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PowerPoint ® Lecture Slide Presentation by Patty Bostwick-Taylor, Florence-Darlington Technical College Copyright © 2009 Pearson Education, Inc., publishing.

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Presentation on theme: "PowerPoint ® Lecture Slide Presentation by Patty Bostwick-Taylor, Florence-Darlington Technical College Copyright © 2009 Pearson Education, Inc., publishing."— Presentation transcript:

1 PowerPoint ® Lecture Slide Presentation by Patty Bostwick-Taylor, Florence-Darlington Technical College Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings 10 Blood

2 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood  The only fluid tissue in the human body  Classified as a connective tissue  Components of blood  Living cells  Formed elements  Non-living matrix  Plasma

3 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood  If blood is spun down in a centrifuge  Erythrocytes sink to the bottom (45% of blood, a percentage known as the hematocrit)  Buffy coat contains leukocytes and platelets (less than 1% of blood)  Buffy coat is a thin, whitish layer between the erythrocytes and plasma  Plasma rises to the top (55% of blood)

4 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.1 (1 of 2) Blood

5 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.1 (2 of 2) Blood

6 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Physical Characteristics of Blood  Color range  Oxygen-rich blood is scarlet red  Oxygen-poor blood is dull red  pH must remain between 7.35–7.45  Blood temperature is slightly higher than body temperature at 100.4°F  In a healthy man, blood volume is about 5–6 liters or about 6 quarts  Blood makes up 8% of body weight

7 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Plasma  Composed of approximately 90% water  Includes many dissolved substances  Nutrients  Salts (electrolytes)  Respiratory gases  Hormones  Plasma proteins  Waste & products of cell metabolism

8 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Plasma  Plasma proteins  Most abundant solutes in plasma  Most plasma proteins are made by liver  Various plasma proteins include  Albumin—regulates osmotic pressure  Clotting proteins—help to stem blood loss when a blood vessel is injured  Antibodies—help protect the body from pathogens

9 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Plasma  Acidosis  Blood becomes too acidic  Alkalosis  Blood becomes too basic  In each scenario, the respiratory system and kidneys help restore blood pH to normal

10 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Photomicrograph of a Blood Smear Figure 10.2

11 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Characteristics of Formed Elements of the Blood Table 10.2 (1 of 2)

12 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Table 10.2 (2 of 2) Characteristics of Formed Elements of the Blood

13 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Erythrocytes (red blood cells or RBCs)  Main function is to carry oxygen  Anatomy of circulating erythrocytes  Biconcave disks  Essentially bags of hemoglobin  Anucleate (no nucleus)  Contain very few organelles  5 million RBCs per cubic millimeter of blood  Measure of the amount of blood cells is called a hematocrit

14 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Hemoglobin  Iron-containing protein  Binds strongly, but reversibly, to oxygen  Each hemoglobin molecule has four oxygen binding sites  Each erythrocyte has 250 million hemoglobin molecules  Normal blood contains 12–18 g of hemoglobin per 100 mL blood

15 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Homeostatic imbalance of RBCs  Anemia is a decrease in the oxygen-carrying ability of the blood  Low RBC count or…  Deficient haemoglobin content in RBC  Sickle cell anemia (SCA) results from abnormally shaped hemoglobin  Polycythemia is an excessive or abnormal increase in the number of erythrocytes  Bone marrow cancer or…  Living at high altitudes.

16 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements Table 10.1

17 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.3 Formed Elements

18 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Leukocytes (white blood cells or WBCs)  Crucial in the body’s defense against disease  These are complete cells, with a nucleus and organelles  Able to move into and out of blood vessels (diapedesis)  Can move by ameboid motion  Positive Chemotaxis: Can respond to chemicals released by damaged tissues  4,000 to 11,000 WBC per cubic millimeter of blood

19 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Abnormal numbers of leukocytes  Leukocytosis  WBC count above 11,000 leukocytes/mm 3  Generally indicates an infection  Leukopenia  Abnormally low leukocyte level  Commonly caused by certain drugs such as corticosteroids and anticancer agents

20 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic Imbalance  Leukemia  Bone marrow becomes cancerous, turns out excess WBC  Anemia and other bleeding problems can occur

21 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  List of the WBCs from most to least abundant  Neutrophils  Lymphocytes  Monocytes  Eosinophils  Basophils  Easy way to remember this list  Never  Let  Monkeys  Eat  Bananas

22 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Homeostatic ImbalancesWhite Blood Cells or Notes

23 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Types of leukocytes  Granulocytes  Granules in their cytoplasm can be stained  Possess lobed nuclei

