--- module: 011-02 language: en chapter: 11 title: "Red Cells, Anaemia, Haemostasis, Thrombosis, and Transfusion" module_title: "Marrow response, clot architecture, and transfusion physiology" source_sha256: 921ca31c4cb7b5fa1371080098098ae7241d8ac51ff7767d42e3ecbc36687d81 --- # Marrow response and clot architecture ## Quantifying red-cell production ### Percentage must be read against the anaemia #### A normal percentage can still mean underproduction #### Correct for haematocrit and maturation delay ### Production can fail despite abundant erythropoietin #### Missing iron, vitamins, or healthy progenitors #### Inflammation suppresses response, raises hepcidin #### Kidney disease adds uraemic stress #### Marrow infiltration disrupts haematopoiesis ### Iron circuit: absorb, carry, use, recover, store #### Hepcidin internalises ferroportin #### High hepcidin restricts pathogens and erythropoiesis ### Low ferritin strongly supports deficiency ### Normal ferritin cannot exclude it in inflammation ### Transferrin saturation estimates circulating supply ### Finding the cause outranks replacement alone ## Morphology as a mechanism map ### Mean cell volume hides mixed populations #### Iron plus vitamin B twelve: normal average, wide spread #### Reticulocytosis raises the average ### Target cells: membrane area exceeds volume ### Schistocytes mark mechanical fragmentation ### Spherocytes: membrane defect or immune removal ### Intravascular destruction spills haemoglobin into plasma #### Haptoglobin consumed, haemoglobinuria possible ### Extravascular destruction in spleen and liver #### Splenomegaly and rising bilirubin ### Both raise lactate dehydrogenase and reticulocytes ### Direct antiglobulin test finds antibody or complement #### It grades no severity and finds no cause ## Haemostasis on cell surfaces ### The cascade organises the laboratory, not the body ### Tissue factor generates a small initial thrombin ### Thrombin activates platelets and cofactors ### A larger burst follows on platelet phospholipid ### Fibrin stabilises the platelet plug ### Endothelium normally resists clotting #### Nitric oxide, prostacyclin, anticoagulant proteins #### Glycocalyx separates blood from procoagulant structures ### Injury shifts the surface toward thrombosis ### Von Willebrand factor protects factor eight ### It mediates platelet adhesion under shear ### Platelet count measures no platelet function ## Coagulation tests and mixing logic ### Clotting times start under artificial conditions ### They omit platelets, vessels, factor thirteen, fibrinolysis ### A normal result cannot exclude bleeding disease ### Mixing study adds normal plasma #### Correction suggests factor deficiency #### Failure to correct suggests an inhibitor #### Drugs and time-dependent inhibitors confuse it ### Lupus anticoagulant prolongs tests yet causes thrombosis ### Fibrinogen falls with consumption, dilution, liver failure ### It can rise first as an acute-phase protein ### Serial testing tracks disseminated intravascular coagulation ## Thrombotic risk and anticoagulant control ### Venous thrombi begin in slow valve pockets ### Local hypoxia activates the endothelium ### Cancer releases procoagulant material and compresses veins ### Surgery combines injury, immobility, and inflammation ### Test thrombophilia only when it changes management ### Acute clot, pregnancy, and drugs distort assays ### Anticoagulants prevent extension more than they dissolve ### Fibrinolysis remodels the existing thrombus ### Duration weighs recurrence against bleeding ### Kidney injury can make a stable dose excessive ### Bleeding needs resuscitation and source control ## Transfusion as transplantation of function ### Benefit depends on output, saturation, and demand ### Stored cells also add circulating volume ### Congestion calls for slower rate or alternatives ### Haemorrhage calls for speed and balanced replacement ### Circulatory overload is hydrostatic pulmonary oedema ### Acute lung injury is permeability oedema ### Haemolytic reactions may be immediate or delayed #### Clerical mismatch is preventable at the bedside #### Delayed alloantibodies complicate future compatibility ### Massive transfusion brings dilution and hypothermia #### Citrate lowers ionised calcium ### The endpoint is perfusion and haemostasis restored ### Patient blood management begins before transfusion ### Document indication, response, and new antibodies ### A haemoglobin threshold alone does not decide transfusion ### Restart thromboprophylaxis individually once bleeding stops