primary exam reports 2011 to 1999

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852 EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION AUGUST /SEPTEMBER 2011 Please note that this report is prepared to provide candidates and their teachers and supervisors of training with information about the performance of candidates in the recent examination, 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. PHARMACOLOGY – WRITTEN SECTION ________________________________________________________________________________ MULTIPLE CHOICE QUESTIONS: 76% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: 1. Compare and contrast the clinically significant cardiovascular and central nervous system effects of desflurane and sevoflurane. 66% of candidates passed this question. Most correctly appreciated the changes in systemic vascular resistance (SVR), myocardial contractility and consequent changes blood pressure due to sevoflurane and desflurane. Also changes in cerebral blood flow, cerebral metabolic rate and intracranial pressure were well understood. However a deeper level of understanding was not universal, a common error being that falls in SVR equates to a fall in cardiac output whereas this tends to be well maintained with these agents initially due to a preserved baroreceptor reflex. Also a loss of cerebral autoregulation at higher MAC values was not universally acknowledged. More than half recognised the effect of myocardial preconditioning which was awarded marks due to a broad definition of the term 'clinically significant'. Better answers correctly discussed differences without getting too bogged down as of course there is a remarkable similarity between the two agents. Only two candidates discussed the QT interval and none mentioned that impaired diastolic function is also a cause of a reduction in stroke volume.

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Page 1: Primary Exam Reports 2011 to 1999

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

AUGUST /SEPTEMBER 2011

Please note that this report is prepared to provide candidates and their teachers and supervisors of training with information about the performance of candidates in the recent examination, 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.

PHARMACOLOGY – WRITTEN SECTION ________________________________________________________________________________ MULTIPLE CHOICE QUESTIONS: 76% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: 1. Compare and contrast the clinically significant cardiovascular and central nervous

system effects of desflurane and sevoflurane. 66% of candidates passed this question. Most correctly appreciated the changes in systemic vascular resistance (SVR),

myocardial contractility and consequent changes blood pressure due to sevoflurane and desflurane. Also changes in cerebral blood flow, cerebral metabolic rate and intracranial pressure were well understood. However a deeper level of understanding was not universal, a common error being that falls in SVR equates to a fall in cardiac output whereas this tends to be well maintained with these agents initially due to a preserved baroreceptor reflex. Also a loss of cerebral autoregulation at higher MAC values was not universally acknowledged. More than half recognised the effect of myocardial preconditioning which was awarded marks due to a broad definition of the term 'clinically significant'. Better answers correctly discussed differences without getting too bogged down as of course there is a remarkable similarity between the two agents. Only two candidates discussed the QT interval and none mentioned that impaired diastolic function is also a cause of a reduction in stroke volume.

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2. What is meant by the term "two compartment model" in pharmokinetics? Use PROPOFOL as an example in explanation. 12% of candidates passed this question.

A systematic approach is needed to answer such a broad question. Areas which could be addressed include: What the model attempts to do, the structure of this kind of model and the mathematics of the model. Properties of propofol which suggest it might fit a multi, rather than a one compartment model. A description of the model, implications of the model, what such a model might be used for and how this model differs from other pharmacokinetic models. Assumptions implicit in using this model, and how this might affect its clinical application. Sources of error in collecting data to test the model. It was not necessary to cover all of these areas to obtain full marks. Many candidates wasted time writing random pharmacokinetic data, details on the structure and use of propofol, definitions of pharmacokinetics, or frameworks for pharmacokinetic answers such as absorption, distribution, metabolism & excretion. Commonly misunderstood concepts included: Compartments being a theoretical construct only. Models fit a curve to observed plasma concentrations plotted against time. No-one described how such a curve might be fitted. The y axis of the plasma concentration time curve is not half life. The words “saturated”, “equilibrium”, “steady state”, and “context sensitive half time”. It is difficult to explain the offset of propofol if the effect site is considered to be in the peripheral compartment. Calculating a loading dose of propfol using the Vdss would be fatal. A two compartment model is conventionally drawn with two, rather than three or four compartments. Diagrams often depicted excretion as being bi-directional, or occurring through the brain. Both practices are discouraged.

3. What is the mechanism of action of β-adrenoreceptor antagonists? Outline the

therapeutic uses and side effects of these drugs. 78.3% of candidates passed this question. Generally this was a very well answered question and most candidates covered all that was asked of them. There was usually sufficient detail on the various cardiovascular uses of the drug, and many candidates added other uses of beta blockers such as treatment of glaucoma and migraine prophylaxis. With regard to the mode of action, obviously they act by blockade of the beta receptor, but extra points were gained by pointing out that this is a form of competitive antagonism and that this group of drugs have very selective action on the beta receptors alone. There were some minor areas of confusion. While beta adrenergic antagonists can be used to suppress the physical stigmata of anxiety, such as dry mouth and tremor, they have no significant anxiolytic properties per se – the patient (or candidate!) is just as anxious on the inside. In fact

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most of the CNS effects of these drugs are quite deleterious and include, insomnia and sleep disturbance as well as vivid dreams. The effects on the peripheral circulation are complex. Older, non selective agents cause peripheral vasoconstriction (not dilatation) and can worsen or precipitate Raynaud’s disease, because the blockade of peripheral beta 2 receptors allows the vasoconstricting alpha effects to predominate unchecked. However, newer agents that are used in the management of cardiac failure, often possess vasodilating properties, possibly mediated through nitric oxide release. Lastly confusion also reigned with regard to the effects of these drugs on the uterus, with candidates claiming that beta blocking drugs possessed both oxytocic and tocolytic effects.

4. Describe the pathogenesis and management of paracetamol toxicity. 50.7% of candidates passed this question.

This question was phrased in 2 parts, “Describe the pathogenesis and management of paracetamol toxicity”. Equal marks were allocated for each half of the question. The pathogenesis of paracetamol toxicity requires a detailed discussion of the metabolism of paracetamol and how it changes when toxic doses of paracetamol are ingested. Mechanisms of toxicity primarily involving the liver and N-acetyl-p-benzoquinone imine (NAPQI) were also important. Mention of typical doses of paracetamol that could cause toxicity and subpopulations at increased risk of toxicity with lower doses of paracetamol also attracted marks. Candidates who described paracetamol metabolism in overdose using applied principles of pharmacokinetics generally scored well. Discussion of management of paracetamol toxicity needed to be balanced and mention general measures such as resuscitation and early consideration for liver transplantation as well as the specific therapies such as N-acetyl cysteine and methionine and the specific principles relating to their use. Candidates who were able to discuss these aspects of the question in sufficient detail achieved a pass mark. Some answers were held back by too much discussion about other aspects of paracetamol pharmacodynamics and unrelated pharmacokinetics.

5. Describe the mechanism of action of protamine when used to reverse effects of

heparin. Outline the side-effects of protamine. 21% of candidates passed this question.

Candidates were required to describe the mechanism of a basic cationic binding protein combining with an acidic anionic compound to form a stable salt complex including some indication of relative doses required and the time course of the drugs actions. Higher marks were awarded for explanations of why excessive doses may cause hypocoagulability and the inconsistent reversal of Xa activity. Side effects which required outlining were not only that it causes allergy but the types of allergy caused and the side effects that would be observed because of it. Similarly hypotension either due to rapid infusion or IgE mediated effects, the problems of

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thromboxane mediated pulmonary oedema and pulmonary vasoconstriction and the phenomenon of heparin rebound attracted higher marks.

6. Discuss the relative advantages and disadvantages of using morphine and fentanyl for post-operative Patient Controlled Analgesia (PCA). 43.5% of candidates passed this question.

This question was not well answered. A pass answer needed to demonstrate both a clear understanding of the objectives of Patient Controlled Analgesia, knowledge of the relative pharmacokinetics and pharmacodynamics of morphine and fentanyl, and translation of that knowledge to the PCA technique to indicate the relative advantages and disadvantages of the opioids. An opening statement outlining that the aims of post-operative PCA using opioids aimed for effective analgesia with rapid onset and a duration of action that could maintains analgesia, without causing sedation, was well regarded, but infrequently given. Discussion of pharmacological parameters of morphine and fentanyl, including differences, needed to be in the context of their administration by PCA, highlighting how the pharmacology determined their advantages and disadvantages. Indicating differences in lipophilicity, redistribution profile, metabolism and elimination of the opioids and their metabolites was important. These features then related to the advantages and disadvantages including relative onset and offset times, speed of redistribution, half-life, accumulation of the opioid or metabolites and safety, including in specific settings, such as PCA in the elderly, hepatic or renal impairment. Some candidates appreciated that advantages in some contexts could be disadvantages in another. Answers suffered from lack of any statement relating to objectives of PCA, inadequate consideration of pharmacokinetics, lack of translation of the relative opioid pharmacology to the PCA method of administration, errors of fact, and inclusion of imprecise comments. Statements relating to clinical experience were considered where the pharmacological principles behind these statements were provided.

7. Briefly outline the acute management of malignant hyperthermia (during a relaxant

general anaesthetic). Describe the important aspects of dantrolene pharmacology relevant to treating malignant hyperthermia. 62 % of candidates passed this question. Equal weighting was given to each part of the question. Most of the candidates who did not attempt the second part of the question did not achieve a pass mark. A brief definition of malignant hyperthermia (MH) was expected. Lengthy discussion of the different ryanodine receptors was not required. The acute management of malignant hyperthermia was generally well described. An outline of specific tasks and actions was required, such as “hyperventilate with 100% oxygen at flows of greater than 10 litres per minute”. Statements like “provide airway support” or “obtain an ICU consult” are too nonspecific. It was pleasing to see descriptions of the anaesthetist in recruiting help, and as leader and coordinator of the team response in theatre. Most candidates understood the pharmaceutical aspects of dantrolene. With respect to pharmacokinetics, candidates often resorted to guesswork.

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Dantrolene is metabolised in the liver. The major pathway produces 5 hydroxy dantrolene (which is active). A minor pathway produces an inactive metabolite. Both metabolites are cleared renally. The half life of dantrolene is variably reported between 5-10 hours. Further dantrolene doses may be required in intensive care. Dantrolene binds to the ryanodine receptor in skeletal muscle, inhibiting calcium release from the sarcoplasmic reticulum. Side effects of dantrolene are rare. The alkaline solution can cause thrombophlebitis, and skin necrosis can occur if the solution extravasates. Hepatic dysfunction (including fatal hepatic failure), sedation and gastrointestinal side effects have been described. Mild to moderate skeletal muscle relaxation occurs. Dantrolene has no direct cardiac effects. The diluent volume required to administer large doses of dantrolene may precipitate acute pulmonary oedema. Co-administration of verapamil is associated with marked hyperkalaemia, which may precipitate ventricular fibrillation. Dantrolene potentiates the skeletal muscle relaxation of non-depolarising muscle relaxants.

8. Describe the terms train-of-four stimulation and double burst stimulation with

respect to the peripheral nerve stimulator. Describe their advantages and disadvantages when used to evaluate non-depolarising neuromuscular blockade. 67.4% of candidates passed this question.

Train of Four is delivered by 4 identical supramaximal stimuli at about 20 – 50 milliamps, each of .1 sec duration, at 2Hz (2 per second); the sequence may be repeated every 10 – 20 seconds if used ‘continuously’. A synopsis of the twitch height and receptor blockade along with a description of the ratios was well described. Interpretation of depth of blockade based on TOF count/ratio was also well discussed Confusion about millivolts and milliamps often cropped up. Double Burst Stimulation described as 2 bursts of 3 tetanic stimulations (.2 msecs duration each) 20 msecs apart at 50 Hz bursts separated by 750 msecs pause. The repeatability takes into account the ‘fatigue’ of the junctions following tetanic stimuli. Discussion of advantaged vs. disadvantages including such topics such as ease of use, accuracy to manual / visual assessment, need for extra objective measurement with eg accelomyography, painful or not, able for awake patients, painful or not, use for depth of block, use for assessing presence of residual blockade, use in reversibility of blockade, need or value of a baseline measurement form a choice of headings to make a comment on. Most candidates were able to mention a few to demonstrate the physical/pharmacological/clinical rationale for the choice of technique used. Detailed descriptions of where and how to place electrodes, comparison of depolarising and non-depolarising blocks were not part of the question.

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 66.9% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: 9. Outline the physiological roles of prostaglandins in the body.

25.6% of candidates passed this question.

This question was answered very poorly, which was surprising as it a recycled question that has been asked relatively recently Many candidates scored poorly by answering it as a Pharmacology question – The insertion of prostaglandin pessaries and the use of intravenous prostaglandins for neonatal Duct closure have no place in a Physiology answer… Other common errors were a very “narrow” answer – particularly focusing on one system (commonly renal) Candidates who scored well wrote legibly, had a well-laid out/ presented answer and used a system-based approach

10. Describe the effects of resonance and damping on an invasive arterial blood pressure

tracing. 42% of candidates passed this question.

Basic material required to pass: Description of the measurement system was useful only if related to the following discussion Definition of resonance and damping Explanation of their importance and their effect on the timely measurement of the components of the blood pressure (systolic pressure, diastolic pressure, mean pressure)

Advanced material: Quantification of the effects

Common errors/omissions/unnecessary inclusions: Equations without definition of symbols Input frequency is not 0 – 40Hz! Natural resonant frequency is a property of the measuring system

Details of transduction were not required “directionless relationships”; in a connected universe, everything influences everything else. To be of use, a relationship should include a direction of the effect, and a qualitative/quantitative indicator of the importance/magnitude

Organisational errors: Planning in the margins or on the back of the cover is a waste of time (headings can be used in the answer)

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Long lists of definitions before any factual content is a poor use of time (definitions should be embedded within the answer itself)

11. Describe the ionic basis of automaticity of cardiac pacemaker cells.

69% of candidates passed this question. Most candidates provided a reasonable account of the relevant sodium, calcium and potassium fluxes that occur in the sinoatrial node of the heart and could relate these to the action potential. Extra marks were awarded for discussion of factors that influence automaticity. Many candidates discussed the effects of the autonomic nervous system and some were able to provide details on the mechanism of these effects. However, no candidate discussed the effects of age or fever on automaticity. Several candidates described the anatomy of the conducting system of the heart, which did not attract any marks for this question.

12. Outline the similarities and differences between myoglobin and adult haemoglobin,

explaining the physiological relevance of the differences. 24.2% of candidates passed this question. Some candidates used a tabular format, others an essay format to answer this question. Both were equally effective strategies. A brief description of the structure and location of these proteins, their respective dissociation curves and P50’s with a simple overview of the function of each of these proteins would round out a good answer. An answer offering more detail about the environments these proteins function in was awarded with further marks. Additional credit was given for answers that explored the buffering and nephrotoxicity of these proteins. The most common reason for not passing this question was simply because not enough relevant content was included. Many candidates spent a lot of time describing in detail the process of buffering and the process of oxygen binding. This detail was not asked for and only received a few marks. The P50 given for myoglobin was frequently incorrect and many answers indicated that myoglobin WAS NOT a haeme containing protein. There was also a misconception in the minds of many that both haemoglobin and myoglobin bound four oxygen molecules. No answer mentioned that myoglobin is located in cardiac muscle in addition to skeletal muscle.

13. Outline the physiological role of cerebro spinal fluid, including a description of its

production and fate. 44% of candidates passed this question. This question had 3 distinct sections that needed to be addressed in the answer. Main points included the amount of CSF and where it is distributed, its role in protection of

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brain, and its role in compensation for physiological changes in intracranial pressure, acid base regulation, maintenance of stable ionic environment, role nutrition and waste removal. Also, the chemistry of CSF and how it differs from plasma, how much is produced and where; its circulation and where it is absorbed, and finally, describing the relationship between ICP and the production and absorption of CSF. Additional points were awarded for explaining CSF’s protective role, its method of production, and describing the relationship between the chemistry of CSF and its role. Common mistakes included inclusion of pathology or pharmacology, detailed descriptions of Monroe Kellie Doctrine without outlining the role of CSF, defining terms before answering the question rather than as part of the answer, incorrect anatomical understanding of production, circulation or absorption of CSF and equating ICP measurement mm of CSF to mm of Hg.

14. Describe the changes in respiratory function tests that occur with long term increases

in small airways resistance. 12.5% of candidates passed this question. This question required an answer that was focused on the respiratory function tests that help assess the effects of chronic increased airway resistance. Changes in the following tests needed to be discussed: • Forced expiratory volumes • Flow volume loops • Pressure volume loops Appropriate diagrams and graphs were expected with a description of the changes that happen when airway resistance is raised. Indicating which test provided a quantitative assessment of raised airway resistance was important. Candidates also gained marks for discussing simple peak flow meter testing, simple spirometry changes, and closing volume changes. Arterial blood gas changes and reduced oxygen uptake on exercise testing all gained additional marks. Care needs to be taken when drawing and labelling graphs so that they are accurate. Simply listing some respiratory changes but not relating the changes to a test was not sufficient to score marks. Details on factors that determine resistance and flow was not part of the answer and in depth descriptions on how to perform a test was not required. Some candidates confused obstructive lung disease with restrictive lung disease.

15. Outline the physiological changes that may explain why an otherwise well patient

may have a reduced urinary output intraoperatively 77.6% of candidates passed this question. On the whole, this question was generally well answered. Candidates who demonstrated a clear understanding of renal physiology appropriately mentioned the determinants of urinary output, renal blood flow, glomerular filtration rate and factors affecting it, as well as the Starling's forces acting across the glomerular capillaries. Marks were awarded to candidates who recognised that surgery is a stressful "condition" which results in secretion of various stress hormones. Humoral factors, in

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fact, play an important role in maintaining water and sodium homeostasis but some candidates failed to even mention the hormones in this setting. The commonest mistake was the assumption that a reduction in urinary output is ONLY a reflection of a reduction in blood pressure. In reality, physiological processes that serve to conserve water and sodium are already in place even prior to any noticable drop in blood pressure. This is because osmoreceptors in the anterior hypothalamus are very sensitive to the plasma osmolality and a change as little as 1% due to a fasting state will cause increased antidiuretic hormone secretion. This results in a concentrated urine with a low volume. Extra marks were given to candidates who were able to explain in detail the actions of ADH and other hormones such as the renin-angiotensin-aldosterone system. However, an extensive list of plausible causes of hypotension does not translate to an outline of physiological changes that result in reduced urinary output.

16. Describe the formation, fate and role of lactate in energy production.

45% of candidates passed this question. A good answer followed the headings of the question thereby obtaining max marks. Many candidates spent a lot of their answer on describing the citric acid cycle and aerobic metabolism, which gained no marks. Lactate is produced daily by red blood cells and during strenuous exercise where a patient is not hypoxic. It supplies a rapid energy source when oxygen demand is not met by supply but is not sustainable over a prolonged period. It can be reutilised by the cells it is formed in(when pyruvate is able to enter the citric acid cycle the equilibrium shifts to allow lactate -> pyruvate) when oxygen is resupplied or can diffuse out of cells into the plasma for transfer to the 1.liver, to under go gluconeogensis(from pryuvate), this glucose can a)enter into the ATP inefficient cori cycle for further energy production during anaerobic conditions in the muscle, b) be stored as glycogen and c)enter the citric acid cycle, and 2.heart as an energy substrate. There was some confusion where the ATP is produced during anaerobic metabolism, ie; during glycolysis not on the conversion of pyruvate to lactate, and the enzyme for this is lactate dehydrogenase. Concepts such as the Law of mass action and including recycling of the substrates for biochemical equations (particularly NAD+) were appreciated.

PHARMACOLOGY – ORAL SECTION ________________________________________________________________________________ OPENING PHARMACOLOGY QUESTIONS: Pharmacodynamics

• What is ED 95?

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Drug variability

• How can the liver affect pharmacokinetics? Inhalational agents

• Factors influencing the rate of rise of Fa/Fi (speed of induction of an inhalational induction). Metabolism. Why recovery different from induction.

Local anesthetics

• Factors that affect the onset of action. • What additives are found in L.A. solutions and why? • Calculate amount of drug in 2% solution. Toxic amount. Effects on RMP. Mechanism

of action. Differential block. Frequency dependent block. Pain

• Classification of drugs to treat neuropathic pain. • Side effects of TCA. • Opioid sparing drugs. • Why is pethidine unpopular? • Advantages, s/e tramadol. • Duration of action and side effects of NSAI’s.

Opioids

• Compare fentanyl to alfentanil. • Time to peak effect of opioids. • Structure of morphine, receptor interaction. • Oxycodone.

Neuromuscular blocking drugs

• Effects on fast c.f. slow twitch muscles. • What is a nondepolarising block? • Fatal effects of suxamethonium.

Anticholinesterase agents

• Does neostigmine cross the BBB? • Onset and duration of neostigmine. • Anticholinesterases other than neostigmine.

Anticholinergics

• Side effects of atropine. Atropine c.f. glycopyrrolate. Autonomic nervous system

• Compare metaraminol, ephedrine and phenylephrine (effects at alpha and beta receptor, heart rate changes).

• Effects in labour.

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• Overdose of phenylephrine. • What is tachyphylaxis? • What are beta 2 effects? • Structure activity relations of catechols. • Vasopressin.

Antiarrhythmics

• Classes. What is type 3. Amiodarone, why loading dose? Is it used in torsade? Why not?

CPR guidelines

• Outline the CPR guidelines. • Mono phasic c.f. biphasic defibrillation. • Why is adrenaline used?

Anti emetics

• Classify antiemetic drugs. Side effects. Prolonged QT syndrome Obstetric drugs

• Tocolytic drugs. • Oxytocin side effects

Diuretics

• Classification Anticoagulants

• Classification of antiplatelet drugs. • Why is a loading dose of clopidogrel required? • Low versus high dose aspirin. • Side effects heparin.

Endocrine

• Insulin side effects GIT

• Drugs affecting gastric acidity IV fluids

• What is tonicity? • What is meant by isoosmolar? • What is a colloid? • Excretion HES, T ½ c.f. gelofusine, HAS. • HES – what is substitution grade? • HES side effects. • HAS – does it require cross match? Why? Can it contain viruses?

Statistics

• Types of data.

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• When is ANOVA used? What is one way ANOVA? • Chi square test? • What is meant by degrees of freedom? • When would Fisher exact test be used? • Paired and unpaired T- test. • Systematic review vs meta-analysis. • Measure of dispersion from central tendency. 95% C.I. when used?

Phases of a clinical trial.

PHYSIOLOGY – ORAL SECTION ________________________________________________________________________________ OPENING PHYSIOLOGY QUESTIONS: Measurement / Physics

• What is a normal adult temperature? • What is a pulse oximeter? • Oximetry • Capnography • How is CO2 analysed • Temperature measurement methods • Draw a Capnograph trace

Respiratory

• Comment on this Blood gas Analysis (Resp acidosis with increased A-a Do2) • When we exercise, oxygen consumption increases. How much can it increase?

Compare to cardiac output and explain how there can be a difference. • What is a normal Pulmonary Artery pressure? Why does it not increase with

exercise? • What do you understand about shunts in the lungs? • What do you understand by the term oxygen flux? • What are the causes of arterial hypoxaemia? • Control of Ventilation • Oxygen cascade • Carbon dioxide carriage • Aging and Respiratory Function • Lung compliance definition and factors affecting • Causes of hypoxeamia • Effects of Alveolar ventilation on PCO2 • Dead space • oxygen stores breathing air and 100% oxygen • ventilation distribution in lateral position • capnography

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Cardiac • Draw a Pressure-Volume Loop for adult LV. Superimpose changes caused by

clamping the abdominal aorta • What heart rate would you expect in a person with all the nerve supply to the heart

removed? • What are determinants of cardiac output? • What are the determinants of coronary blood flow? • Starlings law of the Heart • Distribution of Cardiac Output • Pressure Volume Loop of Left Ventricle • Cardiac contractility and frank-starling curve • Define afterload and what factors contribute to afterload • What changes occur in the CVS as we age • Afterload • What is Contractility • Draw lead 2 of a standard ECG trace. • determinants of venous return

Renal/Acid-base • What is a normal serum Na? What physiological mechanisms can be responsible for

development of hyponatraemia. • What is Clearance • renal excretion of an acid load • effects of changing afferent and efferent tone on renal blood flow and GFR

Nervous system • What would happen to my heart rate and blood pressure if I was woken up by an

earthquake? • Pain transmission • Sleep • Autonomic Nervous System • How can nerves be classified • Factors affecting cerebral blood flow • normal cerebral blood flow and measurement

Gastrointestinal

• Gastric Emptying Endocrinology / Prostaglandins

• What hormones are secreted by the posterior pituitary? • Control of Blood Glucose

Haematology

• When you have a sharp cut in your hand, what stops it from bleeding continuously? • Blood Cross Matching • Platelet function

Muscle

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• Microscopic appearance of skeletal muscle. Action potential for skeletal and smooth muscle

Neonatal/Maternal • Describe the features of the foetus that allow for maximization of oxygen delivery to

the brain. • What are the various stimuli for the baby to make its first breath? • Take me through the foetal circulation. • What factors affect the movement of oxygen across the placenta

Immunology

• Hypersensitivity Reactions • What different immune systems protect the body

Metabolism.

• What are the effects of a 48-hour fast in an otherwise healthy adult? • How is calcium distributed in the body? • What is a normal blood sugar level? • Fasting • heat gain and loss in operating theatre and sauna

Associate Professor Ross MacPherson CHAIR Primary Examination Sub-Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

FEBRUARY /APRIL 2011 Please note that this report is prepared to provide candidates and their teachers and supervisors of training with information about the performance of candidates in the recent examination, 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. General comments relating to ALL short answer questions. Many examiners have written the same comments for their question and for the general information of candidates the following suggestions are provided. The main mistake that candidates continue to make is a failure to answer the question asked. Much time is spent providing pages of information that is irrelevant to the question being asked and for which no marks can be awarded. Examiners are unable to award marks for illegible handwriting. Answers can be validly presented as diagrams, lists or a mini essay. When the former two methods are used, the labelling must be clear and the answer to the question made obvious. In order to obtain marks from graphs, these must be accurately drawn, clearly labelled, and be able to demonstrate understanding of the question asked. It may be necessary to include a sentence to demonstrate understanding with respect to a graph. Where essay form is used, correct spelling, especially relating to pharmacological or physiological terms is important. If candidates have contradictory statements in their answers, no marks will be awarded for correct information that is later contradicted. If candidates elect to draft an answer plan, and later cross out the plan, no marks will be awarded for material that is included in the plan, but not in the answer proper. In practising for the short answer question examination, candidates should consider whether using part of their time to write a detailed plan before writing a ten minute answer is optimum use of the time available. The syllabus lists basic sciences in anaesthesia and intensive care. Where appropriate, aspects of clinical application of physiology and pharmacology that may appropriate in an answer can be included. However, caution must be exercised not to overemphasise clinical information at the expense of the underlying scientific principles.

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PHARMACOLOGY – WRITTEN SECTION

________________________________________________________________________________ MULTIPLE CHOICE QUESTIONS: 71% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: Q1 . Describe the factors which increase the risk of systemic toxicity with amide local anaesthetic agents. This question was passed by 34.6% of candidates. This question requires an understanding that systemic toxicity is due to an excess in the plasma concentration of local anaesthetic, which is dependent on the rate of absorption into the systemic circulation, drug distribution and clearance. Successful candidates organised their answers into drug factors including pharmacodynamic and pharmacokinetic factors and patient factors. Listing factors such as pKa, lipid solubility and protein binding without a clear explanation of how these contributed to toxicity did not gain high marks. Factors which affect systemic absorption were well explained, however, drug distribution was poorly understood especially in the context of patient factors such as age and cardiac status. Repeating a concept under different headings such as pKa, degree of ionisation and ion trapping in the foetus or acidotic patient did not gain more marks. Local anaesthetics bind to many proteins which affects systemic toxicity. Binding to plasma proteins alters drug distribution, affinity for receptor proteins affects dwell time and binding to tissue proteins affects release of drug into the systemic circulation. Candidates were expected to know the relative toxicities between different amide anaesthetics. Quantifying the differences gained extra marks. An understanding of why certain amide anaesthetics are more toxic than others based on factors such as lipid solubility, chirality, intrinsic vasoconstrictive properties and sodium channel affinity were expected. Defining the CNS/CVS ratio without explaining why different amide anaesthetics have different values did not gain marks. Q 2. Classify non-opioid drugs used for the treatment of neuropathic pain and indicate proposed mechanisms of analgesic action and potential adverse effects. This question was passed by 35.1% of candidates. This question was very clear in what was required. Discussion of neuropathic pain, opioids, and non-drug treatments did not attract marks. Many candidates omitted the mechanism of action, used vague statements such as, ‘affects the receptor’, or described a non-analgesic mechanism of action. When discussing adverse effects avoid statements such as, ‘many side effects’ or ‘many interactions’, without providing additional detail. Writing ‘sedation’ as the only adverse effect of tricyclics did not attract marks. Many answers contained a long detailed description of simple analgesics, and only a limited discussion of other drugs used for the treatment of neuropathic pain.

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Answers should have included the following main components: Antidepressants (tricyclics), Anticonvulsants (Gabapentinoids), Membrane Stabilisers (lignocaine/mexiletine), NMDA antagonists (Ketamine), and a brief discussion of simple analgesics. Additional marks were gained for discussion of other drugs, or additional detail Q 3. Outline the effects of liver failure on drug kinetics and dynamics. This question was passed by 31.6% of candidates. Most candidates were able to point out that drug metabolism (predominantly phase 1 reactions) is decreased with liver failure. However, few could indicate the change is only significant in drugs with a low hepatic extraction ratio (e.g. benzodiazepines). A number of candidates spent a significant amount of time describing the change in protein binding of drugs. Unfortunately, the direction and magnitude of change in drug effect were vague in most answers. Common omissions include that associated renal failure (hepatorenal syndrome) may decrease renal clearance of drugs and their active metabolites, and that the production of plasma cholinesterase is reduced with liver failure and this may affect metabolism of suxamethonium. Important pharmacodynamic changes should include an increase in sensitivity of anesthetic agents with hepatic encephalopathy, and down regulation of β adrenoreceptors in liver failure. Q 4. Describe the ideal properties of agents used for sedation using two examples. This question was passed by 69.3 % of candidates. Points expected for a pass: Listing the ideal attributes of a sedation agent. Most chose an intraveneous agent, with focus on pharmacokinetics, including rapid onset, short equilibration effect site time, rapid offset, short context sensitive half time (CSHT), and organ independent elimination. Pharmacodynamic qualities should include high therapeutic ratio, minimal cardiovascular and respiratory depression, amnestic and analgesic qualities Most discussed the examples of midazolam and propofol, comparing them to the ideal qualities and/or to each other. Other acceptable alternatives included dexmedetomidine, ketamine, remifentanil and fentanyl. Better answers demonstrated understanding of the pharmacokinetics, why organ independent metabolism was better, how certain drugs had a short CSHT due to redistribution or high metabolism. Some recognised that propofol had a lower therapeutic ratio as compared to midazolam, as the dose required to produced sedation was close to that for producing general anaesthesia. These answers received more marks than just a bare list of ticks and crosses. Those that used only one example or neglected to talk about pharmacokinetics were less likely to gain enough marks to pass. Other mistakes were to regurgitate all known facts about the two agents, without reference to what would make them ideal for use as a sedation agent.

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Additional marks were given for mentioning drug interactions, increased sensitivity with age and pain on injection with propofol. Q 5. List the classes of drugs that may be used to manage hypertensive crisis and briefly outline the mechanism of action. This question was passed by 11.4% of candidates. The main points expected for a pass included a classification of drugs used in anaesthesia to manage a hypertensive crisis, and include a brief description of those drugs’ mechanisms for this particular action. Most answers included only cardiovascular drugs such as sodium nitroprusside whose specific use is in the management of a hypertensive crisis. However, most answers did not include drugs that anaesthetists use every day to manage this problem, such as sevoflurane, fentanyl, propofol and Local Anaesthetic agents. This was the main reason for the low pass rate. Another common error was to overlook the mechanism of action for lowering blood pressure. Reporting that “beta receptor blockade lowers blood pressure”, is too imprecise to score points in a post-graduate specialty examination. Q 6. Write a brief outline on the pharmacology of remifentanil.

This question was passed by 55.3% of candidates.

A clear pass required: Some sort of logical approach to the description of drug pharmacology incorporating: Drug chemistry Uses Pharmaceutic information including presentation and recommended doses A proposed mechanism of action Pharmacokinetics Pharmacodynamics

Key chemistry description needed to highlight: phenylpiperidine derivation from fentanyl, synthetic preparation, unique ester linkage. There are multiple uses of this agent - simply stating “as a component of TIVA” gained marks but did not gain maximum credit. Pharmaceutic information, in addition to describing the “powder filled ampoules” or “vials of remi”, needed to identify the powder as remifentanil hydrochloride and ideally note the presence of glycine (as this has relevance to routes of administration). To score well, both bolus and infusion dosing had to be given. Few candidates correctly stated any mechanism of action, fewer correctly identified mu selectivity, and fewer still the mechanism of mu agonism induced analgesia. The bulk of the available points were allocated to a description of the agent’s pharmacokinetics reflecting its novel features. Whilst some recall of volume of distribution, elimination half life, and context specific parameters was necessary, a clear pass required more than a list of uninterpreted numbers. Candidates needed to describe/explain: remifentanil has a fast onset and why this is so, that offset is dependant on metabolism not redistribution, organ independent high capacity metabolism and

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metabolic products. Pharmacodynamics was not well described - the requirement was for a logical organ system approach outlining key effects in each system. Candidates who stated only that “the effects are those of morphine” could not score well Q 7. Describe the advantages and disadvantages of using nitrous oxide as part of a general anaesthetic. This question was passed by 73% of candidates. Successful candidates structured their answers with a list of advantages and disadvantages from a pharmaceutic, pharmacokinetic and pharmacodynamic perspective. The main advantages that were expected were: rapid onset and offset, second gas effect, reduction in MAC, and analgesic effect. The main disadvantages that were expected were: reduction in FiO2, diffusion hypoxia, expansion of closed air spaces, PONV, increased CBF/ICP, and the long term effects of prolonged or chronic exposure, e.g. megaloblastic anaemia, subacute combined degeneration of cord, and possible teratogenicity. Additional marks were awarded for clear explanations about why nitrous oxide is inappropriate as a sole agent, and other concepts, e.g. second gas effect, and expansion of gas spaces. Common mistakes were to discuss nitrous oxide in isolation rather than as part of a general anaesthetic. There were misconceptions about the mechanism of analgesia, which is described in the prescribed texts. There were inadequate explanations about how nitrous oxide is “cheap”, and very few candidates discussed the set-up and maintenance costs associated with nitrous oxide. Q 8 How may drugs potentiate the action of non-depolarizing muscle relaxants at the neuromuscular junction? This question was passed by 5.7% of candidates. The following answer would have gained a very high mark: Drug interactions are relevant as there is a risk of failure to reverse neuromuscular blockade and residual paralysis. Drugs may interact either at the nerve terminal or the receptor to reduce the effect of acetylcholine (ACh) in competitively overcoming the block. Presynaptically there are at least three mechanisms that might reduce the release of acetylcholine (ACh):

1. Reduced AMP/ATP synthesis – frusemide 2. Blockade of presynaptic ACh receptors – volatiles 3. Blockade of calcium channels – calcium channel blockers, magnesium, aminoglycosides,

volatiles Postsynaptically there are several mechanisms that interfere with ion flux through the nicotinic receptor:

1. Direct blockade of the ACh receptor – volatiles, aminoglycosides, quinidine, other neuromuscular blockers

2. Desensitization block (binding to non-receptor sites) – volatiles, barbiturates, local anaesthetics

The most common error was irrelevance: detailed descriptions of the physiology of neuromuscular transmission and a classification of non-depolarizing relaxants.

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VIVA OPENING QUESTIONS Parmacokinetics/Pharmacodynamics

How can genetics influence drug action?

How are drugs transformed in the liver?

Drug receptors

Tolerance and addiction

What is meant by pharmacogenetics?

What is the law of mass action?

What is a second messenger?

Dose-Response Curves

Therapeutic Index

Drug metabolism

Classify drug interactions

Low cardiac output and drug metabolism

What is potency?

Propofol concentration-time curves

Determination of Vd

Determination of dose of induction agent

What is bioavailoability?

Muscle Relaxants and reversal

Metabolism of suxamethonium

Pharmacology of rocuronium

Cardiovascular effects of NMBs

Prolongation of suxamethonium block

What is in the red syringe?

Drug-receptor kinetics of NMBs

Electrode placement for TOF

How do NMBs work?

What are anti-cholinesterase drugs

How does neostigmine work?

Adverse effects of neostigmine

Clinically useful anti-cholinesterase agents

Features of organo-phosphate poinoning

Effects of atropine

Management of atropine overdose

Autonomic Nervous System

Structure activity relationships of sympathomimetics

Pharmacology of nicotine

Noradrenaline

Ephedrine and mechanism of action

Lipid solubility of beta blockers

ACE inhibitors

Blockade of autonomic nervous system

Drugs fort myocardial ischaemia

Pulmonary hypertension

Metoproprol

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What is an inotrope?

Tell me about nitric oxide

Treatment of anaphylaxis

Anti-arrhythmic agents

Management of ventricular fibrillation

What drugs are used to manage tachyarrhythmias?

Digoxin and toxicity

Amiodarone

Neuropharmacology

Management of Parkinson’s Disease

Anti-epileptic agents

Drugs used to treat Post Operative Nausea and Vomiting

Classification of anti-emetics

Respiratory

Drugs used for asthma management

Manufacture of oxygen

What are the effects of histamine?

Diuretics

Classify diuretics

Mannitol

What are loop diuretics?

Coagulation

Low molecular weight heparin

Fibrinolysis

Heparin metabolism

Adverse effects of heparin

Classify anti-platelet drugs

Reasons for reduced effects of clopidogrel

Classify anti-coagulants

Obstetrics

Pharmacology of magnesium

Drugs affecting uterine tone

Placental transfer of drugs

PK/PD in pregnancy

Endocrine

Side effects of vasopressin

Oral hypoglycaemic agents

Gastrointestinal

How can gastric acidity be controlled?

Drugs affecting gastric pH

Volatile agents

Physico-chemical parameters of volatile agents

Structure Activity relationships of volatiles

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MAC

Additives to volatile agents

Mechanism of action of general anaesthesia

Dose of volatile agents

Dose-response curves for volatile agents

Lipid solubility and potency

Wake up from GA

Wash in and wash out curves

Halothane toxicity

Partition coefficient

Pain

Activity of opioids

Fentanyl and alfentanil

IV analgesia for pain

Alfentanil

Intrathecal morphine

Oral paracetamol

Morphine toxicity

Naloxone

Opioid reversal

Pharmaceutical aspects

Contents of an ampoule of thiopentone and propofol

Why are substances added to pharmaceutical products?

Stages of drug development

What is a drug?

What additives are added to local anaesthetic solutions?

Statistics

What are categorical data?

What is the difference between meta analysis an systematic review?

Randomised controlled trials

Given a data set and asked to comment

Multi-centre trials

Bias in statistics

Box and whisker plot

Paired and unpaired t-tests

Miscellaneous

Colloids vs crystalloids

Digoxin toxicity

Organophosphate poisoning

Thiopentone and cardiovascular system

Drugs affecting GABA receptors

Dose-response curve for propofol

Mode of action of local anaesthetics

EMLA cream

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 82.8% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: Q 9. Describe the ways in which CO2 is carried in the blood This question was passed by 27% of candidates. In order to pass, candidates were expected to provide a detailed description of the three methods by which CO2 is carried in the blood, i.e. dissolved, as converted to bicarbonate, and combined with proteins. Extra marks were awarded to those candidates who explained the importance of red blood cells/haemoglobin, reasons for differences between arterial and venous carriage, and clear concise descriptions of Haldane effect. Common errors included incorrect units in describing the carriage of CO2, and chemical equations that did not balance with respect to chemical elements or electrical stability. Q 10: Describe the factors that oppose left ventricular ejection. This question was passed by 25% of candidates. As previously, this question was misinterpreted by many candidates and answered as for determinants of left ventricular ejection fraction: descriptions of preload and contractility attracted no marks. The main points expected included: recognition that afterload opposes left ventricular ejection, definition of afterload, the contribution of SVR and factors determining SVR, and the application of the law of LaPlace and the use of the Hagen-Poiseuille equation to describe factors which contribute to afterload. Additional marks were awarded for the role of the aortic valve, aortic compliance, IPPV, and for demonstrating understanding of the relative changes in pressure and tension within the ventricle during systole. Common mistakes included repetition, vague or non-directional statements, and incorrect formulae. 11. Describe the functions of the loop of Henle, including the physiological mechanisms involved. This question was passed by 37% of candidates.

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The question asked for both the functions of the loop of Henle, and physiological mechanisms involved. Both these points needed to be addressed to pass this question. Well structured answers included a brief relevant anatomical description of the loop of Henle, and a description of the functions which included the physiological mechanisms. Very few candidates mentioned functions apart from the development of a concentration gradient, and many candidates were unable to describe the physiological process whereby that gradient is developed. There was often confusion regarding the osmolality at various anatomical locations within the loop. Many candidates did not mention or were unable to explain the role of the vasa recta in the physiological mechanisms of concentration. Many answers were focussed on the collecting duct rather than on the loop of Henle, and several answers listed general functions of the kidney rather than those of the loop of Henle. The examiner was aware of controversy relating to tubuloglomerular feedback in different textbooks, and marks were awarded accordingly. Many candidates obtained near-maximal marks for an accurate and well-labelled diagram explaining the physiological mechanisms. Q 12. Compare and contrast a single twitch and a tetanic contraction in a skeletal muscle fibre.

This question was passed by 25% of candidates. Better answers included a brief description of a skeletal muscle fibre and its contractile mechanism, definitions of a single muscle fibre twitch and titanic contraction, an explanation of the difference between the membrane electrical refractory period and fibre relaxation time and the implications of each, the reasons re-stimulation within fibre relaxation time results in additional contraction, the role of calcium, the impact of relaxation times for different fibre types on the frequency required to create a titanic contraction (with example values for each), and the differences between single twitch and titanic contractions with respect to the reasons that relaxation occurs, force achieved, and energy requirements. Common mistakes included providing excessive detail about synaptic events or excitation-contraction coupling and missing the important points above, describing summation and tetany as electrical events rather than mechanical events, and writing about the use of a nerve stimulator. Q 13. Describe the determinants of work of breathing in an adult human at rest. This question was passed by 43% of candidates.

This question was best answered with an accurate labelled and annotated pressure-volume graph. Previous examination reports have detailed the main points expected and these have not changed. There were many poor diagrams that highlighted candidates’ lack of understanding. A common mistake was to describe the determinants of FRC, not those of work of breathing. Discussing how work of breathing changes when not at rest or in disease garnered marks if it helped to explain the underlying concept that was asked for in the question.

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Q 14. Describe the physiological effects of general anaesthesia on temperature regulation This question was passed by 44% of candidates. In order to pass this question, candidates were expected to discuss temperature regulation with induction, maintenance, and recovery from general anaesthesia. An understanding of dose dependent, agent dependent, and age and sex dependent factors were required. Additional marks were awarded for describing the differences between elderly patients and neonates, for a correct description of the role of non-shivering thermogenesis, and for a description of the additional effects of neuraxial blocks in conjunction with general anaesthesia. Many candidates were confused by the differences between the interthreshold range and the thermoneutral zone. Very few candidates mentioned temperature regulation during the recovery phase. Graphs were often incorrectly drawn, and the thermoneutral zone was frequently incorrectly defined. Some candidates gave a detailed account of the normal physiology of thermoregulation, rather than answering the question as relevant to anaesthesia. The main reason for candidates failing this question was insufficient core knowledge. Q 15. Describe the functions of the gastric secretions. This question was passed by 69% of candidates. In general this question was well answered. Good answers were often in tabular format with headings for secretion and function. Equally good answers were short notes under secretion headings. Poor answers gave lengthy descriptive prose that added no detail to the answer. Some candidates discussed other digestive secretions from the mouth, pancreas and intestine. These carried no marks and wasted valuable time. Repetitive statements also carried no extra marks. Q 16. Explain the difference between viscosity and density. Outline the effects of changes in viscosity and density on the flow of gases and liquids. This question was passed by 72% of candidates. In general this question was well answered. Points required for a pass were to demonstrate some understanding of the definitions of viscosity and density, the differences between laminar and turbulent flow and their dependence on viscosity and density respectively, and the factors that might influence the transition between laminar and turbulent flow. Additional marks were given for illustrative examples taken from physiology or anaesthetic equipment, understanding of flow-resistance relationships, and deeper understanding of the underlying physics (e.g. inertial vs. resistive forces). A common fault was that many candidates erroneously thought that density was defined as mass per unit area.

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VIVA OPENING QUESTIONS OPENING PHYSIOLOGY QUESTIONS: Measurement / Physics

What are the SI units?

What is the difference between heat and temperature?

What are the physical mechanisms by which the body loses heat?

How can you measure intracellular water?

What does a pulse oximeter measure?

What is humidity?

What is a transducer?

Draw a tracing from a capnometer.

What factors affect the flow of fluid through a tube?

What is osmolarity?

How would you measure pH?

What is a resistor? Respiratory

What respiratory function tests are commonly measured?

What is diffusion capacity?

How does the body control ventilation?

What are the physiological effects of IPPV?

How much blood goes through the lungs per minute?

How does oxygen get from the lung to the cell?

What is normal PaO2 ?

What is normal PaCO2?

Can you interpret this arterial blood gas result??

What will happen to the PaO2 if you hold your breath for 1 minute?

What is the effect of posture on lung perfusion?

What are the factors that affect airway resistance

What is pulmonary vascular resistance?

What is shunt?

What is surfactant?

What do you understand by the term “closing capacity”?

What do we mean by the term “work of breathing”?

Define the functional residual capacity of the lungs? Cardiac

What is the function of the circulation?

How is the cardiac output distributed?

Draw the action potential for the SA node.

Draw a lead II ECG.

Describe the coronary circulation.

What is the Frank-Starling Mechanism?

Draw a left ventricular pressure versus time curve.

How would you define afterload?

What are the cardiovascular changes associated with ageing?

What is venous return?

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What happens to cardiac output if you increase venous return?

Show me the waveforms you see when you pass a pulmonary artery catheter?

How does the cardiovascular system respond to haemorrhage?

Draw a central venous pressure trace.

Draw the flow of blood in the aortic root. Renal/Acid-base

How is renal blood flow controlled?

What is the glomerular filtration rate?

What is clearance?

How does the body clear a water load?

How does the body handle potassium?

What is the renal response to a metabolic acidosis?

What is renal response to metabolic alkalosis?

What is a colloid? Nervous system

What is normal cerebral blood flow?

How is cerebrospinal fluid formed?

Describe a myelinated nerve.

What types of nerves do you know?

What happens if you stub your toe?

What are the mechanisms of visceral pain?

What is sleep? Gastrointestinal

What are the functions of the liver?

Describe gastric emptying?

What are the physiological effects of fasting for 48hrs?

Describe the blood supply of the liver. Endocrinology / Prostaglandins

What is a hormone?

What are the functions of adrenal medulla?

What are the functions of the thyroid gland?

How do insulin and glucose interact?

What is the role of prostaglandins in the body? Haematology

Describe the processing of donated whole blood.

What is the body’s response to a damaged blood vessel?

What are the effects of storage on red blood cells? Muscle

Describe sequence of events in neuromuscular contraction.

What is a muscle spindle?

Where do we find smooth muscle in the body? Neonatal/Maternal

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What are the functions of the placenta?

What are the cardiovascular changes in the third trimester of pregnancy?

What are the respiratory changes in pregnancy? Immunology

What is the difference between innate and acquired immunity? Metabolism.

What is in total parenteral nutrition?

What are the physical mechanisms by which the body loses heat? Associate Professor Ross MacPherson Chairman, Primary Examamination Sub-Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

JULY/SEPTEMBER 2010

Please note that this report is prepared to provide candidates and their teachers and supervisors of training with information about the performance of candidates in the recent examination, 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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 83% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: Question 1 : Compare and contrast the pharmacokinetics of orally and intravenously

administered morphine and oxycodone. 26% of candidates passed this question.

Main Points expected for a Pass:

Both Morphine & Oxycodone are full- agonist opioid analgesics used peri-

operatively

They both can be administered orally or intravenously

They are roughly equipotent when administered intravenously but their oral

bioavailability differs.

Morphine has a high hepatic extraction, so Oxycodone is more potent when given

orally

Major differences or similarities in basic pharmacokinetic (PK) parameters such as

volume of distribution, clearance, protein binding, metabolism & half-life

Additional Points which attracted higher marks:

Actual numbers & content for PK parameters such as morphine’s bioavailability

being 30% compared to oxycodone which is 50-87%

Demonstrate an understanding of the role of pKa in ionization & lipid solubility in

comparing the 2 drugs.

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Be able to calculate the dose adjustments & relative conversion between the 2

drugs based on their bioavailabilities.

Be able to discuss accurately volume of distribution & plasma concentration

Discuss the different pathways of metabolism & clearance

Question 2 : Describe the composition of 4% albumin and Normal Saline. Compare and

contrast the pharmacology of each. 67% of candidates passed this question. Candidates are reminded that where a question is asked in two parts, as with this one, it is best to answer it clearly in two parts. Most candidates were able to describe the composition of normal saline, although some added other molecules such as potassium and calcium to the mixture, and of albumin. Albumin also contains a reasonable about of sodium chloride, which was often neglected. Most answers correctly demonstrated an understanding of the distribution of normal saline between the intravascular and extra cellular compartments, and of the oncotic effects of albumin. Although albumin is a product derived from human plasma, it is treated heating to 60 degrees C for 10 hours, thus virtually eliminating the risk of transmission of disease. Extra marks were gained by giving details about the mechanism of hyperchloraemic acidosis seen with infusion of large volumes of sodium chloride.

Question 3: Describe the mechanism of action, pharmacokinetics and major side

effects of intravenously administered amiodarone.

70% of candidates passed this question.

A structured approach was expected and marks were distributed to the three main areas – MOA, pharmacokinetics and adverse effects. Candidates were expected highlight the various mechanisms of action such that amiodarone can fit within most elements of the Vaughan Williams classification. A clear structure addressing the main areas relating to pharmacokinetics was helpful. It was expected candidates would appreciate the very long half life, high protein binding, significant tissue binding and large volume of distribution. Specific comments regarding the main toxicities were expected. In particular, the pulmonary toxicity (both acute and chronic variations) is important. In addition a variety of other issues should be mentioned, including thyroid changes and the well described skin and ocular changes. Cardiac toxicity with bradycardia, QT prolongation and this risk of Torsades that this may pose was mentioned by many candidates and gained specific credit. Additional credit was given for more detailed explanations, comments on enzyme metabolism and examples of drug interactions. Comments on dosing and infusions gained additional marks. Well organized answers such as those with an ordered list of subheadings were rewarded.

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Question 4 : Briefly outline the effects of sevoflurane on skeletal, smooth and cardiac

muscle tissues. Include how these effects are mediated and their clinical significance.

38% of candidates passed this question. On first glance the question looks intimidating, as the exact mechanisms of these actions are complex. The mechanisms, however, were only part of the question. A systematic approach addressing each key issue easily scored enough marks to pass. Areas which could have been covered included: Skeletal muscle: Direct effect, interaction with muscle relaxants, malignant hyperpyrexia, effects on muscle blood flow. Smooth muscle: Effects on vascular smooth muscle, including regional circulations, the uterus and the bronchioles. More marks were awarded for understanding the clinical significance of these effects. Cardiac: The direct effect, the overall effect on the circulation, overall effects on myocardial work, ischaemic preconditioning and arrythmogenesis. Candidates often confused the direct effect of volatiles on skeletal muscle, the interaction with muscle relaxants, and surgical immobility. Many thought that the contraction of skeletal muscle was controlled by the sympathetic nervous system. The effects of sevoflurane on the pulmonary vasculature and hypoxic pulmonary vasoconstriction was poorly understood. The risks of sevoflurane were commonly overstated, particularly in the areas of coronary steal, myocardial ischaemia, heart rate, hypotension; as well as bleeding following Caesarean Section. The structure, physicochemical properties and anaesthetic uses of sevoflurane were not part of the question and so did not attract marks. The question was not an essay on malignant hyperpyrexia, the cerebral effects of sevoflurane, or muscle relaxants. We no longer use general anaesthesia for labour, nor is sevoflurane used for treatment of premature labour. Rewriting the question at the top of the paper is unnecessary.

Question 5 : Describe the pharmacodynamic effects and clinical uses of

anticholinesterase drugs.

65%% of candidates passed this question. A brief definition of an anti-cholinesterase and its effect on acetylcholine concentrations at cholinergic receptors was expected. Subsequently the marks were divided evenly between pharmacodynamics and clinical applications. Briefly an increase in acetylcholine levels at muscarinic receptors results in bradycardia, hypotension, salivation, bronchospasm, increased gut and urinary motility, miosis and central effects if the drug crosses the blood brain barrier.

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Only a few candidates mentioned that muscarinic effects occurred at lower concentrations than nicotinic effects. However the single largest error in answering this question was candidates discussed structure activity relationships and pharmacokinetics of individual agents at length and failed to mention any pharmacodynamics. Clinical uses of these agents are legion and were very well discussed. No value would be gained in repeating these here. Some candidates spent an inappropriate amount of time discussing organo-phosphates but by elaborating the adverse effects of these agents ('SLUDGE' acronym) they gained marks en passant for the pharmcodynamic effects

Question 6 : Describe the principles of how a computer-controlled infusion device targets and maintains a constant effect site concentration of propofol.

73% of candidates passed this question.

Principles relevant to this question included: - Propofol’s pharmacokinetic parameters making it suitable for this technique are rapid equilibration between the central compartment (i.e. the vessel rich group) and the effect site. Especially after the initial bolus producing only a short lag time. A 3 compartment model is described and it is as well to consider the added effect site compartment albeit small. Volumes of distribution of all those compartments have been mathematically derived plus the constants describing the kinetics of transfer using relevant studies on healthy volunteers. This diagram explains the concept : - (Miller Chapter 12) That time to equilibrate with the central compartment correlates with the Keo (high for propofol indicating a short time to peak effect). Clinical effects by the agent at the effect site compartment were equated with a measurable effect on the volunteers eg by using a BIS or EEG. This is a closed loop system but most cases are done on the basis of a set plasma concentration desired for a given procedure. Candidates did describe the different models available (Schneider, Marsh, and Bristol) The driver computer software incorporates derived algorithms, with information using entered patient parameters such as weight, age, sex, height of the patient. The driver calculates and delivers a loading dose, followed by a pause, then a maintenance dose and fluctuation in dosage delivery as the compartments become saturated followed by transfer of the excess into the central compartment. Ultimately the agent is made water soluble, metabolised and renally excreted. A

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target effect site concentration around 3 – 4 mcgm/ml, is also programmed into the machine. The machine alters the infusion rate based on its own mathematical calculations taking into consideration the redistribution amongst compartments and the central compartment, and the metabolism, clearance, and elimination which is pre-programmed into the computer algorithm. The anaesthetist may alter rates for effect or need to alter due to change of plasma concentration requirement. The graph explains the concept: - (Miller Chapter 12) Describing the terms of the context sensitive half time and/or the clinically relevant context decrement time helped to indicate an understanding of the kinetics and dynamics at the end of the infusion.

