|
| A) | Opium | ||
| B) | Cocaine | ||
| C) | Menthol | ||
| D) | Novocaine |
Today, cocaine is recognized as a harmful illicit drug, but it was also the predecessor of the current group of local anesthetics used in dentistry. Cocaine is derived from the coca plant (Erythroxylum coca or Erythroxylum novogranatense) native to western South America [1]. Indigenous groups would chew the leaves of the coca plant to elevate mood, aid digestion, and suppress the appetite [2]. In 1859, the chief alkaloid of coca was isolated and named "cocaine."
| A) | ester or amide type. | ||
| B) | short- or long-lasting. | ||
| C) | first or second generation. | ||
| D) | immediate or delayed release. |
The pharmacologic properties of local anesthetics are directly related to their molecular structure. The basic chemical structure of a local anesthetic consists of an aromatic ring (which enhances lipid solubility) and an intermediate ester or an amide chain and a terminal amine [8]. As such, all of these agents are classified as either an ester type or an amide type.
| A) | Ester-type local anesthetics have a slightly greater risk of systemic toxicity. | ||
| B) | The injectable local anesthetics commonly used in dentistry today are all classified as amides. | ||
| C) | The risk of an allergic reaction is significantly lower with ester-type local anesthetics compared with amide-types. | ||
| D) | The ability to obtain profound intraoral anesthesia is facilitated with the use of ester formulations compared with amide formulations. |
Procaine is an ester-type local anesthetic, as is the topical anesthetic benzocaine. However, the injectable local anesthetics commonly used in dentistry today are all classified as amides, including articaine, bupivacaine, lidocaine, mepivacaine, and prilocaine. Although articaine is technically classified as an amide-type local anesthetic, it is the only one that contains a thiophene (sulfur-containing) ring and an additional ester ring [9,46].
Amide-type local anesthetics have the same basic chemical structure of the ester types, but with an intermediate amide group (rather than an ester) and a terminal amine that enhances water solubility. The ability to obtain profound intraoral anesthesia is facilitated with the use of amide formulations compared with ester formulations, and as noted, they are greatly favored in the United States [11]. The risk of an allergic reaction is also significantly lower with amide-type local anesthetics compared with ester-types, but the amide-type has a slightly greater risk of systemic toxicity, usually dose related. The positive attributes of amide-type local anesthetics outweigh the potential for adverse systemic effects.
| A) | facial nerve. | ||
| B) | abducens nerve. | ||
| C) | trigeminal nerve. | ||
| D) | vestibulocochlear nerve. |
Local anesthetics used in dentistry induce a temporary loss of sensation in the various divisions of the maxillary and mandibular branches of the trigeminal nerve (i.e., cranial nerve V). Local anesthetics prevent the generation and propagation of nerve impulses in response to painful stimuli from procedures such as oral or periodontal surgery, restorative dentistry, or endodontic treatment.
| A) | Axon | ||
| B) | Cell body | ||
| C) | Dendrites | ||
| D) | Hypothalamus |
Neurons are the basic structural cell of the nervous system and can be broadly categorized as either primary sensory (afferent) or motor (efferent). Sensory neurons are responsible for the transmission of sensory impulses, including painful stimuli, to the central nervous system (CNS). These neurons have three major components: the dendrites, the axon, and the cell body. The dendrites, also referred to as the peripheral process, are composed of branched terminal endings of the nerve that propagate stimulation received from other cells and conduct an impulse to the CNS. The impulse continues along the axon, a cable-like, myelinated structure that conducts the message to the brain or spinal cord. While an axon may appear to be a continuous, uninterrupted structure, there are small gaps in the myelin sheath at intervals of about 1 mm, known as nodes of Ranvier. The cell body is not involved in the transmission of neural impulses but functions to provide the metabolic needs of the neuron. The terminal endings of the axon form synapses with various nuclei of the CNS for the interpretation of the initial stimulus.
| A) | Vasopressin | ||
| B) | Epinephrine | ||
| C) | Levonordefrin | ||
| D) | Norepinephrine |
Most commonly, the vasoconstrictor epinephrine is added in a 1:100,000 concentration. Concentrations of 1:200,000 and 1:50,000 also exist, though the latter is rarely used due to its strong sympathomimetic (stimulant) cardiovascular effects. Epinephrine in its varied concentrations is used in conjunction with all local anesthetics except mepivacaine, with which a 1:20,000 concentration of levonordefrin is used. Levonordefrin in its 1:20,000 concentration has the approximate pharmacologic potency of 1:100,000 epinephrine [15,46]. Though the 1:100,000 concentration of epinephrine appears to offer no advantage in prolonging anesthesia compared to a 1:200,000 concentration, an improved ability to achieve hemostasis is facilitated with concentrations of 1:100,000 or greater [16].
