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MRCP PART 1 · HAEMATOLOGY

Haematology questions
for MRCP Part 1.

Clinora has 261 haematology single best answer questions covering 254 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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Question 1Macrocytic/haemolytic anaemiaMedium

A patient has anaemia with a raised mean corpuscular volume, raised reticulocyte count, raised unconjugated bilirubin, raised lactate dehydrogenase and low haptoglobin. Which process best explains this combination of findings?

  1. AIron deficiency
  2. BHaemolysis
  3. CBone marrow aplasia
  4. DVitamin B12 deficiency alone, without haemolysis
  5. EChronic kidney disease-related anaemia
Show answer and explanation

Answer: B Haemolysis

Each result tells part of the story. Low haptoglobin means free haemoglobin is being released and bound, which is the most specific marker of haemolysis. Raised LDH and unconjugated bilirubin reflect red-cell breakdown. The raised reticulocyte count shows a healthy marrow responding. The raised MCV fits too, because reticulocytes are larger than mature red cells, so brisk reticulocytosis raises the measured MCV. The key discriminator is the reticulocyte count. Severe B12 or folate deficiency can also raise LDH and bilirubin and lower haptoglobin, through intramedullary haemolysis (ineffective erythropoiesis), but the reticulocyte count is low because the marrow cannot make cells properly. Next steps would be a blood film (spherocytes, schistocytes, bite cells), a direct antiglobulin test to separate immune from non-immune causes, and urinalysis for haemoglobinuria.

Key clue
Raised reticulocytes, raised bilirubin/LDH, low haptoglobin
What it means
Active haemolysis
What to do
Investigate the cause of haemolysis (for example, direct antiglobulin test, blood film, haemoglobinopathy screen) and manage accordingly

Why the other options are less appropriate

  • A Iron deficiency gives a microcytic anaemia with a low reticulocyte count and none of the haemolysis markers.
  • C Aplasia gives pancytopenia with a very low reticulocyte count, the opposite of a brisk marrow response.
  • D B12 deficiency can mimic the breakdown markers through ineffective erythropoiesis, but the reticulocyte count is low, not raised.
  • E Anaemia of CKD is normocytic and caused by low erythropoietin, with a low reticulocyte count and no haemolysis markers.

Source: StatPearls: Hemolytic Anemia

Question 2Blood components/reactionsMedium

A patient develops fever, rigors, hypotension and back pain within minutes of starting a red cell transfusion. What is the most appropriate immediate action?

  1. ASlow the transfusion rate and continue, since mild reactions are expected
  2. BStop the transfusion immediately, maintain intravenous access, and check patient/unit identification while assessing for an acute haemolytic transfusion reaction
  3. CGive paracetamol only and continue the transfusion unchanged
  4. DRestart the transfusion after 10 minutes without further evaluation
  5. EDiscard the notes on the reaction, as it is not clinically significant
Show answer and explanation

Answer: B Stop the transfusion immediately, maintain intravenous access, and check patient/unit identification while assessing for an acute haemolytic transfusion reaction

Fever, rigors, hypotension and back (loin) pain within minutes of starting red cells suggest an acute haemolytic transfusion reaction. This is usually caused by ABO incompatibility after an identification error. Recipient antibodies bind the donor cells, activate complement and cause intravascular haemolysis, with a risk of shock, DIC and acute kidney injury. Severe bacterial contamination of the unit and anaphylaxis can look similar early on. The BSH guideline on acute transfusion reactions advises stopping the transfusion at once, keeping the IV line open with 0.9% sodium chloride through a new giving set, and checking the patient's identity against the unit and the paperwork. Call for senior help and resuscitate with fluids, oxygen and support for the circulation. Send the unit and giving set to the laboratory with samples for repeat group and crossmatch, direct antiglobulin test, full blood count, renal function, LDH, bilirubin, haptoglobin, coagulation and blood cultures. Monitor urine output, and report the event through SHOT and MHRA SABRE.

