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Pharmacology > Nervous system ( 15% ) > Flashcards

Nervous system ( 15% ) Flashcards

1
Q

. Termination of irreversible neuromuscular block involves

  • a. Regeneration of receptors
  • b. Increase in end plate Ach
A

a. Regeneration of receptors

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2
Q

atracurium

  • a. has a longer duration of action than vecuronium
  • b. is not associated with histamine release.
  • c. is a steroid derivative.
  • d. is eliminated by non renal/liver dependent mechanisms
A

d. is eliminated by non renal/liver dependent mechanisms

Undergoes Hoffman degeneration

Is an Isoquinolone derivative

Is associated with histamine release, and all the potential side effects (bronchospasm, hypotension, tachycardia)

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3
Q

regarding pancuronium – which is INCORRECT?

  • a. It is a steroid
  • b. It does not release histamine
  • c. It is renally excreted
  • d. It has a shorter duration of action than vecuronium
A

d. It has a shorter duration of action than vecuronium

Pancuronium has renal elimination and a long half-life and duration of action

Vecuronium has liver metablism (along with roc)

Isoquinolone derivatives (atracurium and mivacurium) cause histamine release

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4
Q
  1. dantrolene is a good choice in treatment of malignant hyperpyrexia because
  • a. it antagonizes the effects of suxamethonium
  • b. it inhibits prostaglandin formation
  • c. it decreases calcium release from sarcoplasmic reticulum in skeletal muscle
A

c. it decreases calcium release from sarcoplasmic reticulum in skeletal muscle

MH - genetic problem causing uncontrolled calcium release when given sux -> prolonged muscle contraction -> hyperthermia, lactic acidosis, circulatory collapse

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5
Q

vecuronium, all of the following are true EXCEPT

  • a. has minimal CVS effects
  • b. is predominantly renally excreted
  • c. has a shorter duration of action than pancuronium
A

b. is predominantly heptically metabolised

DoA = 25-30min

Pancuronium is renally excreted and has DoA 45-60min

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6
Q
  1. which is true of neuromuscular blockers?
  • a. Gentamicin increases their efficacy.
  • b. Gallium is eliminated by the liver
  • c. Vecuronium is an isoquinolone derivative
  • d. Atracurium causes hypotension in volume depleted people
  • e. Pancuronium causes histamine release.
A

d. Atracurium causes hypotension in volume depleted people

?via histamine release (isoquinolone derivative)

a. Gentamicin increases their efficacy.

(“enhances NMB” unsure why this is not true)

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7
Q
  1. The duration of action of which of these drugs is NOT significantly prolonged in renal failure?
  • a. Tubocurarine
  • b. Pancuronium
  • c. Gallamine
  • d. Atracurium
  • e. Suxamethonium
A

d. Atracurium

Initial answer was sux, but atracurium undergoes Hoffman degeneration and is not impacted in renal or livef failure

e. Suxamethonium

Plasma-cholinesterases break it down very quickly, but has 10% renal elimination

Really could be either but likely atracurium is the best answer here. Probably just a bad question.

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8
Q

suxamethonium

  • a. has a prolonged duration of action
  • b. is reversed with neostigmine in phase I.
  • c. causes Ach release at the neuromuscular junction.
  • d. causes muscle fasciculation
  • e. is primarily metabolized at the neuromuscular junction.
A

d. causes muscle fasciculation

  • a. has a short duration of action (4-8min)
  • b. is reversed with neostigmine in Phase II (neostigmine is an anticholinesterase inhibitor)
  • c. causes K+ release at the neuromuscular junction.
  • e. is NOT metabolized at the neuromuscular junction - it diffuses away and is degraded by plasma cholinesterases (not NMJ acetyl-cholinesterases)
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9
Q

. non-depolarising muscle relaxants:

  • a. which are hepatically metabolized, generally have a shorter half life than those which are renally excreted
  • b. cause insurmountable blockade
  • c. decrease the amount of depolarizing muscle relaxant which is required for blockade
  • d. all cause hypotension via histamine and ganglionic blockade.
  • e. cause hyperkalaemia.
A

a. which are hepatically metabolized, generally have a shorter half life than those which are renally excreted

Can be overcome with increasing ACh levels (competitive antagonist)

Atrocurium (as an isoquinolone derivative) causes hypotension via histamine release and ganglionic block, but others such as roc do not

Only depolarising muscle relaxants causes hyperkalaemia

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10
Q

which of the following statements is FALSE regarding vecuronium?

