EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION FEBRUARY/APRIL 2008

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS
ABN 82 055 042 852
EXAMINATION REPORT PRIMARY FELLOWSHIP EXAMINATION FEBRUARY/APRIL 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 UESTIONS

63% of candidates achieved a pass in this section of the PharmacoLogy Examination.


SHORT ANSWER UESTIONS


QUESTION I An 80 year old woman is undergoing major emergency surgery. Describe the maintenance inhaled concentration of sevoflurane you would choose and the factors that might influence this.

30% of candidates passed this question.

This question seemed to cause a Lot of difficuLty for many candidates who struggLed to reLate their answer to the cLinicaL situation. Common mistakes were the discussion of uptake factors or Listing the pharmacoLogy of sevofLurance without putting it into context. Pregnancy does affect MAC, but not in 80 year oLds.

In order to pass candidates were expected to cover the need to provide enough sevofLurane to prevent awareness and movement whiLe minimising its undesirabLe cardiovascuLar effects. The patient’s age, preoperative condition, type of surgery, and use of other MAC reducing agents or drugs needed to be mentioned. Very few candidates considered that differences between the inhaLed and end-tidaL concentration of sevofLurane.





AdditionaL marks were awarded for awareness monitoring, other factors affecting MAC, and more detaiLs about the cardiovascuLar side effects of sevofLurane. WeLL-structured answers that were cLinicaLLy reLevant scored better marks.



QUESTION 2 List the classes of drugs that are useful in inducing diuresis clinically.
Outline their mechanism of action.


38% of candidates passed this question.

This question integrated the GeneraL InstructionaL Objective and aspects of aLL the Required
AbiLities Laid out in the Primary SyLLabus section on diuretics.

For just over 70% of the marks avaiLabLe it was expected that candidates wouLd List the cLasses - osmotic, carbonic anhydrase inhibition, Loop, thiazide, aLdosterone antagonism, and potassium sparing, then outLine the mechanism of action. The remaining marks were approximateLy evenLy spLit between other drug cLasses exhibiting significant diuretic action and their mechanisms, and overaLL understanding demonstrated of the interpLay of renaL physioLogy, diuretic pharmacoLogy, and cLinicaL effect.

HighLy detaiLed expLanations of mechanism of action were not required, but answers demonstrating an understanding of both the channeL/enzyme/receptor site and the LocaL, and more distaL, tubuLar consequences of that action scored very weLL. Many candidates described onLy the site of action
and stated this “reduced sodium reabsorption“.

CeLLuLar LeveL mechanism of action was most commonLy misunderstood for carbonic anhydrase inhibition where, amongst other probLems, the majority of candidates faiLed to mention the decreased bicarbonate removaL from the fiLtrate and resuLting metaboLic acidosis.

The question asked about diuretics that were “usefuL....cLinicaLLy.” Very few candidates mentioned, or showed understanding of, the reLative potencies, the common conditions diuretics are used to treat, nor reLated diuretic action to the pathophysioLogy of those conditions.



QUESTION 3 Describe the ideal pharmacokinetic and pharmacodynamic properties of agents used for sedation. Outline the pharmacology of midazolam and propofol with reference to these ideal properties.

66% of candidates passed this question.


The main points expected for a pass incLuded a description of the ideaL pharmacokinetic and pharmacodynamic features of an agent specificaLLy suited to the cLinicaL situation of providing sedation. Therefore, pharmacokinetic features that resuLt in a rapid onset and offset of effect with boLuses or infusion is ideaL. ALso the effects of anxioLysis, amnesia and arousabLe sedation were considered desirabLe, with Low propensity to inadvertentLy progress to generaL anaesthesia.

A discussion about other ideaL features such as anaLgesia and stabLe cardio-respiratory effects of the sedation agents were aLso expected.
An outLine of how midazoLam and propofoL fitted this ideaL agent’s features was aLso required. Extra marks were awarded for an opinion comparing the suitabiLity of midazoLam and propofoL
suitabiLity for the provision of sedation, based upon the profiLes generated above.



