Blood Composi2on 17 A. Blood Composi2on. Func2ons of Blood 3/23/15. Physical Characteris2cs and Volume. : a fluid connec2ve 2ssue composed of.

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Blood Composi2on 17 A Blood : a fluid connec2ve 2ssue composed of Plasma Formed elements (red blood cells, or RBCs) Leukocytes (white blood cells, or WBCs) Platelets Blood Composi2on Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females 1 Withdraw blood and place in tube. 2 Centrifuge the blood sample. Formed elements Plasma 55% of whole blood Least dense component Buffy coat Leukocytes and platelets <1% of whole blood 45% of whole blood Most dense component Figure 17.1 Physical Characteris2cs and Volume S2cky, fluid Color scarlet to dark red ph 7.35 7.45 38 C ~8% of body Average volume: 5 6 L for males, and 4 5 L for females Func2ons of Blood 1. Distribu2on of O 2 and nutrients to body cells Metabolic wastes to the lungs and kidneys for elimina2on Hormones from endocrine organs to target organs 1

Func2ons of Blood 2. Regula2on of Body temperature by absorbing and distribu2ng heat Normal ph using buffers Adequate fluid volume in the circulatory system Func2ons of Blood 3. Protec2on against Blood loss Plasma proteins and platelets ini2ate clot forma2on Infec2on An2bodies Complement proteins WBCs defend against foreign invaders Blood Plasma 90% water Proteins are mostly produced by the 60% albumin 36% globulins 4% fibrinogen Blood Plasma Nitrogenous by- products of metabolism lac2c acid, urea, crea2nine glucose, carbohydrates, amino acids Electrolytes Na +, K +, Ca 2+, Cl, HCO 3 Respiratory O 2 and CO 2 Hormones Formed Elements Platelets Monocyte Only s are complete cells RBCs have no nuclei or organelles Platelets are cell Most formed elements survive in the bloodstream for only a few Most blood cells originate in bone marrow and do not divide Neutrophils Lymphocyte Figure 17.2 2

Biconcave discs, anucleate, essen2ally no Filled with hemoglobin (Hb) for gas transport Contain the plasma membrane protein spectrin and other proteins Provide flexibility to change shape as necessary Are the major factor contribu2ng to blood Side view (cut) 2.5 µm 7.5 µm Top view Figure 17.3 Structural characteris2cs contribute to gas Biconcave shape huge surface area rela2ve to volume >97% hemoglobin (not coun2ng water) No mitochondria; ATP produc2on is anaerobic; no O 2 is used in genera2on of ATP A superb example of complementarity of! Erythrocyte Func2on RBCs are dedicated to respiratory gas Hemoglobin binds reversibly with oxygen Erythrocyte Func2on Hemoglobin structure Protein globin: two alpha and two beta chains Heme pigment bonded to each globin chain atom in each heme can bind to one O 2 molecule Each Hb molecule can transport four O 2 β Globin chains Heme group α Globin chains (a) Hemoglobin consists of globin (two alpha and two beta polypeptide chains) and four heme groups. (b) Iron-containing heme pigment. Figure 17.4 3

(Hb) O 2 loading in the lungs Produces oxyhemoglobin (ruby red) O 2 unloading in the 2ssues Produces deoxyhemoglobin or reduced hemoglobin (dark red) CO 2 loading in the 2ssues Produces carbaminohemoglobin (carries 20% of CO 2 in the blood) Hematopoiesis Hematopoiesis (hemopoiesis): blood cell Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur Hematopoiesis Hemocytoblasts (hematopoie2c stem cells) Give rise to all Hormones and growth factors push the cell toward a specific pathway of blood cell development New blood cells enter blood sinusoids Erythropoiesis : red blood cell produc2on A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts Erythropoiesis Phases in development 1. Ribosome synthesis 2. Hemoglobin accumula2on 3. Ejec2on of the nucleus and forma2on of re2culocytes Re2culocytes then become mature erythrocytes Stem cell Committed cell Developmental pathway Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Hemocytoblast Proerythroblast Early Late erythroblast erythroblast Normoblast Reticulo- Erythrocyte cyte Figure 17.5 4

