Neuromuscular blocking agents MCQs With Answer

Introduction

Neuromuscular blocking agents MCQs With Answer are essential for B. Pharm students learning clinical pharmacology of anesthesia and critical care. This concise collection emphasizes mechanisms of action, classification into depolarizing and non‑depolarizing agents, pharmacokinetics, metabolism (plasma cholinesterase and Hofmann elimination), monitoring by train‑of‑four and post‑tetanic count, drug interactions, adverse effects such as hyperkalemia and malignant hyperthermia, and reversal strategies including neostigmine and sugammadex. Questions probe deeper concepts like phase I versus phase II block, organ dysfunction considerations, and steroidal versus benzylisoquinolinium structures to build clinical reasoning. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What is the primary mechanism of action of non‑depolarizing neuromuscular blocking agents?

• Activation of presynaptic muscarinic receptors to reduce acetylcholine release
• Competitive antagonism at nicotinic acetylcholine receptors at the neuromuscular junction
• Irreversible inhibition of acetylcholinesterase at the synapse
• Opening of sodium channels causing prolonged depolarization

Correct Answer: Competitive antagonism at nicotinic acetylcholine receptors at the neuromuscular junction

Q2. Succinylcholine produces neuromuscular blockade primarily by which action?

• Blocking acetylcholine release from presynaptic terminals
• Acting as a depolarizing agonist at nicotinic receptors causing persistent end‑plate depolarization
• Inhibiting acetylcholinesterase to increase synaptic acetylcholine
• Directly blocking voltage‑gated calcium channels in muscle

Correct Answer: Acting as a depolarizing agonist at nicotinic receptors causing persistent end‑plate depolarization

Q3. A phase II block after repeated succinylcholine doses is best explained by which mechanism?

• Increased acetylcholinesterase activity at the synapse
• Voltage‑gated sodium channel inactivation in motor neurons
• Receptor desensitization and channel blockade following prolonged exposure
• Enhanced presynaptic acetylcholine release leading to receptor saturation

Correct Answer: Receptor desensitization and channel blockade following prolonged exposure

Q4. Which neuromuscular blocker is rapidly hydrolyzed by plasma (pseudo)cholinesterase?

• Rocuronium
• Vecuronium
• Succinylcholine
• Pancuronium

Correct Answer: Succinylcholine

Q5. Which neuromuscular blocking drug is effectively reversed by sugammadex?

• Atracurium
• Succinylcholine
• Rocuronium
• Mivacurium

Correct Answer: Rocuronium

Q6. Which agent typically has the fastest onset of neuromuscular blockade?

• Cisatracurium
• Rocuronium (standard dose)
• Succinylcholine
• Pancuronium

Correct Answer: Succinylcholine

Q7. A train‑of‑four (TOF) ratio of 0.9 indicates what clinically?

• Complete paralysis with no muscle function
• Deep block requiring additional NMBA dosing
• Partial recovery but still inadequate for safe extubation
• Adequate recovery of neuromuscular function for safe extubation

Correct Answer: Adequate recovery of neuromuscular function for safe extubation

Q8. Which complication is most classically associated with succinylcholine use?

• Severe hypokalemia
• Hyperkalemia due to potassium efflux from skeletal muscle
• Pancytopenia
• Renal excretion accumulation causing prolonged block

Correct Answer: Hyperkalemia due to potassium efflux from skeletal muscle

Q9. Which neuromuscular blocker undergoes Hofmann elimination and ester hydrolysis making it organ‑independent?

• Pancuronium
• Atracurium
• Rocuronium
• Vecuronium

Correct Answer: Atracurium

Q10. Which class of drugs commonly potentiates the effect of non‑depolarizing neuromuscular blockers?

• Beta‑blockers
• Aminoglycoside antibiotics
• Loop diuretics
• Proton pump inhibitors

Correct Answer: Aminoglycoside antibiotics

Q11. Which neuromuscular blocker is notable for histamine release and potential hypotension?

• Cisatracurium
• Pancuronium
• Atracurium
• Rocuronium

Correct Answer: Atracurium

Q12. Neostigmine reverses non‑depolarizing blockade by which mechanism?

• Direct antagonism at the nicotinic receptor
• Increasing acetylcholine concentration by inhibiting acetylcholinesterase
• Encapsulating the neuromuscular blocker in plasma
• Blocking presynaptic calcium channels to increase acetylcholine release

Correct Answer: Increasing acetylcholine concentration by inhibiting acetylcholinesterase

Q13. What is the molecular mechanism by which sugammadex reverses rocuronium?

• Inhibition of acetylcholinesterase
• Competitive antagonism at nicotinic receptors
• Encapsulation (binding) of rocuronium molecules to form an inactive complex
• Allosteric modulation of the nicotinic receptor to restore function

Correct Answer: Encapsulation (binding) of rocuronium molecules to form an inactive complex

Q14. In severe renal impairment which neuromuscular blocker is preferred due to organ‑independent elimination?