Question 7 : List the physical properties of oxygen. Discuss the potential adverse

effects associated with oxygen administration.

67% of candidates passed this question. The question was similar to that asked in a previous exam, and clearly some candidates used this to their advantage. Generous margins were accepted for some of the numerical physical properties of oxygen, but marks could not be awarded for significant disparities. Although not specifically asked for on this occasion, marks were awarded for descriptions of how oxygen is manufactured where this was adequately linked to the relevant physical property. The adverse effects portion of the question was generally well done, but insufficient to compensate for the absence of an answer for the first half of the question.

Question 8 : Discuss the statistical methods which can be used for analysis of groups

of categorical data.

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15% of candidates passed this question. Categorical data involves primarily nominal data but can include ordinal data (ranked groups). Many candidates failed to provide a clear definition. Marks were awarded for providing brief examples. Descriptive statistics were often omitted, but could involve table of counts or graphical techniques such as bar graphs or pie charts. Inferential analysis could be divided into techniques for nominal data and ordinal data. Chi-squared analysis forms the backbone of analysis for nominal data. A discussion about how the test statistic is calculated and the underlying assumptions involved was expected. Extra marks were also awarded for the appropriate discussion of Fisher’s Exact Test and Yates correction. Ratio analysis was rarely discussed, but extra marks were awarded for discussion about relative risk and odds ratio. A frequent mistake was to discuss parametric analysis for categorical data (eg. Student T test, ANOVA). Categorical data do not generally meet the assumptions required for parametric analysis. A discussion about non-parametric analysis in relation to some types of ordinal data (eg. Wilcoxon Rank Sum test and pain scores) was awarded extra marks.

PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS: Volatile agents

1. Inhalational agents 2. Wash out curves for volatile agents 3. Problems with halothane 4. Sevofluorane chemistry 5. ADR’s and Volatile Agents. 6. Nitrous oxide 7. Define MAC 8. Types of MAC

Neuromuscular Blocking drugs 9. ED95 in NMB’s 10. Fate of suxamethonium 11. Choice of muscle relaxant 12. Classification of neuromuscular blocking drugs 13. Effects of suxamethonium 14. Compare vecuronium and rocuronium 15. Dose Effect curve for vecuronium

Analgesics 16. How are NSAID’s classified? 17. What is the definition of pain?

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18. Paracetamol pharmacology 19. Epidural morphine 20. Speed of onset of opioids.

Statistics

21. Student’s t test 22. Normal distribution 23. Classification of data

Local anaesthetic agents

24. Drug for IV regional analgesia 25. Toxicity of Local Anaesthetics agents 26. Physico chemical properties of lignocaine 27. Describe some local anaesthetics

Miscellaneous

28. Stages of clinical trial design 29. What are the effects of glyceryl trinitrate 30. Classify diuretics 31. Pharmacology of anti-coagulants 32. Pharmacokinetics of phenylephrine 33. Classify catecholamines 34. What is the role of additives 35. Benzodiazepines chemistry 36. The dose- effect curve 37. Classification of inotropes 38. Placental transfer of drugs 39. Management of anaphylaxis 40. Drug tolerance 41. Management of Hypotension 42. What is an isomer 43. Treatment of Parkinson Disease. 44. Name some Anti hypertensve agents 45. Classify antiseptics 46. Contents of an ampoule of Pentothal 47. Anti platelet agents 48. Bronchoconstriction management 49. Pharmacology of aspirin 50. Adverse effects of atropine 51. Chirality in Anaesthesia 52. Drug selection in liver failure 53. Syntocinon pharmacology 54. Describe ketamine and its uses

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 64% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: Question 9 : Describe the factors that affect respiratory system compliance.

31% of candidates passed this question. A definition of compliance followed by a statement of the types of compliance along with normal values for these would have completed a good introduction. A compliance graph with an explanation of the importance of surfactant and how it acts to reduce compliance followed by simple statements as to compliance changes related to: a) lung factors: aging, posture, changes in pulmonary blood volume, airways resistance, emphysema, lung fibrosis, and b) chest wall factors: obesity, scarring, fractures as well as compliance changes occurring during anaesthesia would have rounded out a good answer. Additional marks were awarded for more detail on static and dynamic compliance, compliance at high and low lung volumes and changes in compliance seen from the top to the bottom of the lung in the erect position. The most common reason for not passing this question was because of a paucity of information provided. Additionally, there were frequent errors as to the effect of some of the above factors on compliance, in particular, the effect of age and the effect of emphysema. Complex and detailed discussions regarding the interactions between chest wall and lung compliance were only minimally rewarded.

Question 10 : Discuss the factors that influence coronary blood flow.

This question was passed by 28% of candidates. Many candidates did not perform well in this question as a result of failing to develop a structured answer. In order to pass, candidates were required to provide normal values for coronary blood flow, a basic anatomical outline of the coronary blood supply, note the high oxygen extraction and its consequence, and demonstrate an understanding of Ohm’s law. Having demonstrated Ohm’s law, the factors affecting pressure and resistance (within both the left and right ventricles) could then be further explained. Further marks were allocated for clinical applications and the consequences of

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common pathophysiological disturbances, including hypo/hypertension, coronary artery disease, and severe valvular disease. Common errors included discussing oxygen flux rather than coronary blood flow, and failing to apply Ohm’s law to the coronary circulation. Many applicants spent significant time explaining all the factors of the Hagen-Poiseuille equation, which gained minimal marks. A well labelled graph of the right and left coronary blood flow with respect to the cardiac cycle often scored more highly than attempts to explain the flows in prose. The description of coronary blood flow differs between the different recommended text books, especially with respect to values and labelling of graphs. All variations were considered acceptable within the examiner’s marking scheme.

Question 11 : Explain the physical principles of ultrasound imaging.

57% of candidates passed this question. Important points to include were a description and explanation of the principles from initial signal formation to tissue effects to signal reception to image formation. This should cover both standard imaging and Doppler ultrasound. Better answers explained the Doppler effect and the implications of the Doppler equation

Question 12 : Describe the function of the muscles involved in ventilation.

39% of candidates passed this question. The principal muscles of ventilation are the diaphagm and the intercostals (internal, external). Other important muscles are the abdominals and the accessory muscles of the neck which are recruited in times of need. A precise description of the mechanical effects of these muscles was expected i.e. how these muscles increase or decrease the intrathoracic volume. Desciption of the anatomy of the diaphragm and the chest wall was also helpful. Mention of the pharyngeal and laryngeal muscles and their role in ventilation was also expected. Most candidates who failed did so because they did not name and describe the actions of most of these muscles or did so but only in vague terms. Extra marks were available for the following: effects of posture; special patient groups, including pregnancy and neonates; co-ordination in the medullary respiratory centre; non-ventilatory actions of these muscles (cough, vomiting and defaecation); muscle subtypes; smooth muscle.

Question 13 : Describe the cardiovascular changes in the neonate that occur at birth.

90% of candidates passed this question.

The cardiovascular changes that occur in the neonate at birth was well answered with most candidates providing an adequate account of the effects of the first few breaths and cessation of umbilical blood flow on the pulmonary and intracardiac circulations, along with the sequence and timing of these events.

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Extra marks were awarded for more detailed descriptions of the foetal circulation at term and neonatal haemodynamics at birth, and the factors that modify them (such as the inhibition of ductus arteriosus closure by hypoxia and prostaglandins).

Question 14 : Discuss the effects on intracranial pressure when a person is placed in

a head down tilt.

39% of candidates passed this question. A good answer would have included a definition of intracranial pressure and it’s regulation, including an accurate (not abridged) summary of the Monroe-Kellie doctrine, then would have gone on to describe the effects of head down tilt, ie the increase in hydrostatic pressure on the three elements within the fixed cranial vault, ie: blood volume( both arterial and venous components), cerebrospinal fluid and brain tissue, and finally described the ability to compensate for the increase. Some quantification of the degree of increase in hydrostatic pressure rise vs. degree of head down tilt was useful. Unfortunately a number of candidates confused cerebral perfusion pressure with cerebral blood flow in their explanations, therefore reproducing erroneous equations. Graphical representation of concepts were useful to demonstrate knowledge when labelled correctly and included in the discussion. If axis were unlabelled they gained no marks. The effects of general anaesthetic agents on the three components that generate intracranial pressure was not asked for in the question and gained no marks in a physiology question.

Question 15 : Explain the role of haemoglobin as a buffer.

This question has been asked previously and this time the pass rate was 27%. Marks were awarded for a buffer definition, a brief description of haemoglobin structure, and listing the factors that create an effective buffer. Haemoglobin acts as an effective buffer for CO2 due to the solubility of CO2 , presence of carbonic anhydrase, and the capacity of haemoglobin. Important points that needed to be covered included; the importance of the large volume of haemoglobin, the role and amount of the imidazole side chains on the histidine residues, the effect that their pKa (6.8) has on buffering ability, and a clear description of the reactions within the red cell that involves CO2 conversion to HCO3

-

and H+ and the fate of these two products. Discussion about why the deoxy form of haemoglobin is a better buffer due to it’s change in pKa (7.9), and that this occurs where buffering is needed most, which limits the pH drop for venous blood. Some candidates correctly identified that the dissociation of carbamino compounds within the red cell adds H+ which then needs to be buffered. Discussing the haemoglobin oxygen dissociation curve, carbon dioxide dissociation curve, and other buffers in the body did not attract marks.

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Question 16 : Outline the clinical laboratory assessment of liver function. 29% passed this question.

Basic points to include to achieve a pass included a description of the battery of tests commonly referred to as liver function tests; a description of what they tested and an appropriate interpretation of an change. Extra marks were available for suggestions of more sensitive clinical tests of liver function, (Prothrombin time or INR) and integrating the understanding of common derangements of hepatic function. Common mistakes included listing all the functions of the liver and discussing how these might be assessed.

PHYSIOLOGY - VIVA SECTION PHYSIOLOGY TOPICS: Measurement / Physics

1. SI units

2. What is an electrical resistor?

3. What is heat?

4. Measurement of intracellular water.

5. Pulse Oximetry.

6. Measurement of saturated vapour pressure

7. Measurement of oxygen.

8. BP measurement

9. Principles of arterial pressure measurement.

10. Measurement of temperature

11. What factors determine flow

12. Osmolarity / Colligative properties.

13. CO2 measurement /capnograph

14. pH measurement

Renal/Acid-base

1. Control of renal blood flow

2. What is the glomerular filtration rate

3. Define clearance.

4. How does the body clear a water load?

5. Physiologic effects of renal dysfunction

6. What is extra-cellular pH range?

7. Describe renal handling of a metabolic acid.

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8. What is renal response to metabolic alkalosis?

Endocrinology / Prostoglandins

1. What is a hormone

2. What are the functions of adrenal medulla?

3. Pituitary hormones.

4. Thyroid hormones

5. Interaction of Insulin & Glucose

6. Glucose handling

7. What is normal blood sugar

8. Prostaglandins in the body

Nerve

1. Nernst Equation

2. Describe a myelinated nerve

3. Types of nerves

4. Pain transmission.

5. What is sleep

6. What is the blood brain barrier?

Haematology

7. Describe the processing of donated whole blood.

8. Describe red cell antigens.

9. Response to damaged blood vessel

10. Effects of storage of red blood cells

Muscle

11. Describe sequence of events in neuro muscular contraction.

12. What is a muscle spindle

Cellular

13. Features of a cell

14. Cellular energy sources

Neonatal/Maternal

15. Oxygen delivery to foetus

16. Cardiovascular response to pregnancy.

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17. Respiratory changes in pregnancy

Immunology

18. What is the difference between innate and acquired immunity?

19. Mechanisms to stop bacteria reaching alveoli

20. Hypersensitivity

Metabolism/Thermal homeostasis

21. Normal body temperature

22. What is in Total Parenteral Nutrition?

23. Metabolic consequences of sepsis

Gastro-intestinal

24. Describe swallowing (physiologic principles)

25. Describe gastric emptying

Respiratory

26. Respiratory function tests

27. What is diffusion capacity

28. What affects the diffusion capacity of the lung

29. Control of ventilation

30. Dead space

31. Aging + respiratory function

32. Pulmonary circulation

33. O2 cascade

34. What is the alveolar gas equation

35. O2 supplies in body

36. What is normal PO2

37. What is normal PaCO2

38. Carriage of CO2

39. Interpretation of blood gases

40. Consequences of apnoea

41. Effect of posture on lung perfusion

42. Interpretation of capnography

43. Describe airway resistance

44. What is “O2 extraction”?

45. Why do we produce CO2

46. Compare Pulmonary & Systemic circulation

47. What is pulmonary vascular resistance?

48. What is shunt?

49. What is surfactant?

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50. Lung mechanics

51. Hb O2 dissociation curve?

52. Ascent to altitude

53. Describe work of breathing

Cardiac

1. What is the function of the circulation

2. Distribution of cardiac output

3. Draw the action potential for the SA node

4. Arterial P waveform – changes with age?

5. Describe ECG

6. Frank Starling Mechanism – describe

7. Cardiac cycle

8. Draw left atrial pressure cycle

9. Draw an LV Pressure vs. Time curve

10. What is automaticity

11. Define afterload

12. Cardiovascular changes associated with aging

13. What is anaemia

14. Effects of chronic anaemia

15. Describe venous return

16. Interdependence of venous return and cardiac output

17. Starling curves – draw

18. Pulmonary artery catheter

19. Effects of haemorrhage

20. Control of peripheral blood flow

21. What is the microcirculation

Dr. C Noonan Chairman, Primary Examination Sub Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

MARCH/MAY 2010 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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 75% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Describe how the chemical structure of local anaesthetic drugs determines their

efficacy and safety. 36% of candidates passed this question. This could be considered core material, although many candidates lost marks by spent a time on non-relevant information such as describing local anaesthetic toxicity, mechanisms of action, and routes of administration. Other common errors included: making imprecise statements (for example, „the structure determines what the pKa and lipid solubility will be‟, without saying how), writing lengthy introductions that don‟t make a point, repeating the same point multiple times, and stating that prilocaine is an ester local anaesthetic. The answer needed to be related to the structure of local anaesthetics and could be divided into effects on efficacy and safety. This means looking at the lipophilic, intermediate, and hydrophilic components. Increases in side chain length generally result in increased lipid solubility, potency, and protein binding up to a point. This also increases toxicity, duration of action, and slows the onset/offset. The differences between the ester and amide link in regards to metabolism, allergy, and duration of action need to be covered. Other aspects needed to gain marks included the effects of chirality and acid-base changes.

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QUESTION 2 Describe the methods of determining depth of neuromuscular block and list the advantages and limitations of each. 64% of candidates passed this question.

This question covers material asked in previous questions. The main points expected for a pass include: Neuromuscular blockade can be assessed by both clinical means and by using the nerve stimulator. Some examples of clinical means (eg head lift for 5 seconds) was expected, however clinical methods are unreliable. The characteristics of the required impulses from the nerve stimulator afforded the candidates points. Marks were awarded for the different modes of stimulation, such as single twitch, train of four count and ratio, double burst stimulation, tetany and post tetanic count. It was expected that candidates would describe their requirements, their advantages and disadvantages and how best to clinically utilise them for e.g. for reversal, in deep block. Some candidates went into great detail about the neuromuscular junction, which afforded them no marks. The concept that the strength of the muscular twitches produced is related to receptor occupancy by the neuromuscular blocker and at what levels of occupancy one could expect how many twitches. A few candidates did not appreciate that with a train of four count of 4, there was still a 70% receptor occupancy by the drug. Some thought that with a post tetanic count of 10, it was reasonable to reverse the patient with conventional reversal agents. Bonus marks were awarded if there was demonstration of how the depolarising and non-depolarising blocks differed in their responses to the nerve stimulator, the different sensitivities of different muscle groups to the neuromuscular blocker and mention of acceleromyography or more sophisticated methods. Use of diagrams implied understanding and where appropriate, garnered marks. Some candidates were confused about the TOF ratio, saying it was the ratio of the height of the first twitch compared to the fourth twitch QUESTION 3 Discuss the adverse effects that may occur with the administration of

desflurane.

44% of candidates passed this question. This question was poorly answered by the majority of candidates. Better answers discussed adverse effects by system or divided their response in to those effects peculiar to desflurane and those common to many volatile agents. Even better answers compared some adverse effects to other volatile agents. No marks were awarded for details which were clearly unrelated to the answer such as chemical structure and physical characteristics. The following material needed to be covered for a clear pass. Desflurane is a volatile agent used mainly for the maintenance of general anaesthesia. An adverse effect is an unwanted side effect of a drug. Desflurane reduces systemic vascular resistance and thus mean arterial pressure in a dose dependant manner, however cardiac output is usually well-maintained by an increase in heart rate. Sudden increases in the inspired concentration can cause a marked sympathetic response with tachycardia, hypertension and activation of the renin-angiotensin system. Cerebral blood flow increases above 1.0 MAC but the rise in ICP is quite small (about 7mmHg). At higher doses there is uncoupling of oxygen supply and demand. It is not known to trigger seizure activity. There is a dose-dependent reduction in tidal volume and increase in respiratory rate (overall decrease minute ventilation) and an impaired response to hypoxia and hypercarbia. Desflurane is

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pungent and can cause coughing and breath-holding so it is infrequently used for inhalational induction. It can increase airways resistance (especially in smokers). It can cause a fulminant antibody-mediated hepatitis (like halothane) through neoantigen formation from metabolites, but this is very rare – probably due to the very low rate of metabolism. It reduces uterine tone (potentially worsening postpartum haemorrhage). It is a trigger for malignant hyperthermia. It can interact with carbon dioxide absorbants to produce toxic levels of carbon monoxide (especially with high temperatures and low flows over dessicated Baralyme ®). QUESTION 4 Describe the time course between an intravenous injection of a general

anaesthetic agent to loss of consciousness. Explain the delay using pharmacokinetic principles.

60% of candidates passed this question. The delay to loss of consciousness after intravenous injection of an induction agent is a very specific event that requires detailed knowledge of pharmacokinetics. Descriptions of the time course had to indicate that the delay involved the build up of an adequate or threshold concentration at the effect site for loss of consciousness to occur. There were many facts that attracted marks in this question with the better answers providing fuller justifications. For example simple knowledge such as using a bolus or loading dose and injecting the dose faster attracted marks but explaining that these practices led to a higher dose of agent in the central compartment which then leads to a larger concentration gradient driving the agent into the effect site (CNS) more quickly attracted higher marks. Similar discussions about the importance of cardiac output and pathological situations where the cardiac output may be altered, injecting into a larger vein closer to the heart instead of a peripheral vein, about smaller volume of distribution leading to a larger concentration in the central compartment (despite the paradox that a lower lipid solubility is often associated with a smaller Vd) all attracted marks. Many candidates showed an appreciation of the complexity of pharmacokinetics, describing how redistribution and metabolism begin to occur simultaneous to delivery and may slow the build up of central compartment concentration and delay onset of action to a small degree. Diagrammatic representation of a 3 compartment pharmacokinetic model with correct descriptions with highlighting and description of the importance of the Keo also attracted marks. Comparisons of Keo‟s between differing intravenous induction agents were also central to the question. Graphs depicting the change in plasma and superimposed effect site concentrations with time attracted marks, with the better graphs indicating the threshold level needed at the effect site for loss of consciousness to occur. A discussion of the potential for speed of effect to be influenced at the neuronal membrane and by the specific molecular characteristics of the induction agent and how this related to Fick‟s Law and to unionized drug was also considered relevant. Candidates often ran into difficulties with their answer if they spent too much time discussing how the effect of induction agents wore off or how they were cleared from the circulation, or spoke at length about unrelated facts concerning specific agents.

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QUESTION 5 Describe how Non Steroidal Anti-Inflammatory Drugs exert their clinical effects. Outline the advantages and disadvantages in using COX-2 selective agents.

29% of candidates passed this question. Candidates were expected to describe how the inhibition of cyclo-oxygenase results in both positive and negative clinical effects of NSAIDs. Many candidates did not link the reduction in prostaglandins, leukotrienes, thromboxane and interleukin to specific NSAID actions such as anti-pyrexia, analgesia and anti-inflammation. Physiological actions of prostaglandins and thromboxane were described but did not gain marks unless related to the clinical effects of NSAIDs. Marks were awarded for differentiating the isoforms of cyclo-oxygenase and the logic behind preferentially inhibiting COX-2. A structured approach naming the clinical effects of NSAID‟s and how they occur through manipulation of eicosanoid production gained higher marks. Confusion occurred regarding the effect of COX-2 selective agents on asthma. Generally the precipitation of asthma is reduced. Omitting the allergic potential of COX-2 inhibitors and the fact that Parecoxib is a pro-drug were common. Extra marks were awarded for describing the effects of NSAIDs on bone formation, the ductus arteriosus, the pregnant uterus and bowel cancer. QUESTION 6 List the main drug groups used in the treatment of diabetes mellitus. For each group explain the mechanism of action and give examples. 60% of candidates passed this question. Diabetes mellitus is a common condition faced daily by anaesthetists. A thorough understanding of its management is a clinical necessity. This is a two parts question requiring candidates to list the various groups of drug for the treatment of diabetes mellitus, and to describe their mechanisms of action. It is important that sufficient details, such as molecular and metabolic effects after drug administration, are included for the latter part of the question. While most candidates were able to describe the classical oral hypoglycemic agents (i.e. sulphonylureas and biguanides) in detail, it was surprising that a substantial proportion of candidates did not consider insulin as a drug for the treatment of diabetes mellitus. Most answers were also vague regarding the different preparations of insulin that produce variation in the speed of onset and duration of action. Candidates who included the newer agents, such as thiazolidinediones, alpha glucosidase inhibitors and meglitinides, were rewarded with extra marks. QUESTION 7 Briefly describe the pharmalogical role of the nicotinic cholinergic receptor.

38% of candidates passed this question. The key points that needed to be included were:

The types of the nicotinic receptor, their location and function

Structure activity relations of the receptor which account for drug specificity (e.g.why

ganglion blockers do not cause muscle relaxation), pharmacodynamics (e.g. prejunctional

receptors causing fade) and side effects (e.g. hyperkalaemia with suxamethonium)

Drugs can act either directly or indirectly as either agonists or antagonists (correct examples

attracted marks)

Many candidates failed to write that there is a structural difference between the neuronal and muscle nicotinic receptor, this is important in understanding the specificity of action of neuromuscular blockers. There was a frequent misconception that anti-muscarinic drugs act primarily at the nicotinic receptor. Some candidates wrote at length about the physiology of the nicotinic receptor without mentioning drugs and were thus unable to achieve a pass mark.

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QUESTION 8 Classify drugs used in the treatment of depression. Outline the interactions between antidepressant drugs and drugs that are commonly used during the peri-operative period.

32% of candidates passed this question.

The main points expected for a pass included a classification of antidepressants according to mechanism of action, and therefore making some mention of the amine hypothesis of antidepressant effect. Then an outline of antidepressant – perioperative drug interactions was expected: including pharmacokinetic and pharmacodynamic interactions. Many relevant interactions attracted marks, however, the important MAO inhibitor interactions were especially rewarded. Although most candidates classified antidepressants according to mechanism of action, few connected this pharmacodynamically to the therapeutic antidepressant effect. Pharmacokinetic drug interactions were rarely included in answers and an explanation of what type of sympathomimetic that could be utilized perioperatively in patients taking MAO inhibitors was often omitted. Similarly, serotonin syndrome was frequently discussed as a SSRI interaction (where the severity is usually minor), but rarely so as a MAO inhibitor interaction where it can be severe. Detailed descriptions of the pathology of depression were not expected.

PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS: IV Induction agents Why do you believe propofol is widely used as an anaesthetic agent? What are the pharmacodynamics of propofol? What is in an ampoule of thiopentone? How do you determine an induction dose of propofol? Compare the pharmacokinetics of an infusion and a bolus of a drug Thiopentone as an induction agent What IV agents act on the GABA receptor? Induction of anaesthesia in a volume depleted patient. Pharmacokinetics and pharmacodynamics Gaseous induction with sevoflurane Dose Response curves What drugs are administered by infusion Wash out curve for a volatile agent Concentration-time curve for fentanyl Definition of half life Pharmacokinetic parameters for propofol Drug nomograms Transdermal medications Anaesthesia and liver failure Modifications of drug dosage Draw a quantal dose-response curve Endotracheal administration of drugs Mechanisms of drug clearance. Changes in drug response with age. How can genetics influence metabolism?

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Anti-emetics What drugs can be used for Post-Operative nausea and vomiting? Compare anti-emetics Pharmacology of ondansetron Local anaesthetics Cocaine What drugs are added to local anaesthetics? What drugs are used in topical anaesthesia? Kinetics of local anaesthetics in CSF What is lignocaine? Local anaesthetic toxicity Inhalational agents How do you select an inhalational agent? Draw a wash in curve for isoflurane Draw a wash out curve for an agent Manufacture of nitrous oxide What are the advantages of sevoflurane? When to avoid nitrous oxide Fa/Fi curves How does the addition of nitrous oxide affect inhalational agent uptake? Changes in uptake of volatile agents Effects of sevoflurane on the CNS Isoflurane and the CVS How does cardiac output affect inhalational uptake? Autonomic Nervous System and Adrenoreceptor Blocking drugs Alpha 2 agonist drugs What drugs increase blood pressure? How do you classify beta blockers? What is an inotrope? Anti-arrhythmic effects of beta blockers Effects of clonidine Adverse effects of adrenaline What drug act on the renin-angiotensin system? What is a catecholamine? What is a beta blocking drug? Hydrallazine and clonidine Digoxin Ephedrine Statistics Data types and study limitations Box plots Scatter plots Regression analysis Hypothesis testing Case controlled studies Data interpretation What is probability? Clinical trial design Meta analysis Students t test What is a 95% confidence interval? Neuromuscular Blocking Drugs and reversal Monitoring of neuromuscular blocking drugs Classification of NMB‟s

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Pharmacology of suxamethonium ED95 of muscle relaxants What receptors exist at the NMJ? Dose-response curves to NMB‟s Receptor regulation Changes in response to NMBs Organo phosphate poisoning Atracurium and rocuronium Cardiovascular effects of NMBs Dose response curve with anticholinergics Analgesic agents Non-opioid analgesics COX-2 inhibitors Structure and function of opioids NSAID toxicity Paracetamol pharmacokinetics Parecoxib Post-operative analgesic options Onset time of analgesics Ketamine as an analgesic Methadone Pharmacokinetics of fentanyl Compare alfentanil and remifentanil Tramadol pharmacology How does paracetamol work? IV analgesic drugs Blood levels following oral paracetamol What determines a dose of morphine Miscellaneous Topics What drugs relax the uterus? How does drug development occur? Allergic reactions in anaesthesia How do you treat atrial fibrillation? Pharmacology of amioderone Management of hypertension Classification of anti-hypertensive agents Management of poisoning Management of myocardial ischaemia Principles of antibiotic prophylaxis What is the difference between an anti-septic and a disinfectant? How can we change the pH of stomach contents? What types of heparin do you know of? What anti-platelet agents do you know of? What drugs are used in cardiac arrest? With diuretics, how does site of action influence efficacy? Classification of diuretics What colloid IV fluids do you know of? Classes of IV fluids Classify drug interactions What are the stages in drug development Principles of clinical trials Nitric oxide How do anti-coagulants work Tolerance and tachyphylaxis

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 68% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Explain the physiological factors that may lead to a decrease in mixed venous

blood oxygen saturation. 30% of candidates passed this question. This question required candidates to explain a decrease in mixed venous oxygen saturation. The key issue in this question is the fact that the value of mixed venous saturation is the result of a balance between oxygen delivery to the cells (oxygen flux) and cellular consumption of oxygen. The net value of mixed venous saturation can thus be explained by unpacking the elements of delivery and consumption, and explaining how their variation results in a change in mixed venous saturation. Not acknowledging this issue made it difficult for candidates to accumulate sufficient marks to pass the question. A significant number of candidates approached this by providing flux equations or variants of Fick‟s Law. This readily identified the elements, and their contributions could be clearly explained. These candidates tended to comfortably accumulate sufficient marks to pass. However, some candidates spent significant time on detailed derivations of formulae, leaving less time to address more important aspects or to accumulate bonus marks for more detailed information. Further, detailed derivations not uncommonly introduced simple errors. Simply using a formula or equation to identify the elements or principles involved was sufficient. Many candidates did not identify this basic principle of supply and demand, and therefore struggled to pass the question. Instead, a significant number of candidates focused on details such as the oxygen dissociation curve in both arterial and venous blood, sometimes in great depth and with detailed figures. Some candidates focused on little else. The time spent on this aspect left little opportunity to address more fundamental issues. It was notable that the terms oxygen tension, saturation and content were used carelessly in a significant number of answers. These are fundamental issues at this level of physiology. QUESTION 10 Describe how white blood cells defend the body against infection. 40% of candidates passed this question. The question required a description of the different white blood cells in the body and a discussion of their activation and interaction. Successful candidates gave a comprehensive list of white cell types and described how each defended the body. Some understanding of the roles they played in innate and acquired immunity was also necessary. Better candidates structured their answer based on the time course of activation so they could most effectively describe the interplay between white cells. Common areas of confusion were:

roles played by each cell, particularly the natural killer cell the types of infective agent each cell was active against the difference between acquired and innate immunity.

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Marks were not gained for discussing hypersensitivity reactions or non-white cell mediated defence such as physical barriers. QUESTION 11 Describe the changes that occur in the urine and the plasma with renal dysfunction. 30% of candidates passed this question. 28% scored 8 marks or less. Marks were awarded for the following points: That renal dysfunction could refer to abnormal function at any part of the nephron (glomerulus, tubules, interstitium); most commonly a reduction in GFR was involved. Plasma chemistry changes would include increased creatinine, urea, potassium and hydrogen ions. Creatinine rises only after substantial (eg 50%) loss of nephron function and the rise is in a curvilinear fashion, and creatinine clearance can be used to calculate eGFR and GFR. Urea concentrations are subject to too many variables to be useful in estimating degree of renal dysfunction. Potassium levels may rise to fatal levels, particularly in oliguric patients. Metabolic acidosis is often of a raised anion-gap type due to accumulation of titratable acids, but with renal tubular acidosis may not have a raised AG. Typically there is hypocalcaemia and hyperphosphataemia, increased PTH and decreased VitD3, in chronic disease. Chronically, EPO levels fall leading to anaemia. There may be hypoalbuminaemia in nephrotic syndrome. Accumulation of renally-excreted drugs or their metabolites may occur. Plasma sodium levels tend to remain within the normal range, except in rare situations where large volumes of dilute urine are produced, because the reduction in GFR reduces elimination of both salt and water. (The increase in osmolality is mostly due to urea, a point not understood by most candidates who either said osmolality was unchanged or reduced). Urine changes that scored marks included oliguria (preferably with a definition), possibly polyuria (but this is not the same as “non-oliguric renal failure”, i.e. absence of oliguria does NOT imply abnormal polyuria!); inability to concentrate the urine and also inability to dilute the urine, so that in advanced renal failure the urine osmolality is similar to plasma (isotonic urine); in ATN there may be granular casts; RBC casts occur in glomerulonephritis as do “upper tract”RBC; proteinuria indicates glomerular dysfunction. Appropriate use of terms such as Fractional excretion of Na scored marks if there was an indication the candidate understood the term. Common errors included: Failure to mention creatinine and /or urea or oliguria. Many answers spent lots of time discussing polyuric conditions such as nephrogenic diabetes insipidus, (and little or no time discussing any other situation) leaving the examiner to wonder if this was their idea of a common physiological abnormality. By far the commonest urinary change is a reduced volume. Many candidates listed oliguria as occurring with so-called pre-renal failure and then becoming polyuric with established renal failure. Only 2 answers noted that ability to concentrate AND dilute urine was impaired in most situations. Oliguria in renal failure does NOT mean the urine is concentrated, it simply reflects a much-reduced volume of glomerular filtrate and that small volume may hyper, hypo, or isotonic to plasma. The majority also incorrectly suggested that impaired tubular function would lead to Na and H2O loss and polyuria, whereas as GFR is progressively reduced then tubular function bears less and less relevance to urine volume. Hypovolaemia secondary to polyuria was mentioned more commonly than volume overload due to oliguria. As mentioned above, plasma osmolality rises, due to urea in the main. This does not lead to activation of humoral responses to decrease the osmolality because urea is freely soluble across cell membranes, i.e. an ineffective osmole.

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Many candidates wasted valuable time describing normal tubular function, or determinants of GFR. It was also not asked to describe causes of renal impairment, or to give a description of the renin-angiotensin-aldosterone axis. Only a handful realised that Creatinine levels reflect GFR, but that creatinine clearance and eGFR reflect changes better than blood levels alone. A large number of answers dwelt on glucose handling in the PCT, many saying that glycosuria at normal BGL‟s, and even hypoglycaemia, occur in renal dysfunction, because of alteration in Tmax for glucose. The opposite is closer to the truth- reduced filtration of glucose often leads to there being no glycosuria in the presence of significant hyperglycaemia. Too many candidates used vague statements like “alterations in electrolyte balance”, “build up of metabolic wastes” and “impaired acid-base balance”. Creatinine and creatine are not the same thing; Urea does not cause gout; and insulin is not used to measure GFR. The kidney produces ammonia to excrete acid, it is not the site of ammonia elimination, levels of which rise in hepatic failure not renal failure. QUESTION 12 Briefly explain the changes that occur in stored whole blood.

41% of candidates passed this question. Main Points expected for a pass: What is in stored whole blood How it is stored The biochemical changes The cellular changes Additional points could be gained for: The mechanisms of the changes in stored blood How the preservative solution prolongs blood storage Common problems: Illegible handwriting Poor layout and structure Many candidates were unsure about what the current preservative solution is and what the different components were for The main reason for failing this question was insufficient core knowledge QUESTION 13 Describe the autonomic innervation of the heart and the effects of autonomic

stimulation on cardiac function. 47% of candidates passed this question. Main points expected for a pass included: origins & pathways of efferent sympathetic & parasympathetic supply to the heart, including site of ganglia, neurotransmitters & receptors; and, effects of increased sympathetic & parasympathetic tone on heart rate, contractility, AV nodal conduction & coronary vasculature. This information could be effectively presented in tabular format. Additional marks were allocated for mention of: the reciprocal interaction between sympathetic & parasympathetic systems; prevailing tone at rest; and, effect of both systems on propensity to dysrhythmias. Further marks were awarded for indicating the time frame for onset & offset of autonomic effects; and, for explaining changes in automaticity and demonstrating this diagrammatically via the pacemaker potential. Mistakes commonly made included: spelling errors (particularly for inotropy, chronotropy, lusitropy) & failing to demonstrate an understanding of the meaning of such terms; and, poor legibility of key words. Credit was not given for vague, non-directional statements regarding autonomic stimulation, nor for pharmacological effects of drugs on the autonomic system. Many

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candidates included details of afferent limbs or baroreceptor reflexes of the autonomic system, neither of which was required. Furthermore, excessive detail on intracellular messaging systems was not rewarded commensurate with the time taken to write such information. QUESTION 14 Describe the factors that affect static respiratory system compliance. 36% of candidates passed this question. Basic information required included the following:

A definition of static compliance

Respiratory system compliance is determined by elastic forces in the lung and chest wall (rib cage and diaphragm)

Lung elastic recoil – comprises surface tension of alveoli (La Place‟s Law) and the elastic properties of lung tissue

The importance of surfactant

Lung size (child v adult) – compliance increases with increased size but specific compliance is unchanged

Lung volume – compliance is maximum at FRC and reduced at high and low lung volumes

Examples of disease processes (and direction of effect) that influence compliance – e.g. emphysema, pulmonary fibrosis, pulmonary oedema, pulmonary blood volume (but not blood flow), chest wall scarring, increased intra-abdominal pressure, obesity

Additional marks were given for:

Units and a normal value

The equation relating total with lung and chest wall compliance

Influence of posture

Effect of anaesthesia

Effect of gravity on regional lung compliance Graphs were commonly drawn but rarely provided additional information to that which was written. The effects of pregnancy hormones on chest wall compliance were often mentioned but the (opposite and greater) effect of the gravid uterus was ignored. Common mistakes included discussion of time constants, fast and slow alveoli, and airways resistance. Description of the measurement of compliance did not attract marks. QUESTION 15 Explain how cardiac output is measured using a thermodilution technique.

60% of candidates passed this question. Interpretation: This question asked for an explanation of a specific technique of measuring cardiac output. Not directly relevant are:

1) A detailed discussion on cardiac output and the factors affecting it

2) Other techniques of cardiac output measurement

3) Explanation on how a thermistor functions

Content: The main points in the answer should include:

1) A discussion of the basic principles involved.

Thermodilution is based on the law of conservation of matter where heat lost from the

blood = heat gained by injectate

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2) A description on the specifics of the technique mentioning the requirement of a Swan-Ganz

catheter, nature of injectate and temperature measurement using a thermistor in the

pulmonary artery.

3) An appreciation on how cardiac output is calculated from this technique

4) A discussion of sources of errors which might affect the accuracy of the technique

Errors or common mistakes: Some candidates erroneously conclude that cardiac output IS the area under the curve. Other candidates confuse the PiCCO as a thermodilution technique. Organisation: Better answers include a short list of advantages and disadvantages of the technique. Clarity: Good answers mentioned that the thermodilution technique is a variation of the indicator dilution technique which uses the temperature decrease as the indicator. Additional marks were given for a discussion on the Stewart-Hamilton Equation used to calculate flow/Q. QUESTION 16 Describe the processes whereby substances may cross cell membranes, giving

examples. 60% of candidates passed this question. The following were the main points expected in answering the question: Clear descriptions of the following mechanisms of transport across cellular membranes;

- Exocytosis and endocytosis

- Diffusion, with an appropriate explanation. Better answers included relevant application of

Fick‟s Law of Diffusion

- Movement through ion channels and aquaporins, with ion channel subtypes identified

- Carrier mediated transport, with discussion of facilitated diffusion, primary and secondary

active transport.

It was expected that relevant examples of each transport mechanism were included. Extra marks were awarded for a clear, well structured answer, with appropriate examples offered for key processes. Common errors included;

- Detailed discussions of diffusion mechanisms, with inadequate attention to other processes

- Incorrect or absent examples of key processes

- Describing facilitated diffusion as an example of active transport

- Confusing co-transport and counter-transport mechanisms.

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PHYSIOLOGY - VIVA SECTION PHYSIOLOGY TOPICS: 1) What is a normal PaO2 value?

2) What is a normal PaCO2 value?

3) What are the oxygen stores in the body?

4) What is the EEG?

5) Draw a lead II ECG.

6) What is TPN?

7) Draw a radial arterial pressure trace?

8) Describe the coronary circulation.

9) What are the functions of the liver?

10) What are the functions of the stomach?

11) What is the difference between heat and temperature?

12) What determines the arterial blood pressure?

13) What determines the flow of fluid through a tube?

14) Define the functional residual capacity of the lungs.

15) What is the Frank-Starling mechanism?

16) Describe the blood supply of the liver.

17) What does a pulse oximeter measure?

18) How could you measure gas flow?

19) What types of muscle fibres do you know?

20) Draw a CVP trace.

21) What is normal renal blood flow?

22) What are the causes of hypoxaemia?

23) Describe how CO2 moves from the mitochondria to the air.

24) What are the mechanisms of visceral pain?

25) What is sleep?

26) What is hypothermia?

27) What are the functions of the placenta?

28) Describe the muscle spindle.

29) Where do we find smooth muscle in the body?

30) What are the causes of hypercapnia?

31) Draw the flow of blood in the aortic root.

32) How does the cardiovascular system respond to haemorrhage?

33) Draw an action potential from a SA node cell.

34) What are the causes of hypoxemia?

35) How does the body handle potassium?

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36) What are the physiological effects of fasting for 48hrs?

37) What are the SI units?

38) What are the physiological effects of an increase in airways pressure?

39) Describe the fetal circulation.

40) Describe the valsalva maneuver

41) What is a colloid?

42) How can you be hypercapneic in the presence of a supernormal minute ventilation?

43) What is the range of urine osmolality?

44) Where does the body produce lactate?

45) What is the definition of afterload?

46) What is the definition of cardiac contractility?

47) What do you understand by the term „closing capacity‟?

48) Can you interpret this arterial blood gas result?

49) What is a transducer?

50) What are the functions of the thyroid gland?

51) How could you measure cerebral blood flow?

52) How much oxygen does the body use in a minute?

53) What is a hormone?

55) Describe the principles of the use of ultrasound in medical practice.

56) What are the physiological effects of aging on the cardiovascular system?

57) What are the physical mechanisms by which the body loses heat?

58) How does the body control ventilation?

59) Why don‟t you faint when you stand up?

60) What is a normal blood glucose level?

61) Describe the pulmonary circulation.

62) Draw a pressure volume loop for the left ventricle.

63) How does oxygen uptake increase with exercise?

64) Can you draw the action potential in a skeletal muscle?

Dr. C Noonan Chairman, Primary Examination Sub Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

JULY/SEPTEMBER 2009 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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 72% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Sevoflurane and fentanyl are a common anaesthetic drug combination. Discuss

pharmacological reasons why it is useful to use them together. 30% of candidates passed this question. This question required candidates to detail the beneficial uses and effects of combining sevoflurane and fentanyl. Most answers began with a brief description of each drug and its usual indications of use. The synergistic drug interaction was the primary focus expected. This included discussions about reductions in MAC, MAC-BAR, MAC-awake. Additional marks were awarded for specifying percentage reductions or proportionally greater reductions in MAC-BAR versus MAC-awake. Successful candidates were able to detail the beneficial consequences of this synergistic interaction, which primarily revolved around reduced drug doses of each resulting in reduced adverse effects. This included discussions about enhanced cardiovascular stability with airway instrumentation or surgical stimulation, reductions in sevoflurane adverse effects (hypotension, increased CBF/ICP, reduced uterine tone), and reductions in fentanyl side effects (prolonged sedation or respiratory depression, opioid induced nausea and vomiting). Some candidates were confused about the whether sevoflurane provided analgesia. Whilst sevoflurane in high enough doses can ablate responses to surgery via its global CNS depressant effect, it does not have a specific analgesic action. Bonus marks were awarded for discussion about the possibility of using fentanyl as a sole anaesthetic and the benefit of adding a volatile to an opioid based anaesthetic.

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QUESTION 2 What are the potential side effects of propofol and its formulations? 74% of candidates passed this question. Expected was a brief description of the clinical uses and the most common formulation of propofol. At this point candidates who performed well divided their answer to adverse effects due to propofol and those secondary to the formulation. Common cardio-respiratory effects of propofol were well described. That propofol resulted in sedation and anaesthesia was almost universally recognised but few commented on the narrow therapeutic window between the two. Again, most candidates identified excitatory movements with induction but fewer correctly described the mechanism or explained the contradictory EEG effects and the use of propofol for status epilepticus. Common side effects related to the formulation including pain, bacterial contamination, use of preservatives were well discussed. Metabolic effects from prolonged infusion including lipaemia, propofol infusion syndrome and the propensity to produce green coloured hair and urine was discussed by the majority. Few however mentioned alternative solvents including liposomes, medium chain triglycerides and cyclodextrins. That subclinical doses of propofol produce euphoria and explain the abuse potential unique to this drug also received a mark. Common mistakes were to discuss the pharmacokinetics of propofol, adverse effects related to the formulation only and beneficial central nervous system effects. QUESTION 3 Discuss classes of drugs that influence Post-Operative Nausea and Vomiting

(PONV) including mechanisms where known.

77% of candidates passed this question. Approaches to answering this question include choosing and naming a class followed by an example of the group, acting especially at which receptor, where known, followed by designating the location of action eg agents acting at D2 receptor at the chemoreceptor trigger zone. To add a comment specific to the agent named would then complete a discussion for each agent eg droperidol and the Q-T interval lengthening. Lateral thinking would include agent groups which often induce PONV eg opioids such as morphine acting at mu receptors in the area postrema increases the likelihood of PONV in a dose related manner. Quite rightly, mention of N20, volatiles, ketamine or ergometrine is relevant, as all are agents to which some of our patients are exposed.

The well known groups of 5HT3 antagonists, D2 antagonists including the benzamides to which metoclopropamide belong, formed the nucleus of agents discussed. The use of propofol, use of benzodiazepines and antihistamines all earned marks. Even the new group NK1 Antagonists received mention by quite a few candidates.

The responses which explained very clinical information or extensive dosage regimes or opted to

leave out naming classes of drugs deprived themselves of credit focussing on the question at hand. QUESTION 4 Describe the effect of obesity on pharmacokinetics and the potential clinical

implications, providing relevant examples. 45% of candidates passed this question. This was a question with which most candidates struggled, possibly because it required bringing together information from a variety of areas. Most candidates started off, appropriately, with a definition of obesity and then went on to point out that it was often associated with a range of other co-morbidities such as diabetes and gastric reflux. Then, possibly relying on clinical experience, candidates often remarked that in the obese patient FRC can be reduced, thus affecting uptake of volatile anaesthetic agents and that transdermal, intramuscular and subcutaneous drug absorption was also likely to be affected.

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Many candidates also mentioned that some computer based programmes for TCI could give variable results when actual (rather than lean) body weight was entered. However there were few instances where specific examples were given (as asked for in the question). Pharmacokinetic handling of some opioids are altered in the obese patient, and only a few candidates mentioned the possible pharmacokinetic advantages of poorly lipid soluble volatile agents such as desflurane over other volatile agents in the obese patient. With regard to non-depolarising muscle relaxant drugs, although their polarity generally restricts their distribution, volume of distribution may be increased in the obese, simply by virtue of increased absolute total body water. There will be differences in the distribution, and hence duration of action depending on whether dosage is calculated on the basis of ideal body weight or total body water. From a clinical context, obese patients are comprising an increasing proportion of our population, and candidates should be aware of how this condition influences drug disposition. QUESTION 5 Describe the factors that may decrease the clinical response to nondepolarising

neuromuscular blocking agents. 36% of candidates passed this question. Candidates were expected to briefly mention the important measurable clinical responses (eg. onset, depth and duration of neuromuscular blockade), and briefly mention how these might be measured. Candidates who classified factors into such groups as physiological, pathological, drug factors and drug interactions, with multiple examples usually scored well. Extra marks were awarded for noting that the clinical response depends on which muscle group is monitored, and that the clinical response is less intense and briefer in patients anaesthetised without volatile or sedated in critical care.

Some candidates mistakenly listed factors that contribute to prolongation of neuromuscular blockade (such as atypical plasmacholinesterase, aminoglycosides). Marks were not awarded for arguing that absence of these factors leads to a (relative) decrease in clinical response. Nonspecific pharmacokinetic statements (―clinical response is determined by differences in absorption, volume of distribution, protein binding and clearance‖) without clinical examples and explanation were not awarded high marks. There was general confusion about the effect of various muscle disorders on neuromuscular blockade.

QUESTION 6 Discuss the pharmacodynamics of drugs that affect uterine tone.

48% of candidates passed this question. Candidates interpreted this question in a variety of different ways. The marking scheme was structured so that it was possible to do well with any reasonable interpretation. As the question clearly relates to uterine pharmacology, however, some part of the answer had to pertain to the actions of the drug on the uterus. It was not possible to pass, for example, by writing an essay purely on the non uterine effects of volatile agents. A suitable approach would have been to list the common drugs which affect uterine tone, noting which increase and which decrease tone, and then to discuss the important drugs in more detail. Points which could be elaborated on include, a) the mode of action, b) the effect on basal tone and contractions, both force and frequency, c) how that effect varies with stage of pregnancy and dose of the drug, d) other actions on the uterus and cervix, e) important side effects—particularly those on the uterus, or those which might limit the drug’s use.

Common mistakes were to confuse smooth and skeletal muscle; beta agonists and beta blockers; ,

1 and 2 effects; and the effects of nitrous oxide, volatile agents and intravenous anaesthetic agents. Many candidates were unsure as regards the relationship between systemic vascular resistance, heart rate and blood pressure. Candidates often included unnecessary information on dosage, pharmacokinetics and usage. Vague answers attracted no marks.

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QUESTION 7 Outline the pharmacological management of ventricular fibrillation in an adult with reference to: drugs, dose, mechanisms of action, and potential adverse effects.

51% of candidates passed this question. Overall, the responses to this important question were disappointing. There was wide ranging depth and breadth of understanding of the pharmacological management of ventricular fibrillation (VF). The syllabus clearly states that candidates should be able to describe the international cardiopulmonary resuscitation guidelines, and also the pharmacology of adrenaline, vasopressin, amiodarone and lignocaine with reference to cardiopulmonary resuscitation; these areas of study should enable candidates to understand the pharmacological management specific to VF. A complete answer required that candidates address the drugs used for VF, and dose, mechanisms of action and adverse effects specific to VF, and understood the role of these in current international and local VF management guidelines. Description of the role and current use of adrenaline, amiodarone, vasopressin, lignocaine, magnesium and bicarbonate were expected. Few mentioned the specific role and supporting evidence for each agent in VF resuscitation algorithms. Additional points which attracted higher marks included specific indications for each agent in VF, alternate routes of administration with dosages, understanding of current controversies in medication selection, and management of VF in specific clinical scenarios, for example, local anaesthetic toxicity with VF. In general, there was poor understanding of the mechanisms of action pertinent to resuscitation from VF, of drug dose and timing regimes in this clinical situation, and of adverse effects of acute administration. There was great variability in dosage regimes. Common mistakes included misinterpretation of the question as general resuscitation for cardiac arrest with inclusion of drugs such as atropine, and excessive focus on details of defibrillation and basic CPR technique with little information on pharmacological therapy. QUESTION 8 Mean arterial blood pressure has been measured in two groups of patients one

hour after the administration of either a placebo or an antihypertensive drug. Explain how these data could be analysed.

35% of candidates passed this question.

This question examined basic knowledge regarding the ways in which data from two groups of subjects is evaluated and then compared using statistical testing. The question required that candidates apply their knowledge Points that attracted marks included:

a) Discussions regarding the determination of a hypothesis and its relation to the aim of the research: to disprove the null hypothesis (of no difference between groups)which indicates that the medication may influence blood pressure in a significant way.

b) Detailed characterization of the data into numerical, ratio, discrete or continuous

depending on how it was measured, its distribution and ways of analysing the data if its distribution were not clear on first evaluation. Marks were also given if candidates discussed other ways of organising data to allow evaluation by other types of statistical tests e.g. categorical by conversion of blood pressure measurements into discreet categories

c) Attempts to identify study and data characteristics in the best way possible to select most

accurate test to evaluate hypothesis. Note that all such information was not given with the blood pressure readings allowing candidates to discuss different contingencies and different

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tests which may be used. Mentioning characteristics such as independent measurement, normal distribution, similarity of variances, number of observations etc.

d) Finally the tests which could be used to evaluate the data as well as their specific characteristics : Students –T for parametric, Mann Whitney U and Wilcoxon signed ranks for non-parametric.

e) A brief description of the way the test was evaluated and the conclusions drawn from the

result. f) The creation of and use of confidence intervals to indicate clinical significance.

The most common mistakes involved misinterpretation of the question with detailed discussion of conduct of randomized controlled trials, power analysis, and use of contingency tables to determine specificity and sensitivity. Lack of application of knowledge to the specific example of the blood pressure readings was also a common characteristic of many answers.

PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS: Pharmacokinetics and pharmacodynamics:

1. Placental transfer of drugs 2. Drug handling in liver failure 3. Pharmacokinetics of phenytoin 4. What drugs are administered by infusion? 5. Draw dose- response curve for morphine 6. Tell me about remifentanil 7. Pharmacokinetics of propofol 8. Factors affecting effect site concentration 9. Draw a dose – response cure.

Inhalational Agents:

1. Physical properties of isoflurane 2. FA/FI curve 3. Compare sevofluorane and desflurane 4. Sevoflurane in patients with heart disease 5. How do you define MAC? 6. Metabolism of the volatile anaesthetic agents 7. How does the addition of nitrous oxide affect the uptake of sevoflurane? 8. What are the advantages and disadvantages in using nitrous oxide? 9. Wash in curve for isoflurane. 10. How are inhaled anaesthetics removed from the body?

Intravenous Anaesthetic Agents:

1. Metabolism of benzodiazepines 2. Classify I.V. induction agents 3. Draw a concentration-time curve following an I.V. injection of propofol.

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Local Anaesthetics:

1. Local anaesthetic toxicity 2. What is ropivacaine? 3. Structure – Activity Relationships of local anaesthetics

Pain:

1. NSAIDS and drug interactions 2. Adverse effects of NSAIDS 3. Structure & function of opioids 4. Opioid agonists & antagonists 5. Where does morphine come from? 6. What kind of drug is aspirin? 7. What are the advantages of paracetamol? 8. Where does morphine act? 9. Epidural morphine 10. Tramadol and its effects 11. What are some of the advantages of tramadol as an analgesic?

Neuro Muscular Blocking Drugs and associated topcis:

1. What things can increase the response to NMB’s? 2. Side effects of suxamethonium 3. Adverse effects of atropine 4. Atropine versus glycopyrrolate 5. Classification of anticholinesterase 6. Mechanism of action of anticholinesterase agent 7. Reversal of NMB 8. Compare vecuronium and rocuronium 9. What sort of drug is neostigmine? 10. What is meant by the term ―depolarising blockade‖? 11. How do you classify anti-cholinesterase agents? 12. Side effects of suxamethonium.

Autonomic Nervous System:

1. Draw a muscular cholinergic receptor 2. Naturally occurring sympathomimetic drugs 3. Structure activity relationship of sympathomimetic amines

Neuropharmacology:

1. What is GABA? 2. How do anticonvulsants work? 3. Pharmacokinetic of serotonin

Therapeutic Gasses:

1. Oxygen Toxicity 2. Diffusion hypoxia 3. Oxygen as therapeutic gas

Coagulation:

1. What sort of heparin do you know of? 2. What are the main group of anti-platelet agents? 3. Heparin & Protamine

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4. What is protamine? 5. What is heparin?

Miscellaneous:

1. Aspirin toxicity 2. Outline the drug treatment of anaphylaxis. 3. What are some members of the H2 antagonist group? 4. How do you classify corticosteroids ? 5. What is meant by the word ―addiction‖? 6. What is the appropriate dose of paracetamol? 7. What are the contents of a Hartmann’s solution? 8. Describe the phases of clinical drug development.

Statistics

1. Normal distribution 2. Meta analysis 3. Clinical trial 4. Randomisation in clinical trials – both signs and symptoms must be present or this can be

diagnose. 5. What is meant by the term ―power‖ in statistics? 6. What is meant by the term sensitivity & specificity?

Opioids and analgesics:

1. What are the features of opioid overdose? 2. What are the options to manage opioid induced constipation? 3. What is the cause of differences in speed of onset between fentanyl & alfentanil? 4. Concentration time curve for alfentanil? 5. What the first role of ketamine in pain management? 6. What is the base of ketamine to use in pain management as approach to anaesthetic dosage? 7. What are the adverse reactions associated with ketamine?