Key clue
Fever, rigors, hypotension and back pain shortly after starting transfusion
What it means
Possible acute haemolytic transfusion reaction
What to do
Stop the transfusion, maintain IV access, recheck identification, send samples for investigation, and manage supportively with senior and blood bank involvement

Why the other options are less appropriate

  • A Slowing the rate still gives more incompatible blood. With hypotension and back pain the transfusion must be stopped.
  • C Paracetamol may treat a mild febrile reaction, but hypotension and back pain mean a serious reaction, so the transfusion cannot continue.
  • D Restarting without investigation could give more incompatible blood. A severe reaction needs full laboratory investigation first.
  • E Every serious reaction must be documented and reported to haemovigilance schemes. Discarding the record removes the chance to learn from it.

Source: British Society for Haematology guideline on the investigation and management of acute transfusion reactions

Question 3Sickle cell/thalassaemiaMedium

A 24-year-old woman with known sickle cell disease presents to hospital with severe bone pain typical of her previous vaso-occlusive crises. What is the most appropriate approach to initial analgesia?

  1. AWithhold opioids due to concern about dependence
  2. BOffer strong analgesia, including opioids if needed, within 30 minutes of arrival
  3. CUse pethidine as the preferred opioid
  4. DDelay opioids until the full blood count and reticulocyte count are available
  5. ETreat with antibiotics alone, with no specific analgesia
Show answer and explanation

Answer: B Offer strong analgesia, including opioids if needed, within 30 minutes of arrival

Severe bone pain like her previous crises in a woman with known sickle cell disease is an acute painful (vaso-occlusive) episode. It should be treated as a medical emergency. Sickled red cells block small vessels and cause bone ischaemia, and delay causes avoidable suffering. NICE CG143 advises that analgesia is offered within 30 minutes of arrival, using her individual care plan if she has one. Assess pain severity. If a strong opioid is needed, give a bolus, and consider patient-controlled analgesia if repeated doses are needed. Offer regular paracetamol, and an NSAID unless it is contraindicated. Reassess pain, sedation, vital signs, respiratory rate and oxygen saturation every 30 minutes until pain is controlled, then at least every 4 hours. Pethidine should not be used. Prescribe a laxative, an antiemetic and an antipruritic as needed. Watch for acute chest syndrome, which can develop during an admission for pain: look for new chest signs, fever, breathlessness or falling saturations, and assess urgently if any appear.

Key clue
Known sickle cell disease with a typical vaso-occlusive pain crisis
What it means
Acute painful sickle cell crisis
What to do
Give prompt analgesia per the WHO pain ladder, avoid pethidine, and monitor for complications such as acute chest syndrome

Why the other options are less appropriate

  • A Withholding opioids because of dependence fears causes needless suffering. NICE treats these episodes as emergencies needing effective analgesia.
  • C Pethidine should not be used. Its metabolite norpethidine can accumulate and cause seizures.
  • D Blood tests help to look for complications, but they should never delay analgesia, which NICE advises within 30 minutes of arrival.
  • E Antibiotics are given only if infection is suspected. Analgesia is the priority in a painful episode.

Source: NICE CG143 Sickle cell disease: managing acute painful episodes in hospital

Question 4Thrombotic microangiopathyHard

A 34-year-old woman presents with confusion, thrombocytopenia (platelets 12 x10^9/L), and a blood film showing numerous schistocytes. Haptoglobin is undetectable and LDH is markedly raised. Renal function is only mildly impaired. ADAMTS13 activity has been sent but the result will not be available for several hours. What is the most appropriate immediate step?

