Ealing Paces Revision Guide

MRCP (UK)
EXAM PREPARATION GUIDE
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Contents
Welcome to Ealing PACES ..................................................................................................................... 4
Exam Outline......................................................................................................................................... 5
Course Structure ................................................................................................................................... 8
Course Timetable .................................................................................................................................. 9
The individual colour-coded groups will rotate through stations A-G as follows: ............................... 9
Station 1: The Respiratory System ...................................................................................................... 10
1. Most Common Cases .................................................................................................................. 10
2. Inspections and Observation ...................................................................................................... 10
3. Respiratory Examination of the Chest ........................................................................................ 12
4. Key Diagnostic Test ..................................................................................................................... 12
5. Management............................................................................................................................... 14
6. Presentation................................................................................................................................ 19
Station 1: Abdominal System .............................................................................................................. 20
2. General Inspection ...................................................................................................................... 20
3. Common Differential Diagnoses ................................................................................................. 21
4. Presentation................................................................................................................................ 22
Station 2: History-Taking Skills ............................................................................................................ 23
2. Introduction ................................................................................................................................ 23
3. Interview Structure ..................................................................................................................... 24
4. Presentation................................................................................................................................ 25
Station 3: Neurology & Cardiovascular Stations ................................................................................. 26
2. Introduction ................................................................................................................................ 26
3. Cranial Nerves ............................................................................................................................. 27
4. Speech Examination.................................................................................................................... 33
5. Presentation................................................................................................................................ 38
Station 4: Cardiovascular .................................................................................................................... 39
2|Page MRCP – REVISION COURSE

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2. General Approach ....................................................................................................................... 39
3. Strategy for Examination ............................................................................................................ 39
4. Introduction ................................................................................................................................ 40
5. General Inspection ...................................................................................................................... 40
6. Presentation................................................................................................................................ 46
Station 4: Communication Skills & Ethics ........................................................................................... 47
2. Format of Station ........................................................................................................................ 48
3. How to Conduct the Interview.................................................................................................... 48
4. Driving Regulations ..................................................................................................................... 49
5. Consent ....................................................................................................................................... 50
6. Criteria for Brainstem Death ....................................................................................................... 51
7. How to Pass the Ethics Station ................................................................................................... 51
Station 5: Integrated Clinical Assessment .......................................................................................... 52
1. Ophthalmology Station ............................................................................................................... 52
2. Endocrinology Station ................................................................................................................. 58
3. Dermatology & Rheumatology Stations ..................................................................................... 61
Contributing Authors .......................................................................................................................... 67
Appendix – Mark Sheets ..................................................................................................................... 68

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Welcome to Ealing PACES
The Ealing PACES MRCP course has been running since 1992 and is the leading course in the
country. You will have the opportunity to see over 80 system examinations (short cases), as
well as receive advice on examination technique and skills for the exam.
This guide has been written by our highly experienced teachers to help you prepare in
advance for the course and your exam. Please read thoroughly as part of your preparation.
Getting there:
By public transport: For details on how to get here, please visit either
journeyplanner.tfl.gov.uk (TFL) or http://www.lnwh.nhs.uk (Ealing Hospital).
By car: Please follow the ‘Ealing PACES MRCP Car Park’ signs, which are clearly displayed up on
entering the hospital grounds. The free parking allocated for you is shown by the X on the
map. Follow the road coloured red and leave your car anywhere within the parking area
coloured orange. No parking ticket or pass is needed. Walk back along the way you drove in to
the main entrance of the building.
On arriving at the building’s main entrance: Follow the signs marked ‘Ealing PACES MRCP
Registration’, which will be in the lecture theatre on the third floor.
If you need to get in touch with one of the co-ordinators on the day, please call 020 3330
0031.
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Exam Outline
Before attending the Ealing PACES Course, it is essential that you have a detailed
understanding of the MRCP UK exam and marking scheme.
The MRCP (UK) PACES website has video demonstrations that are worth watching before you
attend www.mrcpuk.org/PACES/Pages/CandidateVideo.aspx.
In addition you should review the following exam outline:
Station 1 Respiratory System Examination (10 minutes)

Examination of the Abdomen (10 minutes)
Make sure that you have thoroughly revised your examination skills so that you can perform both
of these examinations in 6 minutes, giving yourself a further 4 minutes to present your findings and
discuss the differential diagnoses with the examiners.
Station 2 History-Taking Skills (20 minutes)
The history-taking skills station aims to assess your ability to gather data from the patient,
construct a differential diagnosis, deal with concerns the patient may have, construct a
management plan that is explained to the patient clearly and treat the patient with dignity and
respect. Instructions for the case are given to the candidate during the 5-minute interval before the
station, usually in the form of a letter from the patient's GP. 14 minutes are allowed for the history-
taking, followed by a 1-minute period of reflection, followed by 5 minutes for discussion with the
examiners.
Station 3 Cardiovascular (10 minutes)

Neurology (10 minutes)
You should make sure that you can examine the entire cardiovascular system and each part of the
neurological system in 6 minutes, giving yourself 4 minutes for “discussion”. There are stations
dedicated to cardiovascular and neurological examinations and, to get the most out of these, you
need to arrive already knowing how to examine each of these systems.
Station 4 Communication Skills and Ethics (20 minutes)
The communication skills and ethics station aims to assess your ability to guide and organise the
interview with the subject (who may be a patient, relative, or surrogate, such as a healthcare
worker), explain clinical information, apply clinical knowledge, including knowledge of ethics, to the
management of the case or situation, provide emotional support and treat the patient with dignity
and respect.
Instructions for the case are given to the candidate during the 5-minute interval before this station
with two examiners present throughout. Fourteen minutes are allowed for the patient interaction,
followed by 1 minute to reflect, followed by 5 minutes for discussion (after the patient has left the
station).
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Station 5 The Integrated Clinical Assessment 1 (10 minutes)
The Integrated Clinical Assessment 2 (10 minutes)
This station is the one that has worried candidates most, but for the well prepared, it is a gift. The
idea is to mimic a typical 8-minute outpatient consultation, including a possible examination.
Although any examination can come up, it transpires that cases with rheumatological,
dermatological, endocrine and ophthalmological diseases come up most often. A brief examination
is thus possible in patients with arthritis, and the case may go on to discuss the management of the
patient, including new drugs.
It is thus worthwhile spending a short time making sure you are up to date on the following
conditions:
 Psoriasis
 Eczema
 Thyroid lumps and Graves’ disease
 Acromegaly
 Cushing’s syndrome
 Osteoarthritis
 Rheumatoid arthritis
 Diabetic retinopathy, including the step up of treatment of poorly controlled type 2
diabetes, where worsening eye disease suggests that control is poor.

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Course Structure
The Ealing PACES course has been carefully designed to prepare you for the MRCP (UK) Examination.
Over the weekend you will see a wide variety of typical exam cases and be taught and assisted by a
team of highly experienced teachers.
The course is structured into seven distinct stations, each lasting one hour:
Station A Exam Station 1 Mainly respiratory and abdominal cases
Station B Exam Station 2 History-taking
Station C Exam Station 3 Mainly cardiovascular
Station D Exam Stations 3 & 5 Short cases in skin, locomotor, cardiovascular and neurology
Station E Exam Station 4 Communication skills
Station F Exam Station 3 Mainly neurological short cases
Station G Exam station 5 Eyes, endocrine, neurology and short cases, which in the
current exam has two 10-minute Stations.
Before attending, please read through the above details, and practice your examination skills. We
look forward to seeing you on the course.

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Course Timetable
Saturday
08:00 – Registration
08:30 – Introductory clinical lecture by Course Director Professor Karim Meeran
09:15 – Helpers will direct you to your first station based on your coloured badge
Sunday
There is no lecture on Sunday. Please arrive at 9.00am to start at the relevant station for 9.20am.
On both days the sessions each last an hour and the timings are:
Session
9.20 1
10.20 2
11.20 Refreshments
11.35 3
12.35 4
1.35 Lunch
2.15 5
3.15 6
4.15 Refreshments
4.30 7
5.30 Close
The individual colour-coded groups will rotate through stations A-G as follows:
Session
1 2 3 4 5 6 7
Blue A B C D E F G
Pink B C D E F G A
Red C D E F G A B
Green D E F G A B C
Yellow E F G A B C D
White F G A B C D E
Orange G A B C D E F

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Adhering to timescales will benefit both yourself and your fellow candidates. Staff will identify
when a session changeover is about to happen.
Station 1: The Respiratory System

(10 minutes)
1. Most Common Cases
 Interstitial lung disease (fibrosing alveolitis)

 Pleural effusion
 Chronic bronchitis and emphysema
 Pneumonectomy/lobectomy
 Dullness at the lung bases
 Rheumatoid lung
 Bronchiectasis
 Old tuberculosis
 Yellow nail syndrome
 Chest infection/pneumonia
 Kyphoscoliosis
2. Inspections and Observation
Before doing anything else take a moment to look around the bedside to look for helpful clues.
2.1 Environment
Look around the patient area, specifically note if any of the following are present:
 Inhalers, nebulisers: Suggestive of obstructive airways disease.

 Sputum pot: If a large volume of sputum, does the patient have bronchiectasis?
 Oxygen cylinders/concentrators – this instantly tells you that the respiratory condition is so
severe that the patient has significant chronic respiratory failure/hypoxia.
 CPAP or BiPAP machine. Home CPAP implies OSA. Home BiPAP is suggestive of a ventilation
problem like a neuromuscular disorder, or obesity hypoventilation syndrome.
2.2 Expose the patient
 Respiratory pattern and rate: Is the patient breathless at rest? Are they breathing through
pursed lips? A prolonged expiratory time is suggestive of obstructive lung disease.
 Nutritional status
 Chest expansion:
- Is there any obvious asymmetry? The side with reduced chest expansion is likely to be the
side with the pathology.
10 | P a g e MRCP – REVISION COURSE
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- Is the thorax hyper-inflated with decreased expansion? – highly suggestive of an
obstructive pathology with significant air-trapping.
- Is there any deformity of the chest wall?
2.3 Surgical scars for the physician
While thoracic scars are largely the domain of the surgeon, they often provide a valuable clue to
the underlying medical pathology. For this reason YOU MUST FULLY EXPOSE THE PATIENT AND
INSPECT THE BACK AND UNDER THE ARMS. If you fail to fully expose the patient you will risk
missing important signs.
 Thoracotomy scars: Very important but easily missed. Can be anterolateral or posterolateral.
You will have to ensure that the patient is fully exposed and inspect the back to ensure that you
don’t miss these scars. Typical operations, wedge resections, lobectomy, pneumonectomy,
decortication, single lung transplant.
 Bilateral anterolateral thoracotomy combined with transverse sternotomy – aka The Clam shell:
This will look like bilateral thoracotomy scars that meet in the middle over the sternum. This
incision is often used for bilateral lung transplants, but also for other procedures that require
access to the thorax.
 Chest drain scars: Easily missed, look in the triangle of safety (under the axilla between the
pectoralis and lat dorsi muscles. Implies previous pleural effusions or pneumothorax.
 VATS (video-assisted thoracoscopic surgery) scars: Indistinguishable from a chest drain scar. If
you suspect that pulmonary fibrosis is on the differential diagnosis, then the patient may have
undergone a VATS lung biopsy to get a tissue diagnosis. Also used for pleural biopsies,
decortication, pleurodesis.
 Tracheostomy scars: Imply previous invasive ventilation on the intensive care unit.
 Mediastinoscopy scars: A horizontal scar about 1 cm above the sternal notch, very easily
mistaken for a tracheostomy scar. Used for the investigation of mediastinal lymphadenopathy.
e.g. Sarcoid, TB, lymphoma, staging of primary lung cancer.
 Thoracoplasty: Will be obvious, with marked thoracic asymmetry, deformity and a thoracotomy
scar. Some ribs may be missing. A treatment for TB before current therapies were available.
Rarely performed for severe pleural infections.
 Phrenic nerve crush scars: A small scar seen in the supraclavicular fossa, an old treatment for TB
– A few patients with these scars can still be found. The patient may have reduced air entry on
the base of the affected side.
2.4 Other markings
 Radiotherapy tattoos: Can be easily missed, but will tell you that the patient has had
radiotherapy for a thoracic malignancy.
 The hands
 The face

