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BASIC EXAM Part I | Question Bank > PHARMACOLOGY | Local Anesthetics > Flashcards

PHARMACOLOGY | Local Anesthetics Flashcards

1
Q

The Na-K-ATPase pump pumps _____ in and _____ out

A. 2 K in and 2 Na out

B. 2 K in and 3 Na out

C. 2 Na in and 3 K out

A

B. 2 K in and 3 Na out

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2
Q

The key target of local anesthetics is:

A. voltage-gated sodium channel

B. voltage-gated calcium channel

C. voltage-gated potassium channel

A
  • voltage-gated sodium channel
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3
Q

The binding is intracellular and is mediated by what interaction?

A. Lipophilic interactions

B. Hydrophobic interactions

C. Hydrophilic interactions

A
  • Hydrophobic interactions
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4
Q

What mechanism keeps cell membranes at a resting potential?

A. Na-K-ATPase pump

B. Voltage-gated calcium pump

C. Voltage-gated potassium pump

A
  • Na-K-ATPase pump
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5
Q

Individual nerve fibers within each fascicle are surrounded by this layer which is a LOOSE connective tissue containing GLIAL cells, fibroblasts, and blood capillaries:

A. Endoneurium

B. Epineurium

C. Perineurium

A
  • Endoneurium
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6
Q

A dense layer of collagenous connective tissue called that surrounds EACH FASCICLE:

A. Endoneurium

B. Epineurium

C. Perineurium

A

Perineurium

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7
Q

Encases GROUPS OF FASCICLE into a cylindrical sheath:

A. Endoneurium

B. Epineurium

C. Perineurium

A

Epineurium

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8
Q

True or false:

Myelin sheaths shield nerve fibers from local anesthetics, thus making them less sensitive to local anesthetics?

A

FALSE

Local anesthetics bind at the nodes between myelin segments, making myelinated fibers MORE sensitive to Local Anesthetics

  • Myelin improves the electrical insulation of nerve fibers and permits more rapid impulse transmission via SALTATORY CONDUCTION
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9
Q

Sequence blockade of nerve fibers in the differential block:

A. B fibers > C fibers > A fibers

B. C fibers > B fibers > A fibers

C. A fibers > C fibers > B fibers

A

A. B fibers > C fibers > A fibers

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10
Q

C FIBERS are small-diameter nonmyelinated which are primarily for:

A

Pain, Temperature, and Autonomic functions

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11
Q

What is the basic chemical structure of local anesthetics?

A

1) Benzene ring
2) Link
3) Amine

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12
Q

True or false:

Local anesthetics are weak acids and become uncharged by giving a proton away on the amine part.

A

FALSE

Local anesthetics are weak BASES and become CHARGED by ACCEPTING a proton on the amine part

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13
Q

TRUE or FALSE

The resting membrane potential, approximately −70 to −90 mV in neurons is derived predominantly from a difference in the intracellular and extracellular concentrations of potassium and sodium ions

A

FALSE

The resting membrane potential is -60 to -70 mV

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14
Q

TRUE or FALSE

The spike in membrane potential peaks around +50 mV, at which point the influx of sodium is replaced with an efflux of potassium, causing a reversal of membrane potential, or repolarization.

A

TRUE

+50 mV is the spike to push Na in and push K out => REPOLARIZATION

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15
Q

TRUE of voltage-gated sodium channel EXCEPT:

A. Each voltage-gated sodium channel is a complex made up of one principal α-subunit and one or more auxiliary β- subunits

B. B -subunit is a single-polypeptide transmembrane protein that contains most of the key components of the channel function

C It has four homologous α-helical domains (D1 to D4) that form the channel pore and control ion selectivity, voltage-sensing regions that regulate gating function and inactivation, and phosphorylation sites for modulation by protein kinases

D. A triad of highly hydrophobic amino acids (isoleucine, phenylalanine, and methionine [IFM]) appears to be an important structural determinant of fast activation

A

B . B -subunit is a single-polypeptide transmembrane protein that contains most of the key components of the channel function

The a-subunit contains MOST of the key components of the channel function.

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16
Q

The variant of Voltage-gated Na channel involved in Hyperkalemic periodic paralysis:

A

Voltage-gated Na channel 1.4

Nine isoforms of voltage-gated sodium channels (NaV 1.1 to NaV 1.9)
have been identified; each relates to a unique α-subunit subtype.

NaV 1.4 is expressed in skeletal muscles and primarily affected in Hyperkalemic periodic paralysis

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17
Q

The variant of Voltage-gated Na channel involved in Brugada syndrome, a long QT syndrome.

A

Voltage-gated Na channel 1.5

Nine isoforms of voltage-gated sodium channels (NaV 1.1 to NaV 1.9)
have been identified; each relates to a unique α-subunit subtype.

NaV 1.5 is expressed in cardiac muscles and embryonic neurons. It is primarily affected in Brugada Syndrome

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18
Q

True of the LIPID MEMBRANE bilayer EXCEPT:

A. The natural “local anesthetic” tetrodotoxin (TTX) binds at the external
surface of the sodium channel and actively interact with the clinically used local anesthetics

B. The neutral base (N) is more LIPID SOLUBLE preferentially partitions into the lipophilic membrane interior, and easily passes through the membrane.

