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Textbook The Final Frca Structured Oral Examination A Complete Guide 1St Edition Bobby Krishnachetty Ebook All Chapter PDF
Textbook The Final Frca Structured Oral Examination A Complete Guide 1St Edition Bobby Krishnachetty Ebook All Chapter PDF
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The Final
FRCa
Structured Oral examination – a Complete Guide
BOBBy KRiShnaCheTTy
and
DaRShinDeR SeThi
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efforts have been made to publish reliable data and information, neither the author[s] nor the publisher
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The information or guidance contained in this book is intended for use by medical, scientific or health-
care professionals and is provided strictly as a supplement to the medical or other professional’s own
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section 01
clinical Viva 1
01.1 Long case: Epilepsy and learning difficulties 2
01.2 Short case: Complete heart block 7
01.3 Short case: Nutrition in ICU 11
01.4 Short case: Electroconvulsive therapy 14
section 02
clinical Viva 37
02.1 Long case: Foreign body aspiration in a child 38
02.2 Short case: Anaesthesia for lung resection 42
02.3 Short case: Amniotic fluid embolism 45
02.4 Short case: Postoperative eye pain 47
section 03
clinical Viva 65
03.1 Long case: Pregnant woman with diabetic ketoacidosis 66
03.2 Short case: ICU weakness 72
03.3 Short case: Consent issues 75
03.4 Short case: WPW syndrome 78
iii
section 04
clinical Viva 93
04.1 Long case: Guillain Barre syndrome 94
04.2 Short case: Intrauterine fetal death 99
04.3 Short case: Eisenmenger’s syndrome 101
04.4 Short case: Myotonic dystrophy 104
section 05
section 06
iv
section 07
section 08
section 09
section 10
Appendix 1 323
Appendix 2 345
Appendix 3 373
Appendix 4 379
Appendix 5 383
Appendix 6 391
index 399
vi
Justiaan swanevelder
Professor and Head of Department of Anaesthesia
Health Sciences Faculty
University of Cape Town
South Africa
Previous Examiner for Royal College of Anaesthesia Primary and
Final Examinations – 2003–2012
Present Examiner for the Faculty of Anaesthesia,
College of Medicine of South Africa – 2012–present
vii
ix
Francoise Iossifidis
Consultant Anaesthetist
Darent Valley Hospital
xi
xii
First part of the question will be about summarising and discussing the investigation
results. Write down your punchy summary so you have a confident start. Find the abnormal
investigations, think why they are abnormal, derive possible reasons etc. Anaemia is one
such example… almost always expect them to ask you the causes of anaemia if the patient
is anaemic.
Second part would be the anaesthetic management of the patient. Prepare your answers
with the possible headings in mind.
Preoperative
• Is it emergency or urgent… have you got time for preoptimisation?
• Further history and examination
• Investigations
• Preoperative risk stratification and optimisation
• Premedication
Intraoperative
• Preparation
• Senior help
• Monitoring – invasive
• Emergency drugs and equipment
• Induction
• Maintenance
• Emergence
• Analgesia – regional technique
• Antiemesis
• Fluids
• Temperature
• Positioning
Postoperative
• Destination HDU/ITU
• oxygen
• Analgesia
• Antiemesis
• Fluids
• DVT prophylaxis
Third section of the clinical long case viva is about a critical incident whilst in theatre or
recovery – hypoxia, confusion, agitation etc.
xiii
short cases
A mix of obstetric, general, intensive care, and chronic pain cases for just over
20 minutes… and you are done with the clinical viva!
Anatomy
In a 7-minute anatomy viva, 2-3 minutes are given to pure anatomy questions… remember
this is Final FRCA, hence what is important is the application and implications related to
anaesthesia.
The chosen strategy for being successful on applied anatomy is to learn it, one topic a day
and to recite it the next day to someone who will listen.
‘It does not matter how slowly you go so long as you do not stop’
Have a set format to answer some kinds of question. For example – factors affecting blood
flow of any organ the following classification always works.
• Factors inherent to the circulation
• Pressure or myogenic autoregulation
• Chemical/metabolic factors
• Neural factors
• Humoral factors
• others
Determinants of cerebral blood flow are
1. Autoregulation by the myogenic mechanism
2. Chemical/metabolic – o2 and Co2 and local metabolites like prostanoids
3. Neurohumoral – ineffective
4. others – blood viscosity and temperature
I have jotted down the anatomy questions in the order of recurrence. It is wise to look at the
rarities too as ‘the cautious seldom err’.
xiv
Fairly common
Pituitary – hormonal/pressure effects and transsphenoidal surgery
Cervical plexus
Paravertebral space
Liver anatomy – blood supply
Bowel circulation and abdominal compartment syndrome
occasional popups
Bone – for Io circulation
Foetal circulation
Spleen
T10 cross section
Mediastinum
Coeliac plexus
xv
chest X-ray
done two months ago
Fig. 1.1
sleep studies
done two months ago
The polysomnogram demonstrated an apnoea-hypopnoea index (AHI)
of 15 events/hr and a nadir oxygen saturation of 78%; supine AHI was
44 events/hr. Definitive obstructive events were not observed in the non-
supine position. The total sleep time was 337 minutes, with a sleep time
in the supine position of 113 minutes. A 2-minute epoch from the patient’s
polysomnogram is shown in Figure 1.2.