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 61% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Classify the causes of hypotension in the early post-operative period, giving

relevant examples. 37% of candidates passed this question. The minimum requirement to pass this question was to discuss the causes of hypotension and to provide at least one example relevant to the postoperative period. Most successful candidates classified the causes of hypotension by physiological mechanism (reduction in systemic vascular resistance or cardiac output). This provided a logical framework to discuss the relevant causes of reduced preload, contractility, heart rate and systemic vascular resistance. Provided that these areas were covered adequately, those candidates who provided a clinical classification of the causes of postoperative hypotension were also successful. Few candidates correctly defined hypotension as a 20% fall in the patient’s mean or systolic blood pressure or commented on its significance. Detailed descriptions of differing clinical situations producing hypotension by the same mechanism (eg. causes of hypovolaemia) did not attract extra marks. QUESTION 10 Compare and contrast the neonatal respiratory system with the adult. 36% of candidates passed this question. The neonatal period is from 0-28 days and this question predominantly concerned term neonates. This is not a question about the transition from intra- to extrauterine life nor is it a question about the pathophysiology of prematurity. This is a wide ranging question concerning many aspects of respiratory physiology:- physiologically relevant anatomy; ventilation and gas exchange; lung volumes; mechanics of breathing; pulmonary circulation; control of breathing; and haemoglobin. The low pass rate resulted from most candidates not producing enough relevant detail in each of these areas. Differences and similarities are both absolute (neonates are small) and relative (values indexed to weight or FRC). Mention of clinical implications gained extra marks. Well organised answers were frequently in a table form. QUESTION 11 Describe the role of insulin in fat metabolism

36% of candidates passed this question. The following were the main points expected for a pass: description of insulin and its actions as an anabolic hormone, and consequences of activation of

insulin receptors, the effects of insulin on liver: increased uptake glucose; production of glycerol and free fatty

acids; and decreased ketogenesis, the effects of insulin on adipose tissue: glucose uptake; synthesis of fatty acids and glycerol

and the activation of lipoprotein lipase and inhibition of hormone sensitive lipase.

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Bonus marks were given for a structured approach to insulin’s action in fat metabolism, key enzymes involved in liver and adipose tissue, lipoprotein transport in blood and breakdown and uptake by adipose tissue. Common mistakes included: only focusing on one of the following: fat uptake from gut, fat synthesis in liver or adipose

tissue, or the role of increased glucose uptake; confusing anabolic and catabolic actions, providing information about actions of other hormones, providing information about diabetes and carbohydrate metabolism while neglecting to cover

fat metabolism.

QUESTION 12 Discuss the production and function of red blood cells

48% of candidates passed this question. Candidates who did not address both parts of the question were unlikely to pass, as approximately half the marks were awarded for each part of the question. RBCS are derived from a common precursor in the bone marrow and liver in adults This precursor is a pleuripotential cell ie can differentiate into all blood cell lines. It differentiates into various cell lines, including the Colony-Forming-Unit Erythrocyte (CFU-E), which is stimulated by various colony stimulating factors to differentiate into smaller and smaller cells. Haemoglobin concentration increases as differentation continues. Marks were obtained for correctly detailing actions and production of erythropoietin; the structure of haemoglobin, and other structural factors unique to RBCs (eg lack of nucleus and mitochondria). The function of the RBC is related to its content of haemoglobin. RBCs transport oxygen and carbon dioxide, and have a major role in the buffering capacity of the extracellular fluid. Candidates were expected to briefly outline how the cells carries out these functions. Common errors included mention of: "half life of RBCs as 120 days" - rather than average life span "myeloid stem cells" rather than erythroid. Giving numerical ranges for Hb levels - but listing it as the RBC count. reticulocytes having a nucleus - they do not QUESTION 13 Explain the physiological processes that cause oliguria in response to

hypovolaemic shock 64% of candidates passed this question. This is the fourth time that this question has been asked. The main points would be: a brief definition of oliguria and of hypovolaemic shock followed by an appreciation that oliguria occurs secondary to two main effects, namely a decreased RBF and GFR and an associated increased sodium and water retention. Subsequent explanation as to why the RBF and GFR drop and the neuro-endocrine responses occasioning the sodium and water retention would result in a good pass. The answer would include a brief discussion of the systemic influences on RBF and GFR as well as a description of the role of the sympathetic system, the Renin-Angiotensin-Aldosterone system and of ADH on salt and water homeostasis. Additional marks were rewarded for a mention of renal autoregulation, differential afferent and efferent arteriolar effects, effects of ACTH and ANF and the effects of age. Only two candidates mentioned the possibility that this situation could progress to acute renal failure.

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A frequent error was to state that afferent constriction was greater than efferent. Many answers gave incorrect values for the range in which renal autoregulation is seen, believing it occurs down to a MAP of 50 mmHg. Better answers demonstrated a structured and methodical approach to answering the question with minimal repetition. Some of these answers were in narrative form, others in a graphical format. Correct information, appropriately structured was rewarded regardless of the format chosen to answer the question. The main reasons for candidates not passing this question were either poor organisation, repetition of information or just not enough substance in their answer. QUESTION 14 Outline the central nervous system effects on an awake person breathing air

containing carbon dioxide. 42% of candidates passed this question. Good answers included several effects including stimulating central respiratory centres, increased cerebral blood flow, increased intracranial pressure, and stimulation of the sympathetic system. Other points were that inspired air has negligible amounts of CO2 and that high partial pressures can produce CO2 narcosis. QUESTION 15 Describe the complement system.

57% of candidates passed this question. The examiners were aware that there were several different descriptions of complement pathways in different textbooks, and marking schemes reflected these variations. In order to achieve a pass, candidates required a broad knowledge of the actions of complement and the pathways by which these actions are initiated. Further marks were obtained for more detailed descriptions of the pathways, and clinical implications of the actions of complement. Additional marks were given for clinical relevance of abnormalities in the pathways. Common omissions included a lack of knowledge or understanding of the actions of complement, and the methods of activation. Although additional marks were awarded for a detailed description of the complement cascade, it was possible to achieve a high mark without this information as marks were weighted towards demonstrating an understanding. QUESTION 16 List the gastric cell types and their secretions and the functions of these

secretions. 72% of candidates passed this question. In general this was quite well answered. Many candidates had well structured answers which enabled easy marking. Candidates who did poorly were less organised and many candidates confused the secretions and the cells which decreased their overall score. Some candidates did not answer all parts of the question and this was reflected in their mark. Other poor strategies included writing detail which was not required and repeating the same statements.

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PHYSIOLOGY - VIVA SECTION PHYSIOLOGY TOPICS: Cardiovascular: Changes in the cardiovascular system with exercise. Coronary blood flow. Oxygen flux in coronary circulation Cardiovascular effects of aging on arteries. Relationship of VR to CO Measurement of contractility Wigger’s diagram Frank-Starling mechanism Control of regional circulations LA volume vs. time Afterload: definition and measurement Contractility: definition and measurement Respiratory: Respiratory mechanics Alveolar gas equation Effect of altitude on alveolar oxygen content Control of pulmonary blood flow Mixed venous blood gases Factors affecting pulmonary vascular resistance Factors affecting airway resistance Changes in upright lung Dynamic airway compression Changes in oxygen saturation with aging Oxygen flux V/Q changes in lung in upright posture Oxygen stores in the body Oxygen cascade Dead space and effect on blood gases Measurement of FRC Closing volume A-a gradient Control of ventilation Nutrition/Metabolism: Efficiency of anaerobic vs. aerobic metabolism Consequences of fasting Glucose homeostasis Principles of total parental nutrition Basal metabolic rate Thermoregulation: Effect of general anaesthesia on temperature Comparison of heat and temperature

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Renal: Renal handling of water Renal handling of metabolic acid Define GFR and how measured Physiological effects of renal dysfunction Principles of glomerular filtration Measurement: Measurement of intracellular water What is a transducer? Calibration of arterial line Describe a capnogram trace Principles of non-invasive blood pressure measurement Describe the principles of pulse oximetry Utility of pulse oximetry Utility of ECG Role of the balloon in a PAFC. SI units, examples of derived units. EEG Measurement Principles of temperature measurement Principles of CO2 measurement CNS: Principles of cerebral blood flow Autonomic nervous system anatomy Blood- brain barrier Nerve: Classification of peripheral nerves Nerve action potential Changes in autonomic nervous system with aging Endocrine: Hormones of the posterior pituitary Physiological roles of prostatglandins Classes of hormones and their actions. Muscle: Cellular anatomy of skeletal muscle Skeletal muscle contraction Liver: Laboratory assessment of hepatic function Immunology: Defence against bacterial infection Specific and non-specific immunological defence mechanisms Classification of hypersensitivity reactions.

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Pain: Acute pain pathways Obstetric: Changes in cardiovascular physiology during pregnancy Changes in respiratory physiology Haematology: Preparation of stored blood Changes associated with stored blood Role of platelets in clotting Fluid & electrolytes: Distribution of water in the body. Interpretation of blood gases Role of calcium in the body Acid- Base: Handling of metabolic acid load Assessment of acidosis

Dr. C Noonan Chairman, Primary Examination Sub Committee

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Page 110: Primary Exam Reports 2011 to 1999

10/07 11.1.2.2

Australian and New Zealand College of Anaesthetists

ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

JULY/AUGUST 2007

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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 79% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Describe the adverse effects that may occur with the administration of

desflurane. 61 % of candidates passed this question. Answers formulated around the adverse effects of desflurane on various organ systems achieved most marks. Marks were not awarded for provision of pharmacokinetic data and structural formula. Discussion of the need for a special vaporiser because of desflurane's low boiling point was correct but did not answer the question. It was important to mention basic physiological changes and not focus on the unique adverse effects of desflurane. For instance virtually all answers mentioned desflurane's pungency but many failed to discuss its respiratory depressant properties. A reduction in minute ventilation is manifested by reduced tidal volume and increased respiratory rate. Many mentioned tachycardia with increased inspired concentrations of desflurane but only a minority correctly teased out cardiovascular changes. Volatile anaesthetic agents typically result in cerebral vasodilaltion with a rise in ICP. In this regard desflurane is no exception though changes are less significant. Many answers however stated that ICP falls with desflurane. Carbon monoxide production from carbon dioxide absorbents was mentioned by most but only half correctly stated that desflurane is a trigger for malignant hyperthermia.

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Other points for a complete answer were hepatotoxicity, minor renal effects, uterine relaxation and activation of the sympathetic nervous system with rapid increases in desflurane concentrations. QUESTION 2 Outline the important pharmacological considerations when stopping

warfarin and commencing prophylactic (low dose) low molecular weight heparin (LMWH) in the peri-operative period.

22% of candidates passed this question. Candidates generally performed poorly on this question. Often mainly warfarin or LMWH were discussed with little discussion of the other drug. Unfractionated heparin was frequently discussed. Better answers included an introduction outlining the issues of balancing the risks of thrombo-embolism Vs bleeding and a summary of the relevant pharmacology of warfarin and LMW heparins. An outline of the relevant pharmacology is summarised below. This degree of detail was not required for a pass. The summary is provided to assist candidates with future exam preparation. Warfarin Long acting agent, inhibits Vit K reductase production of Factors 2,7,9,10,Protein C,S Metabolised in liver, low clearance, T 1/2 40 hrs Thus clearance of warfarin and resynthesis of new factors 2,7,9,10 required for offset Approximately 3-5 days required for offset Warfarin action potentially prolonged in; Decreased warfarin metabolism- liver impairment, cytochrome inhibition e.g. amiodarone, fluconazole, metronidazole Decreased synthesis of clotting factors- liver impairment, Vit K deficiency, cephalosporins Check INR day before surgery Small dose Vit K, e.g. 1mg can reverse but potential problems with warfarin effect post op FFP will reverse but risk with blood products Recommence after surgery when minimal risk of surgical bleeding May be initially hyper coagulable due to inhibition of protein C,S (endogenous anticoagulants), thus continue LMWH until INR therapeutic LMWH Activates anti-thrombin 3, inhibits factors 10 and 2 but much greater inhibition of Factor 10 Commence 2-3 days after warfarin ceased Predictable and reliable, doesn’t require monitoring, once daily administration due to longer T1/2 compared to heparin S.C admin, high bio-availability, at home administration feasible Prophylactic dose enoxaparin 40 mg daily, dalteparin 5,000 units daily Decrease dose in renal impairment, renally excreted Last prophylactic dose minimum of 12 hours before surgery, neuraxial blockade QUESTION 3 Outline the important pharmacological considerations concerning

choice of opioid and dosage when converting from intravenous morphine to oral opioid analgesia in the post-operative period.

48% of candidates passed this question. The question asked about the science behind our choice and dosage of oral opioids. The other information in the question was that the patient had been on intravenous morphine in the post-operative setting.

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Good answers covered the rationale of what drugs we use, how and when we use them and why. Patient factors included the fact that acute pain is usually diminishing, the importance of the oral route and gut function returning, patient illness, type of surgery, age and previous opioid use. Dosage of the drugs can be calculated from intravenous morphine requirements in the previous period, usually using a prn (as required) dosing schedule and erring on a lower conversion dose and longer dosing interval for safety. Use of adjuvant drugs such as paracetamol and NSAIDs reduces the dose of opioid and use of sedative drugs increases the risk of side effects such as respiratory depression. Many candidates answered the question using a template; Pharmaceutics / Pharmacokinetics / Pharmacodynamics. In many cases it was possible to change the word “opioid” to any other drug and still have a correct statement. However, if this did not answer the question, no marks were awarded. QUESTION 4 A new test called the “intubation score” has a reported 90% sensitivity

and 70% specificity when used to predict difficult intubation. Describe how this information and other statistics related to this test can be used in predicting difficult intubation. How will the incidence of difficult intubation affect the performance of this test?

43% of candidates passed this question. This question asks candidates to apply knowledge of statistical analysis related to screening tests. It guides the candidates to discuss “intubation score” in relation to reported sensitivity and specificity and asks how “disease incidence” effects test performance. Answers that provided definitions of sensitivity, specificity, positive and negative predictive values with reference to predicting difficult intubation and described the relationship between incidence and testing achieved a pass. This was most easily achieved through reference to a contingency table, which highlighted possible outcomes of diagnostic testing. Clarification of each cell in the table attracted marks, for example the situation of positive prediction in the presence of difficult intubation being described as a true positive. Finally a definition of incidence and its influence on positive and negative predictive value was needed. Errors that were evident included confused, incomplete answers and answers that did not make reference to the scenario of difficult intubation. Some were answered incompletely or the question was misinterpreted. QUESTION 5 Describe the factors which increase the risk of systemic toxicity with

amide local anaesthetic agents. 37 % of candidates passed this question. The focus of this question was on CVS and CNS toxicity related to excessive serum plasma levels of drug. Successful candidates structured their answers along pharmacokinetic and pharmacodynamic factors. Concise descriptions of pharmacokinetic factors such as dosage limits, site of administration and rate of administration vs clearance were expected. There appeared to be confusion regarding how pH/pKa applied to toxicity. Marks were awarded for describing how weakly basic drugs with a high pKa would become more ionized and potentially “trapped” in

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acidic environments. This would exacerbate myocardial toxicity in cardiac arrest or other causes of acidosis. At times, the role of plasma protein binding was not clearly explained. Reductions in plasma protein binding via displacement or reduced production would have greater proportional effects on the unbound levels of highly protein bound drugs. The role of changes in volume of distribution was commonly omitted. This would apply in situations such as cardiac failure or the elderly. Succinct descriptions of why certain amides had greater risk of toxicity were expected, e.g. Na channel affinity, lipid solubility, duration of action, lack of vasoconstrictive properties. Commonly, there was confusion between amide and ester local anaesthetics. Marks were awarded for descriptions of a scale of toxicity vs. specific plasma levels and relating it to CVS:CNS toxicity ratios, but general descriptions of local anaesthetics and their mode of action did not accrue any marks. Extra marks were awarded for describing the role of isomers, specific drug interactions, and the role of various physiological factors (pregnancy, neonate, elderly) and pathological factors (tachycardia, electrolyte disturbances, hypoxia, hypercarbia). QUESTION 6 Describe how suxamethonium produces neuromuscular blockade. What

is the mechanism of recovery of neuromuscular function and what mechanisms may be involved in Phase II block?

75% of candidates passed this question. In general this question was well answered. In order to gain maximum marks it was important that candidates specifically answered the three parts of the question i.e. mode of action, mechanism of termination of effect and the mechanism of Phase II block. Most candidates explained the salient features of the ion channel comprising the Ach receptor at the neuromuscular junction (NMJ) and the role of the alpha sub-units. There was some confusion as to why the post-junctional membrane remained resistant to further depolarization by Ach, but most correctly stated that this is because it remains in a continual state of suxamethonium induced inactivation. With regard to termination of action the main error was to suggest metabolism of suxamethonium by pseudocholinesterase at the NMJ. Pseudocholinesterase is not found at the NMJ - the main route of termination of action is simple diffusion away from the NMJ into the plasma following its concentration gradient. With regard to the mechanism of Phase II block it is acknowledged that this can’t be stated with certainty. However, the recommended texts suggest at least four mechanisms that could be involved and points were awarded for mentioning any of these. Unfortunately many candidates spent a great deal of time writing about how a Phase II block can be produced clinically and the means by which it can be identified using the nerve stimulator. QUESTION 7 Outline the mechanisms of action and potential adverse effects of the

oral hypoglycaemic agents. 47% of candidates passed this question. A discussion of the two main groups and their side effects achieved a pass. Sulphonylureas act at potassium ATPase ion sensitive channels in the beta cells resulting in depolarisation and increased calcium concentration which causes increased insulin release. The biguanides decrease hepatic and renal gluconeogenesis, decrease glucose absorption from the gut and increase glucose uptake. Side effects were well described. The propensity for hypoglycaemia will vary amongst sulphonylureas depending on their clearance and site of metabolism along with liver or renal

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pathology. The basis of lactic acidosis with biguanides needed some mention of the action of the drugs at mitochondrial membranes and the increased risk in renal, hepatic impairment and states of decreased perfusion. Other points worth mentioning relate to the degree of protein binding with resultant displacement of other highly bound drugs e.g. warfarin and the potential for altered drug activity, some agents cross the placenta – causing fetal hypoglycaemia and the theoretical potential for inhibition of ischaemic and pharmacological pre-conditioning with sulphonylureas. Many candidates outlined the mode of action and side effects of the meglitinindes and thiazolidinediones. They were rewarded for their knowledge. QUESTION 8 Write short notes on anti-hypertensive drugs that exert their action via

blocking the effects of angiotensin. 73% of candidates passed this question. The core answer required a brief account of the two main classes of drugs (angiotensin converting enzyme inhibitors and angiotensin receptor blockers) that block the effects of angiotensin, including their mechanism of action, clinical use, side effects and essential differences between the two classes of drugs. There was a very broad spread of marks. This was the last question in the exam and a number of candidates gave very brief answers. Some candidates also gave detailed accounts of the physiology of the renin-angiotensin system without explaining how or where in the system these drugs work or what their effects are. Vague statements such as, side effects include electrolyte disturbances, the drugs decrease BP without explaining how, that the drugs have differing half lives or the drugs cause ventricular remodelling without explaining when this is useful do not contribute much to answers. The most frequent omission was any account of when these drugs are used clinically.

PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS: General topics

• Pharmaceutics; thiopentone, lignocaine, propofol, solubility, emulsions • Pharmacokinetics; absorption, bioavailability; hepatic clearance; renal drug handling,

pharmacokinetic modelling, clearances, volumes of distribution, context sensitive half time, variability with age

• Tolerance • Hepatic biotransformation • Dose response

Inhalational agents

• Induction kinetics • Recovery • Washout curves • Inhalational depth • Measurement of depth • MAC; MAC awake • Structure-activity relationships • CNS effects • Metabolism, toxicity • Physical properties

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Local anaesthetics

• Structure activity • Physicochemical properties

Induction agents • Factors affecting induction dose and maintenance infusion rate • Propofol pharmaceutics • Propofol pharmacokinetics • Propofol pharmacodynamics • Mechanisms of action • Ketamine, mechanism of action, pharmacodynamics, adverse effects

Neuropharmacology • Anti-convulsants, classification, mechanisms of action, phenytoin, barbiturate,

benzodiazepine pharmacology • Benzodiazepines, midazolam pharmacology

Neuromuscular blocking agents • Factors affecting clinical choice and dose • Compare rocuronium and vecuronium • Neuromuscular monitoring • Inter-individual variability • Factors effecting onset • Non-depolarisers, mechanism of action • Recovery, drug interactions

Anticholinesterase and anticholinergics

• Classification • Mechanism of action • Compare anticholinesterases • Compare anticholinergics

Opioid agonists and antagonists

• Classification • Mechanism of action • Receptors • Factors effecting clinical choice and dose • Compare fentanyl, alfentanyl, remifentanil • Tramadol

Pain and NSAIDs

• NSAIDs, MOA, classification, adverse effects • Aspirin • COX 2 inhibitors • Paracetamol

Cardiovascular drugs • Anti-hypertensive agents • Catecholamines • Vasopressors • Alpha 2 agonists • Antiarrhythmics; classification, amiodarone, digoxin, adenosine, adverse effects

• Drug therapy of myocardial ischemia • Anaesthetic agents and cardiac output

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Diuretics • Classification • MOA • Loop diuretics

Drugs and coagulation

• Anti platelet drugs, MOA, adverse effects • Aspirin • Clopidogrel • Glycoprotein IIb/IIIa receptor antagonists

Statistics

• Data type • Clinical trial design • Power • Drug development and trials • Selection of appropriate statistical tests • Students T test • Correlation • Evidence based medicine

Obstetric pharmacology

• Placental drug transfer • Fetal adverse effects • Tocolytics • Oxytocics; adverse effects

Miscellaneous topics

• Drugs and gastric acidity • Metoclopramide • Insulin • Intravenous fluids, clinical choice, pharmacokinetics and dynamics • Serotonin and drug action, serotonin syndrome

PHYSIOLOGY – WRITTEN SECTION MULTIPLE CHOICE QUESTIONS:

72% of candidates achieved a pass in this section of the Physiology Examination.

SHORT ANSWER QUESTIONS:

QUESTION 9 Briefly explain the cardiovascular responses to central neural blockade. 42% of candidates passed this question. To achieve a pass, candidates were expected to describe the effects of sympathetic blockade on arterial and venous vessels, how these lead to a drop in cardiac output and blood pressure, and compensatory reflexes involving the various baroreceptors and atrial naturetic peptide. Explanations should have included effects of potential α and ß blockade, and the fact that venodilation (venous side contain 75% of blood volume) and consequent decreased venous return is more significant than vasodilation. Many candidates failed to explain why hypotension is more

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pronounced with ascending block height, and/or effects seen with blockade of cardio-accelerator fibres (T1 – 4). Additional marks were allocated for explaining: - Effects of sympathetic blockade at different levels e.g.

Sacral blockade alone – little effect as parasympathetic fibres involved only; lumbar blockade vs high thoracic blockade “high” block affecting brainstem;

- Mid-thoracic block and renal compensatory mechanism to increase blood flow via JG cells (and not an increase in sympathetic outflow from brainstem vasomotor centre as described by a number of candidates);

- Possible contribution of Bezold-Jarisch reflex; - Afferent/efferent nerves and central control response of high and low pressure baroreceptors; - Consequences of age, hypovolaemia. Answers describing “vasodilation” were read as meaning arterial dilatation alone. Detailed descriptions of drugs or techniques used to attain an epidural/spinal block did not attract marks. QUESTION 10 Briefly describe the factors that affect the partial pressure of carbon

dioxide in mixed venous blood. 38% of candidates passed this question. The partial pressure of carbon dioxide in mixed venous blood depends on the carbon dioxide content of the blood and represents a balance between CO2 production in the tissues and content in the arterial blood. Good answers demonstrated an understanding of this and provided details about these aspects The partial pressure is related to the content by the carbon dioxide dissociation curve the position of which is determined by the state of oxygenation of haemoglobin, the Haldane effect. Carbon dioxide is present in the blood in three forms, dissolved, bicarbonate and carbamino compounds. Carbon dioxide production is related to aerobic metabolism in cells and the total production is defined by the metabolic rate. Production may be increased (e.g. exercise, fever, MH, pregnancy) or decreased (e.g. anaesthesia, hypothermia). The partial pressure of carbon dioxide in mixed venous blood is related to the pressure or content in arterial blood. This is determined by alveolar ventilation and normally controlled by chemoreceptor and the brainstem respiratory centre. Other relevant material included definitions of mixed venous blood, normal values, the effect of temperature and cardiac output. The most common error was discussing PCO2 without making it clear whether it was venous or arterial. The Fick equation was often used but required “solving” for CvCO2 to demonstrate the factors or importance to this question. QUESTION 11 Explain the physical principles of ultrasound imaging. 60% of candidates passed this question.

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Main points expected: Definition of ultrasound and range of frequencies. Principle of ultrasound genesis, tissue passage and reception (piezoelectric crystal understanding) Mention of acoustic impedance (density and sound velocity), reflection (intensity related to degree of differences in tissue density, latency related to depth). Appreciation of relationship between velocity, frequency and wavelength. Ability to correctly describe relationship of wavelength (or frequency) regarding penetration versus resolution. Extra marks: for mention of Doppler mode and correct description of Doppler effect. Doppler equation was awarded points where the values were correctly explained. Ability to calculate cardiac output was only credited when the principle behind the calculation using Doppler and M Mode to calculate area of aortic valve was explained. Simple statements such as Doppler can be used to measure cardiac output scored no marks. Definition of attenuation and thus need for gel at air/tissue interface Understanding that 2D pictures require an array of crystals Common mistakes: Incorrect formulas Incorrect statements such as Doppler is used to measure flow followed by the equation which is solving for velocity. M mode is used for 2D or 3 D or 4 D! imaging. Many candidates spent wasted time listing advantages and disadvantages (not asked for and not worth any marks). Others spent too much time drawing sine waves with amplitude, wavelength and frequency and not enough time discussing the relationship between these. QUESTION 12 Outline the mechanisms by which the kidney maintains potassium

homeostasis. 25 % of candidates passed this question. Main points expected for a pass included an outline of how potassium is handled as the glomerular filtrate passes along the nephron and a brief appreciation of the mechanisms of secretion and reabsorption of potassium. Additional marks were allocated for more detail on the actual cellular mechanisms for secretion and the cellular processes that are influenced by aldosterone. The most common reason for not passing this question was the lack of any structure and a paucity of relevant information. Very few candidates appreciated that reabsorption of potassium is fixed and that altering potassium secretion is the regulatory process. Credit was not given for elaborate discussions of the determinates of glomerular filtration or for detailed descriptions of the systemic control of aldosterone secretion. QUESTION 13 Outline the physiology of blood groupings that allows O negative blood

to be safely transfused to most patients.

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34% of candidates passed this question. Interpretation: The question specifically asked about physiology of blood groups Discussion about type, screening or cross-match were not directly relevant. Points to be covered: Statement of aims of transfusion and usual problem of previously formed recipient antibodies reacting against donor cells, and consequences thereof. Discussion of ABO system and origin of antibodies. Discussion of Rh system and origin of antibodies. Better answers: Mentioned issue of donor antibodies and recipient cells, other potential antigens and antibodies. Clarity: The terms antigen and antibody appeared to be frequently confused. Sources of antigen and antibody were often unclear. Errors: Some candidates’ essays were unclear about whether groups A,B and O have antibodies. There are no anti-AB antibodies. Expression of an antigen is associated with tolerance and prevents development of an antibody. Anti-A and anti-B antibodies are developed in early childhood and do not require blood exposure. QUESTION 14 Describe the cardiovascular changes in the neonate that occur at birth. 35% of candidates passed this question. Interpretation: The question asked for a description of changes; this potentially allows inclusion of a functional description, mechanism of change (where known), time course and consequences. Discussion of changes at birth does not include the gradual replacement of HbF with HbA. Points to include: A discussion of the changes as above. Better answers: Indicated the above and showed the relevance of the changes. Included comments about the transitional nature of some changes Clarity: Diagrams were often of poor quality, and thus unhelpful. Information in diagrams was often repeated longhand in written form (gaining no extra marks). Handwriting was sometimes illegible. Organization: Ten minute questions probably don't require planning notes in the margin, nor should summaries be included, as repetition will not gain extra marks. Highlighting of key points is not part of a traditional SAQ. Errors:

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Terminology was often loose and the sequence of changes and mechanisms was poorly described. Confusion in the use of the terms; flow, pressure, resistance and volume was common. The placenta is NOT the reason that the foetal circulation is described as parallel. The pulmonary circulation initially has high resistance. The high negative pressure at inspiration is NOT the direct cause of the fall in PVR. The ductus arteriosus does not connect the right ventricle to the aorta, neither does the ductus venosus connect the IVC to the brain. QUESTION 15 Outline the clinical laboratory assessment of liver function. 19% of candidates passed this question. This question is taken directly from the syllabus objectives and it was important to have a structured answer to cover all the main points. Suggested structure.

1. Synthetic function 1.a. Prothrombin ratio (acute injury) 1.b. Albumin (chronic) 1.c. Bilirubin formation (conjugation / jaundice / haemolysis)

2. Hepatocellular injury

2.a. Aminotransaminases (aspartate / alanine) 2.b. Lactate dehydrogenase 2.c. Cell death releases enzymes

3. Cholestatic

3.a. Alkaline phosphatase (ductal cells / T1/2 7 days / other sources) 3.b. Gamma-glutamyl-transpeptidase (ductal cells / inducible enzyme/alcohol) 3.c. Unconjugated bilirubin / poorly water soluble

4. Higher marks

4.a. Albumin transport of unconjugated bilirubin 4.b. Albumin loss from other causes 4.c. Plasma concentrations of albumin / bilirubin and jaundice 4.d. Glutathione-S-transferase and centrilobular damage 4.e. Ammonia levels in liver failure

“Outline” does not mean list and there needs to be a connection between what is measured and how that changes with liver dysfunction. Clarity about “increases” and “decreases” is important for showing understanding. A simple list of tests was not enough to answer the question and demonstrate knowledge. Normal plasma concentrations of albumin and bilirubin were infrequently mentioned and enzyme abbreviations without explanations were common. Information not relevant to the question includes:

• Excessive detail on the coagulation pathway • Hepatic blood flow measurement • Clinical signs of liver failure • Functions of the liver and albumin • Explaining how to perform a laboratory test

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• Ultrasound investigations QUESTION 16 Draw and label a lead II electrocardiogram (ECG) tracing for one cardiac

cycle, indicating normal values. What is the PR interval and what factors influence it?

50% of candidates passed this question. The answer to this question should include:

1) A diagram of a typical lead 2 ECG trace, with axes, and labels on P, QRS, and T waves, PR and QT intervals, and ST segments.

2) Quantification of the normal values of duration of PR, QRS and QT interval. 3) Definition and explanation of the significance of the PR interval – in particular the

importance of the AV node. 4) A list of factors that increased or decreased the PR interval – autonomic system, cardiac

abnormalities/disease (WPW, ischaemia), drugs, other physiological derangements (hypothermia, hypokalemia)

Additional marks were given for detailed description of cellular mechanisms of changes in the PR interval and an outline of the allowable normal deviation from isoelectric values of the ST segment, and size of the Q wave. Common mistakes made by the candidates included:

1) Inability to quantify the time intervals. These values are essential to the clinical interpretation of the ECG for the rest of an anaesthetist’s career.

2) Confusion of milliseconds with seconds was very common. 3) The PR interval was not accurately described – it is from the start of the P wave to the

start of the QRS complex (which is usually the Q wave, not the R wave).

PHYSIOLOGY - VIVA SECTION

PHYSIOLOGY TOPICS: Cardiovascular

• Draw the radial artery waveform. • Gross anatomy of the coronary circulation. • Oxygen consumption of the heart. • Draw a flow vs. time curve for the left coronary artery. • Draw a left ventricular pressure vs. time curve. • Function of the microcirculation. • Draw a Swan-Ganz pressure trace as it floats into position. • Role of the balloon in a pulmonary artery catheter. • Definition of contractility. • Changes that occur with aging. • Definition of afterload.

Respiratory

• Physiological effect of a pneumothorax. • Determinants of arterial PCO2 • Determinants of the work of breathing. • Changes associated with high altitude. • Alveolar gas equation. • Draw the oxygen cascade.

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• Draw a spirometer trace. • Draw a pressure vs. time curve for a ventilated patent. • Consequences of apnoea. • Definition of compliance. • Draw a capnogram trace. • Draw an expiratory flow-volume curve.

Renal/Acid-base

• Definition of GFR. • Definition of an acid. • Renal resorption of bicarbonate. • Range of urine osmolarity. • Functions of the kidney. • Value for renal blood flow.

Measurement

• Calibration of an arterial line. • Justify the use of pulse oximetry in anaesthesia. • Difference between heat and temperature. • Definition of pressure. • Units of pressure.

Nervous system

• Normal values of ICP. • Normal values of cerebral blood flow. • Examples of excitatory neurotransmitters. • Value of the resting membrane potential.

Haematology

• Processing of a unit of donated blood. • Role of platelets in haemostasis.

Pregnancy

• Physiological effects of pregnancy.

Endocrine • Iodine utilisation

Pain

• Pathways associated with a painful stimulus.

Immunology

• Functions of the immune system Cellular physiology

• Role of oxygen in the body. • Process of protein synthesis

Integrated physiology

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• Physiological effects of obesity Dr N. Roberts Chairman, Primary Examination Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

FEBRUARY/APRIL 2007 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. ________________________________________________________________________________

PHARMACOLOGY – WRITTEN SECTI ON

MULTIPLE CHOICE QUESTIONS: 87% of candidates achieved a pass in this section of the Pharmacology Examination.

SHORT ANSWER QUESTIONS: QUESTION 1 Describe the potential adverse effects of administering neostigmine post

operatively. 68% of candidates passed this question. This question examined the pharmacology of neostigmine, a drug that is being used in anaesthesia on a daily basis. An adequate description of adverse effects was therefore expected for candidates to obtain a pass mark. The main points should include a discussion on the accumulation of acetylcholine at muscarinic (at low dose) and nicotinic (at higher dose) receptor sites after administration of neostigmine. The muscarinic effects are severe and hence the co-administration of antimuscarinic agent is important. The most worrying adverse effects are bradyarrhythmia with hypotension. Bronchoconstriction, salivation, tracheobronchial hypersecretion, postoperative nausea and vomiting, and enhanced peristalsis (and potential damage on bowel anastomosis) should be mentioned.

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Additional marks were awarded for including potential drug interaction with suxamethonium and mivacurium. Marks were also awarded for depolarizing block after excessive doses of neostigmine. No credit was given for description of neuromuscular monitoring. QUESTION 2 After epidural injection in a health term pregnant woman, discuss the

factors influencing the distribution of bupivacaine to (a) the maternal CSF and spinal cord; (b) the maternal circulation; (c) the foetus.

46% of candidates passed this question. The main points expected for a pass included a discussion of the factors affecting diffusion as described in Fick's Law and how these pertained to the three diffusion interfaces outlined in the question. Solubility, ionization, tissue and protein binding, amount of drug, and concentration gradient all affect the distribution of bupivacaine from the epidural space to the CSF and maternal systemic circulation, and subsequently to the foetus. Demonstration of comprehension that there are physiological differences between these four compartments and how these determine bupivacaine's distribution was expected. Additional marks were awarded for the consequences of the addition of adrenaline or bicarbonate to the bupivacaine solution, a discussion on epidural depot of drug, the biphasic nature of systemic absorption and foetal acidosis effect on bupivacaine protein binding. Common errors included discussing elements of bupivacaine that were not requested; such as drawing its structure or a pharmacodynamic discussion of its toxicity. Also, reproducing factual information, such as the pKa of the drug, without discussing how this affects its diffusion at the three interfaces, did not attract marks. QUESTION 3 Discuss factors contributing to inter-individual variability in the

therapeutic response to opioid analgesic medications. 69% of candidates passed this question. A structured approach was expected dividing the issues along pharmacokinetic / pharmacodynamic lines. A patient factors approach or other structure was also acceptable. The discussion was expected to relate the underlying factors to opioid analgesics. The question was specifically related to inter-individual variability and a simple discussion of mechanisms of action or side effect profiles for varying opioid agents scored no additional marks. Candidates were expected to outline that variability can be seen in areas of absorption, distribution, metabolism and elimination of these agents. Credit was given to candidates who outlined the potential impact of liver or renal disease with specific examples. The discussion would also include the impact of factors such as age, pregnancy, coexisting medical disease or concurrent medication use. Discussion of genetic influences on enzymes and receptors was expected and was well covered by most candidates. Discussion of tolerance, prior drug exposures and previous pain experiences in influencing individual responses attracted extra marks. QUESTION 4 Discuss the suitability of ketamine as a total intravenous anaesthetic agent

in comparison with propofol. 25% of candidates passed this question. To reach a pass standard simple, relevant information on the pharmacokinetics and the neurological, cardiovascular and respiratory pharmacodynamics of both agents was sufficient.

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Almost no candidates explained that ketamine is an effective, sole anaesthetic agent used widely in unsophisticated medical settings, nor the relevance of its particular pharmacodynamic properties in this situation. Many candidates understanding of total intravenous anaesthesia was limited to the use of propofol with pharmacokinetic model driven infusion pumps. Frequently the "comparison" aspect of the answer was not well organized. Answers using parallel columns for each agent's features were generally more complete in their comparisons. In contrast, poorly laid out answers were also more likely to focus predominantly on either kinetic or dynamic features, and to commonly have incomplete comparisons between the two drugs. QUESTION 5 Classify non-opioid drugs used for the treatment of neuropathic pain and

indicate proposed mechanisms of analgesic action and potential adverse effects.

34% of candidates passed this question. The key to successfully dealing with this question was to address each of the three components: classification, mechanisms, and adverse effects. The main points expected were a classification system that was coherent; for example: simple analgesics, anticonvulsants, antidepressant, membrane stabilizers and so on. Proposed mechanisms of action should have included how the drugs work, and (importantly) why this reduces pain. There are many drugs that can be used and there are many potential adverse effects. For this component of the question, emphasis on the more specific drugs (e.g. anticonvulsants and antidepressants), and on specific (e.g. anti-cholinergic effects with antidepressants) rather that generic (e.g. rash, gastrointestinal upset) adverse effects, were rewarded. No marks were awarded for a definition of chronic pain, a description of the pathophysiology of chronic pain, or non–pharmacological therapies as these were not asked. QUESTION 6 Briefly outline the acute management of malignant hyperthermia (during a

relaxant general anaesthetic). Describe the important aspects of dantrolene pharmacology relevant to treating malignant hyperthermia.

54% of candidates passed this question. Equal marks were devoted to each half of the question. Inclusion of the following points would have scored a good pass mark. Management: life-threatening emergency, call for help and dantrolene, cease triggers (e.g. volatile agents), hyperventilate with oxygen, maintain anaesthesia with non-triggering agents, give dantrolene 2.5 mg/kg, repeat up to 10 mg/kg, active cooling to <38 degrees. Pharmacology: skeletal muscle relaxant presented as orange powder containing dantolene 20 mg, mannitol 3g and sodium hydroxide to bring pH >9 with 60mls water. Difficult to mix. Metabolized by liver enzymes, eliminated in urine and bile with a half-life of about 10 hrs. Inhibits calcium release from sarcoplasmic reticulum. It can cause phlebitis, use of verapamil contraindicated. Most candidates who did not achieve a pass mark wrote very little on dantrolene pharmacology. Many candidates gave long, detailed accounts of the etiology and pathology of malignant hyperthermia but this was not asked in the question and attracted minimal bonus marks. QUESTION 7 Describe the pharmacology of midazolam including its mechanism of

action. 66% of candidates passed this question.

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Better answers were well organized and outlined the important aspects of midazolam pharmacology including: • Pharmaceutics, pH dependent “ring opening”, ampoule pH

• Pharmacokinetics, administration, oral bio-availability, high lipid solubility and moderately fast onset, moderate hepatic clearance 7 mls/kg/min approx (cf diazepam), active metabolite, offset dependent on re-distribution and clearance, relatively short elimination half life

• Mechanism of action (MOA), benzodiazepine receptor on alpha subunit of GABAa receptor, enhanced action of GABA, increased chloride entry and neuronal hyper-polarization

• CNS effects, sedation, hypnosis, anxiolysis, amnesia, anti-convulsant, muscle relaxant

• CVS effects, hypotension, vaso-dilatation

• Respiratory effects, respiratory depression, potential airway obstruction, hypoxemia, interaction with opioids

• Clinical uses, pre-medication, sedation, induction agent, anti-convulsant, antagonized by flumazenil

Extra marks were awarded for an outline of; kinetics of offset including context sensitive half time, metabolism and excretion including CYP 3A4 and accumulation of metabolites, the GABA receptor and alpha sub-unit selectivity, effects on cerebral blood flow, oxygen requirements and the EEG, factors potentiating CVS and respiratory effects, dosages for particular clinical applications and clinically important structure activity. Common errors included; not mentioning MOA, describing MOA as direct activation of GABA receptor, describing NMDA or cyclic AMP effects, frequent citing of very inaccurate kinetic data with no mention of clinical implications and frequent omission of adverse effects. QUESTION 8 List the classes of drugs used clinically to treat chronic left ventricular

failure. Outline their mechanisms of action. 65% of candidates passed this question. Only 32% of candidates complied with the first part of the question, to LIST the classes of drugs used. In order to satisfy the requirements of this question, candidates need to relate facts about drugs to their mechanisms of action. Many answers included a definition of heart failure then attempted to relate the benefits of classes to this, however since no mention was made of diastolic dysfunction, many responses were incomplete. It was common for candidates to outline the effects of an agent but not describe the mechanisms of those effects or their consequences. This information needs to be explicit. Thus many failed to acknowledge the influence of renin and how its levels are affected by different agents (eg. beta blockers). Most candidates gave the mechanism of action for the management of myocardial ischaemia for nitrates and beta blockers; while this is often relevant, it is not the prime therapeutic goal for these agents in heart failure. Beta blockers are not used to achieve a decrease in cardiac output. Pre- and after load were frequently confused with few candidates mentioning Starling curves. Although this question related to chronic failure, many candidates discussed drugs typically used for acute systolic dysfunction. Credit was given for a description of digoxin and its benefits in atrial fibrillation and other after-load reducing agents including prazosin and hydralazine.

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PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS/INTRODUCTORY QUESTIONS: General topics

• Pharmaceutics; thiopentone, local anaesthetics, benzodiazepines • Pharmacokinetics; absorption, bioavailability; hepatic clearance; renal drug handling,

pharmacokinetic modelling, clearances, volumes of distribution, AUC • Concentration-time curves • Hepatic biotransformation • Mechanism of drug action • Dose response • Pharmacogenetics • Drugs and gastric acidity • Treatment of poisoning • Chemotherapeutic agents, adverse effects, drug interactions

Inhalational agents

• Induction kinetics • Recovery • Washout curves • Inhalational depth • Measurement of depth • MAC; MAC awake • Structure-activity relationships • CVS effects • Children and adults, kinetic, dynamic differences

Local anaesthetics • Structure activity • Pharmacokinetics • Toxicity, factors affecting toxicity, toxic doses • Mechanisms of action • Cocaine toxicity • Topical anaesthesia

Induction agents • Factors affecting induction dose and maintenance infusion rate • Propofol pharmaceutics • Propofol pharmacokinetics • Thiopentone

Neuropharmacology • Anti-convulsants • Phenytoin • Benzodiazepines

Neuromuscular blocking agents

• Classification • Atracurium, cisatracurium • Isomers • Factors affecting clinical choice and dose

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• Recovery from neuromuscular blockade • Neuromuscular monitoring • Inter-individual variability • Potency • Suxamethonium; dose response curve, side effects

Opioid agonists and antagonists

• Mechanism of action • Receptors • Effect site concentration • Tramadol

Anticholinesterase and anticholinergics

• Classification • Drug interactions and myasthenia gravis • Scopolamine, atropine

Cardiovascular drugs • Drugs that increase blood pressure • Catecholamines • Vasopressors • Alpha 2 agonists • Antiarrhythmics; classification, lignocaine, amiodarone • Beta blockers • Drug therapy of myocardial ischemia • Anaesthetic agents and cardiac output • Nitric oxide • Vasodilators; GTN and SNP

Diuretics • Classification • MOA • Mannitol

Respiratory pharmacology

• Anti-asthma drugs • Nitric oxide

Drugs and coagulation

• Unfractionated heparin, low molecular weight heparin • Warfarin • Antiplatelet drugs • Protamine

Pain

• Oral analgesics • Mechanisms of action • Bio-availability • Paracetamol

Statistics

• Data

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• Clinical trial design • Power • Bias • Regression, correlation • Drug development and trials • Selection of appropriate statistical tests • Randomised controlled trials • Confidence intervals • NNT

Endocrine • Oral hypoglycaemic agents • Insulin • Corticosteroids

Obstetric pharmacology

• Tocolytics • Magnesium, salbutamol • Oxytocics; adverse effects

Antiemetics

• Clinical effectiveness • Adverse effects • 5HT3 antagonists, ondansetron, tropisetron • Dexamethasone

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PHYSIOLOGY – WRITTEN SECTION MULTIPLE CHOICE QUESTIONS:

84% of candidates achieved a pass in this section of the Physiology Examination.

SHORT ANSWER QUESTIONS: QUESTION 9 Define “Venous Admixture”. Briefly explain how venous admixture

influences arterial oxygen tension and how an increase in inspired oxygen concentration may effect this.

43% of candidates passed this question.

Main points expected for a pass included: definition, sources of venous admixture with brief description of each, appreciation that venous admixture is a concept which may be expressed by the shunt equation, statement of effect on PaO2 of venous admixture with reference to the oxyhaemoglobin dissociation curve (demonstrating relation of oxygen tension to haemoglobin saturation), and the effect of increased inspired oxygen concentration on venous admixture.

Additional marks were allocated for more detail with respect to sources of venous admixture (e.g. relative contribution, magnitude effect), demonstration that small and large amounts of venous admixture affect PaO2 differently, explanation of relative effect of high versus low V/Q units, reference to isoshunt diagram and quantifying effect of increased inspired oxygen.

Mistakes commonly made included: imprecise or interchangeable use of terms (e.g. oxygen content for PaO2 and shunt or mixed venous blood for venous admixture); and use of oxyhaemoglobin dissociation curve to justify arguments regarding the effect of increased PaO2 on oxygen content. Credit was not given for vague, non-directional statements of effect, or for discussion of carbon dioxide or factors which affect mixed venous PO2.

QUESTION 10 Explain the mechanisms that prevent blood clotting in intact blood vessels

(do not draw the clotting cascade). 57% of candidates passed this question. For a pass, an understanding of the balance between pro and anticoagulant processes that occur in the blood, and a brief outline of the mechanisms that prevent blood from clotting was required. Candidates who followed the structure of Virchow’s triad to elucidate these factors tended to score well by demonstrating understanding. Many candidates would have benefited by providing a clear introductory statement, outlining the balance between pro and anticoagulant factors, and then explaining the factors that prevent coagulation. As general advice regarding examination technique, candidates may wish to consider that if confronted by a question that they may not have considered in preparation for the examination, by considering the basis of everyday clinical practice, they may yet be able to achieve a good score. In this case, common clinical practices for prevention or perioperative deep venous thrombosis may have provided the key to an answer.

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QUESTION 11 Discuss how the body handles a metabolic acidosis. 57% of candidates passed this question. The main points to be covered were a definition of a metabolic acidosis, discussion of extracellular and intracellular buffering systems, respiratory compensation, the renal mechanisms to excrete non-volatile acids (titratable acidity, ammonium and ammonia), and resorption and regeneration of bicarbonate. Extra marks were awarded for the mechanism of respiratory compensation, explaining that respiratory compensation does not lead to acid excretion, description of buffering by long as well as short term mechanisms, specific details of ammonia and ammonium production and bicarbonate regeneration, understanding that H+ ions can not be excreted unbound, the amount of acid that can be excreted by different renal mechanisms, and aldosterone’s effect on H+ excretion. QUESTION 12 Explain the physiological principles underlying the use of peritoneal dialysis

in a patient with chronic renal failure with this dialysate solution. Na 132 mEq/L Mg 0.5 mEq/L K 0 mEq/L Lactate 40 mEq/L Cl 96 mEq/L glucose 2.5 g% Ca 3.5 mEq/L 17% of candidates passed this question. The purpose of this question is to show an understanding of basic physiological principles involved in peritoneal dialysis and not its clinical applications or indications. The main points expected for a pass were: PD takes places across a membrane (peritoneum) by exchange between dialysate and the patient’s blood. The main processes are:

a) Osmosis - movement of solvent from low to high solute concentration b) Diffusion – movement of solute from region of high to low concentration c) Solvent drag

Definitions of these processes were required. Many candidates showed a lack of understanding of these basic processes. The factors which influence these processes are:

a) movement of solvent • tonicity – definition, dialysate is hypertonic mainly due to it’s hight glucose

concentration, osmolarity approx. 400 mmol/L (2[Na]+ 0.055 [Glucose]+ 0.36 [BUN] b) movement of solute

• Fick’s law of diffusion • Donnan effect – due to effect of charged plasma proteins

Many candidates wasted time on detailed description of what happens to individual solutes at the expense of explaining the basis physiological principles of diffusion and giving an example e.g. K+ Other points which gained marks:

• purpose of PD- i.e. achieve balance of fluids, electrolytes, acid-base and excretion of toxins wastes

• osmosis is a relatively fast process compared to diffusion • glucose absorption can cause hyperglycaemia

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• lactate is provided for conversion to bicarbonate by the liver helping with acid/base balance

• protein transfer into dialysate can result in loss QUESTION 13 Describe the determinants of Venous Return and the effect general

anaesthesia would have on these. 60% of candidates passed this question. In general candidates answered the question fairly well, reflecting an understanding of a physiological variable of major clinical relevance to anaesthetists. The most successful approach used to answer this question was to address specific physiological and anatomical factors, which influence venous return (e.g. blood volume, venous tone, posture). The inclusion of simple formulae (e.g. VR = MSFP-RAP/RVR, Guytonian model) allowed these factors to be related to an effect on VR, and readily demonstrated a good comprehension of the issues. Whilst obvious factors (such as venous tone) were usually mentioned, common omissions included intrathoracic pressures, venous valves and muscle pumps, all important factors both physiologically and in a clinical anaesthesia setting. Guyton curves were used by some candidates. They did illustrate some factors quite well, but for some candidates the time spent with these curves came at the expense of descriptions of either how some determinants actually affected VR or ommission of specific determinants such as venous valves or posture. Most candidates were able to relate the responses to the first part of the question to the second part (effects of anaesthesia). Major omissions or errors in answering the first part often carried over into effects of anaesthesia. A few candidates provided the answer in table form, with each determinant listed along with its effects on VR and changes with anaesthesia. Whilst this approach provided succinct answers, it sometimes proved difficult to describe the net effect of individual determinants using this somewhat abbreviated format. QUESTION 14 Explain the mechanisms whereby oxygen transfer is facilitated at the

placenta. 59% of candidates passed this question. Oxygen passes from the mother to the fetus at the placenta by diffusion. This process is facilitated by a large number of factors including:

1. The placental structure is designed to facilitate diffusion, best summarised by the factors in the Fick equation.

2. The increased affinity for oxygen of fetal compared to maternal haemoglobin 3. The increased concentration of fetal haemoglobin. 4. The (double) Bohr effect.

Other factors which could be discussed included the potential role for maternal hyperventilation (with increased maternal PaO2 and changes in acid base metabolism) associated with pregnancy and the (double) Haldane effect (relevant due to the increased carbon dioxide flux amplifying the Bohr effects). The commonest difficulties with the question arose from taking too narrow a focus. Many candidates confining themselves to describing the double Bohr effect almost in isolation, perhaps supplemented with reference to the differences between fetal and adult haemoglobin oxygen affinity. How the

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structure of the placenta facilitates diffusion and the role of the high concentration of fetal haemoglobin were the commonest omissions. The double Bohr effect was generally well described, but, those that had difficulty mostly misunderstood the concept that the Bohr effect concerned:

1. The decrease in haemoglobin oxygen affinity from arterial to venous on the maternal side of the placenta due to increased concentration of carbon dioxide, and

2. Increase haemoglobin oxygen affinity from arterial to venous on the fetal side due to decreased carbon dioxide concentration.

QUESTION 15 Describe the effects of resonance and damping on an invasive arterial blood

pressure tracing. 21% of candidates passed this question. For a pass, most of the following information was required:

• Some attempt at a definition of the concepts • Evidence of understanding that the system’s f0 needs to be several fold the frequency of the

pulse and the consequences for the pressure waveform of not being so • Means whereby the f0 of the system can be maximised • Effects of under, over and optimal damping on the arterial pressure waveform • Causes of damping in the system

Marks were awarded for other information, including that the measured MAP tends not to be affected by resonance and inappropriate damping; clear diagrams explaining the waveform changes; correct explanation of damping co-efficients and the meaning of the term, especially if a correct diagram of the response to a step change in pressure was included; that the transducers used today have high natural resonant frequency but the other components of the measuring system are the main cause of low f0 in the system; correct use of an equation relating f0 to mass, elasticity and area and especially if this could then be related to practical means of increasing f0 in the measuring system; difference between optimal and critical damping. Common problems in the answers were: • Very few answers included a good attempt at defining the concepts especially damping (delay in

response due to frictional resistance, or similar)

• Discussion of resonance and damping without any attempt at describing the effects on an arterial waveform (at least half the candidates)

• Wasting time with long descriptions of the components of the measuring system or of zeroing or of indications for arterial line placement. Zeroing is irrelevant to the question;

• Quoting figures for damping coefficients with no evidence of any understanding of the meaning of the term

• Using vague terms like “interfere with the trace” with no mention of in what way;

• Stating that damping is used or added to the transducer in order to combat resonance-damping and resonance are features of any oscillating system and the measuring systems used must in some way optimise these inherent features;

• Those candidates who attempted a diagram demonstrating response to a step change in pressure in various damping situations were often wrong

• Several dozen answers compared the radial and aortic pressure traces and described the differences in terms of resonance and damping in the arterial tree. When this information was correct, marks were given but it was not possible to get a pass mark for this information only.

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QUESTION 16 Briefly outline the components of parenteral nutrition, explaining the rationale for the use of each component.

42% of candidates passed this question. A good answer would have included a definition of parenteral nutrition and a rationale for its use. Normal daily requirements should have been described. The components of parenteral nutrition include water and electrolytes, a common omission in many papers. Most candidates covered well the caloric components of lipids, carbohydrates and proteins with a rationale for use. Many answers also included the addition of vitamins, minerals and trace elements, which was pleasing, but the rationale of “to maintain normal levels” was insufficient to score marks. Extra marks were awarded for discussing how the patients requirements alter in normal physiological circumstances, for example age, gender and pregnancy and in disease states such as sepsis and burns.

PHYSIOLOGY - VIVA SECTION

PHYSIOLOGY TOPICS/INTRODUCTORY QUESTIONS: Cardiovascular

• Draw LV pressure vs. time curve. • What useful information can be obtained from the ECG? • What is an electrocardiogram? • What are the determinants of cardiac output? • Draw a pressure-volume loop for the LV. • What controls regional circulation? • Draw an LA pressure wave versus time. • Draw a sino-atrial node action potential. • Discuss the determinants of pulmonary blood flow. • What are the assumptions associated with capillary wedge pressure measurement? • What are the determinants of myocardial perfusion? • Discuss the role of arterioles in the CVS. • What does the term "venous capacitance" mean? • What are the determinants of RV function? • What is the coronary sinus blood oxygen level? • Draw a PA catheter tip pressure trace as the device is inserted. • Draw an ECG and an RA pressure trace. • What is the blood supply to the heart? • Factors determining cerebral blood flow. • Changes in the CVS with aging.

