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Anaemias & haemolysis flashcards

14 high-yield MRCP Part 1 cards from the Intellect Medicos Haematology & Oncology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. What is the preferred first screening blood test for suspected iron deficiency anaemia?

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    Serum ferritin.

    Why? A low ferritin is the most specific single marker of depleted iron stores.

  2. What is the first-line treatment for uncomplicated iron deficiency anaemia?

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    Oral iron, e.g. ferrous sulfate or ferrous fumarate.

    Why? Oral iron is cheap and effective, so it is first-line (NICE/BSG). IV iron is kept for intolerance of oral iron, CKD, IBD or malabsorption.

  3. A 34-year-old man renovating an old Victorian house has colicky abdominal pain, constipation and wrist drop. His film shows a microcytic anaemia with basophilic stippling. Once exposure is removed, which ORAL chelating agent is the usual treatment?

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    DMSA (succimer).

    Why? Lead blocks ALA dehydratase and ferrochelatase in haem synthesis. Chelators bind lead so it can be excreted in urine.

  4. What is the B12 replacement regimen for pernicious anaemia WITHOUT neurological involvement?

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    IM hydroxocobalamin 1 mg three times a week for 2 weeks, then 1 mg every 2–3 months.

    Why? B12 absorption needs intrinsic factor; in pernicious anaemia the antibodies block this, so oral replacement is unreliable and lifelong IM therapy is used.

  5. Name three drugs that can trigger haemolysis in G6PD deficiency.

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    Any three of: primaquine, ciprofloxacin, nitrofurantoin, sulphonamides (e.g. co-trimoxazole), sulfonylureas, sulfasalazine.

    Why? These cause oxidant stress. Without G6PD the red cell cannot make enough NADPH to keep glutathione reduced, so Heinz bodies and bite cells form.

  6. Warm autoimmune haemolytic anaemia is caused by ______ antibodies, and cold AIHA by ______ antibodies.

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    IgG; IgM

    Why? Warm (37 °C) IgG-coated cells are removed in the spleen (extravascular). Cold IgM fixes complement and can cause intravascular haemolysis.

  7. What is the mechanism of action of eculizumab in paroxysmal nocturnal haemoglobinuria (PNH)?

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    Monoclonal antibody against complement C5, which prevents formation of the membrane attack complex.

    Why? PNH cells lack CD55 and CD59 (PIGA mutation), so complement lyses them. Blocking C5 stops the intravascular haemolysis.

  8. What is the standard treatment for severe aplastic anaemia in a patient NOT suitable for stem cell transplant?

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    Horse anti-thymocyte globulin (ATG) plus ciclosporin (± eltrombopag).

    Why? Acquired aplastic anaemia is usually immune-mediated, so immunosuppression can let the marrow recover.

  9. In anaemia of chronic disease, serum ferritin is ______ and TIBC is ______ — the opposite pattern to iron deficiency.

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    normal or raised; low

    Why? Hepcidin (driven by IL-6) blocks ferroportin, trapping iron inside macrophages (ferritin up), while the liver makes less transferrin (TIBC down).

  10. Which anti-tuberculosis drug can cause sideroblastic anaemia, and what is the treatment?

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    Isoniazid; treat with pyridoxine (vitamin B6).

    Why? Isoniazid antagonises pyridoxine, the cofactor for ALA synthase (the first step of haem synthesis), so iron cannot be built into haem and collects as ring sideroblasts.

  11. In suspected pernicious anaemia (autoimmune gastritis), which antibody test is more SPECIFIC?

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    Anti-intrinsic factor antibodies.

    Why? Intrinsic factor antibodies are highly specific but found in only about half of patients; parietal cell antibodies are more common but also occur in other autoimmune diseases and healthy older people.

  12. Which test is recommended to confirm hereditary spherocytosis when the diagnosis is uncertain?

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    Eosin-5-maleimide (EMA) binding test by flow cytometry.

    Why? Spherocytes have less band 3 protein in their membrane, so they bind less EMA dye.

  13. A 9-year-old with hereditary spherocytosis had a febrile illness with a "slapped cheek" rash last week. Hb is now 52 g/L (baseline 105 g/L) and the reticulocyte count is very low. What has caused this crisis?

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    Parvovirus B19 infection causing an aplastic crisis.

    Why? Parvovirus B19 infects red cell precursors and halts erythropoiesis for about a week — trivial normally, but dangerous when red cells already survive only a short time.

  14. Which first-line test separates immune from non-immune causes of haemolytic anaemia?

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    Direct antiglobulin test (DAT, direct Coombs test).

    Why? The DAT detects IgG and/or complement (C3) already bound to the patient's red cells in vivo.

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