Primary FRCA OSCE-SOE exam January 2012 Coventry collection ...

Primary FRCA OSCE-SOE exam January 2012 

SOE set 1 

Pharmacology 

Local anaesthetics – more interested in the different bonds (ester & amide) and what 

characteristics this gave the local anaesthetics. Wanted to know what affects potency, 

length of action and speed of onset (didn’t allow you to get into a flow – just kept 

asking separate questions) and also how you can change these to improve speed of 

onset, potency etc. 

Pharmacokinetics – asked to draw a graph of how concentration changes with time 

for an infusion and then explain why a portion of the graph has a steep gradient and 

then plateaus. Moved onto compartment models and what happens when the infusion 

is switched off. 

Diuretics – what different diuretics are there? Talk about thiazide diuretics – what 

they are used for what side effects one can get. How they work, which pump they act 

on and how this causes the metabolic disturbances often common with thiazides. 

Physiology 

Cardiac action potentials - draw and compare the action potentials for ventricular 

myosite and pacemaker cell. Explain the differences between phases and types of 

calcium channels. Explain why the shape for the ventricular myosite is beneficial ie 

not able to produce tetany. Explain how a muscle contraction happens. 

Glucose metabolism – glycolysis, TCA cycle, oxidative phosphorylation. Wanted to 

know where each take place and how many molecules of ATP are produced at each 

part. Moved onto anaerobic metabolism. How the body gets glucose for metabolism 

– wanted to know about control (insulin, glucagon etc) and glycogenolysis, 

gluconeogenesis etc. 

Lung compliance – define compliance, draw a lung pressure, volume curve – explain 

the shape and why on expiration it does not follow the same path (hysteresis – explain 

this). Surfactant and the roles and how this helps in respiration. 

Clinical 

Scenario – 35ish year old woman for an elective TAH, fit and well. Only medication 

she takes is lansoprazole. On examination you notice she can only open her mouth 2 

fingers wide. 

How would you proceed – history and what I would focus on – reflux vs heartburn, 

when it came on, has it helped following medication. Any other medical problems – 

anaemia in association with menorrhagia (this could be the reason she was having the 

TAH). Smoking history. Examination – full airway assessment – explained what I 

would do and why and if I mentioned grading systems, I was asked to define the 

grades (eg MP scoring, thyromental/sternal distance, Wilsons). What are my 

anaesthetic options – CSE vs general pros and cons for both. She was insistent on GA 

– how would I proceed – would I give a premedication? explained I would do a 

awake fibre optic with consultant. They then moved on to ask how I would manage 

her presuming her mouth opening was OK – I explained RSI in face of reflux – how 

would I do this etc. 

Coventry collection: Many thanks to the candidates from January 2012 

Course 

1


Post op – on extubation, she developed laryngospasm; how would I manage this, how 

would I diagnose laryngospasm, who is more prone to it and what are the causes. 

Physics 

Humidity – why is it important in anaesthetics – prevent drying of gases, prevent heat 

loss, prevent static build up. Define absolute and relative humidity. How can you 

measure humidity – explain how they work. 

Pressure reducing valves – where are they found on an anaesthetic machine – 

cylinder to machine, Ritchie whistle. How they work – (the diagram was in front of 

you so you didn’t have to draw it) but an in depth explanation was needed. 

Force/energy – What is force? What is it measured in? Relationship to other derived 

SI units (I think they were getting onto force, pressure, area relationship). What is 

energy, different types of energy (electrical, mechanical (potential, kinetic), thermal). 

Explain about these and how you can change one form into another. Transducers 

were mentioned then I was asked how does a generator or a motor work – I think they 

were trying to get me to explain a bit more about how it can change one form of 

energy into another. 


Pharmacology viva 

- Differences between Fentanyl and Alfentanil; lipid solubility, pKa, Ionisation, 

dose/potency hence concentration gradient, volume of distribution and clearance 

Gastric acid secretion; drugs that work on that, PPIs, H2 antagonists, Antimuscarinics, 

moved on to antiemetics, prokinetics 

- Population variability in drug metabolism: I started off by talking about where drugs 

are metabolised (liver, kidneys, lung, plasma, gut) and pharmacokinetics. I said that 

what the body does to the drug (pharmacokinetics) can be split into Absorbtion, 

Distribution, Metabolism, Excretion and then went on to discuss each factor 

mentioning the following: genetic variability (Ea:Ea Dibucaine, acetylation, phase 1 

and phase 2 metabolism), lifestyle factors such as smoking and alcohol, physiological 

factors such as old age, neonates, pregnancy and pathological factors such as sepsis, 

renal failure, coealiacs, ileus, liver failure. 

Physiology 

- Oxygen- Hb dissociation curve; p50, what makes it go left and right, what is 2- 

3DPG, why is it sigmoid, Bohr shift, Haldane effect, Hamburger effect 

-How is CO2 stored in the body? Bicarb, carbamino compounds, dissolved 

- Left ventricular pressure trace and draw the aortic pressure trace. How does the 

aortic pressure trace change with aortic stenosis? how can you work out the mean 

arterial pressure from the trace? 


Course 

2


Clinical: 

71 year old female booked to have an emergency laparotomy for acute cholecystitis. 

She is jaundiced and she has abdominal pain. The surgeons say she is septic and they 

suspect that she has a perforated viscus. 

This question threw a lot of people after the exam as it was very medicine orientated 

and less anaesthetics, so I kept calm and went back to medical school basics. 

