Pharmacology Flashcards

A patient on chronic buprenorphine therapy for opioid use disorder requires procedural sedation. Which statement best describes the expected pharmacodynamic interaction with intravenous fentanyl?

Answer: Buprenorphine's partial agonist/antagonist properties at the mu-receptor may attenuate fentanyl's analgesic effect and require higher opioid doses that still may be insufficient

Buprenorphine is a partial agonist with very high mu-receptor affinity and slow dissociation. It occupies and blocks mu receptors, making additional full opioid agonists like fentanyl significantly less effective. Patients may require much higher opioid doses with unpredictable results, and the provider should consult with the prescribing physician before the procedure. Buprenorphine is NOT a pure antagonist, does not act solely at kappa receptors, and cannot be displaced by fentanyl's lipid solubility.

Which mechanism best explains why mivacurium is contraindicated in patients with pseudocholinesterase deficiency, even though it is a non-depolarizing neuromuscular blocking agent?

Answer: Mivacurium is hydrolyzed by plasma pseudocholinesterase, so deficiency prolongs its duration of action dramatically

Unlike most non-depolarizing agents which are metabolized by the liver or excreted renally, mivacurium is uniquely dependent on plasma pseudocholinesterase for hydrolysis—similar to succinylcholine. In patients with pseudocholinesterase deficiency or atypical pseudocholinesterase, mivacurium's duration extends from ~15–20 minutes to potentially several hours, causing prolonged neuromuscular blockade. The other options are pharmacologically incorrect.

A 52-year-old patient taking phenelzine (an MAO inhibitor) for depression is scheduled for office-based oral surgery under sedation. Which analgesic combination poses the greatest risk for a life-threatening serotonin syndrome?

Answer: Meperidine and midazolam

Meperidine is uniquely dangerous in patients on MAO inhibitors because it inhibits serotonin reuptake in addition to its opioid effects. Combined with an MAOI, this creates a severe serotonin syndrome characterized by hyperthermia, agitation, neuromuscular excitability, and cardiovascular instability that can be fatal. Midazolam adds to CNS depression risk. Tramadol also inhibits serotonin reuptake and would be dangerous, but meperidine + MAOI is the classic and most severe interaction. Fentanyl has minimal serotonergic activity and is the preferred opioid in MAOI patients when opioids are necessary.

During deep sedation, a patient's oxygen saturation drops to 88% and capnography shows a flat waveform. The anesthesia assistant administers a jaw thrust, which does not restore ventilation. Flumazenil 0.2 mg IV is given with no response. The most likely explanation is:

Answer: The sedation regimen included an opioid component causing respiratory depression unresponsive to a benzodiazepine antagonist

Flumazenil reverses only benzodiazepine-mediated CNS and respiratory depression. If the sedation protocol included an opioid (e.g., fentanyl), the opioid's contribution to respiratory depression is NOT reversed by flumazenil. In multimodal sedation, inadequate reversal after flumazenil strongly suggests an opioid component is driving the hypoventilation, requiring naloxone. Flumazenil peaks within 1–3 minutes IV; waiting 5–10 minutes is incorrect. Flumazenil's half-life is actually shorter than most benzodiazepines (re-sedation is the real concern, not failure of reversal). Laryngospasm is unrelated to benzodiazepine withdrawal.

Which property of dexmedetomidine makes it uniquely advantageous over propofol or benzodiazepines for procedural sedation in patients with a history of obstructive sleep apnea (OSA)?

Answer: Dexmedetomidine produces sedation without significant respiratory depression by acting on alpha-2 adrenergic receptors in the locus coeruleus

Dexmedetomidine is a highly selective alpha-2 adrenergic agonist that produces sedation by mimicking natural sleep pathways via the locus coeruleus. Crucially, it preserves respiratory drive and hypercapnic/hypoxic ventilatory response at standard sedation doses, making it significantly safer in OSA patients compared to propofol, benzodiazepines, or opioids, which all suppress respiratory centers. It does not produce deeper sedation than propofol at equivalent doses, lacks significant bronchodilatory effect, and does not block laryngeal receptors.

A dental anesthesia team is managing a patient who has received 8 mg/kg of lidocaine with epinephrine (far exceeding the safe limit) and now presents with tonic-clonic seizures, bradycardia, and widening QRS complexes on the monitor. The MOST appropriate first-line pharmacologic intervention for the cardiovascular toxicity is:

Answer: 20% lipid emulsion (Intralipid) infusion to sequester free lidocaine from cardiac tissue

Intravenous lipid emulsion therapy (IVLE) with 20% Intralipid is now the definitive pharmacologic treatment for severe local anesthetic systemic toxicity (LAST) involving cardiovascular collapse. The 'lipid sink' hypothesis explains its mechanism: the large lipid phase in blood sequesters and extracts the lipophilic local anesthetic from myocardial tissue. Dosing is 1.5 mL/kg bolus followed by infusion. While sodium bicarbonate may help with sodium channel blockade, and atropine may be an adjunct, IVLE is the primary intervention per ASRA guidelines for cardiovascular LAST. Bretylium is no longer available in the US and is not current standard of care.