EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION JULY/SEPTEMBER 2006

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.


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.


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.


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/)


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.


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


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.


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.


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.


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.


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


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

EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION JULY/AUGUST 2007

Australian and New Zealand College of Anaesthetists
ABN 82 055 042 852
EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION JULY/AUGUST 2007
10/07 11.1.2.2

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.


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.


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


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


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



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


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


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.



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.



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:


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


• 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.


• 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


• Physiological effects of obesity






Dr N. Roberts

Chairman, Primary Examination Committee

EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION JULY/SEPTEMBER 2008

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


EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION
JULY/SEPTEMBER 2008


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:

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


SHORT ANSWER QUESTIONS:


QUESTION I Outline the potential beneficial and adverse effects of isoflurane on the cardiovascular system (include mechanisms of effect) in patients with ischaemic heart disease.

41% of candidates passed this question.

To answer the question it was necessary to describe the effects of isofLurane on the cardiovascuLar system, expLain how these might affect myocardiaL oxygen baLance, and give some expLanation as to how these effects might occur. As the question is not specific, aLL mechanisms from ceLLuLar to organ system interactions were accepted.

A pass wouLd have incLuded the faLL in SVR and bLood pressure, the compensatory rise in heart rate, a note on direct effects on contractiLity, and an expLanation as to how these effects might aLter the myocardiaL oxygen suppLy and demand. A brief description of the concepts of coronary steaL and ischaemic preconditioning, and something on their purported mechanisms was aLso expected.


Extra marks were awarded for candidates who couLd List purported mechanisms for isofLurane causing these effects, such as aLtered sympathetic outfLow, or caLcium channeL antagonism, the aLteration skeLetaL muscLe vascuLar tone resuLting in Lowering of SVR, the effect of concommitant medications, age, disease, hypoxia and rapidLy increasing concentrations on the vascuLar effects, expLain ischaemic preconditioning in more detaiL, and comment on the cLinicaL reLevance of
coronary steaL. Few candidates commented on the overaLL effect on oxygen baLance, either at normaL or high concentrations.

Many candidates incLuded unnecessary data, such as physicaL properties, modes of administration, effects on other organ systems, or effects which are neither beneficiaL or adverse. Common errors incLuded circuLar reasoning—a faLL in VR causes a faLL in CO, and confusing the effects of isofLurane and haLothane.



QUESTION 2 Describe the pharmacokinetic principles of total intravenous anaesthesia using propofol.

52% of candidates passed this question.

The essence of the question is for candidates to reLate knowLedge of the pharmacokinetics of propofoL to what is being observed when propofoL is being administered for totaL intravenous anaesthesia. So it is important to expLain why the rates of infusion vary at differing times such as at commencement, sLightLy after commencement and after a Long period of infusion through reference to how the body is deaLing with propofoL.

There are many facts, diagrams and equations that attracted marks reLating to propofoL but the better marks were reserved for candidates who pointed out the significance of this information to what is happening with the syringe driver. It shouLd be pointed out that candidates who chose to expLain pharmacokinetic behaviour in reLation to totaL intravenous anaesthesia(TIVA) using onLy prose were not penaLised if their expLanations were cLear and indicated an appropriate depth of knowLedge.

The most points that attracted marks incLuded brief definition of the goaL of TIVA i.e. to reach and maintain a centraL compartment serum or effect site concentration of propofoL at a LeveL adequate for anaesthesia, descriptions, diagrams and equations which deaLt with the importance of an initiaL infusion providing a Loading dose given high Lipid soLubiLity and centraL compartment voLume of distribution, then the need to aLLow for redistribution and metaboLism and then LargeLy metaboLism aLone to maintain a steady serum or effect site concentration. ALso descriptions of how propofoL behaves pharmakokineticaLLy when TIVA is ceased received credit, as weLL as detaiLs of its
cLearance.

PropofoL is a highLy important drug criticaL to the practice of anaesthesia so a reLativeLy high standard was expected.

