2009 Second Sitting SAQs

this question. Candidates were expected to explain and provide an example of an antimicrobial agent for mechanisms such as enzyme inactivation of the antimicrobial, alteration of antimicrobial binding/target sites, reduction of antimicrobial drug uptake or active efflux of drug by the bacteria and alteration in enzymatic pathways. Use of a table aided candidates expressing this information. Examples of the methods of spread of antibiotic resistance in bacteria that were expected were: transfer of resistant bacteria from person to person; horizontal gene transfer; transduction - acquisition of bacterial DNA from a phage (a virus that propagates in bacteria); transformation - uptake and incorporation of free DNA released into the environment by other bacterial cells; conjugation - gene transfer (usually on plasmids), by direct cell-to-cell contact through a bridge. Most candidates could name various mechanisms of resistance but many failed to gain marks as they did not provide an example of an organism and antimicrobial. The second part of the question concerning the spread of resistance was generally done quite well. Syllabus - M2a2c Reference: Pharmacology, Rang and Dale Ch 46, Goodman & Gillman, Ch42

this question. To adequately answer this question, candidates must be able to demonstrate that they recognised this to be a major haemorrhage. When a weight and a volume are supplied it is expected the percentage blood loss would be calculated and the shock graded or the haemorrhage at least described as severe. Often the consequences were omitted. Consequences were best described in organ systems e.g. CV, renal, metabolic. Many candidates failed to mention the patient would be hypotensive and tachycardic. A good answer should include mention, and provide explanations, of the mechanisms for the following compensatory responses: • Activation of both baroreceptors and chemoreceptors and their consequences • The sympathetic nervous system response • Fluid shifts • Renal effects - most candidates mentioned the urine output would be decreased but did not provide a mechanism for this Endocrine effects, eg secretion and actions of ADH, ACTH/Cortisol Syllabus - C1e1 Reference: Textbook of Medical Physiology, Guyton and Hall, Foundations of Anaesthesia: Basic Clinical Science, Hemmings and Hopkins

this question. The better candidates had an organised approach to their answer. For example factors could be broadly classified as pharmacokinetic and pharmacodynamic factors or patient and drug factors. For example, pharmacokinetic factors could include dose, the use of a priming dose, patient’s volume status, cardiac output, muscle group and skeletal muscle blood flow. Pharmacodynamic factors expected were those of mechanism of blockade, receptor affinity, agent potency, neuromuscular disorders, age, drug interactions and electrolyte disorders. Many answers listed factors which affect the duration of neuromuscular blockade instead of the onset. Marks were not allocated for information provided by candidates that did not address the question asked. It is important that candidates provide an answer specific to the question asked. Many candidates applied Fick’s Law inappropriately. Lipid solubility and pKa are not relevant as these drugs do not cross the nerve membrane. Syllabus - H2a, 2c Reference: Pharmacology and Physiology in clinical practice, Stoelting Pg 186, Foundations of Anaesthesia: Basic clinical Science, Hemmings and Hopkins ( 2nd ed)

this question. This question sought a candidate’s knowledge of the basic science underpinning a topical area of clinical Intensive Care practice. Candidates were expected to mention normal values of blood glucose and detail the relevant humoral (dominant) and neural (sympathetic) factors. These included mention of, description of and mechanisms for the stimulation/inhibition and actions of humoral factors such as insulin, glucagon, cortisol, etc as the specifically apply to blood glucose control, neural stimulation and the liver’s role as a glucostatic organ. Good candidates would demonstrate a structured response to their answer. Syllabus - N12b Reference: Textbook of Medical Physiology 11th ed Guyton and Hall, Ch. 78

this question This question related to an area of basic respiratory physiology. A good answer necessitated the precise meaning of venous admixture, being that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed pulmonary end-capillary to arterial PO2 difference. Diagnosis required the candidate to mention, a demonstrated increased in the Aa-DO2, what are normal values. For quantification mention and description of the shunt equation was required. Candidates lacked a definition for venous admixture, were inaccurate with their description of the shunt equation and often overlooked mentioning calculation of arterial and mixed venous blood oxygen content.

this question. Good answers to this question directly compared the anatomical differences using two columns: one for the newborn and the other for the adult airway. They further divided the differences anatomically into mouth/naso and oro pharynx, the glottis (and epiglottis), the larynx, and the trachea (main carina and main bronchi). Common omissions were failure to mention that neonates do not have dentition, have more compliant tissues and reduced muscle tone, that the neonates’ larynx lies more cephalad and anteriorly, is covered by a large floppy epiglottis and that the main carina also lies more cephalad. Few candidates were able to list more than 4 differences between the anatomy of the two airways and none mentioned the possibility of disease affecting the neck in the adult. Syllabus – P2e Reference: Anatomy for anaesthetists and T K Oh Chp95, Anatomy at a glance.

