BIOL 320 1 st Edition Lecture 5 Outline of Last Lecture I Female Gonads II Male Gonads III Pineal Gland IV Thymus V Other Hormone Producing Structures VI Developmental Considerations VII Aging Effects I Blood II Composition of Blood III Erythrocytes A Production B Life Cycle C Disorders Outline of Current Lecture VIII Leukocytes A Production B Disorders IX Platelets X Hemostasis A Phases B Disorders XI Human Blood Groups A Transfusion Reactions Current Lecture Leukocytes 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 invaders o Chemotaxis follow a chemical trail of toxic signal from damaged tissues o Diapedesis leaping across squeezing through epithelial layer to damaged tissue Characteristics o Diameter 2 4 microns o Prevalence 1WBC 300 RBC 1 Neutrophils granular 2 Lymphocytes agranular 3 Monocytes agranular 4 Eosinophils granular 5 Basophils granular o Nucleated o Organelles present o 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 Production o Leucopoiesis formation of WBCs o Cytokines interleukines and colongy stimulating factors hormonally stimulate the production of WBC o Formation Hemocytoblast stem cell Myeloid stem cell o Meyloblast committed cell Granular leukocytes Promyelocyte Eosinophilic myelocyte o Eosinophilic band cells Eosinophils Neutrophilic myelocyte o Neutrophilic band cells Neutrophils Basophilic myelocyte o Basophilic band cells Basophils o Monoblast committed cell Promonocyte Monocytes o Some become wandering macrophages tissues Lymphoid stem cell o Lymphoblast committed cell Prolymphocyte Lymphocytes o Some become plasma cells produce antibodies Disorders o Leukemias Named according to the cell involved Myelocytic leukemia lymphocytic leukemia etc Acute leukemia vs Chronic leukemia Acute o Progresses rapidly o Involves the blast cells o Affects kids mostly Chronic o Slower progression o Later development in cell lines o Affects adults elderly more Common characteristics Immature non functional WBCs in bloodstream Bone marrow full of cancerous leukocytes Cause of death o Internal hemorrhage o Infection Treatments o Radiation o Chemotherapy o Bone marrow transplant o Leukopenia Decrease in number of leukocytes Higher risk to get an infection or disease o Leukocytosis Increase in number of leukocytes May be fighting off infection or disease o 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 times Platelets 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 thrombopoietin o Hemocytoblast stem cell Megakaryoblast Promegakaryocyte o 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 aggregation o Calcium required for coagulation pathway o Enzymes needed for coagulation pathway o ADP potent aggregating agent that causes more platelets to stick to the area and release their contents o PDGF stimulates smooth muscle cells and fibroblasts to divide and rebuild the wall Hemostasis 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 vasoconstriction o Platelet Plug Formation injury to lining of vessel exposes collagen fibers platelets adhere o 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 vessels o Vessel endothelium ruptures exposing underlying tissues o Platelets cling and their surfaces provide sites for mobilization of factors o PF3 released by aggregated platelets o Pathway is much longer more steps so takes more time Extrinsic pathway outside the blood vessels o 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 clot o 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 factors o Calcium o 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 Formation o Two homeostatic mechanisms prevent clots from becoming large Swift removal and dilution of clotting factors Inhibition of activated clotting factors Factors Preventing Undesirable Clotting o 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 anticoagulant o Once blood vessel is roughened then more easily lets platelets stick seen in atherosclerosis Sympathetic ANS Response to Blood Loss o If greater than 10 of blood lost o Why The body will increase vasoconstriction to raise blood pressure heart will beat stronger faster because blood needs to be distributed body wide o How effective Until 40 of blood is lost Disorders o Disseminated Intravascular Coagulation DIC Widespread clotting block