MRCP PACES: High-Yield Topics and Common Cases

25 min read

PACES tests clinical skills across a circuit of stations, and while almost any case can appear, a predictable core comes up again and again. This guide breaks down the highest-yield cases station by station, cardiology, respiratory, abdominal, neurology and Station 5, each laid out the way you would present it to an examiner: the dominant sign, the diagnosis, the supporting signs, a sensible aetiology, markers of severity, and a plan. It also covers the communication and counselling scenarios that trainees ask about most. Use it to target your revision, then use the MRCP Part 1 and Part 2 banks and the textbook to lock in the knowledge behind each case.

How PACES is structured

PACES is an OSCE-style exam built around a circuit of stations that assess different clinical skills: physical examination of the respiratory, abdominal, cardiovascular and neurological systems, history taking, communication and ethics, and brief integrated clinical consultations. You rotate through the stations and are marked by examiners at each one.

Examiners are not only scoring whether you reach the right diagnosis. They score clearly defined skills: eliciting and correctly interpreting physical signs, clinical judgement, managing a patient's concerns, maintaining patient welfare, and clear, professional communication. Knowing which skill a station is testing is half the battle.

Cardiology station: the cases in full

The cardiology station rewards a slick routine and, above all, correct interpretation of what you hear. The reliable way through is a structured presentation: lead with the dominant sign, name your diagnosis, then support it with the associated signs, a sensible aetiology, markers of severity, and a plan. The cases below are the ones that come up again and again, each laid out the way you would present it.

Describe every murmur precisely: where it is loudest, when it occurs in the cycle, where it radiates, and what makes it louder or softer. That single skill separates a clear pass from a borderline one.

Prosthetic valve

The striking finding is an audible mechanical click with a midline sternotomy scar, so my leading diagnosis is a prosthetic valve. I would work out which valve it is and whether it is functioning normally.

Key signs

Midline sternotomy scar, plus leg or arm vein harvest scars if bypass was done at the same time.
A crisp metallic first heart sound suggests a mechanical mitral valve; a metallic second sound suggests a mechanical aortic valve.
A bioprosthetic valve sounds essentially normal; a soft flow murmur can be normal.
Look for bruising or a medical alert bracelet as clues to anticoagulation.

Aetiology / differential

Mechanical valve: durable but needs lifelong warfarin.
Bioprosthetic valve: limited lifespan, often no long-term anticoagulation.

Severity markers

A new regurgitant murmur suggests valve dysfunction or dehiscence.
Muffled, non-crisp mechanical sounds suggest thrombosis.
Anaemia and jaundice suggest haemolysis; fever suggests endocarditis.

Investigations & management

Echocardiography (often transoesophageal) to assess valve function.
INR monitoring with valve-specific targets, and a bridging plan around surgery.
Endocarditis awareness and good dental hygiene advice.

Likely examiner questions

Mechanical or tissue, and how can you tell at the bedside?: A crisp metallic click points to a mechanical valve; a valve with no click that sounds essentially normal suggests a bioprosthesis. Younger patients on warfarin usually have mechanical valves.
What INR target would you aim for?: Roughly 2.5 to 3.5 for a mechanical mitral valve and 2 to 3 for a mechanical aortic valve, higher with extra risk factors. Bioprosthetic valves usually need only short-term anticoagulation.
What are the specific complications of prosthetic valves?: Thrombosis, embolism, bleeding from anticoagulation, endocarditis, haemolysis, and structural failure or dehiscence causing a new regurgitant murmur.

Mitral stenosis

There is a low-pitched rumbling mid-diastolic murmur at the apex, loudest in the left lateral position in expiration, with a loud first heart sound, so my diagnosis is mitral stenosis, most likely rheumatic.

Key signs

Malar flush and an irregularly irregular pulse if in atrial fibrillation.
Tapping, non-displaced apex (a palpable first heart sound).
Loud S1 with an opening snap after S2, then a rumbling mid-diastolic murmur at the apex.
Signs of pulmonary hypertension: loud P2 and a left parasternal heave.

Aetiology / differential

Rheumatic heart disease, by far the commonest cause.
Severe mitral annular calcification; rarely congenital.

Severity markers

A longer diastolic murmur and a shorter interval between S2 and the opening snap.
Pulmonary hypertension, atrial fibrillation and right heart failure.

Investigations & management

Echocardiography to confirm and measure valve area and gradient.
Rate control and anticoagulation if in atrial fibrillation; diuretics for congestion.
Percutaneous balloon valvotomy or valve replacement for severe symptomatic disease.

Likely examiner questions

What is the commonest cause worldwide?: Rheumatic heart disease.
How do you assess severity at the bedside?: A longer diastolic murmur, a shorter interval between S2 and the opening snap, and signs of pulmonary hypertension or atrial fibrillation.
What is Ortner's syndrome?: Hoarseness caused by an enlarged left atrium compressing the recurrent laryngeal nerve.

Mitral regurgitation

There is a pansystolic murmur at the apex radiating to the axilla with a displaced apex beat, so my diagnosis is mitral regurgitation.

Key signs

Displaced, thrusting (volume-loaded) apex beat.
Soft first heart sound with a pansystolic murmur at the apex radiating to the axilla.
A third heart sound, and signs of heart failure or pulmonary hypertension in severe disease.

Aetiology / differential

Degenerative or ischaemic disease; mitral valve prolapse (mid-systolic click, late systolic murmur).
Functional (a dilated ventricle), rheumatic, or endocarditis.