-What are the causes of jaundice? I defined that jaundice was due to an increase of 

bilirubin in the plasma and it is a breakdown product of red blood cells and normally 

broken down in the spleen. Causes can be pre-hepatic, hepatic, post-hepatic. 

the examiner asked for examples of each: pre hepatic; haemolytic causes such as 

sepsis or thalasaemia and sickle cell, hepatic; liver disease, cirhosis, hepatitis, 

autoimmune, infective or drug related. post hepatic; obstrucion 

- How would you assess this patient and what is your plan? they particularly probed 

as to how I would assess her fluid balance status and I eventually got that they wanted 

me to say that I would out in invasive monitoring such as CVC line and NIBP and 

take her to HDU for pre-optimisation...I did not expect that they would want me to 

say that because in real life most hospitals don't have this facility. I mentioned I 

would assess her for an epidural but the stern response I got from the examiners, 

"would you put in an epidural in this woman?" I promptly said no because she was 

septic 

- She suddenly becomes hypotensive in theatre; what are your differentials and how 

would you treat? (ABC, call for help, top differentials; anaesthetic, patient or surgical 

causes) 

- post op care? analgesia, ITU/HDU, intubated or extubated? 

Physics 

Vaporisers 

- what are the features of an ideal vaporiser? high heat capacity, high thermal 

conductivity 

why? so it can retain a lot of heat and then give it easily to the inhalational agent to 

vaporise it, talked about latent heat, SVP 

- talked about draw over vs Plenum and how a plenum vaporiser works? how and why 

do they need temperature compensation? talked about the bimetallic strip and that 

SVP is only dependent on temperature hence the need for compensation 

-talk through desflurane vaporiser and the differences. 

How can you give an infusion of a drug? 

- volumetric pump, syringe driver, by hand, drip counter...he asked me anything 

else...I didn't know there was anything else 

- showed me a picture of an alaris syringe driver and asked me for sources of error 

with this: pump factors (servicing, power failure, microshock), programming factors 

(wrong inputted data, wrong programme, no labelling) and patient end (occlusion, 

wrong kind of connecting infusion sets, no anti siphon no anti reflux, disconnection). 

- He then showed me another set of pictures: one was a tci connection tubing that was 

yellow (used for epidural infusions too), one was for PCA connections, one was the y- 

connector tubing we had in the coventry course osce with the two anti reflux valves 


Course 

3


and he asked me to explain the anti reflux and anti siphon mechanisms and what is 

connected to what. 


Physics: 

Laryngoscopes ,shape of layringoscope, 

BPmeasurement , how do u measure bp of patient in ward, why 4th kororkoff. 

Clinical: 

45 yr old obese , problems during anaesthesia , preassesment, wt is obesity, prone 

position and precautions ? Reflux 

How do u anaesthetise and wt drug doses are used, sensitivity to morphine etc 

In recovery desaturating : wt do u do 

Physio 

Hypoxia , types, odc, Wts. Venous point , wt happens in different types of hypoxia to 

venous point. 

Na and it's regulation 

Osmolality and regulation 

Draw nephron and show na in it 

Pharmacology: 

iv anaesthetic agents. Class , draw thio , propofol,, difference b/n them and thio in 

detail, y sulphur. 

Dose response curves , log dose etc 

Colloids and differences between each 


Pharmac 

IV induction agents particularly barbiturate structure 

Dose response, affinity, potency, efficacy 

Colloids, diff between starches and gelatins, properties of ideal colloid 

Physiology 

Sodium handling 

Hypoxia, affects on o2 diss curve. 

Capillaries 

Clinical 

Obese man with OSA for pilonidal sinus. Post op hypoxia 

Physics 

Laryngoscopes 

Osmolality and osmolometer 

Bp measurement, only interested in nibp. 


Course 

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Pharmacology 

Structure and classification of iv induction agents – propofol, thio, ketamine, 

etomidate. Classes of barbiturates inc methohexitone. What is in each vial of iv 

induction agent 

2.Dose response curve, ED50, full agonist graph, efficacy, affinity, and partial agonist 

graph. 

3.Compare and contrast HES with gelatins 

Physiology 

Describe starlings forces in capillaries, specifically in pulmonary capillaries, draw 

graph of art vs venous in lungs. Compare with systemic 

Describe Na control in body. Causes of hyponatraemia, symptoms 

Hypoxia. Oxy Hb curve, changes in histotoxic, stagnant hypoxia. Mixed venous vs o2 

content 

Physics 

BP measurement. Korotkoff sounds, manometer, dinamap 

Compare and contrast different laryngoscopes 

Osmolarity vs osmolality. Calculation of, colligative properties. Ion gap, equation, 

causes of increased 

Clinical: Patient listed for pilonidal sinus 


Physio SoE - 

1. Glucose metabolism - control . Pathways - what it produce. 

2. AP - pace maker , ventricle - details 

3 Compliance - what is hysteresis , etc 

Pharmac - 

1. LA - compare lignocaine , bupicaine , onset , max dose details 

2. Diuretics - classification , details of bendro . 

3. Washin curve - Iv infusion , compartment model , LD , MD - calculations why ? , 

how . 

Physics - 

1.press regulating valve - draw , explain 

2. Force , Newton , energy - in details . 

3. humidity - everything . 


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Physiology: 

1. Cerebral blood flow - factors affecting ICP, Monro-Kellie doctrine, curves for CBF 

vs PaO2 & PaCO2, autoregulation & associated theories. 