A common error was to incLude pharmaceutic information that was not required, and factuaL pharmacokinetic information about each drug was given LittLe credit when not appLied to how it affected the agents profiLe with reference to the ideaL agent.



QUESTION 4 Outline the pharmacologic management if bronchoconstriction in acute severe asthma. Include mechanisms of action and potential adverse effects.

79% of candidates passed this question.


This question was asked in an earLier examination and comments from the examiner’s report remain reLevant.

The main points to be covered incLuded:
• A List of the main drugs usefuL in this situation
• An exampLe in each group and its route(s) of administration
• Sufficient detaiL on how the drug works
• Important side effects


It was expected that most of the answer wouLd be on B2 agonists, incLuding the use of Less seLective agents eg adrenaLine, steroids, anti-choLinergics and methyLxanthines. AdditionaL marks were aLso given for notes on magnesium suLphate, ketamine, voLatiLes, oxygen and heLiox.

Some information on 2nd messengers was expected, here some candidates were confused with the inhibition of cAMP and the direction of intraceLLuLar caLcium fLuxes. Some candidates faiLed to gain marks by not mentioning a mechanism of action or side effects. There were some exceLLent answers that used a tabLe format, succinctLy giving detaiLed and reLevant information. Extra marks were given for answers that showed some perspective eg minimaL side effects of ipratropium if given by metered aerosoL.

Some candidates used time to discuss the pathogenesis of asthma, which attracted no marks. Insufficient detaiL and main points not covered were the main reasons for faiLing this question.



QUESTION 5 Classify drugs that alter activity at serotonin receptors with examples.
Describe their mechanisms of action and clinical indications.


39% of candidates passed this question.


The main points that needed to be made to demonstrate an understanding of this topic were an overview that receptor activity can be aLtered by drugs that are agonists (e.g. metocLopramide, sumatriptan), antagonists (e.g. ergotamine, ondansetron) and drugs that increase the amount of serotonin and in turn increase activity at the receptor by increasing reLease (tramadoL), inhibiting reuptake (fLuoxetine) or inhibiting breakdown of serotonin. ALL of the serotonin receptors are G- protein Linked except 5HT-3 which is Ligand gated. Many answers gave extensive detaiL of the vomiting pathways which was of Limited reLevance. There was confusion over the cLassification of serotonin reuptake inhibitors. They were often described as agonists (this impLies a direct receptor action); others described the same drugs as antagonists because they inhibit re-uptake. The term “indirect agonist” is the best description. Most candidates focused onLy on the serotonin re-uptake inhibitors (SRI) and the 5HT-3 antagonists. The mechanism of action was often described as a tautoLogy (i.e. SRI’s inhibit the re-uptake of serotonin and 5HT-3 antagonists antagonize the 5HT-3



receptor). These expLanations faiLed to attract additionaL marks making a pass impossibLe to achieve.



QUESTION 6 A surgeon wishes to use topical anaesthetic in the nose before surgery in a
30 year old 70 kg man. He normally uses topical cocaine 5% plus lignocaine 2% with adrenaline 1:100,000 injection. What volumes of cocaine 5% and lignocaine can be used safely? What are the potential toxic effects of cocaine and how do lignocaine and adrenaline affect this?

19% of candidates passed this question.


Better answers came from candidates who had gone to more than just one or two of the recommended textbooks to get information on cocaine (some of them contain very sparse information). ConsiderabLe Latitude was given to the range of toxic doses, especiaLLy when accompanied by a correct caLcuLation. Very few candidates noted that 1:100,000 adrenaLine is 10 mcg/mL and that 10 mL wouLd be an appreciabLe dose of adrenaLine.
An answer that contained the foLLowing wouLd have attracted a good pass:
• toxic doses and thus voLumes
• a statement that toxicities are additive so doses shouLd be modified
• mechanism(s) and manifestations of cocaine toxicity
o re-uptake inhibitor of noradrenaLine (and dopamine and serotonin) o sympathetic nervous system activation (tachycardia, hypertension, arrhythmias, coronary vascoconstriction, myocardiaL ischaemia)
o CNS effects (eg. euphoria, deLirium, seizures)
• Lignocaine enhances CNS toxicity
• adrenaLine increases cardiovascuLar toxicity


Long discursions on sodium channeL bLockade, factors that governed uptake of LocaL anaesthetics and the bLood LeveLs of Lignocaine at which different CNS effects might appear did not attract marks.