Severity markers

A displaced apex, a third heart sound, a short mid-diastolic flow murmur, pulmonary hypertension and signs of failure.

Investigations & management

Echocardiography for mechanism and severity.
Treat heart failure; surgical repair (preferred) or replacement for severe or symptomatic disease or a falling ejection fraction.

Likely examiner questions

Where does the murmur radiate, and how does that help?: To the axilla, which helps separate it from aortic stenosis (radiates to the carotids) and tricuspid regurgitation.
How would you distinguish this from aortic stenosis?: Mitral regurgitation is pansystolic at the apex radiating to the axilla with a soft S1; aortic stenosis is ejection systolic at the base radiating to the carotids with a slow-rising pulse.
When would you refer for surgery?: For severe symptomatic disease, or a falling ejection fraction or progressive ventricular dilatation even without symptoms. Repair is preferred to replacement.

Aortic stenosis

There is an ejection systolic murmur at the aortic area radiating to the carotids with a slow-rising pulse, so my diagnosis is aortic stenosis.

Key signs

Slow-rising, low-volume pulse with a narrow pulse pressure.
Heaving, non-displaced apex; soft or absent S2 in severe disease.
Ejection systolic murmur at the upper right sternal edge radiating to the carotids.

Aetiology / differential

Calcific degeneration in the elderly; a bicuspid aortic valve in younger patients; rarely rheumatic.
Aortic sclerosis gives the murmur without the pulse or pressure changes.

Severity markers

Slow-rising pulse, narrow pulse pressure, soft S2, a thrill, a later-peaking murmur, and symptoms (angina, syncope, breathlessness).

Investigations & management

Echocardiography for gradient and valve area.
Aortic valve replacement (surgical or TAVI) for severe symptomatic disease; use vasodilators cautiously.

Likely examiner questions

What are the common causes at different ages?: Calcific degeneration in the elderly, a bicuspid aortic valve in younger adults, and rarely rheumatic disease.
Which symptoms mark severe disease?: Angina, syncope and breathlessness from heart failure; these carry a poor prognosis without valve replacement.
Surgical valve or TAVI, and what decides between them?: Surgical replacement for lower-risk, younger patients and TAVI for higher surgical risk or older patients. The heart team decides using surgical risk, anatomy and comorbidity.

Aortic regurgitation

There is an early diastolic murmur at the left sternal edge with a collapsing pulse and a wide pulse pressure, so my diagnosis is aortic regurgitation.

Key signs

Collapsing (water-hammer) pulse with a wide pulse pressure.
Displaced, thrusting apex beat.
Early diastolic murmur at the left sternal edge, best heard in expiration leaning forward.
Peripheral signs: Corrigan's pulsation, de Musset's head bob, Quincke's nail-bed pulsation.

Aetiology / differential

Chronic: bicuspid valve, rheumatic disease, connective tissue disease (Marfan, ankylosing spondylitis), aortic root dilatation.
Acute: endocarditis or aortic dissection.

Severity markers

A wide pulse pressure, a long murmur, a third heart sound, an Austin Flint murmur, and signs of heart failure.

Investigations & management

Echocardiography and assessment of the aortic root.
Vasodilators can help symptoms; valve replacement for severe symptomatic disease, a falling ejection fraction or a dilating ventricle.

Likely examiner questions

Name the peripheral signs of aortic regurgitation.: A collapsing pulse with wide pulse pressure, Corrigan's neck pulsation, de Musset's head bob, Quincke's nail-bed pulsation, Duroziez's and Traube's signs.
What is an Austin Flint murmur?: A mid-diastolic rumble at the apex from the regurgitant jet fluttering the anterior mitral leaflet; it indicates severe aortic regurgitation.
What causes acute aortic regurgitation?: Infective endocarditis and aortic dissection.

Ventricular septal defect

There is a harsh pansystolic murmur at the left sternal edge, loudest low down, so my diagnosis is a ventricular septal defect.

Key signs

Harsh pansystolic murmur at the lower left sternal edge, often with a thrill.
A small defect can be very loud (maladie de Roger).
Look for cyanosis and clubbing suggesting Eisenmenger physiology in a large longstanding defect.

Aetiology / differential

Congenital, or acquired after myocardial infarction.
Distinguish from mitral regurgitation (radiates to axilla) and tricuspid regurgitation.

Severity markers

A quieter murmur with signs of pulmonary hypertension can paradoxically indicate a large defect; cyanosis and clubbing indicate Eisenmenger syndrome.

Investigations & management

Echocardiography; endocarditis awareness.
Closure (surgical or device) for significant shunts, before pulmonary vascular disease becomes irreversible.

Likely examiner questions

Why might a loud murmur be reassuring?: A loud, harsh murmur usually reflects a small defect with a preserved pressure gradient; a quieter murmur with signs of pulmonary hypertension can indicate a large defect.
What is Eisenmenger syndrome?: A longstanding left-to-right shunt raises pulmonary pressures until the shunt reverses to right-to-left, producing cyanosis and clubbing. It contraindicates closure.

Atrial septal defect

There is wide, fixed splitting of the second heart sound with an ejection systolic flow murmur in the pulmonary area, so my diagnosis is an atrial septal defect.

Key signs

Wide, fixed splitting of S2.
Ejection systolic (pulmonary flow) murmur at the upper left sternal edge.
A tricuspid flow murmur if the shunt is large, and signs of pulmonary hypertension in longstanding disease.

Aetiology / differential

Ostium secundum (commonest) versus primum defects.
Distinguish from pulmonary stenosis.

