Chapter 14.2: White Blood Cells and Platelets

White Blood Cells (WBCs) -Also called leukocytes -Contain a nucleus and other organelles -No hemoglobin -Specialize in protecting body from disease -Two types: 1)Granular 2)Agranular

White Blood Cells (WBCs) -Granulocytes: contain chemical-filled granules 1)Neutrophils 2)Eosinophils 3)Basophils -Agranulocytes: no granules 1)Lymphocytes: B, T, NK cels 2)Monocytes: macrophages

Granulocytes -1 st Respnoders -> Phagocytosis -60% of WBCs -Found in pus of wounds Neutrophils -Inflammatory reaction -Responds to allergic reactions -1% of WBCs Basophils -Phagocytize antigen-antibody complexes -Mainly attack parasitic worms -2% of WBCs Eosinophils

Agranulocytes -Become macrophages -Consume a lot of microbes -7% of WBCs Monocytes -B, T, and NK cells -Main defense against invaders -30% of WBCs Lymphocytes

WBC Life Span -About 5,000 to 10,000 WBC/µL of blood -Life span = a few days -Phagocytosis interferes with normal metabolism -During infection, only a few hours -Leukocytosis: an increase in the # of WBCs -WBC count used to diagnose specific illness -Develop in red bone marrow from myeloid and lymphoid stem cells

Platelets -Pluripotent stem cells in red bone marrow -> megakaryocytes -> platelets -About 150, ,000 platelets/µL blood -Form a platelet plug to prevent blood loss

Chapter Hemostasis

Hemostasis -A series of responses that stops bleeding when blood vessels are injured -Involves coagulation and clotting of blood to seal site of damage -Prevents hemorrhage -Three different mechanisms: 1)Vascular spasm 2)Platelet plug 3)Blood clotting

Vascular Spasm -Smooth muscle around blood vessel contracts immediately -Initial response to smooth muscle damage -Detected by pain receptors -Can reduce blood loss for several hours -Platelets accumulate and release chemicals to enhance vasoconstriction and maintain vascular spasm

Platelet Plug Formation -Platelets in the blood contact and stick to damaged blood vessel -Release chemicals -Activates nearby platelets and makes them sticky -Sustain vascular spasm -Large number of platelets form a platelet plug -Stops blood loss for minor vessel damage

Blood Clotting -Clotting, or coagulation, is a series of chemical reactions that ultimately form fibrin threads. -Too much = thrombosis -Too little = hemorrhage - Released chemicals are clotting factors -Calcium ions -Enzymes made by liver -Platelet associated molecules

Three Stages of Clotting 1)Prothrombinase is formed 2)Prothrombinase converts prothrombin -> thrombin 3)Thrombin converts fibrinogen -> fibrin (threads of clot) PROTHROMBINASE PROTHROMBIN THROMBIN FIBRINOGEN Loose fibrin threads STRENGTHENED FIBRIN THREADS Fibrin threads Red blood cell Ca 2+

Forming Prothrombinase-Two Pathways 1)Extrinsic Pathway -Occurs rapidly (seconds) -Damaged tissue release tissue factor (TF) into blood from outside blood vessel -TF -> Prothrombinase using calcium and clotting factors 2)Intrinsic Pathway -Much slower -Damaged cells lining blood vessel activates clotting factors and platelets (release phospholipids) -Platelet phospholipids -> Prothrombinase + + Tissue trauma Blood trauma Damaged endothelial cells expose collagen fibers Damaged endothelial cells expose collagen fibers TFTF Clotting factors and Ca 2+ Platelet phospholipids (a) Extrinsic pathway (b) Intrinsic pathway PROTHROMBINASE Activated platelets

Three Stages of Clotting 1)Prothrombinase is formed 2)Prothrombinase converts prothrombin -> thrombin 3)Thrombin converts fibrinogen -> fibrin (threads of clot) PROTHROMBINASE PROTHROMBIN THROMBIN FIBRINOGEN Loose fibrin threads STRENGTHENED FIBRIN THREADS Fibrin threads Red blood cell Ca 2+

Clotting in Blood Vessels -Fatty substances accumulating on arterial walls attract platelets -Slow blood flow allows clotting factors to accumulate -Thrombus forms -May become dislodged and swept away in blood -Becomes an embolus