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Gen Principles Exam 3 > M & M CH 16 Local Anesthetics > Flashcards

M & M CH 16 Local Anesthetics Flashcards

1
Q

Na channels exist in at least three resting states

A

Resting (nonconducting)
Open (conducting)
Inactivated (nonconducting)

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2
Q

What are the subunits of Voltage-gated sodium channels

A

One large alpha subunit
One or two Beta subunits

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3
Q

Sensitivity of nerve fibers to inhibition by LAs is influenced by

A

Axonal diameter
Myelination
And other factors

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4
Q

LA potency correlates with

A

Octanol solubility
Ability for LA to penetrate lipid membranes

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5
Q

(T/F) Adding large alkyl groups to LAs decrease potency

A

FALSE it increases potency

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6
Q

(T/F) LA potency can be measured with MAC (minimum alveolar conc.)

A

FALSE no clinical measurement of LAs potency that is comparable to MAC exists

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7
Q

Factors that affect onset of action of LA

A

lipid solubility
relative conc of the nonionized (free-base) form (B) and the ionized water-soluble form (BH+)

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8
Q

The pKa is the pH at which there is an ____
fraction of ionized and nonionized drug

A

equal

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9
Q

What is the significance of the pKa in LA?

A

pKa represents the pH at which there is an equal fraction of ionized and nonionized drug

*plays a crucial role in determining the onset of action.

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10
Q

Mepivacaine and Lidocaine have (faster/slower) onset than more potent more lipid-soluble agents like ropivacaine or bupivacaine

A

Faster

*lipid soluble agents have a longer DOA but slower onset of action bec they slowly diffuse from lipid rich environment to aq. bloodstream

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11
Q

How do less potent and less lipid-soluble LAs compare in terms of onset?

A

Less potent and less lipid-soluble LAs have a faster onset compared to more potent, more lipid-soluble LAs

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12
Q

What determines the elimination and toxicity of local anesthetics in the blood?

A

pharmacokinetic profiles of LAs in blood are important in determining their elimination and toxicity.

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13
Q

Rank order of LA conc in blood and absorption r/t vascularity of site of injection

A

intravenous (or intraarterial) > tracheal > intercostal > paracervical > epidural >
brachial plexus > sciatic > subcutaneous

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14
Q

Which injection site has the highest systemic absorption?

A

Intravenous (or intraarterial) injections

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15
Q

Ester LAs are metabolized by

A

pseudocholinesterase

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16
Q

Amide LAs are metabolized by

A

(N-dealkylation and hydroxylation) by microsomal P-450 enzymes in the
liver.

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17
Q

(T/F) In awake pt’s, rising LA conc in CNS produce signs of LA tox

A

True

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18
Q

(T/F) Major cardiovascular toxicity usually requires about three times the
local anesthetic concentration in blood as that required to produce
seizures

A

True

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19
Q

Intravascular injection of this LA can cause cardiovascular toxicity. Including left
ventricular depression, av heart block, v-tach and v-fib

A

Bupivacaine

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20
Q

Hypersensitivity RXN’s (w/IgG & IgE) to LA are uncommon but can occur with

A

Ester compounds (i.e. procaine, benzocaine)
*PABA derivative compounds

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21
Q

resting membrane potential

A

-60 to -70 mV

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22
Q

transport of three sodium (Na) ions out of the
cell for every two potassium (K) ions it moves into the cell

A

sodium–potassium pump
(Na+-K+-ATPase)

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23
Q

creates a conc gradient that favors movement of K ions from intracellular to extracellular and movement of Na ions in opposite direction

A

sodium–potassium pump
(Na+-K+-ATPase)

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24
Q

(T/F) cell membrane is much more “leaky” to Na
ions than to K ions, so a relative excess of negatively charged ions (anions)
accumulates intracellularly.

A

FALSE

There are more “Leaky” K ions than Na ions

*combined effects of Na+-K+-ATPase and K
ion leak account for the negative resting membrane potential

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25
Q

Can generate action potentials

A

neurons or myocytes

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26
Q

These channels can produce and transmit membrane depolarization following chemical, mechanical and/or electrical stimuli.