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 The JVP and peripheral oedema (cor pulmonale is an important finding suggestive of severe
respiratory disease).
Then proceed with the respiratory examination of the chest.
3. Respiratory Examination of the Chest
 Closer inspection of the thorax

 Chest expansion
 Percussion
 Auscultation
 You can test for either vocal resonance or tactile vocal fremitus if you believe clinically
indicated.
 Thank the patient and offer assistance to re-dress before turning to the examiner and offering
to present your case.
The patient with bibasal creps:
 If you hear bilateral creps, think of two diagnoses: pulmonary fibrosis or bronchiectasis.
 If you see a VATS scar with fine creps, the favoured diagnosis is pulmonary fibrosis/diffuse
Interstitial lung disease.
 If you hear coarse creps, with a sputum pot at the bedside, the favoured diagnosis is
bronchiectasis.
The patient with an area of dullness to percussion:
 Dullness to percussion + increased vocal resonance + bronchial breathing = consolidated lung.
4. Key Diagnostic Test
4.1 Pulmonary function tests
 Standard spirometry for all: This usually includes an FEV1 and FVC and it is a pre-requisite to
differentiate between obstructive and restrictive pathologies. Bronchodilator reversibility
testing and PEFR diaries are simple tests that can help distinguish between asthma and COPD.
 Transfer factors: Will tell you about a problem with gas exchange and will often be low in diffuse
interstitial lung disease.
 6-minute walk tests: A good way of establishing functional status and holds prognostic value.
 Inspiratory muscle testing and cough PEFR: Can be important in patients with neuromuscular
weakness who are at risk of developing chronic respiratory failure.
4.2 Imaging

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 Standard CT Thorax: Will demonstrate mass lesions and lymph nodes, will not reliably detect
interstitial lung disease or bronchiectasis.
 HRCT: will demonstrate interstitial lung diseases and bronchiectasis. It will not reliably
evaluate lymphadenopathy or a mass lesion.

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4.3 Other tests
 Sputum samples. NEVER FORGET to send the sputum for microscopy, culture and sensitivity.
Ziehl-Neelsen stains to look for acid fast bacilli are required when you suspect active
pulmonary TB infection.
 Tuberculin skin tests: The Mantoux test is useful for identifying those who have been in
contact with tuberculosis. It is most useful for contact tracing and diagnosing latent TB.
Interferon-Gamma release assays (IGRAs – like ELISPOT or QuantiFERON-TB Glod tests) have a
similar role to tuberculin skin tests, and are often used in combination with the Mantoux to
screen for TB contacts or latent TB.
 Bronchoscopy: One of the most common tests in the evaluation of a possible lung cancer.
Frequently performed in cases of atypical infections, TB, etc. Sometimes performed in the
work up of ILD. Also starting to develop an interventional role.
Bronchoscopic transbronchial lung biopsies are occasionally helpful in the investigation of some
interstitial diseases, particularly if Sarcoid is suspected.
Endobronchial Ultrasound (EBUS) is a method of sampling mediastinal lymph nodes in cases of

suspected cancer or TB.
 Lung biopsy: If ILD is suspected, the patient will often require an open lung biopsy, this can
often be achieved via a VATS procedure. CT Guided biopsies are only useful for peripheral
pulmonary lesions to exclude neoplasm.
 Allergy Testing: Commonly with simple skin-prick testing. Consider in the atopic individual.
5. Management
It is not possible to cover the management of every respiratory diagnosis that you may see in your
PACES exam. However, it is usual to consider the following basic principles when you try to
construct your presentation.
5.1 Smoking cessation
Smoking will worsen any pulmonary pathology, and cessation should obviously be encouraged at
every opportunity. You should be able to comment on dedicated cessation services and helplines
combined with specific pharmacological therapy such as Nicotine replacement and Champix
(varenicline).

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5.2 Bronchodilators and steroids
Inhaled bronchodilators are broken down into the following categories:
 SABAs: Short acting beta agonists (e.g. Salbutamol) - The first-line bronchodilator in any
obstructive airways disease
 LABAs: Long acting beta agonists (e.g. Salmeterol or Formeterol) - Usually introduced at step 3
in the treatment of asthma. Often used in a combined inhaler with a corticosteroid.
 SAMA: Short acting muscarinic antagonists (e.g Atrovent/Ipratropium) - Rarely used as an
inhaler since the development of LAMAs, now only really used as a nebuliser during acute
exacerbations.
 LAMA: Long acting muscarinic antagonists (e.g. Tiotropium/Spiriva) - Primarily used in the
chronic management of COPD. Not routinely used in asthma. Rarely/occasionally used for
asthma in refractory cases.
 Theophyllines: Usually introduced in cases that are refractory to inhaled therapy.
 Leukotriene receptor antagonists: (e.g. Singulair/Montelukast) - Particularly helpful in
asthmatics with nasal symptoms/allergic rhinitis. Not used in COPD.
Inhaled steroids are frequently used in the management of asthma and COPD.
Systemic steroids are generally reserved for acute exacerbations of airways disease, or sometimes
in the long-term management of refractory disease.
Systemic steroids +/- steroid sparing agents have a role in the chronic management of selected
interstitial diseases (e.g. selected cases of sarcoidosis). Always consider PPI/bisphosphonate
prophylaxis.
It would be unwise to spend too much time talking about the different inhalers and
bronchodilators that are available. You should be able to explain that in the context of obstructive
airways disease, bronchodilators are introduced in a step-wise fashion (as per the British Thoracic
Society Guidelines):
 Asthma Guidelines
www.brit-thoracic.org.uk/Portals/0/Guidelines/AsthmaGuidelines/qrg101 2011.pdf
 COPD Guidelines
guidance.nice.org.uk/CG101

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5.3 Physiotherapy
Physio is very useful for teaching the patient sputum clearance techniques and postural drainage in
cases of bronchiectasis or cystic fibrosis. It also has a role in helping patients achieve better control
over their breathing. There is good evidence that pulmonary rehab can improve both symptoms
and functional status in COPD, and it is probably helpful in many respiratory conditions. Beyond
the exercise training, most pulmonary rehab programmes will also aim to provide both educational
and psychosocial support to their patients.
5.4 Antibiotic therapy
It is unlikely that acute infections will feature in a PACES setting.
Long term/prophylactic antibiotics do have a role in bronchiectasis where patients are suffering
from very frequent exacerbations. A typical regimen might include azithromycin 250-500mg three
times/week. The role for long-term antibiotics in other conditions is less clear. COPD patients are
more likely to be provided with a “rescue pack” of antibiotics and steroids for the next
exacerbation, in the hope that prompt treatment may prevent further hospital admissions.
Long-term nebulised antibiotics have a role in the management of CF, particularly when colonised
with pseudomonas. Some centres will adopt a similar approach for non-CF bronchiectasis, but the
evidence is limited.
TB therapy: Old TB is a common case for PACES, and the candidate would be expected to comment
on a typical regimen for simple pulmonary TB. The candidate should be able to counsel a patient
on therapy, including side effects. You should also be able to discuss the usual diagnostic tests, the
need for contact tracing, HIV testing, and when to isolate a patient.
Expand on isolation, 2 lines and ref to guidelines.
The majority of patients with TB can be safely isolated in the community. They do not need
admission to hospital. After admission, patients who are smear positive should be isolated for 2
weeks. For further information, see the guidelines.
A typical regimen for fully sensitive pulmonary tuberculosis is below. The most common side
effects are also listed below, and the patient should be counselled on these possible side effects
before the initiation of therapy.
Rifampicin: 6 months
 Hepatotoxicity, P450 enzyme induction (often has a major impact on drug interactions),
orange-red discoloration of all bodily fluids.
Isoniazid: 6 months
 Hepatotoxicity, peripheral neuropathy, Vit B6 depletion.

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Ethambutol: 2 months
 Optic neuritis/colour blindness
Pyrazinamide: 2 months
 Hepatotoxicity, arthralgia.
Pyridoxine
 No anti-TB activity, co-administered with Isoniazid to counteract risk of peripheral
neuropathy/B6 deficiency.
Gastro-intestinal symptoms are also common when on all of the above drugs.
It is routine practice to regularly monitor blood tests while on anti-TB therapy, with particular
attention to the LFTs. More information can be found at the following resource:
www.nice.org.uk/nicemedia/pdf/CG33quickreffguide.pdf
5.5 MDT involvement and palliation
Advanced planning and symptom control is an important part of treatment in advanced respiratory
disease, and it is often neglected in non-cancer diagnoses. Many cases of suspected cancer, and all
cases of proven cancer should be discussed in an MDT meeting. The respiratory MDT will often
guide the treatment of many other conditions (e.g. diffuse Interstitial lung disease).
5.6 Long-term oxygen therapy (LTOT)
LTOT is often prescribed for individuals with chronic respiratory failure, typically with a PaO2
<7.3kPa, or a PaO2 between 7.3kPa – 8kPa with coexisting polycythaemia or pulmonary artery
hypertension. Once prescribed, it is usually worn for at least 15 hours/day. Guidelines on the use
of LTOT are found on the following link:
www.brit-thoracic.org.uk/Delivery-of-Respiratory-Care/Oxygen-Use-in-the-Home.aspx
5.7 Long-term ventilator support
The emergency use of CPAP and BiPAP will not be discussed here.
Strictly speaking, non-invasive CPAP (Continuous Positive Airway Pressure) does not offer support
for ventilation. In obstructive sleep apnoea, CPAP acts as a “splint” that will prevent the upper
airways from collapsing during the night. Beyond keeping the airways open, it does not offer any
further assistance to the process of ventilation (i.e. moving air in and out of the thorax).
The most common mode of providing long-term ventilation is through non-invasive BiPAP (Bilevel
Positive Airway Pressure) via a tight-fitting mask.
Nocturnal NIV/BiPAP is becoming increasingly common, particularly in conditions like obesity

hypoventilation syndrome. Long-term NIV/BiPAP for COPD with chronic type 2 respiratory failure is
GUIDE
controversial. BiPAP for COPD is used in some centres as there is some evidence to say that it is of
benefit, but this has not been universally adopted at this time. Another common indication of long-
term ventilation is chronic neuromuscular weakness, but this will always be under the supervision
of a specialist centre.
There are many different methods of supporting a patient’s ventilation, and this topic is beyond the
scope of this text. It will be sufficient to have a basic awareness of the most common indications
for long-term ventilation.
5.8 Pleural Interventions
Patients with lung cancer may often suffer with recurrent pleural effusions. These are often
managed with a VATS procedure with a pleurodesis, but if the patient is too frail for theatre it is
possible to perform a medical pleurodesis on the ward. Alternatively patients with recurrent
symptomatic pleural effusions can be managed with a long-term tunnelled pleural drain.
5.9 Bronchoscopic Intervention
Interventional bronchoscopy is available in a number of centres. The main indication is to relieve

endobronchial occlusion from a malignancy, through the use of cryotherapy, or stents. Some
centres are placing endobronchial valves as an alternative to lung reduction surgery for COPD, but
this is beyond the scope of the PACES exam and confined to a few specialist centres at this time.
6. Presentation
Dullness to percussion + decreased vocal resonance + reduced air entry = pleural effusion or
pleural thickening
Having spent about 6 minutes examining the patient, you then have 4 minutes to summarise your
findings and discuss a management plan with your examiner.

