AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS

EXAMINATION REPORT

PRIMARY EXAMINATION

MARCH/APRIL 1999

PLEASE NOTE THAT THIS REPORT IS PREPARED TO PROVIDE CANDIDATES AND

THEIR TEACHERS AND SUPERVISORS OF TRAINING WITH INFORMATION
ABOUT THE WAY IN WHICH THE PERFORMANCE OF CANDIDATES IN THE
RECENT EXAMINATION WAS ASSESSED BY THE EXAMINERS, SO THAT
CANDIDATES AND TEACHERS MAY PREPARE APPROPRIATELY FOR FUTURE
EXAMINATIONS. THE INDIVIDUAL REPORTS ARE NOT INTENDED TO
REPRESENT MODEL ANSWERS NOR IMPLY THAT ALL POINTS MENTIONED ARE
NECESSARY IN ORDER TO ACHIEVE A PASS. ALL TRAINEES ARE URGED TO
READ THE QUESTIONS CAREFULLY AND ANSWER THE QUESTION ASKED. ALL
TEACHERS AND SUPERVISORS OF TRAINING ARE ENCOURAGED TO DISCUSS
THIS REPORT IN DETAIL WITH CANDIDATES THEY ARE PREPARING FOR
FUTURE EXAMINATIONS.

PHYSIOLOGY

WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS:

53% of candidates achieved a pass in this section of the Physiology Examination.

SHORT ANSWER QUESTIONS:

QUESTION 1 Explain the Bohr and Haldane effects in trans-placental gas exchange.

Approximately 42% of candidates passed this question.

The Bohr and Haldane effects were defined accurately by nearly all candidates and most confined
themselves to the question including little irrelevant information. Good answers also included the
PO2, PCO2 and pH values in the maternal and fetal circulation’s before and after the placenta. The
best way to describe the transfer of oxygen and carbon dioxide was in a narrative form, explaining
each effect eg. the Bohr effect on the maternal side then on the foetal side.

This answer required precision with terms. Many candidates did not make it clear whether they
were discussing maternal or foetal haemoglobin, or maternal or foetal haemoglobin oxygen
dissociation curves. Uterine and umbilical vessels, when included in diagrams were often wrongly
labelled or not labelled at all.

The most common mistake was to try and draw the double Bohr effect diagram. This diagram is
very complicated and takes a lot of time. Very few candidates drew it accurately or labelled the
axes with both numbers and units. Often the diagram was drawn and no attempt made to explain it.
The diagram alone is not an adequate explanation.
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QUESTION 2 Explain the mechanisms that prevent blood clotting in intact blood
vessels (do not draw the clotting cascade).

42% of candidates passed this question and there were few good answers. Most candidates failed
to appreciate that blood clotting (haemostasis) depends on a fine balance between procoagulant and
anticoagulant processes. The activation of platelets and coagulation is minimal in intact blood
vessels with normal blood flow. Even minor activation of the clotting mechanism results in a rapid
escalation of procoagulant processes (positive feedback or amplification). This can result in
uncontrolled clotting unless anticoagulant processes are simultaneously activated to limit clot
formation.

The mechanisms preventing clot formation can be considered under the following headings:

1. Endothelial surface factors include the smooth endothelial surface and glycocalyx layer, which
prevents contact activation of coagulation factors and platelet activation. Thrombomodulin
binds thrombin thus slowing the clotting process and the thrombomodulin - thrombin complex
activates protein C. PGI 2 inhibits platelet aggregation.
2. Blood flow dilutes and removes activated clotting factors, which are then inactivated by the
RES. Laminar flow causes axial streaming of platelets which minimises endothelial contact and
hence activation
3. Natural anticoagulants are present in concentrations, which exceed that of procoagulants.
Heparin combines with antithrombin III increasing its activity up to a thousand fold.
Antithrombin III inactivates factors IIa, IXa, Xa, XIa and XIIa. Protein C inactivates factors Va
and VIIIa and plasminogen activator inhibitor-1 which stimulates fibrinolysis. α2-
macroglobulin inhibits thrombin.
4. Limitation of clot size due to fibrin binding thrombin in the clot and fibrinolysis breaking down
formed clot.

