Midterm Ch. 1-5

Question 1

Identify providers of dental local anesthesia in North America.

Answer 1

In most states and provinces, dentists and dental hygienists provide dental local anesthesia. In some, mid-level and/or expanded function providers are also allowed to administer dental local anesthesia.

Question 2

Identify the fundamentals of pain management

Answer 2

The fundamentals of pain management include conducting comprehensive assessment, recognizing and responding to patient factors, integrating evidence-based knowledge, and understanding relevant drugs and their effects, indications, and contraindications. Fundamentals also include developing clinical decision-making skills and mastering a wide variety of techniques and appropriate modifications.

Question 3

Define the term troubleshooting as it relates to the administration of local anesthesia.

Answer 3

Troubleshooting is the ability to critically assess and resolve anesthesia inadequacies in order to provide comfortable patient care.

Question 4

How does the International Association for the Study of Pain define pain?

Answer 4

The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

Question 5

Identify variables that contribute to an individual’s experience of pain.

Answer 5

Pain is influenced by many variables that contribute to an individual’s experience of pain. The sex of an individual provides genetic and hormonal influence. Gender also adds numerous complex components that include an array of socially constructed roles and relationships, personality traits, attitudes, behaviors, values, relative power, and influence that society ascribes based on a differential basis. Other factors, such as age, physical health, mental health, emotional status, expectations, previous experiences, learned responses, and ethnic and cultural norms also impact the pain experience.

Question 6

Discuss pain as a protective response.

Answer 6

As a physiological response to our environment, pain is a protective response. Physiological pain serves to protect us from harmful experiences. This protective response is a rapid, reflexive, subconscious reaction. However, a less emergent painful annoyance may elicit a slower, conscious-level reaction. Without the protective pain response, the ability to maintain a healthy body would be seriously compromised.

Question 7

Define pain threshold.

Answer 7

Pain threshold is the point at which a stimulus begins to produce a sensation of pain. It is highly reproducible in the same individual and among different individuals.

Question 8

Define pain tolerance.

Answer 8

Pain tolerance is an individual’s reaction to a painful stimulus. A common experience of pain produces a highly variable reaction from one individual to another.

Question 9

Define acute pain.

Answer 9

Acute pain usually lasts for a few seconds to not more than six months, depending on the causative factors. It is generally caused by tissue damage from an injury or disease.

Question 10

Define chronic pain.

Answer 10

Chronic pain is long-term pain that persists for more than six months, with or without an identifiable cause. The longer an acute pain continues the more likely the pain will become a chronic pain experience.

Question 11

Name the three broad classifications of pain.

Answer 11

Pain is generally considered in three broad classifications: nociceptive pain, neuropathic pain, and pain disorders. Subclassifications exist within these broad categories.

Question 12

Define nociceptors.

Answer 12

Nerve fibers have specialized endings to detect and transmit information to the central nervous system. For pain, the receptor fibers are known as nociceptors. Nociceptors are unique because they are polymodal, meaning they respond to all types of stimuli: mechanical, thermal, and chemical.

Question 13

Explain the difference between pain and nociception.

Answer 13

Pain and nociception are not synonymous. Nociception is the body’s neurophysical detection of tissue trauma by nociceptors and the process of transmission of signals of the tissue injury within the nervous system. Nociception is not a conscious process. The process of nociception is influenced by an individual’s age, general health, and genetics. An individual must have conscious awareness to experience pain. Pain cannot exist apart from consciousness and cannot be objectively measured.

Question 14

Define nociceptive pain.

Answer 14

Nociceptive pain is caused by injury or disease in body tissues. Pain may be constant or intermittent and often escalates with movement.

Question 15

Define somatic and visceral pain.

Answer 15

Somatic nociceptive pain occurs on superficial structures such as skin and muscles and is caused by traumatic injuries. The resulting pain may be sharp, aching, or throbbing. Visceral nociceptive pain occurs in internal body cavities and is caused by compression, expansion, stretching, and/or infiltration of internal organs. It usually produces squeezing or gnawing sensations.

Question 16

Define neuropathic pain.

Answer 16

Neuropathic pain is caused by nerve tissue injury or dysfunction of the sensory nerves in central or peripheral nervous systems. There are numerous neuropathic pain types.

Question 17

Define pain disorders with psychological factors.

