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PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 17 Blood.

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Presentation on theme: "PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 17 Blood."— Presentation transcript:

1 PowerPoint ® Lecture Slides prepared by Janice Meeking, Mount Royal College C H A P T E R Copyright © 2010 Pearson Education, Inc. 17 Blood

2 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 Hematocrit Percent of blood volume that is RBCs 47% ± 5% for males 42% ± 5% for females

3 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

4 Copyright © 2010 Pearson Education, Inc. Functions of Blood 1.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

5 Copyright © 2010 Pearson Education, Inc. Functions of Blood 2.Regulation of Body temperature by absorbing and distributing heat Normal pH using buffers Adequate fluid volume in the circulatory system

6 Copyright © 2010 Pearson Education, Inc. Functions of Blood 3.Protection against Blood loss Plasma proteins and platelets initiate clot formation Infection Antibodies Complement proteins (small proteins that amplify other immune cells ability to kill pathogens) WBCs defend against foreign invaders

7 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

8 Copyright © 2010 Pearson Education, Inc. Blood Plasma 90% water Proteins mostly produced by the liver 60% albumin 36% globulins 4% fibrinogen

9 Copyright © 2010 Pearson Education, Inc. Blood Plasma Nitrogenous by-products of metabolism— lactic acid, urea, creatinine Nutrients—glucose, carbohydrates, amino acids Electrolytes—Na +, K +, Ca 2+, Cl –, HCO 3 – Respiratory gases—O 2 and CO 2 Hormones

10 Copyright © 2010 Pearson Education, Inc. Formed Elements (WBC, RBC, platelets)

11 Copyright © 2010 Pearson Education, Inc. Formed Elements Only WBCs are complete cells RBCs have no nuclei or organelles Platelets are cell fragments Most formed elements survive in the bloodstream for only a few days Most blood cells originate in bone marrow and do not divide

12 Copyright © 2010 Pearson Education, Inc. Figure 17.2 Platelets NeutrophilsLymphocyte ErythrocytesMonocyte

13 Copyright © 2010 Pearson Education, Inc. RBCs or Erythrocytes

14 Copyright © 2010 Pearson Education, Inc. Erythrocytes Biconcave discs, anucleate, essentially no organelles Filled with hemoglobin (Hb) for gas transport

15 Copyright © 2010 Pearson Education, Inc. Figure µm 7.5 µm Side view (cut) Top view

16 Copyright © 2010 Pearson Education, Inc. Erythrocytes Structural characteristics contribute to gas transport Biconcave shape—huge surface area relative to volume >97% hemoglobin (not counting water) No mitochondria; ATP production is anaerobic; no O 2 is used in generation of ATP A great example of how structure and function work together!

17 Copyright © 2010 Pearson Education, Inc. Erythrocyte Function Hemoglobin structure Protein globin: two alpha and two beta chains Heme pigment bonded to each globin chain (4) Iron atom in each heme can bind to one O 2 molecule; binds reversibly Each Hb molecule can transport four O 2 Normal Hb: in women, in men

18 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

19 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)

20 Copyright © 2010 Pearson Education, Inc. Hematopoiesis Hematopoiesis (hemopoiesis): blood cell formation Formed in red marrow Red marrow is found mainly in the flat bones, such as pelvis, sternum, cranium, ribs, vertebrae, and scapula. Also in the spongy epiphyseal plates of long bones like the femur and humerus.

21 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

22 Copyright © 2010 Pearson Education, Inc. Regulation of Erythropoiesis Too few RBCs leads to tissue hypoxia Too many RBCs increases blood viscosity Balance between RBC production and destruction depends on Hormonal controls Adequate supplies of iron, amino acids, and B vitamins

23 Copyright © 2010 Pearson Education, Inc. Hormonal Control of Erythropoiesis Erythropoietin (EPO) Direct stimulus for erythropoiesis Released by the kidneys in response to hypoxia

24 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)

25 Copyright © 2010 Pearson Education, Inc. Hormonal Control of Erythropoiesis Effects of EPO More rapid maturation of committed bone marrow cells Increased circulating reticulocyte count in 1– 2 days Testosterone also enhances EPO production, resulting in higher RBC counts in males

26 Copyright © 2010 Pearson Education, Inc. Figure 17.6, step 5 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

27 Copyright © 2010 Pearson Education, Inc. 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 ferritin and hemosiderin Vitamin B 12 and folic acid—necessary for DNA synthesis for cell division