Whilst antithrombin III and protein C were mentioned by most, few could correctly describe their
activation or mechanism of action. Many answers wrongly stated that the natural anticoagulants
inhibited the inactive form of the coagulation factors.

QUESTION 3 Describe the factors that affect the transport of oxygen and carbon
dioxide from the alveolus to blood.

Overall this question was well answered with 44% of candidates achieving a pass.

The factors that affect transport of oxygen and carbon dioxide between alveolus and blood can be
described by Fick’s Law of simple diffusion ie. Diffusion constant, surface area, membrane
thickness, and concentration gradient (or more correctly partial pressure gradient). Marks were
awarded for relating these factors to the alveolus and lung. The influence of solubility and
molecular weight on the diffusion constant for individual gases should have been described, with
comparisons for oxygen and carbon dioxide. Additional marks were awarded for describing the
influence of cardiac output and the rate of combination of oxygen with haemoglobin. Oxygen
diffusion is normally perfusion limited. Increases in cardiac output (eg. with exercise) normally
result in recruitment of alveoli thereby increasing the surface area for diffusion. However, in the
presence of disease or a low partial pressure gradient (eg. at high altitudes), an increased cardiac
output may reduce red blood cell transit time resulting in insufficient time for equilibration of
oxygen, making oxygen, unlike carbon dioxide, diffusion limited. The combination of oxygen with
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haemoglobin is important because it ensures a low capillary partial pressure of oxygen and
maintains a gradient for oxygen diffusion despite a higher oxygen concentration in the blood. In
this way haemoglobin concentration, the affinity of haemoglobin for oxygen, and capillary blood
volume influence the rate of oxygen diffusion.

Many candidates wasted time providing detailed descriptions of oxygen and carbon dioxide
transport in the blood, the haemoglobin-oxygen dissociation curve, alveolar ventilation, or
ventilation-perfusion mismatch. Failure to address the question led to a reduction in scores.

QUESTION 4 Explain how the kidney handles glucose. Describe the physiological
consequences of glycosuria.

49% of candidates passed this question. To answer the question adequately, candidates should
point out that glucose is filtered at the glomerulus and reabsorbed in the proximal tubule by a
secondary active transport mechanism, using energy supplied by Na/K ATPase. Reabsorption
increases as glucose filtration increases up to a transport maximum (Tm), above which glucose
appears in the urine. They should also mention that glycosuria causes an osmotic diuresis, as
glucose holds water and sodium in the proximal tubule, causing urinary loss of water, sodium and
other electrolytes and consequent hypovolaemia and electrolyte and osmotic imbalance. High fluid
flow in the nephron washes out the medullary osmotic gradient, impairing the kidney’s ability to
concentrate urine. Loss of glucose represents a loss of nutrient and energy.

Other points, which gained marks, included discussion of the link between sodium and glucose
absorption, and of the reason for Tm limitation. Discussion of the mechanism of potassium loss
and mention of the body’s response to osmotic effects of glycosuria on the circulation and
extracellular fluid also gained marks.

Common errors included the assumption that glycosuria equals diabetes mellitus, and consequent
irrelevant discussion of ketoacidosis and its consequences. Several candidates incorrectly stated
that glucose was secreted by the nephron. Others repeated, more or less verbatim, the account of
renal glucose handling given in Ganong, with little evidence of understanding.

Exact statements are more likely to gain marks than vague, imprecise ones. Undefined
abbreviations and forms of shorthand (eg “c”) which clearly have some meaning to the candidate,
but not to the examiner, should be avoided.

QUESTION 5 Differentiate between the terms “heat” and “temperature”. Explain

briefly the principles of a mercury thermometer, indicating its
advantages and disadvantages.

82% of candidates passed this question. Most passed well and there were a number of very good
answers. There was a reasonable amount of confusion about the difference between Heat and
Temperature. Mentioning S.I. units and relating the entities via Specific Heat Capacity enhanced
definitions and gained extra marks.

