Pharmacology
Inhaled & IV anesthetics, opioids, NMBDs, reversal agents, anti-emetics, vasoactive drugs, toxicology, drug interactions. ← Back to Q-Bank
Q1. Methemoglobinemia from prilocaine
A 4-year-old undergoing awake fiberoptic intubation receives topical prilocaine 600 mg via the EMLA pathway. Thirty minutes later, SpO₂ reads 84% on the pulse oximeter, but the arterial blood gas shows PaO₂ 320 mmHg on FiO₂ 1.0. Arterial blood is chocolate-brown. Which is the most appropriate next step?
A. Increase FiO₂ and add PEEP
B. Administer methylene blue 1–2 mg/kg IV over 3–5 minutes
C. Administer hydroxocobalamin 5 g IV
D. Administer ascorbic acid IV
E. Initiate exchange transfusion
Show answer
Answer: B. Classic methemoglobinemia from prilocaine (aminophenol metabolites oxidize Fe²⁺ → Fe³⁺). The saturation gap (low SpO₂ with normal PaO₂) is the giveaway — methemoglobin absorbs at 630 nm. Ascorbic acid is the alternative only if G6PD-deficient (methylene blue needs NADPH from the hexose-monophosphate shunt; G6PD-deficient RBCs hemolyze).
Q2. Glucagon mechanism in β-blocker toxicity
A 68-year-old on chronic β-blocker therapy develops refractory hypotension after CPB despite epinephrine and norepinephrine. Which mechanism best supports the use of glucagon?
A. Direct α₁-adrenergic agonism
B. Inhibition of phosphodiesterase III
C. Activation of adenylyl cyclase via a non-β-adrenergic G-protein–coupled receptor
D. Stimulation of cardiac ryanodine receptors
E. Blockade of muscarinic acetylcholine receptors
Show answer
Answer: C. Glucagon bypasses the β-receptor → ↑ cAMP → positive inotropy/chronotropy. Useful in β-blocker overdose, post-CPB low CO, post-MI, refractory anaphylaxis on β-blockers. Contraindicated in pheochromocytoma and insulinoma.
Q3. Pseudocholinesterase deficiency interpretation
A 32-year-old undergoing C-section remains paralyzed 90 minutes after 1.5 mg/kg succinylcholine. Dibucaine number returns at 20. This indicates:
A. Acquired pseudocholinesterase deficiency from severe liver disease
B. Heterozygous atypical genotype
C. Homozygous atypical genotype
D. Normal genotype with pregnancy-related enzyme reduction
E. Phase II block from excessive dosing
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Answer: C. Dibucaine number = inhibition of normal enzyme: ~80 = normal, ~40–60 = heterozygous (20–30 min recovery), ~20 = homozygous (4–8 hours). Pregnancy reduces total activity ~25–30% but doesn't change the dibucaine number.
Q4. Volatile anesthetic blood:gas coefficients
Which inhaled anesthetic has the lowest blood:gas partition coefficient?
A. Halothane
B. Isoflurane
C. Sevoflurane
D. Nitrous oxide
E. Desflurane
Show answer
Answer: E. Blood:gas coefficients: desflurane 0.42 < nitrous oxide 0.46 < sevoflurane 0.69 < isoflurane 1.46 < halothane 2.54. Lower solubility → faster equilibration → faster induction and emergence.
Q5. Nitrous oxide and vitamin B12
A 28-year-old with chronic kidney disease receives 70% nitrous oxide for a 6-hour procedure. Which metabolic process is impaired?
A. Acetylcholinesterase activity at the NMJ
B. Methionine synthase activity via irreversible oxidation of vitamin B12
C. Hepatic CYP3A4-mediated oxidation
D. Plasma cholinesterase function
E. Coenzyme A acylation
Show answer
Answer: B. Nitrous oxide irreversibly oxidizes the cobalt atom of vitamin B12, inactivating methionine synthase and thymidylate synthetase. Prolonged exposure → megaloblastic changes; 4 days → agranulocytosis. CKD patients may have elevated homocysteine — prudent to avoid.
Q6. Desflurane and CO production
Which combination most increases carbon monoxide production from CO₂ absorbents?
A. Sevoflurane with fresh soda lime
B. Desflurane with desiccated soda lime
C. Isoflurane at low fresh gas flow with normal-moisture absorbent
D. Halothane with calcium hydroxide
E. Nitrous oxide alone
Show answer
Answer: B. Desflurane produces the most CO of any volatile. CO production is exothermic and increased by desiccated absorbents, high temperature, and low fresh gas flows. (Sevoflurane produces the most heat and Compound A but less CO.)
Q7. Hepatic injury and volatile anesthetics
Which volatile is most associated with immune-mediated fulminant hepatic necrosis?
A. Sevoflurane
B. Desflurane
C. Isoflurane
D. Halothane
E. Nitrous oxide
Show answer
Answer: D. Halothane hepatitis is the classic immune-mediated fulminant necrosis. Halothane also decreases hepatic arterial blood flow more than other volatiles. Sevoflurane and desflurane are least likely to cause immune-mediated hepatic injury.