QUESTION 7 Describe the terms train-of-four stimulation and double burst stimulation with respect to the peripheral nerve stimulator. Describe their advantages and disadvantages when used to evaluate non-depolarising neuromuscular blockade.

16% of candidates passed this question.


Candidates were expected to provide a cLear description of how train-of-four (TOF) and doubLe
burst stimuLation (DBS) is produced using a peripheraL nerve stimuLator to evaLuate non-depoLarising neuromuscuLar bLockade (NDMB). A good understanding of the reLationship between twitch height, TOF ratio and LeveL of NDMB in the context of reversibiLity and bLock depth is imperative.
A description of the advantages, Limitations and drawbacks of using both techniques was expected to achieve a pass mark.

WhiLst many candidates were abLe to outLine the principLes of TOF and DBS, most faiLed to provide precise or correct description of important technicaL aspects Like frequency, timing and voLtage. The description of advantages and Limitations were vague, patchy and fragmented and showed generaL Lack of understanding of neuromuscuLar monitoring and its appLied pharmacoLogy.



Good candidates were abLe to describe TOF correLates with receptor occupancy and provide comparison with singLe twitch and post tetanic count.



QUESTION 8 Define the mechanisms of action and adverse effects of metoprolol, glyceryl trinitrate and diltiazem when used to manage myocardial ischaemia.

65% of candidates passed this question.


It was expected candidates wouLd discuss the generaL concept of a baLance of suppLy and demand and go on to describe the main determinates of oxygen demand being heart rate and contractiLity. AdditionaL marks were given for discussing the roLe of ventricuLar diLation. For agents that sLow the heart rate extra credit was given for an expLanation about the proportion of the cardiac cycLe spent in diastoLe at high and Low heart rates and the impact this has on coronary bLood fLow and myocardiaL perfusion. It was expected that the mechanism of action for each agent wouLd be outLined. Some discussion of both the generaL cLinicaL effect and more detaiLed mechanism of
action were expected. For exampLe, metoproLoL is a seLective beta 1 receptor antagonist that resuLts in decreased cycLic AMP as a second messenger. The resuLtant cLinicaL effects are primariLy a reduced heart rate and reduced contractiLity. Extra marks were awarded for reiterating why this is beneficiaL for patients with myocardiaL ischaemia. It was expected that the potentiaL adverse
effects for each agent wouLd be mentioned. Extra credit was given for comments regarding the deveLopment of toLerance to gLyceryL trinitrate. AdditionaL marks were gained for discussing the potentiaL adverse impact that inducing tachycardia or hypotension can have on myocardiaL ischaemia. Further credit was given for noting that both the cLinicaL effects and the potentiaL for
adverse effects are synergistic with each of these and other agents.






PHARMACOLOGY - VIVA SECTION



PHARMACOLOGY TOPICS

• What is meant by the term “haLf - Life” of a drug?
• Draw a concentration - time curve after an I.V. boLus of a drug
• What are the basic processes in pharmacokinetics?
• How do you determine the dose of opioid for anaLgesia?
• What drugs can be given transdermaLLy?
• Define potency and affinity
• What is meant by the term “therapeutic index”?
• Factors determining uptake of voLatiLe anaesthetic agents
• What are the uses of nitrous oxide in anaesthesia?
• Given a range of anaLgesics how do you determine speed of onset?
• How does heart faiLure affect pharmacokinetics?
• Kinetics of propofoL
• What is in an ampouLe of thiopentone?
• How is nitrous oxide manufactured?
• How do you choose a voLatiLe anaesthetic agent?
• Draw a Fa/Fi curve for isofLurane
• Define the term partition coefficient



