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52 Cards in this Set

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MB01 [Mar96] [Jul97] With regard to tetanic stimulation by a nerve stimulator:

A. Used to determine residual curarisation

B. Degree of fade is independent of stimulus duration

C. Degree of fade is dependent on stimulus intensity

D. Used to check depth of anaesthesia
ANSWER C

A: false, PTC is used to evaluate depth NMB, not residual curarisation

B: FALSE: the degree of fade will be dependent on the stimulus duration, i.e. if the stimulus duration is short, then the degree of fade seen will be less than with a prolonged stimulus. With the prolonged stimulus, there will be more fade due to depletion of ACh vesicles. (See Miller Fig 39-3

C. TRUE

D. FALSE: Depth of block of depth NOT anaesthesia
MB02 [Mar96] [Apr01] Hyperkalaemia with suxamethonium is associated with:

A. Abdominal infection

B. Parkinson's disease

C. Meningomyelocoele

D. Cerebral palsy

E. Myotonic dystrophy
ANSWER A or E

Sch-induced hyperkalaemia can follow:
1) clinically unrecognised muscular dystrophy
2) unhealed third degree burns
3) denervation leading to skeletal muscle atrophy
4) severe skeletal muscle trauma
5) upper motor neurone lesions.

stoelting adds severe intraabdominal sepsis
MB03 [Mar96] [Jul96] [Jul97] [Mar98] [Mar99] [Jul99] [Feb00] Which of the following is NOT metabolised by plasma cholinesterase?

A. Procaine

B. Cocaine

C. Dibucaine

D. Suxamethonium

E. Esmolol

F. Mivacurium
ANSWER C and E

A. Procaine - false; ester local anaesthetics undergo hydrolysis by cholinesterase enzyme, principly in the plasma

B. Cocaine - false; metabolised by pseudocholinesterase

C. Dibucaine - True; Dibucaine... inhibits plasma cholinesterase" (Peck Hill and Williams p.170) It is "metabolised in the liver and is the most slowly eliminated of all the amide derivatives

D. Suxamethonium; false

E. Esmolol- true, red cell esterases

F. Mivacurium - false; "The cis-trans and trans-trans isomers of mivacurium are hydrolysed by plasma cholinesterase
MB03b [Mar98] [Apr01] Which of the following is metabolised by plasma cholinesterase?

A. Remifentanil

B. Procaine

C. Esmolol

D. Cocaine

E. All of the above
ANSWER B

A. Remifentanil - False; Remifentanil is unique among the opiods in undergoing metabolism by nonspecific plasma and tissue esterases

B. Procaine - correct; see above

C. Esmolol - False; Esmolol metabolised by red cell esterases

D. Cocaine - false: metabolised by liver esterases

E. All of the above - False
MB03c [Jul98] [Feb00] Esterases metabolise all EXCEPT:

A. Remifentanil

B. Dibucaine

C. Pyridostigmine

D. Aspirin

E. Diamorphine
ANSWER B

C. Pyridostigmine - incorrect; Pyridostigmine undergoes hydrolysis by cholinesterases

Plasma Esterase responsible for the metabolism of
* Suxamethonium
* Mivacurium
* Ester local anaesthetics
* Diamorphine [CEACCP 2004 Vol 4(5)]
* Aspirin [CEACCP 2004 Vol 4(5)]

Red cell esterase

Found in cytosol of RBC
Metabolism of esmolol and possibly remifentanil
Not reduced in pt with pseudocholinesterase deficiency

Non-specific plasma esterase

aka tissue esterase
NOT pseudocholinesterase
Metabolism of remifentanil and atracurium
High capacity system
* Not affected by hepatic metabolism
Level reduced in aged patients
MB03d [Feb04] Which drug has a significantly prolonged duration of action in plasma cholinesterase deficiency?