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Station 1: Abdominal System
(10 minutes)
 Polycystic kidneys
 Transplanted kidney
 Chronic liver disease
 Hepatosplenamegaly
 Splenomegaly
 Hepatomegaly
 Ascites
 Abdominal mass
 Hepatomegaly
 Polycythemia rubra vera
 Hepatomegaly
2. General Inspection
2.1 Examination of the hands
The patient in the abdominal station will often either have chronic liver disease or end-stage renal
disease. Occasionally patients with hepatosplenomegaly due to haematological conditions also
appear in this station.
The signs of chronic liver disease in the hands include:
 Asterixis (liver flap)

 Bruising
 Clubbing
 Dupuytren’s contracture
 Erythema (palmar)
Don’t forget to inspect the forearm for AV fistulae (evidence of current or previous renal
replacement therapy).
2.2 Examination of head and neck
Examine the Eyes: for evidence of anaemia; look under the upper eyelid for subtle conjunctival
icterus (jaundice).
Skin: Is there evidence of jaundice or spider naevi?

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Oral examination: Is there evidence of pigmentation? Don’t forget to inspect the gums. (Gum
hypertrophy may be seen in patients who have been on ciclosporine after renal transplant.)
It is best to leave examination of the neck (and axillae) for lymphadenopathy to the end. This will
give you some time to collect your thoughts about your findings before you present to the
examiner!
2.3 Inspection of the chest
Is there evidence of gynaecomastia or hair loss (signs of chronic liver disease)?
2.4 Examination of the abdomen
 Inspection: Are there scars? Is there abdominal distension?

 Initial palpation: You should be able to easily flex the joints in your hand as you palpate. If you
feel that you can’t flex your fingers easily in a particular quadrant, suspect a mass underneath.
 Palpation and percussion: For organomegaly (liver, spleen, kidneys, bladder)
 Percussion: For shifting dullness (evidence of ascites)
 Auscultation: For bowel sounds, bruits
3. Common Differential Diagnoses
3.1 Ascites
Transudate
 Cirrhosis
 Cardiac failure, constrictive pericarditis
 Nephrotic syndrome, renal failure
Exudate
 Malignancy (abdominal, pelvic, peritoneal mesothelioma)

 Infection: e.g. TB, pyogenic
 Pancreatitis
 Budd–Chiari syndrome (hepatic vein obstruction), portal vein thrombosis
 Chylous ascites: obstruction of lymphatics, e.g. surgery, lymphoma
 (Characterized by increased triglyceride level)
 Haemorrhagic ascites: tumour, trauma, acute pancreatitis

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3.2 Hepatomegaly
 Cancer: (primary or secondary deposits)

 Cirrhosis: (early) usually alcoholic, primary biliary cirrhosis
 Congestive cardiac failure
 Budd–Chiari: (hepatic vein thrombosis)
 Polycystic liver disease
 Infections: hepatitis A, B, C, EBV, CMV, toxoplasmosis, leptospirosis, abscess
 (amoebic, pyogenic), hydatid cyst
 Infiltration: fatty infiltration (alcohol), haemochromatosis, amyloidosis,
 sarcoidosis, lymphoproliferative diseases
 Apparent hepatomegaly: lowered diaphragm (e.g. in COPD)
3.3. Splenomegaly
Portal hypertension (Are there signs of chronic liver disease?)
Haematological: Myeloproliferative disorders (chronic myeloid leukaemia, myelofibrosis,

polycythaemia rubra vera, essential thrombocythaemia), lymphoma, leukaemia, haemolytic
anaemia
Infections: Infective endocarditis, infectious mononucleosis, tuberculosis, brucellosis, malaria,

leishmaniasis, schistosomiasis
Inflammatory/connective tissue diseases/infiltration: Rheumatoid arthritis, SLE, sarcoidosis,

amyloidosis, Gaucher’s disease
3.4 Enlarged Kidney
 Cystic kidney
 Carcinoma
 Hydronephrosis
 Pyonephrosis
 Hypertrophy (following contralateral nephrectomy)
 Perirenal haematoma
 Congenital anomaly
4. Presentation
Having spent about 6 minutes examining the patient, you then have 4 minutes to summarise your
findings and discuss a management plan with your examiner.

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Station 2: History-Taking Skills
(20 minutes)
 Abdominal swelling
 Ankle swelling
 Asymptomatic hypertension
 Back pain
 Breathlessness
 Burning of the feet
 Chest pain
 Cold and painful fingers
 Collapse? Cause
 Confusion
2. Introduction
The history-taking station is an important station. It lasts twice as long as most of the other
stations. It is easy to become complacent about this station as history-taking is something that we
do every day but it is easy to underperform on this station if you are not adequately prepared.
2.1 Exam Format
There is a 5-minute rest break before this station. During this rest break, you will be able to read
the scenario that you are about to encounter. You will usually be asked not to write on the
instruction sheet outside the room and there is a separate copy of the instruction sheet inside the
room. When you enter the room, you will have 20 minutes: 14 minutes to talk to the patient (with
a “two minutes left” warning after 12 minutes), 1 minute in silence to gather your thoughts, and
then 5 minutes of questioning from the examiners.
2.2 Ealing PACES Format
We will have a one-hour per day teaching session on history-taking on the course. This teaching
session is carried out in small groups with 3 candidates per instructor. The instructor will aim to get
you to take a full history, ask you some questions in the style of the examiner, and then give you
some feedback within the space of 20 minutes. In the interests of time, we are not going to give
you 5 minutes for preparation beforehand and we will skip your minute of silence. You will hear
some knocking on the door of the room you are in. This is deliberate – it is the course co-ordinators
signalling to the instructors that 12 minutes and then 20 minutes have elapsed.

GUIDE
3. Interview Structure
 Introduce yourself clearly and confidently to the patient.

 Check you have the right patient (their name and age is on the instruction sheet).
 Start with some open questions, e.g. “I understand you have been sent to me because of
shortness of breath. Could you tell me more about this?”
 Wait until the patient has finished answering your open questions, then start asking more
specific questions about the medical problem, exploring how bad the problem is, the likely
causes and any relevant risk factors (e.g. cardiovascular risk factors in a cardiac history).
 Ask about the previous medical history (including operations), drug history (including over the
counter medication), allergy history, social history, family history and review of systems.
 Summarise the important points of the history you have obtained (briefly) to check you have
understood everything correctly and that you have not missed anything.
 Address the issues that the patient wants to discuss.
 Agree a plan with the patient for investigations, further management and follow-up.
 Tell the patient who they can contact if they have questions or more problems before the next
follow-up appointment (which shows that you are trying to maintain patient welfare).
3.1 Tips
 Most centres will give you a clipboard with some paper – you could use this blank paper to jot
down some ideas of what to ask before you go into the room.
 You should think about a list of differential diagnoses before you walk into the room – this list
will help to guide your history-taking.
3.2 During the history-taking
 Do not address the patient by their first name (unless the patient specifically invites you to do
so).
 Avoid using jargon with the patient.
 Listen carefully and follow up any important cues.
 Do not forget to ask about drug allergies and family history (candidates often forget to do
this).
 You must evaluate the effects of the illness and side effects of any treatment on the patient’s
functional status and general well-being (you should ask relevant questions in the history of
presenting complaint and/or in the social history).
 A good question to ask is, “How does this illness affect your day-to-day life?”
 The social history should be detailed – besides the usual smoking and drinking questions, ask
about work, relationships, and accommodation.
 Get a full history before you start addressing the patient’s concerns – some candidates only
take half a history, then start discussing the issues that are highlighted on the instruction
sheet, and then never finish getting the history.
GUIDE
 If you finish taking your history before the 14 minutes is up, you cannot move on to
questioning early – the examiners are under instructions to let you know how much time is left
and not otherwise talk to you; if you finish really early then summarise your history and, in
doing so, you will hopefully discover the areas that you forgot to ask about.
4. Presentation
 In the minute of silence for quiet reflection, think about your differential diagnoses and now
try to order them with the most likely answers first (based on the history you have now
obtained) and create a problem list.
 Do not present your history after the minute of silence – the examiners have just spent 14
minutes listening to you take the whole history – wait and let them ask you a question.
 Listen carefully to the examiners’ questions and answer them concisely (like in a job interview:
pause for a second to decide how you want to answer, deliver the answer, and then be quiet)
– do not “dig a hole for yourself” by talking too much and straying into dangerous territory!
 Try not to argue with the examiners (even if you are sure that you are right and they are
wrong).
NB
 Do not try and whisper answers to another candidate – you will not be in the exam to help
them and the instructors have better hearing than you think!
 After the course, consider practising history-taking in front of colleagues at your own hospital
and getting some feedback – just like the physical examination stations, you need other
people to point out what you might be doing wrong and you need to get in the habit of taking
a history with the pressure of other people watching you.
We would strongly advise you to look at the example scenarios on the MRCP website:
www.mrcpuk.org/PACES/Pages/PacesFormat.aspx
Remember, this station is about you asking a complete and relevant history, answering the
patient’s concerns, and constructing a sensible differential diagnosis and management plan.

GUIDE
Station 3: Neurology & Cardiovascular Stations
(10 minutes)
 Peripheral neuropathy
 Myotonic dystrophy (dystrophia myotonica)
 Parkinson’s disease
 Charcot-Marie-Tooth disease (hereditary motor and sensory neuropathy)
 Abnormal gait
 Spastic paraparesis
 Cerebellar syndrome
 Hemiplegia
 Muscular dystrophy
 Multiple sclerosis
2. Introduction
The neurology station is often the most feared examination station for PACES. However, it
shouldn’t be, and this guide is to help you become confident with it. There are two main
differences from the other stations:
 If you fail to elicit a reflex due to bad technique, the examiner will notice. Honing your
technique, especially for reflexes, is essential in neurology; you must know your routine. Most
of the signs are elicited from inspection or observation, (and not from palpation or
auscultation). Unfortunately we still see many candidates pausing or forgetting steps during
the examination. Time spent pondering over this is time taken away from the focus and
analysis of signs leading to a diagnosis and presentation.
 Neurology actually combines three main examinations – cranial nerves, upper limbs, and
lower limbs – and some special approaches. Correspondingly, there are more possible cases in
neurology than in other stations. This does not mean you need to know all possible differential
diagnoses. It is more important to think systematically about your findings, even if you don’t
reach the diagnosis.

GUIDE
3. Cranial Nerves
Because of time, often you’ll be asked to examine the eyes (CN II, III, IV and VI) or the lower cranial
nerves (V, VII – XII). Remember certain patterns of lesions:
 V, VII, VIII & cerebellar signs in cerebellopontine angle lesions

 III, IV, Va, Vb, VI in cavernous sinus lesions
A systematic examination would be:
3.1 General
 Introduce yourself; confirm patient’s name

 Explain and ask for permission, e.g. ‘I would like to examine the nerves in your head and neck. Is
that all right?’
 Check there is no pain
 Uncover the head and neck: tie back hair, loosen collar, etc.
3.2 Inspection
 Ptosis, glasses, wasting of temporalis, jaw deviation, face asymmetry, scars, etc.
3.3 Cranial nerves
CN I
 ‘Have you noticed any difficulty with your sense of smell or taste?’
CN II
 Check if glasses/contact lenses – test with corrected refractive error
 Visual acuity: Formal (Snellen chart), else reading text.