| A) | a shorter duration. | ||
| B) | impaired ability to achieve hemostasis. | ||
| C) | increased depth and profundity of anesthesia. | ||
| D) | quicker systemic absorption of the local anesthetic. |
Vasoconstrictors stimulate the contraction of the smooth muscle layer in blood vessels, which results in constriction of the blood vessels in the area and decreases the perfusion of blood. This decreased flow of blood to the anesthetized area favors the retention of the local anesthetic for an increased duration, increases the depth and profundity of anesthesia, and delays the systemic absorption of the local anesthetic (thereby decreasing the potential for systemic toxicity). The ability to achieve hemostasis is also facilitated when vasoconstrictors are included in local anesthetic solutions.
| A) | Unstable angina | ||
| B) | Pheochromocytoma | ||
| C) | Untreated or uncontrolled hypertension | ||
| D) | All of the above |
There are relatively few absolute contraindications to the use of epinephrine in local anesthetics. Patients with unstable angina, refractory arrhythmias, untreated or uncontrolled hypertension, or uncontrolled hyperthyroidism should not receive any elective dental treatment until they are medically stabilized. Epinephrine is also contraindicated in patients with pheochromocytoma, a tumor of the medulla of the adrenal gland that results in hypersecretion of endogenous epinephrine, with subsequent elevated blood pressure [19]. Emergency dental procedures for these patients should be performed in a hospital or an outpatient hospital center.
| A) | Procaine | ||
| B) | Articaine | ||
| C) | Lidocaine | ||
| D) | Bupivacaine |
Since its introduction in 1948, lidocaine has become the most commonly used local anesthetic in the United States and remains the "gold standard" to which all other local anesthetics are compared [13]. It is available without epinephrine and with 1:50,000, 1:100,000, and 1:200,000 concentrations of epinephrine. As noted, the formulation with 1:100,000 epinephrine is used most frequently. Lidocaine is available in a 2% formulation in a 1.7-mL cartridge (containing 34 mg lidocaine) or a 1.8-mL cartridge (containing 36 mg lidocaine). The maximum recommended dose (MRD) of 2% lidocaine for adults and children older than 12 years of age is 7 mg per kg of body weight, to a maximum of 300 mg. Children younger than 12 years of age should receive a maximum of 4.5 mg per kg of body weight up to 100–150 mg [14]. The lowest possible dose of 2% lidocaine to provide the anesthesia required should be used, and the MRD should rarely be attained. During full-mouth extractions or full-mouth restorative rehabilitation, it is important to keep an accurate record of the number of cartridges used.
| A) | 1 minute. | ||
| B) | 5 minutes. | ||
| C) | 10 minutes. | ||
| D) | 30 minutes. |
The onset of anesthesia for 2% lidocaine with 1:100,000 epinephrine is about five minutes, with a duration of approximately one hour for pulpal anesthesia and three to five hours for soft tissue anesthesia [46]. Amide-type anesthetics like lidocaine are metabolized by the liver and excreted by the kidneys, so the presence of hepatic and/or renal disease can compromise metabolism. For patients with these conditions, consultation with the patient's physician may be necessary in order to determine the dose of lidocaine that can be metabolized and excreted safely under these conditions. The 2% lidocaine formulation with 1:50,000 epinephrine should not be used for patients with hypertension or cardiovascular disease given the enhanced stimulant effect; a lower epinephrine concentration should be used [21].
| A) | Procaine | ||
| B) | Articaine | ||
| C) | Lidocaine | ||
| D) | Bupivacaine |
The ester side chain also influences the way articaine is metabolized. The other amide local anesthetics are primarily metabolized in the liver. Due to the presence of the ester side chain, approximately 90% to 95% of articaine is metabolized in the plasma by plasma carboxylesterase, with only about 5% to 10% undergoing metabolism by the liver [29]. Because the metabolism of articaine has minimal reliance on hepatic metabolism, it is the anesthetic of choice for patients with compromised liver function, including those with hepatitis C or cirrhosis. Articaine plasma metabolism is much quicker than the hepatic metabolism of other amide-type local anesthetics, resulting in a shorter half-life (20 minutes) compared with lidocaine (90 minutes) [8]. In lengthy dental procedures, when additional doses of a local anesthetic are required, the expedited clearance of articaine minimizes the occurrence of an accumulation of toxic levels of this anesthetic.