Q8. Halothane and arrhythmias
A pediatric patient under halothane anesthesia receives epinephrine for hemostasis and develops premature ventricular contractions progressing to ventricular tachycardia. The underlying mechanism is:
A. Direct β₁ stimulation by halothane
B. Halothane-induced sensitization of the myocardium to catecholamines
C. Coronary steal phenomenon
D. Hypercalcemia from halothane
E. QT prolongation from halothane
Show answer
Answer: B. Halothane sensitizes the myocardium to catecholamine-induced dysrhythmias, especially in the presence of hypercarbia. Sevoflurane has largely replaced halothane in pediatrics — fewer arrhythmias and less bradycardia.
Q9. Propofol mechanism
Propofol's hypnotic effect is primarily mediated through:
A. NMDA receptor antagonism
B. Potentiation of GABAₐ receptors
C. α₂-adrenergic receptor agonism
D. μ-opioid receptor agonism
E. Glycine receptor agonism
Show answer
Answer: B. Propofol potentiates GABAₐ receptors. It decreases CMRO₂, CBF, ICP, and IOP. Causes the largest drop in systemic BP of any IV induction agent. No analgesic property. Strong antiemetic at sub-hypnotic infusions.
Q10. Propofol infusion syndrome
A 14-year-old with traumatic brain injury is sedated on propofol 6 mg/kg/hr for 36 hours. He develops metabolic acidosis, rhabdomyolysis, hyperkalemia, and new bradycardia. The mechanism is:
A. Allergic reaction to soybean emulsion
B. Impaired free fatty acid utilization and mitochondrial dysfunction
C. Direct propofol toxicity to AV node
D. Soybean-derived endotoxin contamination
E. Carrier-induced renal injury from EDTA
Show answer
Answer: B. Propofol infusion syndrome: high-dose (>4–5 mg/kg/hr) and prolonged (>24–48 hr) propofol impairs cellular FFA utilization and mitochondrial activity → cardiac/skeletal muscle damage, rhabdomyolysis, lactic acidosis, hyperkalemia, hypertriglyceridemia. Children > adults. Concurrent catecholamines or steroids increase risk.
Q11. Ketamine receptor profile
Ketamine's analgesia at high doses (1–2 mg/kg IV) is primarily mediated through:
A. NMDA receptor antagonism
B. μ-opioid receptor agonism
C. α₂-adrenergic agonism
D. GABAₐ potentiation
E. Voltage-gated sodium channel blockade
Show answer
Answer: B. At low doses (75–250 mcg/kg), ketamine acts at NMDA receptors; at high doses (1–2 mg/kg IV), the μ-opioid receptor predominates. Ketamine preserves airway reflexes and respiratory drive, increases CMRO₂, and produces indirect sympathetic stimulation via inhibition of norepinephrine reuptake.
Q12. Etomidate and the adrenal axis
A 72-year-old septic patient is induced with etomidate. Which complication is most concerning in the postoperative period?
A. Hypertensive crisis from sympathetic surge
B. Adrenal suppression from 11-β-hydroxylase inhibition
C. Coronary steal
D. Increased CMRO₂
E. Prolonged neuromuscular blockade
Show answer
Answer: B. Etomidate inhibits 11-β-hydroxylase → adrenal suppression detectable even after a single induction dose; clinical significance debated in septic patients. Etomidate also causes pain on injection, myoclonus, PONV, and can induce epileptiform activity. Avoid in seizure disorders.
Q13. Methohexital paradox
In a patient undergoing electroconvulsive therapy, which IV anesthetic is preferred because it facilitates rather than suppresses seizure activity?
A. Propofol
B. Thiopental
C. Methohexital
D. Dexmedetomidine
E. Diazepam
Show answer
Answer: C. Methohexital activates epileptic foci (unlike other barbiturates which suppress EEG activity). Useful for ECT and for ictal mapping during surgery. Etomidate also lengthens seizures and is an alternative if hemodynamics dictate.
Q14. Dexmedetomidine biphasic response
After a 1 mcg/kg IV bolus of dexmedetomidine over 1 minute, what hemodynamic pattern would you expect in the first 3–10 minutes?
A. Sustained hypotension and tachycardia
B. Transient hypertension followed by bradycardia and hypotension
C. Sustained hypertension and bradycardia
D. Tachycardia followed by reflex hypotension
E. No significant change
Show answer
Answer: B. Biphasic response — peripheral α₂B-mediated vasoconstriction (peak ~3 min hypertension), then central α₂A-mediated reduction in sympathetic outflow → bradycardia and hypotension by ~10 min. Slow administration mitigates the hypertensive phase. Dexmed is 1600:1 α₂:α₁ vs. clonidine 200:1.