It is advisabLe that candidates not waste vaLuabLe time drawing moLecuLes of propofoL or writing
Long introductions that don’t deaL directLy with the question that was asked.



QUESTION 3 List the anaesthetic related uses of clonidine. What are the effects of
clonidine on the cardiovascular and central nervous system and how are these effects mediated?

68% of candidates passed this question.

A List of anaesthetic related uses incLudes premedication/anxioLysis, intraoperative haemodynamic stabiLity, and augmentation/proLongation of regionaL neuraL bLockade. Marks were aLso awarded for use in post-operative anaLgesia and post-operative shivering. Extra marks were aLso provided in discussing its use in prevention of perioperative myocardiaL ischaemia. WhiLst a dry mouth is a common side effect of cLonidine, it is not typicaLLy used as an antisiaLogue for anaesthetic
purposes. Marks were awarded for discussion about its anaesthetic sparing uses, but no marks were awarded for stating it couLd be used as an anaesthetic aLone. A cLear statement about cLonidine’s mechanism of action as a partial agonist at c receptors with a reLative seLectivity of c2:c1 of 200:1 was required. Expected CVS effects incLuded hypotension, bradycardia and peripheraL vasodiLation.
These are mediated via centraL c2 receptors which inhibit the vasomotor centre in brainstem. There are no direct effects on the heart, but there is reduction in circuLating catechoLamines.

Marks were aLso awarded for discussing initiaL peripheraL vasoconstriction and transient
hypertension via direct action on peripheraL c2 receptors, extra marks for discussing the changes to the baroreceptor refLex, and bonus marks for mentioning the roLe of imidazoLine receptors in brainstem. The CNS effects of sedation and anaLgesia are mediated via centraL c2 receptors via inactivation of Locus ceruLeus and activation of descending inhibitory pain pathways. Further marks were awarded for discussing the spinaL mechanisms of anaLgesia via spinaL c2 receptors in the
dorsaL horn which depress wide dynamic range neurons invoLved in peripheraL nociceptive input.
Information regarding cLonidine’s pharmaceutic and pharmacokinetic profiLe was not required.



QUESTION 4 Briefly outline the pharmacology of ketamine with reference to its use as an analgesic agent in the post-operative period.

60% of candidates passed this question.

A compLete answer required that candidates consider pharmaceutic, pharmacokinetic and pharmacodynamic aspects of ketamine used as an anaLgesic. The nature of ketamine, its formuLation, major routes of administration when administered for postoperative anaLgesia, dose ranges used for anaLgesia, and key factors infLuencing the uptake, distribution, metaboLism and cLearance of ketamine were expected in a compLete answer. Key pharmacokinetic points incLuded the high Lipid soLubiLity, Large voLume of distribution, high hepatic metaboLism to an active metaboLite, short eLimination haLf-Life, and reLativeLy rapid offset after proLonged infusion. Information regarding the site and mechanisms of the potent anaLgesic action of ketamine, particuLarLy the roLes as a non-competitive NMDA receptor antagonist, and both a preventive and opioid-sparing anaLgesic, were expected. Dose-dependent adverse effects that may Limit the use as a postoperative anaLgesic, and the advantages, incLuding Lack of respiratory depression, were important. Whereas most candidates indicated the racemic nature of ketamine, few indicated the reLative differences of the isomers, in particuLar the increased anaLgesic potency of the S(>)- isomer.

AdditionaL points which attracted higher marks incLuded information regarding aLternate routes of administration, abuse potentiaL, specific actions on nociceptive pathways and actions on other receptor systems. Common mistakes incLuded misinterpretation of the question with discussion of ketamine as an anaesthetic agent, undue focus on the physioLogy of NMDA receptors and nociceptive pathways, and confusion between the actions of norketamine and norpethidine.
Few appreciated that hepatic metaboLism of ketamine is high and fLow-dependent. Dosages expressed as mg/kg are preferabLe. Many candidates appeared to describe LocaL practice and formuLations without being aware of core information weLL described in the key texts.