Regula2on of Erythropoiesis Too few RBCs leads to 2ssue Too many RBCs increases blood viscosity Balance between RBC produc2on and destruc2on depends on controls Adequate supplies of, amino acids, and B vitamins Hormonal Control of Erythropoiesis Erythropoie2n (EPO) Direct s2mulus for erythropoiesis Released by the in response to hypoxia Hormonal Control of Erythropoiesis Causes of Hemorrhage or increased RBC destruc2on reduces RBC numbers Insufficient hemoglobin (e.g., iron deficiency) Reduced availability of (e.g., high al2tudes) Hormonal Control of Erythropoiesis Effects of EPO More rapid matura2on of commioed bone marrow cells Increased circula2ng re2culocyte count in 1 2 days also enhances EPO produc2on, resul2ng in higher RBC counts in males 5 O 2 - carrying ability of blood increases. IMBALANCE 4 Enhanced erythropoiesis increases RBC count. Homeostasis: Normal blood oxygen levels 3 Erythropoietin stimulates red bone marrow. IMBALANCE 1 Stimulus: Hypoxia (low blood O 2 - carrying ability) due to Decreased RBC count Decreased amount of hemoglobin Decreased availability of O 2 2 Kidney (and liver to a smaller extent) releases erythropoietin. Dietary Requirements for Erythropoiesis Nutrients amino acids, lipids, and carbohydrates Iron Stored in Hb (65%), the liver, spleen, and bone marrow Stored in cells as ferri2n and hemosiderin Transported loosely bound to the protein transferrin Vitamin B 12 and folic acid necessary for DNA synthesis for Figure 17.6 5

Fate and Destruc2on of Life span: days Old RBCs become fragile, and Hb begins to degenerate Macrophages engulf dying RBCs in the spleen Fate and Destruc2on of Heme and globin are separated Iron is salvaged for Heme is degraded to yellow the pigment bilirubin Liver secretes bilirubin (in bile)) into the intes2nes Degraded pigment leaves the body in feces as stercobilin Globin is metabolized into 1 Low O 2 levels in blood stimulate kidneys to produce erythropoietin. 2 Erythropoietin levels rise in blood. 3 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 4 New erythrocytes enter bloodstream; 5 Aged and damaged function about 120 days. red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin Hemoglobin is broken down. Heme Globin Bilirubin Iron stored Amino as ferritin, acids hemosiderin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis. Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria, and excreted in feces. Circulation Erythrocyte Disorders : blood has abnormally low O 2 - carrying capacity A sign rather than a disease itself Blood O 2 levels cannot support normal metabolism Accompanied by fa2gue, paleness, shortness of breath, and chills Food nutrients, including amino acids, Fe, B 12, and folic acid, are absorbed from intestine and enter blood. 6 Raw materials are made available in blood for erythrocyte synthesis. Figure 17.7 1. Insufficient Hemorrhagic anemia: acute or chronic loss of blood Hemoly2c anemia: RBCs rupture prematurely Aplas2c anemia: destruc2on or inhibi2on of red bone marrow 2. Low content Iron- deficiency anemia Secondary result of hemorrhagic anemia or Inadequate intake of iron- containing foods or Impaired iron absorp2on 6

anemia Deficiency of vitamin B 12 Lack of intrinsic factor needed for absorp2on of B 12 Treated by intramuscular injec2on of B 12 or applica2on of Nascobal 3. hemoglobin Thalassemias Absent or faulty globin chain RBCs are thin, delicate, and deficient in hemoglobin anemia Defec2ve gene codes for abnormal hemoglobin (HbS) Causes RBCs to become sickle shaped in low- oxygen situa2ons (a) Normal erythrocyte has normal hemoglobin amino acid sequence in the beta chain. 1 2 3 4 5 6 7 146 (b) Sickled erythrocyte results from a single amino acid change in the beta chain of hemoglobin. 1 2 3 4 5 6 7 146 Figure 17.8 Erythrocyte Disorders : excess of RBCs that increase blood viscosity Results from: Polycythemia vera bone marrow cancer Secondary polycythemia when less O 2 is available (high al2tude) or when EPO produc2on increases Blood doping 7