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Daddy Pharm > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

lipophilicity of the ______ controls the compounds ability to ….

A

aromatic group
penetrate the nerve sheath and enter the nerve membrane

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2
Q

Most LAs are ____ & can exist as …. (2)

A

ionizable weak bases

freebase
or
positively charged form

(this will affect their action at the site)

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3
Q

MoA as antiarrhythmic

A

decrease sodium entry
alters conductivity
can increase/decrease HR

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4
Q

Which part of neuron do they act on?

A

axon (lipid soluble)

can cross at other places but the axon has high [ ] of Na channels

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5
Q

why their lipophilicity is so important?

A

determines ability to penetrate nerve membranes

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6
Q

Most preparation solutions are ____.

A

weakly acidic

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7
Q

T/F
Most LAs have an amide structure.

A

False
they’re amines
(ionizable weak bases)
can bond to another H and become charged

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8
Q

What happens to an LA in acidic conditions?

A

LA = weak base
will pick up + (H) in an acidic environment
become charged/ionized
now harder to cross lipid bilayer (nerve)

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9
Q

The non-pronated form of an LA is also called

A

the freebase form

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10
Q

How to get quicker onset

A

alkalinization prior to use (add bicarb)

↑ free base form = ↑ lipid solubility & ↓ onset

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11
Q

Placing LAs in an acidic environment makes it more (water/lipid) soluble.

A

water

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12
Q

which compounds show the greatest benefit of alkalinization prior to use?

A

LAs with longer onset

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13
Q

Once the LA crosses the axon, what must happen?

A

must convert to ionized form so it can bind to the inside of the Na channel and exert its effects

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14
Q

T/F
alkalization prior to use increases lipid-soluble molecules that can penetrate the axon & also increases the amount that can be converted to ionized form and bind to the inside of the channel.

A

True
more will enter the cell and thus more is available to convert to ionized and bind to inside of channel

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15
Q

T/F
LAs irreversibly block the generation and propagation of nerve impulses.

A

False
reversibly

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16
Q

primary location of effect

A

the axon
d/t its high density of sodium channels

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17
Q

T/F
LAs can alter both sensory & motor fxn.

A

true

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18
Q

bi-directional blockade

A

block function in all excitable cells
can alter sensory and motor function

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19
Q

The decrease in pain, temperature, and touch perception, skeletal muscle tone is mostly d/t….

A

decreased stimulation of the muscle’s motor neuron

local effect plays a part but not primary

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20
Q

Level of effect depends on

A

agent used
route of administration
drug concentration at site (prob #1)
lipophilicity

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21
Q

T/F
A drug can still be a good LA even if its not lipophilic

A

False
has to cross the membrane

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22
Q

routes

A

topically: skin. mucous membranes
parenteral: peripheral, central, spinal
rectally
ophthalmically

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23
Q

Cocaine isolated from

A

South American plant
Erythroxylon coca
1800’s

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24
Q

first synthetic local developed

A

Procaine

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25
Q

What gives cocaine its medical use?

A

potent vasoconstrictor

ie: nasal packing (LA effect & reduces bleeding)

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26
Q

Cocaine’s basic structure led to …

A

development of synthetic compounds that did not have its toxic or addictive action

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27
Q

Noted for its high [ ] of Na channels

A

the axon

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28
Q

Normal resting potential

A

~ -80 mv (most cells)

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29
Q

Ion [ ]
ICF & ECF

A
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30
Q

Primary contributor to resting charge

A

K+ channels

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31
Q

only channel open at rest

A

K+ channels (some of them, not all)

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32
Q

Dendritic Conduction
is a (passive/active) electrical process

A

passive

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33
Q

Axonal Conduction
is a (passive/active) electrical process

A

active

“Axon = Active”

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34
Q

Response from the cell body depends on… (2)

A

how many Na ions enter

where they enter (closer to body = more likely response)

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35
Q

Cell body vs Axon
signal regeneration

A

no regeneration in cell body

axon = signal constantly regenerated

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36
Q

Axonal Conduction

A

-Active electrical process

-voltage-gated Na+ & K+ channels
-Some Ca++ also (mostly terminal)
-Na/K/ATPase: restore chemical (ionic) equilibrium

-Signal initiated at axon hillock by internally ligand-gated Na+ channels

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37
Q

T/F
At the axon, the charge slowly diffuses out.