  • a. It has minimal cardiovascular effects
  • b. It is predominantly renally excreted
  • c. It has a significantly longer duration of action than pancuronium
A

c. It has a significantly longer duration of action than pancuronium

This question appears twice, and the answer alternates between c) and b (renally excreted). The answer is both here.

Pancuronium is renally excreted and has a longer duration of action then vecuronium, which is hepatically metabolised.

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11
Q

the muscle relaxant most commonly associated with tachycardia is low dose

  • a. suxamethonium
  • b. atracurium
  • c. vecuronium
  • d. pancuronium
  • e. tubocurare
A

d. pancuronium

Suxamethonium is associated with tachycardia at high doses, or bradycardia if a repeat dose is given within 5 minutes

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12
Q

the muscle relaxant with the longest duration of action is

  • a. atracurium
  • b. mivacurium
  • c. pancuronium
  • d. vecuronium
  • e. rocuronium
A

c. pancuronium

Renally excreted

Roc and Vec are hepatically metabolised

Atracurium undergoes Hoffman degeneration

Mivacurium is metabolised by plasma esterases (as is sux)

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13
Q
  1. Regarding local anaesthetics
  • a. Adrenaline increases systemic absorption.
  • b. Maximal blood level is independent of site of administration.
  • c. Blockade of Ca2+ channels augments effects.
  • d. Bupivacaine has a short duration of action.
  • e. None of the above are true
A

Nick thinks none are right

a) Adrenaline decreases systemic absorption
b) Maximal blood level does depend on site of administration
c) Increasing ECF Ca2+ reduces the effect of LAs

Blocking Ca2+ channels will reduce efflux of Ca, and thus cause a reduced ECF Ca concentration which should increase the effect of LA

d) Bupivicaine has a long duration of action

2-4 hours

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14
Q
  1. Local anaesthetics:
  • a. May cause blockage of motor nerves before sensory nerves in large mixed nerves
  • b. Preferentially block larger fibres.
  • c. Preferentially block unmyelinated nerves
  • d. Will block A-a fibres before A-d and C fibres
  • e. Have no cardiac effects.
A

Nick thinks a), doesnt seem right but everything else is wrong

a)May cause blockage of motor nerves before sensory nerves in large mixed nerves

‘preferentially blocks small, myelinated, sensory nerves’

b) as above
c) as above
d) C fibres most susceptible, then A-d, then A-a
e) Do have cardiac effects - can cause cardiac arrest, lignocaine is a class 1B antiarrythmic

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15
Q
  1. Which local anasthetic causes methaemoglobinaemia?
  • a. Lignocaine
  • b. Tetracaine
  • c. Bupivacaine
  • d. Procaine
  • e. Prilocaine
A

e. Prilocaine

Ortho-toludine, a metabolite, can cause methaemoglobinaemia in some people.

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16
Q
  1. Which is an ester local anaesthetic?
  • a. Tetracaine
  • b. Lignocaine
  • c. Bupivacaine
  • d. Etidocaine
  • e. Prilocaine
A

a. Tetracaine

Along with cocaine, procaine, and benzocaine

Lignocaine, ropivicaine, bupivicaine, prilocaine are all amides

Amides all have 2 I’s in their name

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17
Q

The local anaesthetic agent prilocaine:

  • a. Is metabolized by butyrylcholinesterase
  • b. Has a very short duration of action
  • c. Has the same intermediate chain as procaine
  • d. Is more likely to cause toxicity in patients with liver disease. Applies to all amides
  • e. Should not be used in patients with a known hypersensitiviy to p-aminobenzoic acid
A

d. Is more likely to cause toxicity in patients with liver disease.