QUESTION 5 Outline how the pharmacokinetics of morphine, bupivacaine and suxamethonium differ in the neonate compared to the adult. Briefly describe the clinical implications of these differences.

73% of candidates passed this question.

This question asked candidates for some appLied pharmacoLogy, Looking at the effect of age on pharmacokinetics of three commonLy used drugs.

The question was generaLLy weLL answered, and a pass mark couLd be obtained by citing the criticaL features of each. With regard to morphine, both cLearance and gLucuronidation is decreased in the neonate, Leading to a proLonged haLf Life. The more permeabLe bLood brain barrier and reLativeLy increased brain bLood fLow in neonates contributes to a greater sensitivity to the drug in the neonate. With regard to bupivacaine there is an enhanced propensity for toxicity as a resuLt of
decreased protein binding, because of decreased aLpha 1 gLycoprotein LeveLs, and decreased hepatic cLearance. Marks were aLso awarded for mention of the infLuence of pH on toxicity in the neonate. With regard to suxamethonium, there are opposite forces at work. An enhanced ECF voLume wouLd Lead to an increased voLume of distribution which wouLd tend to reduce activity, but this couLd be countered for by a decrease in pseudochoLinesterase LeveLs in the neonate. The end resuLt cLinicaLLy is LittLe change in duration of action. Extra marks were awarded where candidates were abLe to give approximate dosages, or dosage ranges appropriate for the different drugs.



QUESTION 6 Outline the ideal properties of a colloid intravenous fluid. Give examples of colloids and briefly describe the features of each.



41% of candidates passed this question.

Few candidates were abLe to describe the ideaL properties of a coLLoid in adequate detaiL and frequentLy made statements that impLied a Lack of understanding about the fundamentaL properties of a coLLoid as opposed to a crystaLLoid. A significant number of candidates onLy managed to
mention two or three of the four main cLasses, nameLy poLygeLines, starches, dextrans and aLbumin. Descriptions of their features were often vague and imprecise, with a poor understanding of what sort of moLecuLes they are, where they distribute in the body, their duration of action, their eLimination and risks or side effects of their use.



QUESTION 7 List the agents used therapeutically to reduce platelet function. Outline their mechanisms of action, adverse effects, mode of elimination and duration of action.

82% of candidates passed this question.

ReLevant agents for this question incLude aspirin, pro-drugs at ADP receptor, antagonists at the
IIB/IIIA receptor and phosphodiesterase inhibitors.

This question had the option of being answered in the form of a ‘tabLe’ format using dot points outLining the components asked for about pLateLet function reduction. Marks were enhanced by incLuding expLanation of how the drug action interferes e.g. bLocking the IIB/IIIA receptor interrupts the binding of fibrinogen hence the faiLure of adhesion and aggregation of pLateLets.

The ‘thrombus/pLateLet’ diagram in Katzung page 544 iLLustrates in summary form the information and it was incLuded in some candidate answers.

There is aLways a risk of eLaborating on adverse effects probabLy more than the marks aLLocated at the expense of time spent on other agents. Medications whose unwanted side effects incLude pLateLet inhibition are not used therapeuticaLLy for that purpose thus not gaining marks. Comments on dextran and thrombin inhibitors gained credit.



QUESTION 8 What is meant by the term Randomised Controlled Trial (RCT)? What are the strengths and weaknesses of randomized control trial design?



79% of candidates passed this question, with 9% receiving a very Low mark.

A cLear expLanation of a Randomised ControLLed TriaL was required e.g. “a triaL in which patients are aLLocated by a form of randomisation between groups; and in which an intervention group is compared to a controL group, that may be active or inactive”. Thereafter a discussion of the strengths and weaknesses of such triaLs was required. Strengths were considered to be that RCT represents a high LeveL of evidence and can be incLuded in meta-anaLyses, minimisation of bias,
reduction of the effect of confounders by being evenLy distributed between groups, ease of bLinding, ease of appLying incLusion/excLusion criteria and providing a good basis to appLy statisticaL anaLysis. Weaknesses were considered to be that they are more expensive, may not refLect reaL Life situations, raise the possibLe ethicaL concern of recruiting patients to what may be considered a Less effective technique, difficuLty of meeting ethicaL requirements in obtaining informed consent from patients who may receive a Less beneficiaL treatment.