A

False
This applies to dendrites

axon = constant regeneration; no concern for charge diluting out or slow process of diffusion

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38
Q

T/F
The charge first initiated at the axon will equal the charge that reaches the nerve terminal.

A

True
charge from dendrite → axon may not be equal
but
charge from axon → terminal will be equal

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39
Q

T/F
As the signal is passed down the axon, Na+ comes in & K+ exits. This restores ion concentrations.

A

False
this restores net voltage

Na/K/ATPase restores ion [ ]s

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40
Q

Na/K/ATPase
MoA

A

cleaves ATP to obtain energy for:
3 Na out
2 K in

restores ion [ ]s

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41
Q

Signals are initiated at ____ by …

A

axon hillock
internally ligand-gated Na+ channels

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42
Q

The axon hillock contains ___ gated Na channels while the axon contains ___ gated Na channels

A

hiLLock = Ligand
axon = voltage

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43
Q

Are C fibers myelinated?

A

No

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44
Q

T/F
Myelination decreases the amount of energy needed.

A

True

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45
Q

Schwann cells vs Oligodendrocytes

A

Schwann cells: wrap their membrane around nerve (PNS)

Oligodendrocytes: 1 cell can myelinate multiple nerves (brain); helpful bc limited space in brain

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46
Q

what allows for saltatory conduction?

A

deficit in charge
proper spacing of myelin sheaths

(too far = charge can’t jump
too close = don’t get max benefit)

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46
Q

T/F
a signal generated at the hillock can travel backwards towards the cell body.

A

False
but
if we take a probe and stimulate near terminal the signal can travel backwards toward the cell body/axon hillock

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47
Q

Factors leading to increased conduction rates:

A

-Myelination (most important)
(↓ Capacitance; Saltatory Conduction)

-less neg. resting potential (closer to threshold)

-↑ Na+ channel density

-↑ Axonal diameter (less resistance to flow)

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48
Q

MoA
mainly believed to be…

A

(Classical hydrophilic pathway):
-enters axon by diffusion in uncharged form
-re-ionizes in cytoplasm
-binds to the inside opening of open, inactivated sodium channels

blocks channel & repulses Na entry d/t positive charge

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49
Q

MoA
Hydrophobic pathway

A

uncharged LA molecule enters
binds to locations on sodium channel that are located within the membrane

(e.g. Benzocaine)

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50
Q

MoA
Alternative hydrophilic pathway

A

permanently charged LA can interact with other channels triggering their opening and allowing a pathway for the charged local anesthetic to enter

(ie: QX-314)

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51
Q

Quaternary amine

A

Nitrogen w/ 4 bonded Carbon structures
not ionizable bc it is permanently charged

won’t solubilize across membranes
can use pores/channels
can then bind to inside of channel bc its charged

Ie: QX-314

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52
Q

The (uncharged/charged) form of an LA is the active form.

A

charged

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53
Q

QX-314 acts on which receptor?

A

TRPV1 (vanilloid, capsaicin)

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54
Q

benefit of using permanently charged (quat amines)

A

once inside cells, can bind to inside of Na channel (if they’re the correct shape)

not directly limited by lipophilicity

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55
Q

All agents act to…

A

decrease the permeability of the membrane to sodium ions

Some K+ inhibition also

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56
Q

LAs bind to ____ gated Na channels, and inhibit Na inflow during ___.

A

voltage
depolarization

“holds” the plug & makes it harder for channels to open up completely again

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57
Q

T/F
LA bonding is covalent.

A

False
competitive
so its dependent on [ ]

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58
Q

T/F
LAs can diffuse out of the cell if ECF [ ] is much lower than ICF, restoring normal conduction.