• MetaboLism of voLatiLe agents
• How does nitrous oxide addition affect uptake of voLatiLe agents?
• Draw a wash-out curve
• What is meant by the term “isomer”?
• PharmacoLogy of ketamine
• CLassification of intravenous anaesthetic agents
• What are the advantages in using propofoL as an induction agent?
• Discuss the GABA receptors
• Disadvantages of thiopentone as an induction agent
• PharmacoLogy of Lignocaine
• What is the fate of an injection of intrathecaL LocaL anaesthetics?
• Toxicity of LocaL anaesthetics
• EMLA cream
• Compare aLfentaniL and fentanyL
• Advantages of NSAIDs
• Compare paracetamoL and NSAID’s
• Mechanism of action of opioids
• How do you define pain?
• CLassification of NeuromuscuLar BLocking drugs
• What is meant by the term “margin of safety” with regard to neuromuscuLar bLocking drugs
• What sort of drug is suxamethonium?
• DepoLarising and non depoLarising bLockade
• What sort of drug is neostigmine?
• Compare atropine with hyoscine
• Describe drugs used to treat hypertension
• Toxicity of sodium nitroprusside
• What are the uses of digoxin
• Management of ventricuLar fibriLLation
• Drugs used in cardiac arrest
• Management of intra-operative hypotension
• PharmacoLogy of aLpha2 agonists
• Drugs affecting seizure threshoLd
• MetocLopramide
• Drugs affecting uterine tone
• Different types of heparin
• Antacids
• Disinfectants and Antiseptics
• What are the uses of steroids?
• PrevaLence and Incidence
• What are the stages of drug deveLopment?
• CLinicaL triaLs
• Forrest pLot
• Measures of centraL tendency
• Discuss 2 x 2 tabLe





PHYSIOLOGY - WRITTEN SECTION



MULTIPLE CHOICE UESTIONS

69% of candidates achieved a pass in this section of the PhysioLogy Examination.



SHORT ANSWER UESTIONS



QUESTION 9 The skin, the kidneys, and the carotid bodies are examples of where specific organ blood flow is far in excess of that organ’s metabolic requirements. For each example, explain what the physiological role of the high organ blood flow is, why this high flow is an advantage to the person and a brief description of the mechanisms involved.

11% of candidates passed this question.


To answer this question, candidates had to expLain the roLe of the high organ bLood fLow, the advantage of this high fLow, and the mechanism creating the high fLow for aLL three organs.

Skin: ThermoreguLation roLe with heat conservation / Loss. Normothermia aLLows normaL enzyme function. High fLow via superficiaL arterioLe network and arterio-venous anastomosis with sympathetic nervous system controL. AdditionaL marks for roLe as a bLood reservoir, correct vaLue of bLood fLow, and importance of sweating.

Kidneys: RoLe is to excrete waste products and sodium / water baLance. Advantage is the maintenance of constant internaL environment. High fLow via short Large renaL arteries, paraLLeL interLobuLar arteries and paraLLeL afferent arterioLe branches. AdditionaL marks for renaL bLood fLow vaLue.

Carotid bodies: High fLow means organ oxygen requirements do not interfere with measuring PaO2. The advantage is earLy detection of hypoxia. High organ fLow occurs due to the smaLL size of the organ and fLow directLy from the carotid artery. AdditionaL marks for organ bLood fLow rate and Lack of effect from anaemia or carbon monoxide poisoning.

A common mistake was to describe in detaiL how bLood fLow is controLLed or aLtered, especiaLLy when referring to the kidney and this was not asked for. Descriptions of physioLogicaL pathways and their end organ responses were aLso not asked for. Re-writing the question was not heLpfuL. Carotid bodies were often incorrectLy described as having a baroreceptor function.



QUESTION 10 Define “thermoneutral zone”. Briefly explain how the body regulates temperature when the ambient temperature exceeds the thermoneutral zone.

50% of candidates passed this question.


Most candidates were abLe to define “thermoneutraL zone“ and many were abLe to give normaL vaLues for aduLts and neonates. Better answers demonstrated the Linear increase in metaboLic rate above and beLow the thermoneutraL zone in graph form.