Q15. Morphine metabolites in renal failure
A 65-year-old with ESRD on hemodialysis receives morphine for postoperative pain and develops myoclonus, prolonged sedation, and respiratory depression. The most likely culprit is accumulation of:
A. Normorphine
B. Morphine-6-glucuronide
C. Norfentanyl
D. Hydromorphone-3-glucuronide
E. Naloxone metabolite
Show answer
Answer: B. M6G is nearly 100× more potent than morphine at μ-receptors and accumulates in renal failure → myoclonus, sedation, seizures, respiratory depression. M3G (lower μ-affinity) is neuroexcitatory at high doses → myoclonus, allodynia. Avoid morphine in ESRD; consider hydromorphone (still has H3G concerns) or fentanyl.
Q16. Meperidine and SSRI
A patient on fluoxetine receives meperidine for postoperative shivering. He develops hyperthermia, agitation, and clonus. The mechanism is:
A. Anaphylaxis from meperidine
B. Serotonin syndrome (meperidine inhibits serotonin reuptake)
C. MAO-B substrate accumulation
D. Direct dopaminergic stimulation
E. Histamine release
Show answer
Answer: B. Meperidine is a serotonin reuptake inhibitor as well as a κ-opioid agonist. Coadministration with SSRIs, MAOIs, tramadol, or methadone can precipitate serotonin syndrome. Meperidine's metabolite normeperidine is neurotoxic (seizures) and renally excreted.
Q17. Remifentanil metabolism
Remifentanil's ultra-short context-sensitive half-time is due to:
A. Hepatic CYP3A4 metabolism
B. Renal excretion of parent drug
C. Nonspecific tissue and plasma esterase hydrolysis
D. Plasma cholinesterase hydrolysis
E. Hofmann elimination
Show answer
Answer: C. Remifentanil is hydrolyzed by nonspecific plasma and tissue esterases — independent of hepatic and renal function. Context-sensitive half-time ~3–4 min regardless of infusion duration. Not metabolized by plasma cholinesterase (so unaffected by pseudocholinesterase deficiency).
Q18. Alfentanil characteristics
The rapid onset of alfentanil relative to fentanyl is best explained by:
A. Higher lipid solubility
B. Higher unionized fraction at physiologic pH (low pKa)
C. Lower protein binding
D. Smaller volume of distribution
E. Faster receptor binding
Show answer
Answer: B. Alfentanil has the lowest pKa (~6.5) of the fentanyl family → ~90% unionized at physiologic pH → rapid BBB crossing. Less lipid-soluble than fentanyl (which prolongs offset) → quick onset and offset. Rule of 4s: 4× faster onset, ¼ duration and potency vs. fentanyl.
Q19. Methadone unique properties
A 45-year-old with neuropathic pain after spinal surgery is started on methadone. Beyond μ-opioid agonism, which property contributes to its efficacy for neuropathic pain?
A. δ-opioid receptor agonism
B. NMDA receptor antagonism
C. α₂-adrenergic agonism
D. COX-2 inhibition
E. Sodium channel blockade
Show answer
Answer: B. Methadone is an NMDA antagonist + serotonin/norepinephrine reuptake inhibitor + μ-agonist — useful in opioid tolerance and neuropathic pain. Key risk: QT prolongation and torsades, especially with CYP3A4 inhibitors. Unpredictable plasma half-life 13–58 hours; analgesic effect 4–8 hours.
Q20. Butorphanol and biliary spasm
Compared with morphine, which opioid is least likely to cause biliary spasm and sphincter of Oddi contraction?
A. Fentanyl
B. Hydromorphone
C. Meperidine
D. Butorphanol
E. Oxycodone
Show answer
Answer: D. Butorphanol (κ-agonist, partial μ-agonist) does not increase pressure in the common bile duct. Morphine, fentanyl, and meperidine all cause sphincter of Oddi contraction. Butorphanol also has a ceiling effect on respiratory depression and is renally safe (no active metabolites).
Q21. Naloxone half-life mismatch
A patient who took an overdose of long-acting morphine is given naloxone in the ED and is awake and breathing. Why is continuous infusion or repeat dosing necessary?
A. Naloxone is rapidly metabolized by pseudocholinesterase
B. Naloxone has a half-life of only 1–2 hours, shorter than most opioids
C. Naloxone induces upregulation of μ-receptors
D. Naloxone undergoes enterohepatic recirculation
E. Naloxone is highly protein-bound
Show answer
Answer: B. Naloxone half-life 1–2 hr; many opioids (especially methadone, sustained-release formulations) last far longer. Renarcotization is the rule unless infusion is started. Side effects of abrupt reversal: severe pain, hypertension, pulmonary edema.
Q22. Succinylcholine contraindications
In which of the following is succinylcholine most contraindicated due to risk of hyperkalemic cardiac arrest?
A. Acute trauma 1 hour after injury
B. Burn injury 5 days post-injury covering 35% TBSA
C. Hyperkalemia of 5.5 from chronic ACE inhibitor
D. Family history of myasthenia gravis
E. Pregnancy at term
Show answer
Answer: B. Upregulation of immature (extrajunctional) ACh receptors begins ~24–72 hr after burn, denervation, prolonged immobility, or stroke and peaks at 5–6 weeks. Succinylcholine causes massive K⁺ efflux. Avoid in burns >24 hr old, denervating disorders (MS, ALS, muscular dystrophies), and prolonged immobility. Acute trauma <24 hr is generally still safe.