C. The charged form (NH+) is more WATER SOLUBLE and binds to the sodium
channel at the negatively charged membrane surface

D. The N form can cause membrane expansion and closure of the sodium
channel.

E. The NH+ form will directly inhibit the sodium channel by binding with a local
anesthetic receptor.

A

A. Tetrodotoxin (TTX) binds at the external
surface of the sodium channel and actively interact with the clinically used local anesthetics.

  • The natural “local anesthetic” tetrodotoxin (TTX) binds at the external surface of the sodium channel and has NO INTERACTION with the clinically used local anesthetics
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19
Q

This THEORY proposes that local anesthetics bind to the open or the inactivated channels more avidly than the resting channels:

A. Modulated-receptor Theory

B. Guarded-receptor Theory

A

Modulated-receptor Theory

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20
Q

Refers to the reduction in the number of sodium channels for a given drug concentration present in the open state at equilibrium.

A

TONIC BLOCKADE

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21
Q

This theory assumes that the intrinsic binding affinity remains essentially CONSTANT regardless of a channel’s conformation:

A. Modulated-receptor Theory

B. Guarded-receptor Theory

A

Guarded-receptor Theory

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22
Q

Which of the following is true of ORDER of BLOCKADE in terms Differential Block:

A. Autonomics > cold sensation > pinprick > proprioception > Motor loss

B. Autonomics > sensory loss to touch > cold sensation > proprioception > Motor loss

C. Motor function > proprioception > sensation to touch/pinprick > followed by the return of sympathetic tone

D. Sympathetic tone > cold sensation > proprioception > pinprick > Motor

A

A. Autonomics(Sympathetics) > cold sensation > pinprick > proprioception > Motor loss

Upon exposure to local anesthetic, the temporality of nerve blockade varies. First, blockade of the autonomic nerve fibers results in increased skin temperature or decreased sensation to cold, followed by sensory loss to touch/pinprick, followed by loss of proprioception. Lastly, a differential spinal blockade results in motor loss.

Regression of blockade as the local anesthetic wears off results in the return of nerve fiber conduction in the reverse order: Motor function, proprioception, sensation to touch/pinprick, followed by the return of sympathetic tone.

23
Q

Which is correct in terms of the order of REGRESSION of blockade as the local anesthetic wears off:

A. Autonomics > cold sensation > pinprick > proprioception > Motor loss

B. Autonomics > sensory loss to touch > cold sensation > proprioception > Motor loss

C. Motor function > proprioception > sensation to touch/pinprick > followed by the return of sympathetic tone

D. Sympathetic tone > cold sensation > proprioception > pinprick > Motor

A

C. Motor function > proprioception > sensation to touch/pinprick > followed by the return of sympathetic tone

  • Regression of blockade as the local anesthetic wears off results in the return of nerve fiber conduction in the reverse order: Motor function, proprioception, sensation to touch/pinprick, followed by the return of sympathetic tone.
24
Q

TRUE of FALSE

Autonomic blockade extends roughly two or more dermatomes above the level of skin analgesia

A

TRUE

25
Q

TRUE or FALSE

Motor blockade extends roughly two or more levels below the level of skin analgesia

A

TRUE

26
Q

SHARP pain

A

myelinated Aδ fibers

27
Q

DULL pain

A

nonmyelinated C fibers

28
Q

Aminoamides are degraded by:

A

Hepatic Carboxylesterases

29
Q

Aminoesters are hydrolyzed by:

A

Plasma cholinesterases

30
Q

TRUE of Local Anesthetic physioproperties except:

A. The cationic form is principally responsible for blockade of sodium channels

B. The tertiary amide on local anesthetics can accept a proton at low affinity; thus, these compounds are classified as WEAK bases

C. The proportion of the lipid-soluble form can be increased by alkalization of local
anesthetic solution and thus accelerate the onset of action

D. Lipid solubility of local anesthetics is conferred by the composition of alkyl substitution on the amide and the benzene groups

E. Para-aminobenzoic acid(PABA), can induce immunologic reactions and are
responsible for the slightly greater incidence of severe allergic reactions
associated with aminoamides.

A

E. Para-aminobenzoic acid(PABA), can induce immunologic reactions and are
responsible for the slightly greater incidence of severe allergic reactions
associated with aminoamides.

PABA is associated with AMINOESTERS.

