective tests showing no response to pulp stimulation. Complications can include hematoma, trismus, or transient facial paralysis if the facial nerve is contacted.
Techniques of local anesthesia [autosaved]
This document discusses various techniques for local anesthesia in dentistry. It describes different nerve blocks for anesthetizing specific regions of the maxilla and mandible, including the posterior superior alveolar nerve block, middle superior alveolar nerve block, and anterior superior alveolar (infraorbital) nerve block. It also covers maxillary injection techniques such as supraperiosteal injections and palatal anesthesia techniques like the greater palatine nerve block.
Maxillary nerve block
The maxillary nerve block is an effective method of achieving profound anesthesia of the hemimaxilla. It involves injecting local anesthetic near the maxillary nerve as it passes through the pterygopalatine fossa using either the high-tuberosity or greater palatine canal approach. When performed correctly with aspiration, it has a high success rate of over 95% and minimizes the volume of local anesthetic needed to anesthetize the entire maxillary division.
Buccal nerve block
The buccal nerve block anesthetizes the buccal nerve, a branch of the anterior division of the trigeminal nerve (V3), providing anesthesia to the soft tissues and periosteum buccal to the mandibular molar teeth. It has a high success rate and is technically easy to perform. Potential disadvantages include pain upon needle contact with the periosteum during injection. Proper technique involves inserting a long needle through the mucosa distal and buccal to the most distal mandibular molar, aiming for the buccal nerve as it passes over the anterior border of the ramus.
Anterior middle superior alveolar nerve
This document summarizes the anterior middle superior alveolar nerve block and palatal approach anterior superior alveolar nerve block techniques. It describes the nerves anesthetized, areas anesthetized, indications, contraindications, advantages, disadvantages, techniques, and signs of successful anesthesia for each block. Both techniques anesthetize the anterior maxillary teeth using a single injection site in the palate and have advantages of minimizing anesthetic volume and needle punctures compared to individual injections.
Oral surgery
This document contains classifications and tables related to oral surgery. It includes the American Society of Anesthesiologists classification of patient physical status, normal values for screening tests related to bleeding detection, factor VIII levels in blood, instrument mechanisms and uses, suture types and absorption rates, cardiac conditions for endocarditis prophylaxis recommendations, dental procedures requiring or not requiring endocarditis prophylaxis.
Anesthesia
General anesthesia involves inducing a reversible state of unconsciousness through various stages of sedation. There are 4 stages of anesthesia ranging from analgesia and conscious sedation to respiratory paralysis. Different concentrations of nitrous oxide (N2O) produce varying levels of sedation and analgesia. Patient position after general anesthesia depends on their condition, with lateral, reclined, or supine positions used depending on needs like recovery from syncope or cervical spine injury.
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Local anesthesia
- 1. Local anesthesia Local anesthesia is defined as transient reversible loss of sensation in a circumscribed area of the body caused by either a depression of excitation in nerve endings, or an inhibition of conduction process in the peripheral nerves, without lss of consciousness.
- 2. Theories of pain 1. Specificity theory – by Descartes it is based on specific set of peripheral nerve fibres that are nociceptive in function, this theory cannot explain any pathological pain, referred pain and also do nt explain paroxysmal episodes of pain. 2. Pattern theory- by Goldscheider, 1894 This theory explains that pain is produced by the summation of sensory input within dorsal horn of the spinal column. 3. Gate control theory- by Melzack and Wall, 1965 This theory contains elements of both specificity and pattern theory. It proposes spinal gating mechanism in substantia gelatinosa that modulates sensory input by the balance of activity of smaller diameter (A-delta C) an larger diameter (A-delta).
- 3. Theories of local anesthesia Acetylcholine theory- acetylcholine is a neurotransmitter at the nerve synapses , supposed to be involved in nerve conduction. Membrane expansion theory- LA penetrates the membrane , expands it and narrows the sodium channels, thus decreases the permeability to sodium ions. Calcium displacement theory – La molecules displace calcium inside the nerve which in turn controls sodium channels. Electrical potential theory/ surface charge theory- the cations RNH+ of LA align themselves on the nerve membrane and make outside potential more positive , thus the threshold potential increases. Specific receptor theory – the specific receptors are sodium channels which re bound by LA and controls the sodium channels. It is the most acceptable theory which explains the actions of LA.
- 5. Classification of Local Anesthesia
- 7. LA substance according to biological site and mode of action classification Definition Chemical substance Class A Agents acting on the tetradoxin External surface of sacridoxin Nerve membrane Class B Agents acting on the Quarternary ammonium Internal surface of nerve Analogues of lidnocaine membrane Class C Receptor-independent Benzocaine, N-butanol Physio chemical Benzyl alcohol mechanism Class D Both receptor mediated Most clinically And receptor- independent Useful LA agents- physiochemical Lidnocaine, mechanism prilocaine
- 8. LA blocks Nerve block – LA deposited near main trunk Field block – LA is deposited near large branch of peripheral nerves Infiltration- LA is deposited near small nerve endings.
- 10. Composition of Local Amesthesia Lignocaine HCL IP 21.3 mg Anesthetic agent Adrenaline (as Adr. Bitartrate IP 0.09 mg) 0.005 Vasoconstrictor NaCL IP 6.0 mg isotonic Sodium metabisulphite IP 0.5 mg (germicidal) reducing agent, antioxidant for adrenaline Methyl Paraben IP 1.0 mg preservative Thymol Fungicide Distilled water for injection IP to make 0.1mL vehicle