Chapter 22: Structure and Function of the Hematologic System

Blood composition divides into plasma, which constitutes approximately 91 percent water and nine percent dissolved substances, and formed elements including erythrocytes, leukocytes, and platelets. Plasma proteins perform multiple critical roles: albumin maintains oncotic pressure and serves as a transport vehicle, globulins facilitate immunity and molecular trafficking, and fibrinogen provides essential clotting machinery. Red blood cells accomplish oxygen delivery through hemoglobin while their biconcave morphology permits passage through narrow capillaries. White blood cells function through distinct mechanisms: granulocytes including neutrophils, eosinophils, and basophils provide rapid pathogen response, while agranulocytes such as monocytes, macrophages, and lymphocytes mediate longer-term immune surveillance and tissue cleanup. Platelets orchestrate hemostatic responses and tissue healing. The chapter then addresses lymphoid architecture, where the spleen filters circulating blood and serves as an immune response center and blood reservoir, while lymph nodes trap pathogens and activate lymphocytes. Blood cell production originates in bone marrow through hematopoiesis, where stem cells differentiate into myeloid and lymphoid lineages under cytokine and growth factor regulation. Erythropoiesis depends on erythropoietin signaling in response to low oxygen tension, while hemoglobin synthesis requires iron, B12, folate, and cofactors; hepcidin controls iron recycling from aged erythrocytes. Myelopoiesis generates neutrophils and monocytes, lymphopoiesis creates T and B lymphocytes, and thrombopoiesis produces platelets via thrombopoietin stimulation. Hemostasis comprises sequential phases: vascular constriction, platelet aggregation into plugs, coagulation cascade amplification through intrinsic and extrinsic pathways generating thrombin and fibrin cross-links, clot contraction, and fibrinolytic breakdown. Endothelial cells provide antithrombotic protection through nitric oxide and prostacyclin secretion, while platelet activation releases adenosine diphosphate, thromboxane, and mitogenic factors. Endogenous anticoagulants including antithrombin III, protein C, and tissue factor pathway inhibitor restrict excessive clotting, balanced against plasmin and tissue plasminogen activator fibrinolytic activity. The chapter concludes by examining developmental and senescent changes: neonates demonstrate elevated hematocrit from fetal hematopoiesis but face immunologic vulnerability until adaptive immunity matures; aging produces slowed erythrocyte turnover, declining lymphocyte responsiveness, and increased platelet adhesiveness that amplifies thrombotic tendency.