Ten free MRCP Part 2 questions in the real best-of-five format, each with a full explanation of why the answer is right and why the other four are wrong.

These are real questions from the License Medical MRCP Part 2 bank, not simplified samples. Every explanation is written by a UK consultant and referenced to UK guidance. Work through them the way you would in the exam: commit to an answer before you read the explanation, and read the reasoning for the options you rejected as well as the one you chose.

What makes Part 2 different from Part 1

Part 2 stems are longer and carry more data. You are given the history, the examination and usually a set of results, and the question is what to do next rather than what the mechanism is. That changes how you should read: find the decision being asked before you read the options, because the options are usually five reasonable-sounding next steps rather than five diagnoses.

The second difference is that Part 2 rewards knowing guidelines rather than knowing physiology. Where Part 1 asks why a drug works, Part 2 asks which drug, at what point, in this patient.

The questions

Question 1

A 78-year-old man is admitted to the Acute Medical Unit with dizziness and presyncope. His pulse is 38 beats/min and blood pressure is 95/60 mmHg. An ECG confirms complete heart block.

Which of the following findings would indicate the lowest immediate risk of progression to asystole?

  1. Recent episode of asystole
  2. Ventricular pause lasting 5 seconds
  3. Mobitz type II atrioventricular block
  4. Complete heart block with a broad QRS escape rhythm
  5. Complete heart block with a narrow QRS escape rhythm

Answer: E — Complete heart block with a narrow QRS escape rhythm

In complete heart block the patient’s stability depends largely on the site of the escape pacemaker. A narrow QRS escape rhythm usually arises from the atrioventricular junction, at or above the bundle of His. Junctional escape rhythms are typically faster (around 40–60 beats/min), more reliable and more responsive to atropine, so the immediate risk of asystole is lower.

The other options are the recognised risk factors for asystole in the Resuscitation Council UK adult bradycardia algorithm: recent asystole, Mobitz type II atrioventricular block, complete heart block with a broad QRS complex, and a ventricular pause of more than 3 seconds. A broad QRS escape rhythm indicates infranodal (ventricular) escape, which is slow, unreliable and liable to fail suddenly; a 5-second pause and a recent episode of asystole are direct evidence of escape failure.

Management follows the ABCDE approach: correct reversible causes (hyperkalaemia, ischaemia, rate-limiting drugs such as beta-blockers, digoxin, verapamil or diltiazem) and give atropine 500 micrograms IV, repeated to a maximum of 3 mg, if there are adverse features (shock, syncope, myocardial ischaemia or heart failure). If the response is inadequate or a risk factor for asystole is present, consider an isoprenaline or adrenaline infusion and transcutaneous pacing, and seek expert help for transvenous pacing as a bridge to permanent pacemaker implantation.

In older people always review the drug chart: rate-limiting drugs and cholinesterase inhibitors such as donepezil are common, reversible contributors to bradycardia, syncope and falls.

Clinical Tip: In complete heart block a narrow QRS (junctional) escape rhythm carries a lower risk of asystole than a broad QRS escape rhythm, Mobitz II block, recent asystole or ventricular pauses over 3 seconds.

Reference: Resuscitation Council UK Adult Bradycardia Algorithm (2021); ESC Guidelines on cardiac pacing and cardiac resynchronisation therapy (2021).

Question 2

A 76-year-old man is admitted to the Acute Medical Unit with palpitations and dizziness. An ECG shows typical atrial flutter with 2:1 atrioventricular conduction and a ventricular rate of 150 beats/min. He is haemodynamically stable and responds to initial rate-control therapy.

He reports several previous admissions with the same arrhythmia over the past year despite medical treatment.

Which of the following is the most effective definitive treatment?

  1. Amiodarone
  2. Bisoprolol
  3. Digoxin
  4. Electrical cardioversion
  5. Radiofrequency ablation of the cavotricuspid isthmus

Answer: E — Radiofrequency ablation of the cavotricuspid isthmus

Typical atrial flutter is caused by a macro-re-entrant circuit in the right atrium that depends on conduction through the cavotricuspid isthmus (CTI), the strip of tissue between the tricuspid annulus and the inferior vena cava. Radiofrequency ablation of the CTI creates a line of conduction block that interrupts the circuit. It has acute success rates above 95% and long-term freedom from flutter in about 90% of patients, which is far better than any drug. The ESC 2024 AF guideline recommends CTI ablation for patients with typical flutter who have failed antiarrhythmic drugs, and it is reasonable as first-line rhythm control for recurrent symptomatic flutter.

