Prometric Exam Questions for Haematopathology Specialists 2026: 20 MCQs with Answers on Anaemia Work-up, Haemoglobinopathies, Leukaemia and Lymphoma Diagnosis, Flow Cytometry, Coagulation, Transfusion Medicine and Laboratory Quality

The specialist haematopathology paper (HEM4711 at DHA, and the equivalent SCFHS, QCHP and NHRA papers) is 100 to 150 single-best-answer questions in up to three hours with a pass mark of about 60%. Candidates with an MD, DNB, FCPS, FRCPath or Arab Board in haematology or haematopathology sit it after the authority confirms the title; haematology technologists and clinical scientists sit separate papers (MTH4612 and MTH4611) with overlapping content. The Gulf has the world's highest carrier rates for thalassaemia, sickle cell and G6PD deficiency, mandatory premarital screening, and fast-growing transplant and oncology services, and the paper reflects that mix. This set covers what recurs. The licensing route for laboratory physician titles is in the pathologist guide and for scientists and technologists in laboratory scientist titles.

Red cells and haemoglobinopathies

Question 1

A 30-year-old woman has haemoglobin 95 g/L, MCV 62 fL, RBC count 5.9 × 10¹²/L, RDW normal, ferritin 80 µg/L and a blood film with target cells and basophilic stippling. The most likely diagnosis and confirmatory test are:

1. Iron deficiency anaemia; serum iron
2. Thalassaemia trait (beta-thalassaemia trait if HbA2 is raised above about 3.5% on HPLC or capillary electrophoresis; alpha-thalassaemia trait if HbA2 is normal, confirmed by DNA analysis), suggested by a disproportionately low MCV with a high red cell count and normal RDW and ferritin
3. Anaemia of chronic disease; CRP
4. Sideroblastic anaemia; bone marrow

Answer: B. The Mentzer index (MCV/RBC below 13) favours thalassaemia trait over iron deficiency; coexisting iron deficiency lowers HbA2 and must be corrected before interpreting it.

Question 2

A premarital screening sample shows HbS 38%, HbA 58%, HbA2 3%, HbF 1% on HPLC, with a positive sickle solubility test. The interpretation and counselling implication are:

1. Sickle cell disease; the person is symptomatic
2. Sickle cell trait (HbAS); the person is healthy but a carrier, and if the partner is also a carrier of HbS, beta-thalassaemia or another interacting variant, each pregnancy carries a 25% risk of sickle cell disease, which is why Gulf premarital programmes screen both partners and offer genetic counselling
3. HbSC disease
4. Normal result

Answer: B. HbS above about 50% with no HbA indicates homozygous disease or S/beta-zero thalassaemia; HbS with raised HbA2 and microcytosis suggests S/beta-plus thalassaemia. Sickle solubility tests are unreliable under six months of age and after transfusion.

Question 3

A 5-year-old boy develops dark urine, jaundice and anaemia two days after eating fava beans. The blood film shows bite cells and blister cells, and a Heinz body preparation is positive. The diagnosis and the testing caveat are:

1. Autoimmune haemolytic anaemia; direct antiglobulin test
2. G6PD deficiency with acute oxidative haemolysis; the quantitative G6PD assay may be falsely normal during the acute episode because the deficient older cells have lysed and reticulocytes have higher enzyme activity, so testing is repeated after recovery, and the family is counselled on oxidant drugs (primaquine, dapsone, nitrofurantoin, rasburicase), fava beans and naphthalene
3. Hereditary spherocytosis; osmotic fragility
4. Malaria; thick film

Answer: B. G6PD deficiency affects a substantial share of Gulf populations; newborn screening is routine in several states.

Question 4

A 68-year-old has macrocytic anaemia (MCV 112 fL) with hypersegmented neutrophils, mild pancytopenia, raised LDH and low B12 with positive intrinsic factor antibodies. The next steps include:

1. Oral folate alone
2. Diagnose pernicious anaemia and treat with parenteral B12 (never folate alone, which can precipitate neurological deterioration), monitor for hypokalaemia during the reticulocyte response, and note the increased gastric carcinoma risk; bone marrow examination is not needed when the picture is typical
3. Bone marrow biopsy immediately
4. Red cell transfusion in all cases

Answer: B. Macrocytosis without megaloblastic features suggests alcohol, liver disease, hypothyroidism, drugs or myelodysplasia.