A. Remifentanil

B. Procaine

C. Mivacurium

D. Rocuronium

E. Cocaine
ANSWER C
MB04 [Mar96] [Jul02] The action of nondepolarising neuromuscular blocking agents is PROLONGED by:

A. Respiratory acidosis

B. Increased temperature

C. Increased calcium

D. Increased potassium

E. Decreased magnesium
ANSWER A


A. Respiratory acidosis - true; "Respiratory acidosis enhances pancuronium-induced NMB and opposes its antagonism with neostigmine" (Stoelting p202 3rd ed) "prolonged in most, but reduced in gallamine" (Peck Hill and Williams p.173)

* B. Increased temperature - false; HYPOthermia prolongs action (Table 12.3 in Peck Hill and Williams p.173)

* C. Increased calcium - false; calcium channel antagonists prolong duration (Table 12.3 as above) so increased calcium levels will presumably oppose this effect

* D. Increased potassium - false; has an antagonistic effect with non-depolarising agents (Table 12.3 as above)

* E. Decreased magnesium - false; hypermagnesaemia causes prolonged action (Table 12.3)
MB05 [Mar96] Agents prolonging nondepolarising NMBA by desensitising the post-junctional membrane :

A. Phenytoin

B. Halothane

C. Lignocaine

D. Verapamil
ANSWER C

A. Phenytoin - false; "patients treated chronically with phenytoin are resistant to the... effects of NDMB drugs" (Stoelting p.199)


B. Halothane - false; "Volatile anaesthetics most likely enhance the effects... by virtue of anaesthetic depression of the CNS" (Stoelting 3rd ed. p.196)



C. Lignocaine - Best answer; "depending on the dose, local anaesthetics... stablise the post-junctional membrane" (Stoelting 3rd ed. p.197)


D. Verapamil - partly true; CCBs work by reducing Ca2+ influx and preventing ACh release thus working pre-synaptically
MB06 [Mar96] [Jul98] Which drugs (?competitively) inhibit acetylcholinesterase?

A. Neostigmine

B. Pyridostigmine

C. Physostigmine

D. Edrophonium

E. All of the above
ANSWER E

Neostigmine, pyridostigmine and physostigmine form carbamyl ester complexes at the esteratic site of acetylcholinesterase producing reversible inhibition. They act as competitive substrates for the enzymes normal binding site with acetylcholine.

Edrophonium does not have a carbamyl group and produces reversible acetylcholinesterase inhibition by electrostatic attachment to the anionic site and hydrogen bonding to the esteratic site. There is no covalent bond making it easy for acetylcholine to compete.
MB06b [Jul00] [Apr01] The activity of plasma cholinesterase is decreased by the following drugs except:

A. Neostigmine

B. Organophosphates

C. THA

D. Metoclopramide

E. Cimetidine
ANSWER E

THA is tacrine which is a weak cholinesterase inhibitor used in certain forms of dementia. May have implications during anaesthesia eg potentiating depolarizing NM block or resistence to non depolarizing agents.

Metoclopramide has been shown to inhibit cholinesterase in vivo and vitro

Cimetidine has no effect.
MB06c [Jul04] Which decrease plasmacholinesterase activity? (remembered options from 2 questions)

A. Hepatic disease

B. Cyclophosphamide

C. Six weeks post partum

D. Hyperthyroidism

E. Obesity

F. Cytotoxic drugs

G. Pregnancy

H. Dibucaine number of 20
ANSWER A B D F G H

"Aquired factors associated with reduced plasma cholinesterase activity include:

* pregnancy
* liver disease
* renal failure
* cardiac failure
* thyrotoxicosis
* cancer
* drugs - either directly or by acting as a substrate or inhibitor to AChE. Ecothipate, metoclopramide, ketamine, the OCP, lithium, lignocaine, ester local anaesthetics, cytotoxic drugs, edrophonium, neostigmine and trimetaphan"
MB07 [Mar97] [Jul98] [Jul99] [Feb00] [Apr01] Regarding vecuronium:

