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LA > Chapter 5 - Dental LA Drugs > Flashcards

Chapter 5 - Dental LA Drugs Flashcards

1
Q

Drug concentrations are expressed as ______________ that refer to [mass] of a drug in [volume] solution

A

Drug concentrations are expressed as PERCENTAGES that refer to the NUMBER OF GRAMS of a drug in 100 MILLILITERS of solution.
E.g.: 2 % = 2g /100mL
2% = 2,000mg/100mL
2% = 200mg/10mL
2% = 20mg/1mL

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2
Q

Articaine metabolism

A

Unique b/c
-majority by rapid plasma cholinesterase metabolism and
-only 5-10% by hepatic p450 enzymes
=> rapid 1/2-life
=» rapid? Repeat? dosing safer
=»> in case of adverse toxic reactions, they generally resolve fast

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3
Q

Onset lidocaine versus articaine

A

 Despite having a slightly higher pKa articaine 7.8 vs lidocaine 7.7) i.e. having slightly fewer neutral base molecules available initially, articaine is more lipophilic and its base molecules have a higher affinity for nerve membranesand therefore has a faster onset than lidocaine

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4
Q

Relative toxicity of Prilocaine

A

~ 1/2 of Lidocaine due to multiple extra-hepatic metabolic pathways
(much of prilocaine is cleared before it reaches the liver)
(lungs and kidneys are alternate sites when liver is not utilized)

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5
Q

LA w/ epinephrine 1:200,000 (uses and preparations)

A

Can be beneficial when it is useful to limit vasoconstrictor doses, e.g. w/
-Significant cardiovascular compromise
-Tricyclic antidepressant use
-Insulin resistant diabetes with underlying cardiovascular disease

-4% articaine w/ epi 1:200,000
(Septocaine w/ epi 1:200,000)

-0.5% bupivacaine w/ epi 1:200,000
(Marcaine 0.5% w/ epi 1:200,000)

-4% prilocaine w/ epi 1:200,000
(4% Citanest Forte w/ epi 1:200,000)

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6
Q

LA without vasoconstrictors

A

(2% lidocaine plain - not avail. in U.S.)

3% mepivacaine plain (Polocaine)

4% prilocaine plain (Citamest Plain)

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7
Q

Why can 0.5% bupivacaine have less vasoconstrictor?

A

Bupivacaine is 2nd highest in vasodilation (after procaine, I. e. highest of all amides), but it can have 1:200,000 epi because of its strong receptorbinding

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8
Q

Bupivacaine’s risk factors for overdose

A
  1. Lengthy 1/2-life: 2.6 hours (162 min)
  2. Early CVS involvement
    => slows removal of bupivacaine from circulation => ODs are more severe => not easily reversed => prolonged OD
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9
Q
  1. The definition of the MRD of a drug best fits which ONE of the following definitions?
    a. A safe dose to administer in all situations
    b. A dose that a 150-lbs individual can have
    c. A dose that cannot be exceeded under any circumstance.
    d. A safe guideline when administering local anesthetic drugs.
A

d - the MRD of a drug is an ESTABLISHED SAFE GUIDELINE for adminstration

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10
Q
  1. Which ONE of the following best describes articaine’s metabolism?
    a. Articaine is metabolized approx. 25% in the liver.
    b. Articaine is metabolized primarily via plasma cholinesterase.
    c. Much of articaine is excreted unchanged.
    d. Articaine’s metabolism is similar to prilocaine’s.
A

b- Articaine is primarily metabolized via plasma cholinesterase.
- metabolized only 5%-10% in the liver
- very little is excreted unchanged
- its metabolism is not similar to prilocaine’s.

