Term
| What is the ideal local anesthetic? |
|
Definition
Nonirritating to the tissue to which is applied;
Short onset;
Long enough duration, but not too long as to entail a prolonged recovery period |
|
|
Term
| What is the chemical structure of LA? |
|
Definition
Weakly basic in nature;
Lipophilic aromatic ring;
Intermediate group:
(Aminoester/
Aminoamide)
Hydrophilic carbon chain bearing an amino group |
|
|
Term
| WHAT IS THE NOMENCLATURE RULE? |
|
Definition
2 "i"s, it's an amide.
1 "i," it's an ester |
|
|
Term
| Is R or S form of LA more cardiotoxic? |
|
Definition
| R form is 40 times more cardiotoxic. |
|
|
Term
| What is the structure of the sodium channel? |
|
Definition
One larger alpha subunit and 1 or 2 smaller beta subunits
(Alpha subunit is the site of ion conduction and local anesthetic binding) |
|
|
Term
| What occurs at the site of the alpha subunit on the NA channel> |
|
Definition
| Alpha subunit is the site of ion conduction and local anesthetic binding |
|
|
Term
| What are the genetics of the sodium channels? |
|
Definition
| There are 10 sodium channel genes on 4 chromosomes |
|
|
Term
| What changes a sodium channel's configuration? |
|
Definition
| Changes configuration in response to membrane potentials |
|
|
Term
| What is the resting membrane potential? |
|
Definition
A negative electrical potential of 60 to 90 mV exists between the extracellular fluid and the axoplasm
(Larger proportion of K inside the nerve
Larger proportion of Na extracellular) |
|
|
Term
| What is the threshold potential? |
|
Definition
The voltage when continued stimulation is no longer needed and local processes can lead to a complete action potential
(Inward Na flux exceeds outward K ) |
|
|
Term
| Why is there an increase in NA influx? |
|
Definition
All sodium channels change configuration in response to the change in potential;
At rest, the Na channels are in the inactive and resting state;
Depolarization causes these channels to open |
|
|
Term
| Why do LA create a neural blockade? |
|
Definition
Block membrane permeability to Na;
Binds to the internal membrane of the sodium channel;
Ionic gradient and resting membrane potential is unchanged;
Local anesthetics only bind in the open and inactive state |
|
|
Term
| Why does LA NOT work on an absess? |
|
Definition
| LA will become positively charged in an acidic environment. Anethesia won't work bc it won't cross into the nerve ending |
|
|
Term
| What are the effects of the LA's nerve blockade? |
|
Definition
Decrease the amplitude of the action potential;
Slow the rate of depolarization;
Increase the firing threshold;
Slow impulse conduction;
Prolong the refractory period |
|
|
Term
| What is the alpha phase of distribution? |
|
Definition
| rapidly redistributed to the well-perfused tissue |
|
|
Term
| How are esters metabolized? |
|
Definition
| they are hydrolized in Blood plasma by pseudocholinesterase. |
|
|
Term
| What is the breakdown product of esters? |
|
Definition
| para-aminobenzoic acid (PABA) |
|
|
Term
| Where does the metabolism of amides occur? |
|
Definition
|
|
Term
| What are amides metabolized into? |
|
Definition
| tertiary amines are metabolized into secondary amines that are then hydrolyzed by amidases |
|
|
Term
| Therefore, a PT with end stage liver disease is most susceptible to local anesthetic tox from which class of drugs? |
|
Definition
|
|
Term
| How is lipide solubility related to anesthetic potency? |
|
Definition
| the more soluable, the more potent. |
|
|
Term
| How is duration related to lipid soluability? |
|
Definition
| the more lipid soluable are less readily removed by blood stream from nerve membranes |
|
|
Term
| What is the rapidity of onset related to? |
|
Definition
|
|
Term
| a newly discovered local anesthetic was found to have a pKa of 7.4. What % of the anessthetic will be unionized in the plasma? |
|
Definition
|
|
Term
| How do you treat CNS toxicity? |
|
Definition
| stop injection. if seizure occurs, hyperventilate w/ 100% O2, give benzo |
|
|
Term
| What is the main exception to the rule that all LAs will produce CVS tox at sim doses than CSN? |
|
Definition
|
|
Term
| Will you see CNS tox or CVS tox first? What is this a factor of? |
|
Definition
| CNS tox first. This is a factor of lipid soluability. |
|
|
Term
| what can you use to treat cardiac arrest? |
|
Definition
| lipid emulsions, since LAs are lipid soluable. |
|
|
Term
| What is the effect of LA on vascular smooth muscle at low concentration? |
|
Definition
|
|
Term
| What is the effect of LA on vascualr smooth muscle at high concentration? |
|
Definition
|
|
Term
| What is the one exception to the high dose LA--vasodialation rule? |
|
Definition
| cocaine--vasoconstriction |
|
|
Term
| Which local anesthetic should be used to topicalize the naropharynx prior to surgury? |
|
Definition
|
|
Term
|
Definition
| a group of drugs that reversibly block nerve conduction. Their use is followed by a complete recovery in nerve function with no evidence of structural damage to the nerve cell or fiber |
|
|
Term
| Chemically, are all LA acids or bases? |
|
Definition
|
|
Term
| What part of the chemical structure of LA determines which classification it belongs to? |
|
Definition
|
|
Term
|
Definition
| Para-aminobenzoic acid--a primary product of ester metabolism |
|
|
Term
| Do people get drug allergies to amides? |
|
Definition
|
|
Term
| How does benzocaine work? |
|
Definition
| It acts by membrane expansion--which physicially occludes the sodium channels |
|
|
Term
| What determines the magnitude of most initial blood concentrations of LA? |
|
Definition
| the amount absorbed from a tissue depot following injection |
|
|
Term
| What decreases absorption from a site? |
|
Definition
|
|
Term
|
Definition
| vasoconstriction, and decrease absorption |
|
|
Term
|
Definition
| rapid exponential diasppearance of LA from the blood |
|
|
Term
|
Definition
| distribution--LA is taken up into less well perfused tissue |
|
|
Term
|
Definition
| clearance phase (metabolism and excretion) |
|
|
Term
| WHICH IS THE fastest digested amide? |
|
Definition
| prilocaine. prilocaine>etidocaine >lidocaine > mepivacaine > bupivacaine |
|
|
Term
| what drugs with what pKa have a faster onset? |
|
Definition
| Agents with a pKa closer to the body's pH will have the faster onset |
|
|
Term
| Where are LA's major toxic effects" |
|
Definition
|
|
Term
| What does LA CNS tox result from? |
|
Definition
| inhibition of excitatory pathways in the CNS--producing a sterotypical sequence of signs and symptoms |
|
|
Term
| Why does Cardiovascular Tox occur? |
|
Definition
| due to a slowing of conduction in the myocardium, Myocardial depression, and peripheral vasodialation |
|
|
Term
|
Definition
| bc LA produces dose-dependent myocardial depression, possibly from interference with calcium signaling mechanisms within cardiac muscle |
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