A

voltage-gated Na channels in peripheral nerve axons

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27
Q

(T/F) Activation of voltage-gated Na channels causes a very brief (roughly 1 ms)
change in the conformation of the channels, allowing an influx of Na ions and
generating an action potential

A

True

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28
Q

The increase in Na permeability causes temporary depolarization of the membrane potential to

A

+35 mV

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29
Q

T/F When there is no more K+ influx, in voltage-gated Na ion channels the membrane returns to its resting potential

A

FALSE
Occurs with Na ion influx, not K+

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30
Q

when can a signal be transmitted as a wave of depolarization along nerve membrane (impulse)

A

when stimulus is sufficient to depolarize membrane

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31
Q

Baseline conc gradients are maintained by ,

A

the sodium–potassium pump

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32
Q

(small/large) amount of Na ions pass into the cell during an action
potential

A

small

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33
Q

When LA bind to ___ subunit, they prevent channel activation and Na influx
through the individual channels

A

alpha

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34
Q

(T/F) LA binding to Na channels alters the resting membrane potential.

A

FALSE

LA binding to Na channels DOES NOT alter the resting membrane potential

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35
Q

As more LAs bind to Na Channels, the threshold for excitation & impulse conduction in nerves (increases/decreases), the rate of rise and
the magnitude of the action potential (increases/decreases), and impulse conduction velocity slows.

A

Increases
Decreases

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36
Q

Why can action potentials no longer be generated when a sufficient fraction of Na channels have bound to LA?

A

LA prevents the normal influx of Na ions thru Na channels during depolarization, leading to the inability to generate action potentials.

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37
Q

What state of Na channels do LA have a greater affinity for: open, inactivated, or resting?

A

open or
inactivated state

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38
Q

Explain the relationship between LA conc and the loss of action potentials

A

As LA conc increase, more Na channels become blocked, resulting in the loss of action potentials and the termination of impulse transmission.

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39
Q

How does the opening of channels during depolarization impact LA action?

A

As channels open during depolarization, they expose binding sites for local anesthetics.
This increased availability enhances likelihood of LA binding to the channels and blocking sodium influx.

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40
Q

What is the term for the phenomenon where the fraction of Na channels binding a LA increases with frequent depolarization?

A

“use-dependent block” refers to the ↑binding of LAs to Na channels when nerve fibers experience frequent depolarizations.

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41
Q

Why is LA binding greater when nerve fibers experience frequent depolarizations compared to less frequent ones?

A

Frequent depolarizations increase the proportion of Na channels in open or inactivated states.

These states are more susceptible to LA binding.

↑depolarization rates enhance LA efficacy.

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42
Q

What channels and receptors can LA bind and inhibit?

A

Ca++
K+
transient receptor potential vanilloid-1 (TRPV1)
+many other channels and receptors.

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43
Q

tricyclic antidepressants (amitriptyline), meperidine, volatile anesthetics, Ca channel blockers, α2-receptor agonists, and nerve toxins may also inhibit

A

Na channels

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44
Q

Factors that influence the sensitivity of nerve fibers to inhibition by local anesthetics

A

axonal diameter
myelination
and other factors

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45
Q

Which type of nerve fibers are less sensitive to LA: Aα or Aδ fibers?

A

Larger, faster-conducting Aα fibers are less sensitive to local anesthetics than smaller, slower-conducting Aδ fibers.

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46
Q

(T/F) Larger unmyelinated fibers are less sensitive than smaller unmyelinated fibers.

A

TRUE
smaller diameter = ↑sensitivity and ↓conduction velocity

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47
Q

(T/F) Small unmyelinated C fibers are sensitive to LA

A

FALSE
small unmyelinated C fibers are relatively resistant
to inhibition by LA compared to larger myelinated fibers.

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48
Q

What happens at steady state if sensory anesthesia is present?

A

all modalities are inhibited

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49
Q

Typical sequence of LA inhibition in a human peripheral nerve

A

autonomic before sensory before motor.

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50
Q

two main components of LAs

A

lipophilic group (usually an aromatic benzene ring) and a hydrophilic group (usually a tertiary amine) separated by an intermediate chain.

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51
Q

How are LAs classified based on the nature of the intermediate chain?

A

classified as either esters or amides based on the nature of the intermediate chain.

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52
Q

What charge do LAs carry at physiological pH?

A

LAs are weak bases and usually carry a positive charge at the tertiary amine group under physiological conditions.