If unable to read, then count fingers  hand movements  light perception
 Visual fields: Confrontation with finger/white pin

Use a red pin for more sensitive evaluation. The standardised examination
will involve using your finger or a white pin. However, if you are asked, do a
focus examination (a patient with acromegaly).
 Pupil reflexes: Direct and consensual in each eye

‘Swinging light’ test for Relative Afferent Pupillary Defect (RAPD)
Accommodation

GUIDE
CN III, IV & VI
 ‘Tell me if you see double at all’
 Test in all directions using a + or H movement
CN V
 Sensation in all three areas
 Temporalis and masseter bulk
CN VII
 Upper face: ‘Raise your eyebrows’, ‘Squeeze your eyes shut tight’
 Lower face: ‘Keep your lips together’, ‘Puff out your cheeks’, ‘Show me your teeth’
CN VIII
 Cover one ear, ‘Repeat the number that I whisper into your ear’
 If abnormal: Rinné’s & Weber’s tests
CN IX & X
 Uvula elevation
CN XI
 ‘Shrug your shoulders’
 ‘Turn your head to face the left/right’
CN XII
 ‘Stick out your tongue’
 ‘Push it against your left/right cheek’
3.4 General
As for cranial nerves, except:

Ask patient to remove shirt or trousers to expose the shoulder or upper thigh depending on the
examination.
3.5 Limb examination
The upper limb and lower limb examinations are similar in sequence. There is some flexibility in the
order that they can be performed in. We would suggest leaving sensation until the end as it is time-
consuming and often may be normal.
It is critical that you have your own practiced method so that you don’t forget any part of the
examination. All teachers have their own order, which you may or may not follow. By contrast, it
can be useful to perform gait at the start of the examination so that there is some idea of the
diagnosis already.
A typical routine would be:

GUIDE
3.6 Inspection
Walking aids (especially for lower limb exam), fasciculations, scars, wasting, etc.
Upper limbs Lower limbs

Screen Pronator drift with arms Gait, including heel-toe walking
outstretched and Romberg’s test
Tone Passive movement of wrist and Roll legs watching for the foot
elbow swinging, and rapidly flex at the
knee looking for ankle lift-off from
the bed
Power Shoulder abduction – deltoid Hip flexion – iliopsoas

Elbow flexion – biceps Hip extension – gluteus maximus
Elbow extension – triceps Knee flexion – hamstrings
Wrist flexion – flexors carpi ulnaris Knee extension – quadriceps
and radialis Ankle dorsiflexion – tibialis
Wrist extension – extensors carpi anterior (common peroneal nerve)
ulnaris and radialis (radial nerve) Ankle plantarflexion –
Thumb abduction – abductor pollicis gastrocnemius
brevis (median nerve) Great toe extension – extensor
Finger abduction – first dorsal hallucis longus
interosseus (ulnar nerve)
Reflexes Biceps (C5, C6) Knee (L3, L4)

Start at the ankle Supinator (C5, C6) Ankle (S1, S2)
and count from one Triceps (C7) Plantar response
Co-ordination Finger-nose test for intention tremor Heel-shin test for intention tremor
and past-pointing Broad-based, unsteady, slow gait
Alternate hand movements for
dysdiadochokinesis
Sensation Place arms with palms up L2 – upper anterior thigh

C4 – over shoulder L3 – over knee
C5 – outer upper arm L4 – medial aspect of shin
C6 – thumb and distal radial forearm L5 – lateral aspect of shin, dorsum
C7 – middle finger of foot, big toe
C8 – little finger S1 – little toe, sole of foot
T1 – distal ulnar aspect of forearm

GUIDE
T2 – axilla (S2 is a strip over the posterior leg
and thigh)
3.7 Special examinations
Cerebellar examination
 Head
Nystagmus or broken smooth pursuit or ocular dysmetria horizontally (towards the lesion)
Speech for slurring or ‘staccato’/scanning quality (each syllable pronounced separately)
 Upper limbs
Finger-nose testing for intention tremor and past-pointing (dysmetria)
Alternating hand movements for dysdiadochokinesis
 Lower limbs
Heel-shin test

GUIDE
Gait

GUIDE
Truncal ataxia (unable to sit unsupported) is a sign of midline cerebellar disease affecting the
vermis.
‘DANISH’ is a common acronym if stuck: Dysdiadochokinesis, Ataxia, Nystagmus, Intention tremor,

Slurred speech, Hypotonia/Hyporeflexia (note that hypotonia/hyporeflexia are mild).
Parkinsonism examination
Start with demonstration of the core features, then proceed to other signs and signs of ‘plus’
syndromes.
Core features
 Resting tremor, worse on distraction
 Rigidity on testing tone
 Bradykinesia of movements (decrease in speed and amplitude of repeated hand movements)
Gait
 Difficulty initiating and stopping
 Shuffling with small steps (reduced stride length and foot lifting)
 Festinant (appears hurried after initiation)
 Turning en-bloc (turn whole body like a statue)
 Loss of arm swing
Other features
 Quiet speech
 Expressionless facies
 Micrographia
Features of ‘plus’ syndromes

 Cerebellar ataxia (multiple system atrophy)
 Autonomic dysfunction (mention standing/lying blood pressure – multiple system atrophy)
 Restricted vertical gaze (progressive supranuclear palsy)
 Dementia (dementia with Lewy bodies)

GUIDE
4. Speech Examination
Usually this means the patient will have a cerebellar lesion, or a bulbar/pseudobulbar palsy, but
there are other causes too.
Ask a simple question (e.g. ‘What is your full name?’ ‘What did you have for breakfast today?’)
Ask patient to repeat phrases (e.g. ‘British constitution’ ‘West Register Street’)
This should give some idea of where the lesion is, and you can proceed to test from the relevant
step:
Hearing (if no answer)

 Test cranial nerves starting with CN VIII
Understanding (if answer makes no sense)

 Test with non-verbal commands such as ‘Make a fist with your left hand’.
 Problems here are called a ‘receptive dysphasia’.
Word formation (if the wrong words are used)

 If understanding is intact, then listen to the speech for neologisms (new words) or paraphasia
(wrong words). Ask the patient if he/she has trouble finding the right word.
 Problems here are called an ‘expressive dysphasia’.
Phonation (if quiet or hoarse)

 If the speech itself is otherwise normal, test cough and the lower cranial nerves and look for a
thyroidectomy scar that could be consistent with recurrent laryngeal nerve injury.
Articulation (if saying the right words, but not clearly)

 Assess different parts of articulation:
o ‘Baby hippopotamus’ for lip sounds (CN VII)
o ‘Grey geese’ for palatal sounds (CN IX, X)
o ‘Red lorry, yellow lorry’ for tongue sounds (CN XII)
Multiple Sclerosis
This should be suspected if you find upper motor neuron signs or cellebellar signs together with
sensory signs. The disease classically relapses and remits and examination of eye movement can
yield the following:
 Nystagmus (‘Dancing Eyes’)
Is a condition of involuntary eye movement, this occurs when the semi-circular canals are
being stimulated while the head is not in motion. The direction of ocular movement is
related to the semi-circular canal that is being stimulated.
 Inter Nuclear Ophthalmoplegia (INO)
Where on looking to the left, one eye fails to adduct and the other exhibits an ataxic
nyrtagnus.
 Marcus Gunn Pupil

GUIDE
This occurs when there is a relative afferent pupillary defect so that the pupil appears to
dilate when light is moved from the normal eye to the affected one.
CN III lesion
If the pupil is equally reactive, then this could be a ‘medical’ cause sparing parasympathetic fibres.
If the pupil is only ‘out’ instead of ‘down and out’, then there may be a CN IV lesion too. If other
eye muscles or the other eye is affected, then it is a ‘complex ophthalmoplegia’.
CN VII lesion
See if the weakness is forehead-sparing (UMN) or not (LMN). If LMN facial weakness, then check if
CN V and CN VIII are intact (for cerebellopontine angle lesions), and then look for causes of facial
nerve palsy: parotid scar or swelling, and vesicles around the ear
CN VIII lesion
See if the hearing loss is sensorineural or conductive. A 512Hz (or, if not available, 256Hz) tuning
fork is used for the tests. Avoid the 128Hz tuning fork, which is really meant for vibration sense. For
Rinné’s test, place the base of the fork on the mastoid then the fork tip next to the ear canal. Air
conduction should be louder than bone conduction in sensorineural deafness or healthy people.
For Weber’s test, place the base of the fork on the centre of the forehead. It localises towards
conductive deafness and away from sensorineural deafness.
Limb weakness
There are many possibilities and it is first important to identify if it is upper or lower motor neuron
in type, or a muscle disorder.
Remember that the presence of mixed upper and lower motor neuron signs with normal sensation
suggests motor neuron disease.
Upper motor neuron (UMN) weakness
Look for relatively preserved muscle bulk, increased tone, brisk reflexes, upgoing plantar response.
Monoparesis and hemiparesis

 Stroke or, rarely, Brown-Sequard syndrome
 Anterior cerebral artery strokes will affect legs more than arms
 Middle cerebral artery strokes do the opposite (and may cause facial weakness and
hemianopia)
Spastic paraparesis and quadriparesis

 Spinal cord lesion or compression if there is a sensory level
 Must inspect back
 Consider hereditary spastic paraparesis if normal sensation
 Consider MS and Friedreich’s ataxia if abnormal co-ordination

GUIDE
GUIDE
Lower motor neuron (LMN) weakness
Look for wasting, fasciculations, decreased tone, and decreased reflexes.
Flaccid paraparesis
 Cauda equina syndrome
 Would be a neurosurgical emergency, and must ask about bowel and bladder symptoms
Radiculopathy
 Unilateral weakness of specific muscles (eg. foot drop for L5 lesion)
 Associated with sensory loss over the corresponding dermatome (eg. dorsum of foot)
Peripheral neuropathy
 Bilateral, symmetrical weakness often with ‘glove and stocking’ sensory loss
Neuromuscular junction
 Proximal bilateral weakness, which can be asymmetrical
 Fatiguable weakness
 Can affect face and extraocular muscles
 Normal sensation
Myopathy
 Proximal bilateral weakness
 Usually normal tone and reflexes until late in the disease
 Normal sensation
Sensory loss
Glove and stocking

 Symmetrical distal sensory loss usually in the legs first
 Hallmark of peripheral neuropathies
Sensory level
 Loss of sensation below a certain dermatome usually on the trunk or in the arms
 Suggests spinal cord compression at that dermatome level
Mononeuropathy
 Specific patterns of sensory loss may occur due to injury of a particular nerve.
 Median nerve compression at the carpal tunnel is the commonest with loss of or altered
sensation over the lateral 3 and ½ fingers and weakness of the ‘LOAF’ muscles. Do Tinel’s test
and Phalen’s test to check for compression.
 Ulnar nerve injury (usually at the elbow) leads to sensory loss over medial 1½ fingers with
weakness of other intrinsic hand muscles.
 Radial nerve injury (usually along humerus) leads to sensory loss of dorsum of hand with wrist
drop.

GUIDE
GUIDE
5. Presentation
Almost all patients can be subdivided into upper or lower motor neurone diseases, or cerebellar
signs, or peripheral neuropathy. We would recommend that you present this, and then give a
differential diagnosis.
For example: This patient has upper motor neurone signs as evidenced by the increased tone and
brisk reflexes in the left arm. There is also some weakness and some cerebral signs. My differential
diagnosis includes a stroke or a brain tumour and I would like to obtain a history of the speed of
onset to distinguish them and do a brain scan.
Remember that the mark scheme mainly rewards good examination rather than spotting the
diagnosis.