Leukaemia and myeloid neoplasms

Question 5

A 25-year-old presents with bruising, gum bleeding, a white cell count of 3 × 10⁹/L with 60% blasts showing Auer rods, fibrinogen of 0.8 g/L and a prolonged PT. The most urgent diagnostic and treatment implications are:

1. Chronic lymphocytic leukaemia; observation
2. Acute promyelocytic leukaemia (APL) with disseminated intravascular coagulation; this is a medical emergency in which all-trans retinoic acid is started on morphological suspicion before genetic confirmation, with aggressive blood product support (platelets above 30 to 50 × 10⁹/L, fibrinogen above 1.5 g/L), and the laboratory confirms t(15;17) PML::RARA by FISH or PCR urgently; flow cytometry typically shows CD33+, CD13+, HLA-DR−, CD34−
3. Acute lymphoblastic leukaemia; steroids
4. Reactive leukocytosis

Answer: B. Early haemorrhagic death is the main cause of mortality in APL; the laboratory's rapid communication is life-saving.

Question 6

Which flow cytometry profile is most consistent with B-lymphoblastic leukaemia?

1. CD3+, CD5+, CD7+, cytoplasmic CD3+, TdT+
2. CD19+, CD10+, CD34+, TdT+, cytoplasmic CD79a+, with absent surface immunoglobulin and negative myeloperoxidase; T-ALL shows cytoplasmic CD3 and TdT, and AML shows myeloperoxidase, CD13, CD33 and CD117
3. CD19+, CD5+, CD23+, surface Ig weak
4. CD138+, CD38 bright, cytoplasmic light chain restricted

Answer: B. Option C describes CLL and option D plasma cells; the WHO classification integrates morphology, immunophenotype and genetics (for example BCR::ABL1, KMT2A rearrangements and hyperdiploidy in B-ALL).

Question 7

A 55-year-old has a white cell count of 180 × 10⁹/L with a full spectrum of granulocyte precursors, basophilia, 3% blasts, splenomegaly and a low leukocyte alkaline phosphatase score. The diagnosis, confirmatory test and monitoring are:

1. Leukaemoid reaction; treat infection
2. Chronic myeloid leukaemia in chronic phase; confirm BCR::ABL1 by PCR or FISH (Philadelphia chromosome t(9;22)), then monitor response to tyrosine kinase inhibitors with quantitative BCR::ABL1 PCR on the International Scale at three-monthly intervals, with mutation analysis if response is lost
3. Primary myelofibrosis; JAK2 testing only
4. Acute myeloid leukaemia; induction chemotherapy

Answer: B. Accelerated phase and blast crisis are defined by blast percentages, basophilia, platelet counts and cytogenetic evolution; a leukaemoid reaction has a high LAP score.

Question 8

A 70-year-old has refractory macrocytic anaemia, a hypercellular marrow with dysplastic erythroid precursors, ring sideroblasts in 25% of erythroblasts and 2% blasts. Which test most informs classification and prognosis?

1. Serum ferritin only
2. Cytogenetics and a myeloid next-generation sequencing panel (for example SF3B1, which defines a favourable ring sideroblast subtype, and TP53, which is adverse), combined with blast percentage and cytopenias in the IPSS-R or IPSS-M scoring for myelodysplastic neoplasms
3. Coombs test
4. Reticulocyte count alone

Answer: B. The 2022 WHO and ICC classifications place molecular findings alongside morphology; del(5q) defines another treatable subtype.

Lymphoid neoplasms and plasma cell disorders

Question 9

A lymph node shows a diffuse infiltrate of large B cells. Immunohistochemistry is CD20+, CD10−, BCL6+, MUM1+, with MYC and BCL2 rearrangements detected by FISH. The classification and significance are:

1. Burkitt lymphoma
2. High-grade B-cell lymphoma with MYC and BCL2 rearrangements ("double-hit"), non-germinal centre type by the Hans algorithm, which carries a worse prognosis than ordinary diffuse large B-cell lymphoma and is treated with intensified regimens; FISH for MYC, BCL2 and BCL6 is recommended for all large B-cell lymphomas
3. Follicular lymphoma grade 1
4. Classic Hodgkin lymphoma

Answer: B. Burkitt lymphoma is CD10+, BCL6+, BCL2− with Ki-67 near 100% and an isolated MYC rearrangement; EBV-associated lymphomas are also relevant in the region's immunosuppressed and transplant patients.

Question 10

A 62-year-old has back pain, hypercalcaemia, renal impairment, anaemia and a serum IgG kappa paraprotein of 45 g/L. Which laboratory work-up confirms the diagnosis and stages the disease?

1. Serum protein electrophoresis alone
2. Serum protein electrophoresis with immunofixation, serum free light chains, 24-hour urine for Bence Jones protein, bone marrow aspirate and trephine with plasma cell percentage and flow cytometry (CD138+, CD38+, CD56+, CD19−, light-chain restricted), FISH on plasma cells for high-risk abnormalities (del(17p), t(4;14), t(14;16), gain 1q), beta-2 microglobulin, albumin and LDH for the Revised ISS, and whole-body imaging for lytic lesions
3. Skeletal survey only
4. Serum viscosity alone

Answer: B. The CRAB criteria and the SLiM biomarkers (60% plasma cells, light chain ratio above 100, more than one focal MRI lesion) define myeloma requiring treatment; MGUS has a paraprotein under 30 g/L, under 10% plasma cells and no end-organ damage.