this question. Candidates were expected to state the purpose of the blood brain barrier (BBB), define what constituted the BBB, what its function is, and what parts of the brain lie outside of this barrier (and why). Further candidates should have mentioned what substances cross the BBB, and how this is achieved. Common omissions included not mentioning the presence of astrocyte foot processes in addition to the tight junctions between the capillary endothelial cells, the presence of active pumps for sugars amines, and some ions, and what parts of the brain lay outside of the BBB. Characteristics of a drug that will penetrate the BBB included low molecular weight, good lipid solubility, a low volume of distribution, low potency and low protein binding. Also expected was a discussion of Fick’s Law and the drug features that would allow a high concentration gradient in the cerebral blood vessels to be achieved and a high diffusion coefficient and mention of drugs that resemble natural ligands for active transport mechanisms. Syllabus - G12d G2a References: Pharmacology, Rang and Dale 6th edition page 476, Principles of physiology for the anaesthetist, Kam page39-40, Pharmacology and Physiology in Anaesthetic Practice, Stoelting, Pg 681, Textbook of medical physiology, Guyton and Hal11th edition page 766. Foundations of Anesthesia. Hemmings and Hopkins. 2nd edition.

this question. Candidates were expected to identify what compounds are lost during vomiting associated with gastric outlet obstruction and that intravascular volume depletion is likely. Furthermore the candidate was then expected to explain that overall the child’s body will defend volume – then tonicity – then acid base status, in this order. An outline of the major physiological defences of volume status (e.g. the renin-angiotensin-aldosterone system), and how these will perpetuate a metabolic alkalosis (prevent the kidney from clearing the excess bicarbonate in the form of an alkaline urine) was then expected. A common omission was to not appreciate that the preservation of volume (sodium or chloride) by the kidneys conflicts with the physiological mechanisms that would allow bicarbonate loss through the kidneys’ tubules. Restoration of normovolaemia would allow an ‘alkaline tide’ or bicarbonate loss by the kidneys (alkaline urine production). Syllabus - G12d G2a References: Power and Kam. P247-266

this question. Any description of the changes in inspired and alveolar PO2 with altitude required the description of, and an understanding of, the equations for calculation of PiO2 (PiO2=0.21(BMP-47)mmHg or 0.21(BMP-6.3)kPa) and PAO2 (PAO2 =PiO2 – PaCO2/R). It was important to mention alteration in atmospheric pressure (BMP) with altitude and that saturated vapour pressure (SVP) is constant for the same body temperature. A good answer to the second part of the question (respiratory physiological responses to altitude) was one that had some structure, eg responses divided into acute and chronic, respiratory, renal, haematological, cardiovascular and CNS categories, and relevant detail for each category. Candidates were expected to at least mention, but not restrict themselves to the following: acute responses, eg carotid/aortic body chemoreceptor stimulation hyperventilation, proportional to reduced BMP and hypoxia, limitations to hypocarbia (due to alterations in CSF pH) etc: physiological responses to early and chronic acclimatisation (eg renal HCO3-excretion, respiratory centre CO2 response curve resets to left, altered peripheral chemoreceptor sensitivity, 2,3, DPG levels and related right. Shift in HbO2 curve, alterations in pulmonary diffusing capacity due to increased alveolar surface area and pulmonary blood volume, etc). It is important that current and future candidates use the examination reports to guide their learning. Thus it is essential that candidates not just read the feedback provided to each exam question but also refer to the reference(s) supplied below and other relevant sources they find to be useful. Syllabus – B1k, 2i Reference – Nunn’s Respiratory Physiology, Ch 17 and 5. Power and Kam 432-4.

