Membership of the Royal College of Physicians (MRCP UK) Haematology and Oncology Syllabus

Haematology and Oncology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Haematology and Oncology in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Anaemia and Red Cell Disorders

   4 topics

   • Iron deficiency and anaemia of chronic disease
   • Megaloblastic anaemia and B12/folate deficiency
   • Haemolytic anaemias
     • Autoimmune haemolysis
     • Hereditary spherocytosis and G6PD deficiency
   • Haemoglobinopathies
     • Sickle cell disease and crises
     • Thalassaemia
2. 2

   Haematological Malignancies

   5 topics

   • Acute leukaemias
   • Chronic leukaemias
     • CML and tyrosine kinase inhibitors
     • CLL
   • Lymphomas
     • Hodgkin and non-Hodgkin lymphoma
   • Myeloma and plasma cell dyscrasias
   • Myeloproliferative and myelodysplastic disorders
3. 3

   Haemostasis and Thrombosis

   4 topics

   • Bleeding disorders
     • Haemophilia and von Willebrand disease
     • Thrombocytopenia and ITP
   • Disseminated intravascular coagulation
   • Thrombophilia and venous thromboembolism
   • Anticoagulant and antiplatelet therapy
     • Reversal agents and bridging
4. 4

   Clinical Oncology and Supportive Care

   5 topics

   • Principles of cancer staging and treatment
   • Oncological emergencies
     • Neutropenic sepsis
     • Tumour lysis syndrome and malignant hypercalcaemia
     • Spinal cord compression and SVC obstruction
   • Cancer of unknown primary
   • Palliative and end-of-life care
     • Symptom control and opioid management
   • Transfusion medicine and reactions

Haematology and Oncology flashcards for Membership of the Royal College of Physicians (MRCP UK)

22 of 53 cards from the Haematology and Oncology deck — real questions with worked answers.

1. What is the classic laboratory triad of iron deficiency anaemia?

   Low serum ferritin, low serum iron with raised total iron-binding capacity (TIBC), and low transferrin saturation. The blood film shows microcytic, hypochromic red cells (low MCV, low MCH) often with anisocytosis and pencil cells.

2. How do you distinguish iron deficiency anaemia from anaemia of chronic disease on iron studies?

   Iron deficiency: ferritin LOW, TIBC/transferrin HIGH, transferrin saturation low. Anaemia of chronic disease: ferritin NORMAL or HIGH (acute-phase reactant), TIBC LOW, transferrin saturation low/normal. The key discriminator is ferritin and TIBC. ACD is mediated by hepcidin trapping iron in macrophages.

3. What red-cell index and reticulocyte pattern characterise megaloblastic anaemia, and what film features are seen?

   Macrocytic anaemia (high MCV, often $>110\ \text{fL}$) with a low reticulocyte count. Blood film shows oval macrocytes and hypersegmented neutrophils ($\geq 5$ lobes). Bone marrow shows megaloblasts due to impaired DNA synthesis.

4. Compare the neurological features of B12 deficiency versus folate deficiency.

   B12 deficiency causes subacute combined degeneration of the cord (dorsal columns and corticospinal tracts), peripheral neuropathy, and dementia. Folate deficiency does NOT cause neurological disease. This is why B12 must be corrected before/with folate — giving folate alone in B12 deficiency can precipitate or worsen neuropathy.

5. What is pernicious anaemia and which antibodies confirm it?

   Autoimmune gastritis causing loss of gastric parietal cells and intrinsic factor, leading to B12 malabsorption. Diagnosed by anti-intrinsic factor antibodies (specific) and anti-parietal cell antibodies (sensitive but less specific). Associated with achlorhydria and increased gastric cancer risk.

6. What laboratory features indicate haemolysis, and how do you separate intravascular from extravascular haemolysis?

   General markers: raised unconjugated bilirubin, raised LDH, low haptoglobin, raised reticulocytes. Intravascular: haemoglobinaemia, haemoglobinuria, haemosiderinuria, very low haptoglobin. Extravascular (spleen): splenomegaly, spherocytes, less haemoglobinuria.

7. What does a positive direct antiglobulin (Coombs) test indicate, and how do warm and cold autoimmune haemolytic anaemias differ?

   DAT positive indicates immune-mediated haemolysis (antibody/complement on red cells). Warm AIHA: IgG, optimal at $37^{\circ}\text{C}$, idiopathic or due to lymphoma/SLE/CLL/drugs, treat with steroids. Cold AIHA: IgM, optimal at $4^{\circ}\text{C}$, due to Mycoplasma, EBV, lymphoma; treat by keeping warm, rituximab.

8. What is the inheritance and molecular defect of hereditary spherocytosis, and how is it managed?

   Autosomal dominant defect of red-cell membrane proteins (spectrin, ankyrin, band 3). Causes spherocytes, extravascular haemolysis, splenomegaly, raised MCHC, and positive osmotic fragility/EMA binding test. Managed with folate; splenectomy for severe cases (after vaccination).

9. What triggers haemolysis in G6PD deficiency, and what film feature is characteristic?

   X-linked G6PD deficiency causes oxidative haemolysis triggered by fava beans, infections, and drugs (e.g. primaquine, dapsone, sulfonamides, nitrofurantoin). Film shows bite cells and Heinz bodies (denatured Hb). Episodes are self-limiting; test G6PD level after the acute episode resolves.

