2018 Second Sitting SAQs

Answers required a description of the surface anatomy outlining the midline structures including the hyoid bone and cartilages. The tissue layers should have been mentioned as should the relevant tracheal anatomy. The anterior, posterior and lateral relations of the trachea should also have been included along with the relevant nerves and blood vessels. Diagrams were not essential but could have been included. Candidates should note that marks were not awarded for a description of how to perform a tracheostomy.

The answer required an explanation of the causes of the difference between the PaCO2 and ETCO2. This required recognising how the end point of phase 3 of the capnograph trace corresponds with end tidal CO2. The difference is caused by the alveolar dead space. The difference is normally very small in healthy adults with the ETCO2 being lower than the PaCO2. It is increased with increasing alveolar dead space. Many incorrectly attributed anatomical dead space as a contributor to the PaCO2-ETCO2 gradient. Discussion of the various types of dead space did not score marks. Marks were awarded for the processes that cause an increased gradient e.g. low cardiac output and pulmonary embolism. Recognising physiological factors such as increasing gradient with increasing age scored marks. Marks were not awarded for descriptions on how dead space is measured.

A definition of arterial and venous CO2 content (mls and partial pressure) and an outline of the 3 forms of CO2 in the blood and their contribution to the AV difference, followed by a detailed explanation of each form of carriage was required for this question. A good answer included a table of the contribution of each form of carriage to arterial and venous content and the AV difference; explained the concepts of chloride shift when describing carriage as HCO3-; detailed the Haldane effect and its contribution to carbamino carriage and referenced Henry’s law when describing dissolved CO2. West’s Chapter 6 on gas transport details the key information to score well on this question.

Answers should have included a description of the need for a pressure gradient for flow and a discussion on right atrial pressure, mean systemic filling pressure and resistance to blood flow. The discussion of each of these factors included definitions, normal values, factors affecting them and the direction of change on venous return. Diagrams were not essential, but their use assisted some candidates in explaining the effects of RAP on venous return

Descriptions of protein binding were generally too brief (e.g. a statement saying that drugs and hormones bind to proteins in the plasma rather than a description of usually reversible binding with a drug-protein equilibrium). It was expected that the factors which determine protein binding would be described. Marks were attributed if proteins, along with characteristics of the drugs they bind, were named. Candidates achieved better marks if they named the pharmacological parameters affected by protein binding and explained how and why change occurs along with the significance of those changes. Few candidates differentiated between tissue and plasma protein binding and the different effects on the volume of distribution

Candidates were required to provide a description of gastric emptying (40% marks). Although the question showed the allocation of marks, many candidates did not provide sufficient detail for this section. This required some description of what gastric emptying is (the co-ordinated emptying of chyme from the stomach into the duodenum). Better answers provided detail regarding the process of gastric emptying in the fed and fasted state and differentiated between liquids, solids, carbohydrate, protein and fats. Factors regulating emptying included an outline of peristaltic waves, the basal electrical rhythm and its modulation, the migratory motor complex (MMC) and its modulation, neural input, stretch and hormonal control. Many candidates erred by answering the question "the regulation of gastric secretions" rather than the question (the regulation of gastric emptying). Although they scored well for hormonal control, they missed out on marks for the other factors relevant to the regulation of gastric emptying.

This question required a brief introduction of the role the kidney plays in water balance; a more detailed description of how water is handled as it passes through the various segments of the nephron (glomerulus, PCT, Loop of Henle, DCT and Collecting Duct); the modulation of water excretion by the kidney due to ADH (vasopressin) and how this operates; and the stimuli (osmotic and non-osmotic) for ADH secretion. Although worth mentioning in the context of the effect they have on water movement through the kidney, detailed explanations of Starling's forces in the glomerulus, and of the operation and maintenance of the counter-current mechanism, were not required. More important was describing the control of water reabsorption in the collecting ducts (and thus modulation of water excretion by the kidney) under the influence of ADH.

An anatomy question expects the use of anatomical nomenclature to describe relationships. Good answers defined the “safe triangle” for the lateral approach, soft-tissue layers passed through from skin to pleura and relationship of the neurovascular bundle to the ribs and intercostal muscles. Additional marks were gained for describing the anterior approach and related structures. Common omissions included description of deeper structures (relations) including intrathoracic and intra-abdominal organs and level of the diaphragm with regard to rib space. No marks were awarded for a description of intercostal catheter insertion

A definition of normal glucose levels was expected, mentioning how it is regulated despite variable intake. Most answers incorporated the roles of insulin/glucagon and the glucostat function of the liver. Sufficient detail regarding the mechanism of insulin release was often lacking. Extra marks were awarded for description of the role of the satiety centre in the hypothalamus, glucokinase and processes in fasting and starvation that maintain blood glucose levels. Marks were not awarded for describing effects of insulin and glucagon unrelated to glucose control.

A logical approach to answering this question included a definition of hypoxaemia and then a discussion of the sensors, integrators and effectors involved. It was expected that candidates would cover the peripheral chemoreceptor response (including the respiratory, cardiovascular and autonomic effects), time course of the ventilatory response, hypoxia-inducible factors, vascular effects (hypoxic vasoconstriction in the pulmonary circulation and vasodilatation in the systemic circulation) and metabolic changes (switch to anaerobic metabolism). No marks were awarded for discussing the causes of hypoxaemia. Many candidates incorrectly stated that hypoxaemia is detected by the central chemoreceptors.

This question was generally well answered. Better answers noted production including an amount, site and mechanism. Similarly, absorption included the site, the rate and factors which affect the rate. The electrolyte and pH and how they compare to extracellular fluid should have been included in the section on composition.

The expected answer included a clear explanation of Starling’s forces, including an understanding of the importance of the relative difference along the length of the capillary, with approximate values and examples of factors that influence them. Some explanation of what contributed to the hydrostatic or osmotic pressure gained more marks than merely stating there was a pressure. Several candidates digressed to Fick’s law of diffusion or intracellular flow of ions which was not directly relevant to capillary flow.

Whilst most candidates understood that ketones provided an alternative source of substrate for energy production, many lacked a basic understanding of their synthesis and metabolism. Important facts included what ketone bodies are, where they were synthesised, where they were taken up and used as fuel, under what circumstances they are used and the integral role of insulin. Many candidates accurately reproduced the glycolytic and/or the TCA cycle, but this was not being examined, and did not score additional marks. Many candidates incorrectly stated that ketone production was the result of anaerobic metabolism.

Candidates often misinterpreted the question and described determinants of cardiac output. The answer should have focussed on factors affecting/contributing to normal LV function - not pathological states. Some answers showed a lack of appreciation that normal left ventricular function is afterload independent, due to compensatory reflexes. Answers needed to consider intrinsic and extrinsic factors affecting LV function - the latter (e.g. SNS, PSNS, hormones, drugs) was often left out. Answers needed to consider both systolic and diastolic function. An excellent answer included physiological phenomena such as the Treppe effect, Anrep effect and baroreceptor and chemoreceptor reflexes. Mention of normal conduction and pacing as well as blood supply limited by diastole scored additional marks.

Most questions lacked a systematic approach to the question and specific detail. The relationship between systemic toxicity (CNS and CVS) and plasma levels should be described. Many candidates did not clearly state that CNS toxicity occurs at lower plasma levels that CVS toxicity. Factors that affect toxicity (e.g. drug factors, patient factors, interactions) needed to be elaborated with some detail. Patient factors such as age, pregnancy, acidosis, hyperkalaemia, hepatic failure were often omitted. Finally, marks were also awarded for noting methaemoglobinaemia as possible toxicity and the existence of specific therapy (intralipid).