Severity markers

Signs of pulmonary hypertension, right heart overload and atrial arrhythmias.

Investigations & management

Echocardiography; percutaneous or surgical closure for significant shunts.
Consider it in a young patient presenting with an embolic stroke.

Likely examiner questions

Why is the splitting fixed?: The atrial communication equalises the respiratory variation between the two sides, so the A2 to P2 interval stays constant through the respiratory cycle.
Which arrhythmia is associated?: Atrial fibrillation and other atrial arrhythmias.

Hypertrophic obstructive cardiomyopathy

There is an ejection systolic murmur at the left sternal edge that gets louder on standing or Valsalva, with a jerky pulse, so I would consider hypertrophic obstructive cardiomyopathy.

Key signs

Jerky pulse and a double apical impulse.
Ejection systolic murmur at the lower left sternal edge, louder with Valsalva or standing and softer on squatting.
A coexisting pansystolic murmur of mitral regurgitation; there may be an implantable defibrillator.

Aetiology / differential

Distinguish from aortic stenosis, where the murmur softens with Valsalva, and from mitral regurgitation.

Severity markers

A family history of sudden death, syncope, arrhythmia and the outflow gradient guide risk.

Investigations & management

Echocardiography and ECG; avoid dehydration and vasodilators.
Beta-blockers, risk stratification for an implantable defibrillator, and family screening with genetic counselling.

Likely examiner questions

How do dynamic manoeuvres change the murmur, and why?: It gets louder on standing or Valsalva, which reduce preload and worsen outflow obstruction, and softer on squatting. In aortic stenosis the murmur behaves in the opposite way.
How do you assess the risk of sudden death?: A family history of sudden death, unexplained syncope, non-sustained VT, marked left ventricular wall thickness and an abnormal blood pressure response to exercise; high risk warrants an implantable defibrillator.

Coarctation of the aorta

There is radiofemoral delay with upper limb hypertension, so my diagnosis is coarctation of the aorta.

Key signs

Radiofemoral delay with weak, delayed femoral pulses.
Upper limb hypertension and a systolic murmur over the back between the scapulae.
Look for associations: a bicuspid aortic valve, or features of Turner syndrome.

Aetiology / differential

Commonly associated with a bicuspid aortic valve; part of Turner syndrome.

Severity markers

The degree of hypertension, heart failure, and collateral formation (rib notching on imaging).

Investigations & management

Confirm with CT or MR aortography; treat hypertension.
Surgical or stent repair, with lifelong follow up for re-coarctation and aneurysm.

Likely examiner questions

Which conditions are associated with coarctation?: A bicuspid aortic valve and Turner syndrome, and there is an association with berry aneurysms.
Why check blood pressure in both arms and a leg?: To demonstrate upper limb hypertension with lower or delayed pressures below the coarctation, confirming the gradient.

Respiratory station: the cases in full

The respiratory station is about interpreting a pattern: the position of the trachea, the quality of chest expansion, the percussion note and the added sounds. Put those together before you commit to a diagnosis, and always look for clues to the cause and to treatment.

Pulmonary fibrosis (interstitial lung disease)

There are fine, late inspiratory crackles at both bases that do not clear with coughing, with finger clubbing, so my diagnosis is pulmonary fibrosis.

Key signs

Finger clubbing and central cyanosis in advanced disease.
Fine end-inspiratory crackles at the bases, with reduced expansion and a central trachea.
Look for a cause: rheumatoid hands, sclerodactyly, or clues such as oxygen and a Cushingoid appearance from steroids.

Aetiology / differential

Idiopathic pulmonary fibrosis; connective tissue disease.
Drug-induced (methotrexate, amiodarone, nitrofurantoin, bleomycin); occupational (asbestosis); hypersensitivity pneumonitis.
Remember upper-zone causes as well as the commoner lower-zone ones.

Severity markers

Resting hypoxia or oxygen use, and cor pulmonale (raised JVP, oedema, loud P2).

Investigations & management

High-resolution CT and lung function (restrictive with a reduced transfer factor).
Treat the cause; antifibrotics (pirfenidone, nintedanib) for idiopathic pulmonary fibrosis; oxygen; transplant in selected patients.

Likely examiner questions

What are the upper-zone causes of fibrosis?: Coal worker's pneumoconiosis, hypersensitivity pneumonitis, ankylosing spondylitis, radiation, tuberculosis, sarcoidosis and silicosis.
Which drugs cause pulmonary fibrosis?: Methotrexate, amiodarone, nitrofurantoin and bleomycin.
What pattern would you expect on lung function testing?: A restrictive pattern (reduced FEV1 and FVC with a preserved or raised ratio) and a reduced transfer factor.

Bronchiectasis

There are coarse crackles that change with coughing, with clubbing and a sputum pot, so my diagnosis is bronchiectasis.

Key signs

Coarse, shifting inspiratory crackles, often with clubbing.
A sputum pot at the bedside; signs of cor pulmonale in advanced disease.

Aetiology / differential

Post-infective (childhood pneumonia, whooping cough, tuberculosis).
Cystic fibrosis in a young patient; immune deficiency; ciliary dyskinesia (Kartagener with dextrocardia); allergic bronchopulmonary aspergillosis.

Severity markers

Frequency of infective exacerbations, chronic Pseudomonas colonisation, respiratory failure and cor pulmonale.

Investigations & management

High-resolution CT (signet-ring sign), sputum culture, and a cause work-up (immunoglobulins, CF screen).
Airway clearance physiotherapy, prompt antibiotics for exacerbations, and vaccination.