A. It accumulates in renal failure

B. Is a benzylisoquinolinium

C. Is a bisquaternary amine

D. Is more lipid soluble than pancuronium

E. Is predominantly renally excreted
ANSWER D

A. It accumulates in renal failure - correct; see table 8-2 in Stoelting 3rd ed. p.185. Both vecuronium and rocuronium are dependent on renal and hepatic function where atracurium and cisatrurium are not

B. Is a benzylisoquinolinium - false; it is an aminosteroidal compound. The benzylisoquinolonium compounds are the "curiums" such as tubocuraine, atracurium and mivacurium

C. Is a bisquaternary amine - false; it has a "monoquaternary structure" (Stoelting 3rd ed. p.210)

D. Is more lipid soluble than pancuronium - correct; "the monoquaternary structure... increases its lipid solubility compared with pancuronium" (Stoelting 3rd ed. p.210)

E. Is predominantly renally excreted - false; renal excretion 15-25% and biliary excretion 40-75% in Table 8-2 from Stoelting 3rd ed. p185)
MB08 [Jul97] [Jul98] [Mar99] [Jul02] [Mar03] In reversing neuromuscular blockade, which of the following combinations is best matched with respect to time of onset?

A. Atropine & neostigmine

B. Atropine & glycopyrrolate

C. Atropine & edrophonium

D. Atropine & physostigmine

E. Glycopyrrolate and edrophonium
ANSWER C

Onset of action
Edrophonium 1-2 minutes
Neostigmine 7-11 minutes
Pyridostigmine 16 minutes
Atropine 1 minute
Glycopyrrolate 2-3 minutes
MB09 [Jul97] [Jul98] [Mar99] [Jul99] [Jul00] [Mar03] Plasma cholinesterase:

A. Metabolises dibucaine

B. Metabolises esmolol

C. Hydrolyses mivacurium at 80% the rate of suxamethonium

D. Is unaffected by neostigmine
ANSWER C

Most correct answer - ??C

A. Dibucaine is an amide local anaesthetic used to inhibit normal plasma cholinesterase when testing for deficiency of this enzyme. A normal person will have 80% of the enzyme blocked in the presence of dibucaine ie. a dibucaine number of 80. Dibucaine is an amide local and is metabolised by microsomal enzymes in the liver - is the most slowly eliminated of all the amide derivatives (Stoelting & Hillier 4th ed. p186, 219)

B. Esmolol is metabolised by RBC esterases and is independant of plasma cholinesterase activity. It's T1/2 is 9.3 minutes. Metabolites are methanol and a primary acid metabolite (major) which has minimal adrenoceptor antagonist activity but a T1/2 of 3.5 hours. The metabolites are mainly renally excreted and acumulate in renal failure, so despite esmolol's rapid hydrolysis, caution needs to be taken with dosing in patients with severe renal failure. (stoelting 4th p330).

C. Mivacurium is hydrolysed by plasma cholinesterase at 88% of the rate of hydrolysis of Suxamethonium. (Stoelting 4th ed. p242)

D. Neostigmine reduces plasma cholinesterase activity by 50%. This effect may last 30 minutes. (Stoelting 4th ed. p 218)
MB09b [Jul01] [Jul04] Suxamethonium

A. Bigger molecule than vecuronium

B. Needs to occupy 80% of nicotinic receptors to get effect

C. Resistant to hydrolysis by acetylcholinesterase

D. ??Is an antagonist at nicotinic receptors

E. Increasing dose produces similar block
ANSWER C

A. Bigger molecule than vecuronium - false

B. Needs to occupy 80% of nicotinic receptors to get effect - false

C. Resistant to hydrolysis by acetylcholinesterase - correct

D. Is an antagonist at nicotinic receptors - false; it is an agonist at the nicotinic receptors (but is longer acting than Ach due to resistance to metabolism by acetylcholinesterase in the synaptic cleft)

