Exam II. Blood. Tigers 4. 1) RBC loss 2) Low O 2 3) Exercise. Level in Blood. Erythropoietin RBCs Mature More Rapidly. Kidney Releases.
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1 Exam I Today: A. Leukocytes B. Platelets C. Hemostatis D. Heart Anatomy Mariners 3 Exam II Blood Tigers 4 Balance of RBCs important: Low = tissue hypoxia High = viscous blood Iron and B-complex vitamins crucial for RBC development Vitamin B 12 and folic acid = Proper DNA synthesis Iron = Hemoglobin synthesis Stored as ferritin and hemosiderin Transported in blood via transferrins Reserves = hemoglobin (80%), cells (20%), blood (<1%) Controlled hormonally by erythropoietin Produced by kidney (~ 85%) and liver (~ 15%) Low Blood Oxygen Level Normal Blood Oxygen Level Hypoxia 1) RBC loss 2) Low O 2 3) Exercise Normal Blood Oxygen Level Increased O 2 Reduced O 2 Increased O 2 Reduced O 2 RBCs Mature More Rapidly Stimulates Bone Marrow Kidney Releases RBCs Mature More Rapidly Stimulates Bone Marrow Kidney Releases Lifecycle of RBCs: Erythrocyte Disorders: 1) Anemias ( oxygen carrying capacity) Decreased RBCs (e.g. blood loss, marrow destruction) Decreased Hemoglobin (e.g. iron / B 12 deficiency) Abnormal Hemoglobin (e.g. Thalassemia; Sickle-cell anemia) 2) Polycythemia ( RBCs) Bone marrow cancer High altitude living Blood doping (artificial) (Figure 18.7) Whole Blood EPO
2 Blood Components: 3) Leukocytes (White Blood Cells - WBCs) Complete cell Function in defense against disease Utilize blood for transport Perform most functions in tissue (exit = diapedesis) Produced in bone marrow Produced/mobilize quickly Generally < 1 day in circulation Blood Components - Leukocytes: Granulocytes (contain granules): 1) Neutrophils (55-65%) Small granules (hydrolytic enzymes/defensins) Multi-lobed nuclei Engulf bacteria/fungi (respiratory burst) 2) Eosinophils (1-4%) Large granules (lysosomes) Bi-lobed nuclei Attack parasitic worms (e.g. tapeworms) 3) Basophils (< 1%) Large granules (histamines) U-shaped nuclei Vasodilate vessels/attract WBCs Blood Components - Leukoocytes: Agranulocytes (lack granules): 1) Lymphocytes (25-35%) Large nuclei Few in blood (lymph nodes/spleen) Immunity function (Life span = years) T lymphocytes (virus-infected/tumor cells) B lymphocytes (antibodies) 2) Monocytes (3-7%) Largest of WBCs Large U-shaped nuclei Macrophages (phagocytosis) Blood Components - Leukocytes Leukopoiesis (Figure 18.11): proerythroblast Myeloid stem cell Hemocytoblast Hormones: Interleukins Colony-stimulating factors Lymphoid stem cell Myeloblast Monoblast Lymphoblast Eosinophils Basophils Monocytes Lymphocytes Neutrophils Blood Components - Leukocytes: Leukocyte Disorders: 1) Overproduction of WBCs Leukemias (cancers of WBCs) Lymphocytic leukemia Mononucleosis (Epstein-Barr virus - high agranulocyte counts) 2) Underproduction of WBCs (Leukopenia) Induced by drugs (glucocorticoids / anticancer) Blood Components: 4) Platelets (thrombocytes) Cytoplasmic fragments (anucleate) Function in blood clotting Granules clotting chemicals Short-lived (~ 10 days)
3 Blood Components - Platelets: Thrombopoietin Megakaryoblast Megakaryocyte proerythroblast Hemocytoblast Platelets Myeloid stem cell Lymphoid stem cell Platelet Production: Myeloblast Monoblast Lymphoblast Eosinophils Basophils Monocytes Lymphocytes Neutrophils (Figure 18.12) Series of fast, localized reactions to halt blood loss Phases: 1) Vascular Spasms (Vasoconstriction of damaged vessel) Significantly reduces blood loss Activated by: (a) Direct injury to smooth muscle (b) Chemical release (c) Nociceptors 2) Formation of Platelet Plug Temporarily seals vessel break (Positive feedback loop) Hemostasis - Platelet Plug Formation: Attracts more platelets Adenosine Diphosphate (ADP) Rupture of vessel Collagen exposed Vascular Platelets stick to site spasms Platelets release contents Aspirin Thromboxane A 2 Serotonin Phases: 3) Coagulation (Blood clotting) Blood converted from liquid to gel (3-6 minutes) Step 1: Formation of prothrombin activator Step 2: Step 3: Intrinsic pathway outside of body (minutes) Extrinsic pathway in tissues (seconds) Prothrombin (protein) Fibrinogen (protein) Prothrombin activator Thrombin Thrombin (enzyme) Fibrin mesh (seals hole)
4 Events in coagulation: Produced in liver Most require vitamin K (Figure 18.13) Clot Retraction and Removal: 1) Platelets draw wound together (Actin/myosin fibers) 2) Platelet-derived Growth Factor (PDGF - Platelets) Stimulates vessel to rebuild (smooth muscle/fibroblasts) 3) Plasminogen converted to Plasmin Dissolves clot (fibrinlysis) Plasmin activated by tpa (tissue plasminogen activator) Factors preventing undesirable clotting: 1) Endothelium smooth walls 2) Prostacyclin (PGI 2 ) and Heparin (anticoagulants) Inhibit platelet aggregation (produced by endothelial wall) Thromboembolytic Disorders (Undesirable clot formation): Thrombus: Clot develops in unbroken vessel Embolus: Clot floats freely in vessels Drug treatment = Aspirin, heparin, warfarin Bleeding Disorders (e.g. Hemophilia - coagulation factor deficiency) Transfusion and Blood Replacement: 1) ABO Blood Groups Presence / absence of 2 glycoproteins (antigens) Transfusion and Blood Replacement: 2) Rh Blood Groups Presence / absence of 1 glycoprotein Type A Type B Type AB Type O Blood has pre-formed antibodies opposite blood type Type O blood = Universal Donor Type AB blood = Universal Recipient Type Rh+ Type Rh- Antibodies formed after initial contact with antigen Hemolytic disease of the newborn
5 Transfusion Reactions: 1) Clumping of foreign RBCs: 2) RBCs rupture/are destroyed: Hemoglobin Treatment = Alkaline fluids (dilute/dissolve hemoglobin) Diuretics Kidneys
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