Download Free Medical Local Anesthesia PowerPoint Presentation

Local Anesthesia PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Local Anesthesia is a reversible loss of sensation in a limited region of the body by reversibly blocking nerve conduction (inhibition of impulse generation or propagation) in a specific region of the body.

Tags : Local Anesthesia,Anesthesia

Published on : Nov 06, 2020 | Views : 6834 | Downloads : 65

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Local Anesthesia Dr. Mohammed Samir Hussein BCs of Pharmaceutical Science MDs of Clinical Pharmacology
Slide 2-

LOCAL ANESTHESIA Reversible loss of sensation in a limited region of the body by reversibly blocking nerve conduction (inhibition of impulse generation or propagation) in a specific region of the body .
Slide 3-

LOCAL VS GENERAL ANAESTHESIA
Slide 4-

FACTORS AFFECTING NERVE SUSCEPTIBILITY Nerve fibers are classed into : – group A nerve fibers, group B nerve fibers, and group C nerve fibers. Groups A and B are myelinated, and group C are un-myelinated
Slide 5-

FACTORS AFFECTING NERVE SUSCEPTIBILITY Susceptibility of nerve fibers to local anesthetic blockade depends on Type of fiber, Degree of myelination, Fiber length, and Frequency of firing local anesthetics preferentially block smaller diameter fibers first because the distance over which such fibers can passively propagate an electrical impulse is shorter Most notably, myelinated nerves tend to be blocked before un-myelinated nerves of the same diameter. B fibers are blocked before the smaller un-myelinated C fibers involved in pain transmission Blockade of fibers with higher frequencies of depolarization is marked (type A delta and C fibers)
Slide 6-

Order of sensory function block Vasomotor block, dilation of skin vessels, and increased cutaneous flow Block of cold temperature fibers Sensation of warmth by patient Temperature discrimination lost Slow and fast pain Tactile sense lost Pressure sense abolished Loss of proprioception (awareness of body or extremity position) Motor paralysis Recovery in reverse order (recovery usually occurs unevenly)
Slide 7-

CHARACTERISTICS OF LOCAL ANESTHETICS
Slide 8-

CHARACTERISTICS OF LOCAL ANESTHETICS
Slide 9-

COMMON USES OF LOCAL ANESTHETICS
Slide 10-

CHEMICAL STRUCTURES OF LOCAL ANESTHETICS )Ester or Amide)
Slide 11-

CHEMICAL STRUCTURES OF LOCAL ANESTHETICS The lipophilic (attracted to fat) and hydrophilic (attracted to water) portions of the molecular structure are crucial to its ability to cross tissue barriers and reach their site of action. The intermediate bond, either an ester or an amide, determines the type of local anesthetic, affecting metabolism and potential for allergic reactions. Local anesthetics are weak bases and are usually made available clinically as salts to increase solubility and stability More lipophilic- more potent (faster rate of interaction with the sodium channel receptor), longer duration of action and longer time to achieve their clinical effect Bind more extensively to proteins- Longer duration of action
Slide 12-

CLASSIFICATION OF LOCAL ANESTHETICS
Slide 13-

CLASSIFICATION OF LOCAL ANESTHETICS
Slide 14-

Mechanism of Action of local anesthetic Na channel is the main channel for propagation of AP. Local anesthetic is injected outside the neurons then it crosses the cell membrane to the cytoplasm of the cell to block the Na channel from inside. The more lipid-soluble (non-ionized, uncharged) form pass through cell membrane and reaches effective intracellular conc, ionized form blocks Na channel from inside. blocking voltage-dependent sodium channels ►reduce sodium ions influx ►preventing depolarization of membrane ► blocking conduction of action potential. When Na channel is blocked, all characteristics of AP are diminished except RMP (Resting Membrane Potential K channel related) Elevated extracellular Ca2+ antagonizes action of LA .
Slide 15-

Pharmacokinetics of local anesthetic 1. Absorption: Epinephrine which is a well known vasoconstrictor is used with local anesthetic for the following reasons: Slow removal of local anesthetic Reducing the systemic absorption of local anesthetic Causing higher local tissue concentration Reducing CNS and systemic toxicity Epinephrine is used with LAs that have short/intermediate duration of action such as Procaine, Lidocaine & Mepivacaine
Slide 16-