An expLanation of how temperature is reguLated when the ambient temperature exceeds the thermoneutraL zone shouLd incLude the foLLowing:

. PATHWAYS
Sensors, afferent pathways and integration were generaLLy weLL described but many candidates faiLed to mention that cutaneous vasodiLatation was mediated by inhibition of sympathetic adrenergic tone and sweating was mediated by sympathetic choLinergic activation.
. BEHAVIOURAL RESPONSES
. CUTANEOUS VASODILATATION
Main points expected were, transfer of heat from core to skin, the roLe of arterio-venous shunts and deep venous pLexuses and increases in skin bLood fLow up to 30 foLd. Better answers expLained how heat transfer from the skin by conduction, radiation and convection required a temperature gradient.
. SWEATING
Main points expected were that evaporation of water, does not require a temperature gradient, is very efficient at heat transfer due to the high Latent heat of evaporation and is the onLy means avaiLabLe to transfer heat when ambient temperature exceeds skin temperature.



QUESTION 11 Outline the physiological consequences of diabetic keto acidosis.


57% of candidates passed this question.


To achieve a pass, candidates needed an understanding that DKA is a syndrome incLuding metaboLic aspects, fLuid and eLectroLyte abnormaLities, as weLL as severe metaboLic acidosis. Some mention of insuLin Lack and fat breakdown as the cause of ketoacid overproduction, of the ensuing hypergLycaemia and osmotic diuresis with attendant water and eLectroLyte (particuLarLy potassium) derangements, and of the physioLogic consequences of severe metaboLic acidosis were required.

Extra marks were given for more detaiLed information about gLuconeogenesis(GN) from amino acids and gLyceroL and reLated aspects of intermediary metaboLism (many answers contained incorrect information here); ketone accumuLation as Krebs cycLe entry becomes saturated; reaLizing that hypergLycaemia was due both to increased GN and faiLure of ceLLuLar uptake of gLucose; for a summary of the neurohumoraL response to hypovoLaemia; for information about response to acidosis
- hyperventiLation due to stimuLation of peripheraL chemoreceptors, buffering, renaL response and shift to the right of the HbO2 dissociation curve; for information reLating to osmotic shifts incLuding ceLLuLar dehydration and pseudohyponatraemia; and for the presence in advanced cases of a secondary Lactic acidosis due to decreased tissue perfusion.

Common errors. A great many answers focused entireLy on the response to metaboLic acidosis onLy, omitting any reference to hypergLycaemia and its effects.
There were many who had scant understanding of metaboLic processes - for exampLe, ketones are not produced from gLucose or from protein; the brain is abLe to utiLize ketones in states of starvation, but more to the point, is not dependent on insuLin for gLucose uptake, therefore neurogLycopaenia is not a feature of DKA; oxaLoacetate, a-ketogLutarate and various other intermediary metaboLites are not “ketone bodies”; ketones are not produced as a resuLt of anaerobic metaboLism.



Most omitted aLL reference to the metaboLic derangements and few indicated there was a cataboLic state with increased GLucagon and other counterreguLatory hormones.
A Large number of candidates faiLed to mention insuLin Lack, and most did not mention gLuconeogenesis at aLL. DKA is not just severe hypergLycaemia as many suggested. Nor does it occur in Type 2 diabetics.

Candidates shouLd not use terms they do not know the meaning of e.g. OsmoLar Gap (which does
not increase with hypergLycaemia aLone). The osmotic diuresis is LargeLy due to gLucose not ketones aLthough they may contribute somewhat.

Dehydration does not cause hyponatraemia unLess there is concurrent Loss of hypernatraemic fLuid or repLacement of sodium-containing fLuid with water. In DKA the commonLy-seen abnormaLity is pseudohyponatraemia.



QUESTION 12 Describe the physiological changes that occur in respiratory function during pregnancy.

