Haematology & Oncology
23 condition pages in this specialty.
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Iron-Deficiency Anaemia
FreeIron-deficiency anaemia reflects depleted iron available for haemoglobin production; replace the iron, but always investigate the pattern of loss, demand or malabsorption that caused it.
Lymphoma
FreeA heterogeneous group of clonal lymphoid malignancies that may present with persistent lymphadenopathy, splenomegaly, extranodal disease or systemic symptoms; tissue classification and subtype-specific staging determine urgency and treatment.
Leukaemia
4 topicsAcute Lymphoblastic Leukaemia (ALL)
Full accessA maturation arrest in the lymphoid lineage lets lymphoblasts proliferate and fill the marrow, causing rapid marrow failure plus a distinctive tendency to infiltrate the central nervous system and testes; it is the commonest childhood cancer.
Acute Myeloid Leukaemia (AML)
Full accessA maturation arrest in the myeloid lineage lets myeloblasts proliferate and fill the marrow, so normal blood production collapses over days to weeks into the anaemia, infection and bleeding of marrow failure, most often in an older adult.
Chronic Lymphocytic Leukaemia
Full accessA 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.
Chronic Myeloid Leukaemia (CML)
Full accessA single acquired fusion gene, BCR-ABL1 from the Philadelphia chromosome, creates a constitutively active tyrosine kinase that drives myeloid overproduction with preserved maturation, so the blood fills with maturing granulocytes and the spleen enlarges, usually indolently until it is controlled by a targeted inhibitor.
Myeloproliferative neoplasms
3 topicsEssential thrombocythaemia
Full accessA myeloproliferative neoplasm in which clonal megakaryocyte proliferation, usually driven by JAK2, CALR or MPL, sustains a high platelet count; the raised, functionally abnormal platelets cause both thrombosis and, paradoxically at very high counts, bleeding, so it is a diagnosis of exclusion once reactive thrombocytosis is ruled out.
Myelofibrosis
Full accessA myeloproliferative neoplasm in which a clonal marrow drives fibroblasts to lay down reticulin and collagen, so the marrow is progressively replaced by fibrosis; blood production shifts to the spleen and liver (extramedullary haematopoiesis), producing massive splenomegaly, a leukoerythroblastic film with tear-drop red cells, and constitutional symptoms.
Polycythaemia Vera
Full accessA 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.
B12 and Folate Deficiency
Full accessB12 or folate deficiency impairs DNA synthesis and can cause megaloblastic cytopenias; B12 deficiency additionally threatens the nervous system, so it must be recognised and replaced promptly, especially before or alongside folic acid.
Disseminated Intravascular Coagulation (DIC)
Full accessDisseminated intravascular coagulation is a dynamic, acquired syndrome of systemic coagulation activation driven by another serious illness, causing microvascular thrombosis while consuming platelets and clotting factors; treat the trigger first and support bleeding selectively.
Haemophilia
Full accessHaemophilia is an inherited deficiency of factor VIII (haemophilia A) or factor IX (haemophilia B), causing impaired fibrin formation and a characteristic tendency to bleed into joints, muscles and deep tissues; urgent specialist treatment is needed for significant bleeding or procedures.
Hyposplenism and asplenia
Full accessHyposplenism is reduced splenic function and asplenia is absent splenic function; both impair clearance of blood-borne organisms and make rapidly progressive infection, particularly with encapsulated bacteria, a lifelong emergency risk.
Immune Thrombocytopenia (ITP)
Full accessImmune thrombocytopenia is an acquired immune-mediated platelet disorder causing isolated thrombocytopenia and a mucocutaneous bleeding phenotype; diagnosis is one of exclusion, and treatment is guided by bleeding risk, platelet count, comorbidity and treatment burden rather than the count alone.
Myeloma
Full accessA clonal plasma-cell malignancy produces monoclonal immunoglobulin or light chains and damages bone, kidneys, marrow and immunity; diagnosis and treatment depend on a myeloma-defining event, disease biology, fitness and patient priorities.
Neutropenic Sepsis
Full accessAnticancer treatment removes the neutrophils that both contain infection and generate its localising signs, so bacteraemia can progress to shock in a patient who still looks well.
Sickle Cell Disease
Full accessAn inherited haemoglobinopathy in which deoxygenated haemoglobin S polymerises, making red cells rigid and adhesive; vaso-occlusion causes ischaemic pain while haemolysis causes chronic anaemia and progressive organ damage.
Thalassaemia
Full accessThalassaemia is an inherited disorder of reduced alpha- or beta-globin synthesis causing ineffective erythropoiesis, haemolysis and microcytic anaemia; severity ranges from an asymptomatic carrier state to transfusion-dependent disease with lifelong risk from iron overload.
Thrombophilia
Full accessThrombophilia is an inherited or acquired tendency to thrombosis. Testing is selective because most heritable results do not change anticoagulation decisions, whereas antiphospholipid syndrome can alter the choice of anticoagulant, pregnancy management and long-term follow-up.
Transfusion Reactions
Full accessBlood components injure recipients four separate ways, immune destruction of red cells, plasma-protein allergy, bacterial contamination and sheer transfused volume, and at onset they look alike.
Von Willebrand Disease
Full accessVon Willebrand disease is an inherited quantitative or qualitative defect of von Willebrand factor, impairing platelet adhesion and factor VIII stability and causing predominantly mucocutaneous bleeding; treatment depends on the subtype, bleeding phenotype, procedure and a documented response plan.