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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.
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).
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.
Classification of Local Anesthesia
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
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.
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

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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.
  • 4.
  • 6.
  • 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.
  • 9.
  • 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