Q23. Succinylcholine in Duchenne muscular dystrophy
A 6-year-old boy with previously undiagnosed Duchenne muscular dystrophy receives succinylcholine for laryngospasm and develops bradycardia progressing to cardiac arrest. The most likely mechanism is:
A. Direct vagal stimulation by succinylcholine
B. Massive hyperkalemia from rhabdomyolysis and immature ACh receptors
C. Malignant hyperthermia
D. Calcium release from sarcoplasmic reticulum
E. Anaphylaxis
Show answer
Answer: B. Duchenne is X-linked dystrophin deficiency; succinylcholine triggers life-threatening hyperkalemia. Volatile agents can also cause rhabdomyolysis. Sux is essentially contraindicated in children with undiagnosed myopathy — this is why the FDA labeled succinylcholine with a strong warning against routine pediatric use.
Q24. Cisatracurium metabolism
Which property makes cisatracurium attractive in patients with hepatic and renal failure?
A. Plasma cholinesterase hydrolysis
B. Hofmann elimination (pH- and temperature-dependent)
C. Renal excretion of unchanged drug
D. Biliary excretion of glucuronide metabolite
E. Hepatic CYP3A4 metabolism
Show answer
Answer: B. Hofmann elimination is non-organ-dependent. Laudanosine is the breakdown product (can precipitate seizures at very high cumulative doses); cisatracurium is more potent than atracurium → less laudanosine produced. Hofmann is enhanced by alkalosis and hyperthermia.
Q25. Sugammadex dosing
A patient receives 1.2 mg/kg rocuronium for RSI. Five minutes later, the case is canceled. What sugammadex dose is required?
A. 2 mg/kg
B. 4 mg/kg
C. 8 mg/kg
D. 16 mg/kg
E. Sugammadex cannot reverse rocuronium this soon
Show answer
Answer: D. Sugammadex 16 mg/kg reverses immediately after a high-dose intubating bolus (rescue dose). 4 mg/kg for deep block (1–2 PTC); 2 mg/kg for moderate block (TOF count ≥2). Dosing based on actual body weight. Sugammadex is ineffective against benzylisoquinoliniums (cisatracurium, atracurium).
Q26. Neostigmine-glycopyrrolate dosing
For reversal of neuromuscular blockade with neostigmine, glycopyrrolate is preferred over atropine because:
A. Glycopyrrolate has a longer half-life matched to neostigmine
B. Atropine causes bradycardia at the doses required
C. Glycopyrrolate has less CNS penetration and less tachycardia
D. Atropine is ineffective against the muscarinic effects of neostigmine
E. Glycopyrrolate is unaffected by renal function
Show answer
Answer: C. Glycopyrrolate is a quaternary amine (doesn't cross BBB) and onset/duration are better matched to neostigmine. Pair edrophonium (faster onset) with atropine. In pregnancy/peds, atropine is preferred because glycopyrrolate doesn't cross placenta while neostigmine does → fetal bradycardia risk.
Q27. Ondansetron side effect
Which side effect of ondansetron most concerns the anesthesiologist managing a patient on methadone?
A. Headache
B. Constipation
C. QT prolongation and risk of torsades
D. Hepatotoxicity
E. Extrapyramidal symptoms
Show answer
Answer: C. Ondansetron prolongs QT in ~20% of patients. Methadone also prolongs QT. Cumulative risk for torsades. Other QT-prolonging anesthesia drugs: droperidol, haloperidol, amiodarone, class III antiarrhythmics.
Q28. Droperidol mechanism
Droperidol's antiemetic effect is primarily through:
A. 5-HT₃ receptor antagonism
B. Dopamine D₂ receptor antagonism (butyrophenone)
C. NK1 receptor antagonism
D. Muscarinic antagonism
E. Histamine H₁ antagonism
Show answer
Answer: B. Droperidol is a butyrophenone D₂ antagonist. FDA black-box warning for QT prolongation/torsades at psych doses (>25 mg) — the antiemetic doses (0.625–1.25 mg) are still considered safe rescue therapy.
Q29. Aprepitant
Aprepitant is most useful for the prevention of which type of PONV?
A. Early PONV (0–2 hours postoperative)
B. Delayed PONV (12–48 hours postoperative)
C. Motion-induced nausea
D. Chemotherapy-induced acute vomiting
E. Opioid-induced sedation
Show answer
Answer: B. Aprepitant is an NK1 (neurokinin-1) receptor antagonist with a 10-hour half-life — particularly effective for delayed PONV. Give preoperatively PO. Substance P binds NK1 in the nucleus tractus solitarii.
Q30. Scopolamine and physostigmine pitfall
A patient receives a scopolamine patch preoperatively and is on varenicline for smoking cessation. Postoperatively she develops agitation and is given physostigmine. Why is this concerning?
