Alkadhi's Local Anesthetics

Blocking K+ channels

Blocking Ca++ channels

Blocking release of NE

Blocking the extracellular part of Na channels

Blocking the intracellular part of Na channels

Molecule has to be lipid soluble to exert its Na channel blocking effect

Some topical local anesthetics can be absorbed systemically and can cause toxicity

The blocking effect of local anesthetics is gone when the molecule is in the cationic form

Entry of local anesthetics in the brain results in CNS depression initially followed by CNS stimulation

Cocaine also has anti-arrhythmic properties

Antiarrhytmic

Therapeutic nerve block and field block

Stimulant, euphoriant

Anticonvulsant in status epilepticus

None of these. All of the above are clinical uses for local anesthetics

Given with a vasodilator to increase duration of action

Thicker nerve fibers are more sensitive to local anesthetics than thinner ones

The more negative the membrane potential, the greater the degree of Na channel block

An active nerve is more sensitive to local anesthetics than a resting nerve

Local anesthetics alter Na and K permeability in neurons

Initial stimulation and then depression of CNS pathways

Local necrosis from vasoconstrictor actions

Blockage of muscarinic ACh receptors at high concentrations

Urticarial rashes

Decreased electrical excitability in myocardium

Tonic-clonic convulsion

Severe bruxism

Respiratory depression followed by stimulation

Pseudohallucinations

Formication

Procaine is faster and longer lasting than lidocaine

Cocaine is good for topical anesthesia of upper respiratory tract

Bupivacaine and cocaine are the only natural anesthetic products

Procaine is hydrolyzed in vivo to GABA

Lidocaine is very lipid soluble

1, 5, 4, 2, 3

4, 5, 2, 1, 3

4, 2, 5, 1, 3

4, 2, 1, 5, 3

3, 1, 5, 2, 4