Answer 17

Pain disorders are related to mental or emotional problems that affect the experience of pain. Pain disorders with psychological factors are diagnosed after other causes of physical pain have been eliminated.

Question 18

What physiological responses occur as a result of the sympathetic nervous system?

Answer 18

Heart rate and contractions increase, blood pressure increases, and pupils dilate. Bronchodilation and vasodilation of skeletal muscle arterioles occur along with vasoconstriction of mesenteric circulation.

Question 19

What percentage of patients report fear as the main reason for avoiding dental appointments?

Answer 19

It has been reported that the main reason individuals avoid dental appointments is fear. About 40% of patients report some level of anxiety related to dental treatment and roughly 5% avoid dentistry because of fear of injections. Patients experience fear on a continuum ranging from mild anxiety to phobia.

Question 20

How can clinicians create an environment that encourages patients to discuss their dental fears?

Answer 20

To create an environment that encourages patients to discuss their fears, deliberate behavior on the part of clinicians can be helpful in developing successful patient experiences. For example, using controlled, calm speech and a positive demeanor convey comfort and instill confidence. Signs of impatience or disapproval from the clinician should be avoided.

Question 21

Give examples of the PREP strategies that help patients manage anxiety and fear.

Answer 21

PREP strategies help patients cope with anxiety and fear:
Prepare by utilizing relaxation techniques such as deep breathing, distraction such as music or visualization, and muscle relaxation.
Rehearse procedures allowing patients to practice control and self-calming techniques.
Empower patients with strategies that give them control during procedures such as raising a hand to ask the clinician to stop.
Praise patients for using specific coping techniques that are helpful to them.

Question 22

What is the debriefing process?

Answer 22

The debriefing process allows for discussion periods at the end of appointments to provide patients an opportunity to relate which aspects of treatment and which approaches to treatment went well and which did not.

Question 23

Give examples of pharmacological interventions that may be helpful and necessary in providing care for fearful patients who avoid dental treatment.

Answer 23

For some patients, pharmacological intervention may be helpful and necessary. Nitrous oxide-oxygen sedation, oral conscious sedation, intravenous sedation, and general anesthesia should be discussed with patients as the situation warrants. Pharmacological solutions are especially helpful for anxious patients who avoid dental treatment and present only for emergent care.

Question 24

Discuss strategies and provide examples that enhance positive communication with patients.

Answer 24

Strategies and examples that will enhance positive communication with patients include:
• Display a genuinely warm and caring attitude.
• Review treatment plan, addressing fears, including fears of the unexpected and of loss of control.
• Obtain permission to begin, addressing fear of loss of control if necessary.
• Establish patient control strategy (time-out signal such as raising hand to stop).
• Direct the focus on positive outcomes (“You may feel a bit of pressure.”).
• Acknowledge and compliment success (“You did great with the anesthesia today!”).
• Create positive expectations (“That went well today and I expect your next appointment will too.”).

Question 25

Discuss examples of distraction techniques.

Answer 25

Examples of distraction techniques include: • Light, casual conversation or guided relaxation • Gate control strategies and devices • Pressure applied with cotton swab to palatal tissues • Gentle lip shaking during needle insertion • The use of vibration devices • Audio devices with headphones for music or audio books (selected by patient) • Television, video devices, and audiovisual glasses (not for highly anxious)

Question 26

Discuss the relaxation response and its relationship to the parasympathetic nervous system.

Answer 26

The relaxation response is a restful state that modifies physical and emotional responses to stress. Parasympathetic pathways that allow recovery from stress (fight or flight) are activated by this response that lowers heart and respiratory rates, blood pressure, and muscle tension.

Question 27

Discuss the link between hypnosis and the physiology of pain.

Answer 27

Growing evidence suggests a strong link between hypnosis and the physiology of pain for effective management of pain and anxiety. When in a state of hypnosis, patients usually feel calm and relaxed and are able to concentrate intensely on a specific thought, memory, feeling, or sensation while blocking out distractions.

Question 28

Name the four structural areas of neurons.

Answer 28

All neurons have four structural areas: the dendritic zone, axon, cell body, and terminal arborization.

Question 29

What is the composition and function of the neurolemma?