E. Increasing dose produces similar block - false
MB10 [Jul97] [Jul98] With regard to the nerve stimulator in competitive blockade:

A. Fade is dependent on stimulating frequency

B. TOFC of four is a sign of adequate reversal

C. Train of four can be assessed every 5 minutes

D.
ANSWER A

A. TRUE: Fade in response to tetanic stimulation is dependant on degree of NMB, frequency of stimulation, length of stimulation and how often tetanic stimuli applied (ref: Miller)

B. FALSE: TOF ratio is a better indicator of adequate reversal with figures between 0.7-0.9 quoted (see Millers section on neuromuscular monitoring). TOF count indicates whether reversal is safe (some say 1 twitch needed, some say 2).

C. FALSE: must give an interval of 20 minutes

D.
MB11 [Jul97] Anticholinesterase agents:

A. Carbamates duration of action is related to the time required for dissociation from the anionic site.

B. Carbamates act by acetylation of the esteratic site.

C. ?

(See also [[MB11b, [[MD28)
Both incorrect

Carbamates produce reversible inhibition of acetylacholinesterase by carbamylating the esteratic binding site.

They does not associate/dissociate as edrophonium does.

Acteylcholine : acetylates the esterastic site.
Carbamates: carbamylate the esterastic site
Organophospates : phosporylate the esterastic site
MB11b [Jul00] [Apr01] [Jul02] [Jul04] Carbamylation of acetylcholinesterase: (Jul02: Phosphorylation of acetylcholinesterase: )

A. Ionic bonding at anionic site

B. Ionic bonding at esteratic site

C. Covalent bonding at anionic site

D. Covalent bonding at esteratic site

E. None of above
ANSWER D
MB12 [dgj] [Jul00] [Jul02] [Jul04] Mivacurium:

A. Is metabolised at 80% the rate of suxamethonium

B. Takes 15 mins from ED95 dose to recovery of 95% twitch height

C. Has an ED95 of 1.5 mg/kg

D. Trigger for malignant hyperthermia

E. ? Duration of action is increased in renal failure
ANSWER A and E

A: true

B: ??? most text quote times for intubating dose

C: Mivacurium ED95 60-80mcg/kg. Intubating dose 0.07-0.15mg/kg - 0.1-0.2mg/kg for children 2-12yo; Intubating conditions within 2.5min; single dose lasts 10-20min

D: false

E: true, increased duration of blockade
July 2000 version: Mivacurium:

A. Twice the ED95 dose is 1.5mg/kg

B. is metabolised at 80 to 90% the rate of suxamethonium

C. After 2 x ED95 dose 95% return of twitch height after 15mins

D. is a symmetrical molecule with similar structure to suxamethonium

E. When given quickly, does not cause histamine release
ANSWER C

A: false

B: true

C: false Mivacurium says that 95% recovery from 2 x ED95 (about 0.15mg/kg) takes 25 mins (and duration of relaxation is 15 mins)

D. False Mivacurium is a symmetrical molecule although it is a mixture of three of the twenty possible isomers. It is a benzylisoquinoline

E. False, Mivacurium may cause histamine release, especially when relatively large doses are administered rapidly, leading to a decrease in blood pressure and an increase in heart rate
MB12b [Jul00] Mivacurium administered at a dose of 2 times the ED95 dose produces relaxation for:

A. 10 mins

B. 15 mins

C. 20 mins

D. 25 mins

E. None of the above
ANSWER B
MB07 [Mar97] [Jul98] [Jul99] [Feb00] [Apr01] Regarding vecuronium:

A. It accumulates in renal failure

B. Is a benzylisoquinolinium

C. Is a bisquaternary amine

D. Is more lipid soluble than pancuronium

E. Is predominantly renally excreted
ANSWER A most correct

A. It accumulates in renal failure - correct; see table 8-2 in Stoelting 3rd ed. p.185. Both vecuronium and rocuronium are dependent on renal and hepatic function where atracurium and cisatrurium are not