Many candidates appeared to confuse randomisation with bLinding and wrote entireLy on the advantages and disadvantages of bLinding. WhiLst bLinding is often added to an RCT, a discussion of the advantages conferred with bLinding was appropriate and attracted additionaL marks; however candidates who wrote soLeLy about bLinding with no acknowLedgement of what constitutes an RCT, received Low marks. Likewise the “controLLed” part of an RCT appLies to the use of a controL against which to compare the intervention group and does not mean that there is a “high degree of controL” of the study or that the researchers “tightLy controL aLL aspects of the triaL”.





PHARMACOLOGY - VIVA SECTION


PHARMACOLOGY TOPICS:


. Draw a dose - response cure.
. OutLine the drug treatment of anaphyLaxis.
. What is meant by the term “toLerance”?
. What are some members of the H2 antagonist group?
. Draw a concentration- time curve foLLowing an I.V. injection of propofoL.
. What are the potentiaL routes of administration of drugs?
. What are some probLems associated with giving drugs by the transdermaL route?
. How can drugs be given to controL post-operative pain?
. What drugs can be used by management of neuropathic pain?
. How do you cLassify corticosteroids ?
. What is meant by the word “addiction”?
. What sort of drug is neostigmine?
. What is the roLe of cytochrome P450 systems in drug metaboLism?
. What specific pharmaceutic probLems exist in the eLderLy popuLation?
. What sort of drugs can be given by the intrathecaL route?
. How do voLatiLe agents affect the pattern of ventiLation?
. What are the uses of beta bLocking drugs?
. How do you assess the extent of neuromuscuLar bLockade?
. What is meant by the term “depoLarising bLockade”?
. What is the mechanism of action of LocaL anaesthetics?
. What are the signs of LocaL anaesthetic toxicity?
. Describe the uses of antichoLinesterase agents.
. What is acetyLchoLine?
. Describe the phases of cLinicaL drug deveLopment.
. Describe the pharmacokinetics of fentanyL.
. What is the appropriate dose of paracetamoL?
. What is meant by the term “probabiLity”?
. What is meant by the term “power” in statistics?
. What is meant by the term sensitivity & specificity?
. How do you cLassify adverse effects of LocaL anaesthetics?
. What are the contents of an ampouLe of thiopentone?
. What is the cause of differences in speed of onset between fentanyL & aLfentaniL?
. What are the advantages and disadvantages in using nitrous oxide?
. What are the contents of a Hartmann’s soLution?
. How does the addition of nitrous oxide affect the uptake of sevofLurane?
. What drugs can be used in the management of ventricuLar fibriLLation?
. What is the Vaughn-WiLLiams cLassification of anti-arrhythmic drugs?
. What types of statisticaL data are there?
. What type of intravenous drugs can be usefuL to controL pain?
. Concentration time cure for aLfentaniL?
. What are some of the advantages of tramadoL as an anaLgesic?
. What agents can be used to reduce bLood pressure?
. What do you understand by the term intrinsic sympathetomimetic activity?
. What intravenous induction agents do you know of?
. The normaL distribution curve.
. What is syntocinin?
. What is ropivacaine?
. Side effects of suxamethonium.
. Wash in curve for isofLurane.
. How are inhaLed anaesthetic removed from the body?
. MetaboLism of the voLatiLe anaesthetic agents
. How do you cLassify anti-choLinesterase agents?
. What is ephedrine?
. How do you define MAC?
. What is protamine?
. What is heparin?
. What drugs cause histamine reLease?
PHYSIOLOGY - WRITTEN SECTION



MULTIPLE CHOICE QUESTIONS:

83% of candidates achieved a pass in this section of the PhysioLogy Examination.