Answer 29

Nerve membranes, called neurolemmas, are bilayered phospholipid membranes. The function of a bilayered membrane is to act as a barrier. Lipid membranes are composed of phospholipids having both lipophilic (“fat-loving”) and hydrophilic (“water-loving”) ends. The membranes are held together by the attraction of the lipophilic ends at their centers.

Question 30

What is the function of Schwann cells?

Answer 30

Schwann cells, which produce myelin, are specialized connective tissue cells that surround and protect peripheral nerves. Schwann cells insulate and protect the nerve membranes from their surrounding environments. Axons and their associated Schwann cells are collectively referred to as nerve fibers.

Question 31

Describe the significance of the nodes of Ranvier in the administration of local anesthesia.

Answer 31

Local anesthetic solutions cannot diffuse through myelinated nerves except in areas where they come into direct contact with the membrane at the nodes of Ranvier.

Question 32

Define saltatory conduction.

Answer 32

Saltatory conduction is the term for the process by which impulses are more rapidly conducted along myelinated nerves.

Question 33

Which two layers within the fasciculi are the most significant barriers to the diffusion of anesthetic solutions?

Answer 33

The two most significant barriers to the diffusion of anesthetic solutions within the fasciculi are the perilemma and the perineurium, with the perilemma posing the greatest obstacle to diffusion.

Question 34

What is the electrical potential of the nerve axoplasm in the resting state?

Answer 34

The electrical potential of nerve axoplasm in the resting state is approximately -70 mV.

Question 35

Which ions bind to specific protein receptor sites within the ion channels of the nerve membrane in its resting state?

Answer 35

In the resting state, Ca+2 ions bind to specific protein receptor sites in the nerve membrane ionic channels. This causes the channels to be closed or gated by the Ca+2 ions.

Question 36

Describe what occurs to create a firing threshold and impulse generation.

Answer 36

When a nerve is stimulated, the ion channels respond by releasing the gate keeper calcium ions. The channels are then wide enough to allow the positively charged, hydrated Na+ ions to begin to enter through the channels into the more negatively charged axoplasm. The initial influx of positively charged Na+ ions causes, at first, a slow depolarization process. Once there are sufficient Na+ ions in the axoplasm to reduce the electrical potential by approximately 15–20 mV, more Na+ ions flood the axoplasm. When the electrical potential reaches -50 to -55 mV, an impulse is generated.

Question 37

Compare the conduction speeds of Aδ and C nerve fibers.

Answer 37

The Aδ fibers convey more rapid information on sharper pain. C fibers convey information more slowly on duller, aching pain. Both A and C fibers have been found in the dental pulp with a greater distribution of C fibers than A

Question 38

Define refractory state and absolute refractory state.

Answer 38

The inability to successfully restimulate a section of membrane after impulse generation and conduction is known as the refractory state. Initially, the membrane is absolutely refractory to stimulation, and the previously fired section of membrane cannot be restimulated no matter how great the stimulus.

Question 39

How does repolarization occur?

Answer 39

During rapid depolarization, the nerve axoplaxm has attained an electrical potential of +40mV. At this point the influx of Na+ ions is prevented and the Na+ ions begin to return to the extracellular environment through the ion channels. Additionally, sodium ion pumps enhance the movement of sodium from the axoplasm. The reversal of the ion concentration in the recovery phase is called repolarization.

Question 40

How long does the process of depolarization to repolarizion take?

Answer 40

This process may seem long and tedious. In reality, however, it requires only one millisecond for a nerve membrane to react and recover after a successful impulse-generating stimulation.

Question 41

Define impulse extinction related to the use of local anesthetic drugs.

Answer 41

Upon administration of local anesthetic drugs, Na+ ion influx through the nerve membrane is blocked and sodium-dependent depolarization is prevented. Both the generation and conduction of nerve impulses can be inhibited by local anesthetic drugs. Decreased responsiveness to stimuli and the failure to transmit an impulse toward the CNS are direct consequences of impulse extinction due to local anesthetic drugs.

Question 42

Which structures do core and mantle bundles innervate?

Answer 42

Nerve fibers housed in mantle bundles tend to innervate structures in close proximity to them. Fibers housed in core bundles tend to innervate structures at some distance away from them. For example, in the case of the inferior alveolar nerve, fibers from the mantle layer tend to innervate the molar region, while fibers from the core layer tend to innervate the anterior mandible including the chin and lips.

