Pharmacology Flashcards

A patient receiving a propofol infusion for deep sedation begins to show signs of severe metabolic acidosis, new-onset dysrhythmia, and lipemic plasma. Which condition should the dental anesthesia assistant suspect, and what is the priority intervention?

Answer: Propofol infusion syndrome; discontinue propofol immediately and prepare for supportive hemodynamic management

Propofol infusion syndrome (PRIS) presents with metabolic acidosis, cardiac dysrhythmias, rhabdomyolysis, and lipemic/discolored plasma — particularly with high-dose or prolonged propofol infusions. Immediate discontinuation and supportive care are the cornerstone interventions. Dantrolene is specific to malignant hyperthermia, which propofol does not trigger. Naloxone reverses opioid effects but would not address this metabolic picture.

When ketamine is co-administered with a benzodiazepine in an office-based dental sedation setting, which pharmacodynamic rationale best explains the pairing?

Answer: The benzodiazepine reduces the incidence of emergence phenomena such as dysphoria and hallucinations caused by ketamine

Ketamine stimulates the limbic system and can produce unpleasant emergence reactions including dysphoria, vivid dreams, and hallucinations — especially in adults. Benzodiazepines such as midazolam blunt these CNS excitatory effects and are routinely co-administered for this reason. Benzodiazepines do not reverse bronchospasm (ketamine itself is bronchodilatory) and do not meaningfully accelerate ketamine metabolism.

A 62-year-old patient on chronic phenytoin therapy requires IV sedation for a complex extraction. The anesthesia team notes that midazolam's effect appears blunted despite a standard dose. Which mechanism most accurately accounts for this observation?

Answer: Chronic phenytoin therapy induces hepatic CYP3A4 enzymes, significantly increasing midazolam's first-pass and systemic metabolism

Phenytoin is a potent inducer of CYP3A4, the primary enzyme responsible for midazolam metabolism. Chronic induction leads to substantially increased clearance of midazolam, reducing its plasma concentrations and sedative effect. Phenytoin does not directly antagonize GABA-A receptors at clinical doses, and while P-gp effects exist, the dominant clinically relevant mechanism is hepatic CYP3A4 induction.

Dexmedetomidine produces sedation and analgesia through selective agonism at α2-adrenergic receptors. Which hemodynamic sequence most accurately describes its biphasic cardiovascular effect following a rapid IV loading dose?

Answer: Initial hypertension (peripheral α2B vasoconstriction) followed by sustained hypotension and bradycardia (central sympatholysis)

A rapid dexmedetomidine loading dose first activates peripheral α2B receptors on vascular smooth muscle, causing transient vasoconstriction and hypertension. This is followed by the predominant central α2A effect: reduced sympathetic outflow, resulting in sustained hypotension and bradycardia. Clinicians often slow or omit the loading dose to avoid this biphasic hemodynamic response, particularly in patients with cardiovascular disease.

Flumazenil is administered to reverse excessive benzodiazepine sedation after IV midazolam. The patient initially awakens and becomes conversational but then becomes re-sedated 25 minutes later. What is the most pharmacokinetically accurate explanation?

Answer: Flumazenil's elimination half-life (approximately 60 minutes) is shorter than midazolam's, allowing receptor re-occupation as flumazenil clears

Flumazenil has a short elimination half-life of approximately 45–60 minutes, significantly shorter than midazolam's 1.5–2.5 hours. Once flumazenil is cleared, residual midazolam can re-occupy the GABA-A receptor and re-establish sedation — a phenomenon called re-narcotization or resedation. This is why patients must be monitored for at least 2 hours after flumazenil administration and should not be discharged prematurely solely because they awakened after reversal.

A patient with a documented pseudocholinesterase deficiency requires succinylcholine-facilitated intubation during a general anesthetic for a prolonged oral surgical procedure. Which clinical scenario BEST characterizes the risk unique to this enzyme deficiency?

Answer: Prolonged neuromuscular blockade lasting hours because succinylcholine cannot be hydrolyzed to inactive metabolites

Succinylcholine is normally hydrolyzed rapidly (within 5–10 minutes) by plasma pseudocholinesterase (butyrylcholinesterase). In patients with pseudocholinesterase deficiency — whether genetic (dibucaine-resistant variants) or acquired (liver disease, pregnancy, organophosphate exposure) — this hydrolysis is severely impaired. Succinylcholine accumulates at the neuromuscular junction, extending the depolarizing block from minutes to potentially hours, requiring prolonged mechanical ventilation. This is not related to malignant hyperthermia, which is triggered by volatile anesthetics and succinylcholine through a separate ryanodine receptor mechanism.