Ten free MRCP Part 1 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 1 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.

How to get the most out of ten questions

Ten questions will not tell you whether you are ready. What they will tell you is whether you are revising the right way. As you work through them, notice which of the three failure modes you fall into.

The first is not knowing the fact. That is the easiest to fix and the least common cause of failure at this level.

The second is knowing the fact but not recognising it in the stem, because the question describes a patient rather than naming a condition. This is what best-of-five actually tests, and it is why reading a textbook feels productive but does not move your score.

The third is narrowing to two options and choosing wrongly. That is a discrimination problem, and the only reliable cure is reading why the near-miss option is wrong, repeatedly, across hundreds of questions.

The questions

Question 1

A 68-year-old woman has 18 months of slowness, stiffness and a resting tremor of her right hand. Her symptoms now make it hard to dress, cook and write, and she has had to stop her part-time job. Examination shows asymmetrical bradykinesia with rigidity and a 4 to 6 Hz rest tremor. She has no cognitive impairment, falls or hallucinations.

What is the most appropriate initial treatment?

  1. No treatment until symptoms are more severe
  2. Levodopa (with a dopa-decarboxylase inhibitor)
  3. An anticholinergic such as trihexyphenidyl
  4. An ergot-derived dopamine agonist
  5. Amantadine

Answer: B — Levodopa (with a dopa-decarboxylase inhibitor)

Parkinson disease is diagnosed clinically using the UK Parkinson’s Disease Society Brain Bank or Movement Disorder Society criteria, based on bradykinesia with rest tremor and/or rigidity, with supportive features such as asymmetry and a good response to levodopa. Diagnosis should be made by a specialist, and DaTscan (SPECT) can help when the diagnosis is uncertain.

Pathophysiology: loss of dopaminergic neurones in the substantia nigra pars compacta, associated with alpha-synuclein Lewy body pathology, depletes striatal dopamine and disrupts basal ganglia motor circuits; levodopa is converted to dopamine in surviving nigrostriatal terminals, restoring dopaminergic signalling.

NICE NG71 recommends levodopa for people in the early stages of Parkinson disease whose motor symptoms affect their quality of life. For people whose motor symptoms do not yet affect quality of life, a choice of levodopa, a non-ergot dopamine agonist or an MAO-B inhibitor should be considered after discussing benefits and harms. Levodopa gives the best symptomatic control but is associated with motor fluctuations and dyskinesias later on; dopamine agonists carry risks of impulse control disorders, excessive sleepiness and hallucinations. Anticholinergics are not recommended as first-line treatment because of cognitive adverse effects, and ergot-derived agonists should not be used first line.

Clinical Tip: For early Parkinson disease that affects quality of life, NICE recommends levodopa; when symptoms do not affect quality of life, levodopa, a non-ergot dopamine agonist or an MAO-B inhibitor can be chosen.

Reference: NICE NG71 Parkinson’s disease in adults (2017).

Question 2

A 32-year-old woman has difficulty releasing her grip after shaking hands, weakness of her hands and frequent tripping. She has bilateral ptosis, frontal balding, temporal wasting, a long thin face and early cataracts. Her mother had a pacemaker inserted at 50 and her baby was floppy at birth.

HbA1c is 52 mmol/mol. ECG shows a PR interval of 240 ms.

What is the most likely diagnosis?

  1. Myasthenia gravis
  2. Facioscapulohumeral muscular dystrophy
  3. Myotonic dystrophy type 1
  4. Mitochondrial myopathy
  5. Duchenne muscular dystrophy carrier

Answer: C — Myotonic dystrophy type 1

Myotonic dystrophy type 1 (DM1) is the commonest adult-onset muscular dystrophy. It is autosomal dominant and multisystem, causing myotonia (delayed muscle relaxation, such as grip myotonia), distal and facial weakness, ptosis, temporal and masseter wasting, frontal balding, early cataracts, cardiac conduction disease and arrhythmias, insulin resistance and diabetes, hypogonadism, cognitive and sleep problems, and respiratory muscle weakness. Congenital DM1, with severe hypotonia, usually occurs when the condition is inherited from the mother.

Pathophysiology: DM1 is caused by an expanded CTG repeat in the 3’ untranslated region of the DMPK gene on chromosome 19; the expanded RNA accumulates in nuclear foci and sequesters splicing regulators such as MBNL1, causing widespread mis-splicing of genes including the muscle chloride channel (causing myotonia) and the insulin receptor. The repeat shows anticipation, particularly with maternal transmission.

Diagnosis is by genetic testing. Cardiac conduction disease is the main cause of sudden death, so patients need at least annual ECG, with Holter monitoring, electrophysiological study and pacemaker or ICD insertion as indicated. Anaesthetic risks include sensitivity to sedatives and opioids, and suxamethonium should be avoided. Myotonia can be treated with mexiletine if troublesome, after cardiac assessment.

