Test your knowledge of important concepts in local anesthetics
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
Tonic-clonic convulsion
Severe bruxism
Respiratory depression followed by stimulation
Pseudohallucinations
Formication
Blocking K+ channels
Blocking Ca++ channels
Blocking release of NE
Blocking the extracellular part of Na channels
Blocking the intracellular part of Na channels
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
Limits toxicity
Increases concentration of local anesthetic by preventing its metabolism by the liver
Causes tissue edema
May lead to hypoxia and tissue damage
Prevents hypotension
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
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
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
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
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