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