Clinical Tip: Grip myotonia, ptosis, frontal balding, cataracts, diabetes and cardiac conduction disease indicate myotonic dystrophy type 1 (DMPK CTG expansion); annual ECG surveillance is essential.

Reference: Myotonic Dystrophy Foundation consensus-based care recommendations for adults with DM1 (2018); NCBI Bookshelf GeneReviews: Myotonic Dystrophy Type 1.

Question 3

A 46-year-old man with alcohol excess was treated for pneumococcal meningitis with intravenous ceftriaxone and dexamethasone. He has made a good recovery and is due for discharge.

Which long-term complication is most common after bacterial meningitis, and what follow-up should be arranged?

  1. Hydrocephalus; arrange routine CT in 1 year
  2. Sensorineural hearing loss; arrange formal audiology before discharge where possible, and within 4 weeks of being well enough to test
  3. Epilepsy; start prophylactic levetiracetam
  4. Cerebral abscess; arrange routine MRI
  5. Pituitary failure; check hormones annually

Answer: B — Sensorineural hearing loss; arrange formal audiology before discharge where possible, and within 4 weeks of being well enough to test

Bacterial meningitis carries a high risk of long-term sequelae, which affect up to a third of survivors of pneumococcal meningitis. Sensorineural hearing loss is the commonest neurological complication, followed by cognitive impairment, focal deficits, epilepsy and hydrocephalus. Hearing loss can progress rapidly to cochlear ossification, which makes cochlear implantation difficult, so early detection is important.

Pathophysiology: bacteria and inflammatory mediators spread from the subarachnoid space along the cochlear aqueduct into the perilymph, causing suppurative labyrinthitis with damage to hair cells and the spiral ganglion; subsequent fibrosis and ossification of the cochlea (labyrinthitis ossificans) can follow within weeks.

NICE NG240 recommends a formal audiological assessment as soon as possible, preferably before discharge from hospital and no later than 4 weeks after being well enough to be tested, with urgent referral for cochlear implant assessment if profound hearing loss is found. Adjunctive dexamethasone, started with or before the first antibiotic dose, reduces hearing loss and death in pneumococcal meningitis in high-income settings. Survivors should also be offered follow-up for psychological, cognitive and neurological effects, and assessed for predisposing factors such as CSF leak, immunodeficiency or asplenia, with pneumococcal vaccination where appropriate.

Clinical Tip: Sensorineural hearing loss is the commonest complication of bacterial meningitis; arrange formal audiology within 4 weeks, with urgent cochlear implant referral if profound loss is found.

Reference: NICE NG240 Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management (2024).

Question 4

A 68-year-old man presents with progressive lower urinary tract symptoms, including urinary hesitancy, a weak stream, nocturia and a sensation of incomplete bladder emptying. Examination is consistent with benign prostatic hyperplasia (BPH). He is started on finasteride.

Which of the following statements regarding finasteride is correct?

  1. It provides symptomatic relief within 24 hours
  2. It acts by relaxing prostatic smooth muscle
  3. It inhibits conversion of testosterone to dihydrotestosterone
  4. It increases PSA levels
  5. It is associated with immediate reduction in prostate size

Answer: C — It inhibits conversion of testosterone to dihydrotestosterone

Finasteride is a 5-alpha reductase inhibitor. It blocks the conversion of testosterone to dihydrotestosterone (DHT), the androgen mainly responsible for prostatic growth. Lower DHT levels gradually shrink the prostate and slow disease progression, reducing the risk of acute urinary retention and the need for surgery.

Its onset is slow: symptomatic benefit may take up to six months, and patients should be counselled about this. This contrasts with alpha-blockers such as tamsulosin and alfuzosin, which relax smooth muscle in the prostate and bladder neck and improve symptoms within days. Finasteride lowers serum PSA by about 50%, so PSA results must be interpreted accordingly. Adverse effects include reduced libido, erectile and ejaculatory dysfunction, and gynaecomastia.

NICE recommends offering a 5-alpha reductase inhibitor to men with moderate to severe symptoms and a prostate estimated to be larger than 30 g, or a PSA above 1.4 ng/ml, who are considered at high risk of progression. Combination with an alpha-blocker can be considered for bothersome moderate to severe symptoms with an enlarged prostate.

Clinical Tip: finasteride inhibits conversion of testosterone to DHT; it shrinks the prostate slowly and halves the PSA.

Reference: NICE CG97. Lower urinary tract symptoms in men: management.

Question 5

A 45-year-old man presents to ambulatory care with a two-month history of progressive fatigue. He reports unintentional weight loss, early satiety and reduced appetite, and over the past two weeks has had several episodes of night sweats. On examination he has pale conjunctivae and a large, firm mass in the left upper quadrant consistent with splenomegaly. He is haemodynamically stable and afebrile.