  1. AGive a therapeutic dose of low molecular weight heparin while awaiting the ADAMTS13 result
  2. BTransfuse platelets to correct the thrombocytopenia before any other intervention
  3. CObserve on the ward and reassess once ADAMTS13 activity is known
  4. DRequest an urgent renal biopsy to confirm a thrombotic microangiopathy before treatment
  5. EStart plasma exchange and corticosteroids immediately through the specialist TTP pathway
Show answer and explanation

Answer: E Start plasma exchange and corticosteroids immediately through the specialist TTP pathway

Severe thrombocytopenia, schistocytes, undetectable haptoglobin, raised LDH and confusion, with only mild renal impairment, is thrombotic thrombocytopenic purpura until proven otherwise. In immune TTP, autoantibodies against ADAMTS13 stop it cleaving von Willebrand factor multimers. The ultra-large multimers cause platelet microthrombi in the brain, heart and kidneys. Untreated, most patients die, so the BSH guideline advises starting plasma exchange as an emergency, ideally within 4–8 hours, once TTP is suspected, without waiting for the ADAMTS13 result. Give corticosteroids alongside. ADAMTS13 activity below 10 IU/dL confirms the diagnosis. Rituximab is added to reduce relapse, and caplacizumab, which blocks von Willebrand factor binding to platelets, is recommended in immune TTP. Avoid platelet transfusion unless bleeding is life-threatening. Check troponin, because cardiac involvement is a major cause of death. Start thromboprophylaxis once platelets are above 50 x10^9/L. Test for HIV and, in women of childbearing age, pregnancy.

Key clue
Severe thrombocytopenia, MAHA with schistocytes, and new confusion, with ADAMTS13 result pending
What it means
This clinical picture meets criteria for a working diagnosis of TTP, a rapidly fatal condition if untreated
What to do
Initiate plasma exchange and corticosteroids immediately through the specialist TTP/TMA pathway rather than waiting for laboratory confirmation

Why the other options are less appropriate

  • A Anticoagulation does not correct ADAMTS13 deficiency and adds bleeding risk with platelets of 12. It is not first-line treatment.
  • B Platelet transfusion is avoided in suspected TTP unless bleeding is life-threatening, because it may worsen microvascular thrombosis.
  • C Waiting for ADAMTS13 risks death. Plasma exchange should start as soon as TTP is suspected.
  • D A renal biopsy is unnecessary for diagnosis and dangerous with platelets of 12. It would delay life-saving treatment.

Source: A British Society for Haematology Guideline: Diagnosis and management of thrombotic thrombocytopenic purpura and thrombotic microangiopathies

Question 5Anaemia of inflammationEasy

A 59-year-old woman with active rheumatoid arthritis has haemoglobin 101 g/L, low serum iron, low transferrin, low transferrin saturation and ferritin 240 micrograms/L. What is the most likely explanation?

  1. AAnaemia of inflammation
  2. BAbsolute iron deficiency from chronic blood loss
  3. CBeta-thalassaemia trait
  4. DSideroblastic anaemia
  5. EAutoimmune haemolytic anaemia
Show answer and explanation

Answer: A Anaemia of inflammation

Active rheumatoid arthritis with mild anaemia, low serum iron, low transferrin, low transferrin saturation and a ferritin of 240 micrograms/L is the typical pattern of anaemia of inflammation, also called anaemia of chronic disease. Inflammatory cytokines, particularly interleukin-6, increase hepatic production of hepcidin. Hepcidin breaks down ferroportin, so iron is trapped in macrophages and enterocytes and less reaches the marrow. Serum iron falls even though body stores are adequate. Ferritin is an acute-phase protein, so it is normal or raised, and transferrin falls as a negative acute-phase protein. The anaemia is usually normocytic. In absolute iron deficiency, ferritin is low and transferrin rises. Inflammation can mask coexisting iron deficiency, because ferritin rises; in this setting a ferritin up to about 100 micrograms/L with low transferrin saturation may still reflect deficiency, and soluble transferrin receptor or reticulocyte haemoglobin can help. The main treatment is control of the inflammatory disease. Look for NSAID-related blood loss too.

Key clue
Active inflammatory disease with low iron, low transferrin and raised ferritin.
What it means
Hepcidin-mediated iron sequestration produces functional iron restriction despite stored iron.
What to do
Diagnose anaemia of inflammation.