2. Thyroid - hormones produced, feedback mechanism, functions of hormones, 

calcitonin & Ca2+ homeostasis 

3. Showed picture of alveolus with adjacent pulmonary capillary. Asked to write 

down alveolar partial pressures of CO2 & O2, then mixed venous pressures. What 

happens during apnoea - changes in numbers. What happens if alveolus closed off, 

what happens if alveolus left open to air? How can you increase the time of to 

hypoxia during apnoea (essentially asking re. pre-oxygenation). What factors cause a 

shorter time to hypoxia in apnoea (reduced FRC, increased O2 consumption, etc). 

How can you manipulate this in anaesthetics? 

Pharmacology : 

1. Drugs that reverse NMB (anti-cholinesterases, Sugammadex). Classify. How do 

they work? What are the SEs (muscarinic effects). How do we overcome this 

(glycopyrrolate etc). Tell me more about Sugammadex, how does it work, can I use it 

with vecuronium? What about atracurium? Why? 

2. What is volume of distribution? How can it be measured. Draw concentration vs 

time graph. What else can be derived from graph (t1/2, time constant)? What is 

bioavailability? Demonstrate on graph how you can measure it (AUC). 

3. Anti-emetics. Draw diagram of VC, CTZ and receptors involved. Tell me more 

about different drugs on different receptors, effects. Indicate on diagram where 

dexamethasone acts. 

Physics 

1. Peripheral nerve stimulator - components, supramaximal stimulus, which nerves 

can you use, which site is most accurate, ToF (various examples given, difference in 

patterns between non-depol & sux), what frequency & amplitude would you use. 

2. Arterial tourniquet. Uses, components, max pressure used, max time allowed & 

why. What if surgeon needs to keep tourniquet on for longer, what would you do? 

Physiological changes during inflation & after deflation. 

3. Given various equations and asked to draw curve. (y = mx + c, xy = constant). 

When do we see these graphs in our anaesthetic practice? Shown various graphs and 

asked to write equations for them. 

Clinical scenario 

19 year old boy brought into emergency department after falling down stairs outside 

nightclub. He is confused & agitated. 

Differential diagnoses, effects of alcohol & drugs on conscious level & diagnosis. 

What investigations? He requires a CT - how would you manage? Cushing's reflex - 

how would you treat. How do you reduce secondary brain injury. He now needs a 

transfer to neurosurgical unit - how would you manage this. 


Course 

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LA and onset factors 

Henderson Hasselbach 

La toxicity 

Routes of admin drugs 

Focus on first pass metabolism 

Bioavailability and factors affecting it 

Gabapentin what do you know 

Antiepileptics site of action 

Pacemaker cells 

Action potential for myocyte vs pacemaker 

Symp effect 

Water compartments 

Effect of dextrose vs saline 

Osmoreceptors 

Vent perfusion lung graph 

West zones 

Effect of exercise 

Effect on PVR 

Clinical 75 obese strangulated hernia. On metformin and smoker. 

Decreased conscious level in recovery. Differential and mx 

Ways to measure flow 

Hot wire pnemotachograph in detail 

Rotameters 

Doppler principle 

Doppler equation 

Ways to measure cardiac output 

Lidco 


Physiology 

1. Glucose metabolism - control . Pathways - what it produce. 

2. AP - pace maker , ventricle - details 

3 Compliance - what is hysteresis , etc 

Pharmacology - 

1. LA - compare lignocaine , bupicaine , onset , max dose details 

2. Diuretics - classification, details of bendrofluazide. 

3. Washin curve - IV infusion , compartment model , LD , MD - calculations why ? , 

how . 


Course 

7


Physics - 

1.press regulating valve - draw , explain 

2. Force , Newton , energy - in details . 

3. humidity - everything . 


Pharmacology: 

1) Pharmacokinetics: Absorption, Distribution (define Vd, give equations), 

Metabolism, Excretion. Draw a curve of plasma concentration of iv drug against time 

following bolus administration (one-compartment model). Write equation for this 

graph. How could you make analysis of this graph better? (semi-log). Please draw this 

new graph. What parameters can you derive from this graph. Tell me about 

bioavailability. What is time constant, half-life, relationship of one to the other. 

2) Anticholinesterases: Started off with 'what drug would you use to reverse 

neuromuscular blockade'. Then went on to details about each drug ie neostigmine, 

pyridostigmine, physotigmine, edrophonium, organophosphates & how they bind to 

the cholinesterase enz. Which used to treat myasthenia gravis. Sugammadex asked at 

the end. 

3) Receptors involved in vomiting: where centrally & peripherally. Different types of 

anti-emetics, and where they act, side effects. Why is metoclopramide not very 

effective. Why is chlorpromazine not used as anti-emetic. 

Physiology 

1) Cerebral blood flow. What maintains CBF. Monro-Kellie hypothesis. Volume of 

different compartments of skull (ie brain, CSF, blood). Different graphs showing 

effects of differing po2, pC02 on CBF. Mechanisms of autoregulation. 

2) Oxygen cascade. Photo of alveolus & pulmonary capillary - indicate the partial 

pressures of o2 & co2 at different sites. Hypoxic Pulmonary Vasoconstriction. 

3) Thyroid gland. Synthesis of thyroid hormones. Transport and MOA of T4/T3. 

Effects on body. Feedback mechanisms. Calcitonin & Ca metabolism. 

Physics 

1) Peripheral Nerve Stimulator. Where would you place PNS to monitor 

neuromuscular blockade? Why is ulnar crease better than facial nerve? (avoid direct 

muscle stimulation). TOF, DBS, Tetanic, PTC. Mechanism of fade. TOF ratio. 