A. Physostigmine antagonizes varenicline
B. Combined overstimulation of central acetylcholine receptors can precipitate seizures
C. Physostigmine causes severe hypotension with scopolamine
D. Varenicline blocks physostigmine
E. Scopolamine prevents reversal of varenicline
Show answer
Answer: B. Physostigmine (tertiary amine, crosses BBB) reverses central anticholinergic effects of scopolamine. Combined with varenicline (a partial α₄β₂ nicotinic agonist), overstimulation of central acetylcholine receptors → seizures. Caution with concomitant nicotinic drugs (bupropion, dextromethorphan, NMDA antagonists).
Q31. Phenylephrine dose and onset
For an adult with sudden hypotension under spinal anesthesia, an appropriate IV bolus of phenylephrine is:
A. 5–10 mcg
B. 50–200 mcg
C. 500–1000 mcg
D. 2–5 mg
E. 10 mg
Show answer
Answer: B. Phenylephrine 50–200 mcg IV bolus; onset 1 min, duration 5–10 min. Pure α₁ agonist → ↑SVR, reflex bradycardia. IM dose 2–5 mg/kg works in 10–15 min when no IV is available.
Q32. Vasopressin in vasoplegic shock
A patient develops refractory hypotension after CPB despite high-dose norepinephrine. Vasopressin is added. Beyond V₁ receptor agonism, which property makes vasopressin useful in vasoplegia?
A. Direct β₁ stimulation
B. Effective at acidotic pH where catecholamine receptors are desensitized
C. Inhibition of nitric oxide synthase
D. Increased preload via venoconstriction
E. NMDA antagonism
Show answer
Answer: B. Vasopressin retains efficacy in acidotic, catecholamine-desensitized vasoplegia (e.g., post-CPB, sepsis). Acts via V₁ on vascular smooth muscle through IP3. Methylene blue (guanylate cyclase inhibitor) and hydroxocobalamin (NO scavenger) are last-line for refractory vasoplegia.
Q33. Dopamine receptor dose dependence
At which infusion range does dopamine predominantly act on α₁ receptors with generalized vasoconstriction and reduced cardiac output?
A. <1 mcg/kg/min
B. 1–3 mcg/kg/min
C. 3–10 mcg/kg/min
D. >10 mcg/kg/min
E. Dose-independent
Show answer
Answer: D. Dopamine: low (D₁, ≤3 mcg/kg/min) → renal/mesenteric vasodilation; mid (β₁, 3–10) → ↑contractility/HR via norepi release; high (α₁, >10) → systemic vasoconstriction. Not recommended over norepinephrine in shock — higher arrhythmia and mortality in cardiogenic shock.
Q34. Milrinone mechanism and contraindication
A patient with severe aortic stenosis develops low cardiac output. Why is milrinone not an ideal inotrope here?
A. Milrinone increases SVR severely
B. Milrinone causes profound bradycardia
C. Milrinone reduces afterload, worsening the AS gradient
D. Milrinone is metabolized too slowly
E. Milrinone causes pulmonary hypertension
Show answer
Answer: C. Milrinone is a PDE3 inhibitor (inodilator) → ↑cAMP → ↑contractility + lusitropy + arterial/venous dilation. The afterload reduction is harmful in fixed obstructive lesions (AS, HOCM). Renally excreted — adjust in renal failure. Side effects: tachycardia, hypotension, AFib.
Q35. Fenoldopam mechanism
Fenoldopam is useful in hypertensive emergencies particularly when:
A. Tachycardia must be avoided
B. Renal preservation is a priority
C. Pulmonary hypertension is present
D. There is severe aortic stenosis
E. The patient has long QT syndrome
Show answer
Answer: B. Fenoldopam is a selective D₁ agonist → vasodilation (coronary, peripheral, renal, splanchnic) via cAMP. Increases renal blood flow and GFR — useful when renal perfusion is a concern. No α or β activity.
Q36. Nitroprusside toxicity
A patient receives a sodium nitroprusside infusion at 8 mcg/kg/min for 12 hours. He develops metabolic acidosis, altered mental status, and a high mixed venous oxygen saturation. The mechanism is:
A. Methemoglobinemia
B. Cyanide toxicity
C. Coronary steal
D. Carbon monoxide poisoning
E. Lactic acidosis from impaired hepatic perfusion
Show answer
Answer: B. Sodium nitroprusside releases nitric oxide and cyanide. High mixed-venous saturation reflects impaired oxidative phosphorylation. Treat with hydroxocobalamin (preferred), or sodium thiosulfate ± sodium nitrite. Limit infusion <2 mcg/kg/min for >24 hr.
Q37. Nitroglycerin vs nitroprusside
Compared with sodium nitroprusside, IV nitroglycerin is characterized by:
A. Predominant arteriolar dilation
B. Predominant venodilation reducing preload
C. Equal arteriolar and venous dilation
D. Inotropic effect
E. No tachyphylaxis
Show answer
Answer: B. Nitroglycerin is a pure venodilator via cGMP — preload reduction predominates. Useful for angina (coronary vasodilation), CHF, and as a tocolytic in obstetric emergencies (e.g., retained placenta, uterine inversion). Nitroprusside is a balanced arterial+venous dilator.