Most candidates gave a reasonable explanation of the physical principles of the mercury
thermometer, although many omitted calibration principles and did not mention the importance of
the relative volumes of the Mercury Reservoir in the bulb and the capillary column. It is also
critical that the capillary tube is evacuated.
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The concept of a time constant was often mentioned but also often misunderstood. In general,
advantages and disadvantages were well done with a number of candidates having prepared
exemplary lists.

QUESTION 6 Describe the factors influencing hepatic blood flow.

Although the pass rate for this question was 73%, very few candidates scored well. A good answer
should have included a discussion of:

a) anatomical considerations of hepatic blood flow

b) normal values and the autoregulation of hepatic artery flow
c) the difference in perfusion pressures of the hepatic artery and portal vein
d) factors that affect the hepatic vascular resistance, including changes in blood gases,
sympathetic stimulation, anaesthetic agents and hepatic diseases
e) other factors including cardiac output, blood pressure and ventilation.

Although most candidates discussed the anatomical factors and perfusion pressures, very few
included in their answer the factors that change the hepatic blood flow.

QUESTION 7 Describe the autonomic innervation of the heart, and the direct effect of
autonomic stimulation on cardiac function.

59% of candidates passed this question.

Anatomical knowledge was required of the neural innervation of the heart, site of ganglia, pathways
to the heart and differences between the left and right sides of the body. The identity of the
neurotransmitters was relevant as well as the receptors activated. Many answers were more suited
to a question on the effects, on the heart, of adrenergic and cholinergic receptors without
distinguishing between the effects of neural stimulation and blood borne agonists.

The cardiac tissues are specialised and the effect of neural stimulation differs on sinoatrial node,
atria, atrioventricular node, Purkinje cells and ventricular myocytes. Many of the better answers
used this information to structure their answer and succinctly present a large amount of information
on the effects of stimulation.

The sequence of events following receptor activation was well handled.

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QUESTION 8 Explain the significance of plasma oncotic pressure in capillary fluid
dynamics.

This question was successfully answered by 75% of candidates, with some excellent answers.

The osmotic pressure exerted by the unfiltered proteins obviously required definition in relation to
the other Starling forces acting across the capillary membranes. This was successfully done by
those who passed, usually with the aid of the Starling pressures equation common to the standard
texts.

Answers that scored well used some or all of the following, to explain the significance of the
plasma osmotic pressure.

• Comparison of forces in different capillary beds

• Quantification of forces. Allowance was made for the different values by different authors in
the standard texts
• Explanation of significance of filtration and reflection coefficients
• Effects of altered osmotic and hydrostatic pressures
• Lymphatic function

Candidates who failed either did not answer the question, or made significant errors, demonstrating
limited understanding of plasma protein osmotic pressure and its function in capillaries.

VIVA SECTION

Introductory Physiology Questions

• What is the effect of a sustained increase in sodium intake?

