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A) Neostigmine 2.5 mg with glycopyrrolate

B) Sugammadex 2 mg/kg

C) Sugammadex 16 mg/kg

D) Edrophonium 0.5 mg/kg

A) It blocks voltage-gated sodium channels at the motor end plate

B) It causes sustained depolarisation of the nicotinic receptor, producing unsynchronised motor unit firing

C) It releases acetylcholine from presynaptic vesicles in large quantities

D) It competitively displaces acetylcholine from the receptor, generating a partial agonist response

A) Suxamethonium at double the standard dose to compensate for enzyme deficiency

B) Suxamethonium at the standard dose with prolonged post-operative ventilation planned

C) Rocuronium with sugammadex available for reversal

D) No neuromuscular blockade; use high-dose opioid technique

A) Cisatracurium

B) Mivacurium

C) Vecuronium

D) Atracurium

A) TOF ratio 0.4 (or TOF count of 4 present)

B) TOF count of 1 (one twitch visible)

C) Post-tetanic count of 5 or greater

D) TOF ratio 0.9 or greater without pharmacological reversal needed

A) Rocuronium 0.6 mg/kg

B) Pancuronium 0.1 mg/kg

C) Cisatracurium 0.15 mg/kg

D) Vecuronium 0.1 mg/kg

A) Hypercalcaemia and hypermagnesaemia

B) Hypokalaemia, hypothermia, and respiratory acidosis

C) Metabolic alkalosis and hyperthermia

D) Hyperkalaemia and metabolic acidosis

A) Single twitch at 1 Hz

B) Tetanic stimulation at 50 Hz for 5 seconds

C) Train-of-Four stimulation at 2 Hz

D) Double burst stimulation at 50 Hz

A) Anaphylaxis to suxamethonium

B) Malignant hyperthermia

C) Neuroleptic malignant syndrome

D) Phase II block from suxamethonium

A) Sugammadex has no interaction with hormonal contraceptives

B) Sugammadex may reduce the efficacy of the contraceptive pill for up to 7 days, requiring additional contraception

C) Sugammadex permanently binds oestrogen-containing compounds and must be avoided in women of childbearing age

D) Sugammadex accelerates clearance of progesterone, requiring a higher contraceptive dose post-operatively

A) It occurs after small single doses and is characterised by fade on TOF stimulation

B) It develops after repeated or large doses and resembles a non-depolarising block with TOF fade

C) It is caused by receptor up-regulation and occurs within 5 minutes of the first dose

D) It is identical in character to Phase I block but lasts longer

A) Aminoglycosides inhibit hepatic metabolism of NMBAs via CYP3A4 inhibition

B) Aminoglycosides block presynaptic calcium channels and reduce acetylcholine release, potentiating neuromuscular blockade

C) Aminoglycosides competitively bind to nicotinic receptors alongside NMBAs

D) Aminoglycosides alkalinise the plasma, increasing protein binding of NMBAs

A) Maintenance of neuromuscular blockade during prolonged abdominal surgery

B) Routine intubation in a fasted, haemodynamically stable patient

C) Rapid sequence induction where rapid onset and ultra-short duration are required

D) Reversal of residual non-depolarising blockade at the end of surgery

A) Confirming adequate recovery prior to extubation

B) Monitoring block depth during total intravenous anaesthesia in a haemodynamically unstable patient

C) Assessing depth of blockade when the TOF count is zero, particularly during deep blockade for laparoscopic surgery

D) Quantifying residual blockade in the post-anaesthesia care unit

A) Neostigmine 2.5 mg with glycopyrrolate 0.5 mg

B) Sugammadex 16 mg/kg

C) Sugammadex 2 mg/kg

D) Edrophonium 1 mg/kg with atropine

A) Extubate immediately as the patient has four TOF twitches

B) Administer neostigmine 2.5 mg and extubate after 5 minutes

C) Administer sugammadex 2 mg/kg and confirm TOF ratio ≥0.9 before extubation

D) Continue ventilation until the TOF ratio improves spontaneously to ≥0.9

A) It causes significant histamine release, increasing bronchospasm risk in the elderly

B) It has a prolonged duration of action due to renal excretion and accumulation, increasing residual blockade risk

C) It is metabolised by plasma cholinesterase, which is reduced in elderly patients

D) It causes direct myocardial depression, leading to haemodynamic instability in the elderly

A) It indicates receptor up-regulation in response to suxamethonium

B) It reflects presynaptic acetylcholine depletion and is characteristic of non-depolarising blockade

C) It is a sign of complete neuromuscular recovery and indicates safe extubation

D) It is caused by postsynaptic receptor sensitisation following depolarising block

A) Spontaneous non-enzymatic degradation at physiological pH and temperature, independent of hepatic or renal function

B) Enzymatic hydrolysis by plasma cholinesterase, producing inactive metabolites

C) Hepatic microsomal oxidation via the CYP2D6 pathway

D) Renal tubular secretion facilitated by active transport mechanisms

A) Rocuronium at this dose has a faster onset than suxamethonium and does not require reversal

B) Rocuronium at this dose achieves intubating conditions within 60 seconds, comparable to suxamethonium, and can be rapidly reversed with sugammadex 16 mg/kg

C) Rocuronium at 1.2 mg/kg has a shorter duration of action than suxamethonium, reducing residual blockade risk

D) Rocuronium does not cause fasciculations and is therefore associated with fewer adverse haemodynamic effects than suxamethonium at equivalent doses