B. Is a benzylisoquinolinium - false; it is an aminosteroidal compound. The benzylisoquinolonium compounds are the "curiums" such as tubocuraine, atracurium and mivacurium

C. Is a bisquaternary amine - false; it has a "monoquaternary structure" (Stoelting 3rd ed. p.210)

D. Is more lipid soluble than pancuronium - correct; "the monoquaternary structure... increases its lipid solubility compared with pancuronium" (Stoelting 3rd ed. p.210) but both are pretty lipid insoluble due to their quaternary N

E. Is predominantly renally excreted - false; renal excretion 15-25% and biliary excretion 40-75% in Table 8-2 from Stoelting 3rd ed. p185)
MB08 [Jul97] [Jul98] [Mar99] [Jul02] [Mar03] In reversing neuromuscular blockade, which of the following combinations is best matched with respect to time of onset?

A. Atropine & neostigmine

B. Atropine & glycopyrrolate

C. Atropine & edrophonium

D. Atropine & physostigmine

E. Glycopyrrolate and edrophonium
ANSWER C

Onset of action
Edrophonium 1-2 minutes
Neostigmine 7-11 minutes
Pyridostigmine 16 minutes
Atropine 1 minute
Glycopyrrolate 2-3 minutes
MB09 [Jul97] [Jul98] [Mar99] [Jul99] [Jul00] [Mar03] Plasma cholinesterase:

A. Metabolises dibucaine

B. Metabolises esmolol

C. Hydrolyses mivacurium at 80% the rate of suxamethonium

D. Is unaffected by neostigmine
ANSWER C

Most correct answer - ??C

A. Dibucaine is an amide local anaesthetic used to inhibit normal plasma cholinesterase when testing for deficiency of this enzyme. A normal person will have 80% of the enzyme blocked in the presence of dibucaine ie. a dibucaine number of 80. Dibucaine is an amide local and is metabolised by microsomal enzymes in the liver - is the most slowly eliminated of all the amide derivatives (Stoelting & Hillier 4th ed. p186, 219)

B. Esmolol is metabolised by RBC esterases and is independant of plasma cholinesterase activity. It's T1/2 is 9.3 minutes. Metabolites are methanol and a primary acid metabolite (major) which has minimal adrenoceptor antagonist activity but a T1/2 of 3.5 hours. The metabolites are mainly renally excreted and acumulate in renal failure, so despite esmolol's rapid hydrolysis, caution needs to be taken with dosing in patients with severe renal failure. (stoelting 4th p330).

C. Mivacurium is hydrolysed by plasma cholinesterase at 88% of the rate of hydrolysis of Suxamethonium. (Stoelting 4th ed. p242)

D. Neostigmine reduces plasma cholinesterase activity by 50%. This effect may last 30 minutes. (Stoelting 4th ed. p 218)
MB09b [Jul01] [Jul04] Suxamethonium

A. Bigger molecule than vecuronium

B. Needs to occupy 80% of nicotinic receptors to get effect

C. Resistant to hydrolysis by acetylcholinesterase

D. ??Is an antagonist at nicotinic receptors

E. Increasing dose produces similar block
ANSWER C

A. Bigger molecule than vecuronium - false

B. Needs to occupy 80% of nicotinic receptors to get effect - false

C. Resistant to hydrolysis by acetylcholinesterase - correct

D. Is an antagonist at nicotinic receptors - false; it is an agonist at the nicotinic receptors (but is longer acting than Ach due to resistance to metabolism by acetylcholinesterase in the synaptic cleft)

E. Increasing dose produces similar block - false
MB10 [Jul97] [Jul98] With regard to the nerve stimulator in competitive blockade:

A. Fade is dependent on stimulating frequency

B. Double burst is of particular value in assessing blockade when there is no response to the train-of-four

C. Double burst is of particular value in assessing blockade when there is no response to the train-of-four

D. The post tetanic count is particularly useful for assessing the patient's suitability for extubation

E. The ideal nerve for neuromuscular blockade assessment is generally considered to be the facial nerve
ANSWER A
MB13 [Mar98] [Jul99] [Jul01] The Recovery Index 25% to 75% is 7 minutes for which drug?