Renal

• Control of renal blood flow. • Define GFR and discuss its determinants • How is urine diluted? • What is serum osmolarity? • Discuss the renal response to acute haemorrhage.

Respiratory

• Discuss the effects of hypercapnea. • Effect of increasing FiO2 on blood gases. • Determinants of arterial oxygen tension. • How is carbon dioxide transported in blood.

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• Draw the oxygen cascade. • Discuss the control of ventilation. • What is Laplace's law? • Respiratory changes of pregnancy. • What is PEEP? • Discuss FRC and closing capacity. • Discuss the changes that occur with a Valsalva manoeuvre • What is dead space? • Draw a respiratory pressure-volume loop for a paralyzed patient. • Draw a normal capnograph. • Draw an intra-pleural pressure versus time curve during quiet respiration. • Discuss the consequences of a sudden obstruction of the left pulmonary artery. • Discuss the effect of application of CPAP to a spontaneously breathing patient. • Define compliance. • How is diffusing capacity measured? • Define closing capacity. • What are typical values for mixed venous gases? • What is the oxygen tension in fetal umbilical arteries? Veins? • What happens to alveolar ventilation and perfusion as you move from the lung apex to the

base? Nervous

• What is a nerve fibre? • What is sleep? • What is normal cerebral metabolism? • Normal values of cerebral blood flow. • How are membrane resting potentials maintained? • What is the blood brain barrier? • What is CSF?

Measurement

• What waves are seen on an EEG? • What is pulse oximetry? • What is saturated vapour pressure? • What is heat? What is temperature? • When will a pulse oximeter give an incorrect reading? • Define humidity. • Principles of measurement of levels of consciousness.

Hormones/Metabolism

• Definition of a hormone • How are serum glucose levels maintained during a fast • Consequences of a 24 hour fast. • How does the body handle glucose?

Haematology

• Definition of anemia • What are the features of a RBC? • Lifecycle of a platelet • How is a unit of packed cells prepared? • What are blood groups?

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GIT • Functions of the liver • What happens when you swallow? • Regulation of gastric pH • Physiological principles of prevention of gastro-oesophageal reflux • Determinants of gastric emptying

Pain

• What is pain? • Describe the mechanisms that are associated with acute pain • What happens if you touch something hot?

Temperature

• How does an awake subject respond to a decrease in ambient temperature? • Discuss heat loss under anaesthesia.

Acid-base

• What is a buffer? DR NOEL ROBERTS CHAIRMAN, PRIMARY EXAMINATION COMMITTEE

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Australian and New Zealand College of Anaesthetists

ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

JULY/SEPTEMBER 2006

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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 81 % of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Describe the use of different sympathomimetics to treat hypotension

occurring as a result of subarachnoid block. Outline the advantages and disadvantages of these agents.

73 % of candidates passed this question. Given the clinical scenario, a brief summary of pertinent issues resulted in less subsequent repetition.

The hypotension results from a change in tone of resistance vessels (reduced systemic vascular resistance). This is accompanied by a decrease in venous return to the heart and a lowering of cardiac output. There may be a lowering of direct sympathetic tone to the heart, leading to a reduction in heart rate and possibly force of contraction. Answers should have included discussion of ephedrine and adrenaline (epinephrine). Credit was also given for discussion of metaraminol, phenylephrine, methoxamine, noradrenaline, dopamine, dobutamine and vasopressin, even if disadvantages outweighed the advantages of the drug. No marks were given for naming a drug without other information.

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Common features of these agents include: • Pharmaceutical presentation - all require dilution before use. • Agents with strong vasoconstricting effects have a risk of tissue necrosis if extravasation

occurs (including metaraminol). • All the drugs have a risk of causing hypertension. • Many drugs can cause tachycardia via direct effects or reflex bradycardia.

Better answers included a list of relevant patient problems that contribute to the advantages/disadvantages of the drugs including:

• Age/intercurrent illness, particularly cardiovascular disease and antihypertensive medications.

• Pregnancy and childbirth (allowance was made for the differences in prescribed texts regarding ephedrine and phenylephrine).

• Drug interactions - monoamine oxidase inhibitors. QUESTION 2 Compare and contrast the clinically significant respiratory,

cardiovascular and central nervous system effects of desflurane and isoflurane.

70 % of candidates passed this question. Cardiovascular effects were well answered with most correctly describing the effects on heart rate, systemic vascular resistance, contractility and cardiac output; though there were some incorrect statements such as, hypotension at one MAC is primarily due to impaired contractility. Better answers discussed the theoretical risk of coronary steal with isoflurane and the practical risk of increases in catecholamine levels with sudden increased desflurane concentration, however there was no mention of the secondary effect on the renin angiotensin system. Common errors in respiratory effects included unqualified comments that both agents could be used for gaseous induction. Some candidates confused the respiratory effects of these agents with opioids where tidal volume is maintained or increased and respiratory rate is reduced. CNS effects were well answered, though only a minority mentioned the faster return to consciousness with a comparable depth of anaesthesia with desflurane. Some said that these agents usually decrease cerebral blood flow. Presentation was of a good standard with most information for the least effort being conveyed with tables. There were some good answers, though in plain text. Significantly there were no blank answer papers. QUESTION 3 Describe the factors which contribute to the inter-individual variability

in drug response seen with intravenous anaesthetic induction agents. 42 % of candidates passed this question. Better answers classified the factors contributing to variability rather than providing a random list. Factors could be broadly classified as pharmacokinetic and pharmacodynamic in nature. Then within each class further division into physiological, pathological and pharmacological, including drug interaction and pharmacogenomic factors. Other schemes that encompassed these key areas were acceptable. Some indication of the relative importance of these factors in determining variability of intravenous anaesthetic agents was important.

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Key pharmacokinetic factors were those that ultimately influenced the extent or duration of effect site concentration and included factors increasing the rate of drug distribution to effect site (e.g. speed of administration, arm-brain circulation time, cardiac output, distribution of cardiac output, central compartment volume, effect site equilibration time); factors influencing redistribution, offset of initial effect and body drug stores (e.g. regional blood flow, volume of distribution, body habitus, age); factors causing variability in metabolism and clearance (e.g. pharmacogenomic factors; induction, inhibition of enzymes; duration of exposure; age-related changes in metabolism; hepatic and renal function). Key pharmacodynamic factors included drug-receptor interaction, receptor numbers and regulation, acute and chronic tolerance, idiosyncratic reactions. Higher marks were awarded for comprehensive breadth of cover of the topic including pharmacogenomic influences and where a clear understanding of the concepts mentioned was evident. Many candidates did not read the question, and did not relate answers at all to intravenous anaesthetic agents. Common errors included irrelevant emphasis on differences between drugs rather than inter-individual variability, confusion over the nomenclature and roles of the different volumes of distribution, uncertainty regarding the relative roles of redistribution and clearance in offset of drug effect and confusion over the pharmacokinetic changes in the very young and elderly patients. A clear knowledge of pharmacological principles and terminology was expected. QUESTION 4 Describe the advantages and disadvantages of rocuronium for rapid

sequence induction. 28 % of candidates passed this question. Most candidates failed because they wrote about the pharmacology of rocuronium without addressing the advantages and disadvantages with regard to rapid sequence induction. It was noted that the better answers were more focused and usually started by stating that rapid sequence induction was a technique designed to secure the airway quickly in patients at risk of aspiration, classically using suxamethonium to cause rapid paralysis. Rocuronium was usually compared with suxamethonium, but candidates should also have noted why rocuronium is currently preferred to alternative drugs when suxamethonium is absolutely contraindicated. Some candidates wasted pages describing all the side effects of suxamethonium that could be avoided with rocuronium. Answers should have indicated the likely doses required for rapid sequence induction because this would determine the onset and offset of neuromuscular block. There was large variation in the times given for onset and offset of block for both suxamethonium and rocuronium. Some answers did not explain why the long duration of action with rocuronium could be a disadvantage. QUESTION 5 Briefly explain the mechanisms responsible for non-steroidal anti-

inflammatory drug (NSAID) – induced side effects. Outline the advantages and disadvantages of selective cyclooxygenase (COX 2) inhibitors.

62 % of candidates passed this question. This question is in two parts. The first part involves a brief explanation of mechanisms behind NSAID induced side effects. Candidates listing and briefly explaining the most commonly discussed effects of peptic ulceration, renal impairment, tendency to bleeding from platelet inhibition and bronchospasm were able to score most marks allocated from this section. The mention of specific subtypes of prostaglandins involved attracted marks. Absence of such information did not stop an answer from scoring well, as long as the discussion of mechanism was adequate.

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The second half of the question called for a brief discussion of advantages and disadvantages of COX 2 inhibitors. Advantages: reduced peptic ulceration rate, reduced postoperative bleeding, theoretical advantage of action in inflamed tissues, possible absence of bronchospasm etc. Disadvantages: expensive, coronary and cerebral thrombosis with chronic use with rofecoxib and possibly others, similar risk of renal impairment as with undifferentiated COX inhibitors. Extra marks were scored by those who gave a very brief overview of COX action and the role of COX 1 and COX 2, as well as discussion of other side effects such as interstitial nephritis, hypertension, fluid retention, ductus arteriosus closure and sulphur allergy. QUESTION 6 A new clinical test called the “intubation score” has a reported 90%

sensitivity and 70% specificity when used to predict difficult intubation. Describe how the accuracy, predictive value and clinical utility of this test can be evaluated. How will the incidence of difficult intubation affect the performance of this test?

34 % of candidates passed this question. To quote from the syllabus (Section C -Statistics [e]), candidates are expected to: "Describe the features of a diagnostic test, including the concepts of sensitivity, specificity, positive and negative predictive value and how these are affected by the prevalence of the disease in question.". Drawing a 2 x 2 table and defining the terms mentioned in the question obtained a pass mark. Unfortunately less than half the candidates accomplished this. The question as to the effect of the incidence of disease on the positive predictive value of a test is of critical importance. Changing the incidence of a disease does not alter sensitivity or specificity, as many stated, but as the incidence falls so does the PPV - a restatement of Bayes' Theorem. This is one of the reasons why all of the predictive tests for failed intubation, a relatively uncommon event, have such a low PPV. Some candidates invoked p values, alpha and beta errors, power and even "t-tests" in their answers, which failed to address the question asked. There were many blank answers. QUESTION 7 Outline the drug and non-drug treatment of ventricular fibrillation in an

adult. Briefly describe their mechanisms of action. (Do not discuss basic life support, airway therapies and oxygen)

44 % of candidates passed this question. A similar question was asked in July 2005. The pass mark has improved significantly. Hopefully knowledge and understanding of this important syllabus topic will continue to improve. Candidates were expected to describe the current management of ventricular fibrillation with particular reference to defibrillation, epinephrine and antiarrhythmic therapy. Allowance was made for both old and new guidelines given their recent introduction. ILCOR published in 2005 (www.erc.edu/index.php/guidelines_download_2005/en/) and Australian guidelines in 2006 (www.resus.org.au/)

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The important areas to be addressed were: • Defibrillation, early intervention, effective therapy, biphasic vs. monophasic, energy

settings and mechanism of action. • Epinephrine, dose, emphasis on activation of alpha 1 receptors resulting in

vasoconstriction and improved coronary and cerebral blood flow. • Antiarrhythmic therapy, amiodarone and/or lignocaine with description of dose and

mechanism of action. • Prioritisation, a description of the sequence of these therapies and how they fit into a

cohesive management plan or protocol. This could be implied in description of the individual therapies.

Extra marks were gained for a description of the possible role of vasopressin, magnesium, sodium bicarbonate and potassium. Common problems included; no clear sequence of therapies, the importance of defibrillation and energy settings omitted, epinephrine not mentioned or dosage and mechanisms incorrect. QUESTION 8 Describe the pathogenesis and management of paracetamol toxicity. 86 % of candidates passed this question. Most candidates exhibited a sound knowledge of the pathogenesis and toxicity of paracetamol. Many candidates wrote at length about the general pharmacokinetics of paracetamol. This did not attract marks. Marks were given for the following points:

• Toxic dose, expressed ideally in mg/kg or a single toxic dose for adults. • Differentiation between a toxic dose and a fatal dose. • Normal metabolic pathway of paracetamol. • Overdose and relationship of minor metabolic pathway with production of toxic

metabolite. • Conditions which may exacerbate toxicity. • Cellular mechanism of hepatic toxicity. • Other features of toxicity e.g. contribution of paracetamol to chronic renal failure. • General management issues of drug overdose. • Role of N-acetyl cysteine and use of normogram. • Monitoring and tests e.g. risk of hypoglycaemia.

It was hard to score very highly without mentioning a toxic dose. When fatal doses were mentioned, the range given was from 7 to 30g for an adult. No candidate mentioned the importance of dose/kg reflecting ideal body weight, and precautions in obese patients or children on long-term paracetamol use. Very few candidates mentioned renal toxicity. Common errors referred to the metabolism of paracetamol to phenacetin, usefulness of dialysis and urine pH manipulation in overdose.

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PHARMACOLOGY – VIVA SECTION PHARMACOLOGY TOPICS: General topics

• Pharmaceutics; thiopentone, local anaesthetics, benzodiazepines

• Pharmacokinetics; absorption, bioavailability; hepatic clearance; renal drug handling, pharmacokinetic modelling, clearances, volumes of distribution

• Ionisation of drugs • Mechanism of drug action • Pharmaco-genetics • Anti-convulsants • Agents that decrease gastric acidity • Drug chirality

Inhalational agents

• Induction kinetics • Recovery • Washout curves • Inhalational depth, mechanisms of

action • MAC; MAC awake • Structure-activity relationships • Nitrous oxide, advantages and

disadvantages Obstetric pharmacology

• Tocolytics • Magnesium, salbutamol • Oxytocics; adverse effects • Placental transfer of drug

Local anaesthetics

• Structure activity • Pharmacokinetics • Toxicity, factors affecting toxicity,

toxic doses • Mechanisms of action

Induction agents

• Factors affecting induction dose and maintenance infusion rate

• Propofol pharmaceutics • Propofol pharmacokinetics • Cardiovascular effects • Principles of TIVA • Ketamine

Benzodiazepines • Mechanism of action • Pharmacokinetics • Adverse effects • Midazolam • Flumazenil

Neuromuscular blocking agents

• Factors affecting clinical choice and dose

• Recovery from neuromuscular blockade

• Neuromuscular monitoring • Inter-individual variability • Potency • Suxamethonium; dose response

curve, side effects • Malignant hyperthermia and

dantrolene Opioid agonists and antagonists

• Mechanism of action • Structure activity relationship • Pharmacokinetics • Pharmacodynamics • Adverse effects • Morphine, remifentanil • Oxycodone, buprenorphine • Tramadol • Neuraxial opioids

Anticholinesterase and anticholinergics

• Classification • Mechanisms of action • Muscarinic receptors • Adverse effects • Toxicology

Cardiovascular drugs

• Antiarrhythmics; classification, beta blockers, digoxin, amiodarone

• Drug therapy of myocardial ischemia • Anti-hypertensives • Calcium antagonists • Vasodilators; GTN and SNP • Inotropes

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Drugs and coagulation • Unfractionated heparin, low

molecular weight heparin • Warfarin • Antiplatelet drugs • Protamine

Pain

• Oral analgesics • Mechanisms of action • Bio-availability

Statistics

• Clinical trial design • Evidence based medicine • Levels of evidence • Meta-analysis • Selection of appropriate statistical

tests • Randomised controlled trials • Confidence intervals • Drug testing

Endocrine • Oral hypoglycaemic agents • Insulin

Histamine and antihistamines

• Histamine receptors • Anaphylaxis, mechanisms, drug

treatment Antiemetics

• Classification • Mechanisms of action • Adverse effects

PHYSIOLOGY – WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 76 % of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Describe the factors that oppose left ventricular ejection. 14 % of candidates passed this question. A large proportion of candidates misinterpreted this question to be about determinants of left ventricular ejection fraction and wasted a lot of time on describing pre-load, contractility and heart rate for which no marks were awarded. This is essentially a question about determinants of afterload which is the sum of all forces that oppose left ventricular ejection. Important points looked for were:

• Recognition that the sum of factors which oppose LV ejection is afterload. • Afterload can also be described as ventricular wall tension.

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Factors that determine afterload: • Systemic Vascular Resistance. Recognition that this is a major contributor to afterload.

Definition, role of SVR in determining afterload and factors which alter SVR attracted extra marks.

• Left ventricular outflow tract resistance and examples of conditions that change this e.g. aortic stenosis.

• Effect of aortic compliance on afterload. • Ventricular wall factors such as radius and thickness. The relevance of Laplace’s law in

relating ventricular wall radius and thickness to wall tension. • Effect of blood viscosity. • Effect of arterial impedance. • Effect of changes in intrathoracic pressure as a result of IPPV or other states. The fact

that IPPV actually reduces afterload by reducing transmural pressure was rarely stated. QUESTION 10 Describe the determinants of work of breathing in an adult human at

rest. 62 % of candidates passed this question. The main points expected were:

• Work is the product of pressure x volume and the SI unit is the Joule. • Inspiratory work has to overcome elastic and resistance forces. • Elastic work consists of deforming elastic tissues and overcoming surface tension. • Resistance work must overcome airway resistance and viscous forces. • Potential energy is acquired during inspiration and stored elastically to provide energy for

passive expiration. • The components of work of breathing are best illustrated on a pressure-volume diagram.

Additional points:

• The percentage contributions of the components to work of breathing. • The oxygen cost and efficiency of work of breathing.

Common errors included mislabelling axes and writing detailed descriptions of compliance, airway resistance and patho-physiological conditions. QUESTION 11 List the hormones that regulate tubular reabsorption and describe their

action and site of action. 81 % of candidates passed this question.

The five principal hormones of relevance to tubular re-absorption are; Angiotensin II, Aldosterone, ADH, ANP and Parathyroid Hormone. These are hormones affecting the absorption or excretion of Na+, H2O, Ca ++ and K+. In addition to listing these hormones, marks were awarded for clearly stating the action and precisely stating the site and mechanism of action. Many direct effects were relevant but indirect effects were also rewarded where they played a major part in these hormones’ actions on tubular re-absorption. The style of the question suited a highly structured answer. The candidates who used lists, headings, subheadings, space and columns were able to get many marks with relatively little writing. This style of answer was easy to understand.

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Many candidates wrote a lot about the processes involved in the release of these hormones which was not asked for and received no marks. Extra-renal effects were not rewarded e.g. effects of Angiotension II and ADH on systems vasculature. Likewise effects on non-tubular parts of the nephron e.g. renal bloodflow and glomerular filtration were often not relevant. Some candidates forgot Parathyroid Hormone and calcium re-absorption. Overall though, most candidates had a thorough knowledge of the topic, were able to communicate effectively and many good marks were awarded.

QUESTION 12 Explain the difference between viscosity and density. Outline the

effects of changes in viscosity and density on the flow of gases and liquids.

47 % of candidates passed this question. Many more candidates were able to adequately define density than viscosity. Few candidates noted that these are separate properties of gases and liquids and extra marks were awarded for noting that gases of similar viscosity may have differing densities e.g. helium and oxygen. Extra marks were also awarded for describing the effects of temperature on the density and viscosity of gases and liquids. The second part of this question should have included discussion on how both viscosity and density effect laminar and turbulent flow. The effects of viscosity on laminar flow, the Hagen-Poiseuille equation and the Reynold’s number were well described by most candidates. Common omissions were; comment on the effect of density on laminar flow, and comment on the effect of changing viscosity on turbulent flow. A common mistake was to state that turbulent flow was directly (rather than inversely) related to density. Many candidates gave detailed descriptions of the characteristics of laminar and turbulent flow that did not pertain to either viscosity or density and therefore did not attract any marks. QUESTION 13 Briefly describe the structure of a mammalian skeletal muscle fibre and

explain how its structure is related to its contractile function. DO NOT describe excitation-contraction coupling.

35 % of candidates passed this question. There were few high scoring answers. In order to pass this question, a simple outline of the structural components of the skeletal muscle fibre and their related functions as related to contraction would suffice. Additional marks were obtained for a more detailed description of the components of the muscle fibre and for disorders of the fibre structures. Many candidates confused the muscle fibre with myofibril or myofilaments, and as such were not able to obtain sufficient marks to pass. Many candidates failed to appreciate that the skeletal muscle fibre was a cell, and therefore did not mention basic cellular components, especially those modified to have a specific function in skeletal muscle fibres.

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QUESTION 14 Compare and contrast the physiological effects of a six hour fast of fluids and food with a twenty four hour fast in a healthy adult.

33 % of candidates passed this question. To pass this question, candidates were expected to appreciate that a six hour fast occurs daily and is thus well tolerated whilst a twenty four hour fast involves a significant mobilisation of reserves. In doing this, a comparison of the likely water and caloric requirements for each period, with some mention as to the origin of these calories, was required. An appreciation of the total fuel reserves available in a healthy adult, along with recognition of the thirst, hunger, lethargy and other physiological consequences of a twenty four hour fast would round out an acceptable answer. Additional marks were awarded to those candidates who were able to more fully quantify the use of reserves during a short and a longer fast and were able to briefly indicate the pathways the body utilises for glucose and ketone production. Few candidates appreciated that the liver is central in the adaptive process whereby the blood sugar level is maintained by the conversion of fat and amino acids to glucose. The most frequent reasons for not obtaining a pass mark were; the absence of enough information to indicate that the key principals were understood, and failing to mention the actual reserves of energy in the body. Very few candidates mentioned that a twenty four hour fast would render the patient hungry, thirsty and lethargic. Many candidates incorrectly used the words glucagon and glycogen interchangeably. QUESTION 15 Explain how a metabolic acidosis develops in hypovolaemic shock.

Describe the consequences of this metabolic acidosis for the body. 53 % of candidates passed this question. Candidates who scored well answered the question in a structured fashion, with definitions of the issues at hand and answered both sections. Although an understanding of how metabolic acidosis develops in hypovolaemic shock was essential, extra credit was earned for understanding the factors that exacerbate the metabolic acidosis in this situation and for demonstrated knowledge of the metabolic pathways involved. Some candidates demonstrated an excellent understanding of these and how they relate to one another. A common error among candidates was to detail physiological consequences of hypovolaemic shock at the expense of addressing the physiological consequences of metabolic acidosis. There was limited information on the cardiovascular effects of a metabolic acidosis. Many candidates were able to state that a metabolic acidosis results in myocardial depression. Few were able to outline how a metabolic acidosis effects the response of the cardiovascular system to sympathetic outflow, or at what pH these effects may occur. Respiratory and renal compensatory mechanisms, when addressed, were generally well described.

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QUESTION 16 Describe the physiological consequences of acute hypoglycaemia. 57 % of candidates passed this question. This was an applied question asking about hypoglycaemia. The physiological response has two broad components. The first is neurologic because of the brains’ reliance on glucose. These symptoms become increasingly serious as the hypoglycaemia worsens and range from confusion to coma, fitting and death. An early component is significant hunger. Associated with the neurologic response is the sympathetic response that is responsible for several of the signs of a “hypo”. This includes agitation, sweating and pallor. The other component is the endocrine response. The “aim” of this is to increase the blood sugar. This response includes decreased insulin production (if any is usually produced), and increased glucagon, cortisol, and growth hormone. Two errors were to include details of diabetic ketoacidosis and focussing on changes in plasma osmolality based on the equation that includes glucose. A minor point is that the Australian and New Zealand unit for glucose is mmol/l not mg/dl.

PHYSIOLOGY - VIVA SECTION PHYSIOLOGY TOPICS: Cardiovascular

• Determinants of cardiac output • Measurement of cardiac output • ECG • Arterial waveforms, radial and

aortic root • Pulmonary circulation • Pulmonary artery trace and

capillary wedge pressure • Frank-Starling relationship • Contractility • CVP waveform • Pressure-volume loops for ventricles • Myocardial oxygen balance • Blood pressure • Capillary exchange • Effects of IPPV, PEEP

Renal and acid/base

• Renal blood flow, regional variations • Glomerular filtration • Clearance • Renal production of concentrated

urine • Renal handling of water • Response to hypovolaemia • Kidney and acid base balance • Respiratory acidosis • Metabolic alkalosis

Respiratory • Lung volumes • Dead space • Regional lung differences • Alveolar gas equation, universal gas

equation • Oxygen cascade • Respiratory changes at altitude • Spirometry • V/Q mismatch • Mixed venous oxygen tension • Closing capacity, FRC • Respiratory effects of anaesthesia,

positioning • CO2 carriage • Forced expiratory flow loop • Physiological response to

hypercapnia, hypocapnia CNS/Pain

• Blood brain barrier • CSF, composition, production,

absorption • Cerebral blood flow • Sleep • Response to acute pain • Resting membrane potential

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Measurement • Errors in pulse oximetry • Pressure measurement • Arterial pressure monitoring • Damping • Principles of Doppler Ultrasound • Measurement of humidity • Temperature • Capnography • Pneumotachograph

Other • Thermoregulation • Oxygen delivery to the foetus • Principles of parenteral nutrition • Lipid metabolism • CHO metabolism • Amino acid metabolism • The red blood cell • I.V fluids • Functions of the liver • Immune function • Thyroid function • Anaemia, physiological effects • Diffusion, Fick’s law • Gastric contents, emptying • Lower oesophegeal function

Dr. N Roberts Chairman, Primary Examination Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY FELLOWSHIP EXAMINATION

FEBRUARY/APRIL 2006

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.

PHARMACOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 66 % of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Outline the pharmacologic management of bronchoconstriction in acute

severe asthma. Include mechanisms of action and potential adverse effects. 44 % of candidates passed this question. The main points to include were:

• A list of classes of drugs used to treat acute severe asthma • Representative examples of drugs • An explanation of how these drugs work • Significant side effects

The most important drugs that should have been included were β2 agonists, steroids, anticholinergics, volatile agents and methylxanthines. Discussion of leukotriene antagonists, ketamine, magnesium, oxygen and helium attracted additional marks.

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Many candidates wrote extensively about the pathophysiology of asthma which could not be credited any marks. Discussion of the mechanism of action of the drugs was often inadequately dealt with. Many answers either did not address this part of the question or stated that β2 agonism or muscarinic antagonism caused bronchodilatation without any discussion of second messengers. Those who did attempt a more detailed discussion often became confused about the change in cAMP and intracellular calcium level. Many answers were dismissive of the use of volatile agents in the treatment of asthma, despite the fact that they are convenient and readily available to treat bronchoconstriction in the setting of anaesthesia. QUESTION 2 What is an isomer? Briefly write an account of the types of isomers and

their significance in drugs used in anaesthesia. 53 % of candidates passed this question. The main points to include were a definition, classification and a description of specific drugs and the implications of isomerism. Many candidates had incorrect classifications. Some candidates described tautomers as a form of stereoisomers when in fact they are a subtype of structural (or constitutional) isomers. Similarly, a large number of candidates confused geometric isomers with structural isomers. Geometric isomers are stereoisomers that differ in the orientation of groups around a double bond or ring structure. Many of the diagrams were incorrect. It is also noted that many candidates neglected to mention the clinical significance of isomers. Better answers included specific examples such as enhanced analgesia with S-ketamine, lower cardiotoxicity with levobupivacaine and improved solubility of the enol form of thiopentone. QUESTION 3 List the non-ideal features of nitrous oxide. 58 % of candidates passed this question. The main points expected for a pass included: the drugs inability to be used as a single agent, diffusion hypoxia, expansion of gas-filled spaces and cobalt oxidation resulting in reduced activity of vitamin BB12. Additional marks were obtained for a description of additional adverse effects including, but not restricted to, non-ideal pharmaceutic properties, post-operative nausea and vomiting, pulmonary hypertension, increased cerebral blood flow, mild myocardial depression, sympathetic stimulation and increased homocysteine levels. Some candidates also described the difficulties associated with interpreting depth of anaesthesia monitoring when administering N2O and its potential for abuse. Forty percent of candidates failed to mention diffusion hypoxia. Also, there was some confusion regarding the relative solubilities of N2O, O2 and N2 and how this affects expansion of gas filled spaces.

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QUESTION 4 Describe the pharmacodynamic properties of propofol and how this influences its clinical usage.

69 % of candidates passed this question.

It was expected emphasis be placed on the central nervous system effects, followed by the cardiovascular and respiratory effects and marks were allocated accordingly. The question was specifically related to pharmacodynamics and a discussion of pharmacokinetic properties scored no additional marks. Candidates were expected to outline that Propofol is an intravenous anaesthetic agent used for both the induction and maintenance of anaesthesia or sedation. Reward was given to candidates who outlined potential mechanisms of action, the dose dependent nature of effects, the effects on the EEG and on cerebral metabolism. Further credit was given for describing how this might impact on its clinical use (e.g. neurosurgery). A description of the cardiovascular effects was expected to include reference to hypotension, reduced systemic vascular resistance and bradycardia with comment on those patients at risk. Respiratory effects include alterations in ventilatory response, reduction in airway reflexes and bronchial tone. Extra credit was given for discussion of other pharmacodynamic properties including; anti-emetic, anti-pruritic, non MH triggering, pain on injection, lipid/caloric load, reduction in intraocular pressure and risk of propofol infusion syndrome. It was expected that candidates would relate each pharmacodynamic effect to the impact on clinical use and failing to address this was a common omission (e.g. reduction of airway reflexes is useful for LMA insertion or airway manipulation). Well organised answers such as those with an ordered list with subheadings or a table were rewarded. QUESTION 5 Write short notes on factors affecting the speed of onset and duration of

effect of local anaesthetics when used to produce peripheral nerve block. 89 % of candidates passed this question. This question required candidates to write short notes and candidates who simply wrote a list without explanation failed to achieve high marks. Likewise the question clearly required candidates to address the issues of both speed of onset as well as duration of action. Some candidates answered only one part of this two part question and failed to achieve high marks. Better answers attempted to differentiate between the factors that affect speed of onset and those that affect duration. Many of the better answers related the answer to aspects of the Fick Principle. Patient factors include:

• Site of administration • Nerve structure and function • Tissue pH • Pregnancy • Electrolyte disturbances

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Drug factors include: • pKa and its effect on non ionised fraction • Lipid solubility and its effect on potency and protein binding • Concentration and volume added • Intrinsic vasoactive properties • Effect of local and distant metabolism • Effect of different additives

QUESTION 6 Explain the possible mechanisms for prolonged neuromuscular blockade

after a four hour procedure using a non-depolarising muscle relaxant. 34 % of candidates passed this question. The main mechanisms expected to be addressed were:

• Overdose • Pharmacokinetic; hypothermia, hepatic failure, renal failure • Pharmacodynamic

o drug interactions (e.g. volatiles, antibiotics) o physiological disturbance (hypothermia, acidosis, electrolyte abnormalities) o neuromuscular abnormality ( e.g. myaesthenia gravis)

Candidates were asked to "Explain..." the mechanisms by which the various mechanisms produced prolonged neuromuscular blockade. For example, overdosage might be produced by a dose calculation error, repeated bolus or infusion without neuromuscular monitoring, or a drug swap error with a long acting agent. The majority of candidates listed some mechanisms that could prolong neuromuscular block but frequently omitted an adequate explanation. Few answers considered the potential for a combined effect created by the clinical context of the question. A four hour case will commonly require repeated doses of neuromuscular blockers, long exposure to volatile anaesthetic agents, and may result in patient hypothermia and acidosis. QUESTION 7 Briefly outline the pharmacology of naloxone. 73 % of candidates passed this question. The majority of answers were well organized. The main points to include were:

• Pharmaceutics • Pharmacokinetics

o IV and IM administration o High clearance, short half life o High lipid solubility o Clinical implications

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• Pharmacodynamics o Competitive mu opioid receptor antagonist o Clinical applications o Adverse effects

Common problems included; lack of organization, failure to discuss the important pharmacokinetic properties or the potential serious adverse effects of naloxone. QUESTION 8 In a clinical trial, why is adequate power important? What factors affect

the determination of an adequate sample size? 46 % of candidates passed this question. Candidates were expected to provide a definition of what “Statistical Power” is in the context of a clinical trial and to show a good understanding of the concept. Most candidates were able to identify why it is important for a trial to have appropriate power. Many demonstrated inadequate understanding of the relationship between sample size and power. Although mathematical equations for sample size calculation were not required, an understanding of the different factors and their significance were expected. Candidates needed to discuss alpha and beta error, measurement effect and measurement variability. Very few candidates mentioned that different formulas and nomograms are often used and currently computer programs make sample size calculations more precise. Many candidates mentioned the main factors affecting sample size but most failed to give the desired values commonly used for alpha and beta error or how population variability is estimated. Candidates who mentioned why meta-analysis increases statistical power, the issues with multiple outcomes, interim analysis and drop out gained more marks.

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PHARMACOLOGY – VIVA SECTION

PHARMACOLOGY TOPICS: General topics

• Pharmaceutics; thiopentone, local anaesthetics, benzodiazepines • Pharmacokinetics; absorption, bioavailability; hepatic clearance; renal drug handling,

pharmacokinetic modelling, clearances, volume of distribution • Ionization of drug • Mechanism of drug action • IV Fluids, properties and kinetics • Agents that decrease gastric acidity • Paracetamol • Oxygen: therapeutic use, side effects, storage, manufacture of gas

Inhalational agents

• Induction kinetics • Time to awakening • Washout curves • MAC; MAC awake • Structure-activity relationship • Desflurane vs. isoflurane

Obstetric pharmacology

• Tocolytics • Desirable and adverse effects of magnesium • Oxytocics; adverse effects • Placental transfer of drug

Local anaesthetics

• Toxicity, factors affecting toxicity • Topical anaesthesia • EMLA cream, amethocaine gel

Induction agents

• Factors affecting induction dose and maintenance infusion rate • Propofol pharmacokinetics

Benzodiazepines

• Mechanism of action • Pharmacokinetics • Toxicology • Antidotes

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Neuromuscular blocking agents • Factors affecting clinical choice and dose • Neuromuscular monitoring • Potency • Suxamethonium; dose response curve, side effects

Opioid agonist and antagonist

• Mechanism of action • Structure activity relationship • Pharmacokinetics • Adverse effects

NSAIDS

• COX1 and COX2 agents; kinetics, side effects Anticholinesterase and anticholinergics

• Classification • Muscarinic receptors • Adverse effects • Toxicology

Cardiovascular drugs

• Antiarrhythmics; classification, beta blockers, digoxin • Clonidine • Vasopressors; metaraminol, ephedrine, phenylephrine; vasopressin • Vasodilators; GTN and SNP • Inotropes • Drugs used for cardiac arrest

Drugs and coagulation

• Unfractionated heparin, low molecular weight heparin • Antiplatelet drugs • Protamine

Statistics

• Selection of appropriate statistical tests • ANOVA • Nonparametric tests • Diagnostic tests • Relative risk • Odds ratio • Number needed to treat

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Endocrine • Oral hypoglycaemic agents • Insulin

Diuretics

• Mechanism of action • Toxicology • Dose-response relationship

Histamine and antihistamines

• Pharmacodynamic effects • Adverse effects

Chemotherapeutic (including antibiotics) agents

• Mechanism of action • Toxicology • Implications in clinical anaesthesia • Allergy

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PHYSIOLOGY – WRITTEN SECTION

MULTIPLE CHOICE QUESTIONS: 71 % of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Outline the systemic cardiovascular response to exercise. 71 % of candidates passed this question. An overall understanding of the systemic CVS response to exercise was looked for. Very few candidates noted the important difference between isotonic and isometric exercise, with corresponding differences in total peripheral resistance. Some candidates didn’t realise that heart rate increases in exercise. Candidates who scored well demonstrated an overall understanding that exercising muscle needs an increased blood/oxygen/nutrient flow and directed their answers to include all the systems that combine to do so. They included redirection of blood from splanchnic circulation, a right shift in the Oxy haemoglobin curve, 2, 3 DPG, sympathetic and parasympathetic nervous systems, and muscle and thoracic pumps for example. See Ganong 22nd edition pages 632 - 634. QUESTION 10 List the physiological factors which increase respiratory rate and include a

brief explanation of the mechanism by which each achieves this increase. 62 % of candidates passed this question. Points required for a pass were: Listing and understanding of the mechanisms by which hypoxia, hypercapnia, and acidosis induce hyperpnoea plus some of the other common causes of tachypnoea (e.g. exercise, increased BMR, hypotension, activation of skeletal muscle stretch, various pulmonary conditions/receptors/work of breathing, CNS causes - voluntary control and in response to pain, age, pregnancy.. Additional marks were given for: Quantitative description of various stimuli, synergistic interactions. Whilst some marks were awarded for description of the various brain-stem centres that control breathing, the descriptions were often not directly linked to tachypnoea. Some candidates wasted time describing factors that slowed respiratory rate, and the definitions of alveolar ventilation.

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QUESTION 11 Briefly outline the role of platelets in haemostasis. 60 % of candidates passed this question. In general this question was well answered. To achieve a pass, candidates needed to describe the involvement of platelets in both primary and secondary haemostasis i.e. platelet adhesion, release reaction, platelet aggregation and then their involvement in the coagulation cascade. Some answers were very detailed on particular roles but the candidates failed to cover the range of actions of platelets. Some candidates focused on pharmacology of anti-platelet agents, which did not answer this question. Extra marks were allocated for general information on the production of platelets, their size and numbers, for explaining contractile elements of platelets, and their involvement in vessel repair. QUESTION 12 Classify and describe the main cellular and molecular mechanisms by

which chemical neurotransmitters exert their effects. Use examples from cholinergic and adrenergic neurotransmission to illustrate the answer.

42 % of candidates passed this question. There were a wide range of marks for this question; however there were a few very good answers. It was important that candidates read the question. The question was based around cellular and molecular mechanisms, with candidates asked to classify and describe them. Importantly examples from the cholinergic vs. adrenergic systems were expected and it was notable that many candidates chose examples from different systems. In general terms, neuro transmitters can exert their affects on ion channels in cell membranes or through intracellular affects. Ion channels can be affected by receptor agonists or antagonists, directly or indirectly (through, for example, G proteins). Intracellular events are usually mediated via G proteins and second messenger systems. Most candidates addressed the issue of agonists and antagonists at cell membrane receptors affecting ion channels well, most usually citing the neuromuscular junction as an example. Most candidates dealt well with the G protein mediated second messenger system, and cited a number of examples. The effects of G proteins on ion channels were very rarely mentioned. This is relevant for example, M1 muscarinic receptors. Areas such as the relative response times of G protein verses direct ion channel effects, modulation and/or amplification, and other complex affects such as MRNA transcription or other neuro modulators were rarely mentioned.

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QUESTION 13 Describe the factors that influence metabolic rate. 48 % of candidates passed this question. Most candidates provided a reasonable list of factors which influence metabolic rate. Many candidates incorrectly equated “basal metabolic rate” (BMR) with “metabolic rate”. Excessive focus on BMR sometimes detracted from discussion of more general concepts pertinent to metabolic rate. There were significant problems describing the influence of “temperature” on metabolic rate. Ambient temperature was not always distinguished from core body temperature. The distinction between the raised metabolic rate, which accompanies small falls in body temperature versus the lowering of metabolic rate with more severe hypothermia or when muscle metabolic responses are blocked by anaesthesia and muscle relaxants was often not made clear. Few answers provided a good overview and very few demonstrated an understanding of the role of skeletal muscle as the single largest and most variable source of energy production and thus the origin of the greatest changes in metabolic rate in an individual. The effect of consumption of differing food types on metabolic rate was frequently a source of confusion. The “specific dynamic action” (SDA) relates to the energy required to assimilate food, (protein > carbohydrate (1/5 that of protein) > fat (2/3 that of carbohydrate)). SDA is not related to the respiratory quotient (RQ) which also varies with food type. The RQ may be of importance for estimating metabolic rate if carbon dioxide production is being measured as a surrogate for metabolic rate. Neither SDA nor RQ is related to the energy produced per gram of food. QUESTION 14 Explain the physiological processes which cause oliguria in response to

hypovolaemic shock. 38 % of candidates passed this question. This question has been asked on two previous occasions. The Examiner Reports from then are well worth reviewing. The following points and concepts should have been included:

• A simple brief definition of hypovolaemic shock and oliguria • The result is to reduce sodium loss and increase water retention • How renal blood flow is reduced and why this is beneficial • Mechanisms for the reduction in glomerular filtration rate (GFR), and the relationship of GFR

to renal artery pressure • Activation of the renin-angiotensin-aldosterone (RAA) system starting with prorenin and

listing the roles of angiotensin II • Effects of aldosterone and anti-diuretic hormone

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Lack of detail around mechanisms of action was common and many candidates did not mention autoregulation of renal blood flow or the relationship of renal artery pressure and GFR. Afferent and efferent glomerular arteriolar effects of angiotensin II and noradrenaline were often confused. A lengthy description of systemic blood pressure control, the factors comprising Starling’s equation, and the counter-current mechanism was not expected. Details on atrial naturetic peptide were not relevant to the mechanisms of oliguria. This question required a well organised answer so that the major points could be covered in enough detail. QUESTION 15 Briefly describe the measurement of pH in a blood sample using a pH

electrode. 49 % of candidates passed this question. For a pass, the answer needed to include a description of the apparatus used, including the presence of pH sensitive glass, two reference electrodes Ag/AgCl and the same, or calomel (Hg/HgCl2) although more modern machines do not use the calomel electrode, a salt bridge to complete the circuit, connecting the calomel or 2nd Ag/AgCl electrode to the test solution, a buffer solution separated from the sample by pH sensitive glass. The only variable in the circuit, given constant temperature, is the difference in pH between the buffer and sample. The electrode potential depends on the Hydrogen ion activity, so the voltage measured in the circuit is proportional to pH. There is a need to calibrate against two known pH Phosphate solutions, and the system must be temperature controlled to 37C. The device is an example of an ion-sensitive electrode. A clearly-labelled diagram was a great help, and although not required for a pass, most of the better answers did include one. In the absence of a diagram, a very clear description was required. Some answers unfortunately had a diagram at odds with the text, making it very difficult to assess understanding. Better answers included detail about how the glass is pH-sensitive, why saturated KCl is used as the salt bridge, a correct definition of pH, and additional information about minimization of error. Lengthy discussion of CO2 control in hypothermia gained little and usually left minimal information that actually answered the question. Answers which described the Clarke or Severinghaus electrodes gained no marks. Many answers included a reasonable diagram but text that inferred a very poor understanding of what was drawn. The concept of an electrical circuit was absent in most answers that failed. Several dozen answers defined pH incorrectly, as a variable in the Henderson-Hasselbalch equation. No candidate mentioned solid-state ion-sensitive field-effect transistors which have been used in pH measurement for 10 or more years.

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QUESTION 16 Describe the physiological factors that contribute to the competence and tone of the lower oesophageal sphincter.

58 % of candidates passed this question. This question has been asked twice before in recent exam history. The main points sought were:

• The anatomical features that maintain the lower oesophageal sphincter, including the coordination of the diaphragmatic crura and the “pinch-cock” effect with contraction of the diaphragm with breathing and coughing. The importance of the lower portion the oesophagus being intraabdominal. The oblique passage into the stomach allowing the increase in gastric tone to further enhance closing and push the mucosal folds into the lower oesophagus contributing the mucosal flap valve.

• An understanding of the concept of “barrier pressure” to reflux of abdominal contents and normal values for pressures involved.

• The neural innervation of both the internal and external portions of the sphincter, i.e. vagal and phrenic respectively and the part the autonomic nervous system played in maintaining lower oesophageal tone.

• The hormones that alter the tone of the sphincter, including gastrin, secretin, CCK, VIP, motilin, progesterone, oestrogen, PGE2.

• Alteration of tone due to physical factors such as raised intraabdominal pressure, swallowing, and gastric content acidity.

Marks were given for all of the above as facts and additional marks were given for demonstrating the mechanism of action of the anatomical features and how changes in physiology (e.g. with pregnancy, diabetes, vagotomy) or anatomy, (e.g. obesity, pregnancy, hiatus hernia) alter the barrier pressure. Many candidates did not cover the breadth of this question focusing either on the anatomical features or the hormonal control and therefore while obtaining a pass not achieving high marks. Unfortunately, as has occurred with this question in the past, some candidates wasted time writing about pharmacology that was not asked for in a physiology paper.

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PHYSIOLOGY - VIVA SECTION

PHYSIOLOGY TOPICS: Cardiovascular

• Pulmonary capillary wedge pressure • Cardiac Muscle action potential • Determinants of venous return • Determinants of cardiac output • Cardiovascular effects of aging • ECG • Arterial waveforms-radial and aortic root • Pulmonary circulation • Frank-Starling relationship • Contractility • Cerebral blood flow • CVP waveform • Pressure-volume loops for ventricles • Response to sudden vasodilatation • Myocardial oxygen balance • Blood pressure

Respiratory

• Dead Space • FRC • Regional Lung differences • Oxygen cascade • O2 flux at altitude • Response to sudden occlusion of the pulmonary artery • Spirometry • V/Q mismatch • Surfactant • Compliance • Respiratory changes with aging • Respiratory changes with pregnancy. • CO2 carriage • Forced expiratory flow loop • PV loop • Physiological response to hypercapnia • Capnography

Renal

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• Renal handling of acid • Renal blood flow • Clearance • Renal production of concentrated urine • Renal handling of water • Response to hypovolaemia

CNS/Pain

• Intracranial waveform • Cerebral blood flow • Sleep • Arousal • CSF • EEG waveforms • Response to acute pain • Response to acute injury

Measurement

• Errors in pulse oximetry • Arterial pressure monitoring • Damping • Principles of Doppler Ultrasound • Measurement of humidity • Temperature • Capnography • Pneumotachograph

Other

• Thermoregulation • Fasting • Lipid digestion • CHO digestion • The red blood cell • Calcium metabolism • Maternal-foetal oxygen transport • Amino acids • Potassium • Body defence mechanisms • Skeletal muscle • Peripheral nerve • Nerve fibres

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Dr. N Roberts Chairman, Primary Examination Committee

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

JULY/AUGUST 2004

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.

PHARMACOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 71% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Briefly describe how drugs produce their pharmacological effects. Illustrate each

mechanism with examples.

67% of candidates passed this question. Generally discussion of receptor mediated mechanisms was excellent, with ligand gated, G-protein, tyrosine kinase & intracellular DNA receptors being well covered with appropriate examples. Non receptor mechanisms are clearly important also. Some candidates confused local anaesthetics as being ligand gated receptor mediated when in fact they have direct action on ion channels. For a complete answer non-receptor mechanisms also include carrier molecules, effects on enzymes, direct chemical interaction, colligative properties and structural analogues (counterfeiting). Finally mechanisms which are unknown or not fully elucidated are relevant and received marks (eg volatile anaesthetic agents, placebo effect). Some candidates gave erudite discussions on pharmacokinetics but this did not answer the question. Good answers divided the answer into receptor and non-receptor mechanisms and didn’t get bogged down in one area. A common issue was spending too much discussion on G-protein coupled receptors at the expense of other areas.

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QUESTION 2 Write a brief description of the pharmacology of ropivacaine. 46% of candidates passed this question. The main points that should have been included were correct recognition of the drug and its chemistry and basic knowledge of the pharmacokinetics (pKa, T1/2 and protein binding). The unique pharmacodynamic features including differential block, toxicity and the relevance of these to the clinical usage of the drug should have been mentioned. Additional accurate information about the chemical structure, mode of action and kinetics was rewarded. A concise correct answer is preferred; many answers included a large amount of repeated and, at times, inaccurate information. It was concerning that many answers stated that ropivacaine was suitable for intravenous regional anaesthesia. QUESTION 3 List the effects of histamine. Write a brief outline on the pharmacology of the H1

blocking drugs. 26% of candidates passed this question. The first part of the question asked for a list of effects. It was not productive to write notes on the chemistry or distribution of histamine, or discuss its role in anaphylaxis. Less than half the candidates produced a minimal list that included bronchoconstriction, vasodilatation, increased vascular permeability, acid secretion and one central nervous system effect. Better answers were able to ascribe the correct receptor subtypes to a comprehensive list, and also include the effects of histamine at a cellular level. The second part of the question was also handled poorly, with a significant number of candidates leaving it unanswered, discussing H2 blocking drugs, or other drugs that were not antihistamines. Some candidates wrote about only one antihistamine, but because the H1 blockers are a diverse group, it was necessary to include other examples. Specific H1 blockers are relatively new and used mainly for the management of allergic conditions. Older antihistamines are not specific, have more diverse indications, and often have a number of side effects. However, sedation may become a desired effect, as is the case with promethazine that has been used in premedication. Although several uses were often listed for H1 blockers, it was important to match these with an appropriate drug because not every antihistamine is appropriate for every indication. QUESTION 4 Write short notes on tramadol. 50% of candidates passed this question. Many candidates handled this question well. A complete answer was helped by organising the essay around sub-headings such as pharmacodynamics, pharmacokinetics, adverse effects and so on. While most answers recognised that tramadol is presented as a racemic mixture, only a proportion went on to say that each isomer had specific effects contributing to the analgesic effect of the drug. Likewise, while the majority of answers noted that the drug has actions on opioid and non-opioid sites, nobody mentioned that the drug’s analgesic effect is as a result of this somewhat peculiar synergistic activity. As an analgesic, it is useful to compare it to a standard opioid such as morphine and most did so, noting its reduced potential for the development of tolerance and dependence and respiratory depression. Pharmacokinetic aspects were less well handled with many failing to note that tramadol is highly metabolised and that one metabolite (M1 or O-desmethyl tramadol) has considerable activity at the opioid receptor and may contribute to the drugs activity. As with codeine, a proportion of patients deficient in the P450 cytochrome CYP2D6 enzyme will fail to form this product and may exhibit reduced analgesia. Some candidates noted other interesting features of the drug such as an improvement in oral bioavailability with multiple dosing; the suggestion that tramadol might increase the risk of awareness under general anaesthesia and that tramadol’s analgesic effect might be antagonised by 5HT3 antagonists. QUESTION 5 What are the strengths and weaknesses of the randomised controlled trial (RCT)

study design?

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49% of candidates passed this question. Answers needed to include the following points. The RCT is a “gold standard”, level II evidence clinical trial allocating volunteers or subjects to one of two groups i.e. a control and a treatment group. Strengths lie in:

• Ability to assign and administer treatment or intervention in a precise, controlled way (avoiding differing techniques)

• Randomisation of subjects or participants aims at decreasing selection bias and minimizing confounders due to unequal distribution in a chosen population

• Measurements, especially parametric data can be chosen precisely making it easier to make observations consistently

• Blinding is easier in RCT improving credibility plus decreasing patient or observer bias • Controlling of group allocations enhance similarity of baseline features so it is easier to form basis for

statistical hypothesis Weaknesses include:

• The increased expense and time consumption, difficult to organize/supervise if multiple sites/locations • Realization that results may not always mimic real life treatment situation • Risk of choosing treatments or subjects whose consent is not valid or unethical treatment is involved

Some other valid points were made:

• If a small trial can include very stringent parameters which are somewhat of an academic nature but will decrease Type I errors as well as test efficacy. Such RCT may lack applicability and be too specific for a chosen population.

• Can make the trial large o good for detecting small but clinically relevant conclusions o more expensive yet decreasing Type II errors

• RCTs can have subgroup analysis enhancing the usefulness for clinical practice. • A successful RCT with conclusive or inconclusive results is eminently publishable.

QUESTION 6 Compare and contrast neostigmine and the organophosphorus compounds. 52% of candidates passed this question. The main points expected in the answer in order to pass were considered under three main headings – (i) pharmacokinetics (ii) mode of action and (iii) pharmacological effects, mainly due to increased acetylcholine. A common mistake was to not discuss the actions of the drugs. They are both anti-cholinesterases which inhibit both acetylcholinesterase and plasma cholinesterase. There are important differences in polarity and lipid solubility which contribute to contrasting distribution in the body for the two compounds. Neostigmine is not distributed to the central nervous system (CNS) whereas organophosphorus compounds are widely distributed including the CNS. Neostigmine is an ionised water-soluble compound which has hepatic and renal elimination. Organophosphorus compounds depend on synthesis of acetylcholinesterase because of the stability of the enzyme-inhibitor complex and a process called “aging”.

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The mode of action for neostigmine at the target enzyme is similar to the way acetylcholine is handled, except the covalent bond of the carbamoylated enzyme is considerably more resistant to hydration and leads to a prolonged thirty minute duration of effect. Organophosphorus compounds have a half-life of weeks to months because of phosphorylation of the esteratic site covalent bond. Inhibition of acetylcholinesterase not only increases the concentration of acetylcholine at the neuromuscular junction but at all other synapses that use acetylcholine as a transmitter. These include the muscarinic receptors of the parasympathetic nervous system, the nicotinic receptors of the autonomic ganglia, and the smooth muscles especially of the respiratory and gastrointestinal tract. Organophosphorus compounds have CNS muscarinic effects that include excitation, confusion and coma. QUESTION 7 Outline the factors which influence the elimination half-life of propofol. 29% of candidates passed this question. This question focused on the application of pharmacokinetics principles to the systemic elimination of propofol. Therefore, candidates were expected to provide a definition of the determinants of elimination half-life and its mathematical model with factual data representative of propofol. Factors that affected hepatic clearance of propofol in particular liver blood flow, severe liver disease, drugs and age should have been mentioned. Enzymatic activity has little influence in the face of the high hepatic extraction ratio of propofol. Similarly, factors affecting volume of distribution at steady state like body fat content should have been mentioned. Many candidates presented irrelevant information such as indications, comparative kinetics with thiopentone and lengthy description of propofol kinetics by infusion. Candidates who mentioned the effects of individual patient variability, hypothermia and critical illness on elimination half-life gained extra marks. QUESTION 8 List the classes of drugs used clinically to treat chronic left ventricular failure.

Outline their mechanisms of action. 25% of candidates passed this question. A good answer included information on ACE inhibitors, beta-blockers, diuretics, digoxin and nitrates. Mention could also be made of calcium channel blockers, orally administered phosphodiesterase inhibitors and new drugs, but preferably with comments about why they are not often used in the treatment of chronic failure. Ideally, mechanisms included the cellular or receptor mechanism of drug action and effects of preload, contractility, afterload and alterations in renal function. Most candidates omitted one or more of the major drug classes. Many candidates spent a lot of time describing drugs used in the management of acute or acute-on-chronic failure, such as adrenaline, dobutamine, oxygen, calcium, glucagon and phosphodiesterase inhibitors. Some discussed drugs used in the treatment of associated conditions such as hypertension or ischaemic heart disease. Some candidates wrote about drugs that are not used currently in chronic heart failure such as hydrallazine and sodium nitroprusside.