2) Arterial Tourniquets: indications, components, contraindications, complications. 

3) Graphs: shown various graphs and asked to write the equations for each. Also 

asked to give clinical examples of each graph. (ie negative exponential, positive 

exponential, straight-line, rectangular hyperbolic) 

Clinical 

19yo male fell down stairs at nightclub at 2am. Brought into AE confused & agitated. 

Differential diagnoses, how manage, when would you intubate, etc. Straightforward. 


Course 

8


SOE set11 

Pharmacology: 

1. Inhalational agents 

a) Which agents you normally use 

b) Compare and contrast Sevo, Des and Iso 

c) Draw Fa/Fi curve and talk through it 

2. Intrathecal and epidural drugs 

a) Routes of drug administration 

b) Name some drugs that can be given intrathecally and epidurally 

c) Ideal properties of an agent for these routes. 

d) What type of drugs cannot be used 

3. Oral hypoglycaemic drugs 

a) Name all 5 classes 

b) Mechanism of action of all 

c) Pharmacokinetics and side effects of all 

Physiology 

1) Pacemaker and Myocardial muscle Action Potential 

a) Where are the pacemakers situated in heart 

b) Draw AP for a pacemaker cell and talk through all the phases 

c) Draw AP for Myocardial muscle, compare and contrast with pacemaker cell 

2) Buffer (same as the college question) 

a) Define, properties of an ideal buffer 

b) physiological buffers of body 

c) importance of each 

d) how much acid produced daily? 

3) If you accidentally put your leg on a pin , what happens 

Asked about pain pathways, withdrawal reflex and knee jerk 

Clinical: 

1) Non progress of labour in a term gravida with epidural for labour analgesia, posted 

for caserean section. How will you evaluate this patient and proceed. 

2) Lady has been managed with epidural for C Section. If after baby delivery 

develops pain, how will you manage 

3) PDPH: detailed discussion of epidural patch. 

Physics: 

1) Temperature measurement: 

a) Shown a photo which had oesophageal probe, infrared thermometer and mercury 

thermometer. Identify 

b) Principles, advantages and disadvantages of each 


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c) Methods of temperature measurement. Detailed discussion on electrical methods 

with drawing and discusiion of graphs. 

2) Pressure 

a) Define and units 

b) Application in clinical practice 

c) Shown a picture of pressure regulator and asked about its principle (weird picture) 

3) Fibreoptic: 

a) parts, difference between fibreoptic laryngoscope and fibreoptic broncoscope 

b) uses, principle of working , advantage over traditional laryngoscope 

c) cleaning and sterilisation 


Pharmacology 

- opening q: 'what drugs can we give intravenously?' - not a q i had prepared for, but 

started by saying i could classify, then first mentioned iv induction agents, at which 

point he stopped me and took me entirely down that route. all the structures and how 

they relate to the drug characteristics 

- colloids/ ideal colloid 

- dose-response curves and shifts 

Physiology 

- sodium handling in the body (very specific) 

- hypoxia, curves 

- fluid movement across capillaries - gradients. 

This felt like my worst viva, sometimes felt like a tutorial! 

clinical 

- morbidly obese man for pilonidal sinus and flap repair - all the issues 

Physics: 

- laryngoscopes - design, features 

- osmolarity, osmometer, definitions 

- can't remember sorry. 


Pharmacology 

Discuss why you would use sevo or desflurane as alternative to isoflurane. 

Routes of administration of drugs- discussion into intrathecal and why we would 

administer drugs in this way (pharmacokinetics, mechanism of action) 

Type II diabetes mellitus drugs- wanted detail description of how peripheral 

sensitization to insulin occurred. 

Physiology 

Reflex arcs, pain pathways 


Course 

10


Buffers- draw buffer titration curve, different types of buffers. Open/ closed. Gibbs 

Donnan equation 

Cardiac nerve conduction comparing pacemaker and myocyte. How SNS and PNS 

would effect it. 

Physics 

Temperature measurement. Details of transcutaneous measurement and oesophageal. 

Pressure- balloon inflated under water, how will pressures and volumes change. 

Adding nano newtons to milli newtons, discussion of integers. 

Fibreoptic scope. Draw cross section of it. How to use it and clean it. Total internal 

reflection. 

Clinical 

Epidural for labour in primigravida. Needs to go to theatre for failure to progress. 

What would you do? 

Categories of section. Pain intraoperatively. 

PDPH- differential dx, treatment. 


Pharmacology 

1. Opioid receptors, partial agonists, side effects of opioids 

2. Concentration – time curves for IV bolus, infusion, infusion of alcohol(!). VD 

and Clearance. 

3. Inotropes and inodilators. 

Physiology 

1. Baroreceptor response 

2. Functions of the placenta 

3. Lung volumes, FRC, closing capacity 

Clinical 

1. 42 year old with dental abscess, limited mouth opening, asthma 

2. Critical incident – laryngospasm on extubation 

3. Dental anaesthesia, conscious sedation 

Physics 

1. Cylinders inc. how to attach to anaesthetic machine 

2. Cardiac output measurement. Doppler effect, Swan Ganz catheter – 

complications 


Pharmacology 

- Isoflurane vs Sevoflurane 

- Pharmacogenetics 

- Digoxin 

Physiology 

- Vomiting 

- Cardiology: formation of the BP trace, and PV relationships 


Course 

11


- Buffers 

Clinical 

- Emergency laparotomy of 65 yo male, previous PE 6/12 ago (warfarinised), but 

otherwise fit and well. 