GUIDE
Station 4: Cardiovascular
(10 Minutes)
 Mixed mitral valve disease

 Mitral incompetence (Lone)
 Mitral stenosis (Lone)
 Mitral valve prolapse
 Mixed aortic valve disease
 Aortic stenosis (Lone)
 Aortic incompetence (Lone)
 Prosthetic valves
 Irregular pulse
2. General Approach
In all stations it is important to have a structured approach not just to your examination but also
your presentation and thought process. Nowhere is this more essential than the cardiology station
where it is possible to begin your diagnostic thought process from the moment you enter the
room.
Many students consider themselves (often inaccurately!) to have below-average auscultatory skills
– whilst this is rarely the case, it is both possible and important to have a good idea of what you
might hear if you ever put your stethoscope to the patient’s chest.
3. Strategy for Examination
Move in an ordered direction from ‘finger tips to feet’. This will ensure on the day you will look
smooth and practiced:
 Introduction
 General inspection
 Hand inspection
 Radial pulses
 Collapsing pulse
 Blood pressure
 Eyes inspection
 Mouth inspection
 JVP inspection
 Carotid pulse examination
 Praecordial palpation
GUIDE
 Auscultation
 Lung oscillation
 Ankle examination
4. Introduction
As always, introduce yourself to the patient, ask permission to examine them then take a step back
and inspect.
5. General Inspection
The diagnostic process should begin as you walk in the room; the key thing to look for in cardiology
is the presence of chest wall scars. Obviously, this tells you whether they have had an operation or
not but you should also start thinking logically about the likely procedure they could have had and
what other signs you may therefore expect:
5.1 Central Sternotomy Scar
 CABG – With a central sternotomy scar, the next thing to look for is leg scars (for vein harvest)
or site of scars in the arms (for radial harvest scars). It is possible to have had CABG without leg
or arm scars if the patient has had an internal mammary (LIMA) graft.
- Also bear in mind that they may have had a CABG in conjunction with another
structural heart operation (especially valve replacement). Surgeons will look for an
excuse to replace valves at the same time as a CABG (even if they are only moderately
diseased) to avoid a potential repeat operation.
 Valve replacement – listen for a click. If you cannot hear one this does not mean the patient
doesn’t have a metallic valve – they can be quiet, particularly in patients with a thick chest wall.
The patient may also have a biological valve. Look for bruising over the patient’s limbs and
body (warfarin).
 A SIMPLE structural heart operation – such as a VSD or ASD repair. A mitral valve repair is also a
possibility. You are likely to find NO murmurs with these operations.
 A COMPLEX structural heart operation – such as repair of tetralogy of fallots. You are likely to
FIND murmurs with this as although the physiology is acceptable the resultant anatomy
remains imperfect.
5.2 Thoracotomy scar
 Coarctation repair – it is very unlikely that you will meet a patient with an unrepaired
coarctation because they will be left with irreversible hypertension. Instead, you may meet
someone with a thoracotomy scar: focus then on comparing the radial pulses (the left may be
reduced) and examining for radio-femoral delay.

GUIDE
 Blalock-Taussig shunt – performed palliatively as part of the tetralogy repair; however, unlike a
coarctation repair it must have a central sternotomy scar accompanying it to signify they have
gone on to have a complete repair. Again, compare radial pulses (the left may be reduced).
5.3 Sub-mammary scar (right or left side)
 Mitral valve surgery – a mini-mitral valve repair (no murmurs) or mitral valvotomy for mitral
stenosis (MR murmur likely as well as residual mild MS) can be done through this route. Also,
the new TAVI procedure (percutaneous aortic valve replacement) can be performed through a
transapical approach giving a left-sided submammary scar.
5.4 Pacemaker scar
 Either just below the clavicle or in the cephalic groove – can you feel the device?
5.5 Other things to consider in your general inspection
 Age:
- Elderly patients - considering valvular and/or coronary disease – either treated (central
sternotomy scar) or untreated (no scars evident)
- Younger patients – consider structural problems, again treated (scars as above) or
untreated
 Skin changes:
- If on sun-exposed regions think of amiodarone therapy (focus on pulse rhythm)
- Cheeks – malar flush (diastolic murmur)
- Bruising – valve replacement (look for a click and note any scars) or AF (rhythm)
5.6 Other
 Features of heart failure – peripheral oedema, dyspnoea

 Gynaecomastia – think spironolactone or digoxin
 Cyanosis – this is a real rarity as it implies advanced pre-terminal disease, particularly if central
 Do they have an underlying syndrome: tall (Marfans) or short (Noonans, Turners), unusual
facial appearance (Williams)?
Finally, use this opportunity to ensure the patient is positioned appropriately at 45 degrees.
5.7 Hands
Ask the patient to stretch both hands out in front of them. Inspect the dorsum then ask them to
turn them over and inspect the palmar surface. Look for:
 Evidence of endocarditis: splinter haemorrhages, Janeway lesions, Osler’s nodes, clubbing

 Cyanosis – see above regarding rarity; if present look for clubbing
 Tar staining – has the patient a central sternotomy scar and vein harvest (CABG)?
GUIDE
5.8 Radial Pulse
Whilst both hands are outstretched, feel both radial pulses at the same time. Then ask the patient
to rest their left hand on their lap and focus on their right radial pulse:
 Rate
 Rhythm – is the patient in AF?
 Radial-radial comparison – particularly if the patient has a thoracotomy scar (see above).
Other causes of a reduced radial pulse: large vessel arteritis, cervical rib, subclavian stenosis,
iatrogenic (radial harvest or damage during a radial angiogram).
 Avoid performing:
- Radio-femoral delay – this can be too intimate for a lot of patients so do not do as
standard; instead, tell the examiners you would like to examine for it only if you
anticipate it being abnormal (i.e. with a thoracotomy scar).
- Character – other than the collapsing nature, this should be assessed at the carotid
pulse.
5.9 Collapsing pulse
 This is taught in a huge variety of ways (not all of them correct) and therefore can be easily
misunderstood. Think about it pathophysiologically: it is essentially a peripheral manifestation
of a wide pulse pressure, caused by a high stroke volume ejected at the start of systole and
then a rapid fall in blood volume (and therefore pressure) back into the ventricle in diastole
through an incompetent aortic valve.
 Place the flats of your fingers of both your hands on the patient’s forearm and raise the arm
quickly and smoothly upwards after obtaining permission from the patient, beware of
shoulder pain, due to tendinitis arthritis. What you should feel is described as a ‘tapping’
feeling: this means the pulse volume feels larger than normal and falls away rapidly. You are
also likely to appreciate it over a large number of your fingers due to the high stroke volume.
 Practice this on your colleagues – it is important to ‘look good’ whilst doing this and it is
surprisingly easy to look awkward if you position your hands incorrectly to start.
 While you are performing it look at the neck – you can therefore assess for Corrigan’s sign at
the same time.
5.10 Blood Pressure
Ask for a blood pressure at this point. If you wait to the end to do so you may forget in the heat of
the moment.

GUIDE
5.11 Face
 Eyes:
- Conjunctiva - look for anaemia by pulling the eyelids down (you do not need to look at
the upper lid as well, this can be uncomfortable for the patient)
- Xanthalasmata and corneal arcus – (look for a CABG scar)
- Jaundice – valve replacement or aortic stenosis
 Mouth:
- Make a note of dentition: in valve replacement cases this is important to comment on,
even if good.
- High arched palate: if the patient is tall think Marfan’s (AR), if they are short think
Noonan’s (PS) or Turner’s (coarctation).
- Cyanosis
5.12 Neck
5.13 JVP
 If raised, the most likely cause in the exam is right-sided heart failure. You should already have
an idea if their ankles are swollen from your general inspection.
 If you cannot see it, press gently but firmly over the right upper quadrant to elicit the hepato-
jugular reflex. Always check with the patient that they don’t mind you doing this beforehand.
 If you can see the JVP, try and characterise the wave pattern. If you struggle with this,
remember two straightforward things that you can comment on in your presentation:
- You should know their cardiac rhythm by now: if they are in AF, comment on the
absence of a waves.
- Giant v waves occur with tricuspid regurgitation so when you come to auscultate listen
for a systolic murmur that gets louder on inspiration.
5.14 Carotid pulse
 Character:
- Slow rising – aortic stenosis
- Collapsing – aortic regurgitation
- Bisferiens – both slow rising and collapsing – AS and AR
- Jerky – hypertrophic cardiomyopathy
 If a patient has had their valve operated on the pulse character should return to normal as the
pathology that caused it has been corrected.

GUIDE
5.15 Praecordial Palpation
 Apex beat
- With your hand flat to the chest wall, locate the furthest point you can feel the
heartbeat. Make a point to count down the number of rib spaces with your other hand
marking this spot. If you cannot feel the apex at all, remember dextrocardia and swiftly
check it is not palpable on the right side using your free hand.
- Character:
 tapping - mitral stenosis
 thrusting - mitral regurgitation
 heaving - LVH, often from aortic stenosis
- Thrills – this is a palpable murmur so if you are going to comment on it they must have
the appropriate finding on auscultation. Feel across the praecordium with three hand
positions: one as for apical examination feeling the mitral and tricuspid regions, one
across the left of the sternum feeling tricuspid and pulmonary regions and one
covering both aortic and pulmonary regions at the top of the sternum.
 Devices – if there is a device scar GENTLY palpate to feel the device. You are confirming its
presence and assessing its size. Pacemakers are very small but you may be able to recognise
them from ICDs as defibrillators are much larger.
5.16 Auscultation
 General points:
- Valve replacements:
 Metal valves will sound distinctly metallic whereas bioprosthetic valves will
sound like a normal heart sound although they are usually louder.
 In some patients with a metallic valve you will only hear the metallic nature of
the valve in certain regions and not across the whole praecordium.
 Generally speaking all aortic valve replacement patients will have a systolic
flow murmur; mitral valve replacement patients rarely have the equivalent
diastolic flow murmur.
 It is very unusual to replace right-sided heart valves as the physiology does not
need to be as perfect, as it is a ‘low pressured’ system. Therefore if the first
heart sound is metallic mitral is most likely and the second, aortic.
- Timing – time the cardiac cycle with the carotid pulse. If you are REALLY struggling to
feel it, use the brachial. Never use the radial, it will not help and looks unprofessional.
- WHERE things are loudest across the praecordium (i.e. in the respective valve regions)
can only guide your diagnosis as this can be variable even in single valve lesions. WHEN
things are loudest within the cardiac cycle (i.e. in relation to the first or second heart
sound) on the other hand cannot be questioned and are much more objective. So if
you heard a metallic first heart sound loudest in the aortic region it is almost certainly a
prothetic mitral valve.
GUIDE
- Right-sided lesions get louder with inspiration, left-sided with expiration.
5.17 Now listen in the four areas
 Mitral area (the apex)

- MS: start with the bell in this area to listen for mitral stenosis. You should have just
mapped out the apex so can listen immediately to this region. Then roll the patient to
the left side, relocalise the apex beat and listen again for this this murmur.
- MR: roll the patient back and listen for a pansystolic murmur in this region. If the
murmur is mid-to-late systole think of mitral valve prolapse and listen for a click. If
you can hear a murmur here, listen in the axilla to see if it radiates.
 Tricuspid area (left 4th intercostal space)
- Particularly focus on this area if you have noted a raised JVP or heard a systolic murmur
in the mitral region. If it sounds louder in the tricuspid region see if it gets louder on
inspiration to help differentiate these lesions.
 Pulmonary area (left 2nd intercostal space)
- If you suspect pulmonary stenosis (for example in someone with Noonan’s syndrome)
ask the patient to take a breath in and hold and see if the murmur gets louder. This can
distinguish this from aortic stenosis (which also radiates to the carotid). Also listen to
the volume of the second heart sound (pulmonary hypertension).
 Aortic area (right 2nd intercostal space)
- Listen for the characteristic ejection systolic murmur of aortic stenosis here. Other
causes of an ESM include PS (gets louder on inspiration), a small VSD (does not change
with respiration), HOCM (intensity increased with valsalva), supra- and infra-valvular
aortic stenosis (consider in someone with William’s syndrome).
- Listen at the carotids with breath holding – for both carotid stenosis and to see if any
systolic murmur you have heard radiates there.
 Aortic regurgitation (lower left sternal edge)
- After listening to all four areas sit the patient forwards and listen in forced expiration
(“take a breath in, and out, and hold it there”).
5.18 Final steps of the examination
 Lung bases – keep the patient sitting forwards after listening for AR. Auscultate for crackles
signifying left sided heart failure.
 Ankle swelling – press gently, AFTER CHECKING WITH THE PATIENT THEY ARE NOT SORE.
 Inform the examiner you would like to see the temperature, dip the urine and examine for
Roth spot’s.