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53
Q

(T/F) Articaine has a benzene ring

A

FALSE

Articaine has a thiophene ring

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54
Q

The physicochemical properties of LAs depend on

A

substitutions in the aromatic ring
the type of linkage in the intermediate chain
the alkyl groups attached to the amine nitrogen

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55
Q

factors that correlate with clinical LA potency

A

octanol solubility
ability to permeate lipid membranes.

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56
Q

factors that affect the minimum concentration of LA needed to block nerve impulse conduction

A

Fiber size, type, and myelination
pH (an acidic environment antagonizes clinical nerve block)
Frequency of nerve stimulation
Electrolyte concentrations (hypokalemia and hypercalcemia antagonize blockade)

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57
Q

which is more potent due to larger alkyl group: bupivacaine or mepivacaine

A

bupivacaine

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58
Q

Does the onset of action directly correlate with the pKa of local anesthetics?

A

No, onset of action doesn’t directly correlate with the pKa of LA

For example, 2-chloroprocaine has the greatest pKa but has most rapid onset

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59
Q

How does the presence of epinephrine affect LA solutions?

A

Commercially formulated LA solutions w/epi are more acidic (pH 4–5) due to epi’s instability in alkaline environments.
Acidity may result in a lower fraction of free base and a slower onset compared to plain solutions w/out epi

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60
Q

An example of a LA that does not exist in a charged form.

A

benzocaine

61
Q

infected tissues effect on LAs

A

pH in infected tissue is more acidic, so LAs will be more in IONIZED form have a slower onset of action

62
Q

What substance is commonly used for alkalinization n LA?

A

Sodium bicarbonate (8.4% solution) is often added to local anesthetic solutions to achieve alkalinization.

63
Q

recommended ratio of sodium bicarbonate to LA

A

1 mL of 8.4% sodium bicarbonate is added per 10 mL of LA

64
Q

Besides improving onset and quality, what additional benefit does alkalinization of LAs offer during subcutaneous infiltration?

A

alkalinization also decreases pain during subcutaneous infiltration procedures

65
Q

proteins that primarily bind local anesthetics in the blood

A

mostly by α1-acid glycoprotein
to a lesser extent, by albumin.

66
Q

Which local anesthetics display some selectivity for sensory nerves?

A

Bupivacaine and ropivacaine

exhibit some selectivity, especially during the onset and offset of block, for sensory nerves.

However, the conc req. for anesthesia often result in some motor blockade.

67
Q

How does absorption after topical application vary based on the site?

A

Most mucous membranes (such as tracheal or oropharyngeal mucosa) provide a min. barrier to LA penetration, resulting in a rapid onset of action.

intact skin req. topical application of an increased conc. of lipid-soluble LA to ensure permeation and analgesia.

68
Q

This is formulated to overcome the obstacles presented by intact skin.

A

EMLA cream

*A mixture of lidocaine and prilocaine bases in an emulsion

69
Q

Systemic absorption of injected LAs depends on blood
flow, which is determined by

A

Site of injection
Presence of additives
Local anesthetic agent

70
Q

Distribution depends on organ uptake, which is determined by

A

Tissue perfusion
Tissue/blood partition coefficient
Tissue mass

71
Q

The addition of epinephrine causes vasoconstriction at the injection site, resulting in

A

Reduced peak local anesthetic concentration in blood
Facilitated neuronal uptake
Enhanced quality of analgesia
Prolonged duration of analgesia
Reduced toxic side effects

72
Q

(T/F) Vasoconstrictors have more pronounced effects on shorter-acting agents than on longer-acting ones.

A

TRUE

*adding epinephrine to lidocaine (short-acting) extends anesthesia duration significantly, but its effect on bupivacaine (long-acting) peripheral nerve blocks is limited

73
Q

How can dexamethasone or other steroids affect local anesthetic blocks?

A

Coadministration of dexamethasone or other steroids with LAs can prolong blocks by up to 50%.

74
Q

(More/Less) lipid-soluble LAs that are highly tissue bound are more slowly absorbed than less lipid-soluble agents

A

More

75
Q

factors that influence the distribution of LAs in the body

A

tissue perfusion
tissue/blood partition coefficient
and tissue mass.

76
Q

Which organs play a crucial role in the initial rapid removal of local anesthetics from the blood?

A

Highly perfused organs –>brain, lung, liver, kidney, and heart

77
Q

What happens after the initial rapid removal of local anesthetics from the blood?

A

a slower redistribution of local anesthetics to a wider range of tissues

78
Q

Why are patients with right-to-left cardiac shunts more susceptible to toxic side effects of lidocaine?