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VIVA SECTION INTRODUCTORY PHARMACOLOGY TOPICS: General topics

• Bio-availability • Pharmaceutics; thiopentone, propofol, local anaesthetics, • Pharmacokinetics; midazolam, propofol • Anaphylaxis • Isomerism • IV fluids, properties and kinetics

Opioids • Mechanism of action • Adverse effects • Remifentanil; kinetics, dynamics • Advantages, disadvantages • Choice of opioid

Cholinergic, anticholinergic drugs • Atropine

Inhalational agents • Speed of induction • Fa/Fi curves • Time to awakening • MAC • Structure activity • Nitrous oxide • CVS and CNS effects of inhalational agents • Desflurane and sevoflurane

Obstetric pharmacology • Tocolytics and mechanisms of action • Adverse effects of magnesium and salbutamol • Oxytocics • Adverse effects of oxytocics

Local anaesthetics • Factors effecting toxicity • Lignocaine and bupivacaine toxicity • Toxic doses • Management of toxicity • Structure activity • Kinetics

Induction agents • Ketamine; CVS, CNS effects • NMDA receptor • Propofol; CVS, CNS effects • Pharmacokinetics of induction and recovery • Effect site concentration

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Anti-arrhythmic drugs • Classification • Pharmacological management of ventricular fibrillation • Amiodarone • Lignocaine • Sotalol

Neuromuscular blocking agents • Kinetics • Adverse effects • Recovery from non-depolarising relaxants • Assessment of recovery • Neuromuscular monitoring • Cisatracurium and vecuronium

Diuretics • Classify • Mechanism of action

Pain • NSAIDS; classification, kinetics, mechanism of action, adverse effects • Opioids

Anticonvulsants • Classify • Phenytoin

Adrenoceptor blocking agents • Beta blocker pharmacodynamics • Adverse effects

Cardiovascular drugs • Pharmacology of adrenaline • Vasopressin • Drug therapy of myocardial ischaemia • Calcium channel antagonists

Statistics • Types of data • Parametric and non parametric tests

Anticoagulant and anti-platelet agents • Mechanisms of action • Adverse effects • Heparin and LMWH

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PHYSIOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 72% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Describe how carbon dioxide is produced in the body. How does it move from

the site of production to the pulmonary capillary? 60% of candidates passed this question. The points required for a pass included

• Site of production of carbon dioxide • Amount of carbon dioxide produced • A brief description of the mechanism of production • The transfer of carbon dioxide from its site of production to the blood down its concentration gradient • The mechanisms of carriage of carbon dioxide in the blood • The amounts carried in each form

Additional credit was given for

• An explanation of the Haldane effect • The differences in carbon dioxide with different substrates • Situations in which there is greater or less production of carbon dioxide • Normal values for the partial pressure of carbon dioxide in venous blood

Common errors included

• Failure to understand that carbon dioxide is produced with aerobic metabolism • A description of the arterial carriage of carbon dioxide rather than venous carriage • Describing the elimination of carbon dioxide, which was not asked for in the question

Common omissions included

• The transfer of carbon dioxide from the mitochondria to blood • The presence of a concentration gradient down which carbon dioxide moves

QUESTION 10 List the physiological factors which affect left atrial pressure and explain their

effects. 19% of candidates passed this question. Candidates were rewarded one mark for each correct factor they listed. The list of factors could be considered in three categories:

• Venous return: influenced by blood volume, posture, venous tone, intrathoracic pressure and intrapericardial pressure

• Left ventricular emptying: influence by contractility and afterload • Left ventricular filling: influenced by the diastolic compliance and mitral valve disease.

Additionally, listing variations in heart rate and obstruction to pulmonary flow were rewarded with additional marks.

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For the second part of the question, marks were awarded for a statement as to how the left atrial pressure (LAP) would be affected by a change in each of the factors listed by the candidate. Whilst a statement of the range of normal LAP gained further credit, the range of pressures quoted was often incorrect. Many candidates only listed a few of the factors that affect LAP thus limiting the mark they could expect to achieve. A common misunderstanding was the effect of an increase in intrathoracic pressure on the LAP with many candidates concluding that IPPV will increase the LAP. QUESTION 11 Briefly explain how oximetry can be used to estimate the partial pressure of

oxygen in a blood sample. 31% of candidates passed this question. This question required integration and application of knowledge about oximetry and the oxygen haemoglobin dissociation curve. Candidates were expected to briefly cover how an oximeter measured haemoglobin saturation in a blood sample, the Beer Lambert law either as a formula or as a written description and the link between haemoglobin saturation and partial pressure of O2 via the oxygen haemoglobin dissociation curve with some common values. Better candidates also described the assumptions and the inaccuracies made in the link between haemoglobin saturation and partial pressure of O2, eg shift of the oxygen haemoglobin curve with changes in pH, pCO2, temperature, 2,3 DPG, the difficulty in deducing pO2 when haemoglobin is fully saturated due to the flat upper portion of the oxygen haemoglobin curve. Common mistakes included writing about the Clark electrode, oxygen content of blood, discussion of pulse oximetry and its inaccuracies, applying the effects of other types of haemoglobin on pulse oximetry to co-oximetry of a blood sample and claiming that oximetry measured the oxygen in the blood directly. QUESTION 12 Briefly describe the secretion and functions of renin and angiotensin. 48% of candidates passed this question. This question was asked in a slightly different form in July 2002 and attracted a similar pass rate at that time.

The main points that would gain a pass were: • A description of the site of release of renin. • The main stimuli that lead to the release of renin, including a reduction of systemic blood pressure and

extracellular fluid, an increase in sympathetic stimulation and a decreased delivery of solutes to the macula densa.

• The cleaving angiotensin I from angiotensinogen by renin. • The conversion of angiotensin I to angiotensin II by the action of angiotensin converting enzyme,

mainly by contact with pulmonary endothelium. • A description of the main functions of angiotensin II, including vasoconstriction, alteration of

glomerular filtration rate, direct action on the renal tubules and stimulation of aldosterone secretion. • The ability of angiotensin II to inhibit the secretion of renin. • This process leading ultimately to conservation of sodium and water.

Additional information that attracted further marks included:

• Detailed information about the process of renin secretion. • Describing other stimuli for renin secretion over and above those described above. • Explaining the site of synthesis of angiotensinogen. • A description of the size, structure and half-lives of renin and the various subtypes of angiotensin. • Other functions of angiotensin II, over and above those described above. • The relative potency of angiotensin III. • More detailed descriptions of the intimate processes and interactions of the system.

Common mistakes or omissions included:

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• Confusion over the exact cells that secrete renin. • Inexact descriptions or omissions of the interrelationship of renin to angiotensin. • Confusion over the way solute load reaching the macula densa affects renin secretion. • Incorrect associations with the process of tubuloglomerular feedback. • Very detailed and often correct descriptions of the actions of aldosterone and vasopressin, at the

expense of the required information. QUESTION 13 Describe the functions of the gastric secretions. 45% of candidates passed this question. The question asked about gastric secretions and their actions. Lengthy descriptions of the control of gastric secretions did not attract marks and would have consumed a significant component of the time available. Some answers did not go beyond control of gastric secretions and did not answer the question asked. The constituents needed to be identified, namely HCl, pepsinogen, mucus and bicarbonate, intrinsic factor (IF) and gastrin. Additional points were attracted for mention of other constituents e.g. gastric lipase and their functions. The breakdown of the action of each of these components was useful in an organised answer to the question. Example: HCI Main points such as activation of pepsinogen to pepsin by HCl, its direct proteolytic action, its bactericidal property and its effect on ‘innate immunity’. Additional points were attracted for discussion of its effect on ferric ion to its more soluble ferrous form, and its stimulant action on biliary and pancreatic secretions. A similar approach could have been adopted for the other products. QUESTION 14 Briefly describe the difference between a single twitch and a tetanic contraction

in a skeletal muscle fibre. Include in your answer the physiological basis for the development of a tetanic contraction.

54% of candidates passed this question. This question required an understanding of the physiological basis of a single twitch versus a tetanic contraction. In particular, it was expected that the answers made reference to the following concepts with regards a tetanic contraction:

• The requirement for repetitive stimulation • The importance of the frequency of the stimuli • The difference between incomplete tetanic contraction and complete tetanic contraction • The critical frequency required for tetanic contraction and its relationship to the single twitch

duration for that fibre • That the contractile mechanism of skeletal muscle has no refractory period

Candidates also earned marks for outlining the sequence of events from motor nerve action potential to muscle depolarisation and subsequent contraction. Some candidates included a comparison with cardiac muscle action potential and its important differences regarding the question of tetanic contraction. The most common errors related to confusion regarding what is summating or fusing in a tetanic response. This mainly was in relation to whether it was the action potential or the contractile response or both that were summating in tetanic type contractions.

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QUESTION 15 Describe the mechanism of action of G-proteins in the cell. 60% of candidates passed this question. To achieve a pass mark, it was expected that the answer would include:

• An indication of the general concept of G-proteins acting as a kind of transducer, converting an extra-cellular event (ligand associating with a G-protein coupled receptor (GPCR)) into a series of intra-cellular events involving 2nd messenger systems.

• A summary of the sequence of events that occurs in this transduction i.e. ligand binds to receptor, brings about a conformational change such that the α-subunit of the G-protein binds GTP, then dissociates from the βγ subunits. The α-GTP then activates a 2nd messenger system, or directly acts upon an ion channel, in some cases the βγ subunit can also activate ion channels. The intrinsic GTP-ase of the α-subunit acts as a self-limiting step to deactivate and allow recombination of the subunits.

• Mention of at least a couple of different kinds of G-proteins e.g. Gs, Gi, Gq, Gt, etc and their associated 2nd messenger systems e.g. adenylate cyclase/cAMP, PLC/IP3/DAG, cardiac K-channels, etc.

• Preferably, examples of receptors associated with each of the mentioned G-protein types. Extra marks were obtained for a detailed description of the mechanism described above, including for mentioning and understanding such features of the system as amplification, self-regulation, uni-directionality and sustained duration; for more complete lists of G-protein types and associated 2nd messengers; for accurate description of the structure as currently appreciated; and also for mention of the existence of “small G” proteins and their role in intracellular organelle function and gene expression. Common mistakes, none of which precluded passing the question as a whole, were:

• describing the G-protein as either a receptor or as a 2nd messenger. Often answers began by saying the G-protein was a receptor then describing the process outlined above where the GPCR is a separate entity. ,

• stating that G-proteins are guanine nucleotides or similar comments • describing the role of ATP rather than GTP in activation • describing the structure of G-proteins as serpentine, 7-trans-membrane-spanning, or similar

These errors suggest an inability to distinguish between various concepts of signal transduction, receptor function and intracellular functions. Some answers resembled a “lucky-dip” of terms and concepts. Some answers gave great detail on the roles of cAMP, DAG, IP3 etc which while usually correct was not relevant and so did not score marks. QUESTION 16 Explain the physiological processes involved in the development of interstitial

oedema. 76% of candidates passed this question. The main points were: the variables contributing to Starling forces, lymphatics, and mechanisms changing these variables. Amongst others, these mechanisms included decreased arteriolar tone, increased venous tone, and increased permeability and surface area. Additional points were definitions of oedema and the interstial space, and that as oedema develops changes in the interstitial Starling variables limit the formation of oedema. This was an applied physiology question; the most common omission was discussion of how Starling forces contribute to oedema rather than the normal balance of the forces and many candidates repeated information or discussed the consequences of oedema rather than the development of oedema.

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VIVA SECTION

INTRODUCTORY PHYSIOLOGY TOPICS: Cardiovascular

• Radial artery pressure-time waveform o Comparisons to aortic trace o Changes with ageing

• Define preload and afterload o Frank – Starling relationship

• ECG complex • Action potential phases & ion currents in cardiac muscle • Pressure vs. volume loop for left ventricle • Fetal circulation and changes at birth • Cardiac effects of IPPV • Determinants of cardiac output

Respiratory • Respiratory quotient and respiratory exchange ratio • Effects of breathing low FiO2 • The oxygen cascade • Arterial PO2 and changes with age • Ventilatory response to raised CO2 • Shunt • Dead space • FRC and its measurement • Closing volume / closing capacity • Normal capnograph tracing

o Changes with disease states and equipment variations • Expiratory volume vs. time graph • Pulmonary blood flow and its measurement

Renal/Acid-Base • Renal handling of glucose • Renal handling of water balance

o Maximal diuresis • Fluid osmotic changes in the loop of Henle • Metabolic acidosis

o Compensation • Metabolic alkalosis

Liver/Metabolic/Endocrine • Functions of the liver • Hormones released by the thyroid • Changes with fasting • Aerobic vs. anaerobic metabolism • Calcium levels in blood

o Control

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Thermoregulation • Normal body temperature

o Causes of heat loss • Thermoneutral zone

Body Fluids & Electrolytes • Distribution of body water

o Measurement of compartments Haematology / Immunology

• Anaphylaxis • Classification of hypersensitivity reactions • Contents of a unit of packed cells

Measurement • Defining heat / temperature • Measurement of temperature • Methods of measurement of BP • Define transducer

Nervous System • Normal cerebral blood flow • Factors controlling CBF • Measurement of CBF • Define ICP, normal values • Pathways involved in pain transmission • Sleep

Musculoskeletal / Cellular • Contrast different types of muscle • Describe a sarcomere • Resting membrane potential

D B F COTTEE CHAIRMAN PRIMARY EXAMINATION

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

FEBRUARY/MARCH 2004

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.

PHARMACOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 73% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Describe the effects of isoflurane on intracranial metabolism, intracranial

haemodynamics, intracranial pressure and the EEG.

71% of candidates passed this question. This question examined core material relating to a commonly used inhalational anaesthetic agent. The main points expected included; significant dose-dependent reduction in cerebral metabolism by isoflurane, indication of direct and indirect influences on cerebral blood flow with cerebral vasodilatation and increasing cerebral blood flow at 1 MAC, maintenance of autoregulation at low concentrations, increased intracranial pressure in parallel with increasing cerebral blood flow, influence of CO2 on intracranial pressure and EEG features of an initial increase in frequency followed by decreased frequency and increased amplitude then burst suppression and electrical silence with increasing MAC.

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Additional marks were awarded for; demonstrating points with clearly labelled graphs, correlating effects with MAC values, noting increasing supply:demand of cerebral blood flow with increasing MAC, noting possible increased reabsorption of CSF with no effect on CSF production and noting the anticonvulsant action of isoflurane. Some candidates were unclear about the final balance of the major determinants of cerebral blood flow and intracranial pressure, indicating that flow and pressure were reduced by isoflurane. Many did not indicate that the ICP rise could be attenuated by hypocarbia. No credit was given for irrelevant information about the structure and physicochemical properties of isoflurane supplied by many candidates. QUESTION 2 Outline factors determining speed of onset of neuromuscular blocking

agents. 71% of candidates passed this question. This question had been asked in the 1999 July paper. The main factors for a pass mark were:

• Dose of agent noting that multiples of ED95 had faster onset of action compared to lower doses.

• Potency of the agent noting that more potent agents have a slower onset of action compared to equivalent doses of a less potent agent, with an explanation of this effect.

• The effect of cardiac output and the perfusion to muscle groups to distribute the agent. • Relevant physicochemical properties of the agents and an explanation of their relevance.

Additional marks were awarded for identifying and explaining the differences in speed of onset between depolarising muscle relaxants and non-depolarising neuromuscular blocking agents, discussion of the different speed of onset between different muscle types and groups, the effects of different routes and sites of administration and the priming principle on speed of onset, the effects of other drugs and the effects of age and relevant disease states. Three common mistakes were:

• Candidates confused the term dose with the term concentration. The two are significantly different and are not interchangeable.

• Description of Fick’s Law without any attempt to interpret or explain its relevance to the question.

• There appeared to be considerable confusion between the term speed of onset and the term onset time. An increased speed of onset will result in a reduction of the onset time. Great latitude was given in this matter but candidates are advised to consistently refer to one or the other to avoid confusion and not use the terms interchangeably

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QUESTION 3 Briefly describe the factors that determine skin penetration by local anaesthetics. Briefly describe the formulation and pharmacology of EMLA cream.

60% of candidates passed this question. Marks available were divided equally between the two parts of the question. The main points expected were:

• An understanding of Fick's Law of Diffusion related to i) the structure of the skin, and ii) the properties of representative local anaesthetic agents.

• Defining "eutectic", details of how EMLA is formulated and administered to overcome the barriers described in the first part of the question, and aspects of the pharmacology of lignocaine and prilocaine relevant to the use of EMLA.

Candidates achieving high marks presented detailed, integrated information showing a higher degree of understanding in both parts of the question. There was confusion about the definition of "eutectic" with a number of candidates writing that it referred to a lowered boiling point of the mixture. A "eutectic mixture" is the mixture of constituents at a ratio that produces the lowest temperature melting point. Candidates and tutors will find relevant information in "Dermatological Pharmacology" in Goodman & Gilman in addition to texts covering local anaesthetic pharmacology. QUESTION 4 Outline the effects of an opioid injected into the spinal intrathecal space. 64% of candidates passed this question. One good approach to this question was to identify the three main mechanisms by which intrathecal opioids act: (i) local effect at receptors in the dorsal horn of the spinal cord, (ii) higher centres in the brainstem and via bulk flow of CSF, (iii) central effects following systemic absorption via the epidural venous plexus. The main points attracting higher marks included an outline of the spinal opioid receptors and additional discussion of the mechanisms of spinal analgesia, a brief outline of the relevant pharmacokinetics (explaining why a small dose is effective), variation in lipid solubility, and major adverse effects such as pruritis, urinary retention and late respiratory depression. Other points that attracted marks included the differential effect on A-delta and C pain fibres and unique features of some opioids (pethidine, remifentanil). Poorer candidates did not discriminate between the effects of intrathecal and other routes of administration. Specific treatment of each of the adverse effects was not required.

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QUESTION 5 Outline the effects of liver failure on drug kinetics and dynamics. 52% of candidates passed this question. The effects on kinetics to outline included:

• Absorption; decreased absorption eg; Vit K • Bioavailability; decreased first pass metabolism • Metabolism and decreased clearance; decreased enzymatic degradation with decreased

clearance of low extraction ratio drugs, decreased hepatic blood flow and decreased clearance of high extraction ratio drugs, decreased pseudocholinesterase levels, decreased biliary excretion and potentially decreased renal clearance

• Distribution; increased volume of distribution for water soluble drugs, decreased levels of albumin and acid glycoprotein with decreased protein binding

The effects on dynamics to outline included:

• Encephalopathy and potential interaction with CNS depressants • Coagulopathy and potential drug interactions • Potential for increased hepatotoxicity

Candidates frequently did not outline the effects on metabolism, biliary excretion, protein binding and pharmacodynamics. QUESTION 6 Outline the circulatory effects of glyceryl trinitrate. 83% of candidates passed this question. Most candidates understood the drug’s mechanism of action. Good answers included not only the direct effects of glyceryl trinitrate on blood vessels but also how those effects lead to favourable changes in the myocardial oxygen supply and demand ratio. Many candidates also gave a brief description of glyceryl trinitrate’s effects in pathological states, such as in myocardial ischaemia, cardiac failure and hypovolaemia. Fewer candidates outlined the effects of glyceryl trinitrate on other organ circulations such as the pulmonary, uterine and cerebral circulations or possible effects on platelets. QUESTION 7 Describe the mechanisms of action of inotropes and provide examples. 67% of candidates passed this question. Main points expected included:

• Definition of inotropes • Roles of c-AMP and intracellular Ca2+ in promoting cardiac contractility • Beta-1 agonists, cardiac glycosides, phosphodiesterase inhibitors (III) and their mechanisms

of action Credit was given for mention of glucagon and calcium.

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Common errors included: • Failure to define inotropes or stating that inotropes were agents which increased blood

pressure and discussing alpha agonists at length • Many candidates wrote about sympathomimetic agents or catecholamines including those

which act predominantly by vasoconstriction QUESTION 8 Describe briefly the side effects and complications of heparin therapy. 71% of candidates passed this question. The question specifically requested the candidate to address the side effects of heparin therapy. Detailed accounts of the mode of action of heparin were frequently included however only in those answers where this information was related to the mechanism of side effects were these of value. To obtain a pass in this question, it is necessary to recognise that side effects can be predictable and dose related, e.g. bleeding, or idiosyncratic, such as the heparin induced thrombotic thrombocytopenic syndrome. Particular reference to intercurrent pathology and drug interactions was valuable. Although many candidates commented on APTT measurement, its significance relates to the narrow therapeutic range and unpredictable effective dose of heparin; few candidates mentioned this. Differentiating the mechanisms of platelet effects is important in view of therapeutic and prognostic implications. Most candidates were aware of alopecia and osteoporosis as side effects, frequently not mentioning the situations in which these occur. Mention of low molecular weight heparins was appropriate, however comparisons often were omitted. Many candidates gave a fairly detailed account of complications of protamine therapy, which was not asked; the requirement for protamine might better be perceived as a disadvantage of heparinisation, particularly at high doses.

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VIVA SECTION INTRODUCTORY PHARMACOLOGY TOPICS: General topics

• Bio-availability • Adverse drug reactions • Mechanisms of drug action • Anaphylaxis • Drug interactions • Esterases • Drug dose response • Bronchodilators • Isomerism • Poisoning

Opioids

• Mechanism of action • Adverse effects • Pharmacokinetics of morphine • Remifentanil • Antagonists

Cholinergic, anticholinergic drugs

• Muscarinic cholinergic synapse • Drug actions • Acetylcholine receptors • Donepezil, tacrine • Compare the anticholinesterases • Organophosphate poisoning

Inhalational agents

• Speed of induction • Fa/Fi curves • Time to awakening • MAC • Structure activity • Sevoflurane in infants and adults • Sevoflurane compared to halothane • Nitrous oxide

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Obstetric pharmacology • Tocolytics and mechanisms of action • Adverse effects of magnesium and salbutamol • Oxytocics • Adverse effects of oxytocics

Local anaesthetics

• Factors effecting toxicity • Lignocaine and bupivacaine toxicity • Toxic doses • Management of toxicity • Structure activity • Kinetics

Induction agents

• Ketamine; CVS, CNS effects • NMDA receptor • Propofol; CVS, CNS effects • Thiopentone • Pharmacokinetics of induction and recovery

Anti-arrhythmic drugs

• Pharmacological management of ventricular fibrillation • Amiodarone • Lignocaine • Sotalol

Neuromuscular blocking agents

• Kinetics • Adverse effects • Recovery from non-depolarising relaxants • Assessment of recovery • Neuromuscular monitoring • Plasma cholinesterases

Diuretics

• Classify • Mechanism of action • Compare frusemide and spironolactone

Pain

• NSAIDS; mechanism of action, COX-2, offset of action • Paracetamol toxicity • Tramadol

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Antidepressants • Classify • Drug interactions

Adrenoceptor blocking agents

• Classify beta blockers • Esmolol • Adverse effects

Histamine and serotonin

• Classify drugs acting via serotonin effects • Serotonin receptors • Histamine effects and receptors

Vasoactive drugs

• Classify vasoactive drugs • Catecholamines • Pharmacology of adrenaline • Vasopressin

Statistics

• Drug trials • Types of data • Chi squared

Antiemetics

• Mechanisms of action • Adverse effects

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PHYSIOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 67% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Briefly outline the differences between the pulmonary circulation and the

systemic circulation. 26% of candidates passed this question. The main points expected for a pass were differences in anatomy, function, haemodynamics (especially pressure, resistance and the affect of lung volume and gravity) – regulation of the circulation and other functions such as filtering. Common errors were as follows:

• to treat this as a compare and contrast question. Many candidates wrote how the pulmonary circulation was controlled and how the systemic circulation was controlled. Only the differences were required.

• many candidates gave lists of the functions of the pulmonary circulation, not differences eg. The blood reservoir function of the lung which is also present in the systemic circulation.

• to state eg. “pulmonary vascular resistance is affected by lung volume” and not to say how it is affected. A statement like this does not receive marks.

The best candidates were well organised, wrote only the differences between the circulations and gave brief explanations. QUESTION 10 Describe the vasoactive substances released by the endothelium. Explain

the role they play in regulating blood flow through the peripheral circulation.

65% of candidates passed this question. The key vasoactive substances released from the endothelium are nitric oxide, prostacyclin and the endothelins. The main points expected for a pass were to describe the formation of these substances and pathways by which they interacted with vascular smooth muscle. Also required was an understanding that these paracrine substances are vasoactive regulators, helping match regional perfusion to metabolic demand. Additional points were awarded for listing the factors which stimulated or inhibited release of these substances; hormones, local metabolites and changes in wall tension. Common errors were to describe the role of the endothelium in coagulation in fibrinolysis, and to describe the physics of blood flow.

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QUESTION 11 What is 2,3 DPG? How is it produced in the red blood cells and how does it interact with haemoglobin? What is its relevance in altitude exposure, anaemia, and stored blood?

84% of candidates passed this question. Main points expected for a pass included a definition of 2,3 DPG, and a brief description of the metabolic pathway involved in production. Also required was a description of the interaction with haemoglobin defining the right shift in the haemoglobin-oxygen dissociation curve, with extra marks awarded for differences with fetal haemoglobin. The role of pH change in altering the production of 2,3 DPG also attracted additional marks. Required also were the role of 2,3 DPG in allowing increased oxygen delivery in anaemia and during altitude exposure, with additional marks awarded when the effects in the lung in the hypoxic environment were included. The potential deleterious effects of a lack of 2,3 DPG in stored blood was also required, with additional points given for inclusion of time-scale, and discussion of the importance of different additives. Overall the question was answered well by candidates, with problems occurring when parts of the question were unanswered, or unclear. The use of diagrams aided in the explanations for most candidates. QUESTION 12 What are the physiological consequences of decreasing functional residual

capacity by one litre in an adult? 50% of candidates passed this question. This question was last asked in March 2001. As described then, to achieve a pass, candidates were expected to cover the majority of the following points:

• Some definition of FRC, being: • The equilibrium point of the lung & chest wall, or • The lung volume at the end of a normal tidal breath, or • Residual volume + Expiratory reserve volume

• An approximate normal value: FRC ≈ 2.2L, or 30mL/kg. • FRC will fall below closing volume, resulting in:

• Airway/alveolar closing with atelectasis • An increase in V/Q mismatch, shunt and arterial hypoxaemia • Increased work of breathing to open airways/alveoli

• A decrease in lung compliance. • An increase in airways resistance • Increased work of breathing. • Increased pulmonary vascular resistance. • Decreased store of oxygen.

Additional marks were attained for the following:

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• Quantification of “one litre” as a significant (~40-50%) decrease. • Increased work of breathing being multifactorial:

• ↓ compliance, and • ↑airways resistance, and • critical opening pressure for collapsed alveoli

• Decreased O2 store → • Increased breath-to-breath variation in PaO2 • Increased risk of hypoxaemia during induction of anaesthesia

• Increased pulmonary vascular resistance → ↑ RV work • Graphs indicating effect of changing volume/FRC on:

• Compliance • Airways resistance • Pulmonary vascular resistance

Many candidates duplicated material, first listing the functions of FRC in-depth, and then listing the consequences of a decrease. While making a short list is a useful aid, repeating several pages of text gains no additional marks and wastes valuable time. Some candidates wasted time writing about the measurement of FRC, the respiratory changes in pregnancy, which were not asked. Vague answers, such as “may result in ABG deficits” are not considered sufficient in detail. QUESTION 13 Describe the concept of renal clearance and its use to estimate glomerular

filtration rate. 69% of candidates passed this question. Renal clearance is a basic physiological concept, and its translation into glomerular filtration rate is a straight-forward application of this concept. Candidates were expected to provide some definition of clearance, with some detail on how the elements of function of the kidney relate to clearance. These include filtration and tubular reabsorption and secretion. Most candidates were able to provide a reasonable definition of clearance, although there were a significant number of errors. The inclusion of any discussion about glomerular filtration and tubular function was a common omission in a number of answers. In a number of cases, extensive detail was provided on the mechanisms of filtration at the glomerulus, but this did not attract significant additional marks. Inclusion of some basic formula about how clearance relates to plasma concentration and urinary volume and concentration was an important inclusion in the answer. Quite a number of candidates included an extensive derivation of this formula, but omitted more important facts. The properties required of a marker, ideal for use in the measurement of glomerular filtration rate was well described by the majority of candidates, and was an important part of the answer. Most candidates included discussion of specific examples which can be used, such as inulin and creatinine. Whilst this was generally done well, an understanding of the relationship between creatinine concentrations, creatinine clearance, and glomerular filtration rate was not always apparent.

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QUESTION 14 Briefly describe the difference between laminar and turbulent flow. List the factors that increase the probability of turbulent flow.

70% of candidates passed this question. The question most naturally fell into three areas:

• A description (and diagrams) of the nature of laminar and turbulent flow and the significance this might have for passage of fluid through a tube.

• A description of the different ways that laminar and turbulent flow are related to pressure, radius and length of tubing, viscosity and density. These were usually summarized by equations (+/- graphs) with interpretation.

• A description of how diameter, velocity, density and viscosity can be used to predict the likelihood of turbulent flow, as summarized by the Reynold’s number. This section should also include mention of the geometry of the tube potentially affecting the nature of the flow as the Reynold’s number is for parallel-sided cylindrical tubing. Concepts of critical velocity, entrance length and transitional or mixed flow types could also reasonably be included.

There were two main areas which created problems with understanding.

• The relationship of turbulent flow to driving pressure, tube length and density was often poorly described even when an acceptable equation was quoted. The “meaning” of the equation was often not understood and commonly misrepresented in graphical form. Most of the confusion arose from difficulties dealing with the flow tending to vary with the square root of pressure and radius to a power of 2 to 2.5 (i.e. the square root of the power 4 or 5) depending on which source was quoted. If these equations are written as “driving pressure is proportional to”: then flow will be squared and radius to the 4th or 5th power. The fact that turbulent flow can not be described by a simple equation and will vary with the degree of turbulence means that the study sources will have slightly differing summaries of the relationships. These were all acceptable.

• Although the Reynold’s number can be incorporated into complex equations for predicting rate of flow, for the purposes of this question the relevant property of the Reynold’s number was its ability to predict the likelihood of turbulence. This needed to be distinguished from equations for estimating flow rates such as the Hagen Poiseuille for laminar flow or the Fanning for turbulent flow. Some candidates tried to apply the Reynold’s number equation to describe factors affecting rate of turbulent flow rather than likelihood of turbulent flow. This resulted in major errors in describing the factors affecting rate of turbulent flow.

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QUESTION 15 List the physiological factors that determine intracranial pressure. Explain briefly how intracranial pressure is regulated.

57% of candidates passed this question. Main points expected for a pass included the definition, normal value and significance of intracranial pressure, a description of the nature of the vault and its component contents and the factors that influence the magnitude of those contents. Additional points were awarded for discussion of the idea of ICP being non-uniform, the separation of cerebral blood flow from cerebral blood volume and other physiological factors that can change ICP (e.g. posture, intra-thoracic pressure) Common errors included directionless relationships, graphs with unlabelled axes, a misstatement of the Monro-Kellie hypothesis and the inclusion of details about the effects of pharmacological agents on ICP. QUESTION 16 Explain how the kidney handles glucose. Describe the physiological

consequences of glycosuria. 57% of candidates passed this question. Points required for a pass were:

• Glucose is freely filtered in the glomerulus and reabsorbed in the proximal tubule. • The mechanisms of re-absorption involve secondary active transport and facilitated diffusion. • The energy for this process is provided by Na/K ATPase. • The amount absorbed depends on the amount filtered (up to a transport maximum). • Glycosuria leads to:

• Diuresis and dehydration – caused by osmotic effects and medullary dilution • Loss of sodium (and other electrolytes) – leading to hypovolaemia and subsequent

homeostatic responses • Loss of energy substrate

Additional marks were given for:

• Quantification of rate of re-absorption and glycosuria. • Details of (co)-transport mechanisms involved in re-absorption – SGLY and GLUT • Heterogeneity of the saturation of reabsorption mechanisms – manifest as “splay”. • Increased chance of urinary infection with glycosuria.

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VIVA SECTION INTRODUCTORY PHYSIOLOGY TOPICS: Cardiovascular

• Radial artery pressure-time waveform • LV pressure-time trace • RA (CVP) pressure-time trace • Preload

• correlation with PAOP • Determinants of myocardial O2 supply and demand • Body’s response to haemorrhage (15%BV) • Normal coronary blood flow and measurement • Autoregulation • Contractility

• methods for measurement • ECG Complex:

• waves, intervals • action potential phases & ion currents

• Cardiac function curve • Vascular function curve

Respiratory • Classification and causes of hypoxia • Alveolar gas equation • RQ • Arterial blood gas measurement • Shunt • Dead space • Closing volume / closing capacity / FRC

• differences in the neonate & with pregnancy • Work of breathing

• influence of changes in resistance and compliance • Resistance to breathing • Static and dynamic compliance of the lung • Normal flow-volume loop

• changes with various disease states • Pulmonary surfactant • Normal capnograph tracing

• changes with disease states and equipment variations • Intrapleural pressure vs. time • Pneumotachograph • Flow vs. volume during respiratory cycle

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• Oxygen stores in the body • changes breathing ‘X’% O2 for 10 minutes

• Physiological consequences of isolated obstruction of: • the left pulmonary artery • the left main bronchus

• CO2 carriage in the blood • Distribution of PO2, PCO2, pH and V/Q in the upright lung • HbO2 dissociation curve

• normal, pregnant & foetal values Renal/Acid-Base

• Functions of the kidney • Renal handling of water balance

• minimum and maximum urine osmolality • Renal maintenance of intra-vascular volume • Renal handling of acid-base balance

• titratable acidity vs. renal hydrogen excretion • Renal blood flow and regulation of GFR • Tubular fluid osmotic changes along the nephron • Functions and regulation of ADH release

Liver/Metabolic/Endocrine • Functions of the liver • Glycolysis, glycogenolysis, gluconeogenesis • Hormones secreted by the pancreas • Hormones released by the thyroid • Metabolic changes of pregnancy

Thermoregulation • Normal body temperature

• causes of heat loss Body Fluids & Electrolytes

• Distribution of body water • measurement of compartments

Haematology/Immunology

• Anaphylaxis • Classification of hypersensitivity reactions • Immunoglobulins • Haemostasis • Coagulation process and assessment of function • Constituents of fresh frozen plasma

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• Requirements for cross-matching • Changes which occur in stored blood • Fibrinolysis

Measurement • Heat / temperature • Measurement of temperature • Humidity • Principles of pulse oximetry • Principles of end-tidal CO2 measurement • Methods of measurement of BP

• aspects of fidelity for intra-arterial measurement Nervous System/Cellular

• Role of GABA receptors in the CNS • Role of the Nernst equation • Normal cerebral blood flow • Factors controlling CBF • Pathways involved in pain transmission • Normal EEG waveforms

D B COTTEE CHAIRMAN PRIMARY EXAMINATION

Page 194: Primary Exam Reports 2011 to 1999

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

JULY/SEPTEMBER 2003

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.

PHARMACOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 78% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Draw and label, on the same X – Y axis, FA/FI curves for the following

halothane concentrations in oxygen, showing a 30 minute period from starting administration.

(a) Halothane 1%, subject breathing spontaneously. (b) Halothane 6%, subject breathing spontaneously. (c) Halothane 6%, subject paralysed and ventilated.

With reference to the major factors determining the shape of FA/FI curves explain the differences between A and B, and A and C.

29% of candidates passed this question. Most candidates started the three curves from the origin satisfactorily. However the rise in FAFI is in fact more rapid for curve (a) rather than (b) to the end point at thirty minutes.

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Most candidates recognised the significance of the concentration effect on the rise in alveolar concentration. However the effect is more modest on the FA/FI ratio, and textbooks discuss this effect where ventilation is controlled. 6% halothane is a profound respiratory depressant in the unstimulated patient and this overrides the concentration effect that most candidates quoted. Some candidates correctly mentioned the mild reduction in cardiac output which would be seen with 6% halothane which would augment the rise in FA/FI. However the effect on ventilation remains paramount. Most candidates recognised the rapid and sustained rise in the FA/FI which would occur during controlled ventilation with 6% halothane. Here the concentration effect and sustained ventilation act together to produce a rapid rise in the FA/FI ratio. Better answers included the effect of IPPV and 6% halothane on cardiac output, which is profoundly reduced. This further segments the rise in FA/FI. Some candidates who clearly had difficulty with the curves went back to first principles, describing the various factors on FA/FI which earned valuable marks. QUESTION 2 Describe the potential interactions of sevoflurane, desflurane and isoflurane

with carbon dioxide absorbents. 60% of candidates passed this question. The main points expected were: • Different carbon dioxide absorbents exist and they vary with respect to the potential interactions

described. • A description of the specific interactions: sevoflurane resulting in compounds A – E, desflurane and

isoflurane producing carbon monoxide. • Factors that accelerate or minimize these reactions. • The potential toxicity and clinical relevance of the products of these reactions. Several candidates stated that the same factors increased the production of compound A and carbon monoxide. This is only partially correct. Low flow and closed circuit techniques have not been implicated in increased carbon monoxide production from desflurane. Soda lime dehydration actually decreases the production of compound A from sevoflurane, this detail was known by only a very small number of candidates. Credit was also given for mentioning potential absorption and subsequent release of volatile agent by the carbon dioxide absorbents. QUESTION 3 Outline GABA’s role as a neuro transmitter and indicate how its actions may

be modified by pharmacological agents. 63% of candidates passed this question but there were no outstanding answers. This question was also asked in March 2001, when the pass rate was lower. The answer should have recognized the importance of GABA as a major inhibitory neurotransmitter, and given a description of the distribution and function of GABA and its receptors. Many candidates failed to mention that there were different GABA receptors. A brief description of the neurophysiology of the GABA receptors would have facilitated the subsequent description of how different agents modify the action of GABA at different sites or by different mechanisms. Many answers did not clearly distinguish

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the effect of benzodiazepines from that of barbiturates on the GABA receptor. A list of drugs acting on the GABA receptor would not receive credit if the direction of effect was not indicated. Only a few answers mentioned non-anaesthetic drugs that affected GABA. QUESTION 4 Describe how a computer-controlled infusion device targets and maintains

constant blood concentrations of propofol. 33% of candidates passed this question. The main points expected for a pass were: • Device contains microprocessor with algorithms for infusion. • Algorithms based on multi-compartment pharmacokinetic model for propofol. • User enters patient’s age, weight and desired target concentration. Typical concentrations range are 1

– 8 mcg/mL depending on the situation. • User adjusts target according to adjuvant drugs, co-morbidities or degree of surgical stimulation. • Computer designs variable-rate infusion. • Loading dose calculated as volume of distribution of central compartment times target concentration. • Maintenance infusion rate includes component for redistribution and component for elimination. Additional points which attracted higher marks were: • Picture of multi-compartment model. • Graph of infusion rate and target concentration vs. time. • How the infusion rate changes if increased or decreased target entered. • Equation for calculation of maintenance infusion rate (redistribution and elimination). • The fact that the pharmacokinetic data are derived from a small group of volunteers. • Details of device hardware and syringes. • An appreciation of the fact that the “Diprifusor” calculates compartmental volumes and rate

constants based on the weight of the patient and does not use the age of the patient, the clearance or the context-sensitive half-life to make its calculations.

Common mistakes and problems included: • Confusion of physiological models (i.e. vessel rich and poor groups) with the mathematical models

used in the current devices. • Confusion of targeting effect-site and blood concentrations. • Failure to appreciate that these devices achieve targets within 30-60 seconds without overshoot and

then maintain constant concentrations. Very few graphs reflected this accurately. • The current devices do not measure the actual blood concentration of propofol. QUESTION 5 Describe the pharmacological effects of paracetamol. Outline its toxicity and

management. 86% of candidates passed this question. Paracetamol is a commonly used drug in anaesthetic practise and the majority of candidates displayed a good understanding of the drug’s pharmacology and toxicity. All candidates noted the analgesic and anti-pyretic actions of the drug, and the fact that it has little or no anti-inflammatory activity. It is true that there is still some conjecture as to the exact mechanism of action of paracetamol, but pass marks were given for citing the usual explanation of central cyclo-oxygenase inhibition. Candidates who showed evidence of more extended reading and listed alternative theories such as COX-3 inhibition or inhibition of 5HT reuptake at the spinal cord level were given credit.

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With regard to the drug’s toxicity, all candidates had a basic understanding of the mechanisms involved in its adverse effects on the liver. Most were able to name the reactive intermediate produced (N-acetyl-p-benzoquinoneimine) although there were a number of inventive spellings. Hepatic toxicity was the main focus of most respondents, and extra marks were awarded to candidates who were able to list other (less common) adverse effects, such as allergic reactions, skin rash and renal impairment. Again the section on management of paracetamol toxicity was generally well handled with all candidates aware of the role of N-acetyl cysteine and the use of nomograms to predict the likelihood of liver damage. In this part, extra marks were awarded for those who remembered that simple strategies can, in some circumstances, be important in limiting paracetamol toxicity. Such interventions to reduce drug absorption include the administration of activated charcoal and gastric lavage. QUESTION 6 List the potential clinical uses of an alpha-2 adrenoceptor agonist and outline

the limitations of clonidine for each. 60% of candidates passed this question. The list of potential clinical uses for alpha 2 adrenergic receptor agonists should include the following. Anaesthesia and sedation, pain management, treatment of hypertension, premedication using anti-sialogogue and anxiolytic properties, haemodynamic stability with a decrease in circulating catecholamines and the reduction of intraocular pressure. Additional other clinical indications are in post operative shivering and the treatment of opiate withdrawal syndromes. The limitations of clonidine in these situations relate to its reduced potency as a partial agonist, and long elimination half life. Its use is associated with hypotension and bradycardia which can be a disadvantage in all the previously mentioned clinical uses. Most candidates understood and explained the acute hypertension with bolus injection and rebound hypertension on withdrawal of clonidine. Sedation and dry mouth can be a limitation except where desirable in use as a premedication. More selective alpha 2 agonists have greater MAC reducing properties than clonidine. A common omission of many candidates was to not address the limitations of clonidine for each use, or to instead to explain adrenergic receptor molecular pharmacology in great detail. QUESTION 7 Write short notes on factors affecting the speed of onset and duration of effect

of local anaesthetics when used to produce peripheral nerve block. 46% of candidates passed this question. Patient factors include: • Site of administration. • Nerve structure and function. • Tissue pH. Drug factors include: • pKa and its effect on non ionised fraction. • Lipid solubility and its effect on potency and protein binding. • Concentration and volume added. • Intrinsic vasoactive properties. • Effect of local and distant metabolism. • Effect of different additives.

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Common omissions were effect of local metabolism and site of administration. Listing the different factors without indicating the direction of change and why the change is observed doesn’t answer the question. Candidates were awarded more marks if they used the Fick principle to illustrate some of the principles, using examples with correct numbers and if they mentioned physiological or pathological states such as pregnancy and electrolyte disturbances. QUESTION 8 Outline the pharmacological differences between neonates and adults with

reference to sevoflurane, vecuronium and morphine. 42% of candidates passed this question. In order to pass the candidate needed to make a number of correct statements pertaining to the question. These statements may have included, but are not limited to the following: • definition of neonate. • brief description of sevoflurane, vecuroniun and morphine. • definition of pharmacology-pharmacokinetics/dynamics. • kinetics: key differences between neonate and adult i.e. relativities of TBW, ECFV, comparison of

protein binding, renal and hepatic clearance, different ratios of ventilation and FRC. • dynamics: different sensitivities to drugs, permeability of BBB, sensitivity of resp centre. • morphine: in neonate increased t1/2 increased respiratory depression and apnoea. • sevoflurane: more rapid induction in neonate, reduced blood gas solubility, MAC higher in neonate

than adult. • Vecuronium: increased Vd reduced clearance increased t1/2 in neonate with increased sensitivity of

neuromuscular junction. Net effect dose per kg similar to adult. Common omissions include widespread lack of definitions e.g. of neonate, drugs. No candidate referred to the effect of prematurity on neonatal drug effects. Common errors: Many candidates were unclear as to the relative sensitivities of neonates to non-depolarising muscle relaxants NDPMRs. Many stated MAC for sevoflurane is lower in neonates than adults. There was much confusion over the effect of an increase in Vd for a polar drug. Many candidates stated that morphine was a highly polar drug. Many stated that neonates have increased TBW and increased fat content compared to adults. Many answers appeared incomplete; suggesting that time management may have been an issue.

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VIVA SECTION INTRODUCTION TO PHARMACOLOGY QUESTIONS: How can analgesic drugs be grouped?

What is your induction dose of propofol and why?

Draw a concentration- response curve for isoflurane.

What are some of the cardiovascular responses to spinal local anaesthetic?

What physiological factors affect a dose of propofol.

How do anti-platelet drugs work.

A set of data is presented. Asked to discuss what statistical tests should be used to interpret it.

What is heparin?

Discuss anti-cholinergic drugs.

Compare atropine and glycopyrrolate.

What are the CNS effects of propofol?

What variables are involved in time to wake up after ceasing isoflurane?

Local anaesthetic toxicity.

Contents of an ampoule of thiopentone.

What is meant by the term “isomer”?

What sort of a drug is neostigmime?

Draw a nephron and discuss where diuretics work.

What is the function of additives in an ampoule of propofol?

What drugs can be used to treat hypotension?

Describe the fate of a 100mg bolus dose of suxamethonium.

What is meant by the term “normal distribution”?

Discuss where drugs act in the renin-angiotensin system.

What are some of the side effects of nitrous oxide?

What are the differences between rocuronium and vecuronium?

How does theophylline work?

Describe the chemical structure of some inhalational agents.

What is a meta-analysis?

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PHYSIOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 72% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Describe the effects of tachycardia on myocardial oxygen supply and demand

in a normal heart. 40% of candidates passed this question. The main points expected were: • The determinants of myocardial oxygen supply and demand. • The left ventricle is perfused mainly during diastole. • Tachycardia not only reduces the diastolic time and oxygen delivery to the left ventricle but also

increases oxygen demand. • Comparison of left and right ventricles; including coronary flow versus time graphs; and that flow in

the right ventricle is continuous and little affected by heart rate. • Subendocardium is most susceptible to ischaemia. • Vasodilation via metabolic mechanism increases flow Extra points were given for detailing coronary blood flow, the high oxygen extraction, and for explaining that oxygen supply cannot be increased by increasing extraction. Extra marks were also given for describing pressure differentials in both ventricles in systole and diastole. Common omissions or errors were: • To not label the diagrams. • To put no units on the axes. • To draw inaccurate traces. • To not list the determinants of myocardial oxygen supply and demand. • To ignore the right ventricle. • To mix up supply and demand. QUESTION 10 Describe the role of baroreceptors in the control of systemic arterial pressure. 57% of candidates passed this question. This question was asked in July/August 2000 and at that time the pass rate was 54%. An overview of the role of baroreceptors in controlling blood pressure was expected. The high pressure baroreceptors react via a negative feedback arrangement to rapidly regulate blood pressure changes by changing cardiac output and systemic vascular resistance. The low pressure cardiopulmonary receptors have a role in long term blood pressure control by regulation of blood volume.

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Other points expected were: • Afferent pathways. • Central integration, and the reciprocal balance between sympathetic and parasympathetic system • Efferent pathways and effects, including hormonal. Common omissions were to not describe the low pressure baroreceptors at all, or to describe the sympathetic response without mention of the parasympathetic. QUESTION 11 Briefly describe the potential causes of a difference between measured end-

tidal and arterial partial pressure of carbon dioxide. 43% of candidates passed this question. The answer required consideration of both patient factors, and those errors and limitations of the equipment and techniques used to monitor carbon dioxide both in the expired gas and arterial blood. The effect of alveolar dead space on the difference between end-tidal and arterial CO2 was recognised by most candidates, and many included satisfactory explanations of the causes and potential underlying pathologies, gaining extra marks. The commonly observed clinical effect of delayed alveolar emptying with slow rise in expired CO2, leading to failure to obtain a true plateau, was usually overlooked, but attracted extra marks when included. Equipment problems expected to be included were leaks and occlusions, effect of sampling site and other gases, and calibration errors. This area was overlooked completely by many candidates, leading to the low pass rate. Most candidates that addressed both the patient and equipment components obtained a good pass. QUESTION 12 Explain the difference between perfusion limitation and diffusion limitation in

the transfer of gas between alveolus and pulmonary capillary. Outline the factors that determine whether gas transfer is perfusion or diffusion limited.

45% of candidates passed this question. The main points expected were a definition and explanation of both perfusion limitation and diffusion limitation, as well as a description of the factors included in Fick's law of diffusion. It was expected that candidates would provide some indication that diffusion limitation implies that that equilibration of gas between alveolus and pulmonary capillary is incomplete. The factors affecting whether a gas is perfusion or diffusion limited include the solubility of the gas, its partial pressure gradient, and the transit time of blood through alveoli. It was expected that examples would be given, and that carbon dioxide and oxygen transfer would be correctly categorised. Additional marks were given for explaining the significance of the binding of the gas to haemoglobin, and for discussing the effects of increased cardiac output and increased altitude on the transfer of oxygen. A graph comparing the changes in red blood cell partial pressures of carbon dioxide and oxygen during its transit through the pulmonary capillary attracted extra marks. Marks were given also for commenting on the transfer of carbon monoxide, and for explaining that this is used to measure gas transfer. Many candidates failed to provide definitions for perfusion and diffusion limitation, or provided incorrect or opposite definitions. Others incorrectly categorised carbon dioxide and oxygen. Many candidates commented on nitrous oxide or carbon monoxide transfer, without discussing carbon dioxide or oxygen. Others failed to mention the factors included in Fick's law, thereby reducing the total marks possible. QUESTION 13 Describe the factors that affect airways resistance.

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64% of candidates passed this question and there were quite a number of excellent answers. Better answers included a definition of Airways Resistance (AWR), invoking a version of Ohms law and correctly ascribing units (either SI units or more commonly cmH2O/L/sec) and giving some idea of a normal value. Also expected was an outline of the relative contributions of the upper and lower respiratory tracts, the relationship between lung volume and AWR (best demonstrated graphically), the concept of laminar and turbulent airflows and their effect on AWR (including a version of the Hagen-Poiseuille equation and Reynolds number), the differing relationships between AWR, driving pressure, flow and airway calibre in both turbulent and laminar flow states, and examples of physiological factors that effect AWR (e.g. bronchomotor tone, respiratory rate, dynamic airways compression). Common errors included: • Not mentioning units or wrong units (e.g. mmHg/L/min). • Incorrectly stating that the “driving pressure” is intrapleural-alveolar gradient rather than mouth-

alveolar. • Incorrect versions of the Hagen-Poiseuille equations or Reynolds number. • Not explaining the relationship between airway calibre, turbulent flow and AWR. • Discussing lung compliance instead. • Confusing the Lung Volume-AWR relationship with the Lung Volume-PVR relationship and stating

therefore that AWR is lowest at FRC than at TLC. • Ignoring the role of the upper airway in AWR. • Wasting time on an exhaustive classification of all Pathological and Pharmacological factors which

effect airway calibre. QUESTION 14 Outline the role of the kidney in the regulation of body water. 34% of candidates passed this question. Important concepts expected were: • The identification and separation of discussion about sodium chloride and associated water (i.e.

saline) and "pure" water regulation. • Description of the ability and associated mechanisms for production of either hypo- or hyper tonic

urine relative to plasma. • Identification and discussion of the role of ADH within this process. Common errors or omissions included: • Many answers failed to address the question as asked. • Terms such as water, volume and fluid depletion were used in ambiguous ways. • Directionless relationships e.g. a change in X causes a change in Y. • Failure to discuss how dilute urine is produced. Better answers: • Discussed the threshold and gain for hypo-osmolarity vs. hypo volemia. • Set the role of the kidney within the broader scope of water homeostasis.

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QUESTION 15 Briefly describe the NMDA (N-methyl d-aspartate) receptor and its

physiological role in the central nervous system. 55% of candidates passed this question. For a pass mark, candidates needed to provide a general description of the receptor e.g. one of a family of excitatory amino acid receptors, widespread throughout CNS especially in spinal cord and hippocampus, it is a ligand-gated, voltage-dependent, receptor, the naturally-occurring ligand for which is glutamate (not NMDA as several candidates suggested); it is a transmembrane multi-unit structure with a central cation ionophore. It is associated with but not part of AMPA receptor and neurokinin-1 receptor, stimulation of which causes partial depolarisation of the cell membrane which allows an Mg2+ plug to leave the central ionophore. Glycine is also required. Not all of this information was required to pass, but an indication of the general structure and method of activation was. Mention of the roles played by the receptor in chronic pain states, with sensitization and hyperexcitability caused by persistent input from sites of tissue or nerve injury; in the phenomenon of “wind-up”, likely due to changes in spinal cord expression of the c-fos protooncogene; and proposed in learning and memory were expected and in most cases provided. Other proposed roles such as in excitotoxicity, ischaemic cell death, and CNS plasticity attracted extra marks, but a more detailed discussion of the role in pain states scored more heavily. Mention of antagonists e.g. ketamine and phencyclidine scored but was not essential. A diagram of the receptor and its associated structures and interactions was not essential, but generally-speaking; the better answers included such a diagram, clearly labelled. Few answers mentioned the need for AMPA receptor stimulation to partially depolarize the cell membrane, thus releasing the Mg plug. Many answers gave detailed descriptions of structure and activation but scant information on role, or vice versa; and did not score as well. QUESTION 16 Outline the mechanism of secretion of hydrochloric acid by the stomach.

Briefly describe how secretion of hydrochloric acid by the stomach is controlled.

61% of candidates passed this question. The answers to the second part on control were often better than the first part on mechanism. Some candidates only answered the second part. There were several important points that were often best dealt with by appropriate diagrams. • The central role of the hydrogen/potassium ATPase. • Receptors for gastrin, acetylcholine, and histamine. • The role of the vagus. • Multiple stimuli both enhancing and inhibiting acid secretion that many divided into cephalic,

gastric, and intestinal factors. Other issues included detailed descriptions of hydrogen ion formation using carbonic anhydrase and associated ion movements in and out of the parietal cells. Points attracting higher marks included a clear understanding that the stomach fluid is extremely acidic and that the parietal cells must actively secrete hydrogen ions against a considerable concentration gradient. Very few mentioned the role of canaliculi in inserting proton pumps into the cellular membrane when the parietal cells are stimulated.

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VIVA SECTION INTRODUCTION TO PHYSIOLOGY QUESTIONS: Cardiovascular Left ventricle pressure volume loop Determinants of cardiac output Estimation of myocardial contractility Foetal circulation Measurement of cardiac output Thermodilution Autoregulation Cardiovascular changes at birth Cardiovascular effects of IPPV Determinants of net fluid flux across a capillary Normal pulmonary artery pressure Total peripheral resistance Pressure vs time curves for aortic root and radial artery Definitions of systolic, diastolic, and mean arterial pressures Respiratory Alveolar gas Equation Normal expired wave capnogram Compliance and the respiratory system Lung volumes Closing volume Functional residual capacity Control of breathing Chemoreceptors Determinants of tissue oxygen delivery Haemoglobin oxygen dissociation curve Mixed venous PO2 Coronary sinus PO2 Carbon monoxide poisoning Causes of a low PaO2 Difference between shunt and V/Q inequality Respiratory quotient CO2 carriage Effects of altitude Blood Effects of haemorrhage Water division within body compartments Haemoglobin molecule Production and breakdown of haemoglobin Foetal haemoglobin Renal Mechanisms for producing concentrated and dilute urine Antidiuretic hormone Filtration and absorption of bicarbonate

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Neuro Blood brain barrier Cerebral blood flow Intracranial pressure Monro-Kellie doctrine GI Functions of the liver Role of vitamin K Role of liver in glucose homeostasis Immunological functions of the liver Constituents and functions of bile Urea cycle Measurement and physics Colligative properties Heat and temperature Humidity Measurement of blood pressure Wheatstone bridge Osmolality Osmotic pressure Flow and resistance Blood pressure measurement Effects of insulin and glucagons Regulation of blood glucose Insulin and glucose interaction Other Respiratory acidosis Metabolic alkalosis Resting membrane potential Nernst equation Sodium potassium ATPase pumps Primary active transport Temperature control N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION

Page 206: Primary Exam Reports 2011 to 1999

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

MARCH/APRIL 2003

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.

PHARMACOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 80% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Briefly outline the effects of isoflurane on skeletal, smooth and cardiac muscle

tissues. Indicate how these effects are mediated and their clinical significance. Although the pass rate for this question was 74%, many answers were borderline and few candidates (<10%) provided a clear well-considered answer directly addressing all aspects of the question. Knowledge of the potential pharmacological and pathological actions of isoflurane on each type of muscle, the clinical significance and a general concept of the postulated mechanisms of action was expected. Candidates were required to know that isoflurane causes dose-dependent skeletal muscle relaxation and potentiation of neuromuscular blockers, with increased skeletal muscle blood flow and drug delivery. The relaxant effects of isoflurane on vascular smooth muscle including coronary and cerebral circulations and the actions on bronchial, pulmonary and uterine smooth muscle should have been considered. Many were unclear of the mechanism of coronary steal and of the controversy over its clinical significance. Actions on cardiac contractility and conduction should have been included. Possible mechanisms of action including CNS effects, postjunctional effects, effects on calcium channels and intracellular calcium, atypical ryanodine receptors in MH, nitric oxide production and G-protein linked receptors were often not outlined.

QUESTION 2 Outline the neuropharmacology of thiopentone, covering only its site of action,

EEG changes, effects on cerebral blood flow and intracranial pressure. The pass rate for this question was 80%. The question was asked in appreciably the same format on the March 1999 paper. The marking parameters as set out in that Examiner’s Report were still appropriate for this sitting. Candidates are directed to read that Examiner’s Report. Virtually all candidates

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appreciated the question had four sub-sections and ensured that they answered all four sections. Despite the question specifying that only the four sections needed to be answered many candidates gave detailed, additional information on packaging, dosing and the structure of thiopentone without in any way attempting to relate these facts to the question asked. No credit was given for this. Also vague answers such as “EEG changes are dose related” or “thiopentone has an inhibitory affect on the brain via GABA receptors” were deemed inadequate to answer the question satisfactorily without more detailed explanation. QUESTION 3 Explain how lignocaine prevents the conduction of a nerve action potential. The pass rate was 37%. The content areas where marks were available could be split as follows. a) How lignocaine reached the site of action which might include differences between routes of

delivery, nerve sites (e.g. peripheral vs. intrathecal), pH/pKa/ionisation relationships and principles of diffusion.

b) Details of voltage gated sodium channel binding site and function, and lignocaine’s interaction with it.

c) Channels/nodes blocked to prevent action potential propagation. Differential nerve fibre block and why it occurs

Common problem areas were i) An almost universal belief that only ionised axoplasmic lignocaine gains access to the channel

(refer Miller 5th Ed: Ch 13, Cousins & Bridenbaugh 3rd Ed: Ch 2, Rang, Dale & Ritter 4th Ed: Ch 40).

ii) The relationship between pH/pKa/drug ionisation with some candidates producing correct diagrams but incorrectly interpreting them, suggesting rote learning but a lack of understanding.

iii) Lignocaine binding to the various channel states. iv) Unlabelled/inaccurate time axes on action potential diagrams. v) A small, but significant, group stated that lignocaine primarily acted at ligand gated sodium

channels in synapses. Candidates who included correct material on anti-arrhythmic and toxic effects of lignocaine gained no extra marks because the material was not relevant to the question asked. QUESTION 4 Outline the potential problems associated with additives used to make

medicines suitable for intravenous injection. The pass rate was about 43%. Many candidates made no mention of anaphylactic/anaphylactoid reactions, pain on injection, thrombophlebitis, physicochemical inactivation (and crystallization) and manufacturing costs. A pass required a brief description of (at least) four additives found in drug preparations used in anaesthesia, and their potential adverse effects. Good answers named the drug and additive and outlined its problems. Higher marks were obtained if consideration was given to dose-response, actual versus theoretical problems and pharmaceutics (complexity, cost, shelf-life). No marks were given for additives found in halothane, EMLA cream, spinal local anaesthetic solutions or blood. It was not accepted that the mannitol found in vecuronium leads to an osmotic diuresis. The statement "causes toxicity", was considered to be non-specific and did not gain marks. QUESTION 5 Outline the important statistical issues in designing a study to compare the

duration of analgesia of two drugs given for post-operative pain relief.

The pass rate for this question was 38%. The principal points expected to pass would have included the following. The setting of the study should be a randomised controlled clinical trial. A statement defining the Null Hypothesis to answer the question raised, for example that the drug has no

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significant effect on post-operative duration of pain relief. Discussion regarding the appropriate determination of sample size including power analysis and the setting of threshold for type one and two error. Power is only one of the issues in sample size estimation and a common mistake was to give too much emphasis to this point in candidate’s answers. The surgical procedure and anaesthetic technique must be standardised to reduce bias. Other methods to reduce bias include blinding the person responsible for data collection. The definitions of inclusion criteria for endpoints of analgesic effect are important and pain severity scores were mentioned by many candidates. Higher marks were given to answers which addressed which statistical test would be suitable and the reasons why it would be appropriate. The data may not be normally distributed so a non parametric test such as a Mann-Whitney U test might be preferred. Other tests were acceptable provided potential limitations were identified and data suitability was included. QUESTION 6 Explain how differences in the pharmacokinetics of alfentanil and

fentanyl can influence the way they are administered intravenously. The pass rate was 51%. Candidates were expected to provide a pharmacokinetic explanation to the differences in the way fentanyl and alfentanil behave when given intravenously. The differences in onset time, effect site equilibration, pka and diffusible fraction should have been discussed. The differences in offset time (bolus and infusion), context sensitive half time and the kinetics underlying this should have been outlined. Many candidates presented a comparative table of kinetic data of both drugs without any further explanation. Similarly, many candidates presented context sensitive half-time graphs with inaccurate indication of the behaviour of the two drugs. Candidates who provided representative figures on kinetics with their answer and made comments on administration of a single small dose bolus, high dose, repeated bolus and infusion gained extra marks. QUESTION 7 Classify diuretics, briefly explaining their mode of action. 88% of candidates passed this question, and many demonstrated a high level of understanding of this group of drugs. Almost all candidates successfully classified the main groups of diuretics according to their mode of action. Better marks were achieved by candidates that not only mentioned their cellular mechanisms of action but also the net effect of this on electrolyte shifts and therefore how diuresis is actually achieved. QUESTION 8 Describe the onset and offset of neuromuscular block at the diaphragm, larynx

and adductor pollicis after administration of 2.5 x ED95 dose of vecuronium. Comment on the differences observed. What are the clinical implications of these differences?

The pass rate for this question was 50%. In this question the candidate was expected to address the issues of the kinetics of onset and offset of neuromuscular block (NMB) and the known different levels of sensitivity of the muscles mentioned. It was important to mention that although the diaphragm (D) and larynx (Lx) are relatively resistant to competitive NMB with respect to the adductor pollicis (AP), the major determinant of onset under these circumstances is blood flow. Thus onset is more rapid in the Lx and D and slowest in the AP. Candidates needed to define ED95 and that the ED95 referred to is that for the AP. At the time of AP twitch disappearance both the D and Lx may have been maximally blocked and may be beginning to recover. Thus it is also critical to mention that the order of recovery is D, Lx and then AP. Clinical implications that should have been discussed included onset of block and intubating conditions, offset of block and adequacy of recovery and monitoring of block at AP, orbicularis oculi and prediction of block at AP, Lx and D. Useful diagrams (as are found in both Miller and Stoelting) to explain these phenomena were used by some candidates to their advantage.

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VIVA SECTION Common Introductory Pharmacology Questions Introductory topics for Pharmacology:

* Volatile agent FA/FI curves

* Recovery from volatile agent anaesthesia

* Cardiovascular pharmacodynamics of volatile agents

* Nitrous oxide

* Propofol plasma concentration vs. time curves

* Thiopentone

* Onset and recovery from neuromuscular blockade

* Monitoring neuromuscular blockade

* Local anaesthetic toxicity

* Local anaesthetic pharmacokinetics

* Inotropic agents

* Pressor agents

* Antiarrhythmics

* Intravenous fluid pharmacology

* Isomers

* Drugs altering uterine tone

* Meta-analysis

* Inherited conditions causing variation in drug response

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PHYSIOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 74% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Explain the role of haemoglobin as a buffer. Only 38% of candidates passed this question. A definition of a buffer was required, and also

that buffering capacity or effectiveness depends on the concentration of the buffer relative to the ambient pH of the solution. Haemoglobin, although intracellular (within the erythrocyte), functions mainly as an “extracellular” buffer for CO2 (volatile acid) formed from aerobic metabolism. The solubility of CO2, the presence of carbonic anhydrase within the erythrocyte and the buffering capacity of haemoglobin all contribute to make the haemoglobin buffering system extremely efficient. Haemoglobin is a quantitatively important buffer because there is a large amount present in blood – 150gm/L. Also the imidazole groups of the histidine residues of the globin chains are an effective buffer as their pKa of 6.8 is close to the pH within the erythrocyte. The buffering capacity of haemoglobin is greatest when it is needed most, that is when haemoglobin is deoxygenated in venous blood with a higher CO2 content. Deoxygenated haemoglobin is a better buffer than oxyhaemoglobin as it is a weaker acid, and the pKa of its imidazole groups are higher at 7.9. This information was deficient in most answers. The increased buffering capacity of deoxygenated haemoglobin contributes approximately 30% of the Haldane effect. Many candidates incorrectly stated that haemoglobin functioned as a buffer by the formation of carbamino compounds. The dissociation of carbamino compounds within the erythrocyte actually adds hydrogen ions that need to be buffered by haemoglobin and other buffers. Better answers mentioned the fact that the bicarbonate buffer system cannot buffer carbonic acid (CO2) as they form part of the same weak acid – conjugate base pair. QUESTION 10 Describe the factors influencing hepatic blood flow. 55% passed this question. Less than 9% scored well. Candidates are expected to provide anatomical information stating that hepatic blood flow has a dual blood supply: (i) the hepatic artery (25%) and (ii) the portal vein (75%). Normal values of flow and pressure are expected. One is expected to discuss the factors that affect the respective pressures and hepatic vascular resistance, Hepatic arterial flow = [mean arterial pressure – hepatic venous pressure] Hepatic vascular resistance Portal venous flow = [portal venous pressure – hepatic venous pressure] Hepatic vascular resistance

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6 Some better answers stated that there is an inverse relationship between the hepatic arterial and portal venous flow with autoregulation occurring in the hepatic artery and not in the portal system. A few mentioned that metabolic regulation can cause the hepatic artery to supply up to 50% of the hepatic blood flow. Many recognised that factors such as sympathetic stimulation, anaesthetic agents, surgical factors and pathological states will affect blood flow by their effects on arterial pressure or cardiac output as well as their effects on hepatic vascular resistance. However, a number of candidates answered the question only from first principle, discussing the Hagen-Poiseuille equation in some detail without making specific reference to hepatic blood flow. A large number of candidates did not give any normal values or had them wrongly stated. Measurement of hepatic blood flow and functions of the liver were not required QUESTION 11 Define the “thermoneutral zone”. Briefly explain how the body regulates

temperature when the ambient temperature exceeds thermoneutral zone. 38% of candidates passed this question. A satisfactory answer would have included the following points:

• Definition of the thermoneutral zone (TNZ) including some reference to oxygen consumption at rest being minimal. Also acceptable was the recognition that body temperature is able to be maintained by changes in skin blood flow alone. Normal values for adults (22 – 28°C) and neonates (32 – 34°C) were required.

• A brief mention of the neural mechanisms involved. • Mention of the means for losing heat; ie, conduction, convection and radiation with

emphasis on the paramount importance of sweating in the absence of a thermal gradient. • A brief mention on the role of behavioural responses (seeking a cooler environment,

removing clothing and increasing fluid intake). Information that was rewarded with additional marks included:

• A well labelled graph. • Relationship of TNZ to body surface area and age. • Relative importance (in percentage terms) of the modalities of heat loss as the ambient

temperature climbs. • Rates of sweating that can be achieved. • The effect of humidity on sweating.

QUESTION 12 Explain the mechanisms that maintain cerebral blood flow on moving from a

supine to a standing position. The past rate for this question was 60%. There was a broad range of marks, with some candidates doing very well, and a large number doing very poorly. In general, an appreciation of both systemic and cerebral factors relevant to cerebral blood flow changes on changing posture were required. From the systemic aspect, an explanation of the hydrostatic effects of a changing posture, and the mechanical and cardiovascular reflex responses to these effects was required. This was included in most answers, though was the only aspect discussed in quite a number.

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7 From the cerebral perspective, some appreciation of the key determinants of cerebral blood flow was required, and in particular some mention of the factors affecting cerebral perfusion pressure and cerebral vascular resistance. It was noted that whilst many candidates had an appreciation of the changes in the arterial side of cerebral perfusion with changes in posture, many candidates failed to appreciate the importance of a concomitant decrease in cerebral venous pressure. This is a significant contributor to minimising the hydrostatic effects of direct position on cerebral blood flow. Some mention of pressure autoregulation was an important component of the answer and many candidates did not mention this aspect at all. There was sometimes confusion between pressure autoregulation and metabolic-cerebral blood flow “coupling”. The term autoregulation is sometimes used interchangeably in the literature, and this creates confusion in published texts. In reality, both responses may share common mechanisms. It was interesting to note that almost no candidates discussed the time course of cerebral blood flow changes. The figure of a 20 percent reduction in cerebral blood flow was commonly quoted, however, it was not often appreciated that this is a temporary change. QUESTION 13 Briefly describe the principles and sources of error in the measurement of

systemic arterial blood pressure using an automated oscillometric non-invasive monitor.

This question was passed by 81% of candidates. Most candidates demonstrated a good understanding of the principles of the device and the strengths and weaknesses in detection of systolic, diastolic and mean pressures. Some candidates presented their answer as if this device was synonymous with a particular brand. It is very reasonable to present the specifications of a particular brand as an example of such a device but not to imply that there is only one type. Some descriptions of the equipment were problematic. The concept of the bladder within the cuff was often not clear and lead to confusion about describing the positioning and size of the bladder. Descriptions of the recommended dimensions of the cuff (and bladder) often did not specify whether length or width were being presented. There were some instances of confusion between historical two tube and two cuff equipment (particularly oscillotonometry cf oscillometry) and current single cuff and tube equipment. Occasional candidates also confused detection of oscillations with detection of Korotkoff sounds. Modern oscillometry devices have the transducer in the control box not in the cuff. Formulas presented for calculating the diastolic pressure were often presented as variations of Mean Arterial Pressure = Diastolic Arterial Pressure + 1/3 pulse pressure. These were usually technically correct but would be better presented as Diastolic Arterial Pressure = a formula related to directly measured parameters (or other algorithm related to change in percentage size of oscillations detected). QUESTION 14 Describe the factors that affect lung compliance. A pass rate of 39% was achieved for this question. Irrelevancies were uncommon on this occasion, however some basic mistakes and omissions did occur. The answer is best introduced with a definition. Marks were allocated for a value with the correct units *the compliance equation relating the total lung, to chest wall and lung compliance.

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8 *Surfactant and its role on surface tension. *Laplace’s law and its applicability. *The importance of elastic forces and their role in disease states. *Lung size. *Lung volume and its relationship (to FRC) on compliance. *Effect of gravity on the lung and hence on compliance. Mention of various compliances like dynamic, static and specific with their definitions attracted extra marks as did diagrams showing a pressure volume loop, hysteresis, or a compliance curve, with explanations. Clinical relevance is also important and mention of restrictive lung disease, obstructive lung disease: pulmonary emphysema, pleural effusions, or at least some of those was appropriate. Differentiating the effects of emphysema on dynamic vs. static compliance also attracted extra marks. QUESTION 15 Describe the physiological actions of thyroid hormones. 38% of candidates passed this question. The question asked the physiological actions of thyroid hormones, not the synthesis of thyroid hormones. There is a lot to cover by way of physiological actions. Some candidates spent time detailing their synthesis Marks were awarded for noting the forms of thyroid hormones, the relative amounts in the bloodstream and relative activities. An account of their mechanism of action at a cellular level was considered important. An understanding of the implication of this mechanism of action to the time for onset of action and duration of effect scored extra marks. An account of end-organ effects was present in some form in most answers, with a system by system approach often used. Most candidates were able to state that thyroid hormone increases metabolic rate. Many of these were able to go on to state that thyroid hormone had some catabolic effects. Some briefly mentioned the role of thyroid hormone in growth and development. Few picked up on the apparent contradiction between catabolic and anabolic effects, and described that the effects of thyroid hormones can be dose and age dependent. The effect of thyroid hormone to provide a negative feedback on its own synthesis was not often mentioned. QUESTION 16 Describe the functions of the loop of Henle, including the physiological

mechanisms involved. The pass rate for this question was 64%. Points required for a pass were: The main function of the loop of Henle is to establish a concentration gradient in the renal medulla, which allows the collecting duct to regulate water excretion. This is achieved by active ionic transport (associated with impermeability to water diffusion) from the tubular lumen in the thick ascending segment of the loop to the interstitium, coupled with water permeability of the descending part of the loop. Some quantification of osmolalities in various parts of the loop, and mention of counter current mechanisms was also required.

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9 Additional marks were given for comparison of the effects of short and long loops (the physiology of desert rats was popularly mentioned!), the role of urea, and role of the loop of Henle in excretion of other ions. Because there is disagreement between texts as to whether the macula densa is part of the ascending loop of Henle - rather than the DCT - marks were given to candidates who described function of the juxta-glomerular apparatus. VIVA SECTION Common Introductory Physiology Questions

CVS Left ventricular pressure/volume curves Coronary artery flow curves Afterload and Guyton’s curves Cerebral blood flow Left ventricular volume curves Myocardial contractility Draw a Lead II ECG complex and label waves and intervals Valsalva manoeuvre Frank-Starling curve Factors determining feto-maternal exchange Wedge pressure and preload Wiggers diagram

Resp Lung volumes and capacities Closing capacity Respiratory compliance Dead space A-a gradient Effects of altitude on PO2 Arterial blood gases Types of hypoxia Airways resistance Functional residual capacity Work of breathing Effects of lung volume on pulmonary vascular resistance Peripheral chemoreceptors Shunt and venous admixture Effect of occluding the left main bronchus in a ventilated patient Effect of adding 5cmH2O PEEP to a circuit Effect of occluding the left pulmonary artery ETCO2 waveforms Effect of changes in minute ventilation on CO2 Effect of changes in inspired pressure on CO2

CNS Control of intracranial pressure Head down tilt – effects on ICP Monro-Kellie doctrine Formation and flow of CSF

Renal Range of urine osmolalities

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10 Excretion of fixed acids Renal handling of water Forces acting across a glomerular capillary Free water clearance ADH effects Renal response to hypovolaemia Renal blood flow Renal handling of potassium

Blood Haemoglobin-oxygen dissociation curve Buffers Difference between plasma and serum Carriage of CO2 in blood Crossmatching of Blood Carriage of oxygen in the blood

GI Gastric acid secretion Carbohydrate handling in the gut

Measurement Humidity Pulse oximetry – mechanism of measurement ETCO2 measurement Temperature Invasive measurement of blood pressure Pneumotachograph Measurement of intracellular water

Other Iodine metabolism Lactate production Aerobic versus anaerobic metabolism Factors affecting heat loss in a hot environment Pain pathways Determinants of the resting membrane potential Morbid obesity N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS

ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

JULY/SEPTEMBER 2002 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.

PHARMACOLOGY WRITTEN SECTION SHORT ANSWER QUESTIONS: QUESTION 1 Outline the influences of pregnancy on pharmacokinetics.

The pass rate for this question was 39%. Answers framed around the structure of absorption, distribution, metabolism and excretion performed better. It was clear from a large number of answers that candidates who structured their answers around the physiological changes of pregnancy, a more familiar topic, performed poorly. This was not because of factual errors, but rather omission of important areas of pharmacokinetics (eg absorption). The effects of pregnancy on oral absorption should have included a discussion of gastrointestinal motility, nausea and vomiting and gut blood flow. The opposing effects of the changes in ventilation and cardiac output on the uptake of volatile agents should have been presented. The effects of increased cardiac output on transdermal and intra muscular routes of administration were infrequently discussed. Volume of distribution is increased in keeping with the increase in total body water and plasma volume. Distribution of drugs is also affected by the changes in cardiac output and plasma protein binding. Hepatic blood flow is generally stable or slightly increased. The differential effects of oestrogen and progesterone on liver enzyme activity were discussed by some. Most candidates discussed the reduction in pseudocholinesterase with pregnancy but few mentioned that this has minimal effect on the dose of suxamethonium because of the increased volume of distribution. Candidates generally mentioned the effect of increased renal blood flow and renal clearance on drug elimination. QUESTION 2 Briefly describe the factors affecting the uptake of orally administered

medicines. The pass rate for this question was 67%. Factors affecting uptake of orally administered drugs can be related either to the drug itself or to the patient. Subsequent pharmacokinetics including the first pass effect or bioavailability should not have been part of the description of uptake and were not awarded any marks.

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2The answer should demonstrate an understanding that drug uptake is usually dependent on a lipid soluble,

un-ionised compound moving down a concentration gradient.

Drug factors affecting uptake include formulation, pKa and ionised state in the gut and ability to resist degradation.

Patient factors include blood flow to mucosa, compliance, altered gut motility or transit times, absorptive surface area, effects of disease and chemical or microbiological contents of the bowel that may degrade the drug. Ficks Law of Diffusion relates concentration gradient, surface area and permeability coefficient for the passive flux of a drug molecule. This illustrates many of the important principles in oral drug uptake. QUESTION 3 Draw a graph comparing the ratio of inspired to alveolar concentrations

during the first half hour of administration for nitrous oxide, isoflurane, and halothane. Outline reasons for observed differences between the agents and indicate the effects of increases in alveolar ventilation and cardiac output.

This question was passed by 73% of candidates, including a borderline pass in 20%. The wording of the question created some confusion, as inhaled anaesthetic uptake is dependent upon the rate at which the alveolar approaches the inspired concentration, graphically represented as the time-course of the ratio of alveolar to inspired concentrations. Most candidates drew this latter graph, correctly labelling the axes, that was accepted as the correct response to the question. A single candidate inverted the ratio and accurately plotted the equivalent time-course of inspired to alveolar concentrations, gaining full marks. Candidates gained marks for accurate representation of the uptake of each of the specified anaesthetic agents. Reasons for the observed differences between the specified agents include the influences of different concentrations, blood/gas partition coefficients and the effects of the agents on alveolar ventilation and cardiac output. For all agents, increased alveolar ventilation results in more rapid rise of the alveolar to inspired concentration ratio, whereas increased cardiac output reduces the rate of rise of alveolar concentration. QUESTION 4 Briefly outline the potential interactions between volatile agents and carbon dioxide absorbents. This question was passed by 52 % of candidates. The main points expected in the answer were: • The different types of carbon dioxide absorbent with differing likelihoods of interaction with

volatile agents. • Specific interactions with:

- sevoflurane, producing compounds A – E - desflurane, enflurane and isoflurane, producing carbon monoxide - trichloroethylene, producing dichloracetylene, phosgene - halothane, producing difluorovinyl compound

• The influence on these reactions of: - temperature - hydration of the absorbent - concentration of the volatile agent

• The potential toxicity of the various products of the interactions • The practical relevance of these interactions in clinical anaesthesia Credit was also given to those who mentioned the ability of carbon dioxide absorbents to absorb volatile agents, with the possible consequences of: • Slowing of anaesthesia induction • Release of absorbed volatile agent to a subsequent case.

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3QUESTION 5 Outline the possible reasons for prolongation of paralysis induced by an

intravenous dose of 1 mg.kg-1 of suxamethonium. Briefly indicate the consequences of such a prolonged block.

The pass rate for this question was 60%. The main points were as follows:

• Suxamethonium 1 mg/kg is a routine dose. Phase 2 block from overdose therefore is unlikely • Suxamethonium is metabolised by pseudocholinesterase. Alterations in the concentration or

activity of this enzyme can cause prolongation of suxamethonium action. • A discussion of acquired alterations in concentration or activity (i.e. liver disease, pregnancy, drug

interactions etc). Note that these do not often result in clinically signficant prolongations in suxamethonium action.

• A discussion of the inherited alterations in concentration or activity, including the genetics, incidence, effect on duration of action, investigation with dibucaine number and other tests

• The duration of action of suxamethonium can also be altered by other agents or diseases with pharmacodynamic effects.

• Consequences including the need for ventilation and sedation in a suitable environment, monitoring of neuromuscular function, possible treatments, investigation of patient and family and implications for future anaesthesia.

Common mistakes included discussion of the clinical indications and other side-effects of suxamethonium and omission of information about consequences of prolonged block. Many candidates omitted to discuss one of the three main causes (i.e. inherited, acquired or pharmacodynamic interactions). QUESTION 6 Write brief notes on tolerance and dependence in relation to opioid analgesics. The key elements of a successful answer were clear definitions of each term and a discussion of their features and mechanisms. Decreased potency rather than decreased efficacy is generally seen with opioid tolerance. Many candidates described a lack of tolerance to respiratory depression when tolerance to analgesia occurs. This was in contradiction to the common finding of tolerance to analgesia, euphoria and respiratory depression being much more marked than that for constipation and pupillary constriction. While the majority highlighted the relevance of tolerance and dependence in heroin addicts few highlighted the similar importance in chronic pain patients on oral opioids. Overall those who stuck to the topic and provided brief notes on both tolerance and dependence achieved a good mark. QUESTION 7 Outline the potential pharmacological advantages and disadvantages of intra-

operative beta-blockade. 76% of candidates passed this question, although there were few high marks achieved. Good answers included an explanation of how improved myocardial oxygen balance was achieved rather than merely mentioning the fact and distinguished between the normal heart and that with coronary artery disease. Many candidates also distinguished between the physiological explanation of how improved myocardial oxygen balance is achieved and the epidemiological studies that have shown that the theoretical advantages translate into improved outcomes in relevant patients. In general candidates were much stronger on the disadvantages of intra-operative beta-blockade than its advantages. Few candidates mentioned interactions with other aspects of anaesthesia, such as their MAC sparing effects, problems with resistance to vasopressors and their possibly masking cardiovascular signs of inadequate anaesthesia. QUESTION 8 Outline the pharmacological effects of vasopressin. The pass rate for this question was 79%. The question asked for a description of the pharmacological uses of vasopressin. Information relating to these aspects rather than physiological characteristics of the endogenous ligand was therefore given preferential weighting. Candidates should have mentioned the peptide nature of vasopressin and hopefully

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4comment on the implications for administration. Peptides typically have extremely low oral

bioavailability due to intestinal proteases. Details relating to receptor subtypes and specific effects were frequently mentioned. Generally there was a good standard of explanation of sub-cellular events and mediators. Candidates should have discussed the different clinical effects and indications for vasopressin and DDAVP. Commonly omitted was the synergistic activity with catecholamines. Although vasopressin will afford water retention in diabetes insipidus it is preferable to use DDAVP to avoid vasoconstriction. VIVA SECTION Common Introductory Pharmacology Questions

• Adenosine • Atenolol • Amiodarone • Assessment of neuromuscular blockade • Central nervous system effects of volatile

agents • Compare atropine and hyoscine • Contrast atracurium and rocuronium • Calcium channel blocking drugs • Cardiovascular effects of volatile

anaesthetics • Clearance • Changes in pharmacokinetics and

pharmacodynamics with age • Drugs affecting the renin-angiotensin

system • Define drug synergy • Dose response curves • Drug disposition in the neonate • Define sensitivity and specificity • Drugs causing amnesia

• Drugs that affect serotonin receptors • Digoxin • Describe statistical tests you would use

for a variety of data types • Formulations of propofol • Hepatic clearance of drugs • Hepatotoxicity of volatile agents • Local Anaesthetic toxicity • Lignocaine metabolism • Lignocaine infusion • Mechanism of action of benzodiazepines • Nitrous oxide elimination • Nitroprusside • Paracetamol • Renal toxicity of volatile agents • Remifentanil infusion • Tramadol • The effects of a combination of propofol

and fentanyl

PHYSIOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 82% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Draw a pressure volume loop for the left ventricle in a normal adult. Outline

the information that can be obtained from such a loop. 67% of candidates passed this question. The main points expected were an accurate pressure volume loop, with the phases named and the points of valve opening and closing marked. In addition, an outline of the information gained from the loop was expected, such as stroke volume, ejection fraction, left ventricular end diastolic volume (as a measure of preload), left ventricular diastolic pressure/volume relationship (as a measure of elastance), left ventricular

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5end systolic pressure/volume line (as an indicator of contractility), and area within the pressure/volume loop (as a measure of stroke work). A common omission was not including simple information eg. naming the phases of the loop and indicating where the valves open and close. Stroke volume and ejection fraction were often forgotten in favour of complicated elastance lines. A common mistake in the loop was to mark the aortic valve opening at a higher pressure than at which it closed. Also, the diastolic curve often had correct volumes but incorrect pressures. QUESTION 10 List the physiological factors which increase respiratory rate. Include a brief

explanation of the mechanism by which each achieves this increase. 55% of candidates passed this question. The question was quite specific in requiring a list of physiological factors followed by a brief explanation of each factor. It was expected that the effects of hypoxia, hypercapnoea, and acidosis would receive most attention. In addition it was expected that at least two other factors would be mentioned (eg exercise, voluntary control, depression of respiratory centre, pulmonary stretch reflexes). Most candidates neglected to mention that hypoxia and hypercapnoea are synergistic in their effect on increasing respiratory rate. Others made vague statements linking the effects of PaO2, PaCO2 and pH. Some candidates produced detailed descriptions of respiratory control mechanisms which were not required. Many candidates were confused about pulmonary stretch reflexes, which act primarily to limit or prevent hyperinflation, and are less important for controlling respiratory rate. QUESTION 11 Outline the factors that determine coronary vascular resistance. 65% of candidates passed this question. The main points expected were a clear understanding of the link between myocardial oxygen utilisation and blood flow, as well as the effect of systolic extravascular compression of coronary blood vessels, and the role of the autonomic nervous system in controlling coronary vascular tone. Inclusion of the myogenic mechanisms that regulate coronary vascular resistance to maintain flow across a range of perfusion pressures gained extra marks, as did mention of the putative mechanisms involved in metabolic regulation. Additional marks were also gained by illustrating the differences between right and left ventricular systolic and diastolic flow patterns. Some candidates began the answer with an explanation of Ohm's Law, but then were unclear about the relationship of flow to pressure, as determined by the coronary vascular resistance. Many also began with Poiseuille's equation, but did not follow this with a clear explanation of the major role of vessel radius as the primary determinant of resistance. Mention of blood viscosity as a determinant increased the score if included in a relevant context. QUESTION 12 Briefly explain the changes that occur in stored whole blood. 58% of candidates passed this question. Candidates who scored well addressed each of the components of whole blood (red cells, Hb, 2,3-DPG, white cells, platelets, plasma proteins/coagulation factors, electrolytes/acid-base, dissolved gases, additives). They “explained” rather than listed the changes, and provided detail of the magnitude and time course. A number drew tables showing the changes during each week of storage, then explained the underlying causes of these changes.

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6Candidates who failed did so because they omitted major components of whole blood. Several candidates

wasted valuable time writing about the effects of massive transfusion, which was not required. Others did not answer the question, preferring to state that “whole blood is no longer used” and then to describe the storage of packed cells, fresh-frozen plasma and platelets. QUESTION 13 Briefly describe the functions of renin and angiotensin. 46% of candidates passed this question. The function of renin is to convert angiotensinogen to angiotensin I. Angiotensin I is converted to the active angiotensin II by angiotensin converting enzyme (which is found principally in pulmonary endothelium, but also in many other organs). Angiotensin II has direct vasocontrictor and direct renal effects, and also stimulates thirst, as well the release of antidiuretic hormone and aldosterone. The overall effect is to retain salt and water. Additional marks were awarded for a more detailed information on the structure of renin and angiotensin I and II, where and how they are produced, and where and how they produce their effects. Some answers included a discussion of antidiuretic hormone and aldosterone physiology which was not relevant. The most common weakness in answers was the omission of basic aspects of the renin-angiotensin system. QUESTION 14 Explain the physical principles of ultrasound imaging. 25% of candidates passed this question. The main points expected were how ultrasound waves are generated; their passage through tissues (eg. conduction velocity, reflection, attenuation); recording of reflected waves and processing (eg signal noise ratio, gain, modes of display); and the Doppler effect. Extra marks were awarded for factors affecting resolution (frequency, wavelength, attenuation, artifacts), and the role of transoesophageal echocardiography in avoiding technical limitations in transthoracic imaging. Common errors included stating that ultrasound is electromagnetic radiation, and that increasing amplitude always improves resolution. QUESTION 15 Give a brief account of the mechanisms which regulate gastric secretion. Gastric secretions include water, hydrochloric acid, intrinsic factor, pepsin, and alkaline mucus. In addition gastrin is secreted by cells in the stomach antrum. Some candidates chose to pursue the control of each individual component, while others took a more global approach. Both approaches were equally acceptable. The main points expected included the contents of gastric fluid, and the three phases of gastric secretion (cephalic, gastric, and intestinal), including the nervous and hormonal mechanisms involved (eg. vagus, acetylcholine, histamine, gastrin, prostaglandins). Additional marks were awarded for detail of the afferent and efferent pathways, the effect of various food types, stimulatory and inhibitory processes, and the control of the content of gastric secretion (eg. volume, pH).

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7QUESTION 16 Explain the Bohr and Haldane effects in trans-placental gas exchange. 77% of candidates passed this question. The main points expected were a definition of the Bohr and Haldane effects, a description of their molecular basis, a description of placental gas transfer, and mention of the double Bohr and Haldane effects for both the foetal and maternal placental/uterine circulations. Diagrams were useful in efficiently conveying information. Additional marks were awarded for some quantification of the size of the effects (eg. values of foetal and maternal blood gases), the relative importance of the two effects, and the effects of maternal factors (eg. hyperventilation). VIVA SECTION Common Introductory Physiology Questions

• What is a buffer? • Define pH • Regulation of pH • Renal bicarbonate management • Sources of acid in the body / renal

handling of acid • Consequences of acid loss • Functions of the kidney / water balance • Determinants of renal blood flow • Forces acting across a glomerular

capillary • Renal clearance • Carriage of CO2 • Oxyhaemoglobin dissociation curve • Interpretation of arterial blood gas

analysis • Venous admixture. • The pulmonary circulation • Functional residual capacity • Non-respiratory functions of the lung • Dead space • Surfactant • Calculation of alveolar-arterial O2

gradient • Types of cellular hypoxia • Oxygen cascade • Respiratory system compliance • The physiological effects of IPPV • Control of breathing • Peripheral chemoreceptors • Closing volume / closing capacity /

measurement • Resistance to breathing / components /

measurement • Autoregulation • Diffusion / osmosis / osmotic pressure /

colligative properties • Determinants of the resting membrane

potential

• Cardiovascular responses to exercise • Effects of intravenous 2 litre saline load • Physiological changes with exercise • Cardiac function curve / vascular function

curve • Left ventricular pressure curve • Determinants of cardiac output /

contractility / measurement • Draw a radial artery pressure wave /

determinants of mean, systolic, and diastolic pressures

• Draw a Lead II ECG complex & label waves and intervals

• Cardiac action potential • Myocardial contractility • Pulmonary artery pressure trace • Actions of insulin • Blood glucose regulation • Functions of calcium / balance /

regulation • Gastric secretions • Dietary carbohydrate and fat • Effects of prolonged vomiting • Functions of liver / complement • Fat metabolism • Content of a unit of fresh frozen plasma • Cerebral blood flow control • Formation and functions of CSF • Cerebral blood flow/cerebral perfusion

pressure • Classification of neurotransmitters • Foetal circulation • Changes in the foetal circulation at birth • Respiratory changes in pregnancy • Cardiovascular changes in pregnancy • Thermodilution cardiac output

measurement • Pulmonary artery pressure measurement • Thermistors • Measurement of gas flow

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8• Pulse oximetry - mechanism of

measurement • ETCO2 - measurement / A-aCO2 gradient • Temperature measurement

• Gas laws • Measurement of intracellular water

N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION

Page 224: Primary Exam Reports 2011 to 1999

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

MARCH/ APRIL 2002 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: 64% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Explain how oxygen supply of organs is maintained during isovolaemic

haemodilution.

45% of candidates passed this question. A satisfactory answer should have indicated that although haemodilution decreases oxygen carrying capacity (by a decrease in arterial oxygen content), oxygen delivery is usually maintained by an increase in cardiac output. These variables are quantified by the oxygen flux equation. The decrease in blood viscosity as a result of haemodilution causes many of the cardiovascular changes that occur. This was not mentioned by over half the candidates. Decreased blood viscosity simultaneously increases venous return and stroke volume and decreases systemic vascular resistance and afterload, all of which increase cardiac output. From Poiseuille’s law we note that flow resistance is directly proportional to blood viscosity. Other relevant areas include the vasodilation that occurs in organ beds and the mechanisms involved. Also important is the increase in oxygen extraction by most organs and possible changes in the oxyhaemoglobin dissociation curve that enhance tissue oxygenation. Some candidates wrongly indicated that anaerobic metabolism and lactic acidosis (as seen in hypovolaemic shock) occur in moderate isovolaemic haemodilution. Many answers described clinical methods of increasing arterial oxygenation or reducing oxygen consumption which were not relevant to the question asked. Erythropoiesis secondary to increased erythropoietin levels (as occurs in chronic anaemia) was mentioned by many candidates but again has no relevance to this question.

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QUESTION 2 Draw a labelled diagram of a cardiac muscle action potential highlighting the sequence of changes in ionic conductances. Explain the terms “threshold”, “excitability”, and “irritability” with the aid of the diagram.

56% of candidates passed this question. The first part of this question required a diagram of a cardiac muscle action potential with labelled axes, normal values, and phases 0, 1, 2, 3, and 4 identified. An explanation of the ionic fluxes involved with each phase was expected. Additional marks were awarded for drawing a diagram showing changes in conductances of Na+, Ca++, and K+. Threshold, the level of depolarisation at which a self propagating action potential is generated, was well described and illustrated. Excitability and irritability were often confused. Excitability refers to the increased slope and conduction velocity of phase 0 as action potentials are initiated at different stages of the relative refractory period of the preceding excitation. Irritability refers to the diminished potential between resting and threshold. Extra marks were awarded for mentioning that as irritability increases, depolarisation is easier, but there is a decreased gradient and reduced conduction velocity of phase 0. A common omission was to describe the ionic fluxes only in terms of membrane permeability, with no explanation of the electro-chemical forces acting on the various ions during the five phases. Few candidates mentioned the effect of K+ on resting membrane potential. QUESTION 3 Define “Venous Admixture”. Briefly explain how venous admixture

influences arterial oxygen tension and how an increase in inspired oxygen concentration may affect this.

46% of candidates passed this question. The main points expected in the answer were: 1. An adequate definition 2. A brief discussion of shunt and V/Q inequality, both physiological and pathological 3. A brief discussion of the contribution of V/Q inequality and shunt to changes in PaO2 4. A differentiation between true shunt and V/Q inequality 5. An explanation of the effect of cardiac output on venous admixture 6. An explanation of the effects of increased FiO2 on true shunt and on venous admixture due

to V/Q inequality Points that gained extra marks included mention of sources of physiological and pathological shunt and V/Q inequality, the effect of the shape of the Hb saturation curve on the response to increasing FiO2, and mention of extra-pulmonary shunts (normal and abnormal). A correctly labelled iso-shunt diagram or description of the shunt equation also received extra marks. Common mistakes included omission of all mention of V/Q inequality. The axes of the iso-shunt diagram were often incorrectly labelled.

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QUESTION 4 Outline the physiological factors that influence pulmonary vascular resistance.

57% of candidates passed this question. The main points expected included the following:- Approximate normal values (and normal range) with correct units. The relationship between pulmonary vascular resistance (PVR), pulmonary perfusion pressure, and cardiac output. The effects of cardiac output and pulmonary artery pressure on PVR by distension and recruitment of vessels. The influence of lung volume on PVR by its effect on the diameter of extra- and intra-alveolar vessels, with the lowest PVR being at functional residual capacity. The influence of alveolar oxygen tension on regional and global PVR. Candidates who discussed the mechanism of these effects scored higher marks. Additional marks were awarded for describing the role of nitric oxide, the effect of blood viscosity, the effect of autonomic factors, the effect of hormones such as serotonin and histamine, and the effect of changes in posture. Candidates who indicated that PVR was better described as pulmonary vascular impedance, giving reasons, also gained extra marks. Several candidates wasted time providing unnecessary information such as detailed descriptions of West's zones of the lung, the benefits of hypoxic pulmonary vasoconstriction, or the difference between laminar and turbulent flow. QUESTION 5 Outline the factors contributing to the generation and maintenance of

the resting membrane potential.

77% of candidates passed this question. Key concepts expected included the semi-permeable nature of the cell membrane, the uneven distribution of ions/charge across the membrane, the equilibrium (Nernst) potential for each ion (with an explanation of what it means). Some version of the Goldman Field Equation (or similar), emphasizing the importance of permeability, with a brief explanation of the role of Na/K ATPase in both maintenance of, and a contribution to, the RMP, was also expected. It was also anticipated that some mention of the Donnan effect and its minor contribution to RMP would be made. Answers were enhanced by including typical resting membrane potentials of various cells (eg Myelinated Axon, Skeletal Muscle, Ventricular Myocyte, Smooth Muscle or Erythrocyte). A few candidates wasted time on a discussion of Action Potentials, which was not required. QUESTION 6 Explain the physiological processes which cause oliguria in response to

hypovolaemic shock 72% of candidates passed this question. The following areas could have been included: Definition of oliguria and hypovolaemic shock; The way that hypovolaemia is detected (role of low and high pressure baroreceptors); The consequent neuro-endocrine responses which affect the kidney, such as activation of the sympathetic nervous system, the role of the renin-angiotensin system and aldosterone, and release of antidiuretic hormone; Influences on glomerular filtration such as renal blood flow, arterial blood pressure, glomerular permeability; Distribution of blood flow within the kidney, intra-renal factors effecting glomerular and tubular function, and the role of the medulla in concentrating urine; Some over-view of the physiological advantage in producing concentrated urine in response to hypovolaemia; Some indication of the relative importance of the concentration process compared to the other factors. Given that the word “shock” was included in the question it was reasonable to include comment about pathophysiology relating to shock and oliguria.

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The challenge of this type of question is to succinctly provide a broad overview. Difficulty in achieving high marks generally related to the problem of going into too much detail in part of the answer and omitting other major areas or explanation of concepts. QUESTION 7 Outline the principles of a pneumotachograph. What factors affect the

accuracy of this device? 44% of candidates passed this question Several candidates wrote answers on different pieces of equipment, e.g body plethysmograph, capnograph, Bourdon gauge, or others. No matter how correct that information, no marks could be given. Eight candidates wrote nothing at all. For a pass, an answer should have included most of the following points :

• Fixed-orifice device i.e. measurement of pressure drop across a fixed resistance • Design with either a mesh screen or capillaries to encourage laminar flow • With laminar flow there is a linear relationship between flow and ∆P, according to

Poiseuille's equation.

Accuracy is affected by the following factors, • Humidity and condensation • Temperature • Flow greater than maximum recommended for the particular device • Viscosity of gas measured versus calibrated for

Extra marks were awarded for additional relevant information e.g. design features; the low pressure drop (< 1 - 2 cmH2O); the Fleisch screen can incorporate a heater to prevent condensation; There is a range of sizes available (eg suitable for children and adults); if flow is too large for the device chosen then turbulence will result in which case there is no longer a linear relationship between P and Flow; if flow is too low the ∆P may be too small for the transducer to detect. Common errors included listing changes in gas density rather than viscosity as important without mentioning that this was only of relevance to calculation of Reynolds' number. QUESTION 8 Describe the physiological factors that contribute to the competence and

tone of the lower oesophageal sphincter. 42% of the candidates passed this question. The main points expected included the following:- The lower oesophageal sphincter (LOS) at the terminal 4 cm of the oesophagus is characterised by an increased number of nerve cells. It consists of smooth muscle (intrinsic sphincter); which is tonically active, and is under neural control. Acetylcholine leads to contraction of the intrinsic sphincter. The crura of the diaphragm constitute the external sphincter, and are under control of the phrenic nerve. Contraction is coordinated with ventilation and contraction of the chest and abdominal muscles. On swallowing, the LOS relaxes temporarily. The oesophagus enters the stomach at an oblique angle and the diaphragm maintains this angle which forms a pinch valve. The lower oesophagus is in the abdomen and is thus exposed to intra abdominal pressure. Some description of hormonal influences was expected (eg. gastrin, motilin, prostaglandin E2, glucagon, secretin, cholecystokinin, VIP).

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Additional marks were awarded for including the following points: The oblique fibres of the stomach wall functions as a flap valve. There is a pressure differential between the stomach and the oesophagus. Barrier pressure is the difference between the LOS pressure and the intra-gastric pressure. The latter is about 10 cm H2O. Normal barrier pressure is about 26 cm H2O (reflux can occur when this pressure falls below 13 cm H2O). Some candidates listed the hormones without stating how they affect the LOS tone. Most mentioned barrier pressure but some did not state any values. Others discussed pharmacology which was not required. VIVA SECTION Introductory Physiology Questions

CVS Guyton's Curves. Effect of haemorrhage Left ventricular pressure volume loops Myocardial oxygen supply and demand; Coronary sinus PO2 Valsalva manoeuvre. Effects of IPPV and PEEP Preload and Frank-Starling curve Autoregulation Fluid flux across capillary; Lymph formation and flow Haemodynamic changes during pregnancy Foetal circulation and changes at birth Cerebral blood flow Head-down tilt - effects on ICP

Resp Effects of supine position Closing capacity Regional variations in ventilation Static compliance A-a gradient Effects of lung volume on pulmonary vascular resistance Effects of breathing high inspired CO2 Alveolar air equation Effects of increasing altitude on PO2 Arterial blood gases Work of breathing

Blood Changes in stored blood Effects of massive transfusion Prevention of blood clotting in normal blood vessels Difference between plasma and serum Blood Groups Structure and synthesis of Hb O2 carriage in plasma Hb-oxygen dissociation curve

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Renal Range of urine osmolalities Mechanisms of concentration/dilution Excretion of fixed acids ADH effects Total body water and its measurement Effects of increasing renal blood flow on GFR What is in 1L of Hartmann's solution? GI What factors prevent gastro-oesophageal reflux? Lower oesophageal sphincter Functions of the liver Measurement Cardiac output: invasive and non-invasive Invasive measurement of blood pressure Humidity Osmolality Lung compliance: dynamic vs static Other Thermoregulation Effects of 48 hour fast Lactate production Buffers

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PHARMACOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 51% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Outline the toxicity of local anaesthetics. 57% of candidates passed this question Toxicity is defined as the deleterious side effects of a drug. Toxicity may be reversible or irreversible and is usually dose related over a range. It may be systemic or local. The main points expected in the answer were: • Local anaesthetics vary in their toxicity, toxicity correlates with intrinsic potency. • Systemic toxicity relates to the blood level of local anaesthetic. • Blood levels depend on site, dose and rate administered and other factors such as metabolism. • A description of the sequence of events that occurs with increasing blood levels, the CC:CNS

ratio. • Specific examples including a brief discussion of the mechanism of toxicity eg. bupivacaine,

cocaine. Other information that was rewarded included a discussion of factors that predispose to toxicity, maximum dosages, local toxicity and anaphylaxis. A common error was to imply that toxicity was the same for all local anaesthetics, eg, 'arrhythmias caused by local anaesthetics are difficult to treat'. Serum levels were sometimes listed without reference to a particular agent. Cousins and Bridenbaugh’s “Neural blockade in clinical anaesthesia and pain management” is an excellent reference for this topic. QUESTION 10 Outline the factors that determine recovery (offset of action) after

ceasing a drug infusion. The pass rate for this question was 43%. This question was also asked in 1999, 1998 and 1995. The effect of most drugs is related to the drug concentration at the effect site. Thus recovery is dependent on all the factors that influence the concentration at the end of the infusion, the rate of decline in concentration, and the final concentration that no longer has an effect. The concentration at the end of the infusion will be dependent on the dosing regimen up to that time and the drug pharmacokinetics. Diffusion of drug between the blood and the effect site will be affected by the concentration gradient and the physicochemical characteristics of the drug. Although a few drugs may be metabolised at the effect site, most drugs will have to diffuse back to the blood before elimination. The decline in blood concentrations will be determined by drug clearance and distribution (and factors that alter clearance and volumes of distribution). Many answers listed potential factors without indicating whether recovery would be prolonged or shortened.

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Many answers elaborated on the context sensitive half time (CSHT) as an example of the balance between distribution and elimination. The CSHT does not determine recovery (although it is better than the elimination half-life as an indicator); it just predicts a defined specific decline in concentration. It is unlikely that exactly a 50% decrease in concentration is required for recovery, and the CSHT can not be simply scaled for other decrement times. Many answers were confused about the effect of volume of distribution (Vd). A larger peripheral Vd may hasten the decline in plasma concentration if the infusion is relatively short. An increase in lipid solubility does not necessarily mean an increase in Vd. A comparison of the opioid data will illustrate the inter-relationships among all the pharmacokinetic variables. The effect site drug concentration required for recovery may be affected by factors such as individual variability, tolerance and drug interactions. Other factors that may influence actual recovery include active metabolites and patient status. A few drugs bind irreversibly to receptors or inactivate them so that the effect long outlasts their measured blood concentration. QUESTION 11 Briefly outline the effects of thiopentone and ketamine not mediated via

the central nervous system. 77% of candidates passed this question. Passing required attention to both the cardiovascular and respiratory peripheral effect of thiopentone and ketamine. Mention of anaphylactic and anaphylactoid reactions; tissue irritation; enzyme induction and porphyria also gained points. Some candidates were unable to clearly differentiate the central and peripheral direct effects of the drugs. However some were very lucid and described both the peripheral effect and the alteration superadded with central system input. QUESTION 12 Outline the mechanism of action of non-steroidal anti-inflammatory

drugs and their potential adverse effects. The pass rate was 72%. The "mechanism of action" and "adverse effects" parts had equal marks available. A bare pass answer in each part could have included -

Mechanism of Action: The inhibition of metabolism of arachidonate by cyclooxygenase (COX) to subsequent prostaglandins, together with detail about COX-I & II differences, explaining why these might be exploited with selective COX-II inhibitors.

Adverse Effects: Gastric haemorrhage, inhibition of platelet aggregation and renal impairment together with detail about how and when these occur Extra marks were given for greater detail of how the analgesic, anti-pyretic, and anti-inflammatory actions are produced and for non-COX inhibition mediated mechanisms of action. Anti-platelet actions were accepted in either part of the answer but marked only once. NSAIDs, including aspirin and paracetamol, have many other adverse effects. These include general CNS disturbances, Reye's syndrome, elevation of LFTs & hepatitis, PDA closure, inhibition of uterine contraction, displacement of plasma protein bound medications, haematopoietic problems including aplastic anaemia, and overdose toxicity of paracetamol and aspirin.

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Candidates frequently stated that "NSAIDs cause asthma" without further qualification. A subgroup of asthmatic patients (20% to 25% of middle-aged patients with asthma, nasal polyps, or chronic urticaria) show hypersensitivity to even small doses of aspirin, and most other NSAIDs. This is thought to be due to diversion of arachidonic acid to the 5-lipooxygenase pathway and leukotriene production. Lipooxygenase blockade appears to be effective in preventing the problem. (Goodman & Gilman 10th Ed, Ch 27). QUESTION 13 What are the side effects of amiodarone and what problems may develop

during concurrent anaesthesia. 44% of candidates passed this question. The main points expected included the following: Pulmonary fibrosis and/or alveolitis is a common serious toxicity estimated to occur in 5 to 15% of patients on chronic therapy. The cause is not known but it has a high associated mortality. There are two presentations – progressive dyspnoea with infiltrates on chest X-ray or an acute onset cough, hypoxia, and dyspnoea that mimics infectious pneumonia. Postoperative patients are at risk of developing adult respiratory distress syndrome particularly if they have been on cardiopulmonary bypass. Additional marks were awarded for mentioning the potential role of inspired oxygen levels in this postoperative complication. Amiodarone is an antiarrhythmic agent with side effects relating to its multiple sites of action in the cardiovascular system. As a non-competitive blocker of α- and β- adrenergic receptors IV administration induces arteriolar vasodilation resulting in hypotension. General anaesthesia may exacerbate these antiadrenergic effects leading to sinus arrest, AV conduction block, peripheral dilation, hypotension and low cardiac output. Direct myocardial depressive effects are minimal. Bradycardia can occur with chronic therapy and the additive effect of volatile anaesthetics in suppressing myocardial conduction may enhance this effect. Amiodarone prolongs the cardiac action potential, and hence the QT interval, through its suppression of outward K channels. This may lead to life threatening ventricular arrhythmias including torsades de pointes, although the incidence is less than with other class III agents. Hypothyroidism or hyperthyroidism occurs in 2-4% of patients, and is related to the iodine content of amiodarone. Corneal microdeposits occur in almost all patients receiving long term therapy. Photosensitive skin reactions are quite common, slate grey pigmentation that persists after discontinuation of the drug is more rare. Dose dependent mild increases in liver transaminases are common. Peripheral neuropathy can occur in patients on long term high dosage. Additional credit was given for mentioning the pharmacokinetic implications of displacement of drugs such as digoxin from protein binding sites and the potentiation of warfarin. QUESTION 14 Briefly outline pharmacological methods of reducing gastric acidity.

Indicate the mechanisms of action and the advantages and disadvantages of each method.

There was a 59% pass rate for this question. Good answers included discussion of antacids (non-particulate and particulate), histamine-2 antagonists, proton pump inhibitors, prostaglandin analogues (misoprostol) and anticholinergic agents. Areas that were often inadequately discussed were antacids, perioperative reduction of acidity and advantages/disadvantages of the methods outlined.

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QUESTION 15 Describe the mechanism of the anticoagulant effect of coumarin derivatives and what determines the onset and offset of effect.