Fig. 1.2
comment on the chest X-ray. obvious abnormality is the presence of a vagal nerve stimulator
• Reduced lung volumes
• Lung fields otherwise clear except haziness in left lower border
• Normal heart borders, borderline cardio thoracic ratio
How does a vagal nerve • Pulse generator/stimulator that sends regular, mild electrical stimuli to the
stimulator work? vagus nerve
• Used in drug-resistant epilepsy, particularly partial seizures and
treatment-resistant depression
• Often not immediately effective and rarely prevents seizures entirely
• Battery-powered so requires changing every 5–10 years
correlate and comment on the • Hypoxaemia, hypercapnia, and polycythemia, related to OSA
ABG and sleep studies result. • Metabolic compensation (chronic disease)
• Apnea/hypopnea index indicates severe OSA
oxygen Desaturation
Desaturations are recorded during polysomnography. Although there are
no generally accepted classifications for severity of oxygen desaturation,
reductions to not less than 90% usually are considered mild. Dips into the
80%–89% range can be considered moderate, and those below 80% are
severe.
Berlin questionnaire
• Patients can be classified into high or low risk based on their responses
to similar questions.
Anaesthetic technique
• Carry-over sedation effects from longer-acting intravenous sedatives and
inhaled anaesthetic agents
• Use propofol/remifentanil for maintenance of anaesthesia
• Use insoluble potent anaesthetic agents (desflurane, sevoflurane)
• Use regional blocks as a sole anaesthetic technique (not in this case!)
Monitoring
• Use intraoperative capnography for monitoring of respiration (mandatory
anyway!)
• Arterial line if OSA associated with cardiac dysfunction
Postoperative period
• Verification of full reversal of neuromuscular blockade
• Ensure patient fully conscious and cooperative prior to extubation
• Non-supine posture for extubation and recovery
• Resume use of positive airway pressure device with close monitoring
post-operatively
• May require HDU/ITU admission
Fig. 1.3
What does the ecG show? • Regular P waves and QRS complexes are seen but are unrelated to
each other
• No QRS widening
• Voltage criteria for LVH
• No obvious features of coronary ischaemia
The ECG shows third-degree AV block, with a ventricular rate of 34/min.
Would you anaesthetise No. Patient is at high risk of severe peri-operative bradycardia leading to
him now? cardiac decompensation, or even cardiac arrest.
• He requires referral to a cardiologist, and probably electrical pacing,
ideally with a permanent pacemaker.
• Further cardiac investigations to determine the cause (e.g. angiogram)
and to establish his baseline cardiac function (e.g. echocardiogram)
would also be helpful.
• If the surgery is deemed too urgent to wait for further investigation and
PPM implantation, other options include a temporary pacing wire, or
pharmacological chronotropy via an isoprenaline infusion.
How would you manage this if Ask surgeons to stop, check correct attachment of monitoring, and feel for
it occurred intraoperatively? a pulse.
If there is no pulse palpable, start CPR and then treat the underlying
problem.
Pharmacological options
• Trial of antimuscarinic drugs (e.g. atropine or glycopyrollate)
• Carefully titrated adrenaline boluses (10–100 mcg)
• Isoprenaline infusion (β-agonist): 0.02–0.2 mcg/kg/min
Electrical/mechanical options
• Percussion pacing using a clenched fist (rarely achieves electrical
capture)
• Transcutaneous external pacing via defibrillator pads; increase current
until electrical capture achieved. Set rate at 70–80 bpm
• If pharmacological measures fail to restore an adequate heart rate,
a temporary pacing wire (inserted via a central line) will probably be
necessary, but this takes time to organise (and should be done under
aseptic conditions by an appropriately trained cardiologist under X-ray
guidance)
• Transoesophageal pacing is also possible but similarly requires specialist
equipment and expertise to set up
What are the indications for • Any symptomatic bradycardia (i.e. causing collapse/syncope/presyncope)
insertion of a permanent • Complete heart block
pacemaker? • Mobitz type II block
• Sick sinus syndrome
• Hypersensitive carotid sinus syndrome
• Symptomatic bradycardia in transplanted heart
• Severe heart failure (cardiac resynchronisation therapy)
• Some patients with dilated or hypertrophic cardiomyopathy
… And for temporary pacing? All of the above indications for permanent pacemaker insertion are also
indications for temporary pacing in an emergency situation (or if a permanent
pacemaker is unavailable/contraindicated (e.g. systemic sepsis).