A

because the lung extracts significant amounts of LA during the “first pass,” leading to ↑exposure and potential toxicity.

79
Q

How does increasing lipid solubility affect the distribution of LA?

A

Greater lipid solubility is associated with ↑plasma protein binding and enhanced tissue uptake of LA from an aqueous compartment.

80
Q

Which tissue provides the largest reservoir for local anesthetic distribution in the bloodstream?

A

Muscle

*because of its large mass

81
Q

Ester local anesthetics are predominantly metabolized by

A

pseudocholinesterase (aka butyrylcholinesterase)

82
Q

Ester hydrolysis is rapid, and the water-soluble metabolites are excreted in

A

the urine

83
Q

Are patients with genetically deficient pseudocholinesterase at increased risk for toxic side effects from ester local anesthetics?

A

Theoretically, yes.
But, clinical evidence for this increased risk is lacking, likely bec alternative metabolic pathways are available in the liver.

84
Q

How does cocaine differ in terms of metabolism compared to other ester anesthetics?

A

Cocaine is primarily metabolized via ester hydrolysis in the liver

85
Q

What enzymes are involved in the metabolism of amide LAs?

A

by microsomal P-450 enzymes in the liver

86
Q

How do decreases in hepatic function or liver blood flow affect amide metabolism? (e.g., due to cirrhosis, congestive heart failure, β-blockers, or H2-receptor blockers)

A

can reduce the rate of amide metabolism

may lead to ↑blood conc. and an ↑risk of systemic toxicity

87
Q

only local anesthetic that is metabolized to o-toluidine

A

Prilocaine
*produces o-toluidine as a metabolite

88
Q

The production of o-toluidine by prilocaine can result in

A

methemoglobinemia
*in a dose-dependent manner.

89
Q

(T/F) Classical teaching suggested that a defined dose of prilocaine (around 20 mg/kg) must be exceeded to produce significant methemoglobinemia

A

FALSE

dose is around 10mg/kg

90
Q

Recent studies have demonstrated that younger, healthier patients can develop medically important methemoglobinemia even after ___ doses of prilocaine (compared to older, sicker patients).

A

lower

91
Q

What other LA ingredient (besides o-toluidine) can also cause dangerous levels of methemoglobinemia?

A

Benzocaine
*common ingredient in topical local anesthetic sprays

92
Q

Treatment of medically important methemoglobinemia includes

A

intravenous methylene blue (1–2 mg/kg of a 1% solution over 5 min)

**Methylene blue reduces methemoglobin (Fe3+) to hemoglobin (Fe2+)

93
Q

Why can increased circulating concentrations of LAs lead to systemic toxicity?

A

because voltage-gated Na channels, which regulate action potentials in neurons and impulse generation in heart, are affected

94
Q

(T/F) Mixtures of local anesthetics have additive toxic effects

A

TRUE

*injecting a solution combining 50% of a toxic dose of lidocaine and 50% of a toxic dose of bupivacaine is likely to produce toxic effects

95
Q

Why are tables of “maximum safe doses” considered nearly nonsensical?

A

The maximum safe dose of LAs depends on various factors:

including the patient, the specific nerve block, the rate of injection, and other individual considerations.

Therefore, fixed tables of maximal safe doses are not practical

96
Q

Local anesthetic systemic toxicity (LAST) refers to the adverse effects of

A

LAs affecting the CNS

** The CNS is particularly vulnerable to these toxic effects

97
Q

Premonitory signs and symptoms of increasing LA conc. in awake patients?

A

Circumoral numbness
Tongue paresthesia
Dizziness
Tinnitus
Blurred vision
A feeling of impending doom

98
Q

Signs that indicate increasing LA conc. in awake patients

A

Restlessness
Agitation
Nervousness
Garrulousness

99
Q

What typically precedes tonic–clonic seizures in cases of LA toxicity?

A

Muscle twitching
*often occurs before tonic–clonic seizures

100
Q

How does the conc. of LAs relate to the risk of seizures?

A

Potent and highly lipid-soluble LAs can produce seizures at lower blood conc. compared to less potent agents

101
Q

Benzodiazepines, propofol, and hyperventilation can (raise/lower) the seizure threshold

A

Raise

*Propofol (0.5–2 mg/kg) quickly and reliably terminates
seizure activity (as do comparable doses of benzodiazepines or
barbiturates)

102
Q

Both respiratory and metabolic acidosis (raise/lower) the seizure threshold.