A. Vecuronium

B. Rocuronium

C. Mivacurium

D. Suxamethonium

E. Rocuonium
ANSWER C

The mean recovery index : time taken for T1 to recover from 25% to 75% of control

Pancuronium 35 min
Vecuronium 12
Rocuronium 14
Atracurium 12
Cis atracurium 14
Mivacurium 6

Sux N/A
July 2000 version: Release of acetylcholine at motor endplate:

A. Hemicholinium directly interferes with release

B. Only in response to action potential

C. Decreased by aminoglycosides / ?? prejunctional effect

D. Is Ca2+ dependent process

E. Always causes an action potential
ANSWER C


Gentamicin inhibits release of presynaptic Ach and also stabilises post-synaptic membrane. (1. Stoelting 2. Sasada)

Botulinum toxin blocks Ach release by cleaving enzymes that help Ach containing vesicles fuse with the nerve cell wall in the pre-synaptic nerve end. (Rang & Dale p 154)

Hemichlinium interferes with synthesis of Ach by blocking transport of choline into the nerve end. This is the rate limiting step of Ach production. (Rand and Dale p 154)

Action potential is only one mechanism for Ach release at end plate. Random minature end plate potentials (MEPP) occur continuously (Stoelting 4th ed. p 214)

Calcium dependant process - yep. (Rang and Dale 154 and Stoelting 214)

Always causes action potential - not necessarily. As above, small quanta released <1mv = MEPP.
MB16 [Jul98] [Mar99] [Feb00] [Jul01] [Mar03] Rocuronium:

A. Monoquaternary at physiological pH

B. More lipid soluble than pancuronium

C. 30% metabolised (?deacetylated) in the liver

D. Rapid onset is due to its high potency

E. Fastest onset is with 2 times ED95 dose

F. Is bisquaternary
ANSWER A

A : true

B: true, but they are all very lipid insoluble

C: false, It is eliminated in the bile 55%(mostly unchanged) and 35% urine. There is very little hepatic metabolism of rocuronium.

D: false, due to low potency

E: false, give 3-4 times

F: false, monquaternary only panc is bisquaternary
MB18 [Mar99] Which of the following do NOT prolong neuromuscular blockade?

A. Volatile anaesthetics

B. Antibiotics

C. Phenytoin

D. Beta-blockers

E. Hyperthermia
answer C


Prolonged neuromuscular blockade
Volatile anaesthetics
Aminoglycoside antibiotics
Local anaesthetics
Cardiac antidysrhythmic drugs (quinidine)
Frusemide (1mg/kg)
Magnesium
Lithium
Cyclosporin
Hypothermia
Hypokalaemia
Females
Dantrolene

Decreased neuromuscular blockade
Anticonvulsants (phenytoin, carbamazepine)
Frusemide (high doses)
Hyperkalaemia
Hypercalcaemia
Burns
Paresis or hemiplegia
Steroids
Azathioprine
MB19 [Jul98] Malignant hyperthermia causes:

A. Hypertension

B. Whole body rigidity

C. Tachyphylaxis with a suxamethonium infusion

D. ?
ANSWER B
MB20 [Jul99] [Jul01] Edrophonium:

A. Longer halflife than neostigmine

B. Onset slower than neostigmine


C. Binds to anionic site of cholinesterase

D. Relieves symptoms of myaesthenia gravis

E. Is reliable in reversing a Phase 2 block
ANSWER A

A: true longer half life, t1/2 is 110 cf 77 min for neostigmine

B: false: faster onset

C: partially true, also binds to esteratic site

D: partially true, depends on current treatment, if MG is undertreated then symptoms improve, but if overtreated then symptoms get worse.