Amiodarone has limited efficacy in preventing flutter and significant long-term toxicity (thyroid, lung, liver, skin), which is particularly relevant in older people. Bisoprolol and digoxin control ventricular rate only; flutter is notoriously difficult to rate-control and digoxin is a poor choice in active patients. Electrical cardioversion restores sinus rhythm acutely but leaves the circuit intact, so recurrence is common.

Unstable patients need immediate synchronised DC cardioversion. All patients should have stroke risk assessed with CHA2DS2-VA (ESC 2024) or CHA2DS2-VASc (NICE NG196) and be anticoagulated in the same way as for atrial fibrillation, usually with a DOAC. Many patients go on to develop atrial fibrillation after flutter ablation, so ongoing monitoring and anticoagulation decisions remain important. Age alone is not a contraindication to ablation; frailty, comorbidity and the patient’s goals should guide the decision.

Clinical Tip: Recurrent typical (CTI-dependent) atrial flutter is best treated definitively by cavotricuspid isthmus radiofrequency ablation; anticoagulate as for atrial fibrillation.

Reference: ESC Guidelines for the management of atrial fibrillation (2024); NICE NG196 Atrial fibrillation: diagnosis and management (2021).

Question 3

A 74-year-old man with moderate COPD presents with acute breathlessness after collapsing while shopping. He has never had syncope before. Four weeks ago he had bilateral varicose vein surgery, and he had an open cholecystectomy 10 years ago.

He is breathless at rest and apyrexial. Pulse 104 beats/min, blood pressure 110/60 mmHg. Heart sounds are normal, there is scattered wheeze and neurological examination is normal.

ECG: sinus tachycardia with T-wave inversion in V1–V3

Chest X-ray: normal

Oxygen saturation: 92% on 40% oxygen

Peak expiratory flow: 290 L/min

What is the most likely diagnosis?

  1. Acute pulmonary oedema
  2. Acute exacerbation of COPD
  3. Pulmonary embolism
  4. Acute myocardial infarction
  5. Pneumocystis pneumonia

Answer: C — Pulmonary embolism

Syncope followed by sudden breathlessness, marked hypoxaemia despite 40% oxygen, a clear chest X-ray and anterior T-wave inversion (right ventricular strain) four weeks after surgery strongly suggest pulmonary embolism. Recent surgery is a major provoking risk factor and the risk remains raised for up to 12 weeks. Syncope in PE indicates a large clot burden with transient obstruction of right ventricular outflow and is a marker of higher risk.

An exacerbation of COPD would not usually cause syncope or such severe hypoxaemia with a relatively preserved peak flow and minimal wheeze. Pulmonary oedema would show on the chest X-ray. Myocardial infarction is less likely with no chest pain and T-wave changes confined to V1 to V3 in this context. Pneumocystis pneumonia occurs in immunosuppressed patients and develops over days to weeks.

Management follows NICE NG158: assess haemodynamic stability, give interim anticoagulation (for example apixaban or LMWH) while arranging CTPA, and use echocardiography and troponin to stratify risk. Thrombolysis is reserved for PE with haemodynamic compromise. In older people, PE often presents with collapse, falls or delirium rather than classic pleuritic pain, so a high index of suspicion is needed.

Clinical Tip: Syncope with sudden breathlessness, severe hypoxaemia, a clear chest X-ray and right heart strain after recent surgery indicates pulmonary embolism.

Reference: NICE NG158 Venous thromboembolic diseases: diagnosis, management and thrombophilia testing (2020, updated 2023); ESC Guidelines for acute pulmonary embolism (2019).

Question 4

A 29-year-old woman with autoimmune hypothyroidism presents with 4 months of fluctuating weakness, most noticeable in her arms. She reports intermittent double vision that is worse in the evening. A recent optician assessment was normal. Examination between episodes is unremarkable.

What is the most likely diagnosis?

