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Gen Exam 3 + Final > Local Anesthetics: Review > Flashcards

Local Anesthetics: Review Flashcards

1
Q

Local anesthetics interrupt neural conduction by

A

inhibiting Na+ influx through channels or ionophores within neuronal membranes

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2
Q

When the neuron
is stimulated, the channel assumes a ___/___ state, in which sodium ions diffuse into the cell, initiating depolarization.

A

activated/open

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3
Q

What happens in the inactivated state?

A

further influx is denied

active transport returns sodium ions
to the exterior

repolarization

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4
Q

Local anesthetics have greater affinity for receptors within sodium channels during

A

their activated and inactivated states

rather than when they are in their resting
states

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5
Q

(Larger/smaller) fibers are generally more susceptible to LAs.

A

smaller
a given volume can more easily block the requisite number of sodium channels & entirely interrupt signal transmission

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6
Q

which fibers are most sensitive?

A

Most to least:
tiny, rapid-firing autonomic fibers

sensory fibers

somatic motor fibers

(most susceptible: Ag spindle efferents, Ad nociceptive
resistant: myelinated C)

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7
Q

recovery from spinal anesthesia:
Order of returning fxns?

A

First to last:
voluntary motor fxn
sensation
autonomic control (ie: micturition)

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8
Q

How do sensory fibers vary in their sensitivity?

A

Easiest → hardest to block:
sympathetic
temperature
pain fibers
pressure & proprioception
motor

Ex: pt may feel unpleasant pressure despite
complete anesthesia of pain fibers

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9
Q

The molecular structure of all local anesthetics consists of (3)

A

lipophilic aromatic ring
intermediate ester or amide linkage
tertiary amine

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10
Q

concentrations that range typically from

A

0.5 to 4%
d/t differences in lipid solubility

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11
Q

Which is more potent?
bupivacaine
articaine

A

bupivacaine is more lipid
soluble & potent

available as 0.5% [ ] (5 mg/mL)

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12
Q

diffusion through nerve sheaths and neural
membranes is determined by

A

aromatic ring and its substitutions

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13
Q

the most important factor that determines the onset of anesthesia

A

proportion of molecules in a lipid-soluble rather than a water-soluble state

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14
Q

When is an amine charged? uncharged?

A

Tertiary (3 bonds) = lipid soluble

Quaternary (4 bonds) = water soluble; + charge

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15
Q

In their packaging, LAs exist as ___. Why does this affect onset of action?

A

quaternary/water-soluble

-unable to penetrate the neuron
-onset: directly r/t proportion of molecules that convert to tertiary/lipid-soluble @ physiologic pH (H&H equation)

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16
Q

T/F
higher pka = faster onset

A

False
higher pKa = less molecules in lipid-soluble form

This will delay onset

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17
Q

The intermediate chain/linkage tells us…

A

classification
&
elimination

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18
Q

Amide metabolism

A

biotransformed in the liver

aromatic hydroxylation
amide hydrolysis
N-dealkylation

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19
Q

Ester metabolism

A

hydrolyzed in the bloodstream by plasma esterases

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20
Q

Which amide is metabolized as if it was an ester?

A

Articaine
amide according to its intermediate linkage, but also contains an ester side chain on its aromatic ring.

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21
Q

Local anesthetics vary in their duration of action due primarily to differences in their …

A

affinity for protein

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22
Q

T/F
local anesthetics irreversibly bind to plasma proteins while circulating in the bloodstream

A

False
reversibly bind

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23
Q

LA’s percentage of protein binding correlates with

A

its affinity for protein within sodium channels

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24
Q

T/F
greater protein binding = shorter neural blockade

A

False
will prolong blockade

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25
Q

bupivacaine vs mepivacaine
protein binding

A

bupivacaine 95%
mepivacaine 55%

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26
Q

Which drug shortens its own duration by dilating local vasculature?

A

Lidocaine

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27
Q

Plain lidocaine formulation limitations

A

useful for brief procedures following infiltration
but
efficacy for nerve block is poor

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28
Q

How do LAs affect seizure activity?

A

Low serum [ ]: suppress 🩷 arrhythmias & status seizures

higher [ ]: induce seizure activity

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29
Q

the initial life-threatening consequence of local anesthetic overdose

A

convulsive seizures

30
Q

How does LA toxicity cause convulsive seizures?

A

selective depression of central inhibitory tracts
↓
uncontrolled excitatory tracts

31
Q

LA toxicity will first cause ___. If [ ]s increase further what else happens?

A

convulsive seizures

all pathways are inhibited
coma, respiratory arrest, CV collapse

32
Q

Lidocaine toxicity [ ]s

A

> 5 mcg/mL (S/S start)

> 10 mcg/ml (convulsive seizures)

33
Q

Monitor for …. when using LAs with sedatives & opioids.

A

respiratory depression

they potentiate any respiratory
depression a/w sedatives & opioids

34
Q

LAs are CNS ___

A

depressants

35
Q

Which clinical conditions lowers the minimum serum [ ] for LA induced seizures?

