A long medication list before an extraction

Correct answer: C. It reduces hepatic clearance of lidocaine, both by lowering cardiac output and by competing for the same hepatic enzymes

• A. Plasma (pseudo)cholinesterase hydrolyses the ESTER anaesthetics — procaine, benzocaine, tetracaine. Lidocaine is an AMIDE and is metabolised in the liver, which is the entire reason this hepatic interaction exists.
• B. Protein binding displacement is not the mechanism. Lidocaine is roughly 65% protein bound and beta blockers do not displace it to any clinically meaningful degree.
• C. CORRECT, and by TWO distinct mechanisms, which is what the question is testing. First, a non-selective beta blocker reduces CARDIAC OUTPUT and therefore hepatic blood flow; lidocaine is a high-extraction drug whose clearance is flow-limited, so less liver perfusion directly means slower elimination. Second, propranolol and the amide local anaesthetics COMPETE for the same hepatic microsomal enzyme pathways. Both effects raise and prolong the plasma lidocaine concentration — which is why the DURATION OF ACTION of lidocaine is increased in the presence of propranolol, and why the maximum dose should be reduced, injection made slowly, and aspiration performed carefully.
• D. The rate of absorption from the site is governed by the vasoconstrictor concentration and by the vascularity of the tissue, not by a systemic beta blocker.

Note: There is a SECOND and separate propranolol interaction that must not be confused with this one. Epinephrine given to a patient on a NON-SELECTIVE beta blocker produces UNOPPOSED ALPHA-1 stimulation, since the vasodilatory beta-2 response is blocked — the result is a hypertensive response with reflex bradycardia. Limit the epinephrine dose, aspirate, and monitor blood pressure. Cardioselective agents such as metoprolol and atenolol carry considerably less of this risk. Note this patient's resting pulse of 58.

Correct answer: C. Imipramine

• A. There is a clear interaction here, and in fact two — the tricyclic with epinephrine, and the non-selective beta blocker with both epinephrine and lidocaine.
• B. Acetaminophen has no adrenergic activity and no interaction with epinephrine.
• C. CORRECT. IMIPRAMINE is a TRICYCLIC ANTIDEPRESSANT. Tricyclics block the reuptake of noradrenaline at the adrenergic nerve terminal, so an injected vasoconstrictor is not cleared from the synapse normally and its pressor effect is markedly EXAGGERATED — producing hypertension and dysrhythmias. Epinephrine is not absolutely contraindicated, but the dose must be limited (a commonly cited ceiling is about 0.04 mg, roughly two cartridges of 1:100,000), aspiration is essential, and LEVONORDEFRIN and NORADRENALINE must be AVOIDED ENTIRELY, since the interaction with those agents is far more severe. Tricyclics also cause pronounced xerostomia, orthostatic hypotension and a lowered seizure threshold.
• D. Sumatriptan is a selective SEROTONIN (5-HT1B/1D) RECEPTOR AGONIST used for acute migraine. It is not an antidepressant and not an SSRI. It matters medically — it causes coronary vasoconstriction and is contraindicated in ischaemic heart disease and uncontrolled hypertension — but it is not the drug driving the interaction with the vasoconstrictor.

Note: ⚠️ The recall author described sumatriptan as ‘an SSRI I haven't heard of’. It is a serotonin receptor AGONIST, not a reuptake inhibitor. The drug responsible for the exaggerated cardiovascular response in this list is the TRICYCLIC. Keep the classes straight: TCAs exaggerate the epinephrine response; non-selective beta blockers give unopposed alpha stimulation; SSRIs and MAOIs, contrary to older teaching, do NOT require epinephrine restriction in dental doses.

Correct answer: C. A block of the nerve within the infraorbital canal

• A. The FACIAL nerve (CN VII) exits the skull at the STYLOMASTOID FORAMEN and supplies every muscle of facial expression, including levator labii superioris, levator anguli oris and zygomaticus major and minor. A lesion there paralyses the whole half of the face and abolishes lip elevation.
• B. A vestibular infiltration deposits solution among those same terminal facial nerve branches as they run superficially, producing a transient motor weakness of the lip — exactly what alarmed this patient. It is harmless and resolves with the anaesthetic.
• C. CORRECT as the exception. The nerve running in the infraorbital canal is the INFRAORBITAL nerve, the terminal continuation of the maxillary division of the trigeminal nerve (V2). It is purely SENSORY, supplying the lower eyelid, the side of the nose and the skin and mucosa of the upper lip, and giving off the zygomaticotemporal and zygomaticofacial branches along its course. Blocking it NUMBS the upper lip but leaves the motor supply entirely untouched — which is why a patient with a profound infraorbital block still smiles normally on that side.
• D. Within the parotid gland the facial nerve divides into its five terminal branches. The zygomatic and buccal branches are the ones that elevate the upper lip, and injuring them during parotid surgery is a recognised and permanent complication.

Note: The whole trick of this item is SENSORY versus MOTOR. V2 SENSES the upper lip; CN VII MOVES it. The same logic explains the far more frequently examined complication of a misplaced inferior alveolar block — solution deposited too deep and posterior enters the parotid capsule, anaesthetises the facial nerve trunk and produces a transient unilateral facial palsy with an inability to close the eye, which must be protected until sensation returns.

Correct answer: D. Styloglossus

• A. Hyoglossus DEPRESSES the tongue, drawing its sides downward toward the hyoid.
• B. Palatopharyngeus elevates the pharynx and larynx during swallowing and forms the POSTERIOR tonsillar pillar. It is not a muscle of the tongue.
• C. Genioglossus is the PROTRUDER — the so-called safety muscle of the tongue, since it pulls the tongue forward and prevents it obstructing the airway. Bilateral action protrudes; unilateral paralysis makes the tongue deviate TOWARD the affected side on protrusion.
• D. CORRECT. STYLOGLOSSUS runs from the styloid process to the side of the tongue and both ELEVATES and RETRACTS it — the movement that initiates swallowing. PALATOGLOSSUS also elevates, specifically the POSTERIOR part of the tongue, and it is the one extrinsic tongue muscle NOT supplied by the hypoglossal nerve; it is innervated by the vagus through the pharyngeal plexus, because functionally it belongs to the soft palate.

Note: The four extrinsic muscles by function: genioglossus PROTRUDES, hyoglossus DEPRESSES, styloglossus ELEVATES and retracts, palatoglossus elevates the POSTERIOR tongue. The INTRINSIC muscles change the tongue's shape rather than its position — superior and inferior longitudinal shorten it and curl the tip, the TRANSVERSE narrows and lengthens it, and the vertical flattens and widens it. All the intrinsics and all the extrinsics except palatoglossus are supplied by CN XII.