RACP Divisional Written Exam · FRACP

Haematology for the written exam

Everything Physify has for Haematology: short lessons written to Australian guidance, exam-style questions with a worked explanation for each, and Bedside, our AI tutor, under every one. Try a question below, no sign-up.

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Haematology

A 51-year-old woman has protein S activity of 38 per cent (reference 60 to 140) measured 2 days after an acute pulmonary embolism, while taking warfarin with an INR of 2.6 and enoxaparin. She has no family history of thrombosis. Haemoglobin 118 g/L, platelets 194 x 10^9/L, bilirubin 11 micromol/L, ALT 26 U/L. How should this be interpreted?

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What's covered

30 courses, each a set of lessons with a quiz after them. The bar shows how many questions each has. Open a course to see its lesson outline.

From the lessons

24 figures sit in the Haematology lessons: ECGs, diagrams, films and clinical images, each with what to look for. Here are 4. Tap one to enlarge it.

Schematic haematopoietic tree. The haematopoietic stem cell gives a common myeloid progenitor and a common lymphoid progenitor. Stem cell clones (CML with BCR::ABL1, other myeloproliferative neoplasms and myelodysplasia) hang from the stem cell and show in several lines at once. The myeloid progenitor gives erythroblasts, megakaryocytes, myeloblasts and monoblasts; AML arises from myeloblasts or monoblasts (CD13, CD33, CD117, MPO; Auer rods; monocytic AML infiltrates gums and skin), and APL from promyelocytes on the granulocyte line (PML::RARA, DIC). The lymphoid progenitor gives B and T lymphoblasts and NK precursors; B-ALL carries CD19, CD10, CD22 and CD79a, T-ALL CD3 and CD7, both TdT positive. Mature cells and their neoplasms: red cells, polycythaemia vera (an MPN); platelets, essential thrombocythaemia (an MPN); granulocytes, CML with neutrophilia and basophilia; mature B cells, CLL (CD5, CD19, CD23) and hairy cell leukaemia (BRAF V600E); plasma cells, myeloma and other plasma cell disorders; T and NK cells, large granular lymphocytic leukaemia (STAT3, neutropenia, rheumatoid arthritis). Notes: acute leukaemia is a block in maturation with 20 per cent or more blasts in marrow or blood (though some AML-defining genetic abnormalities such as PML::RARA count at any blast percentage), while chronic leukaemia still matures; Auer rods and myeloperoxidase mean myeloid, TdT with B or T markers means lymphoblastic, and flow cytometry settles the lineage; gum and skin infiltration suggest monocytic AML, bone pain, nodes and CNS disease ALL, DIC APL, and incidental lymphocytosis with smudge cells CLL.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Diagnosis & Classification” in Leukaemia

Schematic comparing intravascular and extravascular haemolysis. Intravascular, inside the vessels: red cells rupture and release free haemoglobin; haptoglobin binds it and is cleared, so haptoglobin is very low or undetectable; excess haemoglobin passes into the urine as haemoglobinuria (red or dark urine); renal tubular cells store the iron and shed it later as haemosiderinuria; the film shows schistocytes when the cause is mechanical. Extravascular, in the spleen and liver: macrophages remove antibody-coated or misshapen red cells such as spherocytes; haem is broken down to unconjugated bilirubin, giving jaundice without red urine; little free haemoglobin reaches the plasma, so haptoglobin is low but there is no haemoglobinuria; splenomegaly is common, with gallstones if chronic; the film shows spherocytes in autoimmune and hereditary causes. A table: reticulocytes and LDH raised in both; unconjugated bilirubin raised in both; haptoglobin very low or undetectable in intravascular and low in extravascular haemolysis; haemoglobinuria and haemosiderinuria present only in intravascular haemolysis; the DAT is positive in ABO-incompatible transfusion and in autoimmune haemolysis, separating immune from non-immune causes in either compartment, and a negative test does not exclude immune haemolysis. Example intravascular causes: ABO-incompatible transfusion, PNH, microangiopathy, mechanical valve, severe G6PD crisis, march haemoglobinuria, clostridial sepsis and severe malaria. Example extravascular causes: warm autoimmune haemolysis, hereditary spherocytosis, hypersplenism and most drug induced haemolysis. Some causes, such as G6PD deficiency, do both.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Recognising Haemolysis & Immune Causes” in Haemolysis