Likely examiner questions

What are the causes of bronchiectasis?: Post-infective disease (childhood pneumonia, whooping cough, tuberculosis), cystic fibrosis, immune deficiency, ciliary dyskinesia and allergic bronchopulmonary aspergillosis.
What is Kartagener syndrome?: Primary ciliary dyskinesia with the triad of bronchiectasis, situs inversus (dextrocardia) and chronic sinusitis.
How would you investigate a young patient?: High-resolution CT, sputum culture, immunoglobulins, a cystic fibrosis sweat test and genetics, and tests of ciliary function.

COPD

There is a hyperexpanded chest with reduced breath sounds and a prolonged expiratory phase with wheeze, so my diagnosis is COPD.

Key signs

Hyperexpansion, reduced cricosternal distance, pursed-lip breathing and tar staining.
Reduced breath sounds, wheeze and a prolonged expiratory phase.
Signs of carbon dioxide retention or cor pulmonale in advanced disease.

Aetiology / differential

Smoking-related in most cases; alpha-1 antitrypsin deficiency in a young or non-smoker.

Severity markers

Use of accessory muscles, resting hypoxia, cor pulmonale, and home oxygen or nebulisers at the bedside.

Investigations & management

Spirometry (obstructive and largely irreversible), stepwise inhaled therapy, pulmonary rehabilitation.
Smoking cessation, vaccination, and long-term oxygen for chronic hypoxia.

Likely examiner questions

What causes COPD in a young non-smoker?: Alpha-1 antitrypsin deficiency.
Who qualifies for long-term oxygen therapy?: Non-smokers with a resting PaO2 below 7.3 kPa, or below 8 kPa with cor pulmonale or secondary polycythaemia, confirmed on two occasions.

Pleural effusion

There is stony dull percussion at the base with reduced breath sounds and reduced expansion, so my diagnosis is a pleural effusion.

Key signs

Reduced expansion on the affected side, with stony dull percussion.
Reduced breath sounds and vocal resonance; the trachea is pushed away by a large effusion.
Look for a mastectomy scar or other clues to malignancy.

Aetiology / differential

Transudate (heart failure, cirrhosis, nephrotic syndrome).
Exudate (malignancy, infection or empyema, pulmonary embolism, connective tissue disease).

Severity markers

The size of the effusion, breathlessness, and signs of the underlying cause.

Investigations & management

Chest X-ray and ultrasound-guided aspiration, applying Light's criteria.
Treat the cause; drainage for large or infected effusions.

Likely examiner questions

How do you separate a transudate from an exudate?: By pleural protein: below 25 g/L is a transudate and above 35 g/L an exudate; use Light's criteria for values in between.
What are Light's criteria?: An exudate is likely if the pleural-to-serum protein ratio exceeds 0.5, the pleural-to-serum LDH ratio exceeds 0.6, or pleural LDH is over two-thirds the upper limit of normal serum LDH.

Lobectomy or pneumonectomy

There is a lateral thoracotomy scar with reduced expansion and a trachea deviated towards the scar, so this is likely a previous lung resection.

Key signs

Thoracotomy scar with reduced expansion on the operated side.
The trachea is pulled towards a pneumonectomy, which is dull with absent breath sounds over the space.

Aetiology / differential

Resection for lung cancer, bronchiectasis, or old tuberculosis.

Severity markers

Respiratory reserve on the remaining lung.

Investigations & management

Establish the original indication and monitor the remaining lung.

Likely examiner questions

How do you tell a pneumonectomy from a lobectomy at the bedside?: A pneumonectomy pulls the trachea towards the scar with a dull, silent hemithorax; a lobectomy causes less tracheal shift and better preserved breath sounds.

Lung transplant

There is a bilateral thoracotomy (clamshell) scar in a relatively young patient, so I would consider a lung transplant.

Key signs

Clamshell or bilateral thoracotomy scars.
Signs of immunosuppression (Cushingoid appearance, skin changes, gum hypertrophy).
The underlying disease may be evident, such as cystic fibrosis or fibrosis.

Aetiology / differential

Transplant for cystic fibrosis, pulmonary fibrosis, COPD or pulmonary hypertension.

Severity markers

Signs of rejection or infection, and chronic rejection (bronchiolitis obliterans).

Investigations & management

Lifelong immunosuppression and surveillance, with vigilance for infection and malignancy.

Likely examiner questions

What conditions lead to lung transplant?: Cystic fibrosis, pulmonary fibrosis, severe COPD (including alpha-1 antitrypsin deficiency) and pulmonary hypertension.
What are the risks of long-term immunosuppression?: Infection, malignancy (especially skin cancer and lymphoma), and drug toxicity such as renal impairment, diabetes and hypertension.

Abdominal station: the cases in full

The abdominal station is really about organomegaly, transplants and chronic liver disease. Inspect for scars and the stigmata of chronic disease before you palpate, and always look for an arteriovenous fistula and signs of liver disease.

Chronic liver disease

There are multiple stigmata of chronic liver disease with a nodular or shrunken liver, so my diagnosis is chronic liver disease.

Key signs

Leuconychia, clubbing, palmar erythema, Dupuytren's contracture and spider naevi.
Gynaecomastia, caput medusae, splenomegaly and ascites.
Look for jaundice and asterixis (encephalopathy).

Aetiology / differential

Alcohol, viral hepatitis, non-alcoholic fatty liver disease.
Haemochromatosis, autoimmune hepatitis, primary biliary cholangitis, Wilson's disease.

