usually 2.2ml or 1.8ml anaesthetic agent vasoconstrictor stabilizer / preservative isotonic carrier medium
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What local anaesthetics are esters and amides
esters: procaine and benzocaine amides:lidocaine, prilocaine, mepivacaine, bupivacaine, articaine
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how do LAs work
specific receptor theory- local anaesthetic binds to the sodium channel, inactivates sodium channel
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what must LA be able to do
must be able to pass through lipid membrane, must be able to bind to the Na+ channel
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what does the proportion of charged vs uncharged LA depends on
pKa of the drug, pH of the environment
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LA drugs are ..... soluble in aqueous environment.
poorly
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what are the 2 states of LA and what does each state enable LA to do
Uncharged (lipid soluble) – pass through axon membrane,Charged – binds to sodium channel
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what does it mean if an LA has a low pKa
More uncharged drug,Passes through nerve membrane rapidly
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what does a low pH mean
slow onset, failure
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what are the properties of LA
Protein Binding Increases duration Provides a pool of LA High Protein binding: • Bupivacaine • Articaine. Dissociation and solubility, Vasodilation All are vasodilators Increases rate of systemic uptake Least vasodilatory: Prilocaine + m
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continued
Lipid Solubility Membrane = lipid Speed of onset Drug penetration High lipid solubility: – Articaine
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what does absorption depend on
dose – vasoactivity of the drug – vascularity of the tissue – vasodilator effect vs use of vasoconstrictors
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why are vasoconstrictors used
increase speed of onset counteract vasodilatory effects of the LA agent extend duration of anaesthesia improve depth of anaesthesia lower blood levels of LA reduce haemorrhage
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