  1. Myasthenia gravis
  2. Multiple sclerosis
  3. Thyrotoxic myopathy
  4. Mitochondrial myopathy
  5. Lambert-Eaton myasthenic syndrome

Answer: A — Myasthenia gravis

Fatigable, fluctuating weakness with diplopia worse later in the day is typical of myasthenia gravis, an autoimmune disorder of the neuromuscular junction. It is associated with other autoimmune diseases, especially autoimmune thyroid disease, which affects about 10 to 15% of patients.

Investigation includes acetylcholine receptor antibodies (positive in about 85% of generalised disease), MuSK and LRP4 antibodies if negative, neurophysiology (repetitive nerve stimulation or single-fibre EMG), CT of the chest for thymoma, and thyroid function. Respiratory function should be monitored with forced vital capacity in generalised disease. Treatment includes pyridostigmine, corticosteroids and immunosuppressants, and thymectomy in selected patients.

Multiple sclerosis causes relapsing deficits with objective signs. Thyrotoxic myopathy requires hyperthyroidism. Mitochondrial myopathy causes fixed, slowly progressive weakness and ophthalmoplegia. Lambert-Eaton syndrome causes proximal leg weakness that improves briefly with exercise, autonomic symptoms and reduced reflexes, and is often associated with small cell lung cancer.

Clinical Tip: Fatigable weakness with diplopia worse in the evening suggests myasthenia gravis, which is associated with autoimmune thyroid disease.

Reference: Association of British Neurologists. Myasthenia gravis management guidelines (2015); Narayanaswami P et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology 2021.

Question 5

A 62-year-old man with metastatic melanoma has been receiving a PD-1 inhibitor for 8 weeks. He develops fatigue and mild weight gain. Thyroid function initially showed a suppressed TSH with a raised free T4, followed a few weeks later by a raised TSH and low free T4. Thyroid antibodies are negative.

Which one of the following statements about immune checkpoint inhibitor-related thyroid dysfunction is incorrect?

  1. Hypothyroidism occurs more often with PD-1 inhibitors than with CTLA-4 inhibitors
  2. Combined CTLA-4 and PD-1 or PD-L1 blockade has the highest rate of thyroid dysfunction
  3. Graves' disease occurs in about 10% of patients receiving therapy
  4. A heterogeneous gland on ultrasound is associated with a higher risk of hypothyroidism
  5. Thyrotoxicosis from destructive thyroiditis is much more common than Graves' disease

Answer: C — Graves' disease occurs in about 10% of patients receiving therapy

Thyroid dysfunction is the commonest endocrine adverse effect of immune checkpoint inhibitors. The typical pattern is a painless destructive thyroiditis: a short thyrotoxic phase from release of preformed hormone, often within 4 to 8 weeks, followed by permanent hypothyroidism in many patients, as in this man. Graves’ disease is rare (well under 1%), so the statement that it occurs in about 10% is incorrect.

Thyroid dysfunction is more frequent with PD-1 and PD-L1 inhibitors than with CTLA-4 inhibitors, and highest with combination therapy. Pre-existing thyroid antibodies and a heterogeneous gland on ultrasound predict progression to hypothyroidism.

Management: check TFTs before each cycle; treat the thyrotoxic phase with a beta-blocker (antithyroid drugs are ineffective in thyroiditis); start levothyroxine when hypothyroid. Always check cortisol, because coexisting hypophysitis or adrenalitis with ACTH deficiency must be treated with hydrocortisone before levothyroxine. Immunotherapy can usually continue.

Clinical Tip: Checkpoint inhibitor thyroid disease is usually transient destructive thyroiditis progressing to hypothyroidism; Graves’ disease is rare; exclude cortisol deficiency before starting levothyroxine.

Reference: Society for Endocrinology Endocrine Emergency Guidance: acute management of endocrine complications of checkpoint inhibitor therapy (2018); ESMO Clinical Practice Guideline on management of toxicities from immunotherapy (2022).

Question 6

A 72-year-old man is brought to the emergency department with 2 days of confusion and lethargy. He has poorly controlled type 2 diabetes and hypertension. He appears dehydrated with dry mucous membranes.

Temperature 37.0°C, blood pressure 100/60 mmHg, pulse 110 beats/min, respiratory rate 14/min. His chest is clear, heart sounds are normal, the abdomen is soft and non-tender, and there is no rash. He has mild generalised weakness.