• Describe how the kidney concentrates urine.
• How can one measure liver blood flow?
• What are the effects of a biliary fistula?
• What are the changes in blood volume in pregnancy?
• Draw a muscle spindle
• What blood groups are there?
• What is a buffer?
• What are the effects on the body of tipping the body steeply head down?
• What factors determine the glomerular filtration rate?
• What is complement?
• What is an exponential process?
• What forces are overcome by muscle activity during a tidal breath?
• What is lung compliance?
• What is the resting membrane potential of skeletal muscle?
• How can one measure intravascular pressure?
• What are the effects of releasing a tourniquet?
• What are the effects of a Valsalva manoeuvre?
• What is colloid osmotic pressure?
• What are the causes of hypoxaemia?
• What is meant by the term “basal metabolic rate”?
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• What is Starling’s law of the capillary?
• Draw a pressure trace obtained from the root of the aorta.
• What is the effect of right atrial pressure on venous return?
• What is the meaning of the term “resistance”?
• What is the oxygen cascade?
• What is the structure of the haemoglobin molecule?
• How is pain sensation transmitted in the spinal cord?
• What is the Nernst equation?
• What is the origin of the resting membrane potential?
• What is the difference between resistance and impedance?
• What is the effect of unconsciousness on temperature control?
• What are the constituents of cerebrospinal fluid?
• How can one measure gas flow?
• What respiratory changes occur during pregnancy?
• What is “closing capacity”?
• What are the actions of thyroxine?
• How can one measure dead space?
• What types of hormone receptor are there?
• How does one calibrate a pressure transducer?
• What types of muscle fibre are there?
• What factors influence pulmonary vascular resistance?
• What is the circulating blood volume of a 70 kg adult?
• What are the effects of acute loss of one third of the blood volume?
• What are the effects of transfusion of 2 litres of whole blood?
• What are the effects of lying supine from a standing position?
• What is Von Willebrand’s factor?
• How does the kidney handle bicarbonate?
• What is absolute humidity?
• Interpret a set of blood gases
• What is the lower oesophageal sphincter?
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PHARMACOLOGY

WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS:

59% of candidates achieved a pass in this section of the Pharmacology Examination.

SHORT ANSWER QUESTIONS:

QUESTION 9 In a clinical trial, why is adequate power important? What factors affect
the determination of an adequate sample size?

58% of candidates passed this question.

There was a wide range of marks for this relatively straightforward question, probably indicating
that some candidates do not consider the statistical component of the syllabus worth serious study
time. The majority gave an adequate definition of statistical power, but not many really addressed
the question “why is it important?” The answer is simply related to the ethics of clinical research,
the efficient use of resources and the need to obtain a correct result to the research question.
The provision of actual formulae to calculate sample size was not required, but several candidates
made very creditable efforts. Most correctly defined alpha and beta errors and indicated how the
values chosen influence sample size. Having done that many omitted to mention the effect of
population variability and the need to estimate it in some way. Other made no reference to the size
of the difference that the study hoped to detect. A few good answers also commented on the
possibility of a number of different outcomes being studied in the one trial and the need to consider
sample size for these individually.

QUESTION 10 Write a brief outline on the pharmacology of remifentanil.

47% of candidates obtained a pass mark in this question.

This was a straightforward question that required an overview of information found in any standard
text, with an emphasis on unique properties. Credit was given for information as outlined below,
although it should be emphasised that this represents an exceptionally good answer that would have
gained near full marks.

Introduction - Remifentanil is a relatively potent, selective mu agonist with a short

duration of action.
Pharmacy - A phenyl piperidine derivative, containing two ester bonds which is a
weak base with a pKa of about 7.1 Presented as a powder mixed with
glycine it can be reconstituted with water.
Pharmacokinetics – Predominantly ionised at body pH, with moderately low lipid solubility (cf
fentanyl) and 70-90% plasma protein bound. It has a rapid onset (about
1min.) and a modest distribution volume (about 0.5l/kg). High clearance
(5l/min) rather than redistribution is responsible for its speed of offset
(beta half-life about 10min.). Notable is a context sensitive half-life of
about 4min, independent of the infusion time. Clearance is almost
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exclusively by hydrolysis of one of the ester bonds by “non specific”
blood and tissue esterases (not by red cell esterase alone and not by
“pseudocholinesterase”) producing an almost inactive carboxylic acid
derivative
Pharmacodynamics – Typical of a mu agonist.
CNS – analgesia, sedation, depresses some brain stem regulatory centres
(respiratory/cardiovascular), excites others (causing nausea, pupillary
constriction, truncal rigidity).
CVS – minimal direct effects on myocardium or vasculature, normally no
histamine release (cf. morphine). Bradycardia and decreased vascular
resistance secondary to effects on vagal nuclei and vasomotor centres.
Resp.- decreased airway reflexes and respiratory rate possibly with
increased volume leading to apnoea; decreased response to hypercapnia
and hypoxia.
GI/GU – increased tone (biliary tree and ureter) and/or decreased activity
(stomach and bowel) probably of little clinical significance because rarely
used long term post operatively.
Adverse effects– bradycardia, decrease in blood pressure, truncal rigidity with high
dose/rapid administration; “neurotoxicity” due to glycine and immune
mediated histamine release; nausea/vomiting and severe pain after
cessation of administration in awake patients.
Clinical use – Intraoperative analgesia of rapid onset/offset (0.1- 1.0 microgm/kg/min)
with optional preceding bolus of 1-2 microgm/kg. Need to make provision
for postoperative analgesia before cessation of remifentanil.