45 % of candidates achieved a pass. Most candidates indicated that the anticoagulant effect of coumarins is mediated via vitamin K antagonism and inhibition. However, most candidates failed to describe the nature of this antagonism (competitive) at therapeutic levels and also to mention the coumarin sensitive step in the recycling of vitamin K and its role in the carboxylation of glutamic acid residues to produce biologically competent factors. An understanding of the different half-life of vitamin K dependent factors, II, VII, IX, X and protein C and S, was essential to explain the delayed onset of action of coumarins. The time to peak plasma levels and its relation to biological effect were often omitted. Coumarin appears in the plasma after 1 hour and peaks in 4 to 8 hours after an oral dose but the biological effect takes 3 to 5 days to manifest. Important and clinically relevant determinants of onset were rarely mentioned. The effect of loading dose, age sensitivity, postoperative relative vitamin K deficiency, level of coagulation factors and albumin levels should have been included. The effect of congenitally high levels of coagulation factors, disease states, enzyme induction, ingestion of vitamin K rich food could have been included but were rarely mentioned. Most candidates however, identified external supplementation of vitamin K and fresh plasma as ways of accelerating offset of coumarin effect. Most candidates mentioned INR as a monitor for warfarin therapy; some gave unnecessary details of INR levels needed for different indications. QUESTION 16 Briefly outline the pharmacology of flumazenil. The pass rate for this question was 45%. The question asked for straightforward factual information. To pass, the candidate needed to describe the chemical identity, presentation, pharmacokinetics (briefly) and pharmacodynamics of the drug. It was difficult to score enough points to pass without at least a brief mention of each of these points. Many candidates gave lengthy and often incorrect descriptions of the kinetics of the drug. More complete answers usually gave a dose or dosage range for the drug and referred to the clinical problem of re-sedation, due to the longer half-lives of the most commonly used benzodiazepines- compared with flumazenil. VIVA SECTION Introductory Pharmacology Questions Draw a concentration/time curve after an IV bolus of propofol How do you calculate volume of distribution What is the induction dose of propofol and what is its disposition in elderly patients? Describe the structure/function relationships of local anaesthetics Correlate the pKa of local anaesthetics and their activity Describe the site of action of local anaesthetics What is your recommended dose of paracetamol? What is the toxic dose of paracetamol? How do you express drug safety? What is therapeutic index? What is an emulsion? Outline a chi-squared test

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Draw a wash-in curve for your choice of inhalational agent Draw or describe the concentration/response curve for an inhalational agent Describe the uptake of volatile agents Classify diuretics by their site of action What drugs affect uterine motility? Compare/contrast pancuronium and vecuronium Account for a case of delayed recovery from vecuronium How do you assess reversal of muscle relaxants? Describe the anti-platelet agents Discuss factors affecting awakening from isoflurane Cardiovascular effects of remifentanil Classify inotropes Compare propofol and midazolam as induction agents Discuss the brain concentration of bupivacaine after an epidural dose Discuss the principles of drug interactions using opioids and MAOIs as examples Describe tolerance to opioids Describe the metabolism of morphine Why infuse a drug? Describe the mechanism of action of anti-convulsants Compare neostigmine and edrophonium Describe the distribution of histamine receptors What drugs are used in cardiac arrest? What are some sources of bias Heparin-effects, metabolism Serotonin receptors Pharmacokinetics in heart failure Renal failure and drug metabolism Classify drugs used in cardiac failure N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION

Page 235: Primary Exam Reports 2011 to 1999

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

AUGUST/ SEPTEMBER 2001 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: 80% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Explain the effects of intermittent positive pressure ventilation on left

ventricular output. 55% of candidates passed this question The main points expected for a pass were outlined in previous Examiners' reports, August 1996 and March 1998. In brief they are:- On inspiration;

1. An initial increase in left ventricular stroke volume as the increased intra-thoracic pressure squeezes blood into the left atrium, increasing LV preload.

2. Then a decrease in left ventricular stroke volume as the venous return to the right ventricle decreases and the afterload of the right ventricle increases.

On expiration; 1. The decrease in intrathoracic pressure and increase in pulmonary vascular compliance

initially allows blood from the right to collect in the lungs before it crosses to improve the left ventricular stroke volume

2. The venous return to the right ventricle improves as the intrathoracic pressure decreases.

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Additional marks were given for comments on the left ventricular afterload, compliance and ventricular interdependence, and also for the exaggerated drop in blood pressure seen with hypovolaemia and PEEP. Common mistakes were

1. Failure to organise the information. 2. Ignoring expiration. 3. Writing too much on normal ventilation or reasons for positive pressure ventilation. 4. Writing too much on the long-term responses (hormonal) to positive pressure

ventilation and the baroreceptor reflexes. QUESTION 2 Describe the determinants of work of breathing in an adult human at

rest. The pass rate for this question was 72%. This question was asked in similar form in March/April 2000, when the pass rate was slightly less than 50%. The main points expected were- * that the S.I. unit of work is the Joule, and an explanation of how work is derived (eg. Pressure

times Volume) * a breakup of inspiratory work into elastic and non-elastic components * that elastic work consists of deforming elastic tissue, and overcoming surface tension * that non-elastic work consists of overcoming airway resistance and viscous forces * that resistance work is performed during inspiration and expiration, but that the energy for

expiration is acquired during inspiration * the effects on work of breathing due to changes in compliance, airway resistance, and

respiratory rate Additional marks were awarded for- * correctly labelled pressure-volume diagrams with percentage contributions * the oxygen cost and efficiency of work of breathing * mentioning that energy is also lost as heat Common mistakes were to write detailed answers on compliance, airway resistance, and patho-physiological conditions. A common omission was to describe expiration as passive, without stating that potential energy is acquired during inspiration and stored elastically to provide energy for expiration. QUESTION 3 Describe the fuel sources used during early and sustained fasting in man.

51% of candidates passed this question. A large number of the candidates who did not achieve a pass were borderline fails. The main points expected for a pass included a definition of early and sustained fasting. A wide range of definitions was accepted so long as early fasting was considered less than 24h. A brief description of the conversion of liver glycogen stores to glucose during early fasting was required as was the importance of glucose as a source of energy. Similarly, a brief description of the role of gluconeogenesis, lipolysis, and the production of ketone bodies during sustained fasting was

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expected. The fuel sources could be considered as either the substrates (ie glycogen, protein and fat), or their breakdown products (ie glucose, amino acids, free fatty acids, glycerol, and ketone bodies). The reliance of the brain on glucose or ketone bodies was considered core knowledge. Additional marks were awarded for (1) providing quantitative information, (2) a description of the Cori and alanine cycles, (3) the fuel sources used by individual organs (eg brain, heart, muscle etc), (4) the initial sparing of protein during sustained fasting (due to preferential breakdown of triglycerides), and (5) the time course of changes in fuel utilisation. Candidates who mentioned the continued absorption of food remaining in the gut during early fasting received credit. Common mistakes were to consider ATP or creatine phosphate as 'fuel' sources, to discuss the effects of water deprivation (while the question asked for a description of fuel sources), or to consider other aspects of starvation. Common omissions were to overlook the importance of glucose, especially in early fasting, and free fatty acids in sustained fasting.

QUESTION 4 Describe the physiological changes that occur in respiratory function during pregnancy.

Although almost 60% of candidates passed this question few achieved high marks. Key points expected included changes to the various lung volumes, pattern of respiration, minute ventilation, and the resultant arterial blood gases. Additional marks were gained for outlining the various anatomical changes that occur, explaining the physiological implications, and outlining the changes to oxygen flux. Demonstrating understanding of the ramifications of the various changes enhanced answers. For example the reduction in FRC (and therefore the lung O2 stores), coupled with the increased O2 utilization, increases the rapidity of onset of hypoxaemia. Also the arterial gas tension changes enhance placental gas transfer to the benefit of the foetus. Common misconceptions included tidal volume decreasing or remaining unchanged, significant rises in ventilatory rate, elevation of PaCO2, reduction of PaO2, increased shunt, and significant reduction in vital capacity. A number of candidates wrote in some detail on the clinical anaesthetic implications of the airway and ventilatory changes. This only gained additional marks where clear understanding of the underlying physiology was demonstrated. Candidates are referred to Nunn’s Applied Respiratory Physiology 5th edition Chapter 13 and to the 5th edition of Anaesthesia. Miller R. D (ed). Chapter 57. QUESTION 5 Describe the structure and function of voltage gated ion channels.

59% passed this question. This question asked for a description of both structure and function of voltage gated ion channels specifically. General information on ion channels which did not pertain to voltage gated ion channels did not score marks. 'Structure' was generally covered adequately, with inclusion of the basic concept of a transmembrane protein channel. The inclusion of detail on the subunit components and gating mechanisms was variable, and was often restricted to sodium channels alone. Some candidates provided excessive detail at the expense of other areas. The answers to the 'function' component of the question were much more variable. What was sought was evidence of comprehension of the basic functioning of voltage-gated channels. This included knowledge of their dependence on voltage changes for configurational changes, a resulting alteration in specific ion conductance, and awareness of the concept of channel

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activation and inactivation. Further marks were gained by relating this to specific roles in excitable membranes and organs. Again, quite a few candidates focused solely on sodium channels, but this was accepted if comprehension of the concepts of voltage-gated channels was displayed. Inclusion of details of other channels (e.g. potassium and calcium channels), however, scored additional marks. Some candidates included detail on modulation of receptor function over time, and changes in functioning with drugs/toxins, which gained extra marks.

QUESTION 6 Explain how the kidney handles glucose. Describe the physiological

consequences of glycosuria. 47% of candidates achieved a pass mark. The kidney freely filters glucose and almost completely reabsorbs it in the proximal convoluted tubule. This is an active process, utilising a Na+ co-transport system. Energy for this process comes from Na+/K+ ATPase on the basement membrane, pumping Na+ out of the renal tubular cell. This co-transport system is saturable. Extra marks where attracted for discussion of the SGLT 1 and GLUT 2 transporters and their role. A description of the TM and how glycosuria occurs at a level below the theoretical TM also received extra marks. Glycosuria causes an osmotic diuresis, and details of the mechanism were expected. Candidates who explained the effect on the medullary osmotic gradient and the subsequent failure to concentrate urine received extra marks. Some mention of the systemic implications of these effects was also expected. QUESTION 7 Explain the main difference between the intrinsic and extrinsic pathways

of coagulation. 41% of candidates passed this question. The main points expected in the answer included an account of the coagulation factors involved, a sketch of the pathways demonstrating the cascades of factor activation, and the co-factors involved. Also required was an account of what initiates or triggers the pathways of coagulation, the relative importance of the pathways in vivo, and how blood may coagulate in other settings, such as in a test tube. Additional marks were awarded for information regarding the relative speed of the pathways, interaction between the pathways, implications of specific factor deficiencies, the tests used to measure the activity of the pathways (including how these tests are performed), and where anticoagulants such as heparin and warfarin act. The few candidates who described how sepsis and inflammation activate coagulation received additional marks. Common errors were confusion about what the intrinsic and extrinsic pathways of coagulation are, the triggering mechanisms involved, and the relative importance of the pathways in vivo. Some candidates spent time giving accounts of other aspects of haemostasis at the expense of providing information about the intrinsic and extrinsic pathways of coagulation.

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QUESTION 8 Explain the physiological processes involved in the development of interstitial oedema.

The pass rate for this question was 46%.

Interstitial oedema occurs when the volume of fluid leaving the capillaries and entering the interstitial space is increased, and/or the lymphatic drainage is reduced, and/or the total ECF volume is increased. Many candidates discussed only the Starling forces acting across the capillary and failed to mention the role of impaired lymphatics. No candidate mentioned the effect of increasing total ECF volume. To achieve a pass, candidates were expected to include in their answer

• Starling’s equation (or the main components of the equation), with approximate normal values

• Examples of causes of raised capillary hydrostatic pressure, reduced plasma oncotic pressure, increased permeability, and/or decreased reflection coefficient;

• The role of lymphatics with an example of impaired function.

Additional marks were awarded for including the following points: explaining the concept of oncotic pressure (ie osmotic pressure due to non-diffusable particles); giving examples of reduced interstitial hydrostatic pressure leading to oedema (e.g. negative pressure pulmonary oedema); explaining that the pressure and permeability vary between capillary beds; indicating that hydrostatic pressure can increase by venoconstriction or arteriolar dilation; mentioning that protein leak into interstitium increases πi, thus favouring water movement.

Common mistakes made were:

• 60% of candidates stated that increased blood pressure leads to increased capillary pressure. However, this is not alway the case, because most of the pressure drop in the arterial circulation occurs before the capillaries. In fact, arteriolar dilation increases capillary pressure. This reflects a basic misunderstanding of the nature of pressure drops along the circulation.

• Many candidates stated that oedema occurs when net filtration exceeds net reabsorption in the capillary, whereas this occurs in many capillary beds without formation of oedema.

A few candidates restricted their answer to pulmonary oedema, but they were not penalized if the other required information was present. No candidate mentioned that oedema may be localized or generalized.

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VIVA SECTION Common Introductory Physiology Questions

• Atrial pressure waveform • Factors affecting stroke volume • Determinants of cardiac output • Coronary blood flow • Preload, contractility, afterload • Pressure volume loops of the heart • Aortic and radial artery pressure waveforms • Draw the cardiac cycle • Pressure waveforms during pulmonary artery catheter insertion • ECG – Origin of waveform • Pulmonary blood flow • Control of ventilation • Effects of age on lung function • Ventilation / perfusion matching • Causes of tissue hypoxia • Causes of arterial hypoxaemia • Carbon dioxide carriage in the blood • Respiratory acidosis; alkalosis • Causes of an A-a gradient • Alveolar pressure • Shunt and V/Q mismatch • Functions of liver • Effects of vomiting • The effects of insulin • Control of blood glucose • Response to lack of insulin • Absorption of carbohydrate load • Active transport • Facilitated diffusion • Resting cell membrane potential • Osmolality • Measurement of cardiac output • Measurement of gas flow • Blood gas analysis • Spirometry • Pneumotachograph • Oximetry; pulse oximetry • Measurement of arterial pressure • Humidity • Intracranial pressure • Control of cerebral blood flow • Renal handling of acid load • Renal clearance • Effects of drinking 2 litres of water • Excretion of dilute and concentrated urine • Countercurrent exchange in the kidney • Factors affecting GFR

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• Regulation of potassium • Temperature regulation • Basal metabolic rate • Changes in pregnancy • Oxygen delivery to the foetus • Foetal circulation • Structure of haemoglobin • Blood groups • Haemostasis after finger laceration • Haemoglobin dissociation curve • Loading / unloading of haemoglobin

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PHARMACOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 82 % of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 What do you understand by the term “clearance”. Using propofol as an

example, explain briefly the importance of clearance.

77% of candidates passed this question. It was expected that candidates should provide a definition of clearance including units. Some mention of total body clearance being the sum of individual organ clearances was also expected. The most common mistakes made were to define the elimination rate rather than clearance and/or not to provide units. Some candidates entered into erudite discussion of renal clearance, which was more a discussion of renal physiology than drug pharmacology.

Propofol is a general anaesthetic agent with a high clearance (30ml.kg-1.min-1 ). This is in fact greater than liver blood flow suggesting extra-hepatic sites of elimination. Whilst redistribution is important in drug offset in bolus doses, clearance becomes increasingly relevant with infusions. Clearance is also important in determining steady state infusion rates. Most candidates understood these concepts. Equations were a time efficient method of explaining concepts however this occasionally led to confusion. For example volume of distribution and clearance are independent variables and in effect the half life is a proportionality constant. Answers of a higher standard mentioned context-sensitive half time, compartment model infusion regimens and compared propofol to thiopentone. QUESTION 10 Briefly describe the adverse effects of nitrous oxide. 76% candidates passed this question. To achieve a pass mark, candidates were expected to describe the adverse effects of nitrous oxide resulting from expansion of air-containing spaces, diffusion hypoxia and decreased activity of vitamin B12 and methionine synthetase. Additional marks were obtained for comprehensive descriptions of the aforementioned effects, and for description of additional adverse effects including but not restricted to post-operative nausea and vomiting, pulmonary hypertension, increased cerebral blood flow, mild myocardial depression and sympathetic stimulation. Many candidates also described the potential for adverse effects of impurities in manufacture. QUESTION 11 Describe the required pharmacological characteristics of local

anaesthetic formulations intended for topical use. 41% of candidates passed this question. It was expected that there would be a description of the characteristics of the formulations applied at the different sites where topical local anaesthesia is used.

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The main points expected for a pass were concerned with characteristics common to all topical anaesthetics including those incorporated in Fick’s law of diffusion. However there should have been mention of various possible sites of application (eg skin and mucous membranes) in order to illustrate the differing relative importance of characteristics which could subsequently have been divided into pharmaceutical, pharmacokinetic and pharmacodynamic properties. Pharmaceutical Presentation, (eg aerosol, solution, gel, cream, lozenges), stability during storage, concentration of active component, possible “additives” including those required to optimise kinetics (eg pH adjustment and/or vasoconstrictors), lack of local toxicity. Pharmacokinetic Molecular weight, pKa and intrinsic lipid solubility, rapid onset, appropriate duration, high systemic clearance, no active or toxic metabolites. Pharmacodynamic Effective block of nerve transmission, relevance of intrinsic vasoconstrictor activity, high therapeutic ratio. Additional marks were awarded for explanation of the relevance of the above characteristics, eg buffering of formulation to ensure low ionisation thus further enhancing intrinsic lipid solubility or why vasoconstriction, despite the limits it places on systemic uptake, may be undesirable if venous cannulation is planned. Mention of other characteristics (eg ease and economy of production, preservatives, protein binding and common side effects) could also gain additional marks. The question did not relate only to cutaneous application and EMLA. Unnecessary detail about this formulation, to the exclusion of other information, was the most common reason not to gain marks. Similarly extensive discussion of non-pharmacological topics such as the thickness of the cutaneous barrier or area of application did not gain marks unless in relation to kinetics or dynamics (eg onset times and systemic toxicity). Occasional confusion seemed to exist between potency and concentration. The former is a comparison of the mass of one drug, compared to another, to bring about an effect. In this context potency is of little importance so long as the concentration of the formulation is far enough above the effective concentration to ensure a high concentration gradient. Despite the fundamental nature of the relationship between pH, pKa, ionisation and transmembrane passage of molecules, some candidates still appear not to understand this topic. QUESTION 12 Outline the effects of an opioid injected into the spinal intrathecal space. The pass rate for this question was 18%. Intrathecal opioids act initially on spinal opioid receptors, causing presynaptic and postsynaptic effects at a cellular level such as decreased release of substance P. The resultant analgesia is greater for dull pain mediated by C fibres than sharp pain mediated by A-delta fibres. Urinary retention, pruritis, nausea and delayed respiratory depression are important side effects but few candidates mentioned their expected incidence. Better answers compared different opioids, gave some indication of the duration of analgesia and gave more detail on the different side effects. Some candidates appeared to list the effects of spinal local anaesthetics and stated that intrathecal opioids would cause significant cardiovascular disturbance. Although meperidine has been used as a sole intrathecal anaesthetic and large doses of other opioids such as sufentanil may have significant local anaesthetic effect, this is not usually the case after small doses of intrathecal opioids. Secondary haemodynamic or other effects occurring because of adequate analgesia were not rewarded. However candidates should note there has been concern about intrathecal opioids in labour and fetal bradycardia. Some candidates discussed epidural opioids, and gave unnecessary

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detail about transfer of opioids across the dura and systemic absorption. Many candidates wasted time on a detailed comparison of the pharmacology of different opioids. Candidates scored few marks when they listed all the possible effects of opioids without taking into account the intrathecal route and consequent small dose used. QUESTION 13 Compare and contrast neostigmine and the organophosphorus

compounds. The pass rate for this question was 64 %. The question asked for a comparison and contrast between two drugs and it was essential for candidates to have addressed both agents to achieve a pass mark and not discuss only one of the agents.

It was imperative to define the actions of these drugs and describe the mode of binding with some explanation of their durations of action. An explanation of their actions, clinical effects and the fact that neostigmine does not cross the blood brain barrier unlike organophosphates was considered important to the answer. Candidates who were able to give detailed explanation of the binding characteristics of these agents and how that influenced their duration of action, pharmacodynamic profile and clinical applications attained higher marks. It was considered that a general comment such as neostigmine being short acting and organophosphates being long acting, without detailed explanation, was inadequate to pass QUESTION 14 Outline the direct effects of endogenously released histamine. All candidates attempted to answer this question; the pass rate was 49%. The main points expected were a brief description of histamine’s usual roles, including gastric acid production, central neurotransmission, and vascular tone; and its role in inflammation and allergic reactions. A specific mention of drug allergy was rarely included. Many candidates provided an unnecessary amount of detail about the synthesis and G-protein mediated mechanism of action of histamine, but minimal information about its effects. The specific cardiovascular, respiratory and local effects (eg. skin wheal and flare response, pain), specific identification of H1, H2 (& H3) actions, and gastric acid secretion were the main points required. QUESTION 15 Outline the potential benefits and disadvantages of peri-operative

beta-blockade. The pass rate for this question was 47%. To achieve a pass candidates needed to include the following main points. The potential benefits including: lower incidence of ischaemia secondary to improved myocardial oxygen balance, antihypertensive effects particularly during sympathetic nervous system hyperactivity for example during endotracheal intubation and antiarrhythmic actions in catecholamine induced arrhythmias. Extra marks were given for correctly quoting long-term studies where mortality has been reduced. The concept of how beta-blockers improved myocardial supply and demand by decreased heart rate and decreased contractility should have been included. The disadvantages that should have been mentioned were: negative inotropic effects, especially in patients with cardiomyopathies or when combined with inhalational agents or calcium blockers, bradycardia and possible heart block, perioperative hypotension, bronchoconstriction, and hypoglycemia and delayed recognition in diabetes. The incidence of cardiovascular side effects is generally low.

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A common mistake made by candidates was to discuss at length the pharmacology of individual agents or to describe beta receptors and their actions. QUESTION 16 Briefly describe correlation and simple linear regression, and explain

their differences. What assumptions are common to both? This question has previously been asked in this form. A pass rate of 82% indicates that much of the required information had been identified by reference to previous reports. In order to pass in this question, the answer needed to convey the concept that correlation attempts to assess the degree of association between variables, and that linear regression is a process by which a linear relationship could be examined. In reality, linear regression is simply a modelling process, for which the “goodness of fit” of the model (a straight line relationship) to the data is given by the correlation coefficient. Most candidates could name the Pearson and Spearman coefficients and their respective data requirements. Most candidates also stressed the lack of implied causality with correlation and the danger of extrapolating beyond the data range with regression equations. Commenting on the meaning of various values of “r” from –1 to +1 and particularly zero was essential. A useful diagram showing a scattergram with “data” points, a regression line and 95% Confidence Interval lines was included occasionally, being an efficient mode of expressing several important concepts. The coefficient of determination was seldom mentioned, as was the problem of the inevitable correlation (when y is, in fact, necessarily determined by or a product of x). Although most candidates mentioned the term "method of least squares", few attempted to expand the concept and most were incorrect. VIVA SECTION Common Introductory Pharmacology Questions 1. Effects of isoflurane, propofol, fentanyl on blood pressure, in healthy adults 2. What is meant by “loading dose”? 3. Mechanisms of drug-induced histamine release 4. Effects of lignocaine on nerve conduction 5. Factors affecting onset of muscle relaxants 6. Measurement of muscle relaxant effect 7. Effect of isoflurane on respiration 8. The pharmacology of clonidine 9. Early phase (I-II) drug testing 10. Glyceryl trinitrate and sodium nitroprusside 11. Risk ratio 12. Meta-analysis 13. Bias 14. Offset of action of propofol 15. Propofol bolus concentration-time curve 16. Utility of MAC 17. Choice of drugs to treat hypotension after spinal anaesthesia 18. Volume of distribution 19. Factors that alter induction dose 20. Volatile anaesthetic concentration-response curves 21. Characteristics of intravenous induction agents 22. What is a receptor? 23. Comparison of thiopentone and propofol induction 24. Drug effects on skeletal muscle tone 25. Describe events during onset of depolarising / non-depolarising neuromuscular block

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26. Classification of local anaesthetics 27. Cardiotoxicity of local anaesthetic 28. Stereoisomerism 29. Mechanism of action of benzodiazepines 30. Structure of midazolam 31. Metabolism of midazolam vs diazepam 32. Gas uptake from lungs 33. Types of data 34. Structure-activity relationship of barbiturates 35. Mechanism of action of local anaesthetics 36. Types of vasoconstrictors 37. Determination of, and factors influencing, oral bioavailability 38. Conversion to oral opioids 39. Toxicity of sodium nitroprusside 40. Analgesic actions of ketamine 41. DNA and RNA, and recombinant drugs 42. Drugs influencing ligand-gated vs voltage-gated ion channels 43. G-protein-linked receptors 44. Metabolism of sevoflurane N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION DISTRIBUTION College Council Supervisors of Training Regional Education Officers Panel of Examiners Registered Trainees

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS ABN 82 055 042 852

EXAMINATION REPORT

PRIMARY EXAMINATION

MARCH/APRIL 2001 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: 55% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Outline the determinants and regulation of extracellular fluid volume. 68% of candidates passed this question. The volume of ECF is primarily determined by the total amount of osmotically active solute present in this fluid compartment which is predominantly sodium and chloride. Changes in the amount of chloride are to a large extent secondary to changes in sodium. Hence the amount of sodium in the ECF is the most important determinant of ECF volume. This was not mentioned by 46% of the candidates. These candidates were then less likely to go on and describe the mechanisms that control sodium balance and hence determine ECF volume. The factors that regulate ECF volume include angiotensin (which stimulates aldosterone and ADH secretion), aldosterone which causes renal sodium and chloride reabsorption, and ADH which promotes water retention by the kidneys. Changes in GFR alter the amount of sodium filtered. However, the fraction of sodium reabsorbed is held constant by glomerulotubular balance. This is different to tubuloglomerular feedback (the mechanism by which delivery of sodium and chloride to the macula densa feeds back to alter GFR). These two processes were often confused with each other. Stimulation of osmoreceptors in the hypothalamus cause thirst and also increase ADH secretion. Atrial natriuretic peptide secreted by the atria in response to increased intravascular volume causes natriuresis. Sodium is also lost in sweat. Volume stimuli override the osmotic regulation of ADH secretion and hence water excretion. Those candidates who over-emphasised one area at the expense of others, or who produced irrelevant information gained less marks. For example many candidates offered lengthy

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and irrelevant descriptions of the Starling forces across the capillary and the Gibbs-Donnan effect. The location of the volume receptors and osmoreceptors was incorrect in many answers. QUESTION 2 Briefly describe the effect of resting muscle length and load conditions

on the tension generated by a skeletal muscle. How do these factors affect the velocity of shortening?

19% of candidates achieved a pass in this question. The main points expected for a pass were the relationship of resting muscle length to tension development, and the components of active and passive tension which contribute to total tension as length is increased. The inverse relationship of load to velocity of shortening was also expected. High scoring candidates made effective use of correctly labelled graphs to illustrate points, and explained that developed tension was maximal at resting length. Most candidates were able to illustrate the role of actin/myosin cross-bridge formation in the development of tension, but there was often confusion with cardiac muscle, and a Frank-Starling mechanism was often invoked for skeletal muscle. Diagrams frequently referred to left ventricular haemodynamics rather than skeletal muscle. Muscle spindle control and Golgi tendon organ involvement were not required in the answer and did not attract marks. QUESTION 3 Briefly describe the measurement of pH in a blood sample using a pH

electrode 52% of candidates passed this question.

The main points expected for a pass included:-

• the definition of pH

• use of an ion-specific electrode, based upon the use of H+-ion sensitive glass

• the presence of a buffer solution to maintain a gradient for H+-ion

• the generation of a potential difference, in proportion to H+-ion concentration

• the presence of a reference electrode, completing an electrical circuit through a salt bridge, allowing measurement of this potential with a voltmeter or galvanometer

• the requirement for regular calibration The use of a clearly labelled diagram was beneficial in answering this question, but not essential for a pass. A number of candidates described the electrode based upon "half-cells", c.f. the classical description of ion-specific and reference electrodes. On average, candidates using this approach scored well as they appeared to have a clearer understanding of the underlying principles involved. Many candidates confused measurement of H+-ion concentration with arterial PCO2, or the Clark PO2 electrode. Many candidates went into lengthy discussions of the Henderson-Hasselbalch equation, which was not required. A large number expressed that "the pH electrode produced a current flow which was then measured as pH". Additional marks were awarded for including further details. Examples of additional information presented by candidates are listed below. It was not expected that candidates would include more than a few of these examples in the time available.

• the dependence of H+-ion concentration on temperature and the requirement for temperature control

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• common sources of error.

• the measurement of thermodynamic activity, c.f. concentration

• the physical structure pH sensitive glass and the basis of the potential difference generated

• the magnitude of voltage produced and calibration to H+-ion concentration

• the variation of pH with temperature and Rosenthal's correction factor

• the principles of "pH-stat" and "alpha-stat" measurement

• the composition and concentrations of buffer and salt solutions used

• the standard calibration solutions used

• the use of a thermistor to compensate for temperature changes

• the use of either a differential voltage amplifier or "null deflection circuit" to measure the small voltages produced

QUESTION 4 Indicate the sequence of the physiological changes to the fetal circulation

at birth and briefly describe the mechanisms which account for these changes.

64% of candidates passed this question. The main points expected were a description of the physiological changes occurring at birth, including closure of umbilical vessels and ductus venosus, reduction in pulmonary vascular resistance, reduced right atrial pressure, increased left atrial pressure, increased systemic vascular resistance, closure of the foramen ovale, and closure of the ductus arteriosus. Some explanation of the mechanisms involved was required. Additional marks were given for more detailed explanations of (1) the role of lung inflation and loss of hypoxic pulmonary vasoconstriction in the reduction in pulmonary vascular resistance, (2) the loss of the low pressure placental circulation in the increase in systemic vascular resistance, and (3) the effect of pressure changes, increased oxygen tensions, and reduced prostaglandin activity in the closure of the ductus arteriosus. Similarly, additional marks were given for indicating a physiological sequence for the changes, although a temporal sequence was not required. Credit was given for mentioning the change from parallel to a series circuit, and for mentioning that the initial changes are dynamic and potentially reversible (transitional). Many candidates provided detailed descriptions of the fetal circulation, the stimuli to breathing, or the physiology of the first breath. These were not required. Similarly, detailed descriptions of pathological states were not required. Common errors were ignoring the changes in pulmonary vascular resistance, systemic vascular resistance, or both, or listing the changes without describing the sequence or mechanism. Many candidates incorrectly stated that prostaglandins were responsible for closure of the ductus arteriosus.

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QUESTION 5 Explain briefly the role of the skin in maintaining a normal body temperature.

The pass rate for this question was 71%. It is important to note that this question specifically asked for an explanation of the role of the skin in maintaining normal body temperature. It was expected that candidates briefly mentioned the general concept of a reflex pathway to maintain temperature through a balance of heat production and loss. It was not expected that there be a long and detailed discussion of this reflex system. Similarly, it was valuable to include the sensory function of the skin in maintaining body temperature. However, a detailed description was not expected. The control of skin blood flow, with its role in heat loss as well as conservation, was an important part of this question. Rather than simply listing the responses of skin blood flow, inclusion of how changes in this flow related to the mechanics of thermal exchange added significantly to the answer. For example, the inclusion of the concept that heat exchange via radiation/conduction/convection requires a heat gradient, and that skin blood flow changes can facilitate or impair that exchange, demonstrated a clearer understanding of the issues of the skin in the maintenance of body temperature. Most candidates included comments about sweat production. Very few candidates, however, recognised its increasing importance as ambient temperature increases, or the relevance of ambient humidity to its effectiveness. Credit was given for mentioning piloerection as a means of conserving heat, despite its minimal relevance in man. It was interesting to note, however, that almost every answer included piloerection even when other, and much more important, areas related to the skin and body temperature were omitted. QUESTION 6 Describe the substances released by the endothelium. Explain the role

they play in regulating blood flow through the peripheral circulation. The pass rate for this question was 72%. The key vasoactive substances released from the endothelium are nitric oxide, prostacyclin, and endothelins. Factors affecting coagulation and fibrinolysis should have been included, although some of these substances are not so much released as expressed on the surface of the endothelium. Factors relating to tissue metabolism were accepted (adenosine, hydrogen ion, carbon dioxide and others), although the endothelium would commonly not be the primary source of these substances. The second part of the question primarily required a discussion of role of the vasoactive substances on the peripheral circulation. A discussion of substances which do not affect the peripheral circulation was not required in this part of the answer. The fact that many vasoactive substances such as thromboxane A2, bradykinin, histamine and serotonin do not primarily arise from endothelial cells was commonly either not understood or poorly expressed.

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QUESTION 7 Describe how the body detects and responds to water deficit. The pass rate for this question was 50%. Main points expected were the implications of a water deficit, how this is sensed (emphasising hypothalamic osmoreceptors), and the central role of ADH including its structure, synthesis, transport, release and actions. Other points that attracted additional marks included the distribution of body water (including normal values), the sensitivity of osmoreceptors vs. volume sensors, and the effects of severe water deficit sufficient to cause intravascular depletion. A common mistake was to concentrate solely on hyperosmolarity and contraction of the ECF or hyperosmolarity and hypotension. Many candidates failed to indicate that a water deficit involves contraction of both intracellular and extracellular compartments. Pure water deficit does not include Na+ loss, nor does pure water deficit occur in haemorrhage. Thirst is not a "backup system" in water deprivation. High pressure baroreceptors do not respond to hypovolaemia. There was little appreciation that in pure water deficit, a 10% reduction in intravascular volume would be associated with a water deficit of over 4 litres. QUESTION 8 What are the physiological consequences of decreasing functional

residual capacity by one litre in an adult?

62% candidates passed this question To achieve a pass, candidates were expected to define FRC (ie. equilibrium volume of the lung and chest wall; residual volume plus expiratory reserve volume) and give normal values, such that the physiological effects of a decrease of one litre in FRC could be put in perspective. The main points expected were a decrease in compliance, increase in airway resistance, increase in pulmonary vascular resistance, and small airway closure below closing volume leading to increased work of breathing and V/Q mismatch. The increased work of breathing is due to the additional pressure (positive or negative) required to open airways/alveoli as well as the decreased compliance at low lung volumes. Low V/Q leads to arterial hypoxaemia. Candidates who provided appropriately labelled diagrams attracted higher marks. Additional marks were given to candidates who described functions of FRC and the common causes that lead to a decrease, provided that they continued to discuss how the normal functions are disturbed by the fall in FRC. The common errors were not answering the question (eg providing information about FRC without mentioning the effects with a fall in FRC of 1L, confusing shunt with dead space, mislabelling diagrams, confusing the diagram of lung volumes vs airway resistance and lung volumes vs pulmonary vascular resistance. Some candidates discussed at length the effects of hypoxaemia which was not required. VIVA SECTION

• Alveolar-arterial gradient for oxygen • Anaphylaxis • Aortic vs. radial pressure traces • Autoregulation • Blood gas interpretation • Blood groups • Blood-brain barrier • BMR / MRO2

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• Calcium: functions, regulation • Calibration of arterial lines • Capnography • Cardiac function curves • Causes of low PaO2 • Central chemoreceptors • Cerebral blood flow • Changes in stored blood • CO2 carriage in blood • Colligative properties of solutions • Colloid osmotic pressure • Comparison of pulmonary and systemic vascular resistances • Complement cascade • Control of blood glucose • Control of ventilation • Continuous positive airways pressure • CSF composition, functions • CSF production and absorption • Differences between static and dynamic compliance • Diffusion • Diffusion abnormalities in the lung • Factors affecting O2 transfer from mother to fetus • Frank-Starling mechanism • Functions of the liver • Gastric emptying • Gastric secretions • Glomerular filtration rate • Haemoglobin structure • Haldane effect • Heat and temperature • Henderson-Hasselbalch equation • Humidity • Hypersensitivity • Hypoxia - definition, causes, effects • Impedance • Iron distribution in body • La Place's law • Lung volumes • LV pressure-time curves • LV pressure-volume loop • Measurement of blood pressure (invasive/non-invasive) • Measurement of cardiac output • Measurement of gas flow • Measurement of intracellular water • Measurement of osmolality • Myocardial action potential / ionic fluxes • Myocardial contractility • Myocardial O2 supply and demand • Neuromodulation of pain sensation • Occluded left main bronchus • Occluded left pulmonary artery

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• Osmosis • Oxygen stores • PCWP as an estimate of LV preload • Placental O2 transfer • Pregnancy - cardiovascular changes • Pregnancy - respiratory changes • Preload • Pulmonary compliance • Pulse oximetry • Renal concentrating ability • Renal response in metabolic alkalosis • Resistance in fluid systems • Resistance to breathing • Resistors • Respiratory dead space • Respiratory effects of morbid obesity • Respiratory flow-volume loops • Respiratory quotient • Resting membrane potential • Shunt • Surface tension • Surfactant • Temperature measurement • Temperature regulation • Temporal response to haemorrhage • Thyroid hormone synthesis, action • Titratable acidity • V/Q mismatch • Venous admixture • Venous return curves • Water homeostasis

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PHARMACOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 73% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Briefly describe how drugs may produce their pharmacological effects.

Illustrate each mechanism with examples. 75% of candidates passed this question. To obtain a pass, a brief explanation of the following was required. 1 Receptors - at least two types with correct examples of agonists or antagonists

• Ion channel linked (atracurium) • G-protein coupled (adrenaline) • Kinase linked (insulin) • Cytosolic or nuclear receptors that regulate gene transcription (steroids)

2 Direct Ion channel actions (local anaesthetics)

3 Enzyme inhibition (neostigmine) Other mechanisms of action, with examples, such as those listed below earned additional marks.

• Carrier molecules (diuretics, digoxin) • Colligative properties (mannitol) • Structural analogues / counterfeiting (acyclovir, chemotherapeutic agents) • Chemical reactions (heparin/protamine, antacids) • Chelation (penicillamine, desferrioxamine) • Structural proteins (colchicine)

Mention of differing effects as a result of the stereospecificity of interaction was also noted. A common mistake was the description of voltage sensitive ion channels such as calcium and sodium as ligand gated receptors. The mechanism of interaction between heparin and protamine was often incorrectly used as an example of chelation, rather than a simple physicochemical interaction. The lipid theory of the mechanism of action of inhalational agents was often used as an example of a colligative action. This was used as an example in the Examiners Report of this same question in August/September 1996. However, there is now good evidence that the mechanism of action of inhalational agents is via stereospecific protein interaction in the lipid membrane. It is expected that the best answers would integrate relevant current knowledge.

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QUESTION 10 Outline GABA’s role as a neurotransmitter and indicate how its actions may be modified by pharmacological agents.

53% of candidates passed this question. The major points expected in the answer were mention of:

• the distribution and function of GABA as a major inhibitory neurotransmitter • the distribution and function of GABAA, GABAB (and GABA nonA, nonB) receptors • GABAA is predominantly a postsynaptic ligand gated chloride ion channel. Binding of

the GABAA receptor increases chloride flux and hyperpolarises the cell. Drugs that influence GABAA receptor function include the benzodiazepines, barbiturates, propofol, etomidate, steroidal anaesthetics, ethanol, and possibly volatile anaesthetic agents.

• GABAB is a G-protein coupled receptor influencing calcium ion and potassium ion fluxes Baclofen is the best known agonist at GABAB

QUESTION 11 Define the term “context-sensitive half time”. How does this differ from

the elimination half life? Illustrate your answer by comparing thiopentone vs. propofol and fentanyl vs. remifentanil.

The pass rate for this question was 64%. To obtain a pass mark, candidates needed to accurately define “context-sensitive half-time”, explaining the “context” and the reliance of the half time on both drug distribution and elimination. Candidates had to show that they understood the limitations of the elimination half-life in predicting the duration of action of infused drugs, in contrast to the context-sensitive half time. When comparing thiopentone vs. propofol and remifentanil vs. fentanyl, candidates were required to detail the influence of the duration of infusion on the context-sensitive half times of the contrasting drugs, and to discuss factors influencing the distribution and elimination of the drugs, and hence their rate of decline in the central compartment after infusion. Extra marks were obtained for including graphs with appropriate axes and discussing their clinical importance with respect to drug suitability for infusion, and for discussing further details of drug infusion modelling used to determine context-sensitive half time. Mention of the tendency for the value of the context-sensitive half time to approach the elimination half life after prolonged infusions, depending on the individual drug disposition, indicated an understanding of the terms that earned further marks. Relatively few candidates demonstrated a clear understanding of the clinical uses and limitations of the two terms. Some confusion was evident between effect-site decrement times and the context-sensitive half time applicable to the central, or plasma, concentration. Definitions and discussions of elimination half life were frequently imprecise, and some candidates were confused by various uses of the term “T1/2β”. QUESTION 12 Briefly describe the respiratory effects of the volatile agents. 58% of candidates passed this question. Three key points were required to pass this question. 1 control of ventilation and the altered response to hypercarbia and hypoxia. The use of

graphs was a quick and effective way of presenting this information. However an inaccurately drawn graph indicated a lack of understanding in some cases.

2 change in respiratory pattern, with tachypnoea initially.

3 reduction in airway reflexes and upper airway tone.

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Differences among the volatile agents should be mentioned. Other useful points included reduced hypoxic pulmonary vasoconstriction, reversal of bronchospasm, airway irritation, increased secretions, reduced ciliary activity, and reduced gas exchange efficiency. A common error was to state there was a global reduction in respiratory rate in spite of the daily observation of the reverse even in the presence of opioids. QUESTION 13 Outline the NON-ideal features as an intravenous induction agent of the

current formulations of propofol. The pass rate was 55%. Good answers included discussion of:

1. Pharmaceutics; complex formulation, possible bacterial growth, incompatibilities and difficulty of detection, glass packaging, expense

2. Pharmacokinetics; hepatic (mostly) organ dependent clearance, offset of effect mostly dependent on redistribution, high lipid solubility with consequent easy transfer across placenta

3. Pharmacodynamics; a) Central nervous system; decreased cerebral perfusion pressure, excitatory phenomenon, controversial association with epilepsy, not analgesic, mechanism of action not fully understood, no antidote. b) Cardiovascular system; vasodilation, negative inotrope with higher levels, hypotension, depression of baroreceptor response, bradycardia. c) Respiratory system; decreased CO2 and hypoxic response, depressed minute ventilation with possible apnea, depressed airway reflexes/tone with possible aspiration and/or obstruction. d) other; pain on injection with occasional thrombophlebitis, very rarely anaphylaxis.

Many candidates wasted time by describing all the ideal characteristics of propofol. QUESTION 14 Give examples of drugs that enhance the action of the non-depolarising

neuromuscular blocking agents at the neuromuscular junction. Briefly describe the mechanism of these interactions.

36 % of candidates achieved a pass. Inhalational agents such as isoflurane produce CNS depression and reduction in muscle tone, and decrease the sensitivity of the post-junctional membrane to depolarisation. A comparison of the effects of different agents attracted more marks. Local anaesthetics such as lignocaine interfere with acetylcholine release, reduce Na+ conductance, reduce the action potential in neighbouring areas to the motor end plate (producing stabilisation of the post-junctional membrane) and cause direct muscle depression. Antibiotics such as the aminoglycosides decrease the release of ACh and decrease the sensitivity of post-synaptic membrane to ACh. Drugs that could have been included were diuretics, magnesium, quinidine, trimetaphan, cyclosporine, calcium channel blocking agents and others. Many candidates incorrectly mentioned physiological effects (like temperature and acidosis) and pathological effects like renal and liver impairment. Although an understanding of neuromuscular physiology was essential to answer the question, there was no need for a detailed account of the physiology of the neuromuscular junction with diagrams.

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QUESTION 15 Compare and contrast the pharmacology of esmolol and propranolol 75% of candidates passed this question. Those candidates who took a systematic approach to the answer scored better marks and missed fewer important points. It was not adequate to state that a drug was a β1 selective, or a non-selective β-blocker, without describing what this meant in terms of effects on vital organs. Many candidates scored well in describing the contrasting pharmacokinetics of the two agents, but then gave little or no detail on the pharmacodynamic effects of the drugs, particularly their cardiovascular effects that are the main therapeutic target. Important side effects and contraindications to their use were also frequently omitted. A number of candidates stated that esmolol causes no bronchoconstriction in asthmatics because of its selectivity for β1 receptors. The drug is only selective for β1 receptors at low doses. Few candidates mentioned the exaggerated responses that may occur when sympathetic tone is high. QUESTION 16 Describe the use of the null hypothesis and the P-value in a drug trial.

89% of candidates passed this question. In a drug trial the null hypothesis reflects the supposition that the drug has no effect compared with a control or other drug. Thus the null hypothesis states there is no difference (in the variable of interest) in the populations from which the samples are drawn. Most candidates adorned this definition with unnecessary statements of random chance differences. When we examine our statistical analysis of a data set, we can neither “prove” nor “disprove” the null hypothesis in the strict sense that these terms are used in logic. The null hypothesis is rejected or retained on the basis of likelihood. Although the null (or alternative) hypothesis is commonly said to be “accepted”, this terminology has been criticised as misleading because it may imply that the hypothesis is true. Failure to reject the null hypothesis does not necessarily mean that the study groups are truly the same, only that a difference could not be detected. Although this appears to be a semantic discussion, much of the confusion with answers was due to candidates’ difficulties with these concepts. It was important that candidates clearly differentiated likelihood from truth. The explanation of P-values was less confused. Most candidates stated the notional origins of P<0.05, commenting on the limitations of the application of this expression. The majority of answers included some useful explanation of alpha and beta errors, with many discussing the methods by which P is determined for comparison with alpha. The importance of power calculation was commonly mentioned correctly with marks also being awarded for comparisons with confidence intervals and clinical vs. statistical significance. Frequent mention was made of increasing sample size to improve power. It is also possible (although not always) to improve power by increasing the resolution of the measurement being made. Many candidates included diagrams of distributions to illustrate regions and these were helpful.

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VIVA SECTION Common Introductory Pharmacology Questions Pharmacokinetics and pharmacodynamics

• Bioavailability • Volume of distribution, clearance and half-life • Difference between plasma and biophase concentrations • Pharmacokinetics of propofol infusions • Potency, dose response curves and use of log dose • Definitions of ED95 • Mechanisms of anaesthesia • Changes of induction dose in different patient groups • Induction and recovery with inhalational agents • Kinetics of drugs in the epidural space • Pharmacology in pregnancy • Pharmacology in neonates

General topics

• Definition and clinical utility of MAC, MACawake, MACBAR • Effects of anaesthetic agents on CNS • Adverse effects of nitrous oxide; diffusion hypoxia • Topical use of local anaesthetics • Local anaesthetic toxicity, toxic dose, blood levels • Neuromuscular monitoring • Opioid metabolism • Catecholamines: structure-activity relationships • Metabolism of catecholamines, MAO inhibitors • Acetylcholine, Histamine • Non-steroidal anti inflammatory drugs • Diuretics • Inotropic drugs • Antihypertensive agents • Drugs that affect the uterus

Pharmacology of specific drugs:

• Isoflurane, Sevoflurane, Halothane • Vecuronium, Pancuronium, Suxamethonium • Codeine, Morphine, Fentanyl, Alfentanil, Remifentanil, Tramadol • Paracetamol • Heparin, Protamine, Antiplatelet agents • Ropivacaine, Lignocaine, Bupivacaine, Prilocaine, Cocaine • Adrenaline, Clonidine • Atropine, Glycopyrrolate, Neostigmine • Sodium nitroprusside, Glyceryl trinitrate, Nitric oxide • Adenosine, Amiodarone • Ketamine, Propofol, Thiopentone • Dantrolene

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Statistics: • Clinical trials • Sample size • Sensitivity and specificity • Normal distribution, Measures of central tendency • Parametric and non-parametric data • Odds ratio

N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION DISTRIBUTION College Council Supervisors of Training Regional Education Officers Panel of Examiners Registered Trainees

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JULY/AUGUST 2000 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: 55% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Describe the role of baroreceptors in the control of arterial pressure. 54% of candidates passed this question. The main points expected were an overall view of a negative feedback system to maintain the blood pressure constant including the following:-

• High pressure baroreceptors • Role in beat to beat control (eg. changes in posture) • Afferent pathways • Response to a change in blood pressure (ie sympathetic and parasympathetic) • Low pressure baroreceptors • Role in long term regulation of intravascular volume.

Additional marks were awarded for mentioning that baroreceptors respond to both sustained and changing pressures, respond primarily to stretch, can be reset in hypertensive patients, and can be tested clinically (eg Valsalva manoeuvre). Common omissions were failure to describe the relationship between the blood pressure and the rate of firing in the afferent nerves (and the inhibitory effect this has on the vasomotor centre), and the parasympathetic response. Some candidates gave a detailed account of the response to both an increased and decreased blood pressure, essentially duplicating information. Others spent too much time describing intra-renal mechanisms and hormonal responses.

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QUESTION 2 Briefly describe the principles and sources of error in the measurement

of arterial blood pressure using an automated oscillometric non-invasive monitor.

70% of candidates passed this question. The main points expected were a description of the components of an oscillometric system (eg. cuff, tubing, device for inflating the cuff, a method to gradually deflate the cuff, a transducer for measurement of pressure and oscillations in pressure in the cuff, and a display), as well as an indication of how systolic, diastolic and mean pressures are determined using this system. Explaining that the maximum oscillation corresponded to the mean arterial pressure was considered fundamental. The main sources of error expected included inappropriate cuff size, irregular heart rhythms (particularly atrial fibrillation), patient movement including shivering, low output states, and inaccurate calibration. Some explanation of how these factors introduced error was required. Additional marks were awarded for commenting on the relative accuracy of systolic, diastolic and mean pressures, the limited accuracy in certain clinical scenarios, patient factors that affect accuracy, the use of algorithms to calculate systolic and diastolic pressures, and methods for reducing artifact. Similarly, additional marks were awarded for describing the optimal cuff size. Common mistakes were incomplete descriptions of the technique, or descriptions of different techniques such as detection of pressure changes using audible signals, ultrasonic methods, or oscillotonometry. Many candidates commented on the relative advantages and disadvantages of the technique, or the hazards of the technique. This was not required and no marks were awarded for this information. QUESTION 3 Draw an expiratory flow volume curve for a forced expiration from total

lung capacity. Describe its characteristics in people with normal lungs, as well as those with obstructive and restrictive lung disease.

77% of candidates passed this question. The question asked for a diagram of a forced expiratory flow volume curve and it was expected that this would be done reasonably accurately with correctly labelled axes and values. Additional marks were awarded for description of the effort dependent and independent portions of the curve, as well as for some explanation about effort dependent and independent flow. It was also expected that the candidate would draw the patterns in obstructive and restrictive lung diseases and describe the characteristics in these conditions. The common errors were inaccurately shaped curves, inaccurately labelled axes, or incorrect values. QUESTION 4 Outline the principles of compatibility testing of allogeneic (homologous)

blood for transfusions. 27% of candidates passed this question. Principles of compatibility testing requires:-

• Blood grouping. Determination of the recipient's blood group for ABO and Rh antigens. This is achieved by adding a reagent known to contain a specific antibody and observing for agglutination

• Screening for the presence of antibodies in the recipient to other red cell antigens. This is achieved by adding a panel of red cells of the same ABO and Rh group, which are known to express other antigens, and observing for agglutination.

• Selection of a probably compatible unit grouped by techniques as described above.

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• Crossmatching: Mixing a sample of the potential donor red blood cells from this unit with the recipient’s serum and observing for agglutination:

Additional marks were awarded for information on IgM/IgG (and the difference in techniques for detection), the importance of attention to patient and sample identification, and why some antigen:antibody reactions are more important than others. Common mistakes were to confuse or misuse the following terms:-

• Haemolysis and haemagglutination • Autologous and homologous • Direct and indirect Coombs test • Haemolysis and anaphylaxis • Universal Donor • IgM and IgG antibodies • Immediate and delayed transfusion reactions

A common incorrect statement was that group O red blood cells have no antigens. Several candidates stated that 98% compatibility could be achieved using an abbreviated (and cheaper) testing procedure. While this may be true, it is important to state that a 2% incompatibility rate is unacceptable. 12 candidates wrote on autologous not allogeneic transfusion. QUESTION 5 Briefly discuss the relationship between structure and function in

skeletal muscle. 52% of candidates passed this question. The main points expected were a brief description of the macroscopic, microscopic, and molecular structure of skeletal muscle and how these structures relate to the function of skeletal muscle (isometric contraction, isotonic contraction, movement, maintenance of posture). Some discussion of the molecular contractile elements was required as well as some explanation of how the structure of muscle relates to shortening or the generation of tension. Additional marks were awarded for description of different types of muscle (red/white fibres) with different functions, oxidative capacities and mitochondrial numbers; the concept of motor units with increasing size (depending on the function of the muscle); and how shortening of muscle results in movement of body structures. A common error was to describe the structure of muscle OR the function of muscle, but not to relate the two. Many candidates also concentrated on the contractile elements without covering the other aspects involved. QUESTION 6 Briefly outline the physiological control of intraocular pressure. 30% percent of candidates passed this question. Intraocular pressure depends on the production and drainage of aqueous humour and the volume of blood within the globe, particularly in choroidal vessels. Small changes in these compartments with variable volume can have major effects on intraocular pressure, as the globe has relatively low compliance. Contraction of muscles external to the globe also may cause a rise in intraocular pressure. Description of the normal mechanisms of production and drainage of aqueous humour and the causes of changes in intraocular blood volume were expected. Additional marks were awarded for

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commenting on the physiological importance of maintaining intraocular pressure (to maintain the optical properties of the cornea), for briefly mentioning pharmacological and pathological causes of abnormalities, and the problems associated with excessive intraocular pressure. The anatomy of the eye (and physiology of aqueous flow) was a frequent source of error. The terms “orbit” and “globe”, the anterior and posterior chambers, the aqueous and vitreous humours, the position of the canal of Schlemm, and the mechanism of the potential adverse effects of mydriasis on aqueous drainage were often incorrect. Although there is a relationship between intracranial pressure and intraocular pressure, it was not adequate to state that the factors would be the same and focus the answer on factors effecting intracranial pressure. QUESTION 7 Outline the actions of insulin that affect fat metabolism. 28% of candidates passed this question. Main points expected were:-

• Decreased fat utilisation due to increased intracellular availability of glucose • Increased production of fat which occurs mostly in the liver • Increased uptake of free fatty acids by fat cells • Increased storage of fat • Decreased breakdown of fat.

Some details of these processes were required. For example, in the liver, increased glucose uptake by hepatic cells via activation of glucokinase leads to glucose phosphorylation and glucose trapping in the liver. Initially, glucose is utilised in glycogen production, but excess glucose is broken down via the glycolytic pathway to form pyruvate which is converted to acetylCoA, the substrate for free fatty acids. Free fatty acids are transported in the blood as triglyceride, incorporated in lipoprotein complexes. Insulin increases activity of endothelial lipoprotein lipase, thereby increasing the absorption of free fatty acids into fat cells. Insulin also inhibits hormone sensitive lipase, inhibiting the breakdown of triglyceride in fat cells. Insulin promotes uptake of glucose into fat cells where it is utilised for glycerol synthesis. Additional marks were awarded for greater detail and for some quantification of the processes involved. Similarly, additional marks were given for mention of insulin’s effect on citrate, isocitrate and carboxylase. QUESTION 8 Describe the factors governing glomerular filtration rate. 52% of candidates passed this question. The main points could be covered by a description of the following equation:- GFR = Kf[(PGC-PT) - σ( Π GC - ΠT)] where

• Kf = glomerular ultrafiltration coefficient • PGC = capillary hydrostatic pressure • P T = tubular hydrostatic pressure

Π GC = plasma osmotic pressure • ΠT = tubular osmotic pressure

σ = reflection coefficient A short description of how each of these factors affected GFR was required. A description of Kf, was expected; i.e. the product of the glomerular capillary wall hydraulic conductivity (its permeability) and the effective filtration area.

