National Board Dental Examination / Integrated National Board Dental Examination (INBDE) Pharmacology and Pain/Anxiety Management Syllabus

What is the mechanism of action of local anesthetics?

They reversibly block voltage-gated sodium channels from the intracellular side, preventing sodium influx, depolarization, and propagation of the nerve action potential.

Why do local anesthetics fail in infected (inflamed, acidic) tissue?

Low pH increases the ionized (charged) form of the LA and decreases the uncharged base form that crosses the nerve membrane, so less drug penetrates to block sodium channels.

How are amide vs ester local anesthetics metabolized?

Amides are metabolized in the liver by CYP450 microsomal enzymes; esters are hydrolyzed in plasma by pseudocholinesterase, producing PABA (associated with allergic reactions).

What is the maximum recommended dose of lidocaine with epinephrine, and the absolute mg cap for an adult?

7 mg/kg with epinephrine (and 4.4 mg/kg plain), not to exceed an absolute maximum of about 500 mg with epinephrine in a healthy adult.

A 2% lidocaine cartridge of 1.8 mL contains how many mg of lidocaine?

2% = 20 mg/mL, so 20 x 1.8 = 36 mg of lidocaine per cartridge.

What is the early sign of local anesthetic systemic toxicity (LAST) on the CNS, and how is severe LAST managed?

Early CNS signs include circumoral numbness, tinnitus, dizziness, and lightheadedness, progressing to seizures then CNS depression. Severe LAST is treated with airway support and 20% IV lipid emulsion therapy.

Which local anesthetic is associated with methemoglobinemia, and what is the treatment?

Benzocaine (and prilocaine) can cause methemoglobinemia; treatment is IV methylene blue.

What is the mechanism of action of NSAIDs?

NSAIDs inhibit cyclooxygenase (COX-1 and COX-2), blocking conversion of arachidonic acid to prostaglandins, thereby reducing pain, inflammation, and fever.

Why does aspirin pose a particular bleeding risk before dental surgery?

Aspirin irreversibly acetylates COX-1 in platelets, inhibiting thromboxane A2 and platelet aggregation for the platelet's lifespan (~7-10 days), unlike reversible NSAIDs.

How does acetaminophen differ from NSAIDs in action and key toxicity?

Acetaminophen is analgesic and antipyretic but has minimal anti-inflammatory/antiplatelet effect and acts centrally. Its key toxicity is hepatotoxicity in overdose (max ~4 g/day in adults); antidote is N-acetylcysteine.

What is the mechanism of action of opioid analgesics?

Opioids agonize mu (and kappa/delta) opioid receptors in the CNS, inhibiting ascending pain pathways and altering pain perception; they also cause respiratory depression, sedation, constipation, and miosis.

What is the antidote for opioid overdose and its mechanism?

Naloxone, a competitive mu-opioid receptor antagonist that rapidly reverses respiratory depression and sedation (short-acting, may require redosing).

What is the first-line antibiotic for most odontogenic infections, and the alternative for penicillin-allergic patients?

Amoxicillin (or penicillin VK) is first-line. For penicillin-allergic patients, clindamycin (historically) or azithromycin/clarithromycin; current AHA guidance favors azithromycin/clarithromycin or doxycycline.

What is the AHA recommended antibiotic prophylaxis regimen for infective endocarditis in at-risk patients before dental procedures?

Amoxicillin 2 g orally (50 mg/kg children) 30-60 minutes before the procedure; clindamycin is no longer recommended for penicillin-allergic patients (use azithromycin/clarithromycin or doxycycline/cephalexin).

How does bacterial resistance via beta-lactamase work, and how is it overcome in dentistry?

Beta-lactamase enzymes hydrolyze the beta-lactam ring, inactivating penicillins. It is overcome by adding a beta-lactamase inhibitor like clavulanic acid (amoxicillin-clavulanate / Augmentin).

Which antibiotic is most associated with Clostridioides difficile pseudomembranous colitis?