Severity markers

Signs of decompensation (jaundice, ascites, encephalopathy, variceal bleeding) and the Child-Pugh components.

Investigations & management

A liver screen, ultrasound and endoscopy for varices.
Treat the cause, manage complications, and consider transplant.

Likely examiner questions

What are the causes of chronic liver disease?: Alcohol, viral hepatitis B and C, non-alcoholic fatty liver disease, haemochromatosis, autoimmune hepatitis, primary biliary cholangitis and Wilson's disease.
What signs suggest decompensation?: Jaundice, ascites, encephalopathy (asterixis) and variceal bleeding.

Polycystic kidney disease

There are bilateral ballotable flank masses that move with respiration, so my diagnosis is polycystic kidney disease.

Key signs

Bilateral, irregular, ballotable masses that you can get above but not below.
Hypertension; possible hepatomegaly from liver cysts.
There may be a transplant, an arteriovenous fistula, or a dialysis catheter.

Aetiology / differential

Autosomal dominant polycystic kidney disease.
Distinguish from splenomegaly (you cannot get above it, it has a notch and moves towards the right iliac fossa).

Severity markers

Renal impairment, hypertension, and evidence of renal replacement therapy.

Investigations & management

Ultrasound or CT, blood pressure control, tolvaptan in selected patients, and screening of relatives.
Plan for renal replacement; consider intracranial aneurysm screening where indicated.

Likely examiner questions

How do you distinguish a kidney from a spleen on palpation?: You can get above a kidney but not a spleen; the kidney is ballotable and resonant to percussion (overlying bowel gas), whereas the spleen has a notch, moves towards the right iliac fossa and is dull.
What are the extra-renal associations?: Hepatic and pancreatic cysts, intracranial berry aneurysms, mitral valve prolapse and diverticular disease.

Renal transplant

There is a smooth mass in the iliac fossa with an overlying scar and signs of immunosuppression, so this is a renal transplant.

Key signs

A non-tender, smooth mass in the iliac fossa with a hockey-stick scar.
Signs of immunosuppression (Cushingoid appearance, gum hypertrophy, skin changes).
An arteriovenous fistula, which may be defunct; the native kidneys may be palpable if the cause was polycystic disease.

Aetiology / differential

Establish the cause of the original failure: diabetes, polycystic disease, glomerulonephritis or hypertension.

Severity markers

Signs of graft failure or rejection, and complications of long-term immunosuppression such as skin malignancy.

Investigations & management

Monitor graft function and immunosuppression levels, and screen for infection and malignancy.

Likely examiner questions

What are the signs of immunosuppression?: A Cushingoid appearance, gum hypertrophy (ciclosporin), a fine tremor, skin fragility and warts or skin cancers.
What are the common causes of the original renal failure?: Diabetes, hypertension, glomerulonephritis and polycystic kidney disease.

Splenomegaly and hepatosplenomegaly

There is a left upper quadrant mass that I cannot get above, moves towards the right iliac fossa on inspiration and has a notch, so this is splenomegaly.

Key signs

Splenic characteristics: a notch, moves diagonally on inspiration, dull to percussion, and you cannot get above it.
Assess for hepatomegaly and lymphadenopathy, and look for anaemia.

Aetiology / differential

Massive splenomegaly: chronic myeloid leukaemia, myelofibrosis, malaria, visceral leishmaniasis.
Moderate: lymphoma, portal hypertension, haemolysis. With hepatomegaly, consider myeloproliferative disease, lymphoma or chronic liver disease.

Severity markers

Cytopenias from hypersplenism, and constitutional symptoms.

Investigations & management

Full blood count and film, imaging, and a haematology work-up.

Likely examiner questions

What are the causes of massive splenomegaly?: Chronic myeloid leukaemia and myelofibrosis, and in endemic areas malaria and visceral leishmaniasis.
How do you distinguish spleen from kidney?: You cannot get above the spleen; it has a notch, moves diagonally towards the right iliac fossa and is dull to percussion, whereas the kidney is ballotable and resonant.

Haemochromatosis

There is slate-grey skin pigmentation with hepatomegaly, so I would consider haemochromatosis.

Key signs

Bronze or slate-grey pigmentation with hepatomegaly and stigmata of chronic liver disease.
Clues to complications: diabetes, arthropathy, and cardiac signs.

Aetiology / differential

Hereditary (HFE gene) or secondary iron overload from repeated transfusion.

Severity markers

Cirrhosis, diabetes, cardiomyopathy, hypogonadism, and the risk of hepatocellular carcinoma.

Investigations & management

Ferritin and transferrin saturation, genetic testing, and venesection.
Screen for complications and screen relatives.

Likely examiner questions

What is the classic triad?: Bronze skin pigmentation, diabetes and hepatomegaly, often called bronze diabetes.
How is haemochromatosis treated?: Regular venesection to deplete iron stores, with screening for and management of complications; iron chelation is used if venesection is not tolerated.

Neurology station: the cases in full

Neurology is about localising the lesion. Decide whether the signs are upper or lower motor neurone, and whether the problem lies in the cortex, cord, peripheral nerve, neuromuscular junction or muscle, then match that to a recognisable pattern.

Parkinson's disease

There is an asymmetric resting tremor with bradykinesia and rigidity, so my diagnosis is Parkinson's disease.

Key signs

Expressionless face with reduced blink rate; asymmetric pill-rolling resting tremor.
Cogwheel rigidity and bradykinesia (reducing amplitude on repetitive movements).
A shuffling, festinant gait with reduced arm swing, and quiet monotonous speech.