E: false, not reliable
MB22 [Jul99] [Apr01] Atracurium:

A. Has an active metabolite

B. Ester metabolism is a minor pathway of elimination

C. Metabolism is by Hofmann elimination which is pH dependent (‘Did not include temperature’)

D. ?

E. ?
ANSWER A

A: true, laudanosine has no neuromusclar activity but can cause seizures

B: false, 2/3 by ester hydrolysis and 1/3 by hoffman deg

C: false : as above
MB23 [Feb00] [Jul04] What muscle relaxant has an active metabolite with a half-life twice

that of the parent compound?

A. Rocuronium

B. Vecuronium

C. Pancuronium

D. Atracurium or Cisatracurium

E. None of the above

F. Mivacurium
ANSWER B

A: false, no active metabolites

B: true, vec metabolite has 80% activity with elim 1/2 110 minutes (3xvec)

C: false, panc has meta olite with 50% activity with similar kinetics

D: false no active metabolites

E: false

F: false
MB23b [Jul04] Which of these NDNMB has a metabolite that’s 50-70% as active as its parent drug

A. Atracurium

B. Vecuronium

C. Rocuronium

D. dTC

E. None of the above
ANSWER B
MB24 [Feb00] Succinylcholine can cause:

A. Bradycardia

B. Histamine release

C. Tachycardia

D. Hypertension

E. All of the above
ANSWER E
MB26 [Feb00] Which of the following is associated with a decrease in duration or effect of nondepolarising neuromuscular blocking drugs:

A. Volatile anaesthetic alkanes

B. Volatile anaesthetic ethers

C. Aminoglycoside antibiotics

D. Aminopyridine derivatives

E. Local anaesthetic esters
ANSWER D

D. Aminopyridine derivatives - true; aminopyridine "prolongs action potentials thereby increasing transmitter release at the neuromuscular junction and elsewhere.
Alt version: Which of the following decreases the duration/depth of neuromuscular blockade?

A. Enflurane at 2 MAC

B. Aminoglycosides

C. Bolus doses versus infusion

D. Aminopyridines
ANSWER D

D. Aminopyridine derivatives - true; aminopyridine "prolongs action potentials thereby increasing transmitter release at the neuromuscular junction and elsewhere.
MB26b [Jul01] Neuromuscular blockade NOT prolonged by:

A. Hyperthermia

B. Gentamicin

C. Volatile agents

D. Hypothermia

E. ?
ANSWER A
MB27 [Jul00] [Apr01] [Jul04] Neostigmine's mechanism of action:

A. Binds covalently to esteric site on AChEsterase

B. Binds electrostatically to esteric site on AChEsterase

C. Binds to anionic site

D. Forms complex with AChEsterase with a shorter halflife than acetylcholine

E. (“Some other long winded explanation requiring 30 seconds to read and impossible to remember.”)
ANSWER A
MB28 [Jul00] With depolarising neuromuscular blocker:

A: Is competitively antagonised by NDMR

B: at high doses has no fade on a train of 4

C. at low doses has no fade on a train of 4

D. is adequately revered with atropine and nestigmine

E: Shows post tetanic potentiation
ANSWER C
MB29 [Jul00] Rocuronium administered in 2 times the ED95 dose:

A. Rapid onset, short duration

B. Rapid onset, Intermediate duration

C. Slow onset, intermediate duration

D. Slow onset, long duration

E. (“some other combination.”)
ANSWER B

2ED95 dose is the intubating dose of rocuronium - it has a rapid onset and an intermediate duration of action