A

True

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59
Q

T/F
LAs can damage the axon terminal.

A

False

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60
Q

Effect of LAs @
High vs. Low [ ]
(ICF)

A

Low = ↓ rate of rise & height of AP (fewer Na channels working normally)

Higher = can abolish it totally

↑ Firing threshold & total propagation time

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61
Q

In myelinated fibers, LA effects only occur at …

A

the Nodes of Ranvier

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62
Q

LA binding site

A

intracellular mouth of the transmembrane voltage-gated sodium channels

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63
Q

LA’s are too big to cross through pores into cell so they must diffuse across lipid membrane UNLESS …

A

its small enough to utilize certain pores such as the TRPV1

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64
Q

All LA’s are ____.

A

weak bases
may be ionized at physiologic pH

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65
Q

onset time can be predicted by (2)
which 2 LAs are the exception?

A

pKa & local tissue pH

benzocaine & chloroprocaine

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66
Q

Which LA can we not use internally & why

A

benzocaine
methemoglobenemia

base w/ very low pka 3.5
permanently UNcharged at any phys. pH

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67
Q

Why is chloroprocaine different in predicting onset?

A

relatively weak & nontoxic
so
we use large doses which makes comparison of its onset difficult

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68
Q

Henderson Hasselbach equation for bases (LAs)

A

pH = pKa + log [B]/[HB+]

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69
Q

🔷
All LA’s have pKa’s in range of

A

7.6 – 9.0

Benzocaine is the exception (3.5; almost entirely unionized at physiologic pH)

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70
Q

At physiologic pH (~7.4), the higher the pKa of the LA, the (less/more) ionized it will be and the (faster/slower) the onset.

A

more
slower

71
Q

In cases where the tissue is more acidic (such as in an infected region)

A

lower local pH → LA is more ionized

slows the onset & may decrease effectiveness

72
Q

dont memorize
understand concept/trends

A

higher pka = less unionized = less crossing membrane = slower onset

73
Q

Voltage-gated Sodium Channels
structure

A

alpha subunit: 4 additional subunits
additional beta subunits (external)

alpha subunits open the channel

74
Q

Voltage-gated Sodium Channels
structure at 0 mv

A

inactivated
inactivation gate into mouth of channel

75
Q

The inactivation gate plugs the channel closed until…

A

all protein subunits change conformation to close mouth of channel themselves

(the gate essentially stops ion influx while the proteins work on closing the channel)

76
Q

contains the sodium pore

A

The alpha subunit

77
Q

Local anesthetics bind to & stabilize which form?

A

open, inactivated

78
Q

When is the LA binding site exposed?

A

when the channel is open

79
Q

How do LAs affect the inactivation gate?

A

makes it harder for the gate to separate/unplug the channel

the LA will eventually diffuse away when the channel opens if concentration gradients favor that

80
Q

The beta subunits fxn

A

stabilize the channel

not part of the opening of the channel

81
Q

T/F
The 4 alpha subunits are actually one continuous protein structure.

A

True

82
Q

Selectivity filter

A

selects which particular ions that can pass thru

83
Q

Why are C fibers so much slower?

A

unmyelinated
small diameter

84
Q

Benefit of C fibers

A

unmyelinated = LAs can block easily bc no obstructing myelin

85
Q

T/F
LAs cannot cross the myelin sheath.

A

False
they can, but takes a lot longer

86
Q

First fibers that tend to be blocked

A

C fibers

87
Q

How does diameter affect:
susceptibility to LAs
speed of conduction

A

↑ diameter = less susceptible & faster conduction

88
Q

Autonomic preganglionic fibers

A

B fibers

89
Q

Motor fibers

A

Aa fibers

fastest condxn
myelinated
largest diameter

90
Q

If we give enough LA to block motor fxn….

A

potential respiratory issues

91
Q

Low LA doses are more likely to block (pain/motor)

A

pain

92
Q

T/F
C fibers recover before Aa fibers do.