Q38. Clevidipine
Clevidipine is most distinguished by:
A. Long duration of action
B. Hepatic metabolism by CYP3A4
C. Ultra-short half-life via plasma esterases
D. Renal excretion of unchanged drug
E. Direct β-blockade
Show answer
Answer: C. Clevidipine is a dihydropyridine Ca²⁺ blocker metabolized by plasma/tissue esterases — onset 1 min, duration 5–15 min. Useful when rapid titration matters (neurosurgery, hypertensive emergency, aortic dissection).
Q39. Esmolol pharmacology
Esmolol's short half-life is due to:
A. CYP3A4 metabolism
B. Renal excretion
C. Hydrolysis by RBC esterases
D. Hofmann elimination
E. Plasma cholinesterase hydrolysis
Show answer
Answer: C. Esmolol is hydrolyzed by red cell esterases — half-life ~9 min, onset 1 min, duration ~10 min. Selective β₁ blocker. Useful for tachycardia during laryngoscopy, ECT, intraocular surgery.
Q40. Labetalol ratio
Which best describes labetalol's α:β blockade ratio with IV administration?
A. 1:1
B. 1:7
C. 1:4
D. 7:1
E. Pure β-blocker
Show answer
Answer: B. Labetalol IV: α:β ≈ 1:7 (β predominates). Oral: 1:3. Useful in pregnancy-induced hypertension and aortic dissection. Avoid in bronchospasm, severe bradycardia. Carvedilol is the other α₁+β-blocker.
Q41. Amiodarone toxicities
Long-term amiodarone therapy is most associated with which preoperative concern?
A. Thrombocytopenia
B. Pulmonary fibrosis, hypothyroidism, hepatotoxicity
C. Renal failure
D. Megaloblastic anemia
E. Adrenal insufficiency
Show answer
Answer: B. Amiodarone is 40% iodine by weight → thyroid dysfunction (hypo or hyper). Pulmonary toxicity (interstitial pneumonitis, fibrosis), hepatotoxicity, optic neuropathy, blue-gray skin (hapten effect), peripheral neuropathy. Also: bradycardia, heart block, QT prolongation. Class III but has Class I–IV effects.
Q42. Digoxin and hyperkalemia
A 78-year-old on digoxin develops nausea, confusion, and a serum K⁺ of 6.8 mEq/L after starting spironolactone. Why is hyperkalemia particularly worrisome in digoxin toxicity?
A. Digoxin causes intracellular potassium shift
B. Hyperkalemia is a marker of severe digoxin toxicity (inhibition of Na/K-ATPase)
C. Hyperkalemia potentiates Ca²⁺ binding at the digoxin receptor
D. Digoxin acts directly on K⁺ channels
E. Spironolactone displaces digoxin from albumin
Show answer
Answer: B. Digoxin inhibits the Na/K-ATPase → extracellular K⁺ accumulation. Hyperkalemia >5.5 in digoxin toxicity is an indication for digoxin immune Fab (Digibind). Avoid calcium administration in digoxin toxicity (worsens cellular calcium overload).
Q43. TCA overdose and sodium bicarbonate
An adolescent presents with QRS widening, hypotension, and altered mental status after a tricyclic overdose. The most appropriate initial therapy is:
A. Lidocaine 1 mg/kg IV
B. Sodium bicarbonate 1–2 mEq/kg IV
C. Magnesium 2 g IV
D. Norepinephrine infusion
E. Activated charcoal
Show answer
Answer: B. TCAs block cardiac fast sodium channels → QRS widening, dysrhythmias. Sodium bicarbonate raises serum pH (favors non-ionized drug) and provides extracellular sodium that competes off the channel block. Lidocaine and other sodium channel blockers worsen it.
Q44. Cyanide poisoning antidote of choice
A firefighter rescued from a structure fire is hypotensive with a lactate of 14 and a "cherry-red" skin. Carboxyhemoglobin is mildly elevated. Mixed venous oxygen saturation is 90%. The preferred antidote is:
A. Methylene blue
B. Sodium nitrite alone
C. Hydroxocobalamin
D. N-acetylcysteine
E. Atropine + pralidoxime
Show answer
Answer: C. Smoke inhalation = combined CO + cyanide toxicity. Hydroxocobalamin directly binds intracellular CN⁻ → cyanocobalamin → renal excretion. Preferred because it doesn't impair oxygen-carrying capacity (unlike nitrites, which produce methemoglobin). High mixed-venous SaO₂ is the cyanide tell.
Q45. Organophosphate poisoning
A farmer presents with miosis, bradycardia, salivation, bronchorrhea, and muscle fasciculations. The most appropriate treatment is:
A. Atropine + pralidoxime
B. Physostigmine
C. Edrophonium
D. Glycopyrrolate
E. Activated charcoal alone
Show answer
Answer: A. Organophosphates irreversibly inhibit cholinesterase. Atropine reverses muscarinic effects (secretions, bradycardia, miosis, bronchospasm) but not nicotinic NMJ effects. Pralidoxime regenerates cholinesterase if given before the bond "ages" (24–48 hr). Pyridostigmine is prophylaxis (given before exposure), not treatment.