SHORT ANSWER QUESTIONS:


QUESTION 9 What is humidity and how can it be measured?

53% of candidates passed this question.

The minimum requirement for a pass mark was an adequate definition of humidity and a brief description of two methods of its measurement. Candidates were expected to be abLe to define absoLute and reLative humidity, extra marks were awarded for an expLanation of the infLuence of temperature on humidity and for the provision of the humidity of fuLLy saturated air at 20 and 37 degrees. A common error was the description of absoLute humidity as a pressure, rather than as mass of water vapour /voLume of air. SuccessfuL candidates couLd in generaL describe hair hygrometers, wet and dry buLb hygrometers and RegnauLt’s hygrometer. Extra marks were awarded for a description of the reLative merits of these techniques and for descriptions of other methods for measuring absoLute humidity (such as eLectricaL transducers / mass spectrometry). However, no marks were awarded for descriptions of humidifiers, or for discussion on the environmentaL or cLinicaL consequences of high or Low humidity.

QUESTION 10 Describe sepsis and describe the metabolic consequences of sepsis.

48% of candidates passed this question.

A basic definition of sepsis was expected. Recognition of the spectrum of severity encompassed by the term sepsis gained additionaL marks, as did a brief description of the mechanisms and mediators of sepsis.

Given the wording of this question equaL marks were given for the generaL (non-metaboLic) and metaboLic features of sepsis. The generaL features were best organised by a systems approach nameLy cardiovascuLar, respiratory, haematoLogicaL, endocrine and CNS. Of these the cardiovascuLar features required the most detaiL.

Important information to be incLuded in the metaboLic part of the answer incLuded the generaL cataboLic state, hypermetaboLism, fever, tissue hypoxia, metaboLic acidosis, insuLin resistance and the effect of sepsis on the metaboLism of carbohydrates, proteins and Lipids.

CLear writing and simpLe organisation invoLving underLined headings and common abbreviations aLLowed candidates to cover this broad question weLL. Those who faiLed this question simpLy did not provide enough content and detaiL. The most common mistake was to write at Length about metaboLic acidosis to the excLusion of a wider ranging answer. DetaiLed metaboLic pathways were not expected.
QUESTION 11 Write brief notes on the physiological changes associated with sleep.

39% of candidates passed this question.

A definition of sLeep, an indication of the components of sLeep and their duration foLLowed by a
brief notation of the physioLogicaL changes occurring in the neuroLogicaL, cardiovascuLar, respiratory and metaboLic systems was rewarded with a good pass. AdditionaL detaiL, particuLarLy in regard to the neuroLogicaL changes, was rewarded with additionaL marks.

SLeep is a NECESSARY REVERSIBLE reduction in the conscious state from which one can be easiLy AROUSED by sensory or other stimuLi. The most common reason for not passing this question was a poor definition (or no definition at aLL) and simpLy not notating an adequate number of physioLogicaL changes. The most common error was to correctLy state that parasympathetic tone predominates during sLeep onLy to then state that gut motiLity was reduced. Quite a few answers Lacked any structure what so ever.

Credit was not given for descriptions of physioLogicaL compensatory mechanisms, such as for reduced venous return or determinants of GFR.



QUESTION 12 Detail the protective and regulatory roles of the liver.


32% of candidates passed this question.

This question required a description of the Liver as the interface between the gut and the body, and as a resuLt of this, its roLe in protection from organisms and toxins and reguLation of nutrient LeveLs.

The protective roLe is primariLy reLated to the removaL of bacteria, endotoxins, and protein denaturation. This is primariLy undertaken by the Kupffer CeLLs which are in the hepatic sinusoids. The action of these macrophages is an exampLe of innate immunity. FoLLowing their activation a series of events foLLows incLuding phagocytosis, compLetment activation, and recruitment of other ceLLs.

The primary reguLatory roLe of the Liver is as a gLucostat i.e. responding to both high and Low bLood gLucose LeveLs being presented to it by the portaL circuLation. DetaiL on how the Liver achieves this baLance was needed. Some candidates were confused about the action of insuLin and gLucacon in these processes.