10. Describe the genetics of sickle cell disease and the key acute complications.

    Autosomal recessive, point mutation (Glu→Val) at codon 6 of the $\beta$-globin gene producing HbS. Acute complications: vaso-occlusive painful crises, acute chest syndrome, splenic sequestration, aplastic crisis (parvovirus B19), stroke, and priapism. Hydroxycarbamide increases HbF and reduces crises.

11. Classify the thalassaemias and contrast $\alpha$- and $\beta$-thalassaemia major.

    Thalassaemias are defects in globin chain synthesis. $\alpha$-thalassaemia: reduced $\alpha$-chains (gene deletions); 4-gene deletion is fatal (Hb Barts, hydrops fetalis). $\beta$-thalassaemia major: absent $\beta$-chains, presents after 6 months as HbF declines, with severe microcytic anaemia, raised HbF and HbA2, requiring lifelong transfusion plus iron chelation.

12. What defines acute leukaemia on bone marrow, and what is the blast threshold?

    Acute leukaemia is defined by $\geq 20\%$ blasts in the bone marrow or peripheral blood. It is characterised by rapid accumulation of immature cells, bone marrow failure (anaemia, thrombocytopenia, neutropenia), and is fatal within weeks if untreated.

13. How do you distinguish acute myeloid leukaemia (AML) from acute lymphoblastic leukaemia (ALL)?

    AML: myeloid blasts, Auer rods, myeloperoxidase positive; commoner in adults. ALL: lymphoblasts, TdT positive, myeloperoxidase negative; commonest childhood cancer, may involve CNS and testes. Immunophenotyping/flow cytometry confirms lineage.

14. What is acute promyelocytic leukaemia (APML), its genetic hallmark, and its emergency complication?

    APML is AML subtype M3 with the $t(15;17)$ translocation producing the PML-RARA fusion gene. It commonly presents with disseminated intravascular coagulation (DIC) and bleeding. Treated with all-trans retinoic acid (ATRA) plus arsenic trioxide, which induce differentiation; it has the best prognosis of AML subtypes.

15. What are the diagnostic features of chronic myeloid leukaemia (CML) and its first-line treatment?

    CML: massive splenomegaly, very high white cell count with the full spectrum of myeloid precursors, basophilia, and the Philadelphia chromosome $t(9;22)$ producing the BCR-ABL1 fusion (a tyrosine kinase). First-line treatment is a tyrosine kinase inhibitor such as imatinib. Can transform into blast crisis.

16. What is chronic lymphocytic leukaemia (CLL), its hallmark film finding, and its key complications?

    CLL is a clonal proliferation of mature B-lymphocytes, commonest leukaemia in adults. Film shows lymphocytosis with smear/smudge cells. Complications: autoimmune haemolytic anaemia, hypogammaglobulinaemia/infections, and Richter transformation to high-grade lymphoma. Staged by Binet/Rai.

17. What is the key histological feature distinguishing Hodgkin lymphoma from non-Hodgkin lymphoma?

    Hodgkin lymphoma contains Reed-Sternberg cells (large binucleate cells, "owl-eye" appearance, CD15+ CD30+). It spreads contiguously between nodal groups and has a bimodal age distribution. Non-Hodgkin lymphoma lacks Reed-Sternberg cells and spreads non-contiguously.

18. What are the B symptoms used in lymphoma staging, and what staging system is used?

    B symptoms: unexplained fever $>38^{\circ}\text{C}$, drenching night sweats, and weight loss $>10\%$ of body weight over 6 months. Lymphomas are staged using the Ann Arbor system (stages I–IV; suffix A = no B symptoms, B = present). Alcohol-induced nodal pain is classic for Hodgkin.

19. State the diagnostic CRAB criteria of symptomatic multiple myeloma.

    CRAB indicates end-organ damage: hyperCalcaemia, Renal impairment, Anaemia, and Bone lesions (lytic). Plus clonal bone marrow plasma cells $\geq 10\%$ or a plasmacytoma. Investigations show a monoclonal paraprotein, Bence Jones protein in urine, and rouleaux on film.

20. What is MGUS and what distinguishes it from myeloma?

    Monoclonal gammopathy of undetermined significance: paraprotein $<30\ \text{g/L}$, bone marrow plasma cells $<10\%$, and NO end-organ damage (no CRAB). It is asymptomatic, progresses to myeloma at roughly $1\%$ per year, and requires monitoring rather than treatment.

21. What is Waldenström macroglobulinaemia and its characteristic complication?

    A lymphoplasmacytic lymphoma producing a monoclonal IgM paraprotein. The large IgM causes hyperviscosity syndrome (visual disturbance, headache, confusion, mucosal bleeding). Treated acutely with plasmapheresis. Unlike myeloma it does NOT typically cause lytic bone lesions.

22. List the BCR-ABL-negative myeloproliferative neoplasms and the mutation common to them.

    Polycythaemia vera, essential thrombocythaemia, and primary myelofibrosis. The JAK2 V617F mutation is found in nearly all polycythaemia vera and around half of ET and myelofibrosis cases. They share a risk of thrombosis and transformation to AML.

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