Question 11

Peripheral blood from a 65-year-old shows a lymphocytosis of 40 × 10⁹/L with smudge cells; flow cytometry shows CD19+, CD5+, CD23+, CD200+, weak surface immunoglobulin and weak CD20, with FMC7 negative. Which additional tests guide prognosis and treatment selection?

1. No further tests are needed
2. FISH for del(17p) and del(11q), TP53 mutation analysis and IGHV mutational status, because TP53 disruption predicts chemoimmunotherapy failure and directs treatment to BTK inhibitors or venetoclax; a direct antiglobulin test and immunoglobulin levels are also checked for autoimmune cytopenias and infection risk
3. Bone marrow biopsy in every case
4. JAK2 mutation testing

Answer: B. Mantle cell lymphoma is excluded by CD23 and CD200 positivity and cyclin D1 negativity; the Matutes score formalises the CLL immunophenotype.

Coagulation

Question 12

A pre-operative coagulation screen shows a prolonged APTT of 65 seconds with a normal PT, normal fibrinogen and a normal platelet count, in a patient with no bleeding history. The APTT corrects fully on a 50:50 mix with normal plasma. The most likely explanations and next tests are:

1. A lupus anticoagulant; no surgery
2. A factor deficiency in the intrinsic pathway: factor XII deficiency (no bleeding risk), or factor XI, IX or VIII deficiency and von Willebrand disease (bleeding risk), so factor assays and von Willebrand studies are performed; an inhibitor or lupus anticoagulant would fail to correct on mixing, and heparin contamination is excluded by thrombin time or sample history
3. Vitamin K deficiency; give vitamin K
4. Disseminated intravascular coagulation

Answer: B. A prolonged PT with normal APTT suggests factor VII deficiency, early warfarin or liver disease; both prolonged suggests common pathway deficiency, DIC, severe liver disease or massive transfusion.

Question 13

A patient on unfractionated heparin for seven days has a platelet count that has fallen from 250 to 90 × 10⁹/L and a new deep vein thrombosis. The laboratory approach is:

1. Continue heparin and transfuse platelets
2. Calculate the 4Ts score, stop all heparin (including flushes and LMWH) immediately on clinical suspicion, start a non-heparin anticoagulant (argatroban, bivalirudin, fondaparinux or a DOAC per protocol), send an anti-PF4/heparin antibody immunoassay and confirm with a functional assay (serotonin release or heparin-induced platelet activation) where available, and avoid warfarin until platelets recover
3. Switch to low-molecular-weight heparin
4. Give platelets prophylactically

Answer: B. Heparin-induced thrombocytopenia is prothrombotic; platelet transfusion is avoided unless there is bleeding.

Question 14

Which statement about thrombophilia testing is correct?

1. All patients with a first DVT should have a full thrombophilia screen during the acute event
2. Testing is selective (young patients, unprovoked or recurrent thrombosis, unusual sites, strong family history) and timed: protein C, protein S and antithrombin are unreliable during acute thrombosis and on anticoagulants, lupus anticoagulant testing is affected by heparin and DOACs, while genetic tests (factor V Leiden, prothrombin G20210A) can be done at any time; antiphospholipid antibodies must be persistently positive 12 weeks apart
3. DOACs do not interfere with any coagulation test
4. Protein C deficiency is excluded by a normal PT

Answer: B. Results rarely change acute management; they inform duration of anticoagulation and family counselling, and consanguinity increases homozygous deficiencies in the region.

Transfusion medicine

Question 15

A patient's forward group shows anti-A negative, anti-B positive, and the reverse group shows A1 cells positive, B cells negative. The group and the laboratory's next action are:

1. Group A; issue group A red cells
2. Group B, with forward and reverse groups in agreement; proceed to RhD typing and antibody screen, and resolve any discrepancy before issuing anything other than group O red cells in an emergency
3. Group AB
4. Group O

Answer: B. Discrepancies arise from weak subgroups, cold agglutinins, recent transfusion, stem cell transplant and immunodeficiency; they are investigated, not guessed.

Question 16

The antibody screen of a multiply transfused patient with sickle cell disease is positive. Panel testing identifies anti-C and anti-E, and the patient is also Kell negative. The laboratory should:

1. Issue ABO-compatible units without further matching
2. Issue units negative for C, E and K that are ABO and RhD compatible and antigen-negative by phenotyping, crossmatch by indirect antiglobulin test, flag the record permanently for the antibodies, and recommend extended Rh and Kell matching for all future transfusions in sickle cell disease to reduce further alloimmunisation and delayed haemolytic transfusion reactions
3. Give O negative blood only
4. Warm the units to remove the antibodies

Answer: B. Alloimmunisation rates in sickle cell patients are high; hyperhaemolysis after transfusion is a feared complication in which further transfusion can worsen anaemia.