A

False

C fibers = first to be blocked
Aa fibers = last to be blocked

recovery is in the opposite order

93
Q

Use as antiarrhythmic agents is due to

A

-blockade myocardial Na+ channels
-decreases firing rate
-decreases signal passage thru conductive fibers

94
Q

topical use

A

decrease pain of wounds, burns, mucous membranes

95
Q

infiltration

A

injected around area - i.e. - for surgery

96
Q

regional nerve block

A

injected close to nerve that innervates the area to be anesthetized

97
Q

spinal

A

injected into lumbar subarachnoid space to get to nerves in that area going to various body sites

98
Q

epidural

A

given inside spine above the dura mater

99
Q

intravenous use

A

usually for surgery on a specific limb

100
Q

T/F
Selection of agents is mainly based on its pharmacodynamics.

A

False
pharmacokinetics

101
Q

Which are fast? Which are slower?
Procaine
prilocaine
tetracaine
lidocaine

A

usually fastest: lidocaine & prilocaine

slower: Procaine and tetracaine

102
Q

shortest duration

A

Procaine and chloroprocaine
15 - 30 minutes

103
Q

intermediate durations

A

lidocaine and prilocaine
30-90 mins

104
Q

long duration

A

tetracaine
2-3 hours

105
Q

Effect of epi on doA

A

EPI may be used to increase duration, but is not always effective.

106
Q

fastest onset when applied to mucous membranes

A

Benzocaine

followed by lidocaine & cocaine

107
Q

Topical duration of most

A

30 - 60 minutes

108
Q

Other targets besides Na channels

A

K+ Channels

Ca++ channels

NMDA receptors

G-protein receptor complexes

Nicotinic Ach receptors

109
Q

most common cause for LA cessation of action

A

swept away in bloodstream

moved thru body & metabolized/destroyed

110
Q

This receptor is a/w the anti-inflammatory effect of LAs

A

G-protein receptor complexes

111
Q

K+ Channels

A

-Mainly amides
-more intense blockade

112
Q

Ca++ channels

A

antiarrhythmic action of lidocaine?

113
Q

NMDA receptors

A

Lidocaine antagonism (via a metabolite?)
analgesic-effect

114
Q

Action at this receptor enhances NMB (insignificantly)

A

Nicotinic Ach receptors

115
Q

T/F
Adding epi will increase systemic effects of the LA.

A

False
increases duration of effect at that local site

116
Q

Topical blood flow is (higher/lower) than most other tissues, so the LA is removed (faster/slower) here.

A

higher
faster

117
Q

All agents are ___ or ___.

A

esters
amides

118
Q

All LAs contain

A

an aromatic ring

119
Q

Having an amine makes a compound more (acidic/basic).

A

basic

120
Q

Lipophilic and hydrophilic regions

A

Lipophilic group = aromatic ring

Hydrophilic group usually an amine (ionizable)

121
Q

Lipophilic and hydrophilic groups are joined by…

A

an ester or amide

122
Q

The ester/amide linkage between the lipophilic and hydrophilic regions determine (2)

A

metabolism
allergic potential

123
Q

Increasing lipid solubility results in what 2 effects?

A

faster onset
increased duration

124
Q

Altering groups besides the ester/amide linkage results in…

A

alters metabolism rate and other effects.

125
Q

Most important factor in limiting toxicity

A

metabolic rate

(wont be around long enough to cause toxicity)

126
Q

Esters
Metab

A

-plasma esterases (ie: plasma cholinesterase)

-Also by liver esterases & other tissue esterases

127
Q

Spinal agent
metab

A

spinal fluid lacks esterases

intrathecal injxns remain active until absorbed back into systemic circulation

128
Q

T/F
esters are not metabolized in spinal fluid.

A

True

129
Q

Amide
metab

A

mainly liver CYP enzymes
e.g. CYP1A2, CYP3A4

130
Q

Which is more protein bound?
ester
amide

A

amide

131
Q

Amide
protein binding

A

55-95%
Mostly alpha-1 acid glycoproteins

affects toxicity!
low protein levels = higher tox risk

Lung uptake of amide LA’s also important in limiting toxicity

132
Q

T/F
Lung uptake of ester LA’s is also important in limiting toxicity.