Initial blood tests show haemoglobin 105 g/L, platelets 150 × 109/L and a markedly raised white cell count of 50 × 109/L. CT of the abdomen shows massive splenomegaly. A blood film has been sent, and the on-call haematologist has arranged a bone marrow biopsy and cytogenetic analysis, but results are not yet available.

Which of the following findings would support a diagnosis of chronic myeloid leukaemia rather than myelofibrosis?

  1. t(8;21) translocation
  2. Low leucocyte alkaline phosphatase score
  3. t(15;17) translocation
  4. Raised leucocyte alkaline phosphatase score
  5. Massive splenomegaly

Answer: B — Low leucocyte alkaline phosphatase score

The leucocyte alkaline phosphatase (LAP) score helps distinguish chronic myeloid leukaemia (CML) from other causes of a high white cell count with splenomegaly. It is characteristically low in CML, whereas it is normal or raised in myelofibrosis and in reactive leucocytosis (leukaemoid reaction). A low LAP score therefore supports CML.

Massive splenomegaly occurs in both CML and myelofibrosis and does not help to separate them. Myelofibrosis is suggested instead by a leucoerythroblastic film with teardrop poikilocytes and a dry tap on bone marrow aspiration.

In current practice, the diagnosis of CML is confirmed by detecting the Philadelphia chromosome, t(9;22), or the BCR::ABL1 fusion gene by cytogenetics, FISH or PCR, and the LAP score is now rarely used. BCR::ABL1 encodes a constitutively active tyrosine kinase, the target of tyrosine kinase inhibitors such as imatinib. The other translocations listed are associated with acute leukaemias: t(15;17) with acute promyelocytic leukaemia and t(8;21) with acute myeloid leukaemia.

Clinical Tip: a low LAP score supports CML; diagnosis is confirmed by BCR::ABL1.

Reference: European LeukemiaNet 2020 recommendations for treating chronic myeloid leukaemia (Hochhaus et al., Leukemia 2020).

Question 6

A 62-year-old man with known renal cell carcinoma, currently receiving treatment, presents to the medical take with a one-month history of progressively worsening central lower back pain. The pain is poorly controlled with home analgesia and is worse at night. He has no other new symptoms, and neurological examination is normal.

Which investigation should be performed next?

  1. X-ray whole spine
  2. CT lumbar spine
  3. MRI whole spine
  4. Isotope bone scan
  5. X-ray lumbar and sacral spine

Answer: C — MRI whole spine

This man has a malignancy that commonly metastasises to bone and new, progressive back pain that is worse at night. Spinal metastases must therefore be suspected, and the investigation of choice is MRI of the whole spine. Metastases often occur at several levels, so imaging only the symptomatic region can miss disease.

Plain radiographs are insensitive, as a large proportion of bone must be destroyed before a lesion is visible, and CT or a bone scan cannot reliably assess the spinal cord. Renal cell carcinoma metastases are often lytic, which further reduces the value of a bone scan.

NICE recommends MRI of the whole spine within one week for people with suspected spinal metastases without neurological symptoms. If there are symptoms or signs of metastatic spinal cord compression, such as limb weakness, sensory change or sphincter disturbance, MRI should be performed immediately and within 24 hours, and the patient should be discussed urgently with the MSCC coordinator.

Clinical Tip: suspected spinal metastases need MRI whole spine, within one week without neurology and within 24 hours if cord compression is suspected.

Reference: NICE NG234. Spinal metastases and metastatic spinal cord compression (2023).

Question 7

A 25-year-old female presents with recurrent sinopulmonary infections. Which one of the following investigations is most likely to confirm a primary immunodeficiency?

  1. IgM level
  2. IgG level
  3. B cell level
  4. T cell level
  5. Complement (CH50) assay

Answer: B — IgG level

Recurrent sinopulmonary infections in a young adult strongly suggest a primary antibody deficiency, most commonly common variable immunodeficiency (CVID). Antibody deficiencies predispose to infection with encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae.

Measuring serum immunoglobulins, particularly IgG, is the key investigation. The diagnosis of CVID requires a marked reduction in IgG together with low IgA and/or IgM, plus poor specific antibody responses to vaccination, after secondary causes of hypogammaglobulinaemia (for example, protein loss, haematological malignancy or immunosuppressive drugs) have been excluded.

Other primary immunodeficiencies show different patterns. X-linked agammaglobulinaemia causes absent circulating B cells and usually presents in early childhood. T-cell defects predispose mainly to viral, fungal and opportunistic infections, and complement deficiencies are associated with recurrent Neisseria infections.