Aetiology / differential

Idiopathic Parkinson's disease; drug-induced parkinsonism.
Parkinson-plus syndromes (progressive supranuclear palsy, multiple system atrophy).
Benign essential tremor (postural, symmetrical, improves with alcohol).

Severity markers

Postural instability and falls, autonomic and cognitive involvement.

Investigations & management

A clinical diagnosis; levodopa with a dopa-decarboxylase inhibitor, dopamine agonists, MAO-B inhibitors.
Multidisciplinary support.

Likely examiner questions

How do you distinguish it from essential tremor?: Parkinson's gives a resting, asymmetric pill-rolling tremor with bradykinesia and rigidity; essential tremor is a symmetrical postural or action tremor, often familial, that improves with alcohol.
What are the Parkinson-plus syndromes?: Progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration and Lewy body dementia.

Cerebellar syndrome

There is a broad-based ataxic gait with nystagmus and past-pointing, so my diagnosis is a cerebellar syndrome.

Key signs

DANISH: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred staccato speech, Hypotonia.
A broad-based gait and heel-shin incoordination.

Aetiology / differential

Alcohol, multiple sclerosis, stroke, a posterior fossa tumour.
Hereditary ataxias (Friedreich's), paraneoplastic disease, and phenytoin toxicity.
Unilateral signs point to a lesion in the ipsilateral hemisphere.

Severity markers

The degree of disability and any brainstem involvement.

Investigations & management

MRI of the brain; identify and treat the cause.

Likely examiner questions

What are the signs of cerebellar disease?: DANISH: dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred staccato speech and hypotonia.
Which side is the lesion in unilateral signs?: The same (ipsilateral) side as the signs.

Peripheral neuropathy

There is symmetrical distal sensory loss in a glove-and-stocking distribution with absent ankle reflexes, so my diagnosis is a peripheral sensorimotor neuropathy.

Key signs

Distal, symmetrical sensory loss with wasting and weakness of the small muscles.
Reduced or absent reflexes and a high-stepping gait.
Pes cavus and thickened nerves suggest a hereditary cause.

Aetiology / differential

Diabetes and alcohol are commonest; also B12 deficiency, drugs, chronic kidney disease and vasculitis.
Hereditary: Charcot-Marie-Tooth (pes cavus, inverted-champagne-bottle legs).

Severity markers

Motor involvement, autonomic features, and functional impairment.

Investigations & management

Screen for a cause (glucose, B12, renal and thyroid function, immunoglobulins) and nerve conduction studies.
Treat the underlying cause.

Likely examiner questions

What are the common causes?: Diabetes and alcohol most commonly; also B12 deficiency, drugs, chronic kidney disease, vasculitis and hereditary causes.
What is Charcot-Marie-Tooth disease?: A hereditary sensorimotor neuropathy causing pes cavus, distal wasting (inverted-champagne-bottle legs) and a high-stepping gait.

Spastic paraparesis

There is increased tone with pyramidal weakness, brisk reflexes and upgoing plantars in both legs, so my diagnosis is a spastic paraparesis.

Key signs

Increased tone with clonus, pyramidal-pattern weakness and hyperreflexia.
Extensor plantar responses and a stiff, scissoring gait.
Look for a sensory level, which points to a cord lesion.

Aetiology / differential

Multiple sclerosis, cord compression, trauma.
Motor neurone disease (no sensory signs), hereditary spastic paraparesis, B12 deficiency (subacute combined degeneration), anterior spinal artery syndrome.

Severity markers

A sensory level and sphincter involvement (urgency or retention).

Investigations & management

Urgent MRI of the cord to exclude compression, then investigate for the cause.

Likely examiner questions

What is the most urgent diagnosis to exclude?: Cord compression, which needs an urgent MRI.
What are the causes of a spastic paraparesis?: Multiple sclerosis, cord compression or trauma, motor neurone disease, hereditary spastic paraparesis, B12 deficiency and anterior spinal artery syndrome.

Myotonic dystrophy

There is bilateral ptosis with frontal balding, wasted facial muscles and grip myotonia, so my diagnosis is myotonic dystrophy.

Key signs

A myopathic, long thin face with bilateral ptosis, frontal balding and cataracts.
Wasting of temporalis and sternocleidomastoid, with distal weakness and dysarthria.
Grip and percussion myotonia (slow release of the hand).

Aetiology / differential

An autosomal dominant trinucleotide repeat disorder showing anticipation.

Severity markers

Cardiac conduction defects (needs an ECG), respiratory weakness, diabetes and cognitive involvement.

Investigations & management

ECG and cardiac surveillance, genetic counselling, and supportive care; caution with anaesthesia.

Likely examiner questions

What is myotonia and how do you demonstrate it?: Delayed muscle relaxation; show it with a slow release of grip, or by percussing the thenar eminence and watching for slow relaxation.
Why is an ECG important?: Because cardiac conduction defects are common and can cause sudden death, so patients may need pacing.

Motor neurone disease

There is a mixture of upper and lower motor neurone signs with fasciculations and no sensory loss, so my diagnosis is motor neurone disease.

Key signs

Wasting and fasciculations with brisk reflexes (mixed upper and lower motor neurone signs) in the same limb.
No sensory signs; there may be bulbar features (a wasted, fasciculating tongue and dysarthria).

Aetiology / differential

The combination of upper and lower motor neurone signs without sensory involvement is highly suggestive.
Exclude cervical myelopathy.

Severity markers

Bulbar and respiratory involvement carry the worst prognosis.