54% of candidates passed this question. Main Points expected for a pass:
. A brief mention of reasons for the changes - hormonaL, mechanicaL and increases in metaboLic demand
. Changes in Lung voLume and capacities
. ALterations in ventiLation - what causes the increase, how it is mediated and what are the effects (eg. fuLLy compensated respiratory aLkaLosis)
. Increased metaboLic demand - the magnitude of the increase and how the body adapts to meet the demand
. AnatomicaL changes
. Some mention of the extra stress on the respiratory system resuLting from Labour


AdditionaL points couLd be gained for:
. CLinicaL significance of the changes
. Changes in the hypoxic ventiLatory response curve and CO2 ventiLatory response curve
. BLood gases in pregnancy
. Mention of changes in extraction ratio
. Discussion of work of breathing in pregnancy
. Dead space changes in pregnancy
. Changes to the haemogLobin oxygen dissociation curve
. Dyspnoea of pregnancy


Common probLems:
. ILLegibLe handwriting
. Lack of structure when answering the question
. Changes in airway resistance were poorLy understood with wide variation in answers
. Few candidates mentioned the changes that occur during Labour
. The roLe of reLaxin in mediating changes in the respiratory system was often overstated
. Inaccurate terms were common such as ‘totaL Lung voLume’, ‘functionaL residuaL voLume’
. The main reason for faiLing this question was a faiLure to demonstrate factuaL knowLedge.



QUESTION 13 Describe the production of cerebrospinal fluid, its role and its fate.


24% of candidates passed this question.


To pass this question, candidates were expected to answer aLL parts of the question: the production, the roLe, and finaLLy the fate of CSF. This question required recaLL of factuaL information.
Most candidates who faiLed to pass this question either answered onLy some parts of the question, or had factuaL errors in their answers.

Once the factuaL information was demonstrated, further marks were obtained for cLinicaL
appLications of the physioLogy of CSF reLevant to anaesthesia and criticaL care medicine.



QUESTION 14 Describe the pathways whereby myocardial ischaemia may be experienced as pain in the throat or arm regions.

21% of candidates passed this question.


This question was generaLLy very poorLy answered. A significant number of candidates didn’t answer the question at aLL (bLank answer bookLets) and a number of candidates wrote onLy 1 - 2 Lines.
A number of candidates described myocardiaL work or the components of cardiac output.
Good candidates gave a definition, described the embryoLogicaL derivation, why pain is referred and described the correct pathways invoLved from stimuLus, pain receptors and the end point as pain.

OnLy a very few candidates described the correct nerve roots invoLved. A number described the sympathetic chain.



QUESTION 15 Describe how the kidney establishes the medullary concentrating gradient.

71% of candidates passed this question.


The main points that needed to be addressed for a pass incLude:


1. the Loops of HenLe with their water permeabLe descending part and water impermeabLe ascending part which activeLy removes soLute from the tubuLe Lumen - the counter current muLtipLier system
2. the vasa recta which are paraLLeL to the Loops of HenLe and permeabLe to water and soLute with Low fLow, which aLLows the gradient to be maintained - the counter current exchange mechanism
3. the roLe of urea which is concentrated in the meduLLa by mechanisms which invoLve changes in permeabiLity to urea in different regions of the tubuLes partLy infLuenced by the effects of antidiuretic hormone.

Areas which created probLems for a number of candidates incLuded (1) the fact that the meduLLary gradient refers to a gradient down the meduLLa in the interstitiaL fLuid rather than between the tubuLes and the interstitium (2) The correct use and reLevance of the terms “counter current exchange” and “counter current muLtipLier” (3) The roLe of urea (which is described with some differences in detaiL in the texts) was often overLooked (4) the detaiLs of which sections of the Loop of HenLe were water permeabLe and which were not and where active soLute resorption occurred.



QUESTION 16 Discuss the physiological causes of early post-operative hypoxaemia.


13% of candidates passed this question.


For a pass candidates were expected to define hypoxaemia, indicate normaL vaLues of Pa02, and expLain the significance of hypoxaemia. They were expected to discuss the PHYSI0L0GICAL causes of hypoxaemia and this is most easiLy done using a cLassification

PhysioLogicaL causes of hypoxaemia can be broken down into:
1. Low inspiratory oxygen for the needs for the patient
2. HypoventiLation (eg 2° pain, respiratory depression)
3. V/Q scatter or mismatch (areas Low ventiLation cf perfusion eg ateLectasis vs Loss of areas with high perfusion cf ventiLation eg significant hypotension)
4. Increased 0xygen consumption (eg fever, shivering)
5. Diffusion barrier (which pLays very LittLe part in heaLthy patients).


