Pharm 26- Local Anesthetics

Front 1

local anesthesia defined

Back 1

condition that results when sensory transmission from a local area of the body to the CNS is blocked

Front 2

commonly used local anesthetics physical characteristics

Back 2

weak bases with at least 1 ionizable amine function that can become charged through the gain of a proton

Front 3

pKa of most local anesthetics range

Back 3

8.0-9.0

Front 4

concomitant administration of an a-agonist sympathomimetic for what purpose

Back 4

- readily absorbed into the blood from the injection site
- duration of action limited unless blood flow is reduced
- vasoconstricts

Front 5

which local anesthetic does not need to be co-administered with a sympathomimetic

Back 5

cocaine

Front 6

long acting agents that are less dependent on coadministration of vasoconstrictors

Back 6

bupivicaine, ropivicaine, tetracain

Front 7

surface activity

Back 7

ability to reach superficial nerves when applied to the surface of mucous membranes

Front 8

which local anesthetics display surface activity

Back 8

cocaine, benzocaine, lidocaine, tetracaine

Front 9

metabolism of ester local anesthetics

Back 9

plasma cholinesterases (pseudocholinesterases)

Front 10

rate of metabolism

Back 10

very rapid for procaine- half-life 1-2 min
slower for cocaine
very slow for tetracaine

Front 11

metabolism of amide local anesthetics

Back 11

-liver metabolism
- in part by cytochrome P450 isozymes

Front 12

half-lives of different amide local anesthetics

Back 12

lidocaine and priolocaine- 1.5 hours
bupivacaine and ropivacaine- longest active- half lifes of 3.5 and 4.2 hours

Front 13

how to promote ionization of local anesthetics

Back 13

acidification of urine- charged forms are more rapidly excreted

Front 14

MOA of local anesthetics

Back 14

block voltage-dependent sodium channels and reduce influx of sodium ions- prevents depolarization of membrane and blocks AP

Front 15

which form reaches effective intracellular concentrations

Back 15

- unionized form is effective more quickly

Front 16

which form is more effective in blocking entity

Back 16

- once inside the axon- ionized form is more effective blocking entity

Front 17

affinity of the receptor site within the sodium channel is a function of

Back 17

state of the channel- resting, open, or inactivated

Front 18

all other factors equal- order in which fibers are affected

Back 18

- rapidly firing fibers are blocked before slowly firing fibers
- high concentrations of extracellular K may enhance local anesthetic activity- elevated extracellular Ca may antagonize it

Front 19

determinants of sensitivity of nerve fibers to local anesthetics

Back 19

fiber diameter, myelination, physiologic firing rate, anatomic location

Front 20

effect of local anesthetics on skeletal muscle neuromuscular transmission

Back 20

weak blocking effects

Front 21

clinical use of local anesthetics

Back 21

- minor surgical procedures in
- combination with vasoconstrictors like epinephrine

Front 22

sodium bicarbonate administration effect

Back 22

onset of action accelerated because it enhances intracellular access of the weakly basic compounds

Front 23

local anesthetic with fastest onset of action

Back 23

articaine

Front 24

another use of local anesthetics

Back 24

- spinal anesthesia and to produce autonomic blockage in ischemic conditions
- slow infusion at low concentrations- postop analgesia
- repeated epidural injection may lead to tachyphylaxis
- IV anesthetics may be used for reducing pain in perioperative period
- oral and parenteral forms of local anesthetics are sometimes used in neuropathic pain

Front 25

CNS toxicity of local anesthetics

Back 25

-light-headedness or sedation
- restlessness
- nystagmus
- tonic-clonic convulsions
- severe convulsions followed by coma with respiratory and CV depression

Front 26

CV effects of local anesthetics

Back 26

(except cocaine) all are vasodilators
- preexisting cardiac pts may develop heart block and disturbances of electrical function at high plasma levels

Front 27

tox of bupivicaine

Back 27

severe cardiovascular toxicity- including arrhythmias and hypotension

Front 28

tox of ropivicaine

Back 28

- cardiotoxicity when used for peripheral nerve block

Front 29

cardiovascular toxicity of cocaine result of?

Back 29

ability of cocaine to block norepinephrine reuptake at sympathetic neuroeffector junctions and vasoconstricting actions

Front 30

cocaine tox when used as drug of abuse

Back 30

severe HTN with cerebral hemorrhage, cardiac arrhythmias, and MI

Front 31

toxicity of priolocaine

Back 31

metabolized to products that induce o-toluidine (agent that converts hemoglobin to methemoglobin)
- moderate methemoglobinemia can cause decompensation in patients with cardiac or pulmonary disease

Front 32

toxicity of ester type local anesthetics

Back 32

metabolized to products that can cause antibody formation

Front 33

treatment of toxicity of local anesthetics

Back 33

convulsions- diazepam or short acting barbiturate (thiopental)