Clinical Tip: recurrent sinopulmonary infection points to antibody deficiency; check serum immunoglobulins (IgG, IgA, IgM) first.

Reference: ESID Registry working definitions for the clinical diagnosis of inborn errors of immunity.

Question 8

Which one of the following cytogenetic abnormalities is most strongly associated with acute promyelocytic leukaemia (APL)?

  1. t(9;17)
  2. t(15;17)
  3. t(9;22)
  4. t(15;22)
  5. t(17;22)

Answer: B — t(15;17)

Acute promyelocytic leukaemia (APL) is a distinct subtype of acute myeloid leukaemia defined by the t(15;17) translocation. This creates the PML::RARA fusion gene, which blocks myeloid differentiation at the promyelocyte stage, so abnormal promyelocytes accumulate in the bone marrow and blood.

APL typically presents with bleeding caused by disseminated intravascular coagulation and hyperfibrinolysis, and it is a medical emergency because of the high risk of early haemorrhagic death. Treatment with all-trans retinoic acid (ATRA) should start as soon as the diagnosis is suspected from the blood film, without waiting for genetic confirmation, together with aggressive support of the coagulopathy.

ATRA combined with arsenic trioxide is now standard first-line therapy for non-high-risk disease and achieves cure rates of over 90%. Other translocations in the options are associated with different conditions: t(9;22) with chronic myeloid leukaemia and t(8;21) with core-binding factor AML.

Clinical Tip: t(15;17) and PML::RARA define APL; start ATRA immediately on suspicion.

Reference: European LeukemiaNet recommendations for the management of APL (Sanz et al., Blood 2019).

Question 9

Which type of infection is most likely to be transmitted following a platelet transfusion?
  1. Hepatitis B
  2. Malaria
  3. Syphilis
  4. Bacterial
  5. HIV

Answer: D — Bacterial

Platelet concentrates are stored at room temperature (20–24°C) to preserve platelet function, unlike red cells and plasma, which are stored cold. These conditions favour bacterial growth, so bacterial contamination is the most likely transfusion-transmitted infection after a platelet transfusion.

The usual organisms are skin commensals introduced at venepuncture, such as coagulase-negative staphylococci and Staphylococcus aureus; Gram-negative organisms are less common but cause more severe sepsis. In the UK, platelet units are screened for bacteria before release, which has greatly reduced but not eliminated this risk.

Patients may develop fever, rigors, hypotension or septic shock during or shortly after the transfusion. Stop the transfusion immediately, take blood cultures from the patient, return the unit to the laboratory for culture, start broad-spectrum intravenous antibiotics and report the event. Viral transmission (HIV, hepatitis B and C) is now very rare because of donor selection and testing.

Clinical Tip: bacterial contamination is the commonest transfusion-transmitted infection, and platelets carry the highest risk because they are stored at room temperature.

Reference: Serious Hazards of Transfusion (SHOT) Annual Report; JPAC Guidelines for the Blood Transfusion Services in the UK.

Question 10

Which one of the following organisms is most contagious?

  1. Mycobacterium tuberculosis
  2. Influenza virus
  3. Measles virus
  4. Varicella-zoster virus
  5. Mumps virus

Answer: C — Measles virus

Measles is the most contagious of these infections. Its basic reproduction number (R0) is typically 12–18, meaning one infected person can infect 12–18 susceptible individuals. Transmission is airborne, and the virus can remain infectious in the air of a room for up to two hours after the infected person has left, so outbreaks spread rapidly in non-immune populations.

Varicella-zoster virus is also highly infectious, spreading through respiratory secretions and direct contact with vesicle fluid, but its transmissibility is lower than that of measles. Influenza and mumps have considerably lower R0 values, and Mycobacterium tuberculosis requires prolonged close contact for transmission.

Clinical Tip: measles is the most contagious common infection in clinical practice. Two doses of MMR vaccine are required for reliable protection, and any suspected case should be isolated and notified urgently to the local UKHSA health protection team.

Reference: UKHSA. Immunisation against infectious disease (the Green Book), Chapter 21: Measles.

What the exam actually looks like

MRCP Part 1 is two papers of 100 best-of-five questions, three hours each, with a break between them. 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, not as a fixed percentage, which is why comparing your score with a friend from a different sitting tells you very little.

Two hundred questions across six hours gives you a little under two minutes each. Most candidates who run out of time do so by returning repeatedly to questions they are unsure of rather than committing and moving on.

If you want more than ten

The full bank carries over 2,600 MRCP Part 1 questions across the whole blueprint, each 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: when you have narrowed five options to two, stop and ask which single detail in the stem the examiner put there to separate them. There almost always is one, and finding it is a more reliable method than weighing the options against each other.

MRCP Part 1 question bank · Difference between Part 1 and Part 2 · Specialty Certificate Exams explained · How to interpret an ABG

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