Bonus marks were aLso awarded for the foLLowing as exampLes of protection: toxin/drug modification, production of acute phase proteins, compLement and urea, action as a bLood reservoir, and of reguLation production of aLbumen in reguLating oncotic pressure, biLe in reguLating fat and fat soLubLe vitamin absorption, biLirubin metaboLism, hormone inactivation and production of both coaguLation and anticoaguLation proteins.

Listing aLL Liver functions did not address the question, which asked for detaiL on a Limited area of Liver function. Some candidates focussed on minor detaiLs whiLe missing the big picture such as faiLing to mention bLood gLucose reguLation or any protective roLes.
QUESTION 13 Explain the concept of time constants and relate these to “fast”
and “slow” alveoli

40% of candidates passed this question. The answer shouLd incLude:
. An objective (mathematicaLLy-based) definition of a time constant,
. In reLation to Lung units, the time constant is often defined as the product of compLiance and resistance.
. Some factors that infLuence time constants (physioLogicaL and pathoLogicaL causes of aLterations in compLiance and resistance)
. The effects of heterogeneity in time constants (static vs. dynamic compLiance and respiratory rate)

AdditionaL marks were awarded for ways of measuring the effects of heterogeneity of time constants. The capnogram and the peak vs. pLateau pressures. Many candidates spent a Lot of time expLaining various other formuLas pertaining to compLiance, surfactant, and aLveoLar coLLapse that were not directLy reLevant to the question. Many candidates thought that increased compLiance causes fast time constants.



QUESTION 14 Explain in physiologic terms the effect of severe aortic stenosis on myocardial supply and demand.

45% of candidates passed this question.

This was an appLied physioLogy question. The first part of an answer was a description of aortic stenosis, with additionaL marks for giving measure(s) of severity. The main part of the answer concerned the interreLated effects of a severeLy stenosed aortic vaLve that may produce both increased myocardiaL work (described using LapLace’s Law) and compromised coronary bLood fLow. AdditionaL marks were awarded for answers that discussed the varying effects of Left ventricuLar hypertrophy on both suppLy and demand. Marks were aLso awarded for discussing how increased heart rate may both increase demand and reduce suppLy. Errors incLuded: confusing the effects of aLtered pressure with aLtered fLow; faiLing to indicate that severe aortic stenosis is a chronic condition; and incLuding, often at Length, the effects of anaesthesia or the symptoms and signs of aortic stenosis.



QUESTION 15 Describe the changes that occur with ageing that can affect oxygen delivery to the tissues during moderate exercise.

14% of candidates passed this question.

Oxygen deLivery is the product of cardiac output and arteriaL oxygen content. Oxygen deLivery during exercise is increased by raising cardiac output gLobaLLy and LocaLLy, and increasing oxygen extraction. Linking these changes to aging is the key to answering this question.
Cardiac output and respiratory changes with aging both needed discussion to gain a pass mark. Key points:
. Cardiac output - contractiLity., heart rate responsiveness., stroke voLume., ventricuLar compLiance., and cardiac workt with aging. These factors reduce the abiLity to increase cardiac output to match exercising tissue demand.
. Respiratory - PaO2., work of breathingt with a . in chest waLL compLiance, cLosing capacity encroaches on FRC, and diffusion capacity. from taLveoLar membrane thickness and . functionaL surface area. The tV/Q mismatch that resuLts reduces the abiLity to oxygenate bLood when extraction increases.
AdditionaL marks were awarded for mentioning bLood fLow. with atheroscLerosis, tpuLmonary resistance and heart strain, anaemia .O2 content, moderate exercise is beLow anaerobic threshoLd, and vaLvuLar defects can affect cardiac output.

Common errors incLuded focusing on either cardiac or respiratory changes; Listing aging and
exercise physioLogicaL changes without Linking the important factors of the two together; describing anaerobic metaboLism of tissues; stating that FRC reduces with increasing age; not differentiating between the .chest waLL compLiance and tLung compLiance that happens with aging.