- INR now 5.8, ARF 

- Describe your immediate concerns 

- How would you proceed? 

- Discussion of pre-, peri-, post-operative management 

Physics & Measurement 

- Electrical Safety 

- Transducers 

- Scavenging 


Pharmacology 

Propofol ,thio 

Statistics,type of errors,null hypothesis,formulas of errors,methods to minimise. 

Drugs for asthama,mechanism,leukotrienes inhibitors,aminophylline. 

Physiology 

Role of heart, why four chambers,role of atria,work done,why venous side not 

pulsatile.frank starling curves. 

Foetal circulation explain with diagram,oxygen%,what happens with first breath.how 

and why foraman ovale and ductus close. 

Clinical, 

12 yr boy 65 kg,for post trauma,fall fro swing,for radius MIA,SOS playing past 

history of excema and penicillin allergy. 

All pediatric questions,critical incident,laryngospasm,aspiration and management. 

Physics 

Methods for blood warming,design your own device. 

Fibreoptic,working and principles 

Light measurment,definition,pulse ox.beer lamberts law.other methods where light 

principles are used 

Differential amplifier. 

Biological potentials.how are these measured,why different. 


Pharmacology 

1) The examiner began by asking for 3 clinical effects of Ketamine, which I gave her, 

but then when she went on to ask for more details about the pharmacology of 

ketamine, I drew blanks, I honestly did not revise this to sufficient detail that the 

answers took a while to come out with. Particularly, she had to prompt me about the 

receptors it acted on, and the side effects, and I couldn't answer the question fluently. 

2) Name me the different types of receptors. This was a much better question and I 

managed to show and draw the 4 different receptor types. 


Course 

12


3) Classify anti-angina drugs. Again I was let down by my lack of knowledge. I could 

only recall Nitrates, and tried to steer the discussion towards antihypertensives and 

heart failure medications, but she was having none of it. 

Physiology 

1) The examiner asked me what contributes to resting membrane potential in nerve 

cells. I wanted to write out the Nernst equation but he didn't want me to use that to 

explain it. Then I said the Goldman Field equation, but again he didn't want me to 

reproduce that. In the end he seemed rather annoyed and I offered the answer of intra 

and extra cellular concentrations of ions. He then asked why the concentrations were 

different and I said it was the Na/K ATPase pump, but he said why then does the 

potassium ion contribute more to the membrane potential. I realised after a while that 

he wanted me to say the Gibbs Donnan effect. But by this point the 

miscommunication caused alot of time to be wasted. He asked me to draw an action 

potential and explain how it worked, which I reproduced. All in all, quite frustrating 

that we seemed not to be meeting across the table 

2) He asked what Basal metabolic rate was, which I didn't have a good definition for, 

and I offered something to the effect of basal oxygen requirements and the amount of 

work done by the body to maintain homeostasis. Unprepared for this question and it 

was quite painful 

3) He asked what happens when we breathe in 100% oxygen in the alveolus, and 

wrote out the Alveolar oxygen equation. Thought that this question wasn't too bad, at 

least I could use the equation to answer his hypothetical scenarios. He asked what 

happens at altitude and what happens at high bariatric pressures. 

Clinical 

Patient 28 yrs old with Diabetes for appendicectomy. Temperature of 38 degrees and 

BM of 28. 

I thought this question went quite well, and was confident about my answers 

Physics 

1) Asked what was alveolar dead space, which I responded by saying it parts of the 

airway which is ventilated but not perfused. Then asked how we measure anatomical 

deadspace, which I responded with Fowler's method and drew the graph and 

explained it. Then he asked how we measure physiological deadspace, which I used 

the Bohr equation to answer. but he tried to trick me by saying isn't Vt tidal volume 

and not total lung volume. Asked me to show how to derive it, it started to derive it by 

drawing out the lung and labelling Vt and Vd and Vt-Vd, but when he confused me 

with tidal volume versus total lung volume, I apologised and said I couldn't derive it 

there and then. 

2) Showed me a piece of paper with a number of different electrical symbols and 

asked what some of them were, which I answered. Then asked what devices we can 

find capacitors in, I used the defib as an example. Asked me to draw the circuit, which 

I did, then asked me what the inductor in the circuit was for, and I drew the 2 current 

versus time curves and explained the inductor slows the discharge of the energy. 

3) Asked me what a vacuum was, and asked where we might have vacuums in 

anaesthetic practice, I answered scavenging and suction. He asked me about active 

scavenging. 


Course 

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Physics 1. fluid warming system types inc level one 2. light waves and mechanism of 

fibreoptics. 3. Electrode potentials eg EEG, differences and how they work 

Clinical: 12 y o boy who mum says fell from a swing 15 hours ago. Penicillin allergy. 

Closed # radius for MUA+-.. How would you assess? How would you do the 

anaesthetic? Incident: laryngospasm under LMA and how to manage / differential 

Pharm: 1. Propofol including pharmacokinetics. 2. Type I and II errors, sample sizes, 

bias. 3. Drugs for asthma and mechanisms 

Physiology: 1. Fetal circulation. 2. Curves for CO2 versus MV in both awake and 

ventilated patients (ie reciprocal axes). 3. Functions of the heart; CO determinants; 

what happens if the atria were removed? 


Pharmacology 

- Isoflurane vs Sevoflurane 

- Pharmacogenetics 

- Digoxin 

Physiology 

- Vomiting 

- Cardiology: formation of the BP trace, and PV relationships 

- Buffers 

Clinical 

- Emergency laparotomy of 65 yo male, previous PE 6/12 ago (warfarinised), but 

otherwise fit and well. 

