Anatomy & Physiology: Blood Cells, Hemostasis, and Blood Groups
Termini in questo insieme (26)
Lymphocytes have the longest life span among leukocytes.
Neutrophils have a multi-lobed nucleus (3-6 lobes), light lilac cytoplasm with blue and pink granules, and are 2-3 times larger than RBCs. They phagocytize bacteria.
Eosinophils have a bilobed nucleus (earmuff shape), pink cytoplasm with red granules, 2-3 times larger than RBCs, and kill parasitic worms and play a role in allergy and asthma.
Basophils have a bilobed nucleus covered by large purplish/black/blue granules, 2-3 times larger than RBCs, and release histamine and heparin to promote inflammation and prevent clotting.
Agranulocytes lack visible granules in their cytoplasm, unlike granulocytes which have granules.
Lymphocytes have a large spherical nucleus occupying most of the cell, pale blue cytoplasm, slightly smaller than RBCs, and mount immune responses via direct attack or antibody production.
Monocytes have a U-shaped or kidney-shaped nucleus, gray-blue cytoplasm, are the largest blood cells, and phagocytize pathogens and develop into macrophages in tissues.
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils (Mnemonic: Never Let Monkeys Eat Bananas).
Neutrophils make up more than 50% of circulating white blood cells.
Neutrophils and monocytes are the primary phagocytic white blood cells.
Basophils release heparin and histamine to mediate inflammation and anticoagulation.
Thrombopoietin regulates the formation of platelets from megakaryocytes.
1. Vascular spasm: vasoconstriction reduces blood loss.
2. Platelet plug formation: platelets aggregate at injury.
3. Coagulation: fibrin mesh reinforces the plug.
Activated platelets release ADP (promotes aggregation), serotonin and thromboxane A2 (enhance vascular spasm and aggregation), and platelet-derived growth factor (PDGF) (stimulates vessel repair).
Extrinsic pathway: triggered by tissue factor outside blood, faster.
Intrinsic pathway: triggered by factors within blood, slower with more steps.
Prothrombin activator is formed by both intrinsic and extrinsic pathways to start the common pathway.
Phase I: Prothrombin activator forms.
Phase II: Prothrombin converts to thrombin.
Phase III: Thrombin converts fibrinogen to fibrin, forming a clot mesh.
Platelets contract using actin and myosin, pulling fibrin strands to compact the clot and draw vessel edges together, stabilizing the clot.
Fibrinolysis removes clots after healing; plasmin is the fibrin-digesting enzyme activated from plasminogen.
Clotting is controlled by rapid removal and inhibition of clotting factors, anticoagulants like antithrombin III, protein C, and heparin, and intact endothelium releasing nitric oxide and prostacyclin to prevent unwanted clotting.
ABO blood groups are distinguished by the presence or absence of A and B antigens on red blood cells.
Type A: A antigen
Type B: B antigen
Type AB: Both A and B antigens
Type O: No A or B antigens
Type A: anti-B antibodies
Type B: anti-A antibodies
Type AB: no antibodies
Type O: anti-A and anti-B antibodies
Type A: A, O
Type B: B, O
Type AB: A, B, AB, O (universal recipient)
Type O: O (universal donor)
Anti-Rh antibodies form when an Rh-negative person is exposed to Rh-positive blood, usually after the first exposure sensitizes the immune system.
Occurs when an Rh-negative mother carries multiple Rh-positive babies; maternal anti-Rh antibodies cross placenta and destroy fetal RBCs in subsequent pregnancies, causing anemia and hypoxia in the fetus.