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6. Presentation
This is often thought to be the hardest part of the station. However, if you are considering your
diagnosis from the outset you will find this much easier.
General rules:
 Present the signs you elicited in the order you examined for them: i.e. finger tips to feet.
 Avoid spending too long listing negative points, particularly when found peripherally. As a
general rule, if the following are negative it is worth mentioning them (but keep it brief):
- The patient is comfortable at rest
- The patient is in sinus rhythm
- The patient has no peripheral stigmata of endocarditis
- There are no features of heart failure
- No thrills, heaves and an undisplaced apex
- Any negative relevant to the diagnosis you have made
It is important to show the examiners that you found the positive signs relatively early in your
presentation.
 Finish with a summary of your findings to show the examiners you haven’t missed anything and
to conclude strongly.
 If you have found a sign that doesn’t agree with your diagnosis, either don’t mention it (if you
doubt your finding) or mention it but point out how it disagrees with your diagnosis. For
example: “Although the pulse was collapsing in nature I couldn’t hear a diastolic murmur
therefore I suspect this was just a physiological phenomenon/bounding pulse; I would obviously
like an echocardiogram to confirm my diagnosis”.
 If you don’t think you have found a ‘single’ diagnosis, do not be afraid of presenting your
differential but find a reason to order it in terms of likelihood. For example, if the murmur is
louder in a particular region or a relevant sign of severity is present use this to guide you.
So, for a patient with mild aortic stenosis for example the presentation might be:
I examined Mr Smith’s cardiovascular system. I note he is comfortable at rest and he has no scars
on his chest. He is in sinus rhythm and his pulse character was normal and not slow rising; you have
told me his BP is 130/85 and therefore not narrow. He had no peripheral stigmata of endocarditis.
He had no thrills or heaves and his apex was undisplaced. On auscultation the most obvious finding
was an ejection systolic murmur, which radiates to his carotids but not to his axilla. His second
heart sound was normal in volume. His lung bases were clear and his ankles were not swollen.
In summary, this man appears to have aortic stenosis, which is not severe, and he has no evidence
of endocarditis or heart failure.

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Station 4: Communication Skills & Ethics
(20 minutes)
The course has two mock ethics station, and you will have the opportunity to practice your own
ethics cases. You will be in groups of 3, and will thus have a full mock ethics station of your own on
Saturday, and again on Sunday. As with the history-taking stations, you will thus go through three
history-taking stations, for one of which you will be in the “hot seat”. In general we find that
candidates improve vastly between the first and the second day.
 Informed consent
- Consent for lumbar puncture
- Consent for oesophagogastroduodenoscopy (ogd)
- Emergency treatment under principle of ‘best interests’
- Human immunodeficiency virus testing
 Diagnosis and management advice
- Obesity
- Side effects of cardiac medication
- Presentation of a first seizure
- New diagnosis of type 2 diabetes
- Warfarin treatment
- New diagnosis of tuberculosis
 Breaking bad news
- Communication of immunodeficiency virus positive result
- Malignancy in a young patient
- A chronic illness
 Legal issues
- Driving and heart disease/epilepsy
- Do not resuscitate
- Brainstem death testing
- Organ transplantation
- Hospital postmortem
 Dealing with difficult patients/relatives
- Patient desperate for a diagnosis
- Patient with a functional illness
- Missed tumor
- Unhappy inpatient
 Professional issues and communications with colleagues
- Major incident exercise
- A struggling team of doctors

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- A colleague with hepatitis B
2. Format of Station
 Before commencing the case, you will be given a piece of paper with 2-3 lines explaining the
scenario.
 You will spend 13-14min interviewing the actor.
 There will be a knock on the door at 14min, after which the actor will leave.
 The examiners will ask you to summarise the case to them.
 The examiners will viva you on the case.
 The case finishes after 20min in total.
 In the course, you will have a mock ethics station on both days.
3. How to Conduct the Interview
It is important to do some things to make your ‘performance’ appear more authentic, and get the
right info from the patient:
 Carefully read the scenario you are given.

 Remember to explain who you are. They will not know unless you tell them.
 Agree the purpose of interview with the patient, e.g. you are here to discuss the results of their
blood tests.
 Regularly check that the patient understands what you are saying.
 Do not use ANY jargon at all. Terms like glucose, cardiac and respiratory are all classified as
jargon!
 Always leave a minute at the end to summarise what you have discussed, and ask the patient if
there was anything else they would like to discuss – this is crucial; the actor has a list of things
they should try to talk about, so this gives them an opportunity to raise a detail that you have
missed!
 Make a plan. In real life, you would never see a patient in clinic without giving them an idea
about what was going to happen next. Making a plan (even a fictitious one) makes it easier for
the examiner to picture you as a physician, e.g. I will organise for you to see the MacMillan
Nurses right away, then shall we see you next week in clinic? Please bring your husband if he is
free.

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4. Driving Regulations
Here is some important background information that you need to know:
 To drive a car, you need a Group 1 licence from the DVLA.

 To drive a bus or lorry, you need a Group 2 licence from the DVLA.
 To drive a licensed taxi, you need a licence from the local authority – every council has their
own rules on eligibility, but they are generally as strict as the rules for a Group 2 licence.
4.1 Heart attacks
Group 1. You need to stop driving for 4 weeks, but do not need to tell the DVLA.
Group 2. You need to stop driving, and can only get your licence back if you pass stage 3 of an ETT
off anti-anginal treatment! i.e. you will be off work for a while.
4.2 Seizures
Group 1: Stop driving for 1 year, with 3 exceptions:
 First fit (no driving for 6 months)

 All of your seizures during the last 3 years were nocturnal – you can drive
 Your fit was provoked (e.g. head injury)
Group 2: This is end of your career. You need to stop driving for 10 years, and only regain it if fit
free for 10 years, and are off anticonvulsants when reassessed.
4.3 Diabetes
Group 1: This is generally fine, as long as you do not have poor vision, frequent hypos, severe hypos
(enough to bring you to hospital) or hypoglycaemic unawareness.
Group 2: Until recently, you could not have this type of licence and be on insulin treatment. This
rule has recently been relaxed. You can drive a group 2 vehicle on insulin if:
 You have stable glycaemic control over a 3-month period

 You can demonstrate evidence of this using a glucose monitor with a memory function for
at least 3 months
 You are checking your blood sugars at least twice daily.
Remember, these regulations mean that if you want to start insulin, you must take 3 months off
driving your lorry.

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5. Consent
Competent patient
This is simple. You must gain their consent to perform a procedure/treatment.
Incompetent patient
There are 3 options:
5.1. There is no advanced directive or LPA (vast majority of occasions)
The patient cannot consent, so no one can consent for them. The medical team must make a
decision in the best interests of the patient. This does not mean you make a decision on your own!
You must consider:
 Premorbid state, quality of life, life expectancy, etc.

 Patient wishes – info from relatives and friends about what the patient would have
wanted, are very important. If they tell you the patient is a Jehovah’s witness, clearly that
may influence your decisions about blood transfusions, etc.
 What does your boss think? This is not an exit exam. You are expected to discuss tricky
issues with your consultant, without making a hasty decision. They may ask for a second
opinion from another consultant.
 What does the MDT think? It is curtains to forget asking the nursing staff, physiotherapists,
etc. when making a big decision, especially if they are on ITU or have been in hospital for a
while.
5.2. The patient has made an advanced directive
This is a legal document, which informs medical staff what medical treatment a patient would not
want in the future if they ‘lacked capacity’. For instance, you could say that you would or would not
agree to CPR, if required. The advanced directive needs to be followed if it is relevant to the
management decision.
5.3. The patient has made a lasting power of attorney (formally known as enduring power of
attorney)
This is a legal document, which allows a patient to appoint a person (an ‘attorney’) to make
decisions about medical care, when the patient is no longer able to make these decisions (i.e. they
are incompetent). So doctors need to speak to and gain consent from the lasting power of
attorney.
NB: this has nothing to do with “Power of Attorney”, which just gives someone else the power to
sell or manage your financial asset, e.g. close your bank account.

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6. Criteria for Brainstem Death
(Conference of Medical Royal Colleges 1976-1981)
This is a common viva topic, so please make sure you know the criteria.
 All brain stem reflexes are absent

 Pupils are fixed and non-responsive to light
 Corneal reflex is absent
 The vestibulo-ocular reflexes are absent. No eye movements following slow injection of at least
50mls of ice cold water over one minute into each external auditory meatus).
 No limb response to supraorbital pressure
 No gag reflex
 No respiratory movements when disconnect ventilator (PaCO2 6.65kPa confirmed on ABG)
 Repetition of testing
 2 medical practitioners:
- competent in this field
- registered at least 5 years (at least one of the doctors should be a consultant)
- not members of the transplant team
 2 sets of tests should always be performed, can be done by the two practitioners separately or
together.
 Although death is not pronounced until the second test has been completed the legal time of
death is when the first test indicates brain stem death.
7. How to Pass the Ethics Station
Unfortunately, most candidates do very little or no practice of common ethics cases. There is a
limited number of ethical issues that are likely to be examined. It is therefore difficult to pass if you
are unfamiliar with the issues surrounding these common cases.
 Practice, practice, practice. You need to be comfortable doing the common scenarios – you
have a real head-start if you have done your case before (with a friend/partner).
 Get enough info from the actor. Ask some direct questions. Think about if you need to discuss
things like employment (will it be affected?), social security benefits, patient support groups,
genetic counselling.
 Know the regulations
 Always check they understand you
 Summarise
 Make a follow-up plan

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Station 5: Integrated Clinical Assessment
(10 minutes x2)
In previous years, station 5 patients were four stations each of five minutes approximately included
the following:
 Ophthalmology station
 Endocrinology station
 Rheumatology station
 Dermatology station
Station 5 now consists of two 10-minute “integrated” stations to include history, possible brief
examination (7 minutes), explanation to the patient (1 minute) and then discussion with the
examiners (2 minutes). Patients with the above four conditions are commonly used for this station,
and it is thus worth knowing a bit about each of these.
1. Ophthalmology Station
1.1 Most Common Cases
 Diabetic retinopathy
 Retinitis pigmentosa
 Optic atrophy
 Ocular palsy
 Visual field defect
 Retinal vein occlusion
 Old choroiditis
 Papilloedema
 Cataracts
 Myasthenia gravis
1.2 Introduction
Fundoscopy is not difficult!
Finding the time and inclination to practice it so it becomes easy is the difficult part. The old ‘short
case’ style of examining a fundus and providing a diagnosis or differential diagnosis is no longer
required.
You have 8 minutes with each patient to conduct a history focusing on a particular clinical issue,
carry out appropriate examinations and respond to any concerns from the patient. You may not
even have to examine the fundus; taking a history, examining ocular motility in a patient with
diplopia and discussing your findings will easily take up 8 minutes.

GUIDE
Before we move onto typical scenarios, a reminder on how to carry out fundoscopy:
1. Introduce and explain what you are going to do – make sure the patient is at ease that you will
be coming very close to them and that they should continue to breathe normally. Most
‘professional’ patients will know the drill.
2. Try and ensure adequate positioning of the patient on the chair/bedside, especially if you are
particularly short or tall – being comfortable during the examination is important.
3. Don’t forget the general inspection! It is unlikely that the examiners will allow the very obvious
clue of a guide dog to be in the examination room, but dark glasses and a white stick may mean
the patient has severe sight impairment, so comment on them.
4. Ask the patient to remove their spectacles if they wear any and dim the room lights – it helps
with contrast sensitivity and with patients whose pupils don’t dilate very well. As regards what
to do about your own spectacles, it depends on how comfortable you are examining with them
on. We will talk about refractive errors and any adjustments that might need to be made
during the practical session.
5. Before moving onto fundoscopy, check the red reflex – if there is no red reflex, fundoscopy will
be very difficult, if not impossible. It would be unfair for you to be asked to examine an artificial
eye (this would definitely not have a red reflex!).
6. Ask the patient to fixate on a distant target, slightly above head height (helps to move the
upper lid). You may rest your second hand on the patient’s forehead, but do not hold the
upper lid forcibly open. If the patient cannot blink, they will complain that the eye is
uncomfortable and the cornea drying out will impact adversely on your examination.
7. Looking through the ophthalmoscope, approach the patient’s eye ensuring that the light source
is steady on the pupil as you approach. You need to get close enough, so that your entire view
through the eyepiece is through the pupil. If you can see any of the iris visible, you are either
not close enough or you have veered off target.
8. Unless you have a good reason not to (e.g. blind in one eye), you should examine the patient’s
right eye using your right hand and your right eye and vice versa for the patient’s left eye. It is
difficult to get close enough otherwise.
9. Focus on the retinal features and have a logical method of examination: disc, vessels, macula. If
you get ‘lost’ within the eye, follow the bifurcation of retinal vessels back to the disc. Get the
disc into focus and carry on with your routine.
10. Examine the left eye and present your findings in a consistent fashion (be guided by the history
that you have elicited).

