Local anesthetics reversibly block sodium channels in nerve membranes, preventing the generation and conduction of action potentials. This results in loss of pain sensation and motor function. Local anesthetics exist in both charged and uncharged forms, and the uncharged form readily crosses cell membranes. Once inside the cell, it ionizes and binds to intracellular receptor sites on sodium channels, blocking conduction. Administration methods include surface application, infiltration, nerve blocks, epidurals, and spinals. Common local anesthetics include lidocaine, bupivacaine, and procaine.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
Classification
Mechanism of action
Duration of action
Absorption and distribution
Mode of action
Theories of action of L.A
Pharmacokinetics of local anaesthetics
Routes of administration
Metabolism or biotransformation
Individual agents
Vasoconstrictors
Systemic effects
Toxicity
Advantages
Disadvantages
Maximum allowable dose
Local anaesthetics in community trust services
Lecture slides for undergraduates medical (MBBS) Students. Source material for this presentation is Essentials of Pharmacology, KD Tripathi, Katzung and Goodman and Gillman. It deals with Local anaesthetics with their mechanism of action, pharmacokinetics , adverse effects and therapeutic uses.
Local anesthesia has been defined as loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or inhibition of the conduction process in peripheral nerves.
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
local anaesthesia is defined as a loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings
Or an inhibition of the conduction process in peripheral nerves; no loss of consciousness occurs
Local anesthetics interfere with the excitation process in the nerve membrane in one or more of the following ways:
1) Altering the basic resting potential of the nerve membrane
2) Altering the threshold potential (firing level)
3) Decreasing the rate of depolarization*
4) Prolonging the rate of repolarization
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2. Local Anesthetics (LA)
• L.A. reversibly block impulse conduction along nerve
axons and other excitable membrane.
• A local anesthetic is a drug that causes reversible
local anesthesia and a loss of nociception. When it is
used on specific nerve pathways (nerve block), effects
such as analgesia (loss of pain sensation) and paralysis
(loss of muscle power) can be achieved.
8. Mechanism of action of LA
• They act by blockade of sodium channels so that:
Impulse conduction slow
The rate of rise of the action potential declines,
and
The ability to generate an action potential is
abolished or canceled.
9. SEQUENCE OF EVENTS WHICH
RESULT IN CONDUCTION BLOCKADE
1. Diffusion of the base (nonionized)
form across the nerve sheath and
nerve membrane
2. Re-equilibration between the base
and cationic forms in the axoplasm
3. Penetration of the cation into and
attachment to a receptor site within
the sodium channel.
4. Blockade of the sodium channel
10. Nerve Fiber and
Local Anesthetic Setup
Sequence of clinical anesthesia
Loss of pain and temperature sensation
Loss of proprioception
Loss of touch and pressure sensation
Loss of motor function
11. Effect of PH
• Local anesthetics are weak bases and are usually
formulated as the hydrochloride salt to render
them water-soluble. At the chemical's pKa the
protonated (ionized) and unprotonated (unionized)
forms of the molecule exist in an equilibrium but
only the unprotonated molecule diffuses readily
across cell membranes. Once inside the cell the
local anesthetic will be in equilibrium, with the
formation of the protonated (ionized form), which
does not readily pass back out of the cell. This is
referred to as "ion-trapping".
12.
13. Effect of PH (cont.)
• LA are weak bases and their activity increases by
increasing PH
• This because if large amount of a drug is unpolar, it
will facilitate its penetration through the cell
membrane
• Once the drug has penetrated the lipid barrier and
reach its site of action it ionized and the ionized
form is responsible for LA activity
14. • Acidosis such as caused by inflammation at a
wound partly reduces the action of local
anesthetics. This is partly because most of the
anesthetic is ionized and therefore unable to cross
the cell membrane to reach its cytoplasmic-facing
site of action on the sodium channel.
15. • Local anesthetics block conduction in the following
order: small myelinated axons (e.g. those carrying
nociceptive impulses), non-myelinated axons, then
large myelinated axons. Thus, a differential block
can be achieved (i.e. pain sensation is blocked
more readily than other sensory modalities).
16. Methods of Administration
• Surface anesthesia: direct application of the drug
on the surface such as skin and wounds.
• Infiltration anesthesia: injection of LA in
subcutaneous tissue in order to paralyze nerve
endings at the site of action.
• 3- Nerve block: LA is injected in the vicinity of
major nerve such as teeth
17. Methods of Administration
• 4- Epidural anesthesia: injection of LA into the
epidural space.
• 5- Sympathetic block: inject LA around sympathetic
nerves
• 6- Spinal anesthesia: injection of LA into
subarachnoid space in the lumber region
18. Clinical use
• 1- Systemic use as antiarrhythemic agents e.g.
Lidocaine
• 2- Locally use to produce anesthesia
19. Clinical LA
• Clinical local anesthetics belong to one of two classes:
• 1- aminoamide and 2- aminoester
• Synthetic local anesthetics are structurally related to
cocaine. They differ from cocaine mainly in that they
do not produce hypertension or local vasoconstriction
, with the exception of Ropivacaine and Mepivacaine
that do produce weak vasoconstriction.
20. Classification of LA
1-Esters
A- esters of P- amine benzoic acid e.g. Procaine
B- Esters of benzoic acid e.g. Cocaine
• Benzocaine
• Chloroprocaine
• Cyclomethycaine
• Dimethocaine/Larocaine
• Propoxycaine
• Procaine/Novocaine
• Proparacaine
• Tetracaine/Amethocaine
21. Classification of LA
2- Amide e.g. Lidocaine
• Articaine
• Bupivacaine
• Cinchocaine/Dibucaine
• Etidocaine
• Levobupivacaine
• Lidocaine/Lignocaine
• Mepivacaine
• Piperocaine
• Prilocaine
• Ropivacaine
• Trimecaine
22. Classification of LA
3- Combinations
• Lidocaine/prilocaine
4- Natural local anesthetics e.g. Saxitoxin and
Tetrodotoxin
• Naturally occurring local anesthetics not derived
from cocaine are usually neurotoxins, and have the
suffix -toxin in their names. Unlike cocaine
produced local anesthetics which are intracellular
in effect, saxitoxin & tetrodotoxin bind to the
extracellular side of sodium channels.