Investigations & management

A clinical diagnosis supported by electromyography.
Riluzole, multidisciplinary and respiratory support, and advance care planning.

Likely examiner questions

What is the hallmark combination of signs?: Mixed upper and lower motor neurone signs (wasting and fasciculations with brisk reflexes) with no sensory involvement.
What is the only disease-modifying drug?: Riluzole.

Multiple sclerosis

There are signs disseminated in space, such as optic atrophy with cerebellar and pyramidal signs in a young adult, so I would consider multiple sclerosis.

Key signs

Optic atrophy or a relative afferent pupillary defect, and internuclear ophthalmoplegia.
Cerebellar signs, spastic weakness and sensory disturbance, often in a young patient.

Aetiology / differential

Lesions disseminated in time and space; distinguish from other causes of a mixed neurological picture.

Severity markers

Disability, relapse frequency, and progressive disease.

Investigations & management

MRI of the brain and cord, sometimes lumbar puncture (oligoclonal bands).
Disease-modifying therapy, and steroids for acute relapses.

Likely examiner questions

What is internuclear ophthalmoplegia?: A lesion of the medial longitudinal fasciculus causing failure of adduction of one eye with nystagmus in the abducting eye on lateral gaze.
How is the diagnosis of multiple sclerosis made?: By demonstrating lesions disseminated in time and space, supported by MRI and sometimes oligoclonal bands in the cerebrospinal fluid.

Station 5: common spot diagnoses

Station 5 is two brief clinical consultations that combine a focused history, a targeted examination and communication, all against the clock. A handful of endocrine and rheumatological diagnoses recur because they are visible from the end of the bed. Recognise the pattern quickly, then structure the rest of the encounter around the patient's concerns.

Acromegaly

There are large hands and feet with coarse facial features and prognathism, so my diagnosis is acromegaly.

Key signs

Large spade-like hands, coarse features, a prominent supraorbital ridge and prognathism.
Interdental spacing, macroglossia and skin tags.
Look for a bitemporal hemianopia and carpal tunnel signs.

Aetiology / differential

A growth hormone secreting pituitary adenoma.

Severity markers

Diabetes, hypertension, cardiomyopathy, obstructive sleep apnoea and visual field loss.

Investigations & management

IGF-1 and an oral glucose tolerance test (failure to suppress growth hormone), with pituitary MRI.
Trans-sphenoidal surgery, somatostatin analogues.

Likely examiner questions

How do you confirm the diagnosis biochemically?: A raised IGF-1 and failure of growth hormone to suppress during an oral glucose tolerance test, then pituitary MRI.
What are the complications of acromegaly?: Diabetes, hypertension, cardiomyopathy, obstructive sleep apnoea, arthropathy, carpal tunnel syndrome and visual field loss.

Graves' disease

There is a diffuse goitre with thyroid eye signs and a fine tremor, so my diagnosis is Graves' disease.

Key signs

A diffuse goitre, sometimes with a bruit.
Exophthalmos, lid lag and ophthalmoplegia; a fine tremor, sweaty palms and tachycardia or atrial fibrillation.
Pretibial myxoedema and thyroid acropachy.

Aetiology / differential

Graves' disease; distinguish from toxic multinodular goitre and thyroiditis.

Severity markers

Atrial fibrillation, heart failure, and sight-threatening eye disease.

Investigations & management

Thyroid function tests and antibodies, and an isotope scan.
Carbimazole or propylthiouracil, beta-blockers, and radioiodine or surgery.

Likely examiner questions

Which eye signs are specific to Graves' disease?: Exophthalmos (proptosis) and ophthalmoplegia; lid lag and lid retraction occur in any cause of thyrotoxicosis.
How would you treat it?: Beta-blockers for symptoms, antithyroid drugs (carbimazole or propylthiouracil), and radioiodine or surgery for definitive treatment.

Cushing's syndrome

There is central obesity with a moon face, proximal weakness and thin skin, so I would consider Cushing's syndrome.

Key signs

Moon face and facial plethora, a buffalo hump and central obesity.
Thin skin, purple striae, easy bruising and a proximal myopathy.
Hypertension.

Aetiology / differential

Exogenous steroids (commonest); pituitary (Cushing's disease); ectopic ACTH; an adrenal cause.

Severity markers

Diabetes, hypertension, osteoporosis and psychiatric change.

Investigations & management

Confirm cortisol excess (overnight dexamethasone suppression, late-night salivary cortisol, 24-hour urinary free cortisol), then localise the source.
Treat the underlying cause.

Likely examiner questions

What is the commonest cause of Cushing's syndrome?: Exogenous corticosteroids.
How do you confirm cortisol excess?: An overnight dexamethasone suppression test, late-night salivary cortisol, or 24-hour urinary free cortisol, then localise the source.

Rheumatoid hands

There is a symmetrical deforming arthropathy of the small joints of the hands with ulnar deviation, so my diagnosis is rheumatoid arthritis.

Key signs

Symmetrical swelling of the metacarpophalangeal and proximal interphalangeal joints with ulnar deviation.
Swan-neck and boutonniere deformities, a Z-thumb, and rheumatoid nodules.
Muscle wasting; assess function and look for treatment side effects.

Aetiology / differential

Distinguish from osteoarthritis (distal joints, Heberden's nodes) and psoriatic arthropathy.

Severity markers

Functional impairment, extra-articular disease (lung, eyes, vasculitis), and disease activity.

Investigations & management

Inflammatory markers and antibodies (rheumatoid factor, anti-CCP), and X-rays.
Disease-modifying drugs (methotrexate) and biologics, with a multidisciplinary approach.

