1. Chapter 10 Blood

2. Blood Function: Transportation Protection 4-6 Liters of blood is adult average.

3. Functions of Blood Distribution of O 2 and nutrients to body cells Metabolic wastes to the lungs and kidneys for elimination Hormones from endocrine organs to target organs

4. Functions of Blood Regulation of Body temperature by absorbing and distributing heat Normal pH using buffers Adequate fluid volume in the circulatory system

5. Functions of Blood Protection against Blood loss Plasma proteins and platelets initiate clot formation Infection Antibodies Complement proteins WBCs defend against foreign invaders

6. Current event due Monday Growth hormone in meat

7. Blood Compostition Plasma The liquid (extracellular) portion. Formed elements Cells and cell fragments

8. Blood Composition Blood Composition Hematocrit Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females

9. Hematocrit

10. Compostion and Functions of Blood Formed elements Buffy Coat Hematocrit

12. Physical Characteristics of Blood  Color range - O 2 -rich blood is scarlet red - O 2 -poor blood is dull red  pH must be between 7.35 – 7.45 - acidosis - alkalosis  Blood temp slightly higher than body temp

13. Blood  The only fluid tissue in the human body  Classified as a connective tissue - Living cells = formed elements - Non-living matrix = plasma

15. 8 % of body weight

16. Blood Plasma  55% of blood sample  ~ 91 % water  Many dissolved substances - Salts/electrolytes (metal ions) - Proteins - Respiratory gases - Hormones - Nutrients - Waste products

17. Plasma Proteins  Albumin (60%) - regulates osmotic pressure  Fibrinogen (4%) - involved in blood clotting  Globulins (36%) - are the body’s antibodies

18. 1. Erythrocytes = red blood cells 2. Leukocytes = white blood cells 3. Platelets = cell fragments Formed Elements

19. Figure 17.2 Platelets NeutrophilsLymphocyte ErythrocytesMonocyte

20. 1. Erythrocytes (Red Blood Cells)  Carry O 2 & little CO 2  Anatomy- - Biconcave disks - Essentially bags of hemoglobin - Anucleate (no nucleus) - Contain very few organelles  Outnumber WBCs 1000:1

21. Figure 17.3 2.5 µm 7.5 µm Side view (cut) Top view

22. Hemoglobin  Four protein (globin) chains  Heme pigment bonded to each globin  Iron atom in each heme  Each iron atom can bond to one O 2 molecule so hemoglobin has four oxygen binding sites Females: 12-16 g/100 ml of blood Males: 13-18 g/100 ml of blood

23.  Binds strongly, but reversibly, to oxygen  Each RBC has 250 million hemoglobin molecules  So each RBC carries 1 billion molecules of oxygen.

24. 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

25. Anemia The inability of the blood to carry sufficient oxygen to the body cells.

26. 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

27. Causes of Anemia  Low hemoglobin content  Iron-deficiency anemia  Secondary result of hemorrhagic anemia or  Inadequate intake of iron- containing foods or  Impaired iron absorption

28.  Pernicious anemia - anemia caused by a lack of intrinsic factor in stomach or vitamin B 12

29.  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

30. Figure 17.8 1234567146 1234567 (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.

31. Erythrocyte Disorders  Polycythemia: excess of RBCs that increase blood viscosity  Results from:  Polycythemia vera—bone marrow cancer  Secondary polycythemia—when less O 2 is available (high altitude) or when EPO production increases  Blood doping

33. 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

34. 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

35. Types of Leukocytes Granulocytes  Have granules  neutrophils, eosinophils, & basophils Figure 10.4 Agranulocytes  No visible granules  lymphocytes & monocytes

36.  Granulocytes  Neutrophils  Defend the body against microorganisms by engulfing microbes by phagocytosis. Active during acute infections.

37.  Eosinophils  Increase rapidly during allergies and infections by parasitic worms.

38.  Basophils  involved in allergy reactions.  Secretes histamine, an inflammatory chemical that makes blood vessels leaky and attracts other WBC’s to the area.

39.  Agranulocytes  Lymphocytes  Function in the immune system. Takes up residence in lymphatic tissue.

40.  Monocytes  Migrate into tissues where they become macrophages. Very important in fighting chronic infections.

41.  Leukopenia  abnormally low WBC count (i.e. Aids)Aids  Leukocytosis  abnormally high WBC count (infections, leukemia)

42. 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.

43. 3. Platelets  Derived from ruptured multinucleate cells (megakaryocytes)  Needed for the clotting process  Normal platelet count = 300,000/ml

44. Hematopoiesis  Blood cell formation  Red bone marrow  Hemocytoblast – common stem cell  Differentiation  Lymphoid stem cell make lymphocytes  Myeloid stem cell produces other formed elements

45. Control of Erythrocyte Production (Erythropoiesis)  Rate is controlled by a hormone (erythropoietin)  Kidneys produce most erythropoietin  Negative feedback from blood O 2 levels

46. 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

47. 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

48. 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

49. 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

50. 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

51.  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.

52. Prothrombin activator triggers the conversion of prothrombin into thrombin.

53.  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.

54. Figure 17.15

56. Link

57.  Vitamin K is needed for the liver to produce prothrombin

58. Blood Clotting  Blood usually clots within 3 to 6 minutes  The clot remains as endothelium regenerates  The clot is broken down after tissue repair

59. 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

60. 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

61. 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

62. 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)

63. 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.

64. 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

66. 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

67. Rh System

68. 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

69. 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

70. Animated Blood Types Blood Typing

71. 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