Question 43

Explain why the core bundles that innervate the anterior mandible can be more difficult to anesthetize.

Answer 43

Core bundles which innervate the anterior mandible can be more difficult to anesthetize because the anesthetic solution reaches them only after the solution has penetrated through the mantle layer. It takes longer to reach the core, and the solution does so in a diluted form primarily because of the binding of drug molecules to receptor sites in the mantle bundles. Once at the core, there are fewer molecules remaining to bind to sites in the core

Question 44

Define local anesthesia.

Answer 44

Local anesthesia may be defined as a temporary loss of sensation in a specific, usually small area of the body. A primary distinction between local and general anesthesia is that when local anesthesia alone is in effect, the patient remains conscious.

Question 45

Explain how local anesthetics work.

Answer 45

Local anesthetic drugs all work similarly. Local anesthetic molecules have a greater affinity for protein receptor sites within the nerve membrane compared to Ca+2 ions and they subsequently displace them. Different local anesthetic drugs have varying affinities for these receptor sites, which account for clinically significant differences in drug action.

Question 46

Are both sensory and motor nerves anesthetized by local anesthesia?

Answer 46

Local anesthetic drugs are effective on both sensory and motor nerves. They typically anesthetize smaller nerves before larger nerves and sensory nerves before motor nerves

Question 47

Although the desired effects of local anesthetic drugs are local, what other parts of the body are affected by the drug?

Answer 47

Although the desired effects of these drugs are localized, their inevitable systemic absorption exposes other tissues to their potentially toxic actions, including the central nervous system (CNS), the cardiovascular system (CVS), and skeletal muscle.

Question 48

What is the objective in using local anesthetic drugs in dental treatment?

Answer 48

The objective in using local anesthetic drugs in dental treatment is to produce anesthesia for a specific area and, in some instances, to reduce localized bleeding.

Question 49

What is the primary benefit of local anesthesia?

Answer 49

The primary benefit of local anesthesia is that pain sensations can be suppressed without significant central nervous system depression. This allows the majority of dental procedures, for example, to be performed under local anesthesia without exposing patients to the risks of general anesthesia.

Question 50

What are the legal and ethical requirements for all health professionals administering local anesthesia drugs?

Answer 50

A sound knowledge of local anesthetic drugs and techniques is crucial to safe and successful administration. An understanding of the influences of compromised physiologic function, susceptibility to adverse reactions, and awareness of all drugs the patient may be using whether prescribed or not are equally important. Legal and ethical principles mandate that practitioners licensed to inject drugs into the human body are responsible for these considerations and, ultimately, their consequences.

Question 51

Name two primary routes of delivery of dental local anesthetic drugs

Answer 51

There are two primary routes of delivery of dental local anesthetic drugs: topical and submucosal injection.

Question 52

Explain why the use of topical local anesthesia is more effective on mucosa than on skin.

Answer 52

Topical application of local anesthetic drugs is more effective on mucosa than on skin because of the ease of penetration through thin mucosal barriers in order to reach underlying nerves.

Question 53

Why are injections of local anesthetic more effective than topical routes of administration?

Answer 53

Subcutaneous and submucosal injections are more effective than topical routes of administration due to the direct placement of drugs in close proximity to nerves.

Question 54

List ideal properties of local anesthetic drugs used in dentistry.

Answer 54

An ideal local anesthetic would have the following specific properties: a high level of biocompatibility with no systemic effects; a rapid onset; no toxicity to tissue, including nerve tissue; and a therapeutic duration and potency without inducing hypersensitivity or unconsciousness. Further, an ideal drug would be sterilizable, readily biotransformed, and provide excellent topical effects at low concentrations.

Question 55

List the five injectable local anesthesia drugs currently available in dental cartridges.

Answer 55

The five injectable local anesthetic drugs currently available in dental cartridges include articaine, bupivacaine, lidocaine, mepivacaine, and prilocaine.

Question 56

What are the names of the intermediate chains used to classify injectable anesthetic drugs used in dentistry?

Answer 56

Injectable local anesthetic drugs used in dentistry are classified as either amides or esters.

Question 57

What is a relatively easy way to distinguish between the two formulas of intermediate chains in local anesthesia drugs?

Answer 57

A relatively easy way to distinguish between the two formulas is that the amide intermediate chain contains a nitrogen atom whereas the ester chain does not.