Pharmacokinetics of local anesthetic 2. Distribution Once in the blood, local anesthetics are distributed to all tissues. Brain, head, liver, lungs, kidneys and spleen have high levels of local anesthetics due to their high level of perfusion All local anesthetics cross the blood brain barrier All local anesthetics cross the placenta and enter the blood stream of the developing fetus.
Slide 17-

Pharmacokinetics of local anesthetic 3. Metabolism: Ester-type is hydrolyzed rapidly in blood (by butyrylcholinesterase) to inactive metabolites; short plasma t1/2 (< 1 min). Amide linkage is hydrolyzed by liver cytochrome P450 with different rates order (prilocaine (fastest) > Lid > bupivacaine (slowest). Prilocaine is metabolized in the liver and lung. All ester & amide LAs converted to more water-soluble metabolites & excreted in urine. 4- Excretion Kidneys are the major excretory organs for both local anesthetics
Slide 18-

Pharmacokinetics of local anesthetic Application to highly vascular area increases absorption. Injected into a poorly perfused tissue reduces absorption. They are converted in the liver (amide type) or in plasma (ester type) to more water-soluble metabolites, which are excreted in the urine. Ester-types are inactivated by blood circulating butyrylcholinesterase. Toxicity from amide-types more likely to occur in patients with hepatic disease.
Slide 19-

Pharmacokinetics of local anesthetic Application to highly vascular area increases absorption. Injected into a poorly perfused tissue reduces absorption. They are converted in the liver (amide type) or in plasma (ester type) to more water-soluble metabolites, which are excreted in the urine. Ester-types are inactivated by blood circulating butyrylcholinesterase. Toxicity from amide-types more likely to occur in patients with hepatic disease.
Slide 20-

Factors Affecting local anesthetic
Slide 21-

Clinical Use of local anesthetic Articaine has a fast onset and an intermediate duration of action that make it suitable for use in dental procedures. The onset of local anesthesia can be accelerated by the addition of sodium bicarbonate (1–2 mL) to the local anesthetic solution. Procaine and Lidocaine are used for short duration surgery. Lidocaine is used for epidural spinal anesthesia.
Slide 22-

Clinical Use of local anesthetic Cocaine, because of its excellent penetration and local vasoconstrictor effects, has been used extensively for ear, nose and throat (ENT) procedures. Cocaine is irritating and is therefore less popular for ophthalmic procedures. Since local anesthetics have membrane-stabilizing effects, both parenteral (eg, intravenous lidocaine) and oral (eg, mexiletine, tocainide) formulations of local anesthetics have been used to treat patients with neuropathic pain syndromes. Recent studies suggest that intravenous lidocaine may be useful as an adjuvant for reducing acute pain in the perioperative period.
Slide 23-

TOXICITIES OF LOCAL ANESTHETICS CNS toxicity Central nervous system stimulation followed by CNS depression Excitement: Tremors, shivering, and convulsions characterize the CNS excitement Depression: Respiratory depression and, if enough drug is absorbed, respiratory arrest Signs of toxicity: Tongue numbness, lightheadedness, tinnitus, visual disturbances, muscular twitching unconsciousness, coma, respiratory arrest, then cardiovascular collapse Treatment: Thiopental, Propofol, Midazolam (for epilepsy). Succinylcholine (for muscular manifestations of epilepsy).
Slide 24-

TOXICITIES OF LOCAL ANESTHETICS Cardiovascular toxicity Block cardiac Na+ channels and thus depress : cardiac pacemaker activity Excitability Conduction Extremely high concentrations LA block calcium channels. Bupivacaine and Ropivacaine (Cardiotoxics). Treatment: Propofol
Slide 25-

TOXICITIES OF LOCAL ANESTHETICS Blood toxicity Large doses (> 10 mg/kg) of prilocaine during regional anesthesia may lead to accumulation of the metabolite o-toluidine. An oxidizing agent capable of converting hemoglobin to methemoglobin Leads to cyanotic and the blood "chocolate-colored. Treatment: IV- Reducing agent (eg, methylene blue or ascorbic acid), which rapidly converts methemoglobin to hemoglobin.
Slide 26-

TOXICITIES OF LOCAL ANESTHETICS Sedation Example: large amounts of Lidocaine produce a sedation effect which is due primarily to two metabolites glycine xylidide and Monoethylglycinexylidide Allergic Reactions The ester type local anesthetics are metabolized to p-aminobenzoic acid. Amides are not metabolized to p-aminobenzoic acid, and allergic reactions to agents of the amide group are extremely rare.
Slide 27-

THANK YOU FOR YOUR ATTENTION