Investigations:

Sodium 134 mmol/L

Potassium 5.9 mmol/L

Chloride 101 mmol/L

Bicarbonate 22 mmol/L

Urea 18.6 mmol/L

Creatinine 133 µmol/L

Calcium 2.28 mmol/L

Glucose 59.4 mmol/L

What is the most likely diagnosis?

  1. Hyperosmolar hyperglycaemic state
  2. Diabetic ketoacidosis
  3. Septic encephalopathy
  4. Hypoglycaemia
  5. Alcoholic ketoacidosis

Answer: A — Hyperosmolar hyperglycaemic state

This is hyperosmolar hyperglycaemic state (HHS). There is profound hyperglycaemia with dehydration and altered consciousness but no significant acidosis (bicarbonate 22 mmol/L). Calculated osmolality (2 × Na + glucose + urea) is about 2 × 134 + 59.4 + 18.6, roughly 346 mOsm/kg. The Joint British Diabetes Societies (JBDS) criteria for HHS are hypovolaemia, glucose of 30 mmol/L or more, osmolality of 320 mOsm/kg or more, and no significant ketonaemia (below 3.0 mmol/L) or acidosis (pH above 7.3, bicarbonate above 15 mmol/L). The corrected sodium is around 150 mmol/L, reflecting a large free water deficit. The raised potassium reflects insulin deficiency and shift out of cells; total body potassium is depleted.

Diabetic ketoacidosis requires ketonaemia of 3.0 mmol/L or more and acidosis (bicarbonate below 15 mmol/L or pH below 7.3), absent here, although mixed DKA/HHS occurs. Septic encephalopathy is unlikely with a normal temperature and no focus, although infection is a common precipitant and must be sought. Hypoglycaemia and alcoholic ketoacidosis do not fit the glucose or acid-base results.

JBDS management emphasises gradual correction: 0.9% sodium chloride first, aiming for a fall in osmolality of 3–8 mOsm/kg/hour and in glucose of no more than 5 mmol/L/hour. Insulin (fixed-rate 0.05 units/kg/hour) is started only once glucose stops falling with fluids alone, unless there is significant ketonaemia. Monitor potassium closely and give prophylactic low molecular weight heparin, as thrombotic risk is high.

Older patients are at particular risk because of impaired thirst, cognitive impairment and dependence on others for fluids; they are also prone to fluid overload, cerebral oedema with over-rapid correction, and pressure damage, especially to the heels, which should be checked daily.

Clinical Tip: HHS is defined by glucose of 30 mmol/L or more, osmolality of 320 mOsm/kg or more and no significant ketosis or acidosis; correct it slowly with fluids first and add insulin only when glucose stops falling.

Reference: Joint British Diabetes Societies for Inpatient Care: The management of the hyperosmolar hyperglycaemic state (HHS) in adults (2022 update).

Question 7

A 70-year-old man presents with progressive fatigue, dizziness on standing and reduced exercise tolerance. He has a history of Graves’ disease treated with radioiodine and pernicious anaemia. He takes levothyroxine 150 micrograms daily with good adherence and receives regular vitamin B12 injections.

On examination his blood pressure is 98/60 mmHg with a postural drop. He appears tired but is afebrile.

Investigations:

TSH 8.5 mU/L

Free T4 low-normal

Sodium 130 mmol/L

Coeliac screen negative

Despite recent increases in his levothyroxine dose, his TSH remains elevated.

What is the most appropriate next step in management?

  1. Increase levothyroxine dose further
  2. Start fludrocortisone
  3. Perform short Synacthen test
  4. Arrange thyroid hormone absorption test
  5. Measure reverse T3

Answer: C — Perform short Synacthen test

This man has two autoimmune endocrine/haematological conditions and now has fatigue, postural hypotension and hyponatraemia. This should raise strong suspicion of primary adrenal insufficiency (Addison’s disease) as part of autoimmune polyglandular syndrome type 2. The appropriate next step is a short Synacthen test, with a paired cortisol and ACTH sample taken before it.

Glucocorticoid deficiency removes the normal inhibitory effect of cortisol on TSH secretion, so untreated adrenal insufficiency can produce a mildly raised TSH that mimics under-replaced hypothyroidism. This often settles once hydrocortisone is started. Importantly, increasing levothyroxine before correcting cortisol deficiency accelerates cortisol metabolism and can precipitate an adrenal crisis.