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1.3 Scenarios
1.3.1 Diabetic retinopathy
By far the commonest eye condition to be encountered in an examination setting, as there are lots
of diabetic patients that can be called upon. Ensure you know what laser photocoagulation looks
like and don’t confuse it with retinitis pigmentosa (RP) or choroiditis. The scenario may require you
to think about other areas that may need to be examined as well as the eyes, impact on lifestyle
and treatment modalities for the underlying condition.
Example of 10-minute integrated stations to include diabetic retinopathy.
This patient with long-standing type 2 diabetes has come for an annual review in the diabetic clinic.
You need to perform a brief annual review, including history and ophthalmological examination.
You are NOT required to assess for peripheral neuropathy on this occasion.
Commonly patients with poorly controlled type 2 diabetes will give a history compatible with high
levels of glucose including glycosuria and recurrent urinary tract infections.
Ensure you are aware of NICE guidelines for treatment of type 2 diabetes, and remember to always
mention lifestyle changes in addition to drug treatments. Most patients should be on Metformin,
but you should consider the incremental treatments including sulphonylureas which are second
line to Metformin, and then recognise the thiozolidinediones, the GLP-1 (injectable) analogues, the
DPP4 inhibitors (“gliptins”) and the new SGLT2 inhibitors (Dapagliflozin) which increase glycosuria
and are rarely used. Remember that insulin is also a very effective treatment. Talk to the patient
about their concerns of poor control of diabetes.
Fundoscopy may reveal changes of background diabetic retinopathy, or laser burns commonly.
Make sure you know the features of commonly occurring abnormalities:
 Background diabetic retinopathy: this includes hard exudates and microaneurysms

 Pre-proliferative retinopathy: cotton wool spots
 Proliferation (new vessels)
 Maculopathy (hard exudates near the macula)
 Laser burns in patients who have had pan-retinal photocoagulation.
If you see background retinopathy, then you should inform the patient that you can see changes
that suggest that control can be improved, and then explain to the patient how you can do this
using diet exercise and the drugs above.
In the final 2 minutes, you will need to tell the examiners what you have found, and be prepared
for questions about the different treatments available.

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1.3.2 Loss of vision
 History: acute or slowly progressive? Acute onset suggests a vascular aetiology (e.g. vein
occlusion, ischaemic optic neuropathy). Slower onset may be something as simple as a cataract
(can be picked up checking the red reflex) or something sinister such as a compressive lesion.
 Unilateral or bilateral? Bilateral disease may mean an underlying systemic/genetic cause (e.g.
diabetes or RP)
 Painful or painless? Painful causes (e.g. retrobulbar neuritis, giant cell arteritis)
 Is vision loss generalised or specific? Central vision loss implies macular disease (e.g. diabetic
maculopathy, age-related macular degeneration). Peripheral vision loss (e.g. RP, glaucoma).
Hemianopia/quadrantanopia secondary to previous CVA.
1.3.3 Diplopia
 Monocular (with only one eye open)? Usually due to cataract or corneal pathology.
 Binocular (only with both eyes open)? Usually due to extraocular muscle imbalance:
- Nerve palsies
- Thyroid eye disease (TED)
- Myasthenia
- Ocular myopathies
 Variability? Diplopia in nerve palsies and TED generally doesn’t vary whereas myasthaenia and
ocular myopathies can give rise to variable and intermittent diplopia.
 Direction? Constant horizontal diplopia suggests CN VI palsy, whereas constant vertical diplopia
may be due to CN IV palsy.
 Ptosis? Constant ptosis and diplopia may mean a CN III palsy and a variable, fatigable ptosis with
variable diplopia suggests myasthaenia.
 CN III palsy and pupil: if the pupil is involved (i.e. dilated) with a CN III palsy, this is potentially a
neurosurgical emergency, therefore mandatory to check pupil size with suspected CN III palsy.
There are two uses of the COVER test. If a patient has an obvious squint, you can prove this by
asking them to look at you, and covering the “good” eye.
If a patient develops double vision while you are checking their eye movements, then you can
check which eye is weaker by covering each eye in turn. The weak eye ALWAYS sees the outer
image.

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1.3.4 Pupil reactions
 Equal or not equal? Need to check in dim light as well as bright light. Larger pupil in bright
light or smaller pupil in dim light points to the affected side.
 Ptosis? If associated with smaller pupil may mean Horner’s syndrome (congenital or
acquired). If acquired, need to think about potential causes.
 Ptosis? Associated with larger pupil and abnormal eye movement (pupil involving CN III palsy
– see above).
 Adies pupil is a tonically dilated pupil, probably due to a viral infection. More common in
women. May have loss of deep tendon reflexes (Holmes-Adie syndrome).
 Pharmacological: either iatrogenic or recreational.
 RAPD (Relative Afferent Pupillary Defect): a positive RAPD test is a sign of optic nerve
disease. May be an acute finding (e.g. retrobulbar neuritis) or long-standing (previous
ischaemic optic neuropathy).
 ‘Optic atrophy’ is not a diagnosis. Pale optic nerves may be due to many causes and you
must put this finding into the context of the patient you have in front of you (e.g. if it is a
young woman, then more likely to be 2º to demyelination, whereas if it is an elderly man
with hypertension and diabetes, Non Arteritic Ischaemic Optic Neuropathy (NAION) is more
likely.
HINT: What would you do if (following inspection as you walk into the room) you
suspect a Horner’s syndrome?
Answer: Darken the room enough to be able to see a difference in the pupil size. It is the
failure of dilatation that is the problem. Shining a light into the eye will show normal
constriction, and is a common cause of the diagnosis being missed.
1.3.5 Retinitis Pigmentosa
There are many causes of retinitis pigmentosa. It can occur by itself, and be autosomal dominant,
autosomal recessive or X-linked. At this point you would refer them for a specialist opinion. You
need to know nothing else about the condition. There is some small print about one of the causes
(Refsum’s disease) that you might read for interest.
1.3.6 Small print that you don’t need to know about Refsum’s disease. There are only a few cases
in the UK.
Refsums disease occurs in patients who cannot metabolise phytanic acid, which is a fatty acid,
which is a metabolite of chlorophyll. It is concentrated in the fat of animals that eat grass (lamb,
beef). It causes retinitis pigmentosa. Phytanoyl CoA hydroxylase is absent, so that phytanic acid
levels climb. Patients are managed with a diet low in phytanic acid, so they can’t eat beef or lamb.
As long as they are putting on weight, the fatty acids are safely out of the bloodstream and in

GUIDE
triglyceride, but if they lose weight, then the fatty acids are released into the circulation, and toxic
levels result in worsening retinitis pigmentosa, deafness and neurological signs.
2. Endocrinology Station
 Exophthalmos
 Acromegaly
 Graves’ disease
 Goitre
 Hypothyroidism
 Cushing syndrome
 Addison’s disease
 Hypopituitarism
 Pretibial myxoedema
 Gynaecomastia
Features that suggest that the condition is currently active are important, and as there is time for
discussion, there are a few facts that you need to know. Thus having taken a history and examined
the patient, you need to also consider:
 Is the patient’s condition currently active?

 What signs suggest that the condition is active?
 What investigations should be performed?
 What modalities of treatment are available?
 What complications should you look for on examination?
Acromegaly is probably one of the most over-represented stations in PACES. Patients are stable
with signs, and so get recruited. You can obtain a brief history from the patient, to include
particular questions about ring size (the patient has stopped wearing a wedding ring because it
became tight), shoe size and even hat size. To demonstrate the changes, the patient may even
have with them some old photographs. Ask about headache, an important feature of active
acromegaly, and proceed to examine the hands, feeling for the doughy palm and the spade like
shape of the hands. Inspect the tongue and teeth, looking for increased intradental separation, and
you can then proceed to explain what further investigations the patient needs. Sometimes you
need to make the diagnosis, but more often the rubric on the sheet tells you that the patient is
known to have acromegaly and that they have attended for an annual review.

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2.2 Complications of acromegaly
The tumour of acromegaly can be large enough to cause a bitemporal hemianiopia. Be sure to
check each eye individually, as with both eyes open, the fields will be normal.
2.3 Medical treatment of acromegaly
You need to find out what medication the patient is on, and what treatment the patient has
already had. You may then be asked detailed information about the diagnosis and treatment of
acromegaly, especially if you are doing well, and there are relatively few things that you need to
know to look really good. The facts given here might be useful for your discussion. The usual first
line treatment is transphenoidal surgery followed if the patient is not cured, by radiotherapy, and
sometimes medical treatment. Drugs that help to control growth hormone levels include dopamine
agonists such as bromocriptine or cabergoline, or somatostatin analogues such as lanreotide or
octreotide. GH receptor antagonists can also be used (pegvisomant), but at present this is
extremely expensive.
Also remember to discuss pituitary replacement if the patient has been rendered hypopituitary by
the treatment, so that they might need hydrocortisone, thyroxine or sex steroid replacement (HRT
in females or testosterone in males). Some patients may have diabetes insipidus as a consequence
of surgery, and will then be on DDAVP replacement.
Investigations that are undertaken include assessing GH burden with a glucose tolerance test, and
investigation of pituitary reserve with some form of stress test, usually with insulin
(hypoglycaemia). Imaging of the pituitary may reveal a pituitary adenoma.
2.4 Thyroid disease
Patients with Graves’ disease or a nodular goitre are common. There may be a history of features
of hyperthyroidism or hypothyroidism, and the patient may now be well controlled. For
hyperthyroidism, the diagnosis will either be autoimmune Graves’ disease, or a toxic nodular
goitre. The patient will now have been treated. Proceed as follows:
 Obtain a history of the onset and features of the initial presentation.

 Determine what treatment the patient has taken and what they have been offered.
 Check whether the disease is currently active.
 Carefully examine the neck to determine if the thyroid gland is smoothly enlarged (as in
Graves’ disease) or whether you can feel nodularity. Explain to the patient what you have
found, and what you thus think the diagnosis is. Graves’ disease is the likely diagnosis if you can
see any exophthalmos or pretibial myxoedema, which are thus worth looking for. Graves’
disease can be confirmed by measuring antibody titres if you are asked about this.
 Discuss treatment options with the patient, including advantages and side effects of the
treatments. The options include medical treatment with thionamides (either propyl-thiouracil

GUIDE
or carbimazole), or radioiodine, or surgery. The medical treatments have well known side
effects including a rash and occasionally serious neutropaenia.
 Surgery may cause damage to the recurrent laryngeal nerve, resulting in a possible change in
voice, and there is the risk of hypo-parathyroidism, which is difficult to live with in view of the
resulting hypocalcaemia. Radioiodine is safe, but one needs to know about radiation protection
rules (see radioiodine.info for details). After radioiodine, there is a good chance that the
patient will need lifelong thyroxine replacement.
 A very common choice in the UK is for patients to have an 18-month course of thionamides,
and then a review. Half the patients are in remission at that point and will need no further
therapy. Those that relapse are then offered “definitive” therapy (radioiodine or surgery).
 When males are affected, Graves’ disease is generally more aggressive, and males are thus
more likely to require definitive therapy.
To summarise, with the endocrine cases, you should keep your cool and present with confidence.
The discussion can become a detailed management plan. For example if you know all about Graves’
disease, and have really revised the subject, having stated that the patient obviously has Graves’
disease (“as evidenced by a smooth goitre and exophthalmos”) you can proceed to talk about
investigations and treatment:
I would like to check the patients thyroid function tests and determine whether TSH receptor
antibodies are present, to confirm the diagnosis. There are three treatment options to be
considered, medical treatment, radioiodine or surgery, and all three have advantages and
disadvantages. I will explain these to the patient and allow them to make the choice.
Make the most of your knowledge and enjoy yourself!

