--- module: 011-01 language: en chapter: 11 title: "Red Cells, Anaemia, Haemostasis, Thrombosis, and Transfusion" module_title: "Foundations" source_sha256: 6e14b661008510629411a36a0355cd939c4b2bb7abfaee9b2ee97557a77b7bd6 --- # Red cells, anaemia, haemostasis, thrombosis, and transfusion ## Red-cell production and turnover ### Stem cells generate red cells, white cells, platelets ### Erythropoietin from renal interstitial cells #### Released when oxygen delivery is inadequate #### Supports erythroid precursor survival and maturation ### Erythropoiesis needs iron, vitamins, healthy marrow ### Reticulocytes are recently released red cells #### Raised corrected response suggests marrow compensation #### Poor response suggests impaired production #### Marrow response is not immediate ### Haemoglobin: globin chains and iron-bearing haem ### No nucleus or mitochondria, glycolysis only ### Splenic and hepatic macrophages clear old cells #### Iron recycled, globin reused, haem to bilirubin ## Anaemia by mechanism ### Reduced haemoglobin lowers arterial oxygen content ### Microcytosis: impaired haemoglobin synthesis #### Iron deficiency demands a search for cause #### Ferritin also rises with inflammation #### Thalassaemia preserves the red-cell count ### Macrocytosis: vitamin B twelve, folate, alcohol, liver #### Folate alone risks neurological injury ### Normocytic: bleeding, inflammation, kidney, marrow failure #### Kidney disease: less erythropoietin, shorter survival ### Haemolysis intrinsic or extrinsic #### Membrane, enzyme, or haemoglobin defects #### Antibodies, mechanical injury, infection, hypersplenism #### Bilirubin and lactate dehydrogenase up, haptoglobin down ## Iron from store to marrow ### Ferroportin exports iron from cells ### Hepcidin removes ferroportin from the surface ### Iron stays in stores while marrow supply falls ### Deficiency empties reserve, restriction blocks access ### Circulating iron alone cannot separate them ## Platelets and primary haemostasis ### Injury constricts vessels and exposes matrix ### Von Willebrand factor binds platelets to collagen ### Activation: shape change, granules, thromboxane ### Fibrinogen bridges glycoprotein two b three a ### Count does not measure platelet function #### Drugs, uraemia, bypass, inherited defects ### Petechiae and mucosal bleeding versus deep bleeding ## Coagulation and fibrinolysis ### Tissue factor starts coagulation and makes thrombin ### Thrombin forms fibrin and amplifies itself ### Factor thirteen cross-links fibrin ### Natural anticoagulants restrain the reaction #### Antithrombin, protein C and S, pathway inhibitor ### Prothrombin time monitors vitamin K antagonists ### Activated partial thromboplastin time and heparin ### Normal screens do not exclude bleeding disorders ### Plasmin degrades fibrin and releases D-dimer ### D-dimer excludes thromboembolism in selected patients ## Thrombosis ### Virchow's triad: injury, flow, hypercoagulability ### Arterial thrombi are platelet-rich at high flow ### Venous thrombi are rich in fibrin and red cells ### Venous risk: surgery, immobility, cancer, oestrogen ### Deep-vein thrombosis may be silent ### Pulmonary embolism: dyspnoea, pleuritic pain, shock ### Disseminated coagulation consumes platelets and factors ## Antithrombotic drugs ### Antiplatelet drugs dominate arterial syndromes ### Anticoagulants prevent extension and recurrence ### Fibrinolytics dissolve clot at high bleeding cost ### Reversal needs time, antidotes, or factor concentrates ### Stopping treatment can also be dangerous ## Transfusion ### Red cells add capacity, not a diagnosis ### No single universal haemoglobin threshold ### One unit, then reassess ### Compatibility testing reduces haemolytic reactions ### Acute reactions: haemolysis, fever, allergy, overload ### Suspected reaction: stop, assess, check identity, notify ### Plasma is not a volume expander ### Patient blood management limits avoidable loss ## Blood film and marrow logic ### Film shows shape, fragments, inclusions, parasites ### Schistocytes still need clinical correlation ### Spherocytes: immune haemolysis or membrane disease ### Pancytopenia raises marrow failure or infiltration ### Marrow examination when peripheral evidence falls short ### Splenomegaly sequesters and destroys blood cells