Better answers incLuded:
. An indication of appreciation of the significance of these vaLues, ie the beginning of the “sLipperLy sLope” of the haemogLobin dissociation curve.
. Common mistakes / omissions:
. This was N0T a question about tissue hypoxia, and no marked were aLLocated for discussions regarding stagnant hypoxia, etc.

ExpLanations regarding V/Q scatter were often disjointed and incompLete. Causes of dead space and shunt were often confused. PuLmonary emboLi resuLt in areas of no bLood fLow and therefore physioLogicaL dead space (not shunt).

Few candidates indicated how the vaLue of Pa02 decreases in heaLthy aging.


Few candidates indicated that hypoventiLation and V/Q scatter are the major causes of Low Pa02.






PHYSIOLOGY - VIVA SECTION



PHYSIOLOGY TOPICS.

Cardiovascular
. Describe a VaLsaLva manoevour
. Resting 02 consumption
. CVP and StarLing’s Law of the heart
. Functions of the circuLation
. Interpretation of PCWP
. Determinants of myocardiaL oxygen suppLy and demand
. Coronary sinus oxygen saturation
. Factors affecting puLmonary vascuLar resistance
. ReLationship between eLectricaL and mechanicaL events in the heart
. Response to an acute 20% bLood Loss
. Substances reLeased by endotheLium
. Determinants of oxygen fLux
. Compare arteriaL waveform centraLLy and peripheraLLy



. Pressure-voLume Loop for Left ventricLe
. Determination of C0
. Causes of interstitiaL oedema
. Action potentiaL for SA and AV nodes
. Effect of sympathetic bLockade on cardiovascuLar system
. Determination of SVR
. ReLationship between CVP trace and ECG
. Changes in cardiovascuLar system with aging
. Compare puLmonary and systemic vascuLatures
. Effects of IPPV on cardiovascuLar system


Respiratory
. ALveoLar gas equation
. Effects of ascent to aLtitude
. CLosing capacity
. Venous admixture
. Differences between arteriaL and venous gases
. Compare the apex and base of the Lung in standing patient
. Functions of FRC
. CompLiance
. FLow-voLume Loops
. ControL of breathing
. Phases of a capnogram
. 0xygen utiLisation in the body
. Carriage of C02
. Measurement of dead space
. Measurement of FRC
. Measurement of shunt
. Effects of varying V/Q ratios
. HaemogLobin-oxygen dissociation curve


Renal/Fluid & Electrolytes
. RenaL handLing of metaboLic aLkaLosis
. Water homeostasis
. NormaL vaLues of RBF/GFR
. Define osmosis
. RenaL compensation for respiratory acidosis
. Definition of pH
. Determinants of capacity of a buffer


Hae+atolo,y/I++unolo,y
. Contents of a unit of packed ceLLs
. Prevention of cLotting in circuLating bLood
. ControL of fibrinoLysis
. CLassification of hypersensitivity reactions
. Mechanism of anaphLaxis


Gastro-intestinal/Liver
. Gastric acid production
. Determinants of gastric emptying
. Factors affecting Lower oesophageaL tone
. Functions of the Liver





Metabolism/Endocrine
. Digestion/absorption of carbohydrate
. Effects of 48 hour fast
. Definition of basaL metaboLic rate
. GLucose/fat utiLisation
. CLassify hormones and their mechanisms of action


Measurement
. Waveforms of EEG
. Pressure measurement devices
. PuLse oximetry
. Damping in resonant systems
. CaLibration of arteriaL Lines
. Capnography
. Humidity


Foetal/Placenta/Neonatal
. 0xygen deLivery to foetaL brain
. Functions of the pLacenta


Muscle
. Stretch refLex
. Differences between skeLetaL and smooth muscLe


Pain
. SpinaL moduLation of pain
. Pathways for peripheraL pain transmission