Question 17

Fifteen minutes into a red cell transfusion, a patient develops fever, rigors, loin pain, hypotension and haemoglobinuria. The laboratory investigation includes:

1. Nothing; the ward manages it
2. Checking the unit and patient identification and documentation for a clerical error, repeating ABO and RhD on pre- and post-transfusion samples and the unit, a direct antiglobulin test, visual inspection of plasma for haemolysis, repeat antibody screen and crossmatch, Gram stain and culture of the unit and patient blood for bacterial contamination, and tests for haemolysis (LDH, bilirubin, haptoglobin) and DIC, with the reaction reported to the haemovigilance system
3. Repeat the crossmatch only
4. A chest radiograph for TRALI only

Answer: B. Acute haemolytic reactions are nearly always ABO incompatibility from identification errors; TRALI presents with hypoxia and bilateral infiltrates within six hours, and TACO with hypertension and overload.

Question 18

Which patient requires irradiated cellular blood components?

1. Any patient receiving more than four units
2. Patients at risk of transfusion-associated graft-versus-host disease: recipients of haematopoietic stem cell transplants, patients on purine analogues (fludarabine) or anti-thymocyte globulin, Hodgkin lymphoma patients, those with congenital T-cell immunodeficiency, intrauterine and neonatal exchange transfusions, recipients of HLA-matched or directed donations from relatives, and those with CAR-T or similar therapies per guidelines
3. All neonates regardless of indication
4. Patients with iron overload

Answer: B. Leucodepletion does not prevent TA-GvHD; irradiation (gamma or X-ray) inactivates donor lymphocytes and shortens the shelf life of red cells.

Laboratory practice

Question 19

A haematology analyser flags a sample with a platelet count of 40 × 10⁹/L in a patient with no bleeding and a previously normal count. The first laboratory step is:

1. Report the result as critical immediately
2. Examine the blood film for platelet clumping (EDTA-dependent pseudothrombocytopenia), fibrin strands or giant platelets, check the sample for clots and adequacy, and if clumping is seen, request a repeat in citrate or a heparinised tube or perform a direct count, reporting the result with a comment; genuine new thrombocytopenia is then phoned as a critical value
3. Transfuse platelets
4. Repeat on the analyser only

Answer: B. Film review rules, delta checks and critical value lists are quality requirements under ISO 15189 and CAP accreditation.

Question 20

Which statement about internal and external quality assurance in a haematology laboratory is correct?

1. External quality assurance replaces daily internal controls
2. Internal quality control (commercial controls at two or three levels run each shift, evaluated with Westgard rules and Levey-Jennings charts, with corrective action documented before patient results are released) monitors day-to-day precision, while external quality assessment (proficiency testing such as UK NEQAS, CAP or RCPA surveys) compares the laboratory's accuracy with peers and is required for accreditation; both are documented alongside calibration, maintenance and competency records
3. Westgard rules apply only to chemistry
4. Controls are run weekly

Answer: B. A 1-3s or 2-2s violation triggers rejection and investigation; Gulf authorities require laboratory accreditation for most hospital laboratories.

How to practise

• Know the regional haemoglobinopathy and enzymopathy work-up: indices, HPLC patterns, solubility test limits, G6PD timing, premarital screening logic.
• Learn the WHO classification markers: flow panels for ALL, AML, CLL and myeloma, and the genetic tests that define subtypes and prognosis.
• Interpret coagulation screens systematically: mixing studies, HIT scoring, timing of thrombophilia tests.
• Know transfusion laboratory rules: group discrepancies, antibody panels, reaction investigation, special requirements.
• Practise under time in the Haematopathology bank, or the Haematology Technologist bank and Haematology Clinical Scientist bank for those titles, using the error-log method.

Related sets: anatomic pathology questions, medical microbiology questions, lab technologist questions and oncology questions.

Frequently asked questions

How many questions are in the Prometric haematopathology exam?

Typically 100 to 150 single-best-answer MCQs in up to three hours, with a pass mark of about 60%, varying by authority.

Which haematology topics come up most?

Haemoglobinopathy and G6PD work-up, acute leukaemia and lymphoma immunophenotyping, CML and MDS genetics, myeloma criteria, coagulation screen interpretation, HIT, and transfusion laboratory practice.

Does the exam include blood films and flow cytometry plots?

Yes. Expect image-based morphology questions and immunophenotype profiles to interpret.

Is the haematology technologist exam different?

It shares the laboratory content but focuses on analysers, quality control, film preparation and transfusion bench work rather than diagnosis and classification.

Are these real exam questions?

No. They are original practice questions written to the published blueprint. Real exam content is confidential.