Q46. Acetaminophen toxicity
The antidote for acetaminophen toxicity works by:
A. Inhibiting CYP2E1 metabolism
B. Replenishing glutathione (NAC)
C. Directly binding NAPQI
D. Enhancing renal excretion
E. Blocking acetaminophen absorption
Show answer
Answer: B. Acetaminophen → CYP2E1 → NAPQI (toxic) → normally conjugated with glutathione → safe. In overdose, glutathione is depleted → NAPQI binds hepatocellular proteins → fulminant hepatic necrosis. N-acetylcysteine replenishes glutathione.
Q47. Donepezil and succinylcholine
A 78-year-old on donepezil for Alzheimer disease receives succinylcholine for RSI. What is the expected effect?
A. Resistance to succinylcholine, requiring larger dose
B. Prolonged duration of paralysis from acetylcholine accumulation
C. No effect
D. Profound bradycardia immediately
E. Malignant hyperthermia
Show answer
Answer: B. Donepezil is an acetylcholinesterase inhibitor — increases ACh availability, prolongs succinylcholine effect, and causes resistance to non-depolarizing NMBDs.
Q48. Alpha-methyltyrosine indication
Alpha-methyltyrosine (metyrosine) is used preoperatively in patients with:
A. Pheochromocytoma
B. Hyperthyroidism
C. Carcinoid syndrome
D. Conn syndrome
E. Acromegaly
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Answer: A. Metyrosine inhibits tyrosine hydroxylase (rate-limiting step in catecholamine synthesis) and is used only in pheochromocytoma. Standard preop pheo prep also includes α-blockade (phenoxybenzamine or doxazosin) followed by β-blockade once α-blocked.
Q49. Thiazide diuretic effect on electrolytes
Hydrochlorothiazide therapy classically causes which electrolyte pattern?
A. Hyperkalemia, hypocalcemia, metabolic acidosis
B. Hypokalemia, hyponatremia, hypercalcemia, metabolic alkalosis
C. Hyperkalemia, hypocalcemia, metabolic alkalosis
D. Hypokalemia, hypercalcemia, hyperphosphatemia
E. Hypernatremia, hypokalemia, metabolic acidosis
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Answer: B. "HyperGLUC, hypoKMN": Hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia; Hypokalemia, hyponatremia, hypoMagnesemia, metabolic alkalosis. Mechanism: blocks Na/Cl cotransporter in DCT; also stimulates Ca²⁺ reabsorption. Sulfa allergy contraindication.
Q50. Amiloride / triamterene
Amiloride and triamterene cause potassium retention by:
A. Aldosterone receptor antagonism
B. Blocking the epithelial sodium channel (ENaC) in collecting duct principal cells
C. Inhibiting carbonic anhydrase
D. Blocking the Na/K/Cl cotransporter
E. Inhibiting 11-β-HSD2
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Answer: B. Amiloride and triamterene block ENaC in collecting duct principal cells → no Na⁺ reabsorption → no luminal-negative gradient to drive K⁺ secretion. Spironolactone/eplerenone act via aldosterone receptor antagonism instead. Useful in Liddle syndrome.
Q51. NSAID mechanism for analgesia
NSAID analgesia is primarily mediated through:
A. μ-opioid receptor agonism
B. Inhibition of cyclooxygenase → reduced prostaglandin synthesis → reduced sensitization of nociceptors
C. NMDA antagonism
D. GABAₐ potentiation
E. Sodium channel blockade in dorsal horn
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Answer: B. NSAIDs inhibit COX → ↓ prostaglandins (especially PGE₂) → ↓ sensitization of peripheral nociceptors and ↓ central pain transmission. COX-1 maintains gastric mucosa and platelet TXA₂; COX-2 mediates inflammation. COX-2 selectives spare platelets but increase thrombotic risk.
Q52. Gabapentin mechanism
Gabapentin's analgesic effect is mediated through:
A. GABA receptor agonism
B. Inhibition of α₂δ subunit of voltage-gated calcium channels
C. Sodium channel blockade
D. NMDA antagonism
E. Opioid receptor agonism
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Answer: B. Despite the name, gabapentin does not act on GABA receptors. It inhibits the α₂δ subunit of high-voltage Ca²⁺ channels → ↓ glutamate, ↓ substance P → ↓ pain transmission. Useful for neuropathic pain, postherpetic neuralgia. Sedation, ataxia are main side effects.
Q53. Dantrolene mechanism
Dantrolene treats malignant hyperthermia by:
A. Blocking voltage-gated Na⁺ channels
B. Antagonizing the ryanodine receptor on the sarcoplasmic reticulum → ↓ Ca²⁺ release
C. Increasing Ca²⁺ reuptake into sarcoplasmic reticulum
D. Blocking acetylcholine release at the NMJ
E. Direct β-blockade
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Answer: B. Dantrolene antagonizes RYR1 on the SR → ↓ calcium release → ↓ skeletal muscle contraction. Used in MH, NMS, severe spasticity. Also has been used in serotonin syndrome and ecstasy overdose. Initial 2.5 mg/kg q5–10 min up to 10 mg/kg; then 1 mg/kg q4–6 hr or 0.25 mg/kg/hr × 24–48 hr.