| A) | 0.5% formulation with a 1:200,000 concentration of epinephrine. | ||
| B) | 2% formulation with a 1:50,000 concentration of epinephrine. | ||
| C) | 3% formulation without a vasoconstrictor. | ||
| D) | 4% formulation with a 1:100,000 concentration of epinephrine. |
Bupivacaine has been available in cartridge form in the United States since 1983 [13]. Bupivacaine is an analogue of mepivacaine, another amide-type of local anesthetic, but with a fourfold increase in potency and toxicity [21]. Bupivacaine is only available in a 0.5% formulation with a 1:200,000 concentration of epinephrine. Bupivacaine binds strongly to sodium channel proteins, which causes a protracted closing of these channels and prevents initiation and propagation of nerve impulse for an extended time, resulting in a prolonged anesthetic effect [35]. It takes 6 to 10 minutes for the onset of anesthesia, which is the slowest of all amide anesthetics. As such, this is not the anesthetic of choice for short-to-intermediate dental procedures. It also has the longest duration of both pulpal and soft tissue anesthesia, making it an ideal anesthetic for lengthy restorative procedures and to prevent post-surgical emergence of pain. After an inferior alveolar nerve block, the duration of pulpal anesthesia is approximately 1.5 hours; the duration of soft tissue anesthesia can extend up to 12 hours [20,35].
| A) | 34 mg per appointment. | ||
| B) | 56 mg per appointment. | ||
| C) | 90 mg per appointment. | ||
| D) | 120 mg per appointment. |
A 1.8-mL cartridge of 0.5% bupivacaine contains 9 mg of the drug. The MRD of bupivacaine for adults and children 12 years of age and older is 90 mg per appointment, or 10 cartridges. Although 10 cartridges is allowable, this is a large dose and clinicians should strive to use the minimum dose necessary to provide the appropriate depth and duration of anesthesia required for the procedure. Bupivacaine is not recommended for patients younger than 12 years of age [14,59]. Because bupivacaine preparations include a 1:200,000 concentration of epinephrine, the considerations outlined for this vasoconstrictor should also be taken into account.
| A) | 15 minutes. | ||
| B) | 1 hour. | ||
| C) | 3 hours. | ||
| D) | 6 hours. |
The time for onset of anesthesia and duration of pulpal and soft tissue anesthesia vary depending on the affected arch (maxillary or mandibular), whether infiltration or an inferior alveolar nerve block was used, and whether the plain formulation or the formulation including epinephrine is used. When prilocaine plain is used for maxillary teeth, the onset of anesthesia is two to three minutes, with a duration of pulpal anesthesia of about 15 minutes and soft tissue anesthesia of about 1 to 1.5 hours. When prilocaine with 1:200,000 epinephrine is used for the maxillary teeth, the onset of anesthesia is about 2 minutes, with a duration of pulpal anesthesia of about 45 minutes and a duration of soft tissue anesthesia of approximately 2 hours. When anesthesia for mandibular molars requires blocking the inferior alveolar nerve, the onset of anesthesia for prilocaine plain is 5 minutes or more, with the duration of pulpal anesthesia being 1 to 1.5 hours while soft tissue anesthesia may extend to 2.5 hours. When prilocaine with 1:200,000 epinephrine is used for anesthetizing mandibular molars by the nerve block, the onset of anesthesia ranges between two to four minutes. In this case, the duration of pulpal anesthesia is approximately 1.5 hours, while soft tissue anesthesia can extend to 3 hours. Prilocaine plain is suitable for shorter procedures, and prilocaine with 1:200,000 epinephrine can be used for short and intermediate dental procedures [37,46].
| A) | Articaine | ||
| B) | Prilocaine | ||
| C) | Lidocaine | ||
| D) | Bupivacaine |
As with the 4% articaine solution, concerns regarding the potential for neurotoxicity have also been raised about 4% prilocaine. Studies exploring the relationship between the use of 4% prilocaine for inferior alveolar (mandibular) nerve blocks and the subsequent development of an oral paresthesia of the lip and/or tongue reveal that there is a very slightly increased risk. A 2010 report reviewed 10 years of U.S. cases of oral paresthesia involving articaine, bupivacaine, lidocaine, mepivacaine, and prilocaine [38]. The overall incidence of oral paresthesias for all local anesthetics was one case per 13.8 million cartridges used. Prilocaine alone was associated with an incidence of one case of oral paresthesia for every 2 million cartridges used [38]. A 2015 analysis of the U.S. Food and Drug Administration Adverse Event Reporting System showed similar results, with prilocaine having the greatest association with paresthesia [60]. While the risk of an oral paresthesia after the use of prilocaine for mandibular blocks is small, it is greater than the composite risk of all of the other amide-type anesthetics combined.