Applies to all amides

Amides are made more water-soluble in liver reactions, which is slowed in liver disease

Esters are metabolised by plasma esterases

Both are then excreted by the urine

18
Q
  1. With regard to susceptibility to block by local anaesthetic agents, which is NOT true?
  • a. Dorsal root pain fibres are more sensitive than proprioceptive fibres
  • b. They preferentially block small fibres
  • c. Myelinated nerve fibres tend to be blocked before non-myelinated ones of the same size
  • d. Motor fibres may be blocked before pain fibres in the brachial plexus
  • e. Block starts at the distal parts supplied by the nerve and proceeds proximally.
A

e. Block starts at the proximal parts supplied by the nerve and proceeds distally.

Outer fibres supply more proximal areas, hence tend to be blocked first

19
Q
  1. Lignocaine
  • a. Penetrates the axon in its charged form
  • b. Is more potent than bupivacaine.
  • c. Has a higher affinity for activated than resting sodium channels
  • d. Is a weak acid.
  • e. Blocks voltage gated sodium channels at their extracellular end.
A
  • a. Penetrates the axon in its uncharged form.
  • b. Is less potent than bupivacaine
  • c. Has a higher affinity for activated than resting sodium channels
    • ​Hence rapidly firing nerves are more quickly blocked than non-firing
  • d. Is a weak base
  • e. Blocks voltage gated sodium channels at their intracellular end.
    • Hence needs a basic enviroment to speed onset of action, as only the unionised form can cross cell-membranes
20
Q
  1. Concerning lignocaine toxicity:
  • a. Lignocaine is highly cardiotoxic compared to other local anaesthetics
  • b. Lignocaine exacerbates ventricular arrythmias in about 10% of patients
  • c. Neurological effects are less common
  • d. Hypotension is most common
  • e. Side effects are not dose related
A

b. Lignocaine exacerbates ventricular arrythmias in about 10% of patients

Potentially less cardiotoxic given it is used as an anti-arrhythmic (class 1b, same as amiodarone)

Side effects are dose related

Lip tingling is first effect, likely most common

21
Q
  1. The half life of lignocaine is
  • a. 1 minute
  • b. 5 minutes
  • c. 10 minutes
  • d. 30 minutes
  • e. 120 minutes
A

e) 120minutes

Onset 2min

Duration 1-2 hours (2-3 with adrenaline)

22
Q
  1. All of the following are amide local anaesthetics EXCEPT:
  • a. Lignocaine
  • b. Bupivacaine
  • c. Benzocaine
  • d. Prilocaine
A

c. Benzocaine

Esters: cocaine, tetracaine, procaine, benzocaine

Amides: lignocaine, bupivicaine, ropivicaine, prilocaine

23
Q

Regarding local anaesthetics, which is incorrect:

  • Blood levels will be 30% lower with added vasoconstrictors leading to enhanced neuronal uptake
  • A lower pH means that more of the anaesthetic will be in the uncharged form and thus less effective.
  • Systemic absorption is greater when injecting highly vascular sites like the tracheal mucosa
  • Ester-based local anaesthetics will be rapidly broken down in the plasma
A

A lower pH means that more of the anaesthetic will be in the ionised (LA-H) form and thus less effective.

Need to be unionised (LA-) to cross cell membrane and exert effects

All are weak bases, so an acidic enviroment will mean more are in the charged form (and thus unable to cross cell membranes)

24
Q

The following are all examples of ester local anaesthetics except:

  • Prilocaine
  • Procaine
  • Cocaine
  • Benzocaine
A

Prilocaine

Esters: cocaine, tetracaine, benzocaine, procaine

Amides: lignocaine, bupivicaine, ropivicaine, prilocaine

25
Q

Regarding local anaesthetics, which is correct:

  • Unmyleinated Aδ fibres are the most sensitive to block
  • Primary action is blockade of ligand-gated sodium channels. Voltage-gated
  • Hepatic disease will cause increased toxicity from the ester local anaesthetics. Amide
  • Repeated injections of local anaesthetic can result in tachyphylaxis
A
  • Unmyleinated C fibres are the most sensitive to block
  • Primary action is blockade of voltage-gated sodium channels.
  • Hepatic disease will cause increased toxicity from the amide local anaesthetics.
  • Repeated injections of local anaesthetic can result in tachyphylaxis
26
Q