Question 58

Explain two important functions of the amide and ester intermediate chains.

Answer 58

The amide and ester linkages between the separated chemical components of the drugs serve two important functions. The first is to provide proper spacing between the chemical components, an aromatic (lipophilic) end and a secondary or tertiary amine (hydrophilic) end, which allows the anesthetic to be effective in the tissues. The second is to provide for major pathways of biotransformation.

Question 59

Define the term pharmacodynamics.

Answer 59

Pharmacodynamics refers to the actions of a drug on the body.

Question 60

Define the term pharmacokinetics.

Answer 60

Pharmacokinetics refers to the manner in which the body manages the drug, specifically the mechanisms of absorption, distribution, metabolism (biotransformation), and elimination.

Question 61

What is a major difference between local anesthetic drugs and the majority of other drugs?

Answer 61

A major difference between local anesthetic drugs and the majority of drugs is that systemic effects are not desired with local anesthetic drugs.

Question 62

What are the two chemical forms of local anesthetic molecules in solution?

Answer 62

Once dissolved in sterile water, local anesthetic molecules dissociate into two forms: a positively charged cation and an uncharged or neutral base.

Question 63

Explain the effect of local anesthetic drugs on nerve membranes based on the specific protein receptor theory.

Answer 63

The action of local anesthetics on nerve membranes is largely explained by the binding of local anesthetic molecules to these structural proteins known as specific protein receptor sites in the ion channels. Only one molecule can occupy a receptor site at one time. These receptors temporarily transform nerve membranes to nonexcitable states in which impulse propagation is prevented. Sodium ions cannot pass through channels blocked by anesthetic molecules. Receptor binding results in closing of the channels, preventing the influx of sodium and blocking the transmission of impulses.

Question 64

Explain the effect of local anesthetic drugs on nerve membranes based on the membrane expansion theory.

Answer 64

The membrane expansion theory describes a modification of the membrane structure in the presence of local anesthesia drugs. The diffusion of local anesthetic molecules to lipophilic regions of the nerve membrane causes a narrowing of the diameters of ion channels, which limits the permeability of the membrane to sodium ions, further blocking the transmission of impulses.

Question 65

Which ionic form of a local anesthetic molecule diffuses through the nerve membrane?

Answer 65

The neutral base form (RN) of an anesthetic molecule diffuses through the nerve membrane.

Question 66

Which ionic form of a local anesthetic molecule binds to the receptor sites in the sodium channels of the nerve membrane?

Answer 66

The cation (RNH+) form of a local anesthetic molecule binds to the receptor sites in sodium ion channels of the nerve membrane.

Question 67

How does tissue inflammation affect local anesthetic drugs?

Answer 67

When tissues are inflamed at sites of deposition of local anesthetic drugs, the lowered pH inhibits the production of neutral base molecules. This inhibition may result in insufficient numbers of neutral base molecules (RN) penetrating nerve membranes. Profound anesthesia may become difficult to achieve or, if initially achieved, to sustain. In addition to the increase in hydrogen ions, localized edema and increased circulation may also contribute to failure of profound anesthesia by removing drugs from delivery sites.

Question 68

Define pKa.

Answer 68

The equilibrium concentrations of cationic and base molecules in solution are described by the pKa, also known as the dissociation constant. When pKa = pH, there is an equal distribution of cations (RN+) and neutral base (RN) molecules in solution.

Question 69

What is the clinical application of pKa in local anesthesia drug preparations?

Answer 69

In local anesthesia, narrow pKa ranges of around 7.7–8.1 are common and include all five of the injectable amides available in dentistry. These values provide clinically useful onsets of anesthesia. As a general rule, the higher the pKa, the longer the onset of anesthesia.

Question 70

Explain clinical concerns related to the vasoactivity of local anesthesia drugs.

Answer 70

All dental local anesthetic drugs are peripheral vasodilators. Vasodilation is not a desirable characteristic of local anesthetic drugs as it limits their duration and efficacy while increasing their toxicity. Vasoconstrictors are added to the solutions to oppose vasodilation and block the rapid uptake of drugs into the systemic circulation. Local anesthetic drugs that remain in deposition areas for longer periods are less available to the systemic circulation, thereby reducing the risk of rapid uptake which can lead to rapid overdose.

