Local Anesthetics & Analgesics MCQ

Pain control is the most-used pharmacology in dentistry. Local anesthetics block voltage-gated sodium channels to numb the field; they split into amides and esters with very different allergic profiles. Postoperative pain is managed with NSAIDs (COX inhibitors), acetaminophen (central COX), and, when needed, short courses of opioids. The most important single message is that ibuprofen plus acetaminophen at therapeutic doses outperforms most opioid regimens for routine dental pain with fewer adverse effects. Opioids stay in the toolkit for severe acute pain, with care for codeine's CYP2D6 variability and the naloxone reversal pathway.

Local Anesthetics: Amides and Esters

• Local anesthetics block voltage-gated sodium channels from the inside of the nerve, preventing depolarization and the propagation of the action potential.
• Amides (lidocaine, articaine, mepivacaine, prilocaine, bupivacaine, all spelled with two 'i's in the name) are metabolized in the liver and rarely cause allergy; esters (procaine, benzocaine, tetracaine, one 'i') are metabolized by plasma esterases to para-aminobenzoic acid (PABA) and are the classic ester-allergy culprits.
• Onset depends on pKa (closer to physiologic pH means more unionized drug crossing the membrane); duration depends on protein binding (bupivacaine is highly protein-bound and long acting); inflamed tissue is acidic, ionizes the drug, and lowers efficacy.
• Maximum doses for a 70 kg adult include lidocaine with epinephrine about 500 mg (about 7 mg/kg), articaine about 500 mg (about 7 mg/kg), mepivacaine plain about 400 mg (about 6.6 mg/kg), and bupivacaine about 90 mg (about 1.3 mg/kg).

Local Anesthetic Toxicity (LAST)

• Local anesthetic systemic toxicity (LAST) follows an intravascular injection or an overdose; it starts with CNS excitation (perioral numbness, tinnitus, metallic taste, agitation, seizure) and progresses to CNS depression and cardiovascular collapse.
• Cardiovascular effects of bupivacaine are particularly dangerous because of avid sodium channel binding and difficult resuscitation; bupivacaine is rarely the first choice in routine dentistry for this reason.
• Treatment of LAST is airway and oxygenation, seizure control with a benzodiazepine, and intravenous lipid emulsion (20% Intralipid) for cardiovascular collapse.
• Prevention is the meaningful intervention: aspirate before depositing, inject slowly, stay below the maximum dose for the patient's weight, and reduce the dose in the elderly or in hepatic impairment.

NSAIDs: COX-1 vs COX-2

• NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase enzymes, decreasing prostaglandin synthesis and providing analgesic, anti-inflammatory, and antipyretic effects; COX-2 inhibition drives the analgesic effect.
• COX-1 maintains gastric mucosa, renal perfusion, and platelet thromboxane; COX-1 inhibition is responsible for GI bleeding, renal injury, and antiplatelet effects.
• Aspirin irreversibly acetylates COX-1 on platelets for the life of the platelet (about 7 to 10 days); other NSAIDs are reversible.
• Selective COX-2 inhibitors (celecoxib) spare GI and platelet effects but were associated with cardiovascular events (Vioxx withdrawn), so all NSAIDs (including selective COX-2) carry cardiovascular caution in at-risk patients.

Acetaminophen

• Acetaminophen acts mainly centrally on COX (and other targets); it provides analgesia and antipyresis but little anti-inflammatory effect, so it is paired with an NSAID for inflammatory dental pain.
• The maximum daily dose in a healthy adult is about 4 g; chronic alcohol use, malnutrition, or hepatic impairment lower the safe dose (some labels recommend a 3 g/day cap).
• Overdose generates the reactive metabolite NAPQI, which depletes glutathione and causes hepatocyte necrosis; therapeutic doses are safe because the small amount of NAPQI is detoxified by glutathione.
• N-acetylcysteine restores glutathione and is the antidote; chronic alcohol use induces CYP2E1, generating more NAPQI and increasing toxicity risk.

Opioids: Codeine, Hydrocodone, Oxycodone, Morphine, Tramadol

• Opioids are mu opioid receptor agonists that produce analgesia (and the related effects: sedation, respiratory depression, miosis, constipation, nausea, tolerance, dependence).
• Codeine is a prodrug converted to morphine by CYP2D6; ultra-rapid metabolizers can have opioid toxicity (now a pediatric black-box contraindication after tonsillectomy/adenoidectomy in children) and poor metabolizers get no analgesia.
• Tramadol is a weak mu agonist plus a serotonin and norepinephrine reuptake inhibitor; it lowers the seizure threshold and can cause serotonin syndrome when combined with SSRIs or MAOIs.
• Naloxone is the competitive mu antagonist used for overdose; its half-life is shorter than many opioids, so monitoring for re-sedation is essential. Methadone and buprenorphine are used for opioid use disorder and chronic pain.

The Analgesic Ladder for Dental Pain

• First line for routine dental postoperative pain is an NSAID plus acetaminophen at therapeutic doses; this combination outperforms most opioid regimens for dental pain with fewer adverse effects.
• Reserve opioids for severe acute pain when the NSAID-plus-acetaminophen combination is inadequate or contraindicated; prescribe the lowest effective dose for the shortest duration.
• Tailor analgesia to the patient: an NSAID is avoided in chronic kidney disease, severe heart failure, active GI ulcer, late pregnancy, or in patients on anticoagulants where the bleeding risk outweighs benefit; acetaminophen is dose-adjusted in liver disease.
• Counsel patients on adverse effects, drug interactions (anticoagulants, antihypertensives blunted by NSAIDs), and storage of any opioids; the prescription should be written for the minimum duration and a quantity that matches that duration.