Relatively common mistakes included: failure to appreciate mu selectivity; lack of familiarity with
presentation; confusion concerning enzymes responsible for metabolism; inability to work out
degree of ionisation in vivo when agent has already been identified as a weak base and pKa has
been stated; pharmacodynamics that were simply described as being “fentanyl-like” ( the examiner
has no way of knowing if the candidate knows what fentanyl’s properties are); confusion
concerning cause of “depressant’ cardiovascular effects.

QUESTION 11 Briefly compare and contrast the clinical pharmacology of atropine,

hyoscine (scopolamine) and glycopyrrolate.

Many candidates struggled with this question with 42% passing. There were two main problems:

1. Inadequate attempts to compare and contrast the pharmacology of the three drugs; and
2. Consideration of only one aspect of the pharmacology (eg. pharmacodynamics)

Remarkably, only about half the candidates stated that these drugs act at muscarinic receptors.
Very few identified the drugs as competitive antagonists. The candidates should be very careful not
to omit core information such as this - planning would help.

Historical aspects were not well covered. Some candidates mentioned the sources of atropine and
hyoscine in nature, but very few mentioned the use of atropine with ether or hyoscine with
Omnopon. As far as structure-activity relationships went, most candidates identified the
fundamental differences between atropine and hyoscine, and glycopyrrolate. However, very few
talked about isomers and the relationship of the drugs to the ionic site on the receptor. Only three
candidates attempted to draw the structures.
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Pharmacodynamic and pharmacokinetic differences were discussed fairly well. Toxicity was also
frequently discussed, however, many candidates incorrectly stated that “central cholinergic
syndrome” was a problem. Many candidates failed to mention doses and a surprisingly large
number did not mention the use of these drugs in antagonising neuromuscular blockade.

QUESTION 12 Explain the phenomena known as fade and post tetanic facilitation
associated with the use of neuromuscular blocking agents.

The overall pass rate for this question was about 43%. Most candidates seemed to appreciate that
this question required an explanation of the mechanism of Fade and Post Tetanic Facilitation (PTF)
as seen with the non-depolarising class of neuromuscular blocking drugs. The question clearly did
not call for any discussion about how these phenomena are elicited in clinical practice nor the
clinical relevance or usefulness of the elicitation of these phenomena. A few candidates indicated
that Fade and PTF are restricted to the adductor pollcius muscle alone. Quite a few candidates
ignored the term PTF and wrote entirely on Post Tetanic Count. The two are different and
candidates must be careful to answer the question.

Most candidates furnished a definition of Fade and PTF and whilst this was not explicitly called for,
it did appear to provide a good starting point to their answers. Fade exists when, during a partial
non-depolarising block, administration of frequent repeated stimuli eg. Train of Four, results in a
reduction of twitch height with each of the subsequent stimuli. Post Tetanic Facilitation is seen
during partial non-depolarising blockade when after a tetanic stimulation is applied to a nerve-
muscle unit there is seen after a delay, of classically three seconds, a potentiation of twitch height
with a subsequently applied single supra maximal stimulus.

The explanation of Fade should have included discussion of pre-junctional nicotinic receptors
involved in a positive feedback loop with Acetylcholine (ACh) being blocked by the non-
depolarising neuromuscular blocking agent resulting in reduced production of ACh vesicles and
therefore less vesicles available for release. The explanation of Post Tetanic Facilitation required
some discussion of temporarily increased mobilisation of ACh vesicles into the pre-junctional area
for ready release as a result of tetanus.

