Transcript Ch 10 Blood
Chapter 10 Blood Blood Function: Transportation Protection 4-6 Liters of blood is adult average. Functions of Blood Distribution of O2 and nutrients to body cells Metabolic wastes to the lungs and kidneys for elimination Hormones from endocrine organs to target organs Functions of Blood Regulation of Body temperature by absorbing and distributing heat Normal pH using buffers Adequate fluid volume in the circulatory system Functions of Blood Protection against Blood loss Plasma proteins and platelets initiate clot formation Infection Antibodies Complement proteins WBCs defend against foreign invaders Current event due Monday Growth hormone in meat Blood Compostition Plasma The liquid (extracellular) portion. Formed elements Cells and cell fragments Blood Composition • Hematocrit • Percent of blood volume that is RBCs • 47% ± 5% for males • 42% ± 5% for females Hematocrit Compostion and Functions of Blood • Formed elements • Buffy Coat • Hematocrit Physical Characteristics of Blood Color range - O2-rich blood is scarlet red - O2-poor blood is dull red pH must be between 7.35 – 7.45 - acidosis - alkalosis Blood temp slightly higher than body temp Blood The only fluid tissue in the human body Classified as a connective tissue - Living cells = formed elements - Non-living matrix = plasma • 8 % of body weight Blood Plasma 55% of blood sample ~ 91 % water Many dissolved substances - Salts/electrolytes (metal ions) - Proteins - Respiratory gases - Hormones - Nutrients - Waste products Plasma Proteins Albumin (60%) regulates osmotic pressure Fibrinogen (4%) involved in blood clotting Globulins (36%) - are the body’s antibodies Formed Elements 1. Erythrocytes = red blood cells 2. Leukocytes = white blood cells 3. Platelets = cell fragments Platelets Neutrophils Erythrocytes Monocyte Lymphocyte Figure 17.2 1. Erythrocytes (Red Blood Cells) Carry O2 & little CO2 Anatomy- Biconcave disks - Essentially bags of hemoglobin - Anucleate (no nucleus) - Contain very few organelles Outnumber WBCs 1000:1 2.5 µm Side view (cut) 7.5 µm Top view Figure 17.3 Hemoglobin Four protein (globin) chains Heme pigment bonded to each globin Iron atom in each heme Each iron atom can bond to one O2 molecule so hemoglobin has four oxygen binding sites Females: 12-16 g/100 ml of blood Males: 13-18 g/100 ml of blood Binds strongly, but reversibly, to oxygen Each RBC has 250 million hemoglobin molecules So each RBC carries 1 billion molecules of oxygen. b Globin chains Heme group a 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 Anemia The inability of the blood to carry sufficient oxygen to the body cells. Causes of Anemia Insufficient erythrocytes Hemorrhagic anemia: acute or chronic loss of blood Hemolytic anemia: RBCs rupture prematurely Aplastic anemia: destruction or inhibition of red bone marrow Causes of Anemia Low hemoglobin content Iron-deficiency anemia Secondary result of hemorrhagic anemia or Inadequate intake of ironcontaining foods or Impaired iron absorption Pernicious anemia - anemia caused by a lack of intrinsic factor in stomach or vitamin B12 Sickle Cell Anemia – due to abnormal hemoglobin (one amino acid is different out of 287) Causes RBC’s to become sickle shaped in low oxygen situations (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 Polycythemia: excess of RBCs that increase blood viscosity Results from: Polycythemia vera—bone marrow cancer Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases Blood doping 2. Leukocytes (White Blood Cells) Crucial in defense against disease Have nucleus & organelles move into and out of vessels (diapedesis) ameboid motion Respond to chemicals released by damaged tissues Leukocyte Levels in the Blood Normal 4,000 - 11,000 cells per ml Abnormal leukocyte levels - Leukocytosis Above 11,000 WBC/ml Generally indicates an infection - Leukopenia Abnormally low level Commonly caused by drugs Types of Leukocytes Granulocytes Have granules neutrophils, eosinophils, & basophils Agranulocytes No visible granules lymphocytes & monocytes Figure 10.4 Granulocytes Neutrophils Defend the body against microorganisms by engulfing microbes by phagocytosis. Active during acute infections. Eosinophils Increase rapidly during allergies and infections by parasitic worms. Basophils involved in allergy reactions. Secretes histamine, an inflammatory chemical that makes blood vessels leaky and attracts other WBC’s to the area. Agranulocytes Lymphocytes Function in the immune system. Takes up residence in lymphatic tissue. Monocytes Migrate into tissues where they become macrophages. Very important in fighting chronic infections. Leukopenia abnormally low WBC count (i.e. Aids) Leukocytosis abnormally high WBC count (infections, leukemia) Leukemia • Chronic Leukemia —Early in disease, abnormal blood cells can still work; people may not have any symptoms. Symptoms increase as leukemia cells increase. • Acute Leukemia —blood cells abnormal; cannot work. Abnormal cells increases rapidly. Worsens quickly. • Leukemia can arise in lymphoid cells or myeloid cells. 