Increasing levothyroxine further is therefore unsafe until adrenal insufficiency is excluded. Fludrocortisone is part of treatment once the diagnosis is confirmed, but glucocorticoid replacement comes first and diagnosis should precede treatment in a stable patient. A thyroid hormone absorption test is used for suspected malabsorption or non-adherence, and reverse T3 has no role in routine practice. If the patient is unwell or crisis is suspected, give hydrocortisone 100 mg IV or IM immediately after taking blood, without waiting for results.

In older people adrenal insufficiency is easily attributed to frailty or age; unexplained hyponatraemia with postural hypotension and falls should prompt a cortisol test. Once diagnosed, patients need sick day rules and a steroid emergency card (Society for Endocrinology 2020).

Clinical Tip: Exclude adrenal insufficiency (short Synacthen test) before increasing levothyroxine in a patient with autoimmune disease, rising TSH, hyponatraemia and postural hypotension.

Reference: Society for Endocrinology Adrenal Crisis and Steroid Emergency Card guidance (2020); NICE CKS Addison’s disease (2024); NICE NG145 Thyroid disease: assessment and management (2019).

Question 8

A 48-year-old woman has headaches and fatigue. She has had hypertension for 8 years. Blood pressure is 150/90 mmHg, pulse 90 beats/min. She has central obesity, thin skin and wide purple abdominal striae.

Investigations: random glucose 6.9 mmol/L, potassium 3.3 mmol/L.

Which single test is most appropriate to support the suspected diagnosis?

  1. Overnight 1 mg dexamethasone suppression test
  2. Pituitary MRI
  3. Random serum cortisol
  4. Plasma metanephrines
  5. 09:00 plasma ACTH

Answer: A — Overnight 1 mg dexamethasone suppression test

Central obesity, purple striae, hypertension, hypokalaemia and impaired glucose suggest Cushing’s syndrome. The first step is to confirm hypercortisolism after excluding exogenous glucocorticoids. Recommended screening tests are the overnight 1 mg dexamethasone suppression test (dexamethasone at 23:00, serum cortisol at 08:00 to 09:00; a cortisol below 50 nmol/L makes Cushing’s syndrome unlikely), late-night salivary cortisol (two samples) or 24-hour urinary free cortisol (two collections).

A random cortisol is unhelpful because of diurnal variation. ACTH is measured only after hypercortisolism is confirmed, to separate ACTH-dependent from ACTH-independent causes. Pituitary MRI comes later, because pituitary incidentalomas are common and many corticotroph adenomas are too small to see. Plasma metanephrines test for phaeochromocytoma.

False-positive dexamethasone tests occur with oral oestrogen (raised cortisol-binding globulin), enzyme-inducing drugs, alcohol excess, depression and severe illness. After confirmation, a suppressed ACTH points to an adrenal cause (adrenal CT); a normal or raised ACTH points to Cushing’s disease or ectopic ACTH, separated by MRI, CRH testing and inferior petrosal sinus sampling.

Clinical Tip: Suspected Cushing’s syndrome is first confirmed biochemically, for example with an overnight 1 mg dexamethasone suppression test; ACTH and imaging follow.

Reference: Fleseriu M et al. Consensus on diagnosis and management of Cushing’s disease (Pituitary Society, 2021); Nieman LK et al. Endocrine Society guideline on the diagnosis of Cushing’s syndrome (2008).

Question 9

A 77-year-old woman is referred by her GP with an 8-month history of constipation, lethargy and weight gain. Thyroid function tests show that she is hypothyroid.

Which of the following statements is correct?

  1. The commonest cause of primary hypothyroidism in the UK is Hashimoto's thyroiditis
  2. The most discriminatory clinical feature of hypothyroidism is absent ankle jerks
  3. Cardiac evaluation is unimportant in primary hypothyroidism
  4. The ECG typically shows high-voltage complexes with bradycardia
  5. Liothyronine rather than levothyroxine is preferred in older patients

Answer: A — The commonest cause of primary hypothyroidism in the UK is Hashimoto's thyroiditis

In iodine-sufficient countries such as the UK, autoimmune (Hashimoto’s) thyroiditis is the commonest cause of primary hypothyroidism, followed by previous radioiodine or thyroid surgery. Worldwide, iodine deficiency remains the leading cause. Thyroid peroxidase antibodies are usually positive. Hypothyroidism is common in older women and presents insidiously with fatigue, weight gain, constipation, cold intolerance, dry skin, low mood and cognitive slowing, which are easily attributed to ageing.