A

False
amide

133
Q

Amide LAs
Factors that increase/decrease toxicity

A

Increases: smoking, trauma, cancer, etc

Decreased: oral contraceptives, neonate

134
Q

T/F
Amides are uptaken by the lungs and metabolized partially there.

A

False
yes uptaken
but not metabolized there

135
Q

The Esters

A

Procaine (DC’ed)
Proparacaine (Alcaine) – used as an ophthalmic
Chloroprocaine
Tetracaine
Cocaine
Benzocaine
Cetacaine

136
Q

Procaine (Novocain) (DC’ed)

A

First synthetic local anesthetic.

Slower onset
short duration
weak potency
Fairly low systemic toxicity

Best for infiltration and nerve block.
Use superceded by better agents (amides).

137
Q

Chloroprocaine (Nesacaine)

A

fastest & shortest acting
Low systemic toxicity

pKa 9.0
but
Rapid onset b/c high [ ]s used!

Direct acting vasodilator (shortens doA)

For infiltration, nerve block, IV and epidural use.

138
Q

Used in high concentration solutions (since toxicity is low)

A

Chloroprocaine (Nesacaine)

139
Q

Tetracaine (Synera – w/ Lidocaine for topical)

A

⚠️Ten times more potent than procaine, but also ten times more toxic.

Long duration with slow onset.

spinal anesthesia (decrease diffusion & toxicity)

absorption across mucous membranes limits use as topical

❌sulfonamide Abx: m’lite (aminobenzoic acid) inhibits sulfonamide action

140
Q

Avoid in patients taking sulfonamide antibiotics

A

Tetracaine (Synera – w/ Lidocaine for topical use)

141
Q

applying this agent topically risks crossing mucous membranes

A

Tetracaine (Synera – w/ Lidocaine for topical use)

142
Q

Cocaine

A

C-II
from coca leaves

only topical b/c too toxic

potent vasoconstrictive activity & addiction liability along with LA effect

topically:
-mucous membranes (nasal/oropharyngeal cavities preop)
-packed post-op: decrease bleeding & pain

143
Q

Benzocaine (Oragel) (many other tradenames)

A

Poorly water soluble, so only topical
pKa ~ 3.5

⚠️Excessive absorption risk methemoglobinemia

144
Q

Cetacaine (Cetylite)

A

Topical agent for local skin disorders
for various mucous membranes (except eyes)

mixture of Benzocaine, Tetracaine, and Butyl Aminobenzoate used topically, rectally or as a spray to inhibit the gag reflex
(ie: bronchoscope exam).

145
Q

Amides

A

Lidocaine
Prilocaine
Bupivacaine
Ropivacaine
Mepivacaine
Articaine

146
Q

Lidocaine (Xylocaine)

A

Most common LA

Rapid onset
intermediate duration

-vasodilates so often mixed w/ EPI

147
Q

Transient Neurologic Symptoms
reported worse with which agents?

A

lidocaine and mepivacaine
(versus prilocaine, bupivacaine or procaine)

148
Q

Transient Neurologic Symptoms

A

Transient hyperalgesia after spinal anesthesia

Treat pain w/ NSAIDs
Mechanism unclear (direct neurotoxic effect?)

149
Q

Prilocaine

A

Similar to lidocaine, but less vasodilation

Rapid onset
intermediate duration

Least toxic of the amides, but can still cause methemoglobinemia

150
Q

Least toxic of the amides, but can still cause methemoglobinemia

A

Prilocaine

151
Q

Which has higher risk of methemoglobinemia?
Esters
Amides

A

amides

152
Q

Bupivacaine (Marcaine)

A

Long duration
slower onset
High potency

(More toxic than Lidocaine (cardiotoxic)
Most likely to cause adverse effects

infiltration, epidural, spinal

153
Q

Bupivacaine (Exparel) – liposomal formulation

A

interscalene brachial plexus block
single-dose postop infiltration
postop regional
(not for IT, epidural use)

Not recommended <18 yrs, pregnancy, hepatic disease

154
Q

Which amide is most likely to cause adverse effects?