* Rapid onset
* Intermediate duration


* Rocuronium has an ED95 dose of 0.3mg/kg
* At an intubating dose of 0.6mg/kg, has an onset of 1-2 mins, and a duration of action of 20-35 mins.
* At 3-4x ED95 dose, the onset resembles the onset of suxamethonium (approx 60 secs), but has a duration of action resembling pancuronium (60-90 mins
MB31 [Apr01] Neostigmine:

A. Tertiary ammonium compound

B. Readily causes bradycardia if not given with neostigmine

C. Predominately metabolised by plasma esterases to a tertiarty alcohol

D. Peak effect occurs at 5-7 minutes

E. associated with higher risk of gastrointestinal anastamotic breakdown
ANSWER ??

A. FALSE: a quaternary amine

B. FALSE: variable and depends upon the prevailing autonomic tone

C. FALSE: metabolised by plasma esterases to a quaternary alcohol

D. FALSE: peak effect occurs at 7-11 minutes

E. TRUE
MB32 [Jul01] [Jul04] The dibucaine number for a normal person is:

A. 20

B. 40

C. 60

D. 80

E. 100
ANSWER D
MB33 [Jul01] Muscle relaxants are less likely to cause anaphylaxis if:

A. Injected slowly

B. Suxamethonium is the most common cause

C. H1 and H2 blockers prevent anaphylaxis

D. Always fatal

E. Latex free environment is effective for prevention of an anaphylactic reaction
ANSWER E
MB35 [q[ All of the following result in prolongation of Vecuronium block except:

A. Concomitant insulin and dextrose infusion

B. Prior suxamethonium blockade
ANSWER B

A - false; hypokalaemia potentiates the effect on NDMBs

B - true; "the subsequent duration of action of neuromuscular blockade produced by atracurium or vecuronium is not prolonged by the prior administration of SCh.
MB36(Feb04) Post-suxamethonium myalgia:
A. Preceeded by transient myoglobinuria

B. More common in the elderly

C. Can be prevented by pre-treatment with 0.04 mg/kg of D-tubocurarine "pre-curarisation"

D. Is invariably associated with increased intra-ocular pressure

E. Is associated with hypokalaemia
ANSWER C
MB37 [Feb04] Regarding anticholinesterases:

A. Pyridostigmine is a tertiary amine

B. Quaternary ammonium anticholinesterases have a larger volume of distribution than non-depolarising muscle relaxants

C. Edrophonium has a slower onset of action than neostigmine

D. Neostigmine has a longer duration of action than pyridostigmine

E. Edrophonium binds covalently to the esteratic site of acetylcholine
ANSWER B
MB37b [Jul04] Regarding Antiacetylcholinesterase

A. Given orally to treat glaucoma

B. Edrophonium is a long acting AChE inhibitor

C. Physostigmine is quarternary ammonium

D. Neostigmine covalently binds by its phosphate group to serine group at the active site of the cholinesterase

E.
ANSWER E

A: False, they are given using drops. Rarely given orally.

B: false, shorter acting due to redistribution, but has a longer clearance

c: false, physiostigmine is a tertiary amine; neostigmine, edrophonium and pyridostigmine are quaternary amines

D. False: Neostigmine is a reversible inhibitor at the active site

E. Used for treatment of Alzheimer's disease and Lewy Body Dementia
MB38 [Jul04] Which is the best indicator of adequate reversal?

A. TOF Count of 4

B. No fade on DBS

C. No fade to 200 Hz tetanus

D. Head lift??

E. Evidence of post-tetanic facilitation
ANSWER B
MB38b [Jul04] Residual curarization is best evaluated with:

A. TOF 1:4 > 50%

B. Equal twitch height on DBS

C. Degree of fade is independent on stimulus intensity

D. Used to check depth of anaesthesia

E. PTC
ANSWER B
MB39 [Jul07] Sugammadex binds most avidly to:

A. Pancuronium

B. Rocuronium

C. Vecuronium

D. Atracurium

E. Cisatracurium
ANSWER B