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Copyright © 2010 Pearson Education, Inc. Blood Composition Blood: a fluid connective tissue composed of Plasma Formed elements Erythrocytes (red blood cells, or RBCs) Leukocytes (white blood cells, or WBCs) Platelets
Copyright © 2010 Pearson Education, Inc. Blood Composition Hematocrit Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females
Copyright © 2010 Pearson Education, Inc. Figure Withdraw blood and place in tube. 2 Centrifuge the blood sample. Plasma 55% of whole blood Least dense component Buffy coat Leukocytes and platelets <1% of whole blood Erythrocytes 45% of whole blood Most dense component Formed elements
Copyright © 2010 Pearson Education, Inc. Physical Characteristics and Volume Sticky, opaque fluid Color scarlet to dark red pH 7.35– C ~8% of body weight Average volume: 5–6 L for males, and 4–5 L for females
Copyright © 2010 Pearson Education, Inc. Functions of Blood 1.Distribution of ? 3.Protection against Blood loss Plasma proteins and clot formation Infection Antibodies WBCs defend against foreign invaders
Copyright © 2010 Pearson Education, Inc. Blood Plasma 90% water Proteins are mostly produced by the liver 60% albumin 36% globulins 4% fibrinogen
Copyright © 2010 Pearson Education, Inc. Figure 17.2 Platelets NeutrophilsLymphocyte ErythrocytesMonocyte
Copyright © 2010 Pearson Education, Inc. Figure µm 7.5 µm Side view (cut) Top view
Copyright © 2010 Pearson Education, Inc. Erythrocytes Structural characteristics contribute to gas transport Shape—huge surface area >97% hemoglobin No mitochondria No nucleus
Copyright © 2010 Pearson Education, Inc. Figure 17.4 Heme group (a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups. (b) Iron-containing heme pigment. Globin chains Globin chains
Copyright © 2010 Pearson Education, Inc. Hemoglobin (Hb) O 2 loading in the lungs Produces oxyhemoglobin (ruby red) O 2 unloading in the tissues Produces deoxyhemoglobin or reduced hemoglobin (dark red) CO 2 loading in the tissues Produces carbaminohemoglobin (carries 20% of CO 2 in the blood)
Copyright © 2010 Pearson Education, Inc. Hematopoiesis Hematopoiesis; blood cell formation Occurs in red bone marrow, girdle and proximal epiphyses of humerus and femur
Copyright © 2010 Pearson Education, Inc. Figure 17.5 Stem cell Hemocytoblast Proerythro- blast Early erythroblast Late erythroblast Normoblast Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Reticulo- cyte Erythro- cyte Committed cell Developmental pathway Erythropoiesis:red blood cell production
Copyright © 2010 Pearson Education, Inc. Regulation of Erythropoiesis Too few RBCs leads to tissue hypoxia Too many RBCs increases blood viscosity Balance depends on Hormonal controls Adequate supplies of iron, amino acids, and B vitamins
Copyright © 2010 Pearson Education, Inc. Hormonal Control of Erythropoiesis Erythropoietin (EPO) Direct stimulus for erythropoiesis Released by kidneys in response to hypoxia Testosterone also enhances EPO production, resulting in higher RBC counts in males
Copyright © 2010 Pearson Education, Inc. Hormonal Control of Erythropoiesis Causes of hypoxia Hemorrhage or increased RBC destruction reduces RBC numbers Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of O 2 (e.g., high altitudes)
Copyright © 2010 Pearson Education, Inc. Figure 17.6 Kidney (and liver to a smaller extent) releases erythropoietin. Erythropoietin stimulates red bone marrow. Enhanced erythropoiesis increases RBC count. O 2 - carrying ability of blood increases. Homeostasis: Normal blood oxygen levels Stimulus: Hypoxia (low blood O 2 - carrying ability) due to Decreased RBC count Decreased amount of hemoglobin Decreased availability of O IMBALANCE
Copyright © 2010 Pearson Education, Inc. Fate and Destruction of Erythrocytes Life span: 100–120 days Macrophages engulf dying RBCs in spleen Iron is salvaged for reuse Heme is degraded to yellow bilirubin Liver secretes bilirubin (in bile)) into the intestines Degraded pigment leaves the body in feces as stercobilin
Copyright © 2010 Pearson Education, Inc. Figure 17.7 Low O 2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 3 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 New erythrocytes enter bloodstream; function about 120 days. 4 Raw materials are made available in blood for erythrocyte synthesis. 6 Hemoglobin Amino acids Globin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Food nutrients, including amino acids, Fe, B 12, and folic acid, are absorbed from intestine and enter blood. Heme Circulation Iron stored as ferritin, hemosiderin Bilirubin Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria, and excreted in feces.