Why the other options are less appropriate

  • B Absolute iron deficiency gives a low ferritin and raised transferrin, not a ferritin of 240 micrograms/L with low transferrin.
  • C Thalassaemia trait causes marked microcytosis with normal iron studies and does not explain this inflammatory iron pattern.
  • D Sideroblastic anaemia usually shows raised serum iron and transferrin saturation, with ring sideroblasts in the marrow.
  • E Haemolysis would cause reticulocytosis, raised bilirubin and LDH, and a positive direct antiglobulin test, none of which is described.

Source: Good Practice Paper for the laboratory diagnosis of iron deficiency in adults (excluding pregnancy) and children

That is 5 of 261. Carry on with haematology in the practice bank, with progress tracking, flashcards and timed sessions.

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Topics covered

Show all 254 haematology topics
  • A falsely attractive negative bone scan
  • A normal test used as an exclusion rule
  • A small M-spike is not reassurance
  • A vegan diet does not exclude another B12 cause
  • Abnormal coagulation without bleeding is not an automatic plasma indication
  • Absent or hypofunctional spleen
  • Acquired haemophilia A
  • Acquired von Willebrand syndrome in aortic stenosis
  • Acute ABO-incompatible haemolytic transfusion reaction
  • Acute acquired TTP before ADAMTS13 confirmation
  • Acute leukaemia
  • Acute leukaemia emergencies
  • Acute promyelocytic leukaemia coagulopathy
  • Acute/chronic leukaemia
  • Alpha-thalassaemia trait
  • AML with inv(16)
  • AML with monocytic differentiation
  • Anaemia of chronic inflammation pattern
  • Anaemia of chronic kidney disease
  • Anaemia of CKD
  • Anaemia of inflammation
  • Anaemia with acute coronary syndrome
  • Antenatal haemoglobinopathy screening
  • Antiphospholipid syndrome
  • Antiphospholipid syndrome thrombosis
  • Antithrombin deficiency and heparin resistance
  • Antithrombin deficiency heparin resistance
  • APL coagulopathy during induction
  • APL differentiation syndrome
  • Aplastic anaemia
  • Aplastic anaemia marrow finding
  • APS testing before stopping
  • Aspirin is not an automatic prophylaxis exemption
  • Assessing response after FFP
  • Autoimmune haemolytic anaemia
  • Avoiding a particular opioid
  • Bernard–Soulier syndrome
  • Bleeding disorders
  • Blood components/reactions
  • Burkitt lymphoma
  • Cell salvage during surgery with very high expected blood loss
  • Cerebral venous thrombosis with intracerebral haemorrhage
  • Chest symptoms during a pain admission
  • Choosing injections when oral adherence is unreliable
  • Chronic ATP-deficient haemolysis
  • Chronic lymphocytic leukaemia
  • Chronic myeloid leukaemia
  • Chronic myelomonocytic leukaemia
  • Classic Hodgkin lymphoma immunophenotype
  • CLL lymphocytosis
  • CML molecular abnormality
  • Cold agglutinin disease
  • Cold autoimmune haemolytic anaemia
  • Combined vitamin B12 and folate deficiency
  • Complement-mediated atypical HUS
  • Congenital dysfibrinogenaemia
  • Congenital pure red-cell aplasia with thumb anomaly
  • Copper deficiency mimicking myelodysplasia
  • Correcting an INR before a low-risk procedure
  • Corticosteroids in uncomplicated vaso-occlusive pain
  • Critical-care prevention when drugs are contraindicated
  • Cryoprecipitate for hypofibrinogenaemia
  • Dabigatran-associated major bleeding
  • Daratumumab interference with compatibility testing
  • De novo diffuse large B-cell lymphoma
  • Delayed haemolytic transfusion reaction
  • Diamond–Blackfan anaemia
  • DIC laboratory profile