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11
Q
  1. Patient with significant CV compromise and significant liver damage. Which one of the following LADs would be most appropriate for this pt when anesthetizing the maxillary right quadrant?
    a. 2% mepivacaine, 1:20,000 levonordefrin
    b. 3% mepivacaine plain
    c. 4% articaine, 1:200,00 epinephrine
    d. 0.5% bupivacaine, 1:200,00 epinephrine
A

C - 4% articaine, 1:200,000
- addresses both significant CVS and hepatic compromise
- other 3 are metabolized in liver, incl. 3% mepivacaine, which other would be an excellent choice in CVS compromise
- at 1:200,00 epi, articaine is best overall selection

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12
Q
  1. Periodontist requires hemostasis on palatal tissues in UL quad before elevating a surgical flap. Which of the following drugs would furnish the most vigorous hemostasis?
    a.2% mepivacaine, 1:20,000 levonordefrin
    b. 4% prilocaine, 1:200,000 epi
    c. 2% lidocaine, 1:50,000 epi
    d. 4% articaine, 1:100,000 epi
A

c. 2% lidocaine, 1:50,000 epi
- LADs are irrelevant to hemostasis
- epinephrine provides most hemostasis
- 1:50,000 has highest conc. of epi

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13
Q
  1. which characteristic of a LAD determines how well it works without a vasoconstrictor?
    a. Potency
    b. Vasoactivity
    c. pKA
    d. Lipophilic ability
A

b. Vasoactivity
- weak vasodilators will remain in area of deposition longer
- vigorous vasodilators enhance their own systemic uptake => must have vasoconstrictor

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14
Q
  1. If a patient is taking a tricyclic antidepressant and beta-blocker, which ONE of the following would be most appropriate?
    a. 2% lidocaine, 1:100,000 epi
    b. 2% mepivacaine, 1:20,000 levonordefrin
    c. 3% mepivacaine plain
    d. 4% articaine, 1:200,000 epi
A

c. 3% mepivacaine PLAIN
- levonordefrin is safer than epi with beta-blockers, BUT:
- tricyclic antidepressants require care with vasoconstrictors, ESPECIALLY levonordefrin ((risk of serious elevations in BP)

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15
Q
  1. Methemoglobinemia is a life-threating condition that may be precipitated by which ONE of the following drugs?
    a. Lidocaine
    b. Mepivacaine
    c. Prilocaine
    d. Bupivacaine
A

C - Prilocaine

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16
Q
  1. Arrange the injectable LADs in descending order of overall CNS and CVS toxicity.
    a. Bupivacaine, mepivacaine, lidocaine, prilocaine, articaine
    b. Bupivacaine, mepivacaine, lidocaine, articaine, prilocaine
    c. Bupivacaine, mepivacaine, articaine, lidocaine, prilocaine
    d. Bupivacaine, lidocaine, mepivacaine, articaine, prilocaine
A

B - Bupivacaine, mepivacaine, lidocaine, articaine, prilocaine
- considering overall toxicity to CNS & CVS, prilocaine is the least toxic (7x less than bupivacaine)
- articaine < toxic than lidocaine
- mepivacaine overall more toxic than lidocaine (although not thought to be in doses used in dental)

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17
Q

Q5-1: When was the first amide local anesthetic drug, lidocaine, developed by Lofgren?

A

A5-1: Lidocaine was the first amide local anesthetic drug developed by Lofgren in 1943.

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18
Q

Q5-2: What are the three formulations of lidocaine available for use in dentistry?

A

A5-2: Lidocaine is provided in the following formulations:
2% lidocaine plain (without vasoconstrictor)
2% lidocaine with 1:100,000 epinephrine
2% lidocaine with 1:50,000 epinephrine

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19
Q

Q5-3: What is the duration of anesthetic action for each of the formulations of lidocaine used in dentistry?

A

A5-3:
- 2% lidocaine plain: Very short duration = 5–10 minutes pulpal; 60–120 minutes soft tissue

  • 2% lidocaine with 1:100,000 epinephrine: Intermediate duration = 60 minutes pulpal; 180–300 minutes soft tissue
  • 2% lidocaine with 1:50,000 epinephrine:
    Intermediate duration = 60 minutes pulpal; 180–300 minutes soft tissue
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20
Q

Q5-4: What are key considerations in duration of action for local anesthetics?