A

hypercarbia

caution w/ respiratory depression by concurrent use of
sedatives and opioids!

36
Q

greater potential for direct cardiac toxicity than other agents

A

bupivicaine

(~greater affinity for inactive &
resting Na channel → dissociates more slowly)

37
Q

When using lidocaine or other anesthetics, regardless of their formulated concentration, one must consider ___
administered, not the ___

A

dose (milligrams)
volume (milliliters)

38
Q

In adults, we use ____ to avoid toxicity.
In peds, this value is expressed as ___.

A

adults: have max dose in mg (regardless of age and weight)

peds: max dose is in mg/kg

(large children: dot exceed max dose when calculating mg/kg)

39
Q

metabolite of prilocaine

A

o-toluidine
can oxidize Hgb iron
ferrous ( Fe 2+) → ferric ( Fe 3+)

40
Q

Patients appear cyanotic and become symptomatic when the proportion of methemoglobin exceeds

A

15%

41
Q

prilocaine contraindctns

A

hereditary methemoglobinemia

42
Q

Methemoglobinemia treatment

A

methylene blue
reduces the hemes to their normal state

43
Q

How does Methemoglobinemia affect oxygen monitoring?

A

low pulse oximetry ( SpO2 ) despite effective oxygenation and ventilation

ex: SpO2 90%, but PaO2 is normal

44
Q

Why do pts sometimes falsely assume they’re allergic to an LA?

A

1) syncopal episode a/w the injection

2) 🩷 palpitations from the epi (in the solution or released endogenously)

45
Q

Likely cause of true LA allergy

A

Preservatives (methylparaben)

antioxidants (sulfites)

46
Q

Methylparaben

A

preservative
in multidose vials to prevent microbial growth

46
Q

Sulfites

A

antioxidants
prevent the [O] of vasopressors
(epinephrine or levonordefrin)

47
Q

Allergies
Type I Reactions

A

occur w/in minutes

mediated by antibodies or immunoglobulin E ( IgE ) produced by B lymphocytes

most commonly provoked by components of the formulation

48
Q

Allergies
Type 4 reactions

A

delayed for several days

mediated by sensitized T lymphocytes

rare

49
Q

Drugs must be … to cause allergic rxn, but most do so by…

A

large MW w/ multiple valences

combining w/ carrier molecules
(most drugs are too small)

50
Q

Have the PABA structure in common and risk cross sensitivity

A

sulfa antibiotics
methylparaben
ester LAs

51
Q

T/F
The ester linkage causes the allergic rxn a/w ester LAs

A

False
a molecular component joined by this linkage is the culprit

52
Q

patients claiming allergy to
these foods may experience cross-reactions with LA solutions containing vasopressors bc they contain these same sulfites

A

fresh fruits and
vegetables

53
Q

Meperidine “allergic” response

A

Meperidine simulates histamine release
and NSAIDs may promote synthesis of leukotrienes

Pt response = pseudoallergic
(vs true allergy, which is immune-mediated)

54
Q

How to assess LA allergy

A
55
Q

unverified LA “allergy”
what should we use?

A

mepivacaine or prilocaine
without vasopressor

(avoids esters & sulfites from ‘pressors)

56
Q

Good for length procedures

A

Bupivacaine

but more pain injection

57
Q

Most widely used LA in US

A

Lidocaine

58
Q

Vasopressors are drugs that provide constriction of blood vessels by

A

activating alpha-1 adrenergic receptors

59
Q

Why include Vasopressors with LAs

A

hemostasis in operative field

delay absorption (reduces systemic toxicity risk & prolongs effect)

60
Q

Epi causes considerable cardiac stimulation d/t its..

A

Beta 1 adrenergic agonist

(in addition to the usual Alpha 1)

61
Q

Epi concentrations greater than 1 : 200,000 (5 mg/mL )

A

does not reduce LA serum [ ]

62
Q

Increasing Epi [ ] to 1 : 100,000 (10 mg/
mL ) and 1 : 50,000 (20 mg/mL )

A

may increase site hemostasis

63
Q

Standard Epi [ ]

A

1 : 100,000

64
Q

Epi receptor sites

A

alpha, beta-1, and
beta-2

65
Q

Norepi vs Epi

A

Norepi lacks activity at beta-2

66
Q

T/F
Avoid vasopressors in a pt that regularly uses cocaine

A

True
Not an absolute contraindcation

67
Q

Can increase cardiotonic effects of vasopressors

A

tricyclic & MAOI antidepressants
digoxin
thyroid hormone
any sympathomimetics for weight control or attention deficit disorders

(not a contraindication)

68
Q

Vasopressors in a pt using nonselective B-blocker

A

selective agents only block beta-1 🩷 receptors

nonselective also block vascular
beta-2

pressors’ alpha agonist action increases
↑↑↑DBP & MAP
↓
sudden reflex ↓HR

69
Q

T/F
vasopressors are contraindicated in patients taking nonselective beta blockers

A

False
use caution

Gen Exam 3 + Final (13 decks)

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