Clindamycin, though most broad-spectrum antibiotics can cause it.

What is the first-line topical antifungal for oral candidiasis, and a systemic alternative?

Topical nystatin (suspension or pastilles) or clotrimazole troches; systemic alternative is fluconazole.

What antiviral is used for recurrent herpes labialis/orolabial HSV, and what is its mechanism?

Acyclovir (or valacyclovir/penciclovir); it is phosphorylated by viral thymidine kinase and inhibits viral DNA polymerase, terminating DNA chain elongation.

What is the mechanism of corticosteroids' anti-inflammatory action?

Corticosteroids inhibit phospholipase A2 (via lipocortin/annexin-1), blocking arachidonic acid release and thus both prostaglandin and leukotriene synthesis, plus broad immunosuppressive gene effects.

Why must dental clinicians be aware of long-term systemic corticosteroid use, and what is the concern with abrupt stress?

Chronic steroids suppress the HPA axis, risking adrenal crisis under surgical stress; supplemental ('stress dose') steroids may be considered, and abrupt cessation must be avoided to prevent adrenal insufficiency.

What are common topical and systemic hemostatic agents used in dentistry?

Topical: gelatin sponge (Gelfoam), oxidized cellulose (Surgicel), collagen, thrombin, and tranexamic acid mouthrinse. Systemic adjunct: aminocaproic/tranexamic acid (antifibrinolytics).

What is the mechanism by which fluoride prevents caries and aids remineralization?

Fluoride incorporates into enamel forming fluorapatite (more acid-resistant than hydroxyapatite), promotes remineralization, and inhibits bacterial enzymes (e.g., enolase) reducing acid production.

What are the signs of acute fluoride toxicity and the probable toxic dose?

Nausea, vomiting, abdominal pain, hypersalivation, and in severe cases cardiac arrhythmias/hypocalcemia. The probably toxic dose (PTD) is ~5 mg/kg; treat with milk/calcium and seek care; lethal dose ~32-64 mg/kg.

What is the mechanism of action of benzodiazepines used for dental anxiolysis/sedation?

They bind the GABA-A receptor benzodiazepine site and increase the frequency of chloride channel opening, enhancing GABA-mediated inhibition (sedation, anxiolysis, amnesia, muscle relaxation).

What is the reversal agent for benzodiazepine oversedation?

Flumazenil, a competitive benzodiazepine receptor antagonist (short-acting; monitor for resedation and seizure risk in dependent patients).

What are the advantages of nitrous oxide-oxygen for minimal sedation in dentistry?

Rapid onset and recovery, easy titration, analgesic and anxiolytic effects, minimal cardiovascular/respiratory depression, and quick reversal with 100% oxygen; minimum 30% oxygen must always be delivered.

Why must epinephrine in local anesthetic be limited in patients with significant cardiovascular disease, and what is the cardiac dose limit?

Exogenous epinephrine can raise heart rate and blood pressure and provoke arrhythmias. The cardiac patient limit is ~0.04 mg epinephrine (about 2 cartridges of 1:100,000).

How do warfarin and the direct oral anticoagulants (DOACs) differ in mechanism, and what lab monitors warfarin?

Warfarin inhibits vitamin K epoxide reductase (blocking factors II, VII, IX, X) and is monitored by INR (target ~2-3). DOACs directly inhibit factor Xa (apixaban, rivaroxaban) or thrombin (dabigatran) and need no routine monitoring.

What dental adverse effect is associated with calcium channel blockers (e.g., nifedipine), phenytoin, and cyclosporine?

Gingival hyperplasia/overgrowth.

Which class of antidepressants poses a risk of hypertensive crisis with epinephrine or tyramine, and which antihypertensive interacts with NSAIDs?

Nonselective MAO inhibitors (and tricyclic antidepressants potentiate sympathomimetics) raise hypertensive crisis risk. NSAIDs blunt the effect of ACE inhibitors and other antihypertensives and can raise blood pressure.