QUESTION 13 Describe the neuropharmacology of thiopentone covering its site of

action, EEG changes, effects on cerebral blood flow and intracranial
pressure.

This question was generally well answered with a pass rate of 78%. Many candidates showed
detailed knowledge of the site of action, but there was considerable confusion about the
mechanisms reducing cerebral blood flow and intracranial pressure. Candidates describing other
areas of thiopentone’s neuropharmacology were awarded marks but the emphasis in marking was
on the required content. A number of candidates produced answers similar to the following model -

Site of action:
Thiopentone’s actions are thought to occur at the γ-amino butyric acid (GABA)A receptor complex.
GABAA receptors are ligand gated chloride ion channels, have up to five subunits, and have
benzodiazepine and picrotoxin binding sites. GABA is the principal inhibitory neurotransmitter in
the central nervous system. Barbiturates decrease the rate of dissociation of GABA from the
receptor and increase the duration of GABA mediated channel opening. At higher concentrations
barbiturates directly activate the channels even in the absence of GABA. Channel opening causes
membrane hyperpolarisation and thereby inhibits action potential transmission.
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EEG Changes:
Thiopentone produces a dose-related depression of the electroencephalogram (EEG). The awake
alpha pattern progresses to higher amplitude and slower frequency delta- and theta-waves until
there is burst suppression and finally a flat EEG.

Effect on cerebral blood flow and intracranial pressure:

There is a dose-dependent reduction in cerebral metabolism of oxygen (CMRO2) which reaches a
maximum of 55% with a flat EEG. Note this is due to reduced neuronal, not metabolic, oxygen
consumption. This produces a parallel reduction in cerebral blood flow, cerebral blood volume,
intracranial pressure (ICP), and increased cerebral vasoconstriction, provided that CMRO2 and
blood flow remain coupled. Cerebral perfusion pressure is maintained if the fall in mean arterial
pressure produced by thiopentone infusion is less than the fall in ICP.

QUESTION 14 Briefly outline the pharmacological effects of the volatile anaesthetic

agents on the kidneys.

This question was generally well answered with 64% of candidates passing this question. The most
important aspects were that all volatile agents decrease renal blood flow to some extent, and this
associated with a reduction in glomerular filtration rate and urine flow. These effects are usually
minimal and can be largely negated by maintaining intravascular hydration. The “stress response”
of major surgery may compound these effects.

The metabolism of some agents results in free fluoride ions, which have been associated with
tubular damage and high output renal failure. This is related to the amount and duration of
exposure, as well as their solubility (rate of excretion) and extent of metabolism - this is why
methoxyflurane is particularly nephrotoxic; the critical level for methoxyflurane is about 2 MAC-
hours, and this is usually associated with a plasma fluoride level of 50 µmol/litre.

Sevoflurane metabolism also produces fluoride ions, but there is no clinical evidence that this is
associated with renal damage. This has been attributed to its rapid excretion and low rate of intra-
renal production of fluoride ion. Sevoflurane is also broken down in soda lime (& Baralyme) to
compound A; this is increased at low fresh gas flows. Compound A is nephrotoxic in rats, but
probably not in humans (though this remains controversial).

QUESTION 15 List the drugs used clinically as anticoagulants and antithrombotics.

Write short notes on their mechanisms of actions.

The pass rate for this question was 65%. The majority of the candidates were able to list the
required anticoagulants and antithrombotics namely heparin, the coumarin derivatives and aspirin.
Many received additional credit for discussing dextran 70, dipyridamole, hirudin, ticlopidine, and
abciximab. However many of the answers failed to demonstrate a clear understanding of their
mechanisms of action, and were lacking in precise details. Unfortunately most candidates devoted
a large part of their answer to discussing thrombolytic therapeutic agents such as tissue
plasminogen activator and streptokinase. No credit could be given for such discussion, as this was
not asked in the question.

The references for information on this subject are the relevant section of Katzung and Stoelting 2nd
edition, p467, 472, 474.
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QUESTION 16 Describe the effects of the alpha-2 adrenoceptor agonists relevant to

anaesthesia.