Schematic of iron traffic. The duodenal enterocyte takes iron in through duodenal cytochrome b and DMT1 and exports it through ferroportin with hephaestin, about 1 to 2 mg a day, into plasma transferrin, a pool of about 3 mg that is normally about 30 per cent saturated. Marrow erythroblasts take up diferric transferrin through TfR1 and make red cells, which hold about two thirds of the 3 to 4 g of body iron. Macrophages recycle old red cells and return 20 to 25 mg a day to plasma through ferroportin. Losses are about 1 to 2 mg a day from shed cells and blood loss; there is no regulated excretion. The hepatocyte stores iron as ferritin and makes hepcidin, which degrades ferroportin at both gates, the enterocyte and the macrophage, so absorption and macrophage release stop and saturation falls within hours while the stores stay full. Hepcidin is raised by iron stores through BMP6 and BMP2 to SMAD, with haemojuvelin, HFE and transferrin receptor 2, by inflammation through IL-6 and STAT3, and by reduced renal clearance in CKD; it is lowered by erythroferrone, hypoxia and HIF stabilisation, testosterone and TMPRSS6, which cleaves haemojuvelin. A table reads the results: iron deficiency, ferritin and saturation low; inflammation or CKD, ferritin normal or high with low saturation; TMPRSS6 loss (iron-refractory iron deficiency anaemia, IRIDA), ferritin normal or low with very low saturation; haemochromatosis and ineffective erythropoiesis, both high, saturation often above 75 per cent in haemochromatosis; and loss-of-function ferroportin disease, ferritin very high with normal or low saturation. Above about 75 to 80 per cent saturation, non-transferrin bound iron enters heart and liver.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Iron: Absorption, Transport and the Hepcidin-Ferroportin Axis” in Oxygen Sensing, Iron and Haem

Flowchart classifying anaemia, a haemoglobin below about 130 g/L in men or 120 g/L in non-pregnant women, by MCV and then the reticulocyte count. Microcytic, MCV under 80 fL, sorted by iron studies: iron deficiency (ferritin under 30 micrograms per litre, or up to 100 with inflammation, low transferrin saturation, high transferrin, high RDW, pencil cells); anaemia of inflammation (ferritin normal or high, low transferrin saturation, transferrin low or normal, CRP raised, usually normocytic and microcytic if prolonged); thalassaemia trait (normal iron studies and RDW, red cell count normal or high, Mentzer index under 13, HbA2 raised in beta trait and gene testing for alpha trait); and sideroblastic anaemia (ferritin and transferrin saturation high, ring sideroblasts, dimorphic film, with basophilic stippling in lead poisoning). Normocytic, MCV 80 to 100 fL, sorted by the reticulocyte count: raised, over about 100 x 10^9/L, means haemolysis (bilirubin and LDH up, haptoglobin low) or blood loss; low or inappropriately normal means underproduction, from anaemia of inflammation, CKD, early iron deficiency, mixed deficiency, hypothyroidism, liver disease, marrow infiltration or failure, or myelodysplasia. Macrocytic, MCV over 100 fL, sorted by the film, B12 and folate: megaloblastic (oval macrocytes and hypersegmented neutrophils) from B12 or folate deficiency or drugs such as methotrexate, hydroxyurea, azathioprine and zidovudine; non-megaloblastic from alcohol, liver disease, hypothyroidism, myelodysplasia, reticulocytosis, myeloma and pregnancy. A note says a normal MCV does not exclude combined iron and B12 deficiency.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Approach to Anaemia” in Anaemia

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Haematology in the clinical exam

10 interactive short cases and 3 long cases for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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Haematology on the blog

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