A

Lower

103
Q

intravenous ____ to terminate local anesthetic-induced seizures

A

lipid

104
Q

What is most important in managing LA toxicity?

A

Maintaining a clear airway with
adequate ventilation and oxygenation

105
Q

______ infusions are used to inhibit ventricular arrhythmias

A

Lidocaine

106
Q

Actions of infused LAs?

A

can inhibit ventricular arrhythmias
decrease cerebral blood flow
attenuate the rise in intracranial pressure during intubation for pt’s with decreased intracranial compliance

107
Q

(T/F) Infusions of lidocaine and procaine have been used to supplement general anesthetic techniques, as they are capable of reducing the MAC of volatile anesthetics by up to 60%.

A

FALSE
40%

108
Q

What additional benefits do lidocaine infusions offer?

A

inhibit inflammation and reduce postoperative pain

decrease postoperative opioid requirements, leading to shorter hospital stays after surgery

109
Q

symptoms that indicate an overdose of cocaine

A

restlessness
emesis (vomiting)
tremors
convulsions
arrhythmias
respiratory failure
and cardiac arrest.

110
Q

What complications were associated with unintentional injection of chloroprocaine into the subarachnoid space during epidural anesthesia?

A

total spinal anesthesia
marked hypotension
and prolonged neurological deficits

111
Q

The neural toxicity associated with chloroprocaine may be due to a combination of its low pH and the presence of a preservative

A

sodium bisulfite

*Chloroprocaine is available in a preservative (bisulfite)-free formulation that has been used safely and possibly proves that the compound itself has minimal direct neurotoxicity

112
Q

Administration of this LA in continuous spinal anesthesia has been associated with cauda equina syndrome

A

5% lidocaine

*possibly due to pooling of drug around cauda equina

113
Q

(T/F) Lidocaine depresses the ventilatory response to low PaO2 (hypoxic drive)

A

True

114
Q

apnea after administration of a “high” spinal or epidural anesthetic is nearly always the result of

A

hypotension and brain
ischemia rather than phrenic block.

115
Q

What effect does intravenous lidocaine have on reflex bronchoconstriction associated with intubation?

A

Intravenous lidocaine (1.5 mg/kg) may block the reflex bronchoconstriction sometimes associated with intubation.

116
Q

tachycardia and hypertension can occur with LA concentrations that produce CNS excitation or from

A

injection or absorption of epinephrine (often combined with local anesthetics)

117
Q

How do local anesthetics affect myocardial contractility and conduction velocity?

A

depress myocardial contractility and conduction velocity at higher blood concentrations

118
Q

What causes the depression of myocardial automaticity (spontaneous phase IV depolarization)?

A

direct actions on the cardiac muscle membrane, through inhibition of cardiac Na channels
In intact organisms, it can also occur due to inhibition of the autonomic nervous system.

119
Q

At low concentrations, all local anesthetics inhibit ________ leading to vasoconstriction

A

nitric oxide

120
Q

At higher concentrations, LAs (except cocaine) produce

A

smooth muscle relaxation and arterial vasodilation, including arteriolar vasodilation

121
Q

T/F Major cardiovascular toxicity usually requires about twice
times the LA conc in blood as that required to produce
seizures

A

FALSE
requires THREE times the LA conc

122
Q

How is the HTN associated with laryngoscopy and intubation often attenuated?

A

can be mitigated by intravenous administration of lidocaine (at a dose of 1.5 mg/kg) 1–3 minutes prior to instrumentation.

123
Q

usual presenting signs of cardiac local anesthetic systemic toxicity (LAST) during general anesthesia

A

Cardiac arrhythmias or circulatory collapse

124
Q

Overdoses of lidocaine can lead to marked

A

left ventricular contractile dysfunction

125
Q

What severe cardiovascular complications can result from unintended intravascular injection of bupivacaine during regional anesthesia?

A

severe cardiovascular LAST (local anesthetic systemic toxicity) including:

left ventricular depression, atrioventricular heart block, and life-threatening arrhythmias such as ventricular tachycardia and fibrillation.

126
Q

What are some predisposing risk factors for bupivacaine-induced toxicity?

A

pregnancy, hypoxemia, and respiratory acidosis.
Young children may also be at increased risk

127
Q

How does bupivacaine compare to lidocaine in terms of changes in conduction and arrhythmia risk?