this question. There are a few areas of anatomy that are essential for Intensivist to have a high level of knowledge of. The subclavian vein is one of them. Unfortunately the extent of knowledge displayed by the candidates was very shallow. A good answer required as a minimum, a clear description of the course of the vein. This included the following facts – it is a continuation of the axillary vein, it’s relationship to the first rib, to the medial border of the scalenus anterior, the fact that it arches up, medial, then down and that it joins the internal jugular vein (behind the subclavian joint, anatomical relationships (eg Anterior – clavicle, subclavius muscle, Posterior – first rib, apex lung superiorly, first intercostal space inferiorly, Superior – subclavian artery, thoracic duct medially, phrenic nerve, lower trunk brachial plexus laterally and Medial – brachiocephalic artery, trachea, vagal trunk, thoracic duct and oesophagus posteriorly) and surface anatomy (related to the various available techniques (eg the infraclavicular and supraclavicular approach) Syllabus – C1d, 2g Reference: Anatomy for Anaesthetists, Ellis and Feldman

this question. Antiemetics can be classified by their receptor actions including, dopamine antagonists, serotonin antagonists, antihistamines, anticholinergics, antimotilinic etc or by their drug type – butyrophenones, phenothiazines, benzamides etc. Marks were divided between each class, and for “other/novel” antiemetics – such as, steroids, GABA agonists, alpha 2 agonists, mu receptor antagonists, canabinoids, propofol and NK1 receptor antagonists. Candidates were expected to mention the drug type, receptor interaction, the location of the receptors and the pathways inhibited by the drug – central CTZ, vestibular nuclei, solitary tract nucleus, vagal afferents or GIT motility and secretions. Most drugs work at one or more of these sites and marks were awarded for mention of this. Commonest errors were omission of adequate detail in each class. Antihistamines, anticholinergics and “others/novel” were frequently omitted. Syllabus - Q12e and Q2b2a Reference: Chp 37 Goodman and Gillman

this question. A good answer to this question required the collation of knowledge from broad range of areas, ie drug activity. Marks were divided between each of the following: 8.4%NaHCO3-, insulin/glucose, K+ exchange resin, frusemide/loop diuretics, Beta2 agonists and K+ free fluid rehydration/dilution. Candidates often overlooked the fact that only loop diuretics and K+ exchange resins lower total body K+ content, whilst the others induce an intracellular K+ shift which is not sustained and do not directly result in body elimination of K+. Intravenous fluid rehydration lowers total body K+ if there is a resulting diuresis. Most candidates just passed this question. Common omissions included NaHCO3, loop diuretics and beta 2 agonists. No candidate mentioned rehydration/dilution. Calcium does not lower serum potassium.

this question. A good answer to this question required a discussion that focused on the following key points- Recruitment and distension of pulmonary capillaries. Helps limit pulmonary vascular resistance as pressure and flow increase. Lung volume. Lung inflation is thought to have a dual effect, expanding large vessels by traction while compressing smaller vessels and resistance is dependent upon lung volume, being lowest at approx FRC. Gravity. Perfusion is distributed down a vertical gradient in the lung, reflecting the balance between intra-alveolar pressure and the distending vascular pressure. (West’s Zones) Oxygen. Hypoxia causes pulmonary vasoconstriction. Diverts blood away from hypoxic regions of the lung. Hypercapnia and acidosis vasoconstriction Autonomic innervation. Alpha -adrenergic stimulation - vasoconstrictor, Beta-adrenergic stimulation - vasodilatation, Parasympathetic stimulation - Vasodilatation Local mediators. Vasoconstrictors (Serotonin, histamine, endothelins) and Vasodilators (NO, prostacyclin, isoprenaline) The majority of these points could be efficiently explained through the use of graphs/figures, all of which are commonly found in the majority of physiology books that include respiratory physiology. Those candidates who failed to do so were also those who scored fewer points with this question.

this question Candidates should expect that questions relating to “the pharmacology of ……” are likely to be common. Thus candidates should have prepared structured approach for any such question. For example, one that includes predefined major categories such as pharmacodynamics and pharmacokinetics and sub-categories such as mechanism of action, absorption, preparations, bioavailability, volume of distribution, metabolism, elimination, adverse effect, clinical indications, precautions/interactions, etc. and the information relevant to each category. Failure to take a structured approach to such questions, as was observed amongst some candidates within this exam, risks omission of vital facts (and not gaining marks) and errors. Noradrenaline is such a common drug within intensive care practice and so candidates would be expected to know it in great detail. There are many references for it, such as the ones listed below. Syllabus – G3a, 2b References – Goodman and Gillman Chp 10 and Katzung.

this question. For a good answer it was expected that candidates would mention the relationship of angiotensinogen, angiotensin I, renin and Angiotensin Converting Enzyme to angiotensin II production, the actions and fate of angiotensin II and factors that regulate angiotensin II. It was expected that candidates mention angiotensin acts as a potent vasoconstrictor, stimulates aldosterone secretion, facilitates noradrenaline release, preferentially vasoconstricts Efferent arteriole in nephron, preserving GFR in low perfusion states, increases renal tubular Na + reabsorption and increases secretion of vasopressin and ACTH. Regulation of Angiotensin could be separated into factors increasing angiotensin levels (eg prostaglandins, low K+ levels, Sympathetic stimulation, ↓ Na+ delivery at distal tubule, any factor contributing to reduced renal blood flow (eg hyovolaemia, cardiac failure, renal artery stenosis) and factors reducing angiotensin levels (eg hypervolaemia, afferent arteriolar dilatation and vasopressin). Syllabus - N1 (h), C2b (f) Reference: Textbook of medical Physiology, Guyton, Chp 26, Goodman and Gillman, Chp 30