A

A5-4: The receptor binding strength of a local anesthetic and its vasoactivity are key considerations in duration of action.

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21
Q

Q5-5: Using Table 5-1 in the text, give examples of short, intermediate, and long durations of action for local anesthetic drugs.

A

Table 5-1: Local Anesthetic Duration Comparisons

DRUG CLASSIFICATION (DURATION)
Articaine Intermediate
Bupivacaine Long
Lidocaine Short (without vasoconstrictor)
Intermediate
Mepivacaine Short (without vasoconstrictor)
Intermediate
Prilocaine Short (infiltrations, no vasoconstrictor)
Intermediate
Procaine Short

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22
Q

Q5-6: What is the maximum recommended dose (MRD) of lidocaine per appointment?

A

A5-6: 3.2 mg/lb (7.0 mg/kg); 500 mg absolute maximum .

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23
Q

Q5-7: Describe the relative potency of lidocaine in relation to other local anesthetic drugs used in dentistry.

A

A5-7: Lidocaine is twice as potent as its predecessor procaine, equal in potency to mepivacaine and prilocaine, approximately two-thirds as potent at articaine, and approximately one-fourth as potent as bupivacaine.

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24
Q

Q5-8: Describe the relative toxicity of lidocaine in relation to other local anesthetic drugs used in dentistry.

A

A5-8: Lidocaine is approximately twice as toxic as procaine and prilocaine, similar in toxicity to mepivacaine and articaine, and far less toxic (approximately one-fourth as toxic) as bupivacaine.

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25
Q

Q5-9: How is lidocaine metabolized?

A

A5-9: Lidocaine is metabolized by hepatic enzymes, oxidases, and amidases. This process is complex and involves multiple steps. Hydrolysis accounts for about one-third of lidocaine elimination. Several of lidocaine’s byproducts (metabolites) are pharmacologically active.

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26
Q

Q5-10: What percentage of lidocaine is excreted unchanged by the kidneys?

A

A5-10: Less than 10% of lidocaine is excreted unchanged by the kidneys.

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27
Q

Q5-11: Describe the vasoactivity of lidocaine in relation to other local anesthetic drugs used in dentistry.

A

A5-11: Lidocaine is a potent vasodilator with a very short duration when administered without a vasoconstrictor. It is a less potent vasodilator compared to procaine but greater compared to prilocaine and mepivacaine, which limits the use of lidocaine to very short procedures if used without a vasoconstrictor.

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28
Q

Q5-12: What is the pKa of lidocaine?

A

A5-12: The pKa of lidocaine is 7.7.

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29
Q

Q5-13: What is the pH of lidocaine plain solution?

A

A5-13: The pH of lidocaine plain solution is 6.5.

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30
Q

Q5-14: Using Table 5-2 in the text, what is the onset time of lidocaine with epinephrine?

A

A5-14: The onset time of lidocaine with epinephrine is 2–3 minutes.

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31
Q

Q5-15: How long is the elimination half-life of lidocaine?

A

A5-15: The elimination half-life of lidocaine is 1.6 hours (96 minutes).

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32
Q

Q5-16: Discuss the effective use of lidocaine as a topical anesthetic agent.

A

A5-16: Lidocaine is effective as a topical anesthetic. It is available for use in concentrations ranging from 2% to 10% in various ointments, viscous solutions, and mixtures. When used topically, the onset of anesthesia occurs within 1–2 minutes with peak effects available from 2–5 minutes.

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33
Q

Q5-17: What is the FDA Pregnancy Category for lidocaine?

A

A5-17: Lidocaine is in FDA Pregnancy Category B.

34
Q

Q5-18: Using Table 5-4 in the text, summarize the FDA pregnancy rating for dental local anesthetic drugs.