A

Bupivacaine (Marcaine)

155
Q

Ropivacaine (Naropin)

A

Long duration
(similar to Bupivacaine, but less cardiotoxic)

S-isomer (vs. bupivacaine(racemic) has a more cardiotoxic R-isomer)

Less lipid soluble
more rapidly metabolized (vs Bupivacaine)

Uses similar to Bupivacaine (infiltration, nerve block, epidural, spinal)

156
Q

Ropivacaine vs Bupivacaine

A

Ropiv = less toxic (S isomer)
Bupiv = racemic; has R isomer (more toxic)

ropiv = less lipid sol.; faster metab

BOTH:
infiltration, nerve block, epidural, spinal
similar structures

157
Q

Mepivacaine (Carbocaine)

A

Uses Similar to lidocaine
(infiltration, nerve block, epidural)

Not effective topically

Racemic mixture
(structurally similar to Bupivacaine & Ropivacaine)

❌ OB: biotransformation in fetus is prolonged.
“no Mepiv for Mommy”

158
Q

Racemic mixtures

A

Mepivacaine
Bupivacaine

159
Q

Articaine (Septocaine)

A

Only in U.S. with EPI.

Similar to Lidocaine

short duration
rapid onset
Low systemic toxicity
(rapid breakdown: ester group along w/ amide)

Used for dental and periodontal procedures.

160
Q

Which amide also has an ester group?

A

Articaine (Septocaine)

161
Q

Pramoxine (Proctofoam)

A

Not a true amide or ester
for pts w/ amide/ester sensitivity

Topical:
hemorrhoids, rectal pain, itching (pruritus)

Weak potency (will not totally abolish gag reflex)

Mixed in combination with many products (ex. Hydrocortisone, calamine).

162
Q

Which LA will not cause enough numbing of the gag reflex?

A

Pramoxine (Proctofoam)

mostly for topical hemorrhoids & itching

163
Q

Local hypersensitivity reactions more common with

A

ester type

164
Q

Some preps include ….., which also increase sensitivity risk

A

tartrazine and sulfites

165
Q

Systemic absorption

A

cardiotoxic risk

potential CNS symptoms
(sedation, dizziness, disorientation, tremors, seizures, respiratory arrest)

166
Q

Neurotoxicity more common in

A

epidural/subarachnoid

Cauda Equina syndrome & Transient Neurologic Symptoms

167
Q

T/F
Topical agents are safer as they do not carry risk of methemoglobinemia.

A

False
Methemoglobinemia possible with topical anesthetics

168
Q

Methemoglobinemia
mechanism

A

Oxidize hemoglobin to ferric (+3) instead of normal ferrous (+2) state

(prilocaine, benzocaine, lidocaine, Cetacaine)

169
Q

Agents w/ risk of methemoglobinemia

A

prilocaine
benzocaine
lidocaine
Cetacaine

170
Q

Except for allergic or hypersensitivity reactions, actual risk for most patients is fairly low due to …

A

their use in small amounts in a localized area for most procedures

171
Q

Lipid Rescue

A

-systemic toxicity
-known overdose
-accidental IV injxn

Intralipid: soybean emulsion
10%, 20%, 30%

lacks strong evidence
mechanism not fully understood

172
Q

T/F
Lipid rescue mechanism of action is not completely understood.

A

True
What do we actually know? fr

173
Q

T/F
The antidote for poor regional technique is lipid rescue.

A

False
gotta have skillz

174
Q

Future Local Anesthetics

A

-Exploitation of other mechanisms (QX-314)

-Selective Na channel blockers
(specific to axon & avoid 🩷)

-Targeted dose forms with magnetic carriers
(target specific site)

Daddy Pharm (13 decks)

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