Likely examiner questions

How do you tell it from osteoarthritis?: Rheumatoid affects the MCP and PIP joints symmetrically with soft-tissue swelling and ulnar deviation; osteoarthritis affects the DIP joints (Heberden's nodes) and is bony and often asymmetrical.
What are the extra-articular features?: Pulmonary fibrosis and nodules, episcleritis and scleritis, vasculitis, anaemia, Felty's syndrome and amyloidosis.

Systemic sclerosis

There is tight, shiny skin over the fingers with telangiectasia and a beaked nose, so my diagnosis is systemic sclerosis.

Key signs

Sclerodactyly and tight skin, with calcinosis and telangiectasia.
Microstomia and a beaked nose; Raynaud's phenomenon.
Digital ulcers or pulp atrophy.

Aetiology / differential

Limited cutaneous (CREST) versus diffuse cutaneous systemic sclerosis.

Severity markers

Pulmonary hypertension and lung fibrosis, renal crisis, and gastrointestinal involvement.

Investigations & management

Antibodies (anti-centromere, anti-Scl-70) and organ screening (echocardiography, lung function).
Treat Raynaud's phenomenon and organ complications.

Likely examiner questions

What does CREST stand for?: Calcinosis, Raynaud's phenomenon, oEsophageal dysmotility, Sclerodactyly and Telangiectasia.
What are the life-threatening complications?: Pulmonary arterial hypertension, interstitial lung fibrosis and scleroderma renal crisis.

History taking and brief consultations (Stations 2 and 5)

These stations test whether you can take a focused, structured history under time pressure and reach a safe plan. Common presentations include breathlessness, chest pain, unintentional weight loss, blackouts and funny turns, and joint pain.

The marks are in structure and safety: a clear opening, systematic questioning, screening for red flags, eliciting the patient's ideas and concerns, and a management plan you can justify.

Communication skills and ethics (Station 4)

This station is pure communication: breaking bad news, capacity and consent, confidentiality, DNACPR discussions, and adherence. You are marked on empathy, clarity and professionalism, not on reciting facts.

Hepatitis B in pregnancy

Hepatitis B is screened for in routine UK antenatal care because the main risk is vertical transmission from mother to baby, largely around delivery. In PACES this usually appears as a counselling scenario.

All pregnant women are offered hepatitis B screening as part of routine antenatal bloods.
The risk of vertical transmission rises with a high maternal viral load and e-antigen (HBeAg) positivity.
Antiviral therapy (tenofovir) is considered in the third trimester when the viral load is high, to reduce transmission.
Babies of hepatitis B positive mothers receive a birth-dose vaccine and, where indicated, hepatitis B immunoglobulin, then complete the vaccination course.
Breastfeeding is not contraindicated once the infant has been appropriately immunised.
The skill being tested is explaining the plan clearly and reassuringly, and addressing the mother's fears about harming her baby.

Diabetes and fasting in Ramadan

Many patients with diabetes choose to fast during Ramadan even when they are exempt, so the safe approach is shared decision-making and a pre-Ramadan risk assessment, not simply advising against it.

Risk-stratify first: type 1 diabetes, recent DKA or severe hypoglycaemia, poor control, significant renal impairment and pregnancy are high risk, and fasting may be inadvisable.
The main dangers are hypoglycaemia (especially with sulfonylureas and insulin), hyperglycaemia and DKA, dehydration and thrombosis.
Medication is usually re-timed so the larger dose covers the evening meal (iftar), with reduced doses for the pre-dawn meal (suhoor).
Sulfonylureas and insulin regimens need review to avoid daytime hypoglycaemia; metformin timing is adjusted around the two meals.
Advise breaking the fast if blood glucose falls below 3.9 mmol/L or climbs dangerously high, and safety-net clearly.
The marks are in eliciting the patient's wishes, assessing risk, and giving practical, respectful advice.

Isoniazid resistance and TB adherence

Tuberculosis stations usually test communication around adherence and public health rather than drug trivia. Isoniazid resistance is a useful peg for explaining why completing treatment matters.

Standard treatment is an intensive phase of four drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) followed by a continuation phase of rifampicin and isoniazid.
Isoniazid resistance is one of the commoner forms of resistance, confirmed on drug-susceptibility testing, and regimens are adjusted on specialist advice.
Poor adherence is the main driver of acquired drug resistance, which is why finishing the full course is essential.
Directly observed therapy is offered to patients at higher risk of not completing treatment.
TB is a notifiable disease, so contact tracing and public health involvement are expected.
The skill being tested is explaining, without blame, why every dose matters and how the team will support the patient to finish treatment.

The recurring must-know points

Clubbing and its causes, the stigmata of chronic liver disease, and the features that separate an upper from a lower motor neurone lesion.
Valve lesions: how to describe the murmur, where it radiates, and what raises or lowers its intensity.
Common inheritance patterns and the conditions that go with them, such as polycystic kidney disease and neurofibromatosis.
Safe prescribing and monitoring points, which examiners like to probe in the consultation stations.

How to use MedPrep alongside PACES prep

A guide like this points you at the right topics, but PACES is passed at the bedside. Use it to prioritise, then rehearse examinations and consultations with colleagues on real or simulated patients.

Use the MRCP Part 1 and Part 2 question banks to lock in the medicine behind each case.
Use the textbook to read around any topic here that feels shaky.
Practise your examination routines out loud and against the clock until they are automatic.

Start practising

MRCP Part 1 questions MRCP Part 2 questions