Regarding the effects of local anaesthetics which is incorrect:

  • At least 2 nodes of Ranvier need to be blocked to prevent AP propagation in a myelinated nerve
  • Unmyelinated nerves tend to be blocked before myelinated nerves of the same diameter
  • Sensory fibres are preferentially blocked because they have a higher rate of firing and a longer AP
  • Block of a large nerve will result in sensory analgesia that starts proximally and spreads distally
A

myelinated nerves tend to be blocked before unmyelinated nerves of the same diameter

Myelinated, small, sensory, peripheral most sensitive (c- fibres most susceptible)

27
Q

Toxicity due to local anaesthetics includes all of the following except:

  • Direct neural toxicity
  • Direct and indirect cardiotoxicity
  • Seizures
  • Methaglobulin accumulation
A

Direct and indirect cardiotoxicity

  • Seem to only have direct cardiotoxic effects due to Na-channel block*
  • Prilocaine can cause methaemaglobinaemia*
28
Q
  1. Local anaesthetics
  • a. Act on the most rapidly firing neurons
  • d. have an increased effect on large fibre diameter
A

a. Act on the most rapidly firing neurons
Acts on activated or

29
Q
  1. Which of these drugs increases the steady state concentration of phenytoin?
  • a. Phenobarbitone
  • b. Carbamazepine.
  • c. Isoniazid
  • d. Ethanol
  • e. All of the above
A

c. Isoniazid

Phenobarbitone and carbamazepine are P450 inducers (will reduce levels)

30
Q
  1. Phenytoin
  • a. Is not effective against partial seizures.
  • b. Accumulates in the endoplasmic reticulum of brain tissue
  • c. Is poorly bound to plasma proteins
  • d. Is mostly excreted unchanged by the kidneys.
  • e. Suppresses seizures primarily by its action on channels.
A

b. Accumulates in the endoplasmic reticulum of brain tissue

  • a. Is effective against partial seizures
  • c. Is 80% bound to plasma proteins
  • d. mostly undergoes Hepatic metabolism (zero order)
  • e. Suppresses seizures primarily by its action on channels. Also true – blocks sodium channels
31
Q
  1. phenytoin
  • a. is lowly protein bound
  • b. causes agranulocytosis in 5% of patients
  • e. can cause abnormalities of vitamin D metabolism
A

e. can cause abnormalities of vitamin D metabolism

  • 80% protein bound*
  • Can cause thrombocytopenia*
32
Q
  1. concerning toxicity of phenytoin
  • a. nystagmus is a late complication.
  • b. alopecia is a complication
  • c. increased deep tendon reflexes is a manifestation
  • d. vitamin D metabolism abnormalities can occur
  • e. agranulocytosis is a common manifestation
A

d. vitamin D metabolism abnormalities can occur

  • a. nystagmus is an early complication.
  • b. alopecia is a complication of sodium valproate
  • c. ??increased deep tendon reflexes is a manifestation
  • e. thrombocytopenia is a manifestation
33
Q
  1. carbamazepine
  • a. is metabolized to active metabolites
  • b. in overdose does not cause seizures
  • c. is an enzyme inhibitor.
  • d. is not a tricyclic.
  • e. enhances sodium channel conductance.
A

a. is metabolized to active metabolites

Structurally related to TCAs, with Na-channel blocking effects and can cause a similar toxidrome

  • b. in overdose causes seizures
  • c. is an enzyme Inducer (valproate is an inhibitor)
  • d. is a tricyclic
  • e. Reduces sodium channel conductance as it is a sodium channel blocker
34
Q

A patient started on carbamazepine for episodes of partial seizures. After a month where she was seizure free, she started having further seizures. What is the MOST likely cause?

  • a. The patient has developed a tolerance to carbamazepine
  • b. Carbamazepine is not the drug of choice for such seizures, hence the patient needs to be put on a more suitable anticonvulsant
  • c. Initially carbamazepine has a low systemic clearance, however over time the clearance increases requiring an increase in dose.
  • d. She was not loaded with carbamazepine appropriately
  • e. All of the above
A

c. Initially carbamazepine has a low systemic clearance, however over time the clearance increases requiring an increase in dose.