- INR now 5.8, ARF 

- Describe your immediate concerns 

- How would you proceed? 

- Discussion of pre-, peri-, post-operative management 

Physics & Measurement 

- Electrical Safety 

- Transducers 

- Scavenging 


Physiology 

1) Heat loss and control: Where is heat regulation controlled in body. What happens 

when you are too hot and what happens when you are too cold? What does a dog 

do?! 

2) Cardiac pressure vs time curve: Left ventricle, aorta and ECG on it. What is 

isovolumetric contraction. Starlings Law. 


Course 

14


Pharmacology 

1) How does paracetamol work? Where are it’s receptors and what are they? How 

can it be administered? What happens in overdose? How do we treat overdose. 

Are there any other harmful effects of paracetamol? Because I mentioned COX at 

some point in my answer, they also asked me to draw the arachadonic acid- 

PG/leucotriene flow diagram to show what COX does. Briefly at the end I was 

asked what side effects NSAIDS have that parsacetamol don’t. 

2) This question was sort of about context-sensitive half lives I think, but I didn’t 

really understand it. It was to do with what happened when you stopped an 

infusion that had been maintaining steady state and to draw a concentration time 

graph for fentanyl after stopping the infusion which had been going for 8 hours 

and to draw the same thing but for after a fentanyl infusion that lasted 20mins. 

Also something about half life. 

3) Heparin- mode of action. Different types. What are the molecular weights? What 

kind of chemical is it. Is there any heparin in our body? Where is it? 

Clinical 

Man, 78, for TURP. States he may have had a small MI 6 months ago and had 

some tests done. Now on clopidogrel and aspirin. Also, has a blood pressure of 

190/105. 

- What are the main anaesthetic concerns. 

- How long might someone need to be on clopidogrel after a stent is inserted? 

- How could I find out if he had had an MI (They wanted an immediate test that 

might help- turned out they wanted ECG) 

- What are anaesthetic options? 

- Postpone? 

- How long to wait after stopping clopidogrel before doing a spinal? Why might 

people having this op bleed a lot if they are on anti-coagulants? 

- Assuming it has been postponed and he comes back off clopidogrel and BP is 

controlled, what anaesthetic will I do? 

- Absolute contraindications to spinal 

- Patient becomes SOB and agitated: Diff diagnosis 

- Treatment of TURP syndrome. Investigations that can be done to confirm it. 

- Patient worsens becomes even more hypoxic- management now? Where to 

send after theatre? 


Course 

15


Physics 

1) Ventilator: What are the ideal properties of a ventilator for transport? This 

question was all very vague and I had a lot of trouble answering this one. There 

was a lot about what modes I might want. How much Oxygen would I need for 

the trip: What factors would I need to know before setting off to work this out? 

How would I work out how much to take? 

2) A picture of N2O Isotherms- asked to explain each one. Define SHC, SLH of 

Vaporisation, SLH of fusion. Define BP and freezing point. How do these change 

up a mountain? What is the SHC of water? 

3) Draw a CO2 electrode. How does it work? How is it calibrated? What is the 

relationship between pCO2 and voltage? 


Pharmacology 

1: “Tell me about vecuronium” 

Turned into a comparison with rocuronium, focused on pharmacokinetics especially 

onset speed. Moved into reversal methods. Also discussed antagonism and agonism. 

2: “Draw on concentration-time curve for a single compartment model” 

Discussed time constant, half life, exponential function, then moved to two 

compartment model including equation of it and what could be derived from the 

graph (A, B, compartmental time constants0. 

3. “How do anti-epileptics work?” 

Classify, how and where (on a cellular level) do they work. Any other 

receptors that could be used, started to discuss calcium involvement in nervous 

transmission and potential as a target. Wanted to know any calcium channel blockers 

used in epilepsy. 

Physiology 

1: “What happens if some one breathes 100% oxygen for 5 minutes” 

Led to discussion and manipulation of alveolar gas equation and oxygent 

content equation. Then oxyhaemoglobin dissociation curve. What happens to this 

curve in hyperbaric oxygen? 

2: “Tell me about the pituitary” 

Where is it. Hormones produced and how. How controlled. Where exactly is 

the portal system? What does ADH do? Are renal and peripheral ADH receptors the 

same? 

3: “How does a nerve impulse cause movement?” 


Course 

16


Excitation-contraction coupling. Draw a sarcomere. Where are the t-tubules, 

where is the calcium. What does calcium do? Compare skeletal muscle to cardiac, 

including drawing action potentials. 

Clinical 

83 male, bowel perf, septic, ARF/CRF, hr 120 irregular. 

1: Issues and anaesthetic mangement. 

2: Hypotension interop. 

3: Post op care. Included analgesia. Was not very clear on what was wanted here, 

seemed very diffuse. 


Pharmacology 

1. Muscle relaxant reversals – I talked about anticholinesterases (short, medium & 

long) & Sugammadex. 

2. Anti-emetics – VC & CTZ (all the receptors) & then got asked on 

Metoclopramide, Cyclizine & Ondansetron. Also got asked oculogyric crisis 

which I said I am not sure. 

3. Pharmacokinetics on bioavailability – definition, show on graph, routes of 

administration, first pass metabolism. 

Physiology 

1. Cerebral blood flow – Monro-Kelly doctrine, graphs on CBF v MAP & 

increasing ICP. CPP equation. Management on head injury utilising CPP. 