  • Disseminated intravascular coagulation
  • Do not apply the marrow-failure platelet rule to ITP
  • Duration for an acutely ill medical patient
  • Early symptom response after B12 replacement
  • Emergency treatment of myeloma cast nephropathy
  • Essential thrombocythaemia
  • Essential thrombocythaemia complication
  • Evans syndrome
  • Factor V Leiden mechanism
  • Factor X deficiency in AL amyloidosis
  • Factor Xa inhibitor reversal
  • Factor XI deficiency
  • Factor XIII deficiency
  • Fanconi anaemia
  • Fanconi anaemia clue
  • First-line treatment of severe aplastic anaemia
  • Folate replacement safety
  • Follicular lymphoma
  • Fresh frozen plasma indication
  • G6PD oxidative trigger
  • Gestational thrombocytopenia
  • Glanzmann thrombasthenia
  • Glucose-6-phosphate dehydrogenase deficiency
  • Grey platelet syndrome
  • Haemoglobin M methaemoglobinaemia
  • Haemoglobinopathy screening
  • Haemophagocytic lymphohistiocytosis
  • Haemophilia A inheritance
  • Hairy-cell leukaemia phenotype
  • Hairy-cell leukaemia presentation
  • Heparin-induced thrombocytopenia
  • Heparin-induced thrombocytopenia timing
  • Hereditary elliptocytosis
  • Hereditary spherocytosis
  • Hereditary spherocytosis test
  • Hereditary stomatocytosis
  • High bleeding risk in extended treatment
  • High-affinity haemoglobin
  • Homocysteine is not specific to B12 deficiency
  • Imaging suspected myeloma
  • Immune platelet refractoriness
  • Immune thrombocytopenia
  • Immune TTP remission surveillance
  • Individual red-cell targets in transfusion-dependent chronic anaemia
  • Inherited thrombophilia testing
  • Initial B12 testing during pregnancy
  • Initial follow-up during pregnancy on B12 replacement
  • Iron deficiency anaemia
  • Iron deficiency shortly before planned surgery
  • Iron-deficiency anaemia
  • Iron-deficiency anaemia in pregnancy
  • Irradiated blood components
  • Isolated ICANS after CAR T-cell therapy
  • ITP initial concern
  • Laboratory tests should not postpone interim therapy
  • Lifelong replacement after complete terminal ileal resection
  • Light-chain myeloma
  • Likely DVT, imaging delayed
  • Low fibrinogen without bleeding or a planned procedure
  • Low total B12 in a combined-pill user
  • Lupus anticoagulant mixing study
  • Lymphoma diagnosis
  • Lymphoma/myeloma
  • Macrocytic/haemolytic anaemia
  • Major haemorrhage
  • Mantle-cell lymphoma
  • MDS with isolated deletion 5q
  • Mechanical intravascular haemolysis after valve replacement
  • Megaloblastic anaemia neurological clue
  • Microcytic anaemia ferritin
  • Minimum treatment duration
  • MMA after a borderline initial result
  • Mobile chemotherapy is not a universal LMWH indication
  • Monoclonal gammopathy of undetermined significance
  • Myelodysplastic syndrome clue
  • Myelodysplastic syndromes
  • Myeloid hypereosinophilic neoplasm
  • Myeloma CRAB feature
  • Negative DVT pathway prompts an alternative diagnosis
  • Negative intrinsic-factor antibodies do not exclude autoimmune gastritis
  • Negative proximal scan but positive D-dimer
  • Neutropenic sepsis
  • Neutropenic sepsis definition
  • New dyspepsia in autoimmune gastritis
  • Nitrous-oxide functional vitamin B12 deficiency
  • NPM1-mutated AML response assessment
  • One unit, then reassess
  • Oral B12 dosing when malabsorption is suspected
  • Oxygen threshold during vaso-occlusive pain
  • Pancreatic chemotherapy changes the prevention decision
  • Paroxysmal cold haemoglobinuria
  • Paroxysmal nocturnal haemoglobinuria
  • Paroxysmal nocturnal haemoglobinuria clue