Due to induction of its own CYP enzyme

  • b. Carbamazepine is usually effective for partial seizures
  • d. She was not loaded with carbamazepine appropriately.
    • Long half-life, but a month would be sufficient and would not explain the initial seizure control
35
Q
  1. A patient on phenytoin has a seizure and is found to have a low level, which is least likely to cause this?
  • a. Phenobarbitone.
  • b. Non-compliance.
  • c. Hypoalbuminaemia.
  • d. Disulfiram.
  • e. Erythromycin
A

​e. Erythromycin. Also an enzyme inhibitor

  • *d. Disulfiram - Inhibits metabolism -> high plasma levels**
  • Nick says disulfram - however it appears that this is very specific in what it inhibits as per a Google search (clozapine and benzene), and erythromycin is more commonly used as an example of an inhibitor.*
  • a. Phenobarbitone - Enzyme inducer -> would be likely to cause a low level
  • b. Non-compliance - Most likely cause of low levels
  • c. Hypoalbuminaemia - Decreases the total amount but not the free (active amount) – same as thyroid hormones
36
Q
  1. With rergard to phenytoin, which is NOT true?
  • a. Metabolism is saturable within the therapeutic concentration range
  • b. Small changes in dose may cause swings from toxicity to sub-therapeutic levels
  • c. Steady state can be relied on to be achieved within 7 days of a dose change.
  • d. It may induce microsomal enzymes
  • e. Intravenous doses should be given over at least 20-30 minutes to avoid toxicity
A

c. Steady state can be relied on to be achieved within 7 days of a dose change.

Half-life = 24 hours but may increase at higher doses due to zero order kinetics. Therefore 4 half-lives could easily exceed 1 week

37
Q
  1. carbamazepine is closely related to
  • a. vigabatrin
  • b. quinidine
  • c. sodium valproate
  • d. metoprolol
  • e. imipramine
A

e. imipramine

A TCA

38
Q
  1. Which of the following regarding carbemazepine is FALSE?
  • a. It is greater than 50% protein bound
  • b. It has active metabolites
  • c. It induces p450 liver cytochromes
A

Jokes, theyre all true. Whoever wrote the question could not remember a false answer.

39
Q
  1. Match the drug and effect – which is INCORRECT?
  • a. Phenytoin – gum hypertrophy
  • b. Carbamazepine – ataxia
  • c. Phenobarbitone – enzyme induction
  • d. Ethosuximate – hirsutism
  • e. Valproate – idiosyncratic hepatic toxicity
A

a. Phenytoin – gum hyperplasia

  • Not hypertrophy*
  • Nick said ‘Ethosuximate – hirsutism’, but wikipedia lists this as an ADR (it is an antiepileptic)*
  • Others all seem true - ataxia is one of the first ADRs of carbamazepine; phenobarbitone does induce enzymes; and a major side effect of valproate IS hepatotoxicity*
40
Q
  1. Your patient has abnormal LFTs, in particular an elevated AST. He tells you he is on medication for fits, but can’t name it. Which is MOST likely to be his drug?
  • a. Phenytoin
  • b. Diazepam
  • c. Sodium valproate
  • d. Clonazepam
  • e. Ethosuximide
A

c. Sodium valproate

Hepatotoxicity is a major side effect

41
Q
  1. with regard to the general pharmacokinetics of anticonvulsants:
  • a. they are generally highly protein bound.
  • b. bioavailability is low.
  • c. volumes of distribution are usually many time the free water volume.
  • d. clearance is hepatic
  • e. extraction ratios are high
A

d. clearance is hepatic

  • a. they are generally low protein bound (except the three we need to know well - sodium valproate, phenytoin, and carbamazepine which are about 80% bound)
  • b. bioavailability is High
  • c. volumes of distribution are usually Approx the TBW (~0.5-1L/kg)
  • e. extraction ratios are not high (?low)

Pharmacology (13 decks)

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