GUIDE
3. Dermatology & Rheumatology Stations
 Systemic sclerosis/CREST syndrome

 von Recklinghausen disease (Neurofibromatosis)
 Osler-Weber-Rendu syndrome (Hereditary hemorrhagic telangiectasia (HHT))
 Psoriasis
 Rash of uncertain cause
 Dermatomyositis
 Xanthomata
 Vitiligo
 Adenoma sebaceum in tuberous sclerosis complex
 Pseudoxanthoma
 Rheumatoid arthritis
 Psoriatic arthropathy
 Systemic sclerosis/CREST syndrome
 Diabetic foot/Charcot joint
 Tophaceous gout
 Ankylosing spondylitis
 Paget’s disease
 Osteoarthritis
 Marfan’s syndrome
 Vasculitis
Examination of the hands and deciding whether a patient has rheumatoid arthritis (RA) or
osteoarthritis (OA) is basic and important. RA commonly affects the proximal interphalangeal (PIP)
joints as well as the metacarpophalangeal (MCP) joints. OA affects the distal interphalangeal (DIP)
joints and is important. Other seronegative arthritides are also important to consider. The
treatment hierarchy for rheumatoid disease is also key information. Patients may attend with long-
standing rheumatoid arthritis for a routine follow up, but they may have a new problem or
worsening symptoms that needs review. Thus a patient with stable rheumatoid arthritis might
complain of breathlessness and one should consider infection, pulmonary fibrosis or pneumonitis
relating to their medications.
Tips for Station 5
Always ask for a list of medications, the effects of the condition on the patient's life, functional
limitation, whether they have any questions or worries or concerns.

GUIDE
3.2 Rheumatoid Arthritis
 History
- Duration, which joints, pain worse in the morning
- Is there morning stiffness (duration), functional limitation
- Any rashes (e.g. psoriasis)
- What treatment, any side effects
- Determine whether their RA is active
- Risks and benefits of DMARDs and biologics
 Examination
- Symmetrical, deforming polyarthritis
- Nodules indicate seropositivity (RhF)
- Exclude psoriatic arthropathy (nails, skin)
- Assess activity (red, hot, swollen, painful joints)
- Assess function (e.g. power, precision or key grip)
 Investigations
- ESR, CRP
- X-rays hands and feet and chest (as baseline pre-methotrexate)
- RhF and anti-CCP Antibodies
 Management - early and aggressive to induce remission

- DMARDs - methotrexate (MTX, first line), sulphasalazine, hydroxychloroquine
- Anti-TNFs - must be screened for TB as risk of reactivation of latent TB
Side effects of methotrexate - immunosuppressant therefore risk of infections, myelosuppressive,

hepatotoxic, pneuomonitis (early in MTX use), fibrosis, teratogenic
3.3 Psoriatic Arthritis (PsA)
 Classify the type of PsA (5 types)
- DIP, rheumatoid-like, ankylosing spondylitis-like, mutilans, oligoarthritis
 History - as for RA
 Examination
- Usually extensor surfaces - classical plaques (knees, elbows, behind ears, scalp, naval and
natal cleft), guttate, flexural, palmar-plantar pustulosis
- Nails (pitting, onycholysis, hyperkeratosis, discolouration, ridges)
- - Koebner phenomen (psoriasis in a scar)

GUIDE
 Treatment
- Psoriasis - topicals (coal tar, calcipotriol, dithranol), systemic (methotrexate, ciclosporin),

PUVA, anti-TNFs
- PsA - methotrexate, anti-TNFs
3.4 Systemic Lupus Erythematosus (SLE)
 History
- Rashes, malar rash, photosensitivity, alopecia (?scarring), oral ulceration, dry eyes
(?secondary sjogrens), dry mouth, raynauds, PE/DVT/miscarriage (?secondary
antiphospholipid syndrome)
- Previous kidney or neurological involvement
 Examination
- Vasculitic lesions (nail fold infarct, purpura)

- Jaccouds arthropathy (correctable!, deforming polyarthropathy)
- Rashes (malar, livedo reticularis)
 Investigations
- Urine dip - blood/protein/casts (?glomerulonephritis), Renal biopsy

- ANA (95%), dsDNA (50%), ENAs (Smith, Ro)
- Raised ESR, normal CRP, low C4
- U&Es
 Treatment - depends on organ involvement

Mild (hydroxychloroquine), Moderate (azathioprine, MMF, prednisolone), Severe
(cyclophosphamide, rituximab)
3.5 Scleroderma - systemic sclerosis
Classified by the distribution of skin affected. The face may be involved in both.
- Limited - centromere Abs - scleroderma limited to below elbows, below knees

- Diffuse - SCL70 Abs - scleroderma including above elbows, above knees, trunk
 History & Examination
- Skin changes (itch implies activity, tightening), telangiectasia

- Raynauds, digital ulcers, autoamputation of digits
- Calcinosis

GUIDE
- Small mouth, pinched nose (don't say beaked), peri-oral furrows
- Gastroesophageal reflux
- Dysphagia
- Diarrhoea/constipation (?bacterial overgrowth)
- Interstitial lung disease (bibasal, fine-end inspiratory crepitations)
- Pulmonary hypertension (loud P2, RV heave, TR, raised JVP)
 Investigations
- ANA, centromere, SCL-70

- Respiratory - lung function tests, CXR, HRCT chest
- Cardiac - echocardiogram, ECG, cardiac MRI
- GI - barium swallow, hydrogen breath tests, B12, folate
- Renal - urine dip, renal biopsy
 Management
- Skin - camouflage
- Raynauds - gloves, calcium channel blockers, angiotensin II receptor antagonists,
fluoxetine, iloprost (prostacyclin)
- GI - omeprazole, ranitidine, prokinetics (metoclopramide)
3.6 Gout
The patient may have a history of acute gout with no signs whatsoever, or may have chronic
tophaceous gout.
 History
- Attacks of gout - which joints, how often duration, how many attacks, ?trigger and risk
factors, e.g. diet, alcohol, lympho or myeloproliferative disease
- ?Renal impairment (may dictate management), ?urate stones
 Examination
- Tophi (ears, elbows, Achilles tendon)

- Signs of psoriasis or myelo/lymphoproliferative disease
 Investigations
- Uric Acid - may be normal in 40% cases of acute gout

- U&Es
 Management
- Lifestyle - diet (reduce purine rich foods), alcohol

GUIDE
- Acute - NSAIDs (e.g. naproxen), colchicine
- Chronic - urate lowering therapy (e.g. allopurinol) if recurrent attacks, erosions or urate
stones
-
3.7 Ankylosing spondylitis
 History
- Inflammatory back pain (worse in the morning, better with exercise, NSAID-responsive,
morning stiffness)
- ?Inflammatory bowel disease, ?psoriasis, uveitis
- ?Family history
 Examination
- Shoeber's test - 2 points in midline marked 10cm above dimples of venus and 5cm below.
Expand less than 5cm on maximum forward flexion
- Kyphosis, loss of normal lumbar lordosis, extension at cervical spine
- Measure occiput-wall distance with patient standing against wall
- Look for signs of psoriasis, aortic regurgitation and apical pulmonary fibrosis
 Investigations
- HLA B27, CRP, ESR

- X-ray and/or MRI sacroiliac joints and spine
 Management
- Physiotherapy
- NSAIDs, TNF inhibitors
3.8 Paget’s disease of the bone
Paget’s disease of the bone affects older people, and may cause a warm bowed tibia. The patient
may also have a Pagetic skull. Carefully examine both legs and compare them. If one leg is warm
and bowed, then this is a possible diagnosis.
 History & Examination
- Bone pain, fracture, osteosarcoma (rare)

- Increased cardiac output due to shunting of blood through large bones (high output cardiac
failure is apparently possible, although I have never seen a case).
- Deafness
- Optic atrophy - angioid streaks

GUIDE
 Investigations
- ALP very high (normal calcium, phosphate, liver function tests)
- Bone scan
 Management
- Analgesia, bisphosphonates

GUIDE
Contributing Authors
Prof. J S Kooner MD, FRCP Consultant Cardiologist Imperial College
Dr J Chambers MD, FRCP Consultant Cardiologist Imperial College
Prof K M Meeran MD, FRCP Consultant Endocrinologist Imperial College
Dr J Vaughan MD, FRCP Consultant Neurologist Imperial College
Dr S Lightman MD, FRCP Consultant Ophthalmologist UCL
Dr L Thakuria MD, MRCP Respiratory SPR NW London Trusts
Dr A Sam MD, FRCP Consultant Physician Imperial College
Dr A Eichholz MD, MRCP Clinical Oncologist Oxford University Hospital
Dr C Broyd MD, MRCP Cardiologist SPR Hammersmith Hospital
Dr K Chinthapalli Neurologist SPR Queens Square
Dr C Jayasena Clinical Lecturer Imperial College
Dr B Hussain Consultant Ophthalmologist Moorfields Eye Hospital
Dr P Mehta MD, MRCP Rheumatologist SPR Imperial College

GUIDE
Appendix – Mark Sheets

GUIDE

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MRCP (UK)

EXAM PREPARATION GUIDE

2|Page MRCP – REVISION COURSE

3|Page MRCP – REVISION COURSE

In addition you should review the following exam outline:

Station 1 Respiratory System Examination (10 minutes)

Station 2 History-Taking Skills (20 minutes)

Station 3 Cardiovascular (10 minutes)

Station 4 Communication Skills and Ethics (20 minutes)

7|Page MRCP – REVISION COURSE

Station A Exam Station 1 Mainly respiratory and abdominal cases

Station B Exam Station 2 History-taking

Station C Exam Station 3 Mainly cardiovascular

Station E Exam Station 4 Communication skills

Station F Exam Station 3 Mainly neurological short cases

8|Page MRCP – REVISION COURSE

9|Page MRCP – REVISION COURSE

Station 1: The Respiratory System

1. Most Common Cases

 Interstitial lung disease (fibrosing alveolitis)

2. Inspections and Observation

 Inhalers, nebulisers: Suggestive of obstructive airways disease.

2.2 Expose the patient

2.3 Surgical scars for the physician

2.4 Other markings

11 | P a g e MRCP – REVISION COURSE

Then proceed with the respiratory examination of the chest.

3. Respiratory Examination of the Chest

 Closer inspection of the thorax

The patient with bibasal creps:

The patient with an area of dullness to percussion:

 Dullness to percussion + increased vocal resonance + bronchial breathing = consolidated lung.

4. Key Diagnostic Test

4.1 Pulmonary function tests

12 | P a g e MRCP – REVISION COURSE

13 | P a g e MRCP – REVISION COURSE

Endobronchial Ultrasound (EBUS) is a method of sampling mediastinal lymph nodes in cases of

5.1 Smoking cessation

14 | P a g e MRCP – REVISION COURSE

Inhaled bronchodilators are broken down into the following categories:

15 | P a g e MRCP – REVISION COURSE

5.4 Antibiotic therapy

It is unlikely that acute infections will feature in a PACES setting.

Expand on isolation, 2 lines and ref to guidelines.

16 | P a g e MRCP – REVISION COURSE

5.5 MDT involvement and palliation

5.6 Long-term oxygen therapy (LTOT)

5.7 Long-term ventilator support

Nocturnal NIV/BiPAP is becoming increasingly common, particularly in conditions like obesity

5.8 Pleural Interventions

5.9 Bronchoscopic Intervention

Interventional bronchoscopy is available in a number of centres. The main indication is to relieve

19 | P a g e MRCP – REVISION COURSE

1. Most Common Cases

2.1 Examination of the hands

The signs of chronic liver disease in the hands include:

 Asterixis (liver flap)

2.2 Examination of head and neck

Skin: Is there evidence of jaundice or spider naevi?

20 | P a g e MRCP – REVISION COURSE

2.3 Inspection of the chest

Is there evidence of gynaecomastia or hair loss (signs of chronic liver disease)?

2.4 Examination of the abdomen