Copyright © 2010 Pearson Education, Inc. Erythrocyte Disorders Anemia: abnormally low O 2 -carrying capacity A sign rather than a disease itself Blood O 2 cannot support normal metabolism Accompanied by fatigue, paleness, shortness of breath, and chills
Copyright © 2010 Pearson Education, Inc. Causes of Anemia 1.Insufficient erythrocytes Hemorrhagic anemia: acute or chronic loss of blood Hemolytic anemia: RBCs rupture prematurely Aplastic anemia: destruction or inhibition of red bone marrow
Copyright © 2010 Pearson Education, Inc. Causes of Anemia 2.Low hemoglobin content Iron-deficiency anemia Secondary result of hemorrhagic anemia or Inadequate intake of iron-containing foods or Impaired iron absorption
Copyright © 2010 Pearson Education, Inc. Causes of Anemia Pernicious anemia Deficiency of vitamin B 12 Lack of intrinsic factor needed for absorption of B 12 Treated by intramuscular injection of B 12
Copyright © 2010 Pearson Education, Inc. Causes of Anemia Sickle-cell anemia Defective gene codes for abnormal hemoglobin (HbS) Causes RBCs to become sickle shaped in low-oxygen situations
Copyright © 2010 Pearson Education, Inc. Figure (a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain. (b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin.
Copyright © 2010 Pearson Education, Inc. Erythrocyte Disorders Polycythemia: excess of RBCs that increase blood viscosity Results from: Polycythemia—bone marrow cancer Secondary polycythemia—when less O 2 is available (high altitude) or when EPO production increases Blood doping
Copyright © 2010 Pearson Education, Inc. Figure 17.9 Formed elements Platelets Leukocytes Erythrocytes Differential WBC count (All total 4800 – 10,800/l) Neutrophils (50 – 70%) Lymphocytes (25 – 45%) Eosinophils (2 – 4%) Basophils (0.5 – 1%) Monocytes (3 – 8%) Agranulocytes Granulocytes
Copyright © 2010 Pearson Education, Inc. Table 17.2 (1 of 2)
Copyright © 2010 Pearson Education, Inc. Table 17.2 (2 of 2)
Copyright © 2010 Pearson Education, Inc. Leukopoiesis Production of WBCs Stimulated by chemical messengers from bone marrow and mature WBCs
Copyright © 2010 Pearson Education, Inc. Figure Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast MonoblastMyeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Developmental pathway Eosinophils Neutrophils Basophils Granular leukocytes (a) (b)(c) (d) (e) Monocytes Lymphocytes Agranular leukocytes Some become Some become
Copyright © 2010 Pearson Education, Inc. Leukocyte Disorders Leukopenia Abnormally low WBC count—drug induced Leukemias Cancerous conditions involving WBCs Named according to the abnormal WBC clone involved Myelocytic leukemia involves myeloblasts Lymphocytic leukemia involves lymphocytes Acute leukemia involves blast-type cells and primarily affects children Chronic leukemia is more prevalent in older people
Copyright © 2010 Pearson Education, Inc. Leukemia Bone marrow totally occupied with cancerous leukocytes Immature nonfunctional WBCs in the bloodstream Death caused by internal hemorrhage and overwhelming infections Treatments include irradiation, antileukemic drugs, and stem cell transplants
Copyright © 2010 Pearson Education, Inc. Platelets Form a temporary platelet plug that helps seal breaks in blood vessels Circulating platelets are kept inactive and mobile by NO and prostacyclin from endothelial cells of blood vessels