31
Q

ESTERS

A

Trivia: one ‘i’ ONLY in its name

Chloroprocaine
Prilocaine
Tetracaine (highest LIPID SOLUBILITY among esters)

Etidocaine (highest LIPID SOLUBILITY among amides)

32
Q

Benefits of epinephrine as ADJUVANT in Local Anesthetic:

A

*Prolong BLOCK, increase INTENSITY, Decrease SYSTEMIC ABSORPTION

  1. Prolongation of local anesthetic
    block
  2. Increased intensity of block
  3. Decreased systemic absorption of
    local anesthetic

*antagonizing inherent vasodilating effects of local anesthetics, decreasing systemic absorption and intraneural clearance, and perhaps by redistributing intraneural local anesthetic

33
Q

Coadministration of opioids with central
neuraxial local anesthetics results in synergistic analgesia EXCEPT which local anesthetic:

A. Chloroprocaine
B. Lidocaine
C. Etidocaine
D. Levobupivacaine

A

A. Chloroprocaine

Spinal administration of opioids provides analgesia primarily by attenuating C-fiber nociception and is independent of supraspinal mechanisms. Coadministration of opioids with central neuraxial local anesthetics results in synergistic analgesia. An exception to this analgesic synergy is chloroprocaine, which appears to decrease the effectiveness of opioids coadministered EPIDURALLY.

34
Q

What preservative commonly used for ester and AMIDE local anesthetics is usually responsible for allergies?

A

Methylparaben

Trivia*
AMIDE = Methyparaben
ESTER = PaBa

35
Q

Why does pregnancy predispose one to cardiovascular toxicity from Local Anesthetics?

A

Pregnancy = ↓ plasma cholinesterases and lower plasma proteins

36
Q

Which three drugs are most responsible for cardiac adverse effects when reaching toxic levels systemically?

A

Bupivacaine > Ropivacaine > Lidocaine

37
Q

Which TWO local anesthetic are most often the culprits of methemoglobinemia?

A

Prilocaine
Benzocaine

38
Q

The variant of Voltage-gated Na channel involved in the cardiac manifestation of LAST?

A

Voltage-gated Na channel 1.5

It is widely accepted that local
anesthetics bind and disrupt the normal function of the heart-specific voltagegated
sodium channel, NaV 1.5, in cardiac myocytes; however, there may be
other intracellular targets as well.

39
Q

The following are risk factors in developing LAST except?

A. Male
B. Extremes of age
C. Use of local anesthetics in a Non-hospital setting
D. CNS disease
E. Diabetes Mellitus

A

A. Male

40
Q

The most common and highest incidence of CNS symptoms in LAST?

A. Tinnitus
B. Seizure
C. Loss of consciousness
D. Peri-oral numbess

A

B Seizure

41
Q

The plasma concentration level of LIDOCAINE that corresponds to ANALGESIA?

A

5mg/dL

42
Q

Which of the following plasma concentration level of LIDOCAINE corresponds to Seizure?

A. < 5mg/dL
B. > 25mg/dL
C. 10-15 mg/dL
D. 5-10mg/dL

A

C .10-15 mg/dL

43
Q

Which of the following plasma concentration level of LIDOCAINE corresponds to numbness of the tongue or perioral numbness?

A. < 5mg/dL
B. 5-10 mg/dL
C. > 15 mg/dL
D. > 25 mg/dL

A

B. 5-10 mg/dL

44
Q

The following are true of α2-Adrenergic Agonists as adjuvant to local anesthetics except:

A. CLONIDINE produce analgesia via supraspinal and spinal adrenergic receptors

B. It has direct INHIBITORY effects on peripheral nerve conduction (A and C nerve fibers)

C. On average, clonidine improves the duration of analgesia by about 6 hours

D. Synergy with local anesthetics is expected

A

C On average, clonidine improves the duration of analgesia by 6 hours - This is a wrong statement.

Clinically, the average duration of analgesia when used with LA is 2 hours.

45
Q

Which of the following is least Cardiotoxic?

A. Lidocaine
B. Bupivacaine
C. Levobupivacaine
D. Chloroprocaine

A

D. Chloroprocaine

46
Q

What is the only local anesthetic that causes vasoconstriction?

A

cocaine

47
Q

The maximum dose of LIDOCAINE in tumescent technique is:

A

55mg/kg

48
Q

The recommended or safest dose of LIDOCAINE in tumescent technique is:

A

35mg/kg

49
Q

What is the first step in management of LAST?

A. Airway
B. Get Help
C. Administer 20% Lipid Emulsion
D. Administer Midazolam 0.1mg/kg

A

B. Get Help

50
Q

How does lidocaine affect EKG?

A

Prolongation of PR interval and QRS widening

*This is due to Na blockade

51
Q

Bolus dose of Lipid Emulsion based on the ASRA 2017 guideline?

A

Bolus over 2–3 min 100 mL for patients over 70 kg or 12 mL/kg for less than 70 kg

52
Q

Maintenance dose of Lipid Emulsion based on the ASRA 2017 guideline?

A

infusion over 15–20 min 200–250 mL for patients over 70 kg or 0.25 mL/kg/min for patients less than 70 kg

53
Q

Ceiling dose of Lipid Emulsion?

A

Recommend 12 mL/kg lipid emulsion as the upper limit for initial dosing

54
Q

The following are medications are avoided in the treatment course of LAST except:

A. Vasopressin
B. Calcium channel blockers
C. Beta blockers
D. Depolarizing NMB agent

A

D. Depolarizing NMB agent

  • Seizure management of LAST includes benzodiazepines and consider small dose of succinylcholine for intractable seizures to minimize acidosis and hypoxemia.

BASIC EXAM Part I | Question Bank (30 decks)

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