Q54. Inhaled anesthetic effect on neuromuscular blockade
Which volatile most potentiates non-depolarizing NMB at 1 MAC?
A. Nitrous oxide
B. Halothane
C. Sevoflurane
D. Isoflurane
E. Desflurane
Show answer
Answer: E. Potentiation: desflurane (~60%) > isoflurane ≈ sevoflurane (~40%) > nitrous oxide (~20%). Mechanism: direct skeletal muscle relaxation + synergy at NMJ. More pronounced with aminosteroids than benzylisoquinoliniums.
Q55. Antibiotics that prolong NMB
Which class of antibiotic most prolongs non-depolarizing NMB?
A. Cephalosporins
B. Aminoglycosides
C. Penicillins
D. Fluoroquinolones
E. Vancomycin
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Answer: B. Aminoglycosides, polymyxins, tetracyclines, lincomycin, and clindamycin prolong NMB by inhibiting presynaptic ACh release and depressing postjunctional receptor sensitivity. Calcium administration may partially reverse.
Q56. Lidocaine maximum dose with epinephrine
The maximum infiltration dose of lidocaine with epinephrine is approximately:
A. 3 mg/kg
B. 4.5 mg/kg
C. 7 mg/kg
D. 12 mg/kg
E. 15 mg/kg
Show answer
Answer: C. Lidocaine: 4.5 mg/kg without epi (max 300 mg), 7 mg/kg with epi (max 500 mg). Bupivacaine: 2.5 mg/kg without / 3 mg/kg with epi. Ropivacaine: 3 mg/kg. Chloroprocaine: 11 mg/kg / 14 mg/kg with epi.
Q57. Local anesthetic onset, potency, duration determinants
Which property primarily determines local anesthetic potency?
A. pKa
B. Lipid solubility
C. Protein binding
D. Molecular weight
E. Vasoconstrictor co-administration
Show answer
Answer: B. Lipid solubility → potency. pKa → onset (drugs closer to physiologic pH have more unionized fraction → faster onset; bicarbonate added to lidocaine speeds onset). Protein binding → duration. Vasoconstrictor → duration via slowed absorption.
Q58. Bupivacaine cardiotoxicity vs ropivacaine
Why is ropivacaine considered less cardiotoxic than bupivacaine?
A. Lower lipid solubility
B. Predominantly S-enantiomer with faster sodium channel dissociation
C. Higher pKa
D. Hepatic instead of renal clearance
E. Less protein binding
Show answer
Answer: B. Ropivacaine is pure S(–) enantiomer with faster dissociation from cardiac sodium channels than racemic bupivacaine — wider safety margin in LAST. Both heavily protein-bound (safer in pregnancy than lidocaine).
Q59. Lidocaine for ion trapping in fetus
Why is lidocaine particularly concerning in the setting of fetal acidosis?
A. Lidocaine increases fetal oxygen consumption
B. Acidic fetal serum ion-traps lidocaine, leading to higher fetal levels
C. Lidocaine directly suppresses fetal sodium channels
D. Lidocaine prolongs fetal QT
E. Lidocaine prevents transplacental glucose delivery
Show answer
Answer: B. In fetal acidosis, lidocaine becomes ionized and trapped on the fetal side of the placenta → higher fetal toxicity. Ropivacaine and bupivacaine cross less due to high protein binding.
Q60. CYP3A4 induction and warfarin
Which medication is most likely to decrease the effect of warfarin via CYP3A4 induction?
A. Rifampin
B. Fluconazole
C. Ciprofloxacin
D. Amiodarone
E. Omeprazole
Show answer
Answer: A. Rifampin is a strong CYP inducer — accelerates warfarin metabolism, reducing INR. Other inducers: phenytoin, carbamazepine, phenobarbital, St. John's wort, chronic alcohol. CYP inhibitors (B-E) increase warfarin effect.
Q61. Codeine and CYP2D6
Codeine is converted to its active metabolite morphine by:
A. CYP3A4
B. CYP2D6
C. CYP2C9
D. UGT2B7
E. Plasma esterases
Show answer
Answer: B. CYP2D6 converts codeine → morphine (~5–15%). Ultra-rapid metabolizers can develop respiratory depression at standard doses (relevant in nursing mothers → infant respiratory arrest). Poor metabolizers get little analgesia. FDA contraindicates codeine in tonsillectomy patients <12 years.
Q62. Sevoflurane and Compound A
Compound A formation with sevoflurane is increased by which combination?
A. High fresh gas flow with fresh soda lime
B. Low fresh gas flow with desiccated absorbent containing strong base
C. High flow with desflurane
D. Sevoflurane at room temperature
E. Sevoflurane with calcium hydroxide–only absorbent
Show answer
Answer: B. Compound A formation rises with low FGF, desiccated absorbents, strong bases (NaOH, KOH), and higher temperatures. Theoretical nephrotoxicity in animals — humans appear less susceptible but recommendation remains FGF ≥2 L/min with sevoflurane >2 MAC-hours.