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.

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.

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 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.

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 agents 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

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.

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

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 Parkinsons 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

 Pain

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 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

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.

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 excitationcontraction 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.

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.

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?

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 bodys 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

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