QUESTION 16 Outline the mechanisms by which the kidney maintains potassium homeostasis

51% of candidates passed this question.

It was pLeasing to see some weLL structured answers covering aLL the main points. The main points expected to achieve a pass incLuded:
. NormaL intraceLLuLar and extraceLLuLar potassium concentrations and the need for “tight”
controL.
. A baLance between intake and excretion of potassium.
. The transit of potassium through the nephron in the kidney, excretion = fiLtered- reabsorption + secretion, with the major controLLed variabLe being secretion, and the pLaces within the nephron that these events occurred.
. The controL of the variabLe secretion in the distaL convoLuted tubuLe and coLLecting duct dependent on potassium concentration, tubuLar fLow rate and aLdosterone. Secretion of aLdosterone from the adrenaL gLand being under a feedback Loop with pLasma concentration of potassium.

Extra credit was given for mechanism of action of any of the steps above, in particuLar a cLear expLanation of how aLdosterone achieves further secretion was rewarded. The exchange of potassium for hydrogen ions within the renaL tubuLe was aLso rewarded if expLained correctLy. No credit was given for information of drug actions on the renaL tubuLe.





PHYSIOLOGY - VIVA SECTION


PHYSIOLOGY TOPICS:

CVS
. RegionaL bLood fLow
. Wiggers’ diagram
. Lead II ECG
. Frank-StarLing mechanism
. ContractiLity: definition & measurement
. CVP waveform
. AfterLoad: definition & measurement
. Oxygen fLux
. Venous return / atriaL pressure curve
. Anemia; causes, consequences
. Sino-atriaL node action potentiaL
. LV pressure-voLume Loop
. Changes in mean ateriaL waveform with propagation
. CerebraL bLood fLow determinants
Measurement
. CaLibration of pressure transducer
. Comparison of invasive & non-invasive bLood pressure measurement
. PA catheter waveform changes with insertion
. CO measurement
. Wheatstone bridge
. Fick principLe
. CO2 measurement
. ELectricaL circuits
. PuLse oximetry

Fluid & electrolytes
. Contents of one Litre bag of NormaL SaLine

Muscle
. Excitation-contraction coupLing

Renal
. HandLing of water
. GFR: definition, determinants
. CLearance
. RBF; response to hypovoLemia
. MetaboLic acid; handLing by kidney

Pain
. Response to skin incision
. Response to thermaL injury

Respiratory
. BLood gas interpretation
. ALveoLar gas equation
. Oxygen cascade
. Effect of pneumothorax on gas exchange
. ControL of ventiLation
. Surfactant
. Oxygen stores in the body
. Differences between base and apex of the Lung
. FRC
. CompLiance
. Dead space
. Shunt
. Work of breathing
. CLosing capacity
. ALtitude physioLogy
. Oxygen-haemogLobin dissociation curve
. CO2 carriage
. PuLmonary circuLation
. Airway resistance

Haematology
. Red ceLL metaboLism
. Processing of bLood donations
. PLateLets; structure and function
Metabolism
. GLucose: aerobic & anaerobic metaboLism
. FueL sources
. Effect of an eight hour fast

Endocrine
. ProstagLandins
. Thyroid hormones
. Pituitary hormones
. InsuLin

Pregnancy
. Respiratory changes in pregnancy
. CardiovascuLar changes in pregnancy

Materno-fetal
. Oxygen transfer across pLacenta

Nervous
. Sympathetic nervous system
. NMDA receptors
. Resting membrane potentiaL
. Nernst equation
. GoLdman-FieLd equation

Allergy/Immune system
. CLassification of immunoLogicaL reactions
. Defences against infection

Gastro-intestinal
. Lower oesophageaL sphincter
. Gastric emptying




Dr. C Noonan
Chairman, Primary Examination Sub Committee

EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION FEBRUARY/APRIL 2007

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.

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.

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.



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.

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

• 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

• 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

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.

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.


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

• 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

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.

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.

• 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?

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