A

Dental LAD FDA Pregnancy Rating
Articaine C
Bupivacaine C
Lidocaine B
Mepivacaine B
Prilocaine C

35
Q

Q5-19: A 30-year old mother, Elena Gagarin, is nursing her infant every 3–4 hours. If lidocaine is injected, will the drug be present in her breast milk after her appointment?

A

A5-19: A small amount of lidocaine will enter the breast milk. Most drugs are available in breast milk once introduced. Product information generally states that caution must be exercised when nursing after lidocaine administration.

36
Q

Q5-20: When was articaine available for use in dentistry in the United States?

A

A5-20: Articaine, synthesized in 1969 by H. Rusching, is the most recently approved injectable local anesthetic drug for use in dentistry in the United States (2000).

37
Q

Q5-21: How does articaine’s classification as an amide differ from that of other amide local anesthetic drugs and why is this difference significant?

A

A5-21: Articaine is classified as an amide; however, it has a distinctly different chemical structure with a thiophene ring and an ester component attached. This unique configuration provides several beneficial pharmacologic behaviors. Unlike other amides, the addition of an ester component promotes more rapid biotransformation. The presence of a sulfur atom within the ring structure makes articaine highly lipophilic, easily passing through neural membranes.

38
Q

Q5-22: What are the two formulations of articaine available for use in dentistry?

A

A5-22: Articaine is provided in the following formulations:
4% articaine with 1:100,000 epinephrine
4% articaine with 1:200,000 epinephrine

39
Q

Q5-23: What is the MRD for articaine?

A

A5-23: 3.2 mg/lb (7 mg/kg); no absolute maximum provided (previously 500 mg absolute maximum).

40
Q

Q5-24: What factor makes the metabolism of articaine unique compared to other amide local anesthetic drugs?

A

A5-24:
- 5–10% is metabolized via hepatic p450 enzymes.
- majority via rapid plasma cholinesterase metabolism to articainic acid, its inactive primary metabolite, before reaching the liver.
- Articaine is further metabolized to articainic acid glucoronide, a minor metabolite, also considered to be pharmacologically inert.

41
Q

Q5-25: What is the onset of action of articaine for nerve block anesthesia?

A

A5-25: The onset of action for articaine in nerve block anesthesia is 2–3 minutes.

42
Q

Q5-26: When, where, and by whom was mepivacaine prepared as an alternative to lidocaine?

A

Mepivacaine was introduced in Sweden in 1957 as an alternative to lidocaine by A. F. Eckenstam.

43
Q

Q5-27: Discuss the vasodilation property of mepivacaine and its relationship to the anticipated length of pulpal anesthesia.

A

A5-27: Mepivacaine is a weak vasodilator and is effective for short durations without a vasoconstrictor. The 3% formulation without vasoconstrictor is capable of providing approximately 20–40 minutes of pulpal anesthesia compared with plain solutions of 2% lidocaine, which provide only 5–10 minutes of pulpal anesthesia.

44
Q

Q5-28: What are the two formulations of mepivacaine available for use in dentistry?

A

A5-28: Mepivacaine is provided in the following formulations:
3% mepivacaine plain (without vasoconstrictor)
2% mepivacaine with 1:20,000 levonordefrin

45
Q

Q5-29: What is the duration of anesthetic action of each formulation of mepivacaine used in dentistry?

A

3% mepivacaine plain
Short = 20–40 min pulpal; 120–180 min soft tissue

2% mepivacaine w/ 1:20,000 levonordefrin
Intermediate = 60min pulpal; 180–300 minutes soft tissue

46
Q

Q5-30: What is the MRD for mepivacaine?

A

A5-30: 3.0 mg/lb (6.6 mg/kg); 400 mg absolute maximum.

47
Q

Q5-31: How is mepivacaine metabolized?

A

A5-31: Mepivacaine is metabolized in the liver; however, the pathways are different compared to lidocaine. Unlike lidocaine, amidase activity is insignificant. Its elimination half-life of 1.9 hours reflects its less efficient metabolic pathway.

