Basic Sciences and Anatomy Flashcards

During deep sedation, a patient suddenly develops masseter muscle rigidity following succinylcholine administration. Which combination of findings would most strongly suggest malignant hyperthermia rather than simple masseter spasm?

Answer: Rapidly rising end-tidal CO2 combined with metabolic acidosis and hyperthermia

Malignant hyperthermia (MH) is a hypermetabolic crisis triggered by volatile anesthetics or succinylcholine in genetically susceptible individuals. The hallmark triad is rapidly rising end-tidal CO2 (reflecting uncontrolled cellular metabolism), metabolic acidosis (from anaerobic metabolism and lactic acid accumulation), and hyperthermia (often a late sign). Masseter muscle rigidity after succinylcholine is a recognized early warning, but alone it does not confirm MH. Transient jaw tightness with normal parameters suggests simple masseter spasm. Bradycardia and prolonged QT are not primary MH features.

The glossopharyngeal nerve (CN IX) provides sensory innervation to which specific pharyngeal region that, if inadequately anesthetized, can trigger laryngospasm during airway manipulation?

Answer: Posterior one-third of the tongue and the oropharynx including the vallecula

CN IX (glossopharyngeal) provides general somatic afferent (GSA) innervation to the posterior one-third of the tongue, palatine tonsils, oropharynx, and vallecula. Stimulation of these areas without adequate topical or nerve block anesthesia activates protective reflexes including laryngospasm. The anterior two-thirds of the tongue is CN V3 (lingual nerve). The epiglottis (supraglottic) is primarily CN X (superior laryngeal nerve, internal branch), and the infraglottic larynx is the recurrent laryngeal nerve. The soft palate receives contributions from both CN IX and CN X.

A patient with a history of myasthenia gravis requires sedation for a dental procedure. Which pharmacokinetic property of succinylcholine makes it particularly dangerous in this population compared to non-depolarizing agents?

Answer: Pseudocholinesterase deficiency common in myasthenia gravis patients prolongs succinylcholine's duration unpredictably, risking Phase II block

Patients with myasthenia gravis often have reduced acetylcholine receptor density and may have altered pseudocholinesterase activity, particularly if treated with pyridostigmine (an acetylcholinesterase inhibitor). Pyridostigmine also inhibits pseudocholinesterase, the enzyme responsible for succinylcholine's rapid hydrolysis in plasma. This inhibition can dramatically prolong succinylcholine's duration and increase the risk of Phase II (desensitization) block — a non-depolarizing-like state that cannot be reversed with neostigmine. Additionally, myasthenia gravis patients are exquisitely sensitive to non-depolarizing agents but may show resistance or unpredictable responses to succinylcholine.

Which anatomical landmark defines the boundary between the supraglottic and infraglottic compartments of the larynx, and which nerve supplies sensation exclusively below this boundary?

Answer: The vocal cords (rima glottidis); the recurrent laryngeal nerve

The vocal cords (rima glottidis) form the anatomical dividing line between the supraglottic larynx (above) and the infraglottic/subglottic larynx (below). The recurrent laryngeal nerve (a branch of CN X) provides sensory innervation to the mucosa below the vocal cords and motor innervation to all intrinsic laryngeal muscles except the cricothyroid. The internal branch of the superior laryngeal nerve supplies supraglottic sensation (epiglottis down to the level of the cords). This distinction is clinically critical for transtracheal nerve blocks and topical anesthesia planning during awake airway management.

A healthy 35-year-old patient receives midazolam 2 mg IV and fentanyl 100 mcg IV for moderate sedation. Fifteen minutes later, the patient's respiratory rate drops to 6 breaths/min, SpO2 is 88%, and they are unresponsive to verbal stimulation. After supplemental oxygen, you administer flumazenil 0.2 mg IV with minimal effect. What is the most likely explanation and next step?

Answer: The predominant respiratory depression is opioid-mediated; administer naloxone 0.04–0.1 mg IV titrated

When a patient receives both a benzodiazepine and an opioid and develops significant respiratory depression, the contribution of each agent must be assessed. Flumazenil reverses benzodiazepine-mediated sedation but has no effect on opioid-induced respiratory depression. A minimal response to flumazenil strongly suggests that fentanyl's respiratory depression is the dominant factor. The appropriate next step is titrated naloxone (low doses of 0.04–0.1 mg IV to avoid acute pain, agitation, or pulmonary edema from rapid opioid reversal). Flumazenil's maximum dose is typically 1 mg, but additional flumazenil would not address opioid-mediated depression. Cricothyrotomy is a surgical airway, not indicated as an immediate first step here.

During a dental anesthesia procedure, a patient's blood pressure suddenly drops to 70/40 mmHg, heart rate rises to 130 bpm, and urticarial wheals appear on the chest and neck 8 minutes after IV administration of a colloid fluid. Which immunologic mechanism most precisely explains this reaction, and which mediator is primarily responsible for the vasodilation?

Answer: Type I IgE-mediated hypersensitivity; histamine and prostaglandin D2 from mast cell degranulation cause vasodilation

This presentation — urticaria, hypotension, and tachycardia within minutes of drug administration — is classic anaphylaxis, a Type I IgE-mediated hypersensitivity reaction. On prior sensitization, antigen-specific IgE antibodies bind to high-affinity FcεRI receptors on mast cells and basophils. Re-exposure crosslinks IgE, triggering degranulation and release of preformed mediators (histamine, tryptase) and newly synthesized lipid mediators (prostaglandin D2, leukotrienes). Histamine acting on H1 receptors on vascular smooth muscle and prostaglandin D2 are primary drivers of vasodilation and increased vascular permeability. Type III reactions (serum sickness) are delayed (days). Type IV reactions take 48–72 hours and do not cause urticaria acutely. Some colloids (dextran, gelatins) can also cause direct (non-IgE) mast cell activation (anaphylactoid), but the mechanism involving IgE is the most precise answer for the classic anaphylaxis pathway described.