• Vecuronium
• Pancuronium
• Cisatracurium
• Rocuronium

Correct Answer: Cisatracurium

Q15. Prolonged paralysis after succinylcholine administration is most likely due to which condition?

• Enhanced hepatic metabolism of succinylcholine
• Pseudocholinesterase (butyrylcholinesterase) deficiency
• Rapid renal clearance
• Increased plasma albumin binding

Correct Answer: Pseudocholinesterase (butyrylcholinesterase) deficiency

Q16. When the TOF stimulation shows zero responses, which test helps quantify deep blockade?

• Single twitch at 0.1 Hz
• Post‑tetanic count (PTC)
• Measurement of muscle temperature
• Pulse oximetry waveform analysis

Correct Answer: Post‑tetanic count (PTC)

Q17. Which neuromuscular blocker is associated with vagolytic effects and tachycardia?

• Pancuronium
• Atracurium
• Cisatracurium
• Edrophonium

Correct Answer: Pancuronium

Q18. Which patient factor most significantly affects the onset time of an intravenously administered NMBA?

• Patient hair color
• Peripheral muscle mass only
• Cardiac output and muscle blood flow
• Height but not weight

Correct Answer: Cardiac output and muscle blood flow

Q19. Why is an anticholinergic such as atropine or glycopyrrolate often given with neostigmine when reversing NMBAs?

• To enhance acetylcholinesterase inhibition
• To prevent muscarinic side effects like bradycardia and bronchospasm
• To directly displace the neuromuscular blocker from nicotinic receptors
• To increase renal excretion of the NMBA

Correct Answer: To prevent muscarinic side effects like bradycardia and bronchospasm

Q20. Malignant hyperthermia triggered by certain anesthetic agents involves which primary intracellular event?

• Inhibition of sarcolemmal sodium channels
• Excessive release of intracellular calcium from the sarcoplasmic reticulum
• Autoimmune destruction of acetylcholine receptors
• Excessive acetylcholinesterase activity

Correct Answer: Excessive release of intracellular calcium from the sarcoplasmic reticulum

Q21. Which neuromuscular blocking agent belongs to the benzylisoquinolinium class?

• Vecuronium
• Pancuronium
• Atracurium
• Rocuronium

Correct Answer: Atracurium

Q22. Which statement about potency and onset of NMBAs is generally correct?

• Higher potency agents always have faster onset times
• Onset time is unrelated to potency or dose
• Higher potency often correlates with slower onset due to lower dosing per kilogram
• Low potency agents are always longer acting

Correct Answer: Higher potency often correlates with slower onset due to lower dosing per kilogram

Q23. How does neostigmine affect a phase I depolarizing block produced by succinylcholine?

• It reliably reverses phase I block
• It converts phase I to phase II block immediately
• It may prolong or intensify phase I depolarizing block
• It has no interaction with succinylcholine effects

Correct Answer: It may prolong or intensify phase I depolarizing block

Q24. Which monitoring technique provides objective quantitative measurement of neuromuscular function?

• Clinical judgment based on respiration alone
• Acceleromyography measuring TOF ratio
• Pulse oximetry
• Capnography waveform analysis

Correct Answer: Acceleromyography measuring TOF ratio

Q25. In hepatic failure which neuromuscular blocker is more likely to have prolonged duration due to reduced hepatic clearance?

• Cisatracurium
• Vecuronium
• Atracurium
• Succinylcholine

Correct Answer: Vecuronium

Q26. Which reversal agent is a selective binding agent for steroidal non‑depolarizing neuromuscular blockers?

• Neostigmine
• Edrophonium
• Sugammadex
• Atropine

Correct Answer: Sugammadex

Q27. Which short‑acting acetylcholinesterase inhibitor has been used historically for rapid reversal and diagnostic testing (Tensilon test)?

• Neostigmine
• Physostigmine
• Edrophonium
• Donepezil

Correct Answer: Edrophonium

Q28. Magnesium sulfate potentiates neuromuscular blockade primarily by what action?

• Increasing postsynaptic receptor density
• Blocking acetylcholinesterase
• Reducing presynaptic calcium‑mediated acetylcholine release
• Enhancing hepatic metabolism of NMBAs

Correct Answer: Reducing presynaptic calcium‑mediated acetylcholine release

Q29. Which antibiotic class is least likely to potentiate neuromuscular blockade?

• Aminoglycosides
• Tetracyclines
• Fluoroquinolones
• Cephalosporins

Correct Answer: Cephalosporins

Q30. If succinylcholine is contraindicated for rapid sequence intubation, what is an appropriate alternative strategy?

• Use low‑dose vecuronium without reversal available
• High‑dose rocuronium for rapid onset with availability of sugammadex for reversal
• Delay intubation until succinylcholine becomes safe
• Administer neostigmine before intubation

Correct Answer: High‑dose rocuronium for rapid onset with availability of sugammadex for reversal

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com