2. Thyroid gland – hormones produced & how it is regulated. What happens during 

hypothyroidism. Also on parathyroid hormone & calcitonin. 

3. Alveolar gas equation – wanted to know values of normal PAO2, PACO2, PaO2 

& PaCO2. Then how values change in different conditions eg. Increased O2, 

blocked airway. Then the equation and what is the R component. 

Clinical 

Scenario was a 19 year old man fell down the stairs in the nightclub. Brought into 

A&E confused & agitated. 

Asked on: Different diagnosis of altering level of consciousness. What is GCS & the 

components? Management of this patient? Intubate or not? Initial Ix (I said trauma 

series: c-spine, CXR & pelvis), then preparation for CT scan. In CT scan, BP rising 

with decreasing HR. What will I do & what it means? Dosage of Mannitol. How to 

prepare for inter-hospital transfer? 

Physics 

1. Peripheral nerve stimulator – Explain the physics, different types of mode, shown 

on TOF & DBS diagrams (compare & contrast). 

2. Arterial tourniquet – Usage, components of it, duration of inflation, 

complications & contraindications. 

3. Graphs – draw y=mx + c. Draw exponential graph, compare with hyperbolic. 


Course 

17



Pharmacology viva: compare desflurane and isoflurane, isomers, antiplatelet drugs. 

Physiology viva: functions of the heart, reabsorption processes in the PCT, sorry can't 

remember the last one. 

Physics viva : measurement of anaesthetic agents, ultrasound and Doppler, sorry can't 

remember the last one. 

Clinical: 22 yr old with RIF pain, low BP, tachycardic. Discussed differential 

diagnosis, resuscitation, method of anaesthesia. Critical incident: sudden BP drop 

once in theatre. 

Then discussed management of patients who refuse blood transfusion. 


Pharmacology viva 

- isomerism; types and examples. If an example is give is it pure Or racemic? Why is 

isomerism important. 

- anti platelets inc NSAID and Clopidogrel 

- volatiles; compare the structure of des and sevo. Compare thier physical properties 

Physiology viva 

- function of the heart; pump function and frank starling curve, ANP peptide 

production 

- concentrations from the start to the end of the proximal tube of Na, glucose and 

inulin. Not the numbers but how trends change. 

- spinal reflex pathways specifically pain and then questions on pain pathways 

Physics viva 

- ultrasound; uses, modes, resolution vs depth 

- circle system; draw a diagram what is meant by low flow and what are the 

advantages 

- CO2 absorbers; ideal properties (mesh size, air space in the absorber..), what the 

potential problems 


Pharmacology 

Alfentanil vs fentanyl 

Genetics of metabolism 

Antacids 

Physiology 

Renal blood flow 

OxyHb dissociation curve - how much O2 is bound to Hb at diff points 

on the curve? 

Completely forgotten last one 

Physics 


Course 

18


Types of vaporisers and relative advantages/disadvantages 

Methods of measuring O2 in gases including the equations for reactions 

at each electrode in fuel cell and Clark electrode 

Infusion pumps and different types of connector eg Y connector, 

epidural infusion 

Clinical 

71 y/o lady with acute cholecystitis and jaundiced requiring 

laparatomy for ruptured gallbladder 

Causes of hepatitis 

Perioperative management Inc management of sepsis 


Pharmacology 

What are the effects of ketamine? What is in a vial of ketamine? 

Physiology 

What is basal metabolic rate? What factors increase or decrease it? 

What receptors are you aware of? Mode of action, speed of response. 

Nerve action potentials. Define membrane potential. What determines membrane 

potential. What is absolute and relative refractory period? 

Clinical 

You have been asked to see a young male with type 1 DM for an 

appendicectomy. He is pyrexial, vomiting, with a BM of 24. 

How would you approach this patient. Seperated into – initial resuscitation, brief 

pathophysiology of DKA, Tx of DKA, how would you anaesthetise. Critical incident 

– failure to breath post op. (Due to opiate excess) 

Physics 

Electrical symbols – focused of capacitors, uses, what determines charge held 

Vacuum – what is a vacuum? What is a torricelean vacuum? What uses do 

vacuums have? 


physiology - 

1. Nernst equation (specifically looking for the equation) and an explanation of its 

importance and relevance to an action potential 

2. Basal metabolic rate 

3. Alveolar gas equation 

pharmacology - 

1. ketamine 

2. cell membrane receptors 

3. anti-anginals 


Course 

19


Physics - 

1. dead space 

2. electricity 

3. vacuums (specifically looking for an explanation of vacuums in space, torrcellian, 

domestic applicance and medical vacuum/suction) 


Pharmacology 

1. Discuss the properties of the ideal intravenous anaesthetic agent. 

2. Drug metabolism – other than the liver, where else are drugs metabolised? Zero 

and first order kinetics. Give example of drugs that are metabolised in the plasma, 

lungs. 

3. How are anti-arrhythmics classified? Draw the cardiac action potential and describe 

how each drug can affect it. Questions on amiodarone – how does it work, what is its 

volume of distribution and half life, what are its side effects? 

Physiology 

1. Define the term osmolality. What pressure is exerted by a solution of 1osmol? 

Discussion of osmolality of the plasma, including Starling’s forces. 

2. How are gastric secretions regulated? 

3. Diagram of the cardiac cycle and aortic pressure wave– draw on the LV pressure 

wave, RV pressure wave – would the pulmonary valve open before or after the aortic 

valve? Where do the heart sounds occur? 