Delayed relaxation of the ankle reflex, not absent jerks, is the classical sign, and no single clinical feature is discriminatory; diagnosis rests on a raised TSH with low free T4. The ECG shows sinus bradycardia, low-voltage complexes and flattened T waves, and pericardial effusion may occur. Cardiac assessment matters because hypothyroidism is associated with hypercholesterolaemia and ischaemic heart disease, and starting thyroxine can precipitate angina.

NICE recommends levothyroxine, not liothyronine, for primary hypothyroidism. In people over 65 or with cardiac disease, start at a low dose (25 to 50 micrograms daily) and titrate gradually, checking TSH every 3 months until stable. Over-replacement in older people increases the risk of atrial fibrillation and osteoporotic fracture.

Clinical Tip: Hashimoto’s thyroiditis is the commonest cause of primary hypothyroidism in the UK; in older people start levothyroxine at a low dose and titrate slowly.

Reference: NICE NG145 Thyroid disease: assessment and management (2019); NICE CKS Hypothyroidism (2024).

Question 10

A 38-year-old woman has had amenorrhoea for 2 years; her periods did not return after the birth of her second child. She has mood swings and hot flushes. She has vitiligo, and there is a family history of thyroid disease and type 1 diabetes.

Investigations: FSH 34 U/L, LH 21 U/L, oestradiol below 70 pmol/L, prolactin 550 mU/L (below 500).

What is the most likely diagnosis?

  1. Sheehan's syndrome
  2. Premature ovarian insufficiency
  3. Prolactinoma
  4. Carcinoid syndrome
  5. Polycystic ovary syndrome

Answer: B — Premature ovarian insufficiency

Raised gonadotrophins with a low oestradiol and menopausal symptoms in a woman under 40 indicate premature ovarian insufficiency (POI). The diagnosis requires oligo- or amenorrhoea for at least 4 months and an FSH above 25 U/L on two occasions 4 or more weeks apart. Her vitiligo and family history suggest autoimmune ovarian failure, possibly as part of autoimmune polyglandular syndrome type 2.

Sheehan’s syndrome follows postpartum haemorrhage and causes low gonadotrophins, failure of lactation and other pituitary deficiencies. A prolactin of 550 mU/L is barely raised and would suppress, not raise, gonadotrophins. PCOS causes normal or raised LH with normal FSH and normal oestrogen.

Investigations include karyotype, fragile X (FMR1) premutation testing, thyroid and adrenal antibodies, TSH and, if adrenal antibodies are positive, a Synacthen test. Hormone replacement therapy (or the combined pill) is recommended until the average age of menopause to protect bone and cardiovascular health. Fertility counselling should include oocyte donation, as spontaneous pregnancy occurs in only about 5%.

Clinical Tip: Raised FSH and LH with low oestradiol in a woman under 40 is premature ovarian insufficiency; screen for autoimmune and genetic causes and give HRT until about 51.

Reference: ESHRE, ASRM, CREWHIN and IMS. Evidence-based guideline: premature ovarian insufficiency (2024); NICE NG23 Menopause: identification and management (2015, updated 2024).

How the exam is marked

One mark per correct answer and nothing deducted for a wrong one, so there is never a reason to leave a question blank. The pass mark is set by a panel judging the standard expected of a candidate at that stage rather than as a fixed percentage, which is why comparing your score with a friend from a different sitting tells you very little. Confirm the current paper structure and timings on the Federation site when you apply, as these are periodically revised.

If you want more than ten

The full bank covers the whole MRCP Part 2 blueprint, each question with an explanation of this depth, written by one UK consultant rather than a rotating pool of authors. That consistency is the point: the same standard of reasoning in every explanation, so you learn one way of thinking rather than twelve.

Clinical Tip: in a Part 2 stem, read the last sentence first. It tells you whether you are being asked for the diagnosis, the next investigation or the treatment, and that single piece of information changes which details in the history matter.

MRCP Part 2 question bank · Free MRCP Part 1 questions · Difference between Part 1 and Part 2 · Specialty Certificate Exams explained

Exam marking described here is taken from the Federation of Royal Colleges of Physicians of the UK. Confirm format, dates and fees on their site before applying.