Question 71

What factors can precipitate toxic overdose from local anesthetic drugs?

Answer 71

Factors that can precipitate toxic overdose from local anesthetic drugs include excessive dose, intravascular administration, rapid delivery, and/or slower than normal biotransformation or elimination. Other factors that may contribute to overdose include route of administration and an individual’s age, weight, and health status.

Question 72

List signs and symptoms of CNS overdose toxicity.

Answer 72

``` Signs and Symptoms of CNS overdose toxicity include: Apprehension, excitedness, talkativeness Bilateral numbness of tongue Disorientation Drowsiness more common with lidocaine Elevated BP, pulse, breathing Headache Lightheadedness Loss of consciousness Muscle twitching/tremors in muscles of face, extremities Perioral numbness Shivering, chilled feeling of skin Slurred speech Visual/Auditory disturbances Warm, flushed feeling of skin ```

Question 73

List CVS effects of local anesthesia drug overdose.

Answer 73

``` Effects on the CVS include: Mild depression of the myocardium, which decreases: Electrical excitability Conduction rate Force of contraction Peripheral vasodilation (except cocaine) Relaxation of smooth muscle in vessels: Slight or no change in blood pressure Hypertension with increasing dose Relaxant action on bronchial smooth muscle ```

Question 74

How does the vascularity of an injection site affect the absorption and distribution of local anesthetic drugs?

Answer 74

Injection into highly vascular areas will result in faster absorption and distribution away from sites of deposition. In contrast, less vascular areas with slower vascular uptake prolong the local actions of drugs.

Question 75

What are the two main pathways of biotransformation of local anesthetic drugs?

Answer 75

Biotransformation of local anesthetic drugs occurs primarily in the liver or in the blood.

Question 76

What is meant by the elimination half-life of a drug?

Answer 76

The elimination half-life of a drug may be defined as the rate at which it is removed from the systemic circulation by the kidneys. Within the kidneys, drug elimination occurs over time, as blood recirculates through the organs. Elimination half-life has also been expressed as the time necessary to metabolize and excrete 50% of a drug.

Question 77

Given the half-life of lidocaine as 1.6 hours, what is the approximate total number of hours to effectively eliminate lidocaine from the body?

Answer 77

Lidocaine has a half-life of 1.6 hours. It will take essentially six half-lives to clear this drug or more than nine hours before only a trace remains.

Question 78

When was the first amide local anesthetic drug, lidocaine, developed by Lofgren?

Answer 78

Lidocaine was the first amide local anesthetic drug developed by Lofgren in 1943.

Question 79

What are the three formulations of lidocaine available for use in dentistry?

Answer 79

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

Question 80

What is the duration of anesthetic action for each of the formulations of lidocaine used in dentistry?

Answer 80

1. 2% lidocaine plain (without vasoconstrictor) Very short duration = 5–10 minutes pulpal; 60–120 minutes soft tissue 2. 2% lidocaine with 1:100,000 epinephrine Intermediate duration = 60 minutes pulpal; 180–300 minutes soft tissue 3. 2% lidocaine with 1:50,000 epinephrine Intermediate duration = 60 minutes pulpal; 180–300 minutes soft tissue

Question 81

What are key considerations in duration of action for local anesthetics?

Answer 81

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

Question 82

What is the maximum recommended dose (MRD) of lidocaine per appointment?

Answer 82

3.2 mg/lb (7.0 mg/kg); 500 mg absolute maximum .

Question 83

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

Answer 83

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.

Question 84

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

Answer 84

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.

Question 85

How is lidocaine metabolized?

Answer 85

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.

Question 86

What percentage of lidocaine is excreted unchanged by the kidneys?

Answer 86

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

Question 87

Describe the vasoactivity of lidocaine in relation to other local anesthetic drugs used in dentistry.

Answer 87

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.

Question 88

What is the pKa of lidocaine?

Answer 88

The pKa of lidocaine is 7.7.

Question 89

What is the pH of lidocaine plain solution?

Answer 89

The pH of lidocaine plain solution is 6.5.

Question 90

what is the onset time of lidocaine with epinephrine?

Answer 90

The onset time of lidocaine with epinephrine is 2–3 minutes.

Question 91

How long is the elimination half-life of lidocaine?

Answer 91

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

Question 92

Discuss the effective use of lidocaine as a topical anesthetic agent.