Physics 

1. The gas laws, clinical applications 

2. LASERs – how they work, safety precautions 

3. ECGs – lead placement, CM5, cardiac axis, filtering, common mode rejection 

Clinical 

A 76 year old is scheduled to have inguinal hernia repair. He had a pacemaker fitted 6 

years ago, smokes 30 cigarettes per day, and weighs 51kg. 

Discuss the issues relating to this man’s anaesthetic 

- emergency vs elective 

- under weight 

- cardiovascular disease 

- likely respiratory disease 

What type of anaesthetic would you choose? 

If you elected to perform the surgery under local with sedation, what sedation would 

you choose? What are the problems of using propofol as a sedative? What are the 

problems with using a benzodiazepine? 

The patient becomes agitated after administration of a benzodiazepine. Discuss the 

reasons this might occur. 


Course 

20



1) Pharmacology 

a) Tell us about Alfentanil and Fentanyl. 

Specifics re Pharmacokinetics - Vd/ t1/2/ Onset etc. 

Differences to Morphine. 

b) Pharmacogenetics - Not well worded questions but discussed MH/ Plasma 

Cholinesterase Deficiency. 

Differences of drug behaviour with age. 

c) Tell us about drugs that affect gastric acid secretion. 

Discussed PPIs, H2 antagonists/ other agents that act on gut. 

2) Physiology - 

a) Shown graph of Oxy-Hb Dissociation curve. 

Asked to talk through and label. 

Discussed what moves the curve/ Why sigmoid shape/ relevance to 

anaesthesia. 

b) What affects Renal function. 

Led into discussing GFR/ affecting factors on GFR/ anatomy of nephron 

and what affects each section. 

c) Shown graph and asked to draw cardiac cycle for left ventricle pressure. 

Discussed dicrotic notch and what affects its position. 

Added on CVP/ ECG. 

3) Clinical - 

a) 71 yr old female, admitted with abdominal pain. Jaundiced. Found to 

have a perforated gallbladder and booked for an emergency laparotomy. ON review 

appears septic. 

Questions on jaundice - causes of each type (pre/ intra/ post etc). 

Features of liver failure - examination/ lab. 

Management of patient - pre optimisation etc. 

Taken to theatre - BP drops and HR increases - causes - differences 

between anaphylaxis, hypovolaemia, sepsis. How would you treat each. 

4) Physics 

a) Vaporisers - types/ safety features/ desflurane vaporiser difference. 

b) Gas measurement techniques. 

Oxygen electrodes - shown pictures of clark and fuel cell and asked to 

describe/ equations. 

Describe mass spectrometry. 

c) Infusion devices - types/ uses/ safety features - shown picture and 

asked to find faults (syringe not properly fitted, occlusions of line etc). 


Course 

21



1. Physiology – Action potentials of ventricular contractile muscle and pacemaker 

cells, ion channels associated with both, effect of adrenaline on the curves. 

2. Pharmacology: Sux apnoea, dibucaine number, genetic changes for SUX apnoea, 

management of SUX apnoea, classification of antihypertensives, mech of 

action of ACE inhibitors, rennin-angiotensin-aldosterone system 

3. Physics: venturi and applications, methods of temp measurement 

Clinical: 36 yr lady for lap cholecystectomy, nausea and vomiting with previous 

gynaecological surgery, mouth opening 2 fingers 


Clinical: 25 year Diabetic coming for Appendicectomy. Temp 38.5 deg celcius, Blood 

glucose 25mmol/L. Pain abdomen and vomiting. Questions: Management, Intraop 

management following optimization; Critical incident: delayed reversal. 

Physics: 1. Dead space - measurement etc. 

2. Electricity - resistor, capacitor, defibrillator. 

3. Vacuum and suction. 

Physio: 1. Effect of breathing 100% O2 for 5 mins - details. Hyperbaric chamber. 

Pharma: 1. Ketamine. 

2. Receptors. 

3. Anti-anginal drugs. 


Pharmacology Viva 

Physiochemical differences between Sevoflurane and Isoflurane (wanted a 

table), some details about desflurane also wanted 

Digoxin-where and when used, structure (I didn’t know this but seemed OK 

when said digitalis derivative), how it worked and dose. 

Pharmacogenetics-I mentioned stuff about fast and slow acetylator status but 

they wanted MH and sux apnoea 

Physiology 

Vomiting-neurotransmittors, structures involved, how vomiting occurs 

Buffers and hendersson haselbalch equation 

Arterial waveform and how differs aorta vs radius 

Cardiac pres volume loop 

Clinical 

65 year old, warfarinied for previous PE (6 months ago), admitted for laprotomy 

for perforated viscus, INR of 5.8, AKI 

Causes of high INR 

Pre-op resuscitation and fluid resuscitation 

‘how long would need to be on ITU for optimisation’ 

How would you anaesthetise 

Causes of intra-op hypoxia and tachycardia 


Course 

22


Wanted me to comment on duration of wafarinisation-should have been 3 

months if PE with cause-might have other pathology 

Physics 

Calibration and graphs, 1 point calibration vs 3 point calibration 

Graphs showing drift and non linearity 

Electrical safety and microshock-what amp causes what, pic of CF equipement 

symbol, and what would 2 lines at each side mean (defib safe) 

Scavenging, active and passive – safe concentrations of agents and nitrous 

Some on resonance and damping-what causes an under an overdamped trace in 

an arterial line. 


Course 

23

Primary FRCA OSCE-SOE exam January 2012 Coventry collection ...

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