48
Q

Q5-32: What is the onset of action for mepivacaine?

A

A5-32: The onset of action for mepivacaine is 1.5–2 minutes.

49
Q

Q5-34: What is the FDA Pregnancy Category for mepivacaine?

A

A5-34: Mepivacaine is in FDA Pregnancy Category C. Category C suggests that there should be strong rationale for its use prior to administering.

50
Q

Q5-35: When was prilocaine first prepared and approved for use by the FDA?

A

A5-35: Prilocaine was first prepared by Lofgren and Tegner in 1953 and approved by the FDA in 1965.

51
Q

Q5-36: What are the two formulations of prilocaine available for use in dentistry?

A

A5-36: Prilocaine is provided in the following formulations:
4% prilocaine plain (without vasoconstrictor)
4% prilocaine with 1:100,000 epinephrine

52
Q

Q5-37: What is the MRD for prilocaine?

A

A5-37: 4.0 mg/lb (8.8 mg/kg); 600 mg absolute maximum.

53
Q

Q5-38: What is the special relative toxicity consideration with the use of prilocaine?

A

A5-38: Due to prilocaine’s metabolite orthotoluidine (o-toluidine), some individuals are at an increased risk of developing a potentially life-threatening anemia known as methemoglobinemia. Cautions apply when treating patients at risk for methemoglobinemia as well as any patients with oxygenation difficulties, especially those taking medications which are independently capable of inducing methemoglobinemia.

54
Q

Q5-39: How is prilocaine metabolized compared to lidocaine and mepivacaine?

A

A5-39: Prilocaine has a simpler hepatic metabolism compared with lidocaine and mepivacaine. Much of the drug is cleared before it is able to reach the liver. The lungs and kidneys are alternate sites of breakdown when the liver is not utilized.

55
Q

Q5-40: What year was bupivacaine approved by the FDA?

A

A5-40: Bupivacaine was prepared by A. F. Ekenstam in 1957 and approved by the FDA in 1972.

56
Q

Q5-41: Provide clinical indications for the use of bupivacaine in dentistry.

A

A5-41: Bupivacaine has several important clinical indications:
1. For extended postoperative pain control. Bupivacaine can provide up to twelve hours of relief.
2. In situations where profound and durable anesthesia have proven to be difficult, if not impossible, to achieve with all the other available drugs.
3. For extended procedures requiring longer than normal 60–90 minute durations.

57
Q

Q5-42: Discuss an important postoperative consideration when using bupivacaine.

A

A5-42: Self-injury is an important consideration when using bupivacaine, particularly if the individuals are at higher risk of self-inflicted postoperative trauma, such as young children.

58
Q

Q5-43: What formulation of bupivacaine is provided for use in dentistry?

A

A5-43: Bupivacaine is provided in the following formulation:
0.5% bupivacaine with 1:200,000 epinephrine

59
Q

Q5-44: Explain why bupivacaine with a 1:200,000 concentration of epinephrine is capable of producing prolonged anesthesia for up to twelve hours.

A

A5-44: The strength of bupivacaine’s receptor site binding allows lower concentrations of epinephrine to be used.

60
Q

Q5-45: What is the maximum recommended dose (MRD) for bupivacaine in the United States and in Canada?

A

A5-45: In the United States the FDA recommends a 90 mg absolute maximum; no body weight information is provided. In Canada, Health Canada recommends 0.9 mg/lb; 2.0 mg/kg.

61
Q

Q5-46: Why is bupivacaine effective with a dilute 0.5% concentration?

A

A5-46: Bupivacaine is eight times more potent than procaine, four times more potent than lidocaine, mepivacaine, and prilocaine, and nearly three times more potent than articaine.

62
Q

Q5-47: Why is bupivacaine more toxic compared to other anesthetic drugs?

