Pcol Sem 2 Test 4 Local Anesthetics

Front 1

what is the main MOA of local anesthetics

Back 1

Na channel blockers by interfering w/ propagation of AP

Front 2

what is unique about esters vs amides

Back 2

esters are more prone to hydrolysis and have a shorter duration of action

Front 3

what are the properties of lidocaine

Back 3

AMIDE ANESTHETIC
used for short procedures (epidural/spinal anesthesia)
must be given w/ epinephrine

Front 4

what are the properties of bupivacaine

Back 4

AMIDE ANESTHETIC
used for longer duration procedures

Front 5

what are the properties of procaine

Back 5

ESTER ANESTHETIC
used for short duration procedures (epidural,spinal anesthesia)
must give epinephrine

Front 6

what are the properties of cocaine

Back 6

ESTER ANESTHETIC
blocks Na channels but also has sympathomimetic effects
used in procedures requiring high surface activity and vasoconstriction

Front 7

how are local anesthetics able to interact w/ Na channel blockers

Back 7

they are made as non-ionized weak bases and the uncharged form penetrates the cell wall and binds to the intercellular portion of Rc then gets protonated becoming active

Front 8

why are local anesthetics less effective if injected into infected tissues

Back 8

due to the tissue being acidic the local anesthetic has reduced effectiveness due to limited diffusion of charged form

Front 9

what is the duration of action of local anesthetics proportional to

Back 9

time in contact w/ nerve

Front 10

what kind of local anesthetics work faster

Back 10

lipophilic compounds

Front 11

how does tissue vascularity effect local anesthetic administration

Back 11

the more vascularized a tissue is the more anesthetic must be given due to there being less contact

Front 12

why is epinephrine added to local anesthetics

Back 12

it is a vasoconstrictor and will enhance activity by increasing time in contact w/ nerve

Front 13

what are the disadvantages of epinephrine use

Back 13

sympathomimetics increase O2 consumption/demand

vasoconstriction can lead to hypoxia and tissue damage

not effective in prolonging duration of lipophilic drugs

Front 14

what is occassional caused by vasoconstrictors

Back 14

edema
delayed wound healing
necrosis

Front 15

what is the distribution of Amides

Back 15

get sequestered into lipophilic storage sites (fat)

two phases: rapid (in highly perfused tissue)
slow (in moderately perfused tissue)

Front 16

what is the distribution of Esters

Back 16

no systemic toxicity b/c once they get into blood rapidly metabolized

Front 17

how are esters metabolized

Back 17

hydrolyzed rapidly by Butyrylcholinesterate

Front 18

how are amides metabolized

Back 18

by liver CYP450

Front 19

what is the metabolic rate of prilocane, mepivacaine, lidocaine

Back 19

prolocaine > lidocaine > mepivacaine

Front 20

what disease state enhance toxicity from amide local anesthetics

Back 20

hepatic disease

Front 21

what are the sodium channel characteristics

Back 21

4 domains
6 transmembrane segments per domain
-S4 = voltage sensor
-S5/S6 are around the pore

excessive activation of Na channel leads to inactivation via H blocking

Front 22

how do Local anesthetics effect the propagation of AP

Back 22

act directly on S6 region of Na channel

Front 23

what does it mean that Na channel blockade is voltage and time dependent

Back 23

resting nerve is less sensitive to block than active nerve

the more positive the membrane potential the greater the degree of block

Front 24

what regulates anesthetic rate of onset

Back 24

lipophilicity

smaller more lipophilic anesthetics have a faster rate of interaction w/ Na channel

Front 25

what is potency of local anesthetics correlated to

Back 25

lipophilicity

more lipophilic compounds are more potent

Front 26

what local anesthetics are lipophilic and water soluble

Back 26

lipophilic: tetracaine, bupivacaine, ropivacaine

water soluble: lidocaine, procaine, mepivacaine

Front 27

other than lipophilicity what else affects local anesthetics

Back 27

fiber size (small the fiber the more sensitive to local block)

rate of activity of fiber (more active the fiber the more its effected by local anesthetics)

Front 28

what type of function do local anesthetics effect first

Back 28

sensory function then motor function (type a Alpha)

Front 29

what type of fiber are local anesthetics very effective against

Back 29

type A delta and type C due to their firing frequency

Front 30

what local anesthetics can be used as antiarrhythmic agents

Back 30

lidocaine

Front 31

how do local anesthetics effect other excitable membranes

Back 31

we effect on neuromuscular blocking
potent effect on cardiac cell membrane

Front 32

what local anesthetics can cause lethal arrhythmias

Back 32

bupivacaine
ropivacaine

Front 33

what is a Bier block

Back 33

application of tourniquet to proximal limb to maintain a localized effect of anesthetic by limiting blood flow this is good when you can't use general anesthesia

Front 34

what local anesthetic is applied topically

Back 34

lidocaine

Front 35

what are the routes of administration of local anesthetics

Back 35

topical
bier block
perineural
nerve blocks (trigeminal, opthalmic, brachial)
spinal cord

Front 36

read page 9 on nerve blocks

Back 36

read page 9 on nerve blocks

Front 37

what ester and amide are used for epidural nerve block

Back 37

ester: cocaine and its derivative

amide: lidocaine and its derivatives

Front 38

what are the major forms of local anesthetic toxicity

Back 38

systemic effects: rapid rise in blood levels

direct neurotoxicity from local administration (lidocaine can cause neuropathy)

Front 39

what are the causes of accidental OD

Back 39

major peripheral nerve block (facial surgery)

given IV

Front 40

what are symptoms of local anesthetic OD

Back 40

circumoral and tongue numbness
metallic taste

Front 41

high concentrations of local anesthetics cause what

Back 41

nystagmus
muscle twitching
tonic clonic convulsions
respiratory excitation followed by depression

Front 42

since seizures may occur due to local anesthetic OD what can be done

Back 42

premedicate w/ antiseizure drug such as BZD (diazepam or midazolam)

Front 43

how do you treat seizures caused by local anesthetic OD

Back 43

treat w/ general anesthetics (propofol, thiopental, midazolam)

short acting neuromuscular relaxant drugs (succinylcholine) THESE WON'T BLOCK CENTRAL SEIZURES

tracheal intubation

Front 44

what can be used to treat systemic toxicity of local anesthetics and how

Back 44

lipid emulsion solution

lipids act to capture and sequester lipophilic local anesthetics

Front 45

under what circumstances will cocaine be used as an anesthetics

Back 45

when vasoconstriction is also required

Front 46

how is cocaine a vasoconstrictor

Back 46

it inhibits catecholamine reuptake

Front 47

what is good for topical anesthetsia of upper respiratory tract

Back 47

cocaine

Front 48

cocaine abuse can lead to what

Back 48

tonic clonic convulsions
respiratory stimulation followed by depression
cardiovascular toxicity (tachycardia)
tissue ischemia

Front 49

what cardiovascular effect do most local anesthetics cause

Back 49

arteriolar dilation

Front 50

what local anesthetics has cardiovascular toxicity and is difficult to treat

Back 50

bupivacaine

Front 51

what local anesthetics has hematologic effects; what are they, and how do you treat it?

Back 51

prilocaine's metabolites convert hemoglobin to methemoglobin (cyanosis)

treat w/ reducing agents such as methylene blue or ascorbic acid to convert methemoglobin to hemoglobin

Front 52

how do esters cause allergic reactions

Back 52

as a result of p-aminobenzoic acid derivatives from metabolism