A

bupivacaine is associated with more pronounced changes in conduction and a greater risk of arrhythmias than comparable doses of lidocaine.

128
Q

What is the difference between the R(+) and S(–) optical isomers of bupivacaine?

A

The R(+) optical isomer of bupivacaine blocks more avidly and dissociates more slowly from cardiac sodium channels than the S(–) optical isomer (levobupivacaine or ropivacaine).

129
Q

Is bupivacaine-induced cardiac toxicity be challenging to manage?

A

Yes. Its difficult and resistant to standard resuscitation drugs

130
Q

alternative treatment for bupivacaine-intoxicated patients who do not respond to standard therapy

A

bolus administration of nutritional lipid emulsions at 1.5 mL/kg

*Lipid emulsions are advocated as a first-line treatment for cardiovascular LAST

131
Q

How does ropivacaine compare to bupivacaine in terms of motor block and therapeutic index?

A

Ropivacaine produces less motor block when injected at the same volume and conc as bupivacaine.
appears to have a greater therapeutic index than racemic bupivacaine, likely reflecting its formulation as a pure S(–) enantiomer.

132
Q

How are cocaine’s cardiovascular reactions different from other local anesthetics?

A

unlike those of any other local anesthetic

Inhibits the normal reuptake of norepinephrine by adrenergic nerve terminals, thereby potentiating the effects of adrenergic stimulation.

133
Q

cardiovascular responses are associated with cocaine

A

hypertension and ventricular ectopy

134
Q

initial treatment for systemic cocaine toxicity

A

benzos to reduce central stimulation

135
Q

use of cocaine when applied topically

A

produces vasoconstriction when applied topically
useful agent to reduce pain and bleeding related to nasal intubation in awake patients

136
Q

cocaine-induced arrhythmias treatment

A

with α-adrenergic antagonists and amiodarone

137
Q

Commercial multidose preparations of amides often contain methylparaben, which has a chemical structure vaguely similar to that of

A

PABA

*speculation on whether this preservative may be responsible for most of the apparent allergic responses to amide agents due to its similarity to PABA

138
Q

Local anesthetics are mildly _____ when directly injected into skeletal muscle, either intentionally (e.g., trigger-point injection treatment of myofascial pain) or unintentionally.

A

myotoxic

139
Q

What is the usual regeneration time after injection-induced myotoxicity?

A

Regeneration usually occurs within 4 weeks after the injection

140
Q

Compounding the local anesthetic with steroid or epinephrine (worsens/improves) myonecrosis.

A

worsens

141
Q

When infused into joints for prolonged periods, local anesthetics can produce severe

A

chondromalacia

142
Q

How does lidocaine affect normal blood coagulation?

A

mildly depresses normal blood coagulation, leading to reduced thrombosis and decreased platelet aggregation.

143
Q

What effect do α2-adrenergic agonists (e.g., clonidine) have on LA analgesia?

A

α2-adrenergic agonists potentiate LA analgesia produced after epidural or peripheral nerve block injections

144
Q

What is the role of pseudocholinesterase in the metabolism of succinylcholine and ester LAs?

A

Both depend on pseudocholinesterase for metabolism.

However, no evidence that the potential competition between ester local anesthetics and succinylcholine for the enzyme has any clinical significance

145
Q

How might epidural chloroprocaine interfere with neuraxial morphine’s analgesic actions?

A

may interfere with the analgesic actions of neuraxial morphine, particularly after cesarean delivery

146
Q

How do opioids affect analgesia produced by epidural and spinal local anesthetics?

A

Opioids potentiate the analgesia produced by epidural and spinal local anesthetics

147
Q

Which drugs decrease hepatic blood flow and affect amide local anesthetic clearance?

A

H2-receptor blockers and β-blockers decrease amide local anesthetic clearance by reducing hepatic blood flow

148
Q

What can prolong the metabolism of ester local anesthetics?

A

Pseudocholinesterase inhibitors (e.g., organophosphate poisons) can prolong the metabolism of ester local anesthetics

149
Q

How does dibucaine relate to genetically abnormal pseudocholinesterases?

A

Dibucaine (an amide local anesthetic) inhibits pseudocholinesterase.

The extent of inhibition by dibucaine defines one form of genetically abnormal pseudocholinesterases.

Gen Principles Exam 3 (2 decks)

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