A

A5-47: Bupivacaine is nearly eight times more toxic than procaine, five to six times more toxic than prilocaine, and nearly four times more toxic than lidocaine, mepivacaine, and articaine. Bupivacaine toxicity is nearly equal to both the CNS and CVS. In overdose, two main factors contribute to the increased risk versus other drugs: bupivacaine’s lengthy half-life and early CVS involvement.

63
Q

Q5-48: What is the onset of action for bupivacaine?

A

A5-48: The onset of action for bupivacaine is 6–10 minutes.

64
Q

Q5-49: Explain why it may be advantageous to administer mepivacaine prior to bupivacaine.

A

A5-49: The pKa of bupivacaine is 8.1. Bupivacaine’s higher pKa translates into slower onset times. When the use of bupivacaine is planned, a drug with a more rapid onset such as mepivacaine may be administered initially.

65
Q

Q5-50: Discuss the importance of the introduction of procaine in the early 1900s.

A

A5-50: Procaine was introduced by Alfred Einhorn in the early 1900s as an alternative to cocaine due to the desire to eliminate its addictive tendencies when using it as a local anesthetic drug as well as its systemic toxicity, and the local tissue injury that too often accompanied cocaine’s use.

66
Q

Q5-51: What derivative of procaine is responsible for its relatively high rate of allergenicity?

A

A5-51: Procaine is a derivative of para-aminobenzoic acid (PABA) which is also the metabolite thought to be responsible for procaine’s relatively high rate of allergenicity

67
Q

Q5-52: How is procaine metabolized?

A

A5-52: Procaine is rapidly metabolized via plasma cholinesterase. There are no hepatic pathways for the biotransformation of procaine.

68
Q

Q5-53: Discuss the clinical significance of the high pKa of procaine.

A

A5-53: The pKa of procaine is 9.1; therefore, initially there are fewer base molecules to diffuse through the nerve membrane. Additionally, procaine has poor lipid solubility. The clinical significance is a slow onset of 6–10 minutes.

69
Q

Q5-54: What is the half-life of procaine?

A

A5-54: The elimination half-life of procaine is 6 minutes.

70
Q

Q5-55: Using Table 5-5 in the text, summarize the U.S. Food and Drug Administration’s drug categories in pregnancy.

A

Category A Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities.
Category B Animal studies have revealed no evidence of harm to the fetus; however, there are no adequate and well-controlled studies in pregnant women. Or Animal studies have shown an adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate a risk to the fetus.
Category C Animal studies have shown an adverse effect and there are no adequate and well-controlled studies in pregnant women. Or No animal studies have been conducted and there are no adequate and well-controlled studies in pregnant women.
Category D Studies, adequate, well-controlled, or observational, in pregnant women have demonstrated a risk to the fetus. However, the benefits of therapy may outweigh the potential risk.
Category X Studies, adequate, well-controlled, or observational, in animals or pregnant women have demonstrated positive evidence of fetal abnormalities. The use of the product is contraindicated in women who are or may become pregnant.

71
Q

Gold band on cartridge

A

Articaine HCL 4% w/ epi 1:100,000

72
Q

Blue band on cartridge

A

Bupivacaine 0.5% w/ epi 1:200,000

73
Q

Light blue band on cartridge

A

Lidocaine HCl 2% (w/o epi) (not available in the US)

74
Q

Green band on cartridge

A

Lidocaine HCl 2% w/ eip 1:50,000

75
Q

Red band on cartridge

A

Lidocaine HCl 2% w/ epi 1:100,000

76
Q

Tan band on cartridge

A

Mepivacaine HCl 3%

77
Q

Brown band on cartridge

A

Mepivacaine HCl 2% w/ levonordefrin 1:20, 000

78
Q

Black band on cartridge

A

Prilocaine HCl 4%

79
Q

Yellow band on cartridge

A

Prilocaine HCl 4% w/ epi 1:200,000

80
Q

Silver band on cartridge

A

Articaine HCl 4%w/ epi 1:200,000

81
Q

White band on cartridge

A

Articaine HCl 4% w/ epi 1:400,000 (not available in the US)

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