24 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Types of granulocytes  Neutrophils  Multilobed nucleus with fine granules  Act as phagocytes at active sites of infection  Eosinophils  Large brick-red cytoplasmic granules  Found in response to allergies and parasitic worms

25 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Types of granulocytes (continued)  Basophils  Have histamine-containing granules  Initiate inflammation

26 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings  Agranulocytes  Lack visible cytoplasmic granules  Nuclei are spherical, oval, or kidney- shaped

27 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Types of agranulocytes  Lymphocytes  Nucleus fills most of the cell  Play an important role in the immune response  Monocytes  Largest of the white blood cells  Function as macrophages  Important in fighting chronic infection

28 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formed Elements  Platelets  Derived from ruptured multinucleate cells (megakaryocytes)  Needed for the clotting process  Normal platelet count = 300,000/mm 3 End of Quiz 1 Material

29 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hematopoiesis  Blood cell formation  Occurs in red bone marrow or myeloid tissue, average of one ounce/day containing 100 billion new cells  All blood cells are derived from a common stem cell (hemocytoblast)  Hemocytoblast differentiation  Lymphoid stem cell produces lymphocytes  Myeloid stem cell produces all other formed elements Quiz 2 Material

30 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.4 Hematopoiesis

31 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formation of Erythrocytes  Unable to divide, grow, or synthesize proteins  Wear out in 100 to 120 days  When worn out, RBCs are eliminated by phagocytes in the spleen or liver  Lost cells are replaced by division of hemocytoblasts in the red bone marrow

32 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production  Rate is controlled by a hormone (erythropoietin)  Kidneys produce most erythropoietin as a response to reduced oxygen levels in the blood  Homeostasis is maintained by negative feedback from blood oxygen levels

33 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 1 Normal blood oxygen levels

34 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 2 Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Normal blood oxygen levels Imbalance

35 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 3 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Normal blood oxygen levels Imbalance

36 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 4 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Kidney releases erythropoietin Normal blood oxygen levels Imbalance

37 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 5 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Erythropoietin stimulates Kidney releases erythropoietin Red bone marrow Normal blood oxygen levels Imbalance

38 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 6 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels Imbalance

39 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 7 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Increased O 2 - carrying ability of blood Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels

40 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Control of Erythrocyte Production Figure 10.5, step 8 Reduced O 2 levels in blood Stimulus: Decreased RBC count, decreased availability of O 2 to blood, or increased tissue demands for O 2 Increased O 2 - carrying ability of blood Erythropoietin stimulates Kidney releases erythropoietin Enhanced erythropoiesis Red bone marrow More RBCs Normal blood oxygen levels Imbalance

41 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Formation of White Blood Cells and Platelets  Controlled by hormones  Colony stimulating factors (CSFs) and interleukins prompt bone marrow to generate leukocytes  Thrombopoietin stimulates production of platelets

42 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Stoppage of bleeding resulting from a break in a blood vessel  Response is fast, and localized  Hemostasis involves three phases  Vascular spasms  Platelet plug formation  Coagulation (blood clotting)

43 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Figure 10.6 Hemostasis

44 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis 1 st Step:  Vascular spasms  Vasoconstriction causes blood vessel to spasm  Spasms narrow the blood vessel, decreasing blood loss

45 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6 Injury to lining of vessel exposes collagen fibers; platelets adhere Fibrin clot with trapped red blood cells Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets Fibrin PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) Step 1: Vascular Spasms Step 2: Platelet Plug Formation Step 3: Coagulation +

46 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 1 Step 1: Vascular Spasms

47 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis 2 nd step:  Platelet plug formation  Collagen fibers are exposed by a break in a blood vessel  “sticky” platelets cling to fibers  Anchored platelets release chemicals to attract more platelets  Platelets pile up to form a platelet plug

48 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 2 Injury to lining of vessel exposes collagen fibers; platelets adhere Collagen fibers Step 1: Vascular Spasms Step 2: Platelet Plug Formation

49 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 3 Injury to lining of vessel exposes collagen fibers; platelets adhere Platelet plug forms Collagen fibers Platelets Step 1: Vascular Spasms Step 2: Platelet Plug Formation

50 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 4 Injury to lining of vessel exposes collagen fibers; platelets adhere Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets PF 3 from platelets Calcium and other clotting factors in blood plasma Tissue factor in damaged tissue Step 1: Vascular Spasms Step 2: Platelet Plug Formation +

51 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 5 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

52 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 6 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator ProthrombinThrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

53 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 7 Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) +