| A) | Cyanosis | ||
| B) | Tachypnea | ||
| C) | Hyperactivity | ||
| D) | Excessive caries |
Patients will become symptomatic when the proportion of methemoglobin exceeds 10% to 15% [39]. Cyanosis is usually evident in the nail beds and the lips; other symptoms include fatigue, shortness of breath, and mental status changes. Patients who develop methemoglobinemia require intravenous administration of methylene blue to reverse the problem [36]. Supplemental oxygen is not useful, as methemoglobin does not carry oxygen. Hereditary methemoglobinemia is an absolute contraindication for the use of prilocaine.
| A) | avoided in all cases. | ||
| B) | administered via infiltration. | ||
| C) | started at the greatest safe dose. | ||
| D) | All of the above |
As with all local anesthetics, the lowest cumulative dose possible should be used to achieve anesthesia and complete the dental procedure. This is particularly essential when mepivacaine 3% plain is used in children. The short duration of 3% mepivacaine minimizes the potential for traumatization of anesthetized soft tissue; however, it is 1.5 times more toxic than the 2% formulation [43]. Therefore, the use of mepivacaine 3% plain in children, especially those younger than 5 years of age, should be administered via infiltration and restricted to the smallest dose whenever possible.
| A) | 10% lidocaine patch | ||
| B) | 10% benzocaine spray | ||
| C) | 20% benzocaine gel | ||
| D) | 20% lidocaine microspheres |
Benzocaine gel in a concentration of 20% is the most common topical anesthetic used in dentistry. It is marketed under several brand names and is available in many flavors to enhance patient acceptance. Benzocaine is not water-soluble, so it must be combined with other substances (e.g., alcohol, propylene glycol, polyethylene glycol) in order to make it suitable for application to the oral mucosa [13]. The tissue of the intended injected site should be isolated and dried prior to the application of benzocaine, as salivary contamination can dilute the drug and negate its effectiveness.
| A) | Age older than 60 years | ||
| B) | Weight greater than 150 kg (330 lbs) | ||
| C) | A history of angina or myocardial infarction | ||
| D) | Concurrent use with other medications that cause vasoconstriction |
The expedited return to normal sensation decreases the risk of iatrogenic tissue damage and facilitates the return to normal oral function. However, as with any medication, there are potential adverse effects. Injection site pain and reports of transient paresthesia have been associated with phentolamine mesylate use [14]. Because phentolamine mesylate is a vasodilator, its concurrent use with other medications that cause vasodilation can lead to an unsafe decrease in blood pressure. This includes phosphodiesterase-5 inhibitors (e.g., sildenafil, tadalafil, vardenafil) used in the treatment of erectile dysfunction and nitrates used to treat ischemic heart disease; use of these medications precludes the simultaneous use of phentolamine mesylate. Phentolamine mesylate is also contraindicated in patients who are younger than 6 years of age, who weigh less than 15 kg (33 lbs), who have a history of angina or myocardial infarction, or who have a known hypersensitivity to phentolamine mesylate [42]. The initial use of phentolamine mesylate as an anesthetic reversal agent in dentistry has provided encouraging results. Long-term studies and continued research are essential to determine if any problems or contraindications emerge with its continued use.
| A) | acetamidoglycine. | ||
| B) | cholamine chloride. | ||
| C) | an 8.4% sodium bicarbonate solution. | ||
| D) | citric acid and disodium hydrogen phosphate. |
Local anesthetic solutions that are "plain" (no vasoconstrictor) have a pH of approximately 5.9, while those containing epinephrine or levonordefrin have a pH of approximately 3.5, which classifies these as solutions with weak-to-moderate acidity [51]. The "sting" or "burning" patients feel during the injection of a local anesthetic is a result of this acidity. This may also account for post-injection soft tissue trauma. Manufacturers have addressed this issue by developing a system to increase the pH of a local anesthetic solution to increase patient comfort and minimize the potential for acidity-related soft tissue trauma after the injection.