Answer 92

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.

Question 93

What is the FDA Pregnancy Category for lidocaine?

Answer 93

Lidocaine is in FDA Pregnancy Category B.

Question 94

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?

Answer 94

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.

Question 95

When was articaine available for use in dentistry in the United States?

Answer 95

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).

Question 96

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

Answer 96

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.

Question 97

What are the two formulations of articaine available for use in dentistry?

Answer 97

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

Question 98

What is the MRD for articaine?

Answer 98

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

Question 99

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

Answer 99

Articaine’s metabolism is unique. 5–10% is metabolized via hepatic p450 enzymes. The majority of articaine’s removal is accomplished by 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.

Question 100

What is the onset of action of articaine for nerve block anesthesia?

Answer 100

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

Question 101

When, where, and by whom was mepivacaine prepared as an alternative to lidocaine?

Answer 101

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

Question 102

Discuss the vasodilation property of mepivacaine and its relationship to the anticipated length of pulpal anesthesia.

Answer 102

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.

Question 103

What are the two formulations of mepivacaine available for use in dentistry?

Answer 103

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

Question 104

What is the duration of anesthetic action of each formulation of mepivacaine used in dentistry?

Answer 104

3% mepivacaine plain Short duration = 20–40 minutes pulpal; 120–180 minutes soft tissue 2% mepivacaine with 1:20,000 levonordefrin Intermediate duration = 60 minutes pulpal; 180–300 minutes soft tissue

Question 105

What is the MRD for mepivacaine?

Answer 105

3.0 mg/lb (6.6 mg/kg); 400 mg absolute maximum.

Question 106

How is mepivacaine metabolized?

Answer 106

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.

Question 107

What is the onset of action for mepivacaine?

Answer 107

The onset of action for mepivacaine is 1.5–2 minutes.

Question 108

What is the elimination half-life of mepivacaine?

Answer 108

The elimination half-life of mepivacaine is 1.9 hours (114 minutes).

Question 109

What is the FDA Pregnancy Category for mepivacaine?

Answer 109

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

Question 110

When was prilocaine first prepared and approved for use by the FDA?

Answer 110

Prilocaine was first prepared by Lofgren and Tegner in 1953 and approved by the FDA in 1965.

Question 111

What are the two formulations of prilocaine available for use in dentistry?

Answer 111

4% prilocaine plain (without vasoconstrictor) | 4% prilocaine with 1:100,000 epinephrine

Question 112

What is the MRD for prilocaine?

Answer 112

4.0 mg/lb (8.8 mg/kg); 600 mg absolute maximum.

Question 113

What is the special relative toxicity consideration with the use of prilocaine?

Answer 113

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.

Question 114

How is prilocaine metabolized compared to lidocaine and mepivacaine?

Answer 114

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.

Question 115

What year was bupivacaine approved by the FDA?

Answer 115

Bupivacaine was prepared by A. F. Ekenstam in 1957 and approved by the FDA in 1972.

Question 116

Provide clinical indications for the use of bupivacaine in dentistry.

Answer 116

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.

Question 117

Discuss an important postoperative consideration when using bupivacaine.

Answer 117

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.

Question 118

What formulation of bupivacaine is provided for use in dentistry?

Answer 118

0.5% bupivacaine with 1:200,000 epinephrine

Question 119

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

Answer 119

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

Question 120

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

Answer 120

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.

Question 121

Why is bupivacaine effective with a dilute 0.5% concentration?

Answer 121

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.

Question 122

Why is bupivacaine more toxic compared to other anesthetic drugs?

Answer 122

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.

Question 123

What is the onset of action for bupivacaine?

Answer 123

The onset of action for bupivacaine is 6–10 minutes.

Question 124

Explain why it may be advantageous to administer mepivacaine prior to bupivacaine.

Answer 124

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.

Question 125

Discuss the importance of the introduction of procaine in the early 1900s.

Answer 125

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.

Question 126

What derivative of procaine is responsible for its relatively high rate of allergenicity?

Answer 126

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.

Question 127

How is procaine metabolized?

Answer 127

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

Question 128

Discuss the clinical significance of the high pKa of procaine.

Answer 128

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.

Question 129

What is the half-life of procaine?

Answer 129

The elimination half-life of procaine is 6 minutes.