54 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.6, step 8 Injury to lining of vessel exposes collagen fibers; platelets adhere Fibrin clot with trapped red blood cells Platelet plug forms Platelets release chemicals that attract more platelets to the site and make nearby platelets sticky Collagen fibers Platelets Fibrin PF 3 from platelets Calcium and other clotting factors in blood plasma Formation of prothrombin activator Prothrombin Fibrinogen (soluble) Fibrin (insoluble) Thrombin Tissue factor in damaged tissue Phases of coagulation (clotting cascade) Step 1: Vascular Spasms Step 2: Platelet Plug Formation Step 3: Coagulation +

55 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis 3 rd step  Coagulation  Injured tissues release tissue factor (TF)  PF 3 (a phospholipid) interacts with TF, blood protein clotting factors, and calcium ions to trigger a clotting cascade  Prothrombin activator converts prothrombin to thrombin (an enzyme)  Thrombin joins fibrinogen proteins into hair- like molecules of insoluble fibrin  Fibrin forms a meshwork (the basis for a clot)

56 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Figure 10.7

57 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis  Blood usually clots within 3 to 6 minutes  The clot remains as endothelium regenerates  The clot is broken down after tissue repair

58 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Undesirable Clotting  Thrombus  A clot in an unbroken blood vessel  Can be deadly in areas like the heart  Coronary Thrombosis  Embolus  A thrombus that breaks away and floats freely in the bloodstream  Can later clog vessels in critical areas such as the brain

59 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Bleeding Disorders  Thrombocytopenia  Platelet deficiency  Even normal movements can cause bleeding from small blood vessels that require platelets for clotting  Hemophilia  Hereditary bleeding disorder  Normal clotting factors are missing

60 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Bleeding Disorders  Liver unable to synthesize clotting factors  Vitamin K deficiency: can take supplements. (vitamin K is needed to make clotting factors)  Whole blood transfusions may be needed.

61 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Groups and Transfusions  Large losses of blood have serious consequences  Loss of 15–30% causes pallor, weakness  Loss of over 30% causes severe shock, which can be fatal  Transfusions are the only way to replace blood quickly  Transfused blood must be of the same blood group  Blood can be stored for up to 35 days at a blood bank.

62 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Human Blood Groups  Blood contains genetically determined proteins  Antigens (a substance the body recognizes as foreign) may be attacked by the immune system  Antibodies are the “recognizers” (we produce these)  Blood is “typed” by using antibodies that will cause blood with certain proteins to clump (agglutination)

63 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings 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

64 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings ABO Blood Groups  Based on the presence or absence of two antigens  Type A  Type B  The lack of these antigens is called type O

65 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings ABO Blood Groups  The presence of both antigens A and B is called type AB  The presence of antigen A is called type A  The presence of antigen B is called type B  The lack of both antigens A and B is called type O

66 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings ABO Blood Groups  Blood type AB can receive A, B, AB, and O blood  Universal recipient  Blood type B can receive B and O blood  Blood type A can receive A and O blood  Blood type O can receive O blood  Universal donor

67 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings ABO Blood Groups Table 10.3

68 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Rh Blood Groups  Named because of the presence or absence of one of eight Rh antigens (agglutinogen D) that was originally defined in Rhesus monkeys  Most Americans are Rh + (Rh positive)  Problems can occur in mixing Rh + blood into a body with Rh – (Rh negative) blood

69 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Rh Dangers During Pregnancy  The mismatch of an Rh – mother carrying an Rh + baby can cause problems for the unborn child  The first pregnancy usually proceeds without problems  The immune system is sensitized after the first pregnancy  In a second pregnancy, the mother’s immune system produces antibodies to attack the Rh + blood (hemolytic disease of the newborn)

70 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Rh Dangers During Pregnancy  Danger occurs only when the mother is Rh – and the father is Rh +, and the child inherits the Rh + factor  RhoGAM shot can prevent buildup of anti-Rh + antibodies in mother’s blood

71 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Typing  Blood samples are mixed with anti-A and anti-B serum  Coagulation or no coagulation leads to determining blood type  Typing for ABO and Rh factors is done in the same manner  Cross matching—testing for agglutination of donor RBCs by the recipient’s serum, and vice versa

72 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Blood Typing Figure 10.8

73 Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings Developmental Aspects of Blood  Sites of blood cell formation  The fetal liver and spleen are early sites of blood cell formation  Bone marrow takes over hematopoiesis by the seventh month  Fetal hemoglobin differs from hemoglobin produced after birth  Physiologic jaundice results in infants in which the liver cannot rid the body of hemoglobin breakdown products fast enough


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