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Additional marks were awarded for stating normal values, and for more detail on how GFR is affected by:

• Changes in blood pressure; autoregulation • Tubuloglomerular feedback • Changes in the afferent and efferent arteriolar vascular tone of the glomerular capillaries • Factors affecting afferent and efferent arteriolar vascular tone • Changes in hydrostatic pressure in Bowman's capsule • Effects of oedema within renal capsule • Changes in plasma protein concentration • Permeability of glomerular capillaries in pathological states

The major errors or omissions were to "list" rather than "describe" factors affecting GFR, and to not state the direction in which GFR was affected, i.e. an increase or a decrease. VIVA SECTION

Introductory Physiology Questions • Determinants of intracranial pressure • Control of cerebral blood flow • Composition of cerebrospinal fluid • Potassium distribution in body • Sodium intake/absorption • Total body water distribution • Donnan effect • Nernst equation • Osmolality • Differences between heat and temperature • Temperature measurement • Measurement of gas flow • Basal metabolic rate • Osmotic pressure • Active transport • Carbon dioxide and oxygen measurement • Clot formation • Natural inhibitors of coagulation • Platelet contents and function • Determination of cardiac output • Compensatory effects in chronic anemia • Effects of blood loss • Normal electrocardiograph • Left ventricular pressure wave forms • Arterial pressure waveforms • Coronary perfusion pressure • Pulmonary vascular resistance • Effects of body immersion • Myocardial contractility • Role of baroreceptors

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• Aldosterone • Anti-diuretic hormone • Insulin and insulin receptors • Hormones produced by the kidney • Acid-base changes and buffers • Renal elimination of acid • Renal excretion of potassium • Production of a concentrated urine • Functions of the nose • Lung volumes • Lung compliance • Non-respiratory functions of lung • Control of breathing • Causes of hypoxemia • Alveolar air equation • Arterial blood gases • Ventilation/perfusion mismatch • A-a gradient • Causes of hypercapnoea • Effects of hypercapnoea • Closing capacity • Work of breathing • Liver blood flow • Liver function • Gastric secretions • Lower oesophageal sphincter function • Mechanisms of pain

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PHARMACOLOGY WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 30% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 What is an isomer? Briefly write an account of the types of isomers and

significance in drugs used in anaesthesia. 67% of candidates achieved a pass in this question. A correct definition of an isomer and an explanation of the main types of isomers were expected. Structural isomers are also known as constitutional isomers and they include the tautomers or dynamic isomers such as the keto/enol transformations of thiopentone. Stereoisomers can be classified into enantiomers and diastereoisomers. The commonest error was to define a stereoisomer as a molecule having a chiral centre. Stereoisomers are molecules with identical formulae having a different spatial arrangement, and the geometric isomers need not have a chiral centre. Marks were also given for explaining the nomenclature of chiral centres although this was a common source of confusion. Classification by any of the following systems is completely independent of the others: absolute configuration of a chiral centre [R- and S- by the Cahn Ingold Prelog convention]; optical rotation of polarised light [(+) and (-) or (d-) ,and (l-)]; and relative configuration of simple sugars and amino acids [D- and L ]. Few papers explained clearly that isomers may have different pharmacokinetic and pharmacodynamic properties. Some isomers also have different physicochemical characteristics. Examples of isomeric forms of anaesthetic drugs with correct explanations of the resultant variation in physicochemistry, kinetics, and dynamics were awarded additional marks. Common examples discussed included isoflurane and enflurane, keto and enol forms of thiopentone, bupivacaine, ropivacaine, atracurium and cisatracurium. QUESTION 10 Classify diuretics giving examples and briefly explaining their action. 79% of candidates achieved a pass for this question. While possible to classify diuretics in a ‘uniform way’ by their site of action (action on proximal tubule, loop of Henle, etc.) or mechanism (osmotic, inhibitor of ion exchange, etc.), the majority of standard texts use a mixture of these. Thus acceptable answers for this question could include any of the above, as long as all major types of diuretics were mentioned. The commonest classifications used were: action in proximal tubule (carbonic anhydrase inhibitor); loop of Henle (loop diuretics); distal tubule (thiazide compounds); collecting ducts (potassium ‘sparing’ agents); osmotic agents. A specific example was expected for each of the other ‘major’ classes (e.g. acetazolamide, frusemide, chlorothiazide, spironolactone, mannitol). A brief but clear explanation of the mechanism of action was expected. It was commonly assumed that a description of altered ion flux alone was an explanation of diuresis. This was particularly apparent in descriptions of inhibition of carbonic anhydrase. Few answers mentioned the effect of osmotic diuretics on the renal medulla’s concentration gradient or the difference between the site of action of spironolactone and other potassium sparing diuretics such as triamterene. Mention of diuresis secondary to increases in cardiac output, renal blood flow and glomerular filtration, or to antagonism of the effects of antidiuretic hormone, also received credit. Details of the therapeutic uses of diuretics gained no credit.

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QUESTION 11 Describe the structure and function of G proteins. 50% of candidates achieved a pass for this question. G proteins are so named because they are guanine nucleotide binding proteins (and thus bind GDP and GTP, not ADP and ATP as suggested by some candidates). The most common error was to confuse the structure of the G protein with that of the receptor to which the G protein is coupled. Otherwise the heterotrimeric structure of the G protein and the sequence of events from activation of the receptor to activation of the effector mechanism was well described. Some candidates mistakenly referred to the G protein itself as the second messenger. Better answers were able to give several examples of G protein linked receptors along with the corresponding enzyme systems or ion channels that were the effectors for the different G proteins (e.g. β adrenoreceptor linked to Gs to stimulate adenylyl cyclase to increase cAMP; µ opioid receptor linked to an inhibitory G protein that opens K+ channels, etc.). Many candidates gave unnecessary information on the structure of the G protein linked receptor itself or wasted time describing a long cascade of effects caused by different second messengers. Most candidates knew that G proteins are responsible for transduction and amplification of the original signal but very few mentioned how changes in G protein coupling are involved in the regulation of receptors. QUESTION 12 Explain how differences in the pharmacokinetics of alfentanil and

fentanyl can influence the way they are administered intravenously. 54% of candidates passed this question. It was not sufficient to list the pharmacokinetic parameters of these two drugs without reference to the core of the question, which was to explain how these characteristics influence the way the drugs are administered intravenously. Relative comparisons of the pharmacokinetic values were satisfactory and given the same credence as exact kinetic values. Marks were given for a description of how data such as pKa, lipid solubility, protein binding, volume of distribution and clearance influenced the drugs’ relative potency, onset, and duration of action. The time to peak effect and context sensitive half time of the two drugs could also be compared. All these factors in turn could influence the choice of drug, timing of administration, dose, dosing intervals and dosing regimens that are used in clinical practice. QUESTION 13 Write short notes on factors affecting the speed of onset and duration of

local anaesthetics when used to produce peripheral nerve block. 54% of candidates passed this question. In order to achieve a pass, the following factors should have been mentioned: Drug factors

• pKa and its effect on non-ionised fraction • lipid solubility and its effect on potency (and therefore dose) and protein binding • concentration and volume administered • intrinsic vasoconstrictor properties • effect of local and distant metabolism • effect of additives

Patient factors • site of administration including its vascularity • structure and function of nerve • pH of tissues

Candidates were awarded more marks if they used the Fick equation to illustrate some of the principles, if they used examples with numbers, such as a comparison between lignocaine and bupivacaine, and if they mentioned other patient factors such as pregnancy or electrolyte

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disturbance. High marks were achieved if the candidates addressed some of the complexities, such as that relating to the effect of lipid solubility on the onset of action. Common mistakes included listing the factors which influence onset and duration without describing the actual direction of effect, confusing tissue binding with plasma protein binding, and the use of trade names instead of generic names. QUESTION 14 Write short notes contrasting the cardiovascular effects of propofol and

ketamine seen clinically. 46% of candidates achieved a pass for this question. Key words in the question were ‘contrasting’ and ‘seen clinically’. Marks were awarded for answers structured to clearly contrast the two drugs. Some candidates used tables while others used headings of the various clinically seen effects followed by a discussion of the two drugs in relation to that effect. Candidates describing all the effects of one drug in isolation, followed by the other, gained no marks for ‘contrasting.’ Effects ‘seen clinically’ are those seen during anaesthesia or intensive care, i.e. heart rate, blood pressure. In patients monitored with pulmonary artery catheters, changes in cardiac output and haemodynamic variables can also be seen. A correct description of the direction of most of these clinical effects, and an explanation of why they occurred, achieved a pass in this question. Additional marks were given for noting the differences in dose dependency of effects, cerebral blood flow changes, the differences expected in a range of disease states (e.g. the elderly, hypovolaemia, ischaemic heart disease), and clearly identified in vitro findings relevant to the clinical cardiovascular effects. A number of candidates provided correct, but irrelevant, information about the chemistry and anaesthetic effects of the two drugs. QUESTION 15 Write brief notes on latex allergy. 44% of candidates passed this question. In a previous paper two years ago, the pass rate was 30%. The majority of candidates who failed chose to write extensively on the basic immunology of type 1 hypersensitivity reactions with specific reference to latex. Better answers included information relevant to latex allergy in the perioperative period. This included brief comments on what latex is, identifying ubiquitous sources of latex, methods to reduce exposure, consequences of exposure to latex, and the investigation of latex allergy. QUESTION 16 Compare and contrast the pharmacology of atracurium and cis-

atracurium.

26% of candidates passed this question. This question was best answered in tabular form using a standard pharmacological approach starting with physicochemistry and moving to pharmacokinetics and pharmacodynamics. It was incorrect to write that cisatracurium is the cis isomer of atracurium. Atracurium is a mixture of 10 isomers, 15% by weight being cisatracurium which provides 50% of the relaxant activity. Cisatracurium is the R-cis, R'-cis isomer, where R designates the stereochemistry of the tetrahydropapaverine rings and cis represents the dimethoxy and 2 alkyl ester groups at C1 and N2.

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Pharmacokinetic parameters were poorly presented and many answers stated incorrectly that the drugs have identical kinetics. The effects of age, temperature, pH and advanced liver and renal failure were rarely presented. Metabolic pathways of cisatracurium were a source of confusion in many answers. Cisatracurium is 77% metabolised by Hoffman elimination, with 16% cleared by the kidneys. Atracurium is mainly metabolized by ester hydrolysis. The drugs are not pharmacodynamically similar and it is important to compare the two drugs at ED95 equivalent doses. In fact ED95, duration of action, and recovery times from bolus and infusion regimens were rarely mentioned. VIVA SECTION Common Introductory Pharmacology Questions Pharmacokinetics and pharmacodynamics

• Bioavailability • Volume of distribution, clearance and half-life • Difference between plasma and biophase concentrations • Pharmacokinetics of propofol infusions • Enzyme substrate interactions • Esterases • Potency, dose response curves and use of log dose • Definitions of ED95 • Mechanisms of anaesthesia • Changes of induction dose in different patient groups

General topics • Drug delivery systems • Drugs that affect gastric acidity • Drugs that affect the uterus • Opioids: cardiovascular effects; receptors; duration of action • Definition and clinical utility of MAC and MACawake • Adverse effects of nitrous oxide; diffusion hypoxia • Adverse effects of suxamethonium • Barbiturate structure-activity relationships • Metabolism of catecholamines • Choosing between ephedrine and metaraminol • Interaction of chemotherapeutic agents and anaesthesia • Differences within the penicillin class of drugs • Serotonin and antagonists • Colloids; mannitol • Non steroidal anti inflammatory drugs

Pharmacology of specific drugs: • Sevoflurane Cisatracurium • Codeine Tramadol • Heparin Protamine • Ropivacaine Lignocaine • Clonidine Milrinone • Atropine Glycopyrrolate • Adenosine Sodium bicarbonate

Statistics:

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• Clinical trials • Sample size • Sensitivity and specificity • Normal distribution • Parametric and non parametric data

N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION DISTRIBUTION College Council Supervisors of Training Regional Education Officers Panel of Examiners Registered Trainees

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PRIMARY EXAMINATION

MARCH/APRIL 2000 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: 28% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 Explain how cardiac output is measured using a thermodilution

technique? Half of the candidates passed this question. Main points required included a definition of cardiac output, a definition and description of the Fick principle, an accurate description of the technique, a description of the temperature/time curve generated, advantages and disadvantages, and errors in the technique. Common omissions were failure to describe the Fick principle, the site of injection, to accurately draw the temperature/time curve, or appreciate that the area under the temperature/time curve is inversely proportional to the cardiac output. Many candidates also did not state advantages and disadvantages of the technique. QUESTION 2 Briefly describe the factors that influence the partial pressure of oxygen

in mixed venous blood? 56% of candidates passed this question. It was apparent that candidates had difficulty in sourcing from the relevant areas of respiratory and cardiovascular physiology to present an adequate answer. The following areas were explored in the better answers. A definition of “mixed venous” including sampling site. The relationship between PO2 and O2 content in mixed venous blood. For any mixed venous O2 content the mixed venous PO2 is dependant on the shape of the haemoglobin-

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oxygen dissociation curve. A right shifted HbO2 curve increases mixed venous PO2. Most candidates wrongly stated the reverse. Some candidates interpreted this as a question on the HbO2 dissociation curve and the factors that shift it. This was only a small part of the answer. Also expected was the relationship between mixed venous O2 content, arterial O2 content, oxygen consumption and cardiac output. All are related by modification of the Fick equation:CvO2=CaO2-VO2/Q. Any factor which affects CaO2, VO2 or Q will ultimately affect mixed venous PO2. Of note is the reciprocal relationship between oxygen extraction and cardiac output. As cardiac output falls, O2 extraction increases and mixed venous PO2 falls. Arterial O2 content is also an important determinant of mixed venous PO2. However, some candidates produced a lengthy description of all the factors affecting PaO2 or even drew the oxygen cascade which was not required. A common error was to relate the factors described to the mixed venous O2 content or saturation rather than partial pressure. Terms such as content and concentration were often confused with each other, as were tension and saturation. QUESTION 3 What is a normal value for pulmonary vascular resistance? Outline

physiological factors that influence pulmonary resistance. 49% of candidates passed this question. The first part of the question specifically asked for the normal range of pulmonary vascular resistance (PVR). Common mistakes included presenting only a single value instead of normal range, and using incorrect units. Some candidates completely ignored this section. The units and the normal range are best considered by referring to the relationship between PVR, cardiac output, and the pressure drop across the pulmonary circulation (mean pulmonary artery – pulmonary capillary wedge pressure). In this way the units mmHg/L/min (also known as Wood units) are obtained. Values using dyne/sec/cm5 were also accepted. Even if exact values were not known, it was important to indicate that PVR is much less (1/8-1/10) than systemic vascular resistance. The factors that influence PVR are those that affect resistance to flow anywhere in the body, as well as factors particular to the lung. ie. Resistance is directly proportional to blood viscosity (which is influenced by haematocrit) and inversely proportional to the fourth power of the radius (given that flow is laminar and that length is constant). Most candidates ignored the effects of blood viscosity. Factors particular to the lung that affect radius include lung volume, distension and recruitment of pulmonary vessels (secondary to changes in pulmonary artery pressure), and hypoxic pulmonary vasoconstriction. An outline of at least two of these factors was required for a pass. Additional marks were given for more detail on the mechanism of these effects. Detailed discussion of West’s zones was not required. Credit was given for mentioning the lesser effects of carbon dioxide, pH, and endogenous vasodilators and vasoconstrictors. Few candidates explained that pulmonary vascular impedance is a more appropriate term for the pulmonary circulation due to the relatively greater pulsatility. QUESTION 4 Briefly describe the difference between a single twitch and tetanic

contraction in a skeletal muscle fibre. Include in your answer the physiological basis for the development of a tetanic contraction.

53% of candidates passed this question. The main points expected in the answer were:- • A Single twitch is the response to a single stimulus, whereas a tetanic contraction is the

response to repetitive stimulation above a critical frequency. • The critical frequency depends on the single twitch duration in that muscle fibre. • Repetitive stimulation before complete relaxation causes summation of contractions, and

repetitive stimulation before any relaxation causes tetanic contraction.

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• The physiological basis of tetanic contraction is the maintenance of a high Ca++ concentration in the myoplasm, as repetitive sarcolemmal depolarisation causes Ca ++ to enter the myoplasm faster than it is pumped out into the sarcoplasmic reticulum.

• The contractile mechanism has no refractory period. • The tetanic force is up to 4 times greater than that of a single twitch. • Tetanic contraction continues until the repetitive depolarisation ceases or until fatigue occurs. Other points which gained marks included: • A description of the mechanism by which sarcolemmal depolarisation causes Ca++ to enter the

myoplasm. • Mention of high ATP consumption during tetanus. • A brief description of the role of Ca++ in electromechanical coupling. • Actin-myosin bridge formation (and hence shortening) continue as long as the Ca++

concentration in the myoplasm is high. Several candidates mis-read the question, assuming it to be about the response to use of a peripheral nerve stimulator in the operating theatre, while in fact the question was about normal neuromuscular physiology in the intact human. Failure to discuss the role of calcium was a stumbling block for some candidates. QUESTION 5 Describe the important determinants of work of breathing in an adult

human at rest. Explain how to minimise work of breathing. Slightly less than 50% of candidates passed this question. A number of candidates appeared to be unaware of the ‘work of breathing' as a concept. Better answers defined the work of breathing and gave correct SI units (Joules). A well-labelled pressure-volume graph was an ideal way to clearly and concisely demonstrate an understanding of elastic and non-elastic/resistance work, potential energy stored elastically for passive expiration, and energy dissipated as heat. Percentage contributions to overall work on overcoming elastic forces, airway resistance and tissue viscous resistance enhanced answers. A figure for O2 consumption by the respiratory muscles was expected. The second part of the question related to minimising the work of breathing and was particularly poorly done. Better answers used graphic representation of the work and respiratory rate relationship for elastic work, resistance work and overall work. Comparing work of breathing and optimal respiratory rate in situations of increased resistance work and increased elastic work enhanced answers. A number of candidates wrote very “clinical” answers emphasising patho-physiology, ICU management principles and lists of drugs useful to treat increased airways resistance. This was not required. Simply writing down Poiseiulle’s equation or Reynold’s number with no effort to relate them to work of breathing was also unhelpful. Mentioning FRC and the role of surfactant was useful but not to the exclusion of a discussion of other factors. QUESTION 6 Describe the control of gastric emptying. Just over 50% of the candidates achieved a pass in this question. The main points should have included a discussion of the neural and hormonal factors, both local (gastric and duodenal), as well as extrinsic factors. Many candidates appeared not to know the structure and function of the nervous supply of the stomach and duodenum. The hormonal control of gastric emptying was either not mentioned or was wrong in several answers. The inter-relationship between the stomach and duodenum in the control of gastric emptying was mentioned by only a few candidates.

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QUESTION 7 List the hormones that regulate renal tubular reabsorption and describe their action and site of action.

70% of candidates passed this question. The question required listing the hormones that act directly on the tubule cells to regulate reabsorption of the glomerular filtrate ie. aldosterone, angiotensin 2, atrial natriuretic hormone, antidiuretic hormone, and parathyroid hormone. Locally released hormones, and hormones that indirectly affect reabsorption by, for example, affecting renal perfusion, were listed by some and were accepted if their action was appropriately explained. Calcitonin was accepted, even though its physiological role in the kidney is unclear. There were generally good descriptions of actions, particularly of aldosterone and antidiuretic hormone, at the cellular level. There was less certainty and accuracy in describing site of action within the tubule (eg proximal vs distal tubule vs collecting duct). Parathyroid hormone, when listed, was correctly described by few candidates. There was confusion between it and 25-hydoxyvitamin D, calcitriol and calcitonin, by many candidates. QUESTION 8 Briefly describe the breakdown of haemoglobin after red cell lysis. Overall this question was done poorly, with only 17% passing. Another 20% were close to passing but there were no excellent answers. The main points expected were a discussion of the structure of haemoglobin and the fate of all three of its constituents ie; iron, haem and globin. Details about haemoglobin's survival time and the mechanisms of breakdown of the constituents were required, as well as the relevant transport proteins, and enzymes involved in key reactions. Some comments about the fate of bilirubin should also have been included, such as its secretion into bile, and its enterohepatic circulation. A common misconception was that globin is directly reincorporated into haemoglobin. In addition, the enterohepatic circulation was often incorrectly described. However, the main error was failure to discuss all three of haemoglobin's constituents, or to describe the breakdown processes in sufficient detail. VIVA SECTION Introductory Physiology Questions

Cardiovascular • Determinants of myocardial O2 demand and supply • Myocordial contractility • CVP / RAP trace • LV pressure time curve • LV pressure volume loop • Coronary artery blood flow • Oxygen flux • Circulatory charges at birth • Pressure trace right atrium to ‘wedge’ • Afterload • Myocyte Action Potential • Storlings law of the heart • Radial artery vs Aortic waveform Respiratory Surfactant • Dead space, types and measurement • Hypoxia, definition and classification

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• Compliance • Capnogram • Spirograph • PEFR • Airways Resistance • Flow Volume loops • Blood gases; acute respiratory acidosis • Shunt / Venous admixture • CO2 carriage Fluid & Electrolytes / Renal / Acid Base • Countercurrent systems • GFR; Starling forcers • Atrial Natriuretic Peptide • Mole / Osmole / Osmolality measurement • Colligative properties • 1/3 Blood Volume loss • Renal handling of bicarbonate Measurement / Physics • Mass spectrometer • Transducers • Wheatstone bridge • SI units • Flowmeters; types & principles • Impedance • Pneumotacograph • Humidity • Boiling Point • Heat vs Temperature Cellular • Resting membrane potential • Krebs cycle • Trans membrane transport Gastrointestinal • Dietary fat handling • Bile and its loss • Gastric secretions • Pancreatic secretions • Effects of Insulin Blood • Coagulation • What stops blood clotting ? • Blood groups • Von Willebrand’s factor

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Other • Effect of Tourniquet release • Effect of Steep trendelenberg position • Hormones. Definition. Classification. Secretion • Reflexes

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PHARMACOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 53% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 Compare and contrast the effects of halothane and isoflurane on the

heart. 65% of candidates passed this question. Effects on the heart refers to changes in heart rate, stroke volume and rhythm. A good approach was to divide the effects into direct and indirect. Changes in systemic or pulmonary vascular resistance were relevant to the question provided it was indicated that these would influence stroke volume. Although halothane is not often used in adult anaesthesia practice, it provides a contrast with isoflurane, and is well covered in the standard texts. Important points required for a pass answer were that cardiac output is better maintained with isoflurane (normocapnic ventilated patient) and heart rate is lower during halothane anaesthesia. Good answers had detail of the probable mechanisms of the differences in vascular resistance changes, baroreceptor depression, SA and AV nodes and cardiac conduction, and myocardial depression. Where standard texts and current literature are still conflicting or vague, such as the degree of direct myocardial depression at various concentrations of these agents, any plausible explanation of clinical observations was accepted. Interactions with other drugs could also be included and most candidates compared the agents with reference to adrenaline-induced arrythmias. Some even mentioned malignant hyperrexia, which is a valid interaction. QUESTION 10 Briefly describe the pharmacological effects of paracetamol. Outline the

mechanisms of its toxicity. 70% of candidates passed this question. The better answers were structured into sections on kinetics, dynamics, and toxicity. This was a pharmacology question, not a question about the physiology and biochemistry of pain. Nevertheless, many candidates gave unnecessarily elaborate details of arachidonic acid metabolism and cyclooxygenase inhibition. Although these answers were not penalised for this additional information, many easy marks were lost because basic pharmacological details such as onset and offset of action, and dosage were not included. Many candidates mentioned that paracetamol has a mild antiinflammatory action, yet then wrote extensively about peripheral inhibition of prostaglandin. Explanations of paracetamol toxicity were generally good. Some candidates incorrectly attributed the renal toxicity of paracetamol to the same mechanism to that associated with NSAIDs.

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QUESTION 11 Outline the main biochemical events involved in noradrenergic transmission, and how these may be altered by the use of MAO (mono amine oxidase) inhibitors ?

This question was passed by 57% of candidates. The main points covered in the better answers included:- • The structure of noradrenaline. • A concise outline of the synthesis of noradrenaline from phenylalanine via tyrosine, dopa and

dopamine, including the sites of these processes and the enzymes involved. • The storage function of the granulated vesicles and the calcium ion dependent mechanism(s) of

noradrenaline release via exocytosis into the synaptic cleft in response to an action potential. • The interaction between noradrenaline and post-synaptic receptors. • The breakdown in the synaptic cleft (and elsewhere) or noradrenaline by catechol-o-methyl-

transferase (COMT) to form normetanephrine. • The presynaptic and post-synaptic uptake of noradrenaline, most of the noradrenaline from the

presynaptic uptake being reincorporated into the granulated vesicles. • Metabolism by mono-amine-oxidase(MAO) within the nerve terminal to form 3,4

dihydroxymandelic acid, which is converted by COMT to 3 methoxy-4-hydroxy-mandelic acid (vanillymandelic acid,VMA).

• Inhibition of MAO results in reduced breakdown and increased activity of adrenaline, noradrenaline and serotonin at relevant sites throughout the nervous system.

• The differentiation of sites and functions of MAO A and MOA B, and their specific inhibitors. • Reversible (eg moclobemide) and irreversible inhibition of MAO. • The biomechanical events underlying the various adverse reactions to MAOIs precipitated by

eg. Sympathomimetics, amphetamines, tricyclics, pethidine, and tyramine rich foods. • The blood pressure lowering effected of a MAOI-induced false transmitter (octopamine). • Comments on the putative basis for the antidepressant effects of MAOIs. Several answers included extensive accounts of the physiological functions subserved by noradrenergic transmission but made little or no reference to the relevant biochemical events. QUESTION 12 Outline the pharmacology of oxytocin. There was a high pass rate (77%) with few poor answers, which might reflect the fact that candidates had made good use of examiners' reports from previous years. Oxytocin is an endogenous polypeptide hormone released from the posterior pituitary and is available for clinical use in a synthetic form. In the literature there is some dispute as to whether it is an octapeptide or a nonapeptide and either statement was acceptable. The primary actions of oxytocin are on the gravid uterus and breast milk ducts. It has very poor oral bioavailabilty due to inactivation by chymotrypsin as a first pass effect, and must be administered parenterally but can also be used intranasally. Indications for use are augmentation of labour, uterine contraction post delivery, and as aid in lactation. The common side effect seen is vasodilation resulting in flushing and a drop in systemic vascular resistance that produces hypotension and a reflex tachycardia that elicits a net increase in cardiac output. This hypotension can augment that seen with anaesthetic agents and techniques that produce hypotension. Synthetic oxytocin has very little antidiuretic hormone effect and the syndrome of water intoxication, whilst relevant and important is not a common side effect. It is usually seen after prolonged high dose infusions with significant water infusion, usually in the from

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of 5% dextrose. There are real risks to foetal well being if the full dose of oxytocin is administered prior to delivery. It is stated in texts that oxytocin infusions antagonise the effect of suxamethonium and that it is inactivated if co-administered with blood transfusion. QUESTION 13 Briefly describe correlation and simple linear regression, and explain

their differences. What assumptions are common to both? 70% of candidates passed this question. Many candidates successfully used a set of scatter plots to aid their description of these two concepts. The formula for a straight line [y= a + bx] was noted along with the phrase ‘least squares method’ in describing simple linear regression. The slope of this line [b] which is called the regression coefficient was however commonly confused with the Pearson’s correlation coefficient [r]. While r describes the strength of the association, b does not. They will have the same sign for a given data set but are otherwise completely separate concepts. While discussing the assumptions common to both, most candidates mentioned that data must be normally distributed. Additional marks were given to the few candidates who indicated that a distribution free correlation coefficient, the Spearman’s rank correlation, is applicable to non-parametric data. The examiners' expectation was for an explanation of the concepts rather than detailed knowledge of the statistical equations and their derivations. However, in many cases the use of an equation is most appropriate in quickly explaining the 'concept'. QUESTION 14 Discuss the roles of plasma esterases on drugs used in anaesthesia. 67% of candidates passed this question. Good answers included an overview of the unique properties of the esterases and their pharmacological implications followed by a discussion of pseudocholinesterase (butyrylcholinesterase) and non-specific plasma and red cell esterases. ie. Overview;

Hydrolysis of ester bonds with drug inactivation by esterases High capacity/clearance enzymes produced in liver and red cells Non organ dependent drug metabolism with generally inactive metabolites Exceptions including laudanosine and salicylic acid

Pseudocholinesterase; Metabolism of succinylcholine, mivacurium, and ester local anaesthetics Potential problems with congenital and acquired dysfunction Common congenital pseudocholinesterase variants and clinical implications Acquired dysfunction including physiological, pathological and drug interactions

Non specific plasma esterases; Metabolism of remifentanil, atracurium High capacity systems little effected by hepatic metabolism High clearance of remifentanil with infusion and independent short context sensitive t1/2 Atracurium and laudanosine

Red Cell esterases; Metabolism of esmolol and possibly remifentanil High clearance of esmolol with short duration, titratable

Some problems with answers included; extensive discussion of acetylcholinesterase and detailed discussion of pseudocholinesterase with none of plasma and red cell esterases.

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QUESTION 15 Describe the effects of opioids on the respiratory system. 75% of candidates passed this question, although very few achieved a high mark. The question required a description of the centrally mediated effects of opioids, including site of action, receptors, effects on respiratory rate, tidal volume, responsiveness to carbon dioxide and oxygen concentrations in the blood, and that the drug can cause apnoea. Mention of truncal rigidity, mast cell degranulation, and depression of cough reflex and cilial motility were expected. Better answers included some differentiation of effects of different opioids such as morphine, pethidine, phenylpiperidines and partial agonists. How pharmacokinetics of the drugs and route of administration alter the likelihood and timing of effects, and how other sedative drugs, sleep, disease (such as sleep apnoea), extremes of age, hypothermia and the degree of pain affect the responses in individuals could have been included. Secondary effects of sedation and loss of upper airway reflexes were rarely mentioned. Extremely few candidates mentioned the therapeutic ratio of these effects, the fact that they occur in the dose range of desirable analgesia, that tolerance does not always develop to the respiratory depression, or that the respiratory depression may be fatal. QUESTION 16 Briefly describe the factors that determine skin penetration by local

anaesthetics. What is an eutectic mixture? Briefly describe the formulation and pharmacology of EMLA® cream.

73% of candidates passed this question. However, a large number of answers included a list only, without further explanation, thus scoring poorly on this section. Although most candidates correctly referred to the fick equation, simply writing it down without explanation did not constitute adequate coverage. Furthermore, very few noted that a large surface area was not needed if a small area of anaesthesia was desired. In fact, some comments about uptake and blood flow suggested that many candidates felt that EMLA cream was intended to achieve therapeutic systemic concentrations (this was not a question about trans-dermal opiates; fentanyl in particular). Many candidates referred to “protein binding” without indicating which proteins were they referring to. Plasma protein binding plays little, if any role in the trans-cutaneous action of EMLA. No candidate made use of the structure-solubility relationship of local anaesthetics (2 mentioned amethocaine or benzocaine, but failed to qualify these inclusions adequately), nor did many explain non-ionised fractions well, several suggesting that ionisation increases with increasing pH. Please note that potency correlates with lipid solubility (and toxicity), but is not an independent determinant of absorption. Generally, it appeared that few candidates understood much of the chemistry of these drugs or the definition of an eutectic mixture. Local anaesthetics are not the only compounds to form eutectic mixtures. In fact only 2 candidates correctly defined the mixture as being the composition at the eutectic point. EMLA cream is a CREAM (as written in the question), not an ointment, etc. Knowledge of the constituents, the droplet formation, and the free base content were required to score highly. Most candidates mentioned metHb formation from prilocaine and the low systemic toxicity potential for this preparation. Several candidates confused basic concepts such as melting and boiling points. Details of onset and duration were also poorly covered.

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VIVA SECTION Introductory Pharmacology Questions • What are the side effects of opioids ? • What drug factors influence the side effects of opioids ? • Plasma concentration time graph of morphine. • Change of etCO2 with time after an IV bolus of morphine. • What factors influence the onset of action of volatile agent ? • Why is N2O used ? • Side effects of N2O. • Recognition of structure of lignocaine. Metabolism and protein binding of lignocaine. • Define therapeutic index. • Toxicity lignocaine vs bupivacaine (R + S). • How does liver disease affect the way the body handles drugs. • Side effects of Suxamethonium • α2 agonists pharmcodynamics. • Isoflurane and brain. • Isomerisation of isoflurane. • Isoflurane vs sevoflurane • Structure/activity of sevoflurane. • Classification of vasodilators. • How does GTN work ? • Structure activity relations of catecholamines. • Draw and explain the FA F1 curve. Does the curve reach unity at infinity ? • Differences between midazolam & diazepam. • Diazepam metabolism. • Differences between morphine and fentanyl. • What agents can be used to decrease gastric acidity ? • Discuss one parenteral antihypertensive. • Sodium nitroprusside mechanisms of action and metabolic toxicity. • Margin of safety of neuromuscular function. • Assessment of neuromuscular block. • Dibucaine number. • Suxamethonium apnoea. • Types of anticholinesterase. • Recognise 5-hydroxy typamine. What drugs interact with 5HT ? • Discuss digoxin • Contents of ampoule thiopentone, role of each adjuvent. • Draw barbituric acid nucleus. What are the keto and enol forms ? • pH & pKa, Henderson Hasselbach equation. • What are the effects of cocaine on the heart ? • What is the effect of B2 agonist drugs, how do they work ? • What is in an ampoule of propofol ? • Draw the plasma concentration time curve of propofol and the effect site (brain)

concentration time curve. • How would it vary with age ? • Discuss the pharmacodynamics of atropine. • Dose-response curves of neuromuscular blocking agents. • Define ED95. • Statistical classification of data relating to trial of antiemetic drug and test that may be used to

analyse the data.

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• Statistical classification of data relating to trial to assess potency of inhalational agent and appropriate statistical test.

• Information from confidence intervals versus P-value • Define nonparametric data ? • Pharmacodynamics of tramadol. • Define the term “an Hypnotic drug”. • Classify muscle relaxants. • What is phosphodiesterase. What drugs affect it ? • What is muscle relaxation and how can it be achieved. • Side effects nonsteroidal anti-inflammatory drugs. • Types of anti-cholinesterase drugs. • Catecholamine structure and effects of ephedrine. • Comparision of Thiopentone and Methohexitone. • Actions of adenosine. • Actions of diuretics, comparision of thiazide & loop diuretics ? • Pharmacogenetics – examples related to anaesthesia. • Fate of I.V. bolus of morphine. • Onset of action of Fentanyl. N.M. GIBBS CHAIRMAN PRIMARY EXAMINATION DISTRIBUTION College Council Supervisors of Training Regional Education Officers Panel of Examiners Registered Trainees

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AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS

EXAMINATION REPORT

PRIMARY EXAMINATION

JULY/AUGUST 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: 61% of candidates achieved a pass in this section of the Physiology Examination. SHORT ANSWER QUESTIONS: QUESTION 1 How does a fall in temperature influence blood gas solubility and acid

base values? 28% of candidates passed this question. This question was asked in the March/April examination in 1998, and most of the Examiner's comments from that time apply to this 1999 exam. When temperature is lowered, the solubility of a gas in a liquid increases, since the decreased kinetic energy of the gas particles reduces the partial pressure exerted by a given amount of the gas in the solution. When in equilibrium with a liquid/gas interface, a larger amount of gas will be dissolved at a lower temperature, hence the solubility is greater. Henry's Law defines the proportional relationship of amount of gas in solution, to its partial pressure. The solubility coefficient is inversely proportional to temperature (Ostwald) or defined at a fixed temperature (Bunsen). There was considerable confusion about the basic physical principles involved, in particular concerning Henry's Law. Effects of temperature on haemoglobin/oxygen affinity were also mentioned, and were generally well understood by candidates. pH increases as temperature falls, due to decreased ionic disassociation. The increase in pH in blood follows closely the change seen in neutral water. Decreased temperature also affects pH, which was generally overlooked by candidates when attempting to apply the Henderson-Hasselbach equation to explain this effect. Alpha-stat and pH-stat strategies of blood gas interpretation were again often misunderstood.

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Candidates need to remember that this is primarily an examination of physical and physiological principles, often in the context of patient management, rather than of pathophysiology. Refer to Nunn, Blitt & Hines, and Scurr & Feldman. QUESTION 2 What physiological factors contribute to the competence and tone of the

lower oesophageal sphincter? 42% of candidates passed this question. The standard of answer for this question was relatively poor considering it's importance to anaesthesia. The main points sought were that the area is anatomically indistinguishable from other portions of the oesophagus, although containing an increased number of nerve cells. It is however able to maintain a higher pressure. A discussion of the anatomical factors contributing to the competency was expected. These include: • A functional flap valve of gastric mucosa • Oblique entry into the stomach • Effect of diaphragm • Lower oesophagus exposed to intra abdominal pressure • Increased tone of circular muscle in sphincter A description of the concept of barrier pressure, with the inclusion of physiological pressures encountered was expected. Describing other factors including the hormones that may alter tone of the sphincter e.g. Gastrin, motilin, PGE2, oestrogen, progesterone, glucagon, secretin, cholecystokinin & VIP, gained additional marks. Physical factors such as elevated intra abdominal pressure and reduced gastric pH, should have been mentioned. Many candidates gave excellent papers on the anatomical contributing factors and failed to mention the hormonal or physical factors. The reverse was also the case. Although scoring well on the aspect that they discussed, they often only managed a borderline pass. Some candidates discussed pharmacological manipulation of the sphincter. This was not asked in the question and although done very well in many instances, was not rewarded with additional marks. QUESTION 3 Describe the factors that affect airway resistance. 60% of candidates passed this question. This was a straightforward question that required little more than repetition of textbook material. Although the majority of candidates passed the question, few achieved high marks. The examiners expected a brief description of the following factors which contribute to airway resistance:

The upper airway The calibre of the lower airways. This can be varied by factors in the lumen, the tone of the bronchi, factors in the wall of the airway, and factors external to the airway such as dynamic compression. Examples of these factors were expected. Whether the airflow is laminar or turbulent. The likelihood of turbulent flow is determined by Reynold's number. A description of the factors (preferably with formulas) affecting the resistance to laminar and turbulent flow was expected. The volume of the lung.

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A hyperbolic relationship exists between lung volume and airway resistance. Many candidates wasted time through poor technique. Repeating the question, or writing an introductory paragraph does not answer the question and wastes valuable time. This was a broad topic. Many candidates focused in detail on some parts of the topic but ignored others. This scored full marks for part of the question but no marks for unmentioned parts of the topic. Many candidates gave detailed and impressive accounts of the resistance to laminar and turbulent flow, but ignored other factors contributing to airway resistance, such as lung volume. Some candidates confused factors contributing to lung compliance with airway resistance. Others confused factors affecting pulmonary vascular resistance with airway resistance. Measurement of airway resistance was not asked, and was not required in an answer. QUESTION 4 Outline the role of the kidneys in the regulation of body water. 66% of candidates passed this question. The difficulty in presenting the wide range of pertinent material that could be discussed meant that high marks were difficult to achieve. The key concept was that the kidney is usually the major effector of body water regulation based on the large renal blood flow and glomerular filtration and its capacity to excrete either dilute or concentrated urine in response to the requirements of maintenance of body water volume and osmolality. Most candidates focussed on either the details of renal tubular handling of water, or on how the kidneys function in relation to the body's sensors of intravascular volume and osmolality and how the hypothalamus has a key role in integrating this process. Either approach done well, with reference to the importance of regulation of urine volume and osmolality achieved a pass. Discussion on other sites of water loss and their potential for regulation compared with the kidneys and the effect of various situations which may disturb the kidney's ability to perform its role in regulation of body water were included by some candidates. If integrated with discussion of the kidney's role in body water regulation, these were also considered pertinent material. QUESTION 5 Describe the ways in which CO2 is carried in the blood. 55% of candidates passed this question. The carriage of gases in blood is an area where a good understanding is expected and indeed, some of the answers were outstanding. The relative importance of the ways in which carbon dioxide is carried in arterial and in venous blood, and an account of why the percentages differ on the venous side was expected. A good account of the factors making up the Haldane effect and their relative importance was a feature of the better answers. Many candidates gave an adequate account of carbon dioxide carriage as bicarbonate ions. Fewer discussed the chloride shift and very few went on to mention the implications on venous blood haematocrit. Carriage of carbon dioxide as carbamino compounds was generally not as well accounted for as the other forms of carbon dioxide carriage. Candidates are reminded that carboxyhaemoglobin (carbonmonoxyhaemoglobin) refers to the carriage of carbon monoxide on haemoglobin. A discussion of carboxyhaemoglobin was not requested. QUESTION 6 Explain the mechanisms that maintain cerebral blood flow on moving

from a supine to a standing position. 51% of candidates passed this question. This question explores a topic that is clinically important, the maintenance of cerebral perfusion. The answer should have divided the mechanisms into

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global and local. Since a significant amount of the answer revolves around pressures, its relationship to flow and resistance should have been highlighted. The global response revolves around restoring MAP via baroreceptors. The venous pump and valves minimising the pooling effect is also relevant. Again this needs to be tied in with the question, i.e. CPP=MAP-CVP (ICP). The local factors have to include the autoregulation of cerebral blood flow, with the myogenic and local metabolic theories quickly outlined. The Munroe-Kellie doctrine along with the relationship of the perfusion pressure to ICP and CVP, also helps to explain the postural effect on venous pressure and intracranial pressure favouring flow. This all leaves us with a final balance of about a 20% decrease in cerebral blood flow. QUESTION 7 Describe how the partial pressure of oxygen in a blood sample is

measured using a Clark electrode. 28% of candidates passed this question on basic measurement. There were some good answers, but the results overall indicate that many candidates do not have a satisfactory working knowledge of the principles underlying blood gas analysis. This may be the result of a "black box" approach to automated blood gas analysis. Candidates are again reminded that the theory underlying measurement techniques remains an important component of the syllabus and will continue to be examined. Most candidates included a diagram in their answer illustrating the components and configuration of the Clark electrode. The use of diagrams is encouraged, but candidates are reminded to apply clear and correct labelling. A diagram on its own is not sufficient to achieve a pass. Additional detail is required to demonstrate an understanding of the function of each of the components of the diagram. Some of the common errors that cost valuable marks included the following: the incorrect assignment of materials to the anode and cathode; chemical reactions incorrectly assigned to anode and cathode; unbalanced or incorrect chemical equations outlining the reactions at the anode and cathode; confusion as to the role of current and voltage; the voltage and current relationship plotted with current as the independent variable. Many candidates omitted a description of methods of calibration and factors affecting accuracy and limitations. These included the effects of temperature, consumption of oxygen by the electrode, problems with the membrane (e.g. holes, proteins), non-linearity of voltage and current. QUESTION 8 Draw both aortic root and a radial artery pressure wave forms on the

same axes. Explain the differences between them. 50% of the candidates passed this question. There were very few good answers. Candidates were expected to draw waveforms on appropriately labelled axes. The curves should show the peak and pulse pressures of the radial artery pressure wave to be greater than the aortic root pressure wave (with correct normal values). Furthermore, the radial wave pressure should show a steeper upstroke and a shorter duration than the aortic trace, and with a delay in the time of onset of the initial pressure rise. The differences between the waves are due to the decreased compliance which gave rise to the steeper upstroke in the radial wave form. The higher systolic radial arterial pressure is due to reflection and summation, tapering and faster transmission of pressure waves. Whilst damping in the radial wave causes the loss of anacrotic and dicrotic notches; whereas reflection and resonance lead to a diastolic hump on the radial wave form. In elderly patients, pulse wave may be transmitted unchanged from the ascending aorta to the periphery because of the less compliant vessels. The common errors in the answers were unlabelled axes and a lack of normal values. 16% of the candidates drew wave forms on 2 separate sets of graphs using identical axes rather than one graph

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with superimposed wave forms on the same axes. They were not penalised if the above mentioned points were illustrated. Some showed a grossly exaggerated delay of the radial wave. There was a general lack of understanding of the reasons for the differences in the wave forms. VIVA SECTION Introductory Physiology Questions

Cardiovascular Determinants of myocardial oxygen demand and supply Relationship of pulmonary artery occlusion pressure to left ventricular preload ECG principles Pressure traces from right atrium to pulmonary artery Left ventricular pressure-volume loop Vascular function curves Origins of arterial blood pressure Compare and contrast muscle capillary with glomerular capillary Circulation to muscle Red blood cell production, structure and metabolism Haemoglobin structure and metabolism

Respiratory Changes in gas exchange due to induction of intravenous anaesthesia Ventilation perfusion changes from apex to base of lung when upright Functional residual capacity, role and measurement Spirometry and lung volumes The single breath nitrogen washout test (Dead space and closing volume measurement) Shunt and venous admixture “Shunt equation” Ideal gas equation The oxygen cascade Dead space Oxygen stores, effect of preoxygenation Effect of occlusion of left main bronchus Effect of occlusion of left pulmonary artery

Fluid and electrolytes / Renal / Acid Base Distribution of body water including compartments and content. Effect of intravenous administration of one litre of 3% saline Fate of one litre of 0.9% saline given intravenously What is a buffer? Factors effecting glomerular filtration rate Starling forces in the capillary Antidiuretic hormone Small bowel cutaneous fistula renal handling of bicarbonate pH homeostasis

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Measurement Pulse oximeters: principles and sources of errors Intra-arterial pressure measurement Measurement of anaesthesia circuit gases and vapours Humidity and its measurement What is an exponential function?

Other Gastric emptying Thyroid hormone synthesis Physiological modulators of the “pain pathway” Inducible enzyme systems

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PHARMACOLOGY

WRITTEN SECTION MULTIPLE CHOICE QUESTIONS: 56% of candidates achieved a pass in this section of the Pharmacology Examination. SHORT ANSWER QUESTIONS: QUESTION 9 What is meant by "95% confidence interval"? Explain the practical

applications of confidence intervals and indicate why they may be preferred to P-values?

This identical question has been asked in August 1995 and March 1997 (see previous reports). The pass rate of 48% this time was poor albeit better than in the previous papers. Many answers showed poor understanding not just of confidence intervals (CI) but also the principles of statistical inference concerning samples and populations. Comments from the previous examiners' reports are still applicable. In addition, it was surprising that many answers referred to the 95% CI as a single value, or neglected to mention 95% in their definition. Many statements did not make sense grammatically or logically e.g. "95% certain that the sample mean lies within the population mean". The use of the term "sample population" prevented marks from being awarded because it was not certain whether the candidate meant sample or population. Other common errors were statements such as "95% CI has a 95% probability of containing the sample mean"; and the incorrect formula that 95% CI = 1.96±SEM. There was confusion regarding the significance of a CI containing zero. This depends on what the particular CI is providing an estimate for. Many candidates wrote unnecessary information about P values without comparing them to CI, and many thought incorrectly that CI could not be used for hypothesis testing. QUESTION 10 Outline factors determining speed of onset of neuromuscular blocking

agents. 58% of candidates passed this question. This was a question essentially addressing pharmacokinetics and pharmacodynamcis involved with drug delivery, distribution to the effector site and interaction at the effector site. As a result the better answers presented a balanced understanding of drug and patient related factors. The candidate should be able to provide information regarding: 1. Drug factors: physicochemical properties, dose and potency concepts 2. Patient factors: rate and site of injection, cardiac output and muscle blood flow and receptor

kinetics 3. Other factors: the differences in responses different muscle group that are monitored and the

effect of the priming principle QUESTION 11 Outline the toxicity of local anaesthetics. This basic question was passed by 36% of candidates. Essential features expected in an answer were the causative factors and manifestations of toxicity in both the central nervous system and the cardiovascular system, together with a comparison of the blood levels (e.g. for lignocaine)

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associated with CNS and CVS toxicity. Mention was also expected of the particular risks associated with the use of bupivacaine. A number of answers omitted any reference to CVS toxicity, and some made no reference to CNS toxicity. A few made no mention of either. In addition to an outline of CNS and CVS toxicity good answers included some of the following: • A definition of "toxicity" (needle-induced nerve damage and CSF leak do not fall within any

standard definition) • Kinetic factors influencing toxic plasma levels (e.g. dose, rate and site of administration, lipid

solubility, protein binding, clearance) • Effects on toxicity of both acidosis and elevated PCO2 • Direct toxicity to nerves • Toxic effects at autonomic ganglia • Toxic effects at the neuromuscular junction • Special features of prilocaine • Special features of cocaine • Stereoisomers and the relevant features of ropivacaine and S and R bupivacaine • Toxicity in association with pregnancy • Toxicity in the foetus • Effects of additives (e.g. adrenaline, metabisulfite) • Effects of metabolites (e.g. of esters and of lignocaine) • Immune-based reactions QUESTION 12 Briefly describe the mechanism and treatment of the toxicity of sodium

nitroprusside. 48% of candidates passed this question. A complete answer required not only the description of the primary mechanism of cyanide toxicity but also toxicity associated with thiocyanate, methaemaglobinaemia and excessive hypotension associated with nitric oxide. An indication of the dosage at which this might occur and the relationship of this to metabolic pathways of excretion was appropriate. Treatment was best covered by an explanation of the cessation of infusion of nitroprusside in the presence of warning signs (elevated mixed venous PO2, metabolic acidosis and tachyphylaxis). Further explanation of the use of sodium nitrate to convert haemoglobin to methaemoglobin in severe toxicity and the use of sodium thiosulphate and the use of sodium thiosulphate and hydroxycobalamine in less severe toxicity was necessary. There was considerable confusion amongst candidates as to the structure (and activity) of nitroprusside with many unaware of the presence of a nitric oxide group or iron. Many candidates did not understand the role of methaemaglobin and often had an incorrect understanding of the action of methylene blue believing it to form rather than reverse methaemaglobinaemia. A significant number of candidates made no valid attempt at the question.

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QUESTION 13 Using opioids as an example describe and illustrate with graphs what you understand by the terms "potency", "efficacy", "partial agonist", "competitive antagonist", and "therapeutic index".

77% of candidates passed this question. This question was a challenge to provide a meticulous and systematic explanation of five basic pharmacological concepts. To gain a pass it was expected that a description would be provided for every part of the question. Attention to the phrasing of the question was neglected by candidates who performed poorly. Examples of other substances were not relevant and were ignored during the examiner’s assessment. A graphical illustration of each concept was considered essential. Each of the terms is in common use and well described in any of the standard references. This question was a straight forward memory exercise that enabled well organised candidates to achieve high marks. QUESTION 14 Briefly outline the effects of intravenous induction agents not mediated

via the central nervous system. 24% of candidates passed this question. This question was badly answered, lack of time might have been a factor. Many candidates wasted time on irrelevant details like:

1. Effects of inhalational agents. 2. Centrally mediated effects, mainly respiratory effects. 3. Contraindications of intravenous induction agents

Candidates should be able to provide a systematic answer of the effects of the different agents on different systems. The cardiovascular effects of Ketamine were poorly understood. Ketamine can produce a direct reduction in myocardial contractility especially at high doses while producing a dilator effect on vascular smooth muscle. It also causes a direct increase in coronary blood flow that is unmatched to the central effect of tachycardia, hypertension and increased contractility. The net effect is an unfavourable increase in myocardial oxygen demand and little change in systemic vascular resistance. Similarly the role of nitric oxide in vascular smooth muscle relaxation due to thiopentone and propofol was seldom mentioned. The respiratory effects should include effects on laryngeal reflexes (relatively maintained with thiopentone and depressed with propofol ) as well as effects on bronchial secretions and bronchial smooth muscle. The local effects of pain on injection, local thrombosis, skin necrosis and the effects of intra arterial injection of agents like thiopentone should also be mentioned. Other important effects like allergic reactions, histamine release, metabolic, endocrine, gastrointestinal and uterine effects were not mentioned by many candidates.

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QUESTION 15 Briefly describe the preparation of oxygen for medical use. List the physical properties of oxygen. Outline the potential adverse effects associated with its medical use.

50% of candidates passed this question. Many answers only addressed one part of the question. Preparation, physical properties and toxicity should all have been covered. Better answers covered the following points: Preparation 1. Fractional distillation of liquid air. Based on different boiling pints of oxygen and nitrogen.

Used for commercial production. 2. Oxygen concentrators. Absorption of nitrogen by "artificial zeolite". Used for home use and

remote locations. Physical properties Colourless, odourless gas. Molecular weight 32. Critical temperature – 119oC. Supports combustion. Potential adverse effects Acute pulmonary toxicity, absorption atelectasis, decreased hypoxic respiratory drive in patients with hypercarbic respiratory failure, retrolental fibroplasia, hyperbaric effects including convulsions and pulmonary toxicity. QUESTION 16 Outline the factors that determine recovery (offset of action) after

ceasing a drug infusion. The pass rate for this question was 55%. As always, it was disappointing to see that several candidates had failed to plan the examination, and had left little or no time to answer the final question. An ideal answer would have considered the offset of infusion effects in terms of both pharmacokinetics and pharmacodynamics. Kinetic parameters of importance include re-distribution and clearance. Pharmacodynamic effects would have led to a consideration of the interactions with other drugs. Good answers used several examples, the commonest used being propofol, remifentanil and non-depolarizing muscle relaxants. Answers (and there were many) which concentrated purely on the issue of context-sensitive half time and remifentanil attested more to successful marketing by drug companies, rather than a clear understanding by candidates of the issues raised by this question. VIVA SECTION Introductory Pharmacology Questions Pharmacokinetics and Pharmacodynamics: Receptor theory

Functional properties of receptors Halflife and time-constant First order and second order kinetics Spare receptors Kinetics of Inhalational agents Storage of drugs and potency Tolerance

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Therapeutic Index ED 90

Inhalational agents Structure-activity relationship MAC uses and shortcomings Occupational hazards System effects of different agents

CVS effects Respiratory effects Endocrine and Metabolic effects

N2O properties and contra indications Uptake and wash-out curves

Intravenous agents Barbiturates, structure-activity relationship Propofol uptake and distribution

Ketamine, mechanism of action Metabolism of different agents Determinants of an induction dose

Benzodiazepine receptors Muscle relaxants Principles of neuromuscular monitoring

Characteristics of depolarising and non depolarising block Contraindications and side-effects of suxamethonium,

Cis-atracurium vs atracurium Dose-response curve of different muscle group Narcotics Morphine vs fentanyl vs alfentanil

Epidural and subarachnoid narcotics Remifentanil, kinetics and cardiovascular effects Tramadol, kinetics and effects NMDA receptors Local anaesthetics Additives to local anaesthetics EMLA Foetal LA toxicity Structural-activity relationships Comparative toxicity of bupivacaine vs ropivacaine Systemic toxicity Miscellaneous Bias in clinical research specificity / sensitivity / predictive value Study design and clinical trials Antiemetics Dopamine Serotonin and antagonists Histamine and antagonists Bradykinins

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Prostaglandins, synthesis and inhibition Renin-Angiotensin system Alpha blockers Beta blockers Antibiotics mechanisms of action Structure activity relationships of catecholamines NSAIDs, mechanisms of action

Compare and contrast Paracetamol and Acetylsalicylic acid. Mechanism of action of antiepiliptic drugs Kinetics and side effects of phenytion Uterine relaxants DDAVP, mechanism of action Side effects of sodium bicarbonate Atropine vs glycopyrolate Neostigmine like drugs Anticoagulants Heparin vs LMW heparin Side effects of Protamine

Classification and clinical indications of phosphodiesterase inhibitors , Dose response curve for diuretics Mechanism of action of mannitol

Dextrose vs dextran Clinical toxicity of Mg Sterioisomers

Antihypertensives in pregnancy Nitric Oxide A.W. Quail CHAIRMAN PRIMARY EXAMINATION DISTRIBUTION College Council Supervisors of Training Regional Education Officers Panel of Examiners Registered Trainees

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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