Haematology & Oncology

A malignant clone of immature blast cells expands rapidly in the bone marrow and crowds out normal blood production, so the clinical picture is a predictable marrow failure triad (anaemia, infection and bleeding) appearing over days to weeks.

A deficiency of either B12 or folate stalls DNA synthesis in every dividing cell, so red cell precursors keep growing but cannot divide, producing large, immature megaloblasts, while B12 deficiency alone also strips myelin, adding neurological disease that folate cannot fix and may make worse.

A clonal accumulation of mature but functionally incompetent B lymphocytes that pile up slowly in blood, marrow and nodes rather than dividing rapidly, so most patients are asymptomatic for years and the disease is found incidentally on a routine blood count.

Anaemia arising when iron intake or absorption fails to match losses or demand, so haemoglobin synthesis fails first and red cells emerge small and pale, and in an adult the default assumption is chronic blood loss until a source is found.

A malignant clonal proliferation of lymphocytes that expands within lymph nodes and lymphoid tissue rather than first flooding the marrow, so it presents as painless, progressive lymphadenopathy with cytokine-driven systemic 'B symptoms', behaving very differently depending on whether the clone is Hodgkin's Reed-Sternberg cells or a non-Hodgkin subtype.

A malignant clone of plasma cells expands in the bone marrow and pours out a single monoclonal immunoglobulin, so the clinical picture (bone destruction, renal failure, anaemia and hypercalcaemia) follows directly from marrow infiltration and the toxic paraprotein, summarised as CRAB.

A life-threatening oncological emergency in which chemotherapy-induced collapse of the neutrophil count removes the main defence against bacteria, so a fever after chemotherapy is treated as sepsis and given broad-spectrum antibiotics within one hour, before the neutrophil count is even known.

A clonal myeloproliferative disorder, usually driven by a JAK2 mutation that makes marrow precursors hypersensitive to growth signals, so red cells (and often white cells and platelets) are overproduced independent of erythropoietin, raising blood viscosity and thrombosis risk while erythropoietin itself is suppressed.

An inherited haemoglobinopathy in which abnormal haemoglobin S polymerises when deoxygenated, distorting red cells into rigid sickles that occlude small vessels and haemolyse, so hypoxia, dehydration, cold and infection all precipitate the same vaso-occlusive crisis.