3. Platelets Derived from ruptured multinucleate cells (megakaryocytes) Needed for the clotting process Normal platelet count = 300,000/ml Hematopoiesis Blood cell formation Red bone marrow Hemocytoblast – common stem cell Differentiation Lymphoid stem cell make lymphocytes Myeloid stem cell produces other formed elements Control of Erythrocyte Production (Erythropoiesis) Rate is controlled by a hormone (erythropoietin) Kidneys produce most erythropoietin Negative feedback from blood O2 levels Erythropoiesis • Phases in development (takes 3-5 days) 1. Ribosome synthesis 2. Hemoglobin accumulation 3. Ejection of the nucleus and formation of reticulocytes • Reticulocytes then become mature erythrocytes Fate of Erythrocytes Can’t divide, grow, or make proteins Wear out in 100 to 120 days Eliminated by phagocytes in spleen or liver Replaced by division of hemocytoblasts Hemostasis Stoppage of blood flow Result of a break in a blood vessel Hemostasis involves three phases 1. Vascular Spasms 2. Platelet Plug Formation 3. Coagulation 1. Vascular Spasms Injured smooth muscle in vessels and local pain receptors cause vasoconstriction Platelets release serotonin also causing blood vessels to spasm Spasms narrow the blood vessel, decreasing blood loss 2. Platelet Plug Formation Collagen fibers are exposed by a break in a blood vessel Platelets become “sticky” and cling to fibers Anchored platelets release chemicals to attract more platelets (positive feedback) Platelets pile up to form a platelet plug 3. Coagulation Injured blood vessel creates a rough spot in its lining. Damaged tissue cells release certain clotting factors into the plasma. These factors rapidly react with other factors already present in the plasma to form prothrombin activator. Prothrombin activator triggers the conversion of prothrombin into thrombin. Thrombin then reacts with fibrinogen to change it into fibrin, a fibrous gel that forms a tangled web of fine threads at the clot site causing RBC’s to get caught in the tangle. Figure 17.15 Link Vitamin K is needed for the liver to produce prothrombin Blood Clotting Blood usually clots within 3 to 6 minutes The clot remains as endothelium regenerates The clot is broken down after tissue repair Undesirable Clotting Thrombus Clot in unbroken vessel Deadly in heart Embolus Thrombus that breaks away and floats in bloodstream Can later clog vessels in critical areas such as the brain Bleeding Disorders 1.Thrombocytopenia Platelet (thrombocyte) deficiency normal movements can cause bleeding Petechiae – purple blotches 2. Hemophilia Hereditary bleeding disorder Normal clotting factors are missing Sex-linked genetic disorder Blood Groups and Transfusions Large losses of blood have serious consequences - Loss of 15 to 30 % = weakness - Loss of over 30 % = shock; can be fatal Transfusions = only way to replace blood quickly Transfused blood must be of the same blood group Human Blood Groups Blood contains genetically determined proteins (antigens) A foreign protein (antigen) may be attacked by the immune system Blood is “typed” by using antibodies that will cause blood with certain proteins to clump (agglutination) Human Blood Groups There are over 30 common red blood cell antigens The most vigorous transfusion reactions are caused by ABO and Rh blood group antigens If not matched blood types: Lysed RBCs release hemoglobin which blocks kidneys, causes fevers, vomit, etc. ABO Blood Groups Based on the presence or absence of two antigens (A & B) Blood Types Type A – has A antigen, anti-B antibody Type B – has B antigen, anti-A antibody Type AB – has both A & B antigens, Universal Recipient Type O – lacks A & B antigens, has both anti-A anti-B antibodies; Universal Donor Rh Blood Groups Named because one of eight Rh antigens (agglutinogen D) found first in Rhesus monkey Most Americans are Rh+ Anti-Rh antibodies not automatically formed; formed after exposed to Rh+ Problems can occur in mixing Rh+ blood into a body with Rh– blood Rh System Rh Dangers During Pregnancy Mom is Rh– and Dad is Rh+, and child Rh+ Rh– mother carrying Rh+ baby can cause problems for the unborn child The first pregnancy usually without problems In a second pregnancy, the mother’s immune system produces antibodies to attack the Rh+ blood (hemolytic disease of the newborn) Destruction of RBCs, anemia, brain damage, death Fetal transfusions Blood Typing Blood mixed with anti-A and anti-B serum agglutination or no agglutination leads to determining blood type Cross matching – testing for agglutination of donor RBCs by the recipient’s serum, and vice versa • Animated Blood Types • Blood Typing Developmental Aspects of Blood Sites of blood cell formation - fetal liver and spleen - bone marrow takes over by 7th month Fetal hemoglobin can pick up more O2 Physiological Jaundice – liver can’t keep up with / rapid fetal RBC destruction