• Acute myocardial infarction causing asystole/bradyarrhythmia that entails
haemodynamic compromise
• Drug overdose (e.g. β-blockers, calcium channel blockers, digoxin)
• Surgery/general anaesthesia for patients with stable heart block not
causing haemodynamic compromise but potentially at risk of worsening
bradycardia/asystole
• Following cardiac surgery (usually involves placement of epicardial
pacing wires, rather than transvenous pacing wire, at end of surgery by
surgeons)
What do you want to know Preoperative assessment should be aimed at finding answers to the
before anaesthetising a following questions:
patient with a PPM? • Indication of pacemaker insertion
• Check date (Does it need checking again before theatre?)
• Is the patient pacing dependent?
• Type of PPM (unipolar/bipolar, number of leads, biventricular/
univentricular, etc)
• Programmed mode
Investigations/preparation
• All patients should have CXR (to show PPM position and number
of leads)
• ECG: look for pacing spikes before each QRS to determine whether
pacing-dependent
• Correction of any electrolyte abnormalities (which may cause loss of
capture)
• Switched to fixed rate mode if necessary
• PPM check if any doubts re: function/battery life/failure of capture, etc.
• May need to arrange cardiac-monitored bed post-op (plus another
PPM check)
What hazards arise in theatre • Electromagnetic interference (mainly from monopolar diathermy) may
in patients with a PPM? reprogram the PPM (usually into a fixed rate back-up mode) or inhibit
pacing inappropriately. To reduce the risk of PPM malfunction, use
bipolar diathermy. If monopolar diathermy is unavoidable, the pad should
be placed as far as possible from PPM; diathermy current should flow
perpendicular to PPM current.
• Patient shivering, fasciculations following suxamethonium, and sources
of vibration may cause inappropriate ‘sensing,’ which will inhibit pacing or
rate modulation (if not previously switched to fixed rate mode).
• PPM may be dislodged during patient positioning or CVP line insertion.
• Theoretical risk of microshock via PPM lead, which may induce
arrhythmia.
• All PPM-dependent patients are at risk of asystole or bradyarrhythmias if
the PPM fails for any reason. Emergency drugs and pacing facilities (as
discussed above) should therefore be readily available.
10
Fig. 1.4
comment on the most obvious Nasogastric tube is above the diaphragm and follows the course of the right
finding in the film. lower lobe bronchus.
How can the tube position national Patient safety Agency alert/nice guideline
be confirmed? • Use pH paper.
° pH < 5.5 indicates gastric placement.
11
What are the normal nutrition Measuring energy use requires sophisticated equipment, so nutrition
requirements for a healthy requirements are estimated using formulae.
person?
The Harris Benedict Equation estimates basal metabolic rate (BMR) in kcal/day.
In men: BMR = 13.75 × weight (kg) + 5 × height (cm) − 6.78 × age (years)
+ 66
For women: BMR = 9.56 × weight (kg) + 1.85 × height (cm) − 4.68 × age
(years) + 655
For an afebrile healthy individual, this is around 25 kcal/kg/day.
Conditions such as fever, sepsis, surgery, and burns increase the
requirements.
european society of Parenteral and enteral nutrition (esPen)
The total energy requirements of critically ill patients are given in recent
guidelines issued by the ESPEN in 2006.
• Acute initial phase of critical illness: 20–25 kcal/kg/day
• Recovery/anabolic phase: 25–30 kcal/kg/day
• Protein around 1.5 g/kg/day (2g/kg/day in severely catabolic patients).
• lipid should be limited to 40% of total calories.
• Carbohydrate makes up the remaining calorie requirements.
Glutamine, arginine, fish oils, and ribonucleotides; antioxidants including
Vitamins C and E; selenium and other trace elements are considered useful
for immunonutrition.
Sodium 1.0–2.0 mmol/kg/day
Potassium 0.7–1.0 mmol/kg/day
Calcium 0.1 mmol/kg/day
Magnesium 0.1 mmol/kg/day
Chloride 1–2 mmol/kg/day
Phosphate 0.4 mmol/kg/day
Define malnutrition. Malnutrition is the condition that develops when the body does not get the
right amount of vitamins, minerals, and other nutrients it needs to maintain
healthy tissues and organ function.
Patient has been on ITU for 5 days and has not been fed.
What is he at risk of? Malnutrition is associated with increased morbidity and mortality.
• Increased risk of infection and pulmonary oedema
• Reduced ventilatory drive
• Impaired production of surfactant
• Prolonged weaning due to muscle fatigue
• Impaired wound healing
• Delayed mobilisation resulting from weak muscles
12