BIOL 320 1st EditionLecture 5 Outline of Last Lecture I. Female GonadsII. Male GonadsIII. Pineal GlandIV. ThymusV. Other Hormone-Producing StructuresVI. Developmental ConsiderationsVII. Aging EffectsI. BloodII. Composition of BloodIII. ErythrocytesA. ProductionB. Life CycleC. DisordersOutline of Current Lecture VIII. LeukocytesA. ProductionB. DisordersIX. PlateletsX. HemostasisA. PhasesB. DisordersXI. Human Blood GroupsA. Transfusion ReactionsCurrent LectureLeukocytes- WBC are in Buffy Coat (part of the Formed Elements) and make up less than 1% of whole blood- Function: immune system cells…attack foreign invaderso Chemotaxis: follow a chemical trail of toxic signal from damaged tissueso Diapedesis: “leaping across” squeezing through epithelial layer to damaged tissue- Characteristics:o Diameter: 2-4 micronso Prevalence: 1WBC/300 RBC1. Neutrophils (granular)2. Lymphocytes (agranular)3. Monocytes (agranular)4. Eosinophils (granular)5. Basophils (granular)o Nucleatedo Organelles: presento Classification: based on granular content (either granular or agranular) Granulocytes vs. Agranulocytes- Granules: visible vs. non-staining- Nuclei: lobed vs. unlobed- Life Span: short lived vs. long lived- Productiono Leucopoiesis = formation of WBCso Cytokines (interleukines and colongy stimulating factors) hormonally stimulate the production of WBCo Formation: Hemocytoblast: stem cell- Myeloid stem cello Meyloblast: committed cell (Granular leukocytes) Promyelocyte- Eosinophilic myelocyteo Eosinophilic band cells Eosinophils- Neutrophilic myelocyteo Neutrophilic band cells Neutrophils- Basophilic myelocyteo Basophilic band cells Basophilso Monoblast: committed cell Promonocyte- Monocyteso Some become wandering macrophages (tissues)- Lymphoid stem cello Lymphoblast: committed cell Prolymphocyte- Lymphocytes o Some become plasma cells (produce antibodies)- Disorderso Leukemias Named according to the cell involved- Myelocytic leukemia, lymphocytic leukemia, etc. Acute leukemia vs. Chronic leukemia- Acute:o Progresses rapidlyo Involves the blast cellso Affects kids mostly- Chronic:o Slower progressiono Later development in cell lineso Affects adults (elderly) more Common characteristics:- Immature, non-functional WBCs in bloodstream- Bone marrow full of cancerous leukocytes- Cause of death:o Internal hemorrhageo Infection- Treatments:o Radiationo Chemotherapyo Bone marrow transplanto Leukopenia Decrease in number of leukocytes Higher risk to get an infection or diseaseo Leukocytosis Increase in number of leukocytes May be fighting off infection or diseaseo Mononucleosis Cause: Epstein-Barr virus WBC characteristics: atypical…non-normal…elevated numbers of WBC Symptoms: low grade fever, tired, achy, sore throat… Prognosis: runs course in 3-4 weeks…usually build up resistance…and will only have one timesPlatelets- Thrombopoiesis: production of platelets- Abundance: 250,000 – 500,000/cc blood- Function: blood clotting…- Inhibition: not naturally sticky, kept inactive by nitric oxide and prostaglandins (prostacyclin)- Formation:o Regulated by the hormone, thrombopoietino Hemocytoblast: stem cell Megakaryoblast- Promegakaryocyteo Megakaryocyte (located in bone marrow and release/project platelets into blood vessels) Platelets: formed from degradation of megakaryocyte- Granules in platelets contain:o Serotonin: messenger that enhances vascular spasm and platelet aggregationo Calcium: required for coagulation pathwayo Enzymes: needed for coagulation pathwayo ADP: potent aggregating agent that causes more platelets to stick to the area and release their contentso PDGF: stimulates smooth muscle cells and fibroblasts to divide and rebuild the wallHemostasis- Definition of hemostasis:o Cessation of bleeding- Fast series of reactions for stoppage of bleeding- Steps for Hemostasis:o Vascular Spasms: smooth muscle contracts, causing vasoconstrictiono Platelet Plug Formation: injury to lining of vessel exposes collagen fibers; platelets adhereo Coagulation (blood clotting): fibrin forms a mesh that trap RBCs and platelets, forming a clot Phase I: two pathways to prothrombin activator- Intrinsic pathway: inside the blood vesselso Vessel endothelium ruptures, exposing underlying tissueso Platelets cling and their surfaces provide sites for mobilization of factorso PF3 released by aggregated plateletso Pathway is much longer (more steps) so takes more time- Extrinsic pathway: outside the blood vesselso Tissue cell trauma exposes blood to tissue factor (TF)o Pathway is much faster (fewer steps) so takes less time Phase II: common pathway to thrombin- Prothrombin (II) + Prothrombin activator  Thrombin (IIa) Phase III: common pathway to the fibrin mesh- Fibrinogen (I) [soluble] + Thrombin (IIa)  Fibrin [insoluble polymer]o Fibrin [insoluble polymer]  Cross-linked fibrin mesh- Fibrin strands form the structural basis of a clot- Fibrin causes plasma to become a gel-like trap for formed elements- Cross-links of fibrin strengthens and stabilizes the cloto Clot Retraction and Repair & Fibrinolysis Clot Retraction- 30-60 minutes- Actin & Myosin: pull on edges of the wound towards the middle…causes liquid/serum to lead out of the edges- Serum evacuated- Pulls wound together Repair- PDGF (platelet derived growth factor): stimulated vessel wall to rebuild- Fibroblasts: connective tissue patch- VEGF (vascular endothelial growth factor): stimulate rebuilding of endothelium Clot Destruction- Plasminogen: turns into active form plasmin by plasminogen activator (secreted by endothelium)- Plasmin: dissolves clot- Factors Needed for Clotting:o Clotting factorso Calciumo Vitamin K (needed to make factors in liver)o Platelets- Regulation by a positive feedback until coagulation occurs/plug forms- Factors Limiting Clot Growth or Formationo Two homeostatic mechanisms prevent clots from becoming large Swift removal and dilution of clotting factors Inhibition of activated clotting factors- Factors Preventing Undesirable Clottingo Platelet adhesion is prevented by: Smooth endothelial lining of blood vessels Antithrombic substance nitric oxide and prostacyclin secreted by endothelial cells Vitamin E (quinine), which acts as a potent anticoagulanto Once blood vessel is roughened then more easily lets platelets