Copyright © 2010 Pearson Education, Inc. Figure Stem cellDevelopmental pathway Hemocyto- blast Megakaryoblast Promegakaryocyte MegakaryocytePlatelets
Copyright © 2010 Pearson Education, Inc. Hemostasis Fast series of reactions for stoppage of bleeding 1.Vascular spasm 2.Platelet plug formation 3.Coagulation (blood clotting)
Copyright © 2010 Pearson Education, Inc. Vascular Spasm Vasoconstriction of damaged blood vessel Triggers Direct injury Chemicals released by endothelial cells and platelets Pain reflexes
Copyright © 2010 Pearson Education, Inc. Figure Collagen fibers Platelets Fibrin Step Vascular spasm Smooth muscle contracts, causing vasoconstriction. Step Platelet plug formation Injury to lining of vessel exposes collagen fibers; platelets adhere. Platelets release chemicals that make nearby platelets sticky; platelet plug forms. Step Coagulation Fibrin forms a mesh that traps red blood cells and platelets, forming the clot
Copyright © 2010 Pearson Education, Inc. Figure (1 of 2) Vessel endothelium ruptures, exposing underlying tissues (e.g., collagen) PF 3 released by aggregated platelets XII XI IX XII a Ca 2+ XI a IX a Intrinsic pathway Phase 1 Tissue cell trauma exposes blood to Platelets cling and their surfaces provide sites for mobilization of factors Extrinsic pathway Tissue factor (TF) VII VII a VIII VIII a Ca 2+ X XaXa Prothrombin activator PF 3 TF/VII a complex IXa/VIII a complex V VaVa
Copyright © 2010 Pearson Education, Inc. Figure (2 of 2) Ca 2+ Phase 2 Phase 3 Prothrombin activator Prothrombin (II) Thrombin (II a ) Fibrinogen (I) (soluble) Fibrin (insoluble polymer) XIII XIII a Cross-linked fibrin mesh
Copyright © 2010 Pearson Education, Inc. Figure 17.15
Copyright © 2010 Pearson Education, Inc. Thromboembolytic Conditions Prevented by Aspirin Antiprostaglandin that inhibits thromboxane A2 Heparin Anticoagulant used clinically for pre- and postoperative cardiac care Warfarin Used for those prone to atrial fibrillation
Copyright © 2010 Pearson Education, Inc. Bleeding Disorders Hemophilias include several similar hereditary bleeding disorders Hemophilia A: most common type (77% of all cases); due to a deficiency of factor VIII Hemophilia B: deficiency of factor IX Hemophilia C: mild type; deficiency of factor XI Symptoms include prolonged bleeding, especially into joint cavities Treated with plasma transfusions and injection of missing factors
Copyright © 2010 Pearson Education, Inc. ABO Blood Groups Types A, B, AB, and O Based on the presence or absence of two agglutinogens (A and B) on surface of RBCs Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present
Copyright © 2010 Pearson Education, Inc. Table 17.4
Copyright © 2010 Pearson Education, Inc. Rh Blood Groups Anti-Rh antibodies are not spontaneously formed in Rh – individuals Anti-Rh antibodies form if an Rh – individual receives Rh + blood A second exposure to Rh + blood will result in a typical transfusion reaction RhoGAM containing anti-Rh can prevent the Rh– mother from becoming sensitized
Copyright © 2010 Pearson Education, Inc. ABO Blood Typing
Copyright © 2010 Pearson Education, Inc. Figure Serum Anti-A RBCs Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) Blood being tested Type A (contains agglutinogen A; agglutinates with anti-A) Type B (contains agglutinogen B; agglutinates with anti-B) Type O (contains no agglutinogens; does not agglutinate with either serum)
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