63% of candidates passed this question.

Alpha-2 adrenoceptor agonists have been in use as antihypertensives, as adjuncts and

investigational agents in both human and veterinary anaesthesia for over 20 years. It is therefore
reasonable to expect that the candidates should have some knowledge of which agents are included,
their effects (both specific to anaesthesia and in general), and the likely physiological consequences
following their administration. Areas in which difficulties were encountered included identification
of the relevant drugs (eg. clonidine and dexmedetomidine), the sites of significant action (central
post-synaptic, peripheral pre-synaptic, spinal cord) and the assignment of anaesthesia utility to
various actions and characteristics. The listing of drug effects does not constitute a description, as
the effects may not be clinically useful. Similarly, while the assertion of the high oral availability
of clonidine was frequently made, the significance of this to anaesthesia was seldom encountered.
Better responses were typically legible, well organised with sites and mechanisms clearly stated,
and the effects listed with appropriate comment. Only a few candidates mentioned the problem of
prolonged hypotension after clonidine, although many mentioned the transient hypertension with
intravenous (IV) bolus dosing. No one mentioned the relatively slow onset of central activity of
clonidine or that any of these properties might actually be undesirable for an IV anaesthetic agent.
The frequent assertion that bolus dosing with clonidine produces hypertension with tachycardia was
disconcerting, as it suggested scant regard for baroreflex responses and little awareness of the effect
of alpha-1 receptor stimulation in an intact subject. One further difficulty in interpreting
candidates’ answers was the tendency to use personalised (or local) abbreviations, often without
translation; this also was less frequent in the better responses.

VIVA SECTION

Introductory Pharmacology Questions

• What volatile agent are you most familiar with and can you tell me about that agent?
• Please describe the site of action of neuromuscular blocking agents.
• What are the contents of an ampoule of Sodium Thiopentone?
• Tell me about Aminophylline.
• Can you classify and list the side effects of Suxamethonium administration?
• Can you explain the offset of non-depolarising muscle relaxants?
• Can you describe the effects of Isoflurane on respiration?
• Explain the techniques used to monitor neuromuscular block.
• Tell me about the effects of Morphine on the cardiovascular system.
• Tell me about the effects of Fentanyl on the cardiovascular system.
• Can you explain the concentrating and second gas effects?
• What determines uptake of volatile anaesthetic agents from the alveolus?
• Describe the production of adrenalin in the body.
• Can you define standard deviation and explain confidence levels?
• How is nitrous oxide produced?
• Tell me about the cardiac effects of Adenosine.
• How do benzodiazepines exert their effects in the body?
• Tell me about factors effecting MAC.
• Discuss the clinical uses of long acting opioids.
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• What factors determine variation in doses of induction agents, for example with age and shock?
• Tell me about pharmacogenetic disorders.
• Can you tell me about Phenytoin?
• What do you understand by the term “context sensitive half-life”?
• How does one determine sample size in statistics?
• Can you tell me about Ergometrine?
• What can you tell me about Esmolol?
• Tell me about agents that are used to lower blood pressure.
• Explain the mechanism of action of anticholinesterases.
• Classify drugs that affect the gastric acidity.
• Draw a set of wash in curves versus time for commonly used volatile anaesthetic agents.
• Give a classification of non-opioid analgesic drugs.
• What is meant by the term “volume of distribution”?
• Tell me about the formulation of Propofol.
• What is meant by the Therapeutic Index?
• Explain how Heparin exerts its anticoagulant effect.
• What is meant by meta-analysis?
• Please explain the second gas effect.
• Tell me about neuroleptic malignant syndrome.
• Tell me about the structure-activity relationships of volatile anaesthetic agents.
• Classify the drugs used in the treatment of asthma.

A.W. Quail
CHAIRMAN
PRIMARY EXAMINATION

DISTRIBUTION College Council Supervisors of Training

Regional Education Officers Panel of Examiners
Registered Trainees