  • Perioperative erythropoietin when compatible blood is unavailable
  • Peripheral arterial disease and stockings
  • Persistent symptoms on maximum oral B12 treatment
  • Philadelphia-positive ALL
  • Platelet support before critical-site surgery
  • Platelet support for clinically significant non-major bleeding
  • Platelet threshold before non-critical-site surgery
  • Platelet transfusion before marrow biopsy
  • Platelet transfusion refractoriness
  • Platelet transfusion thresholds
  • Platelets without bleeding
  • POEMS syndrome
  • Polycythaemia vera
  • Polycythaemia vera mutation
  • Polycythaemia vera thrombosis prevention
  • Post-transfusion purpura
  • Post-transplant lymphoproliferative disorder
  • Prekallikrein deficiency
  • Preventing recurrent TACO
  • Primary CNS lymphoma
  • Primary myelofibrosis
  • Primary myelofibrosis splenomegaly
  • Primary plasma-cell leukaemia
  • Prior home analgesia changes the opioid choice
  • Prophylactic FFP before a bleeding-risk procedure
  • Prophylactic fibrinogen replacement before a bleeding-risk procedure
  • Prophylaxis in severe renal impairment
  • Protein C deficiency and warfarin skin necrosis
  • Protein C deficiency warfarin necrosis
  • Provoked event after completed treatment
  • Provoked proximal DVT
  • Pseudothrombocytopenia
  • Pyruvate kinase deficiency
  • Reassessment after a platelet dose
  • Red-cell transfusion threshold in acute coronary syndrome
  • Red-cell volume in a very low-body-weight adult
  • Repeat diagnostic B12 testing during intramuscular treatment
  • Repeated boluses and patient-controlled analgesia
  • Repeated perioperative tranexamic acid in renal impairment
  • Restrictive red-cell transfusion
  • Richter transformation
  • Risk information at diagnosis
  • Secondary erythrocytosis from hypoxia
  • Severe aplastic anaemia definitive treatment
  • Shiga-toxin haemolytic uraemic syndrome
  • Shwachman–Diamond syndrome
  • Sickle cell disease
  • Sickle cell disease complications
  • Sickle cell/thalassaemia
  • Sickle-cell acute chest syndrome
  • Sickle-cell priapism
  • Sickle-cell retinopathy surveillance
  • Sideroblastic anaemia
  • Sinusoidal obstruction syndrome
  • Stable anaemia: threshold versus symptoms
  • Stopping replacement after a reversible dietary cause resolves
  • Supplement use can obscure B12 deficiency
  • Suspected DVT
  • Symptomatic myelofibrosis
  • Systemic AL amyloidosis
  • Systemic mastocytosis
  • TACO distinguished from TRALI
  • TACO recognition
  • Thalassaemia trait indices
  • The admission-to-prophylaxis clock
  • The first analgesic clock
  • The last days of life are a different VTE pathway
  • The stocking no longer fits after oedema
  • Thrombophilia testing during anticoagulation
  • Thrombotic microangiopathy
  • TRALI recognition
  • Tranexamic acid for lower-volume theatre surgery
  • Transfusion acute haemolysis
  • Transfusion-associated circulatory overload
  • Transfusion-dependent thalassaemia
  • Transplant-associated thrombotic microangiopathy
  • TTP pentad treatment
  • Tumour lysis syndrome
  • Type 2B von Willebrand disease
  • Unprovoked VTE
  • Unprovoked VTE and occult malignancy
  • Unstable haemoglobin
  • VHL-related Chuvash erythrocytosis
  • Vitamin B12 deficiency
  • Vitamin K deficiency
  • Von Willebrand disease
  • Von Willebrand disease bleeding
  • Waldenstrom hyperviscosity
  • Waldenstrom macroglobulinaemia hyperviscosity
  • Warfarin reversal
  • Warm autoimmune haemolysis
  • Washed red-cell components
  • When not to treat CLL

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