It is essential that candidates read and respond to the question asked of them. The first part of
the question required simple, accurate definitions, which the majority of candidates were
unable to provide. Marks were awarded for the definition only. Descriptions of
measurement, potential effects on oxygenation, etc. were not asked and gained no marks.

The core of the second part required an outline of the exchange of heat and moisture through
the upper airways and bronchial tree, culminating in fully saturated gas at core body
temperature by level of the 2nd generation bronchi. Whilst the question asked ‘humidity’ and
not temperature, correct definitions in the first part would have dictated a joint outline of
both. The effects of surface area, the nasal turbinates, mucosal secretion and blood flow were
all relevant. The contribution to insensible moisture and heat loss should have been
mentioned. No candidate considered the effects of respiratory rate, mouth versus nose
breathing, or dry medical gases versus room air.

this question. Once again candidates are reminded to read and answer the question presented to them as well as take into consideration the proportion of marks allocated. The expectation from the first section of the question was for candidates to only “list” the hormones secreted by the pituitary gland. The main hormones expected were ACTH, TSH, GH, FSH, LH and prolactin anteriorly; and, ADH (vasopressin) and oxytocin posteriorly. Unfortunately, a number of candidates confused which hormones come from which region and therefore were unable to score marks in the second part. The question clearly asked for factors controlling secretion of hormones from the posterior pituitary, therefore, detailed descriptions of the mechanism of action of ADH in the kidney, or of hormones arising from the anterior pituitary did not relate to the question and were not allocated marks. With respect to ADH, most marks were gained by candidates who described not only osmolality and plasma volume, but the relative sensitivity of the pituitary to these and the pre-potent nature of volume over osmolality; also, the influence of other hormonal axes involved in plasma volume regulation. Marks were also available for other inputs including pain, stress, exercise, etc. A brief description of factors influencing oxytocin was also expected. Syllabus – N12d Reference: Gannong p383, Guyton p359

this question. Candidates were essentially expected to describe the fate of sodium as t passes through the kidney from filtration at the glomerulus to ending up in the urine. Essentially, most Na+ is reabsorbed at the proximal tubule (65%), reabsorption being down an electrochemical gradient (inside cell negative and low Na+ concentration) which is maintained by active Na+/K+ ATPase activity at the basolateral membrane. Then Loop of Henle reabsorbs a further 15% of filtered Na+. At descending limb – no Na+ reabsorption. At ascending limb, thick segment – active process as per proximal tubule, but mostly coupled to K+ and Cl- and paracellular diffusion through tight junctions. Finally the distal convoluted tubule and collecting ducts, a further almost 20% reabsorbed – leaving increase Na+ reabsorption, but minor factors Syllabus – D1, 2f Reference – Textbook of medical Physiology, Guyton, Chp 28

this question. For a good answer candidates were expected to at least mention the following -- Formation and secretion of bile Carbohydrate metabolism (Glycogen synthesis and breakdown, Gluconeogensis) Lipid metabolism (Fatty acid oxidation, Synthesis of cholesterol and phospholipids, Production of ketoacids) Protein metabolism Breakdown Metabolism of toxins, drugs (Phase I reactions - oxidation, reduction, hydrolysis, Phase II reactions- conjugation/glucuronidation) Storage (Vitamins B12, A, D 2, Iron as ferritin, Glycogen) Immunity Endocrine (Synthesis of 25 OH cholecalciferol, Metabolism of steroid hormones, Synthesis of somatomedins, Erythropoietin) Miscellaneous (Acid base role – lactate metabolism, Blood store) Syllabus – I2a Reference: Gannong p485, Power and Kam p185

(11%) of candidates passed this question. For a good answer candidates were expected to account how the placenta allows for effective diffusion to occur. Good answers incorporated the parameters within the Fick equation (eg. area of placental gas exchange, pressure of gas in maternal sinuses (PO2 = 50 mmHg), pressure of gas in umbilical vein (PO2 = 30 mmHg ). Also expected was an explanation of the role of foetal haemoglobin, the double Bohr and double Haldane effects. These were commonly omitted.