28 Copyright © 2010 Pearson Education, Inc. Fate and Destruction of Erythrocytes Life span: 100–120 days Old RBCs become fragile, and Hb begins to degenerate Macrophages engulf dying RBCs in the spleen

29 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1

30 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 2 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Erythropoietin levels rise in blood. 2

31 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 3 Low O2 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

32 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 4 Low O2 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 New erythrocytes enter bloodstream; function about 120 days. 4

33 Copyright © 2010 Pearson Education, Inc. Fate and Destruction of Erythrocytes Heme and globin are separated Iron is salvaged for reuse Heme is degraded to yellow the pigment bilirubin Liver secretes bilirubin (in bile) into the intestines Degraded pigment leaves the body in feces as stercobilin Globin is metabolized into amino acids

34 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 5 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 Hemoglobin Amino acids GlobinHeme 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.

35 Copyright © 2010 Pearson Education, Inc. Figure 17.7, step 6 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. 5 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, B12, 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.

36 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.

37 Copyright © 2010 Pearson Education, Inc. Erythrocyte Disorders Anemia: blood has abnormally low O 2 - carrying capacity A sign rather than a disease itself Accompanied by fatigue, paleness, shortness of breath, and chills

38 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

39 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 Heavy menstruation

40 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 or application of Nascobal Common in elderly and those with GI disorders that cause malabsorption, like Crohn’s, IBD, etc.

41 Copyright © 2010 Pearson Education, Inc. Causes of Anemia 3.Abnormal hemoglobin Thalassemias Absent or faulty globin chain RBCs are thin, delicate, and deficient in hemoglobin

42 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

43 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.

44 Copyright © 2010 Pearson Education, Inc. 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

45 Copyright © 2010 Pearson Education, Inc. Leukocytes or WBCs

46 Copyright © 2010 Pearson Education, Inc. Leukocytes Make up <1% of total blood volume Can leave capillaries via diapedesis Move through tissue spaces by ameboid motion and positive chemotaxis (toward a chemical stimulus) Normal range: 4-11,000/mm 3 Leukocytosis: WBC count over 11,000/mm 3 Normal response to bacterial or viral invasion

47 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

48 Copyright © 2010 Pearson Education, Inc. Granulocytes Granulocytes: neutrophils, eosinophils, and basophils Cytoplasmic granules stain specifically with Wright’s stain Larger and shorter-lived than RBCs Lobed nuclei Phagocytic

49 Copyright © 2010 Pearson Education, Inc. Neutrophils Most numerous WBCs Aka polymorphonuclear leukocytes (PMNs) Granules contain hydrolytic enzymes or defensins Very phagocytic—“bacteria slayers” THE MARINES “FIRST ONES IN”

50 Copyright © 2010 Pearson Education, Inc. Eosinophils Red to crimson (acidophilic) coarse, lysosome-like granules Allergies and digest parasitic worms that are too large to be phagocytized

51 Copyright © 2010 Pearson Education, Inc. Basophils Rarest WBCs Large, purplish-black (basophilic) granules contain histamine Histamine: an inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites Are functionally similar to mast cells

52 Copyright © 2010 Pearson Education, Inc. Figure (a-c) (a) Neutrophil; multilobed nucleus (b) Eosinophil; bilobed nucleus, red cytoplasmic granules (c) Basophil; bilobed nucleus, purplish-black cytoplasmic granules

53 Copyright © 2010 Pearson Education, Inc. Agranulocytes Agranulocytes: lymphocytes and monocytes Lack visible cytoplasmic granules Have spherical or kidney-shaped nuclei

54 Copyright © 2010 Pearson Education, Inc. Lymphocytes Large, dark-purple, circular nuclei with a thin rim of blue cytoplasm Mostly in lymphoid tissue; few circulate in the blood Crucial to immunity

55 Copyright © 2010 Pearson Education, Inc. Lymphocytes Two types T cells act against virus-infected cells and tumor cells (cell mediated immune response) B cells give rise to plasma cells, which produce antibodies (humoral immune response)

56 Copyright © 2010 Pearson Education, Inc. Monocytes The largest leukocytes Abundant pale-blue cytoplasm Dark purple-staining, U- or kidney-shaped nuclei

57 Copyright © 2010 Pearson Education, Inc. Monocytes Leave circulation, enter tissues, and differentiate into macrophages Actively phagocytic cells; crucial against viruses, intracellular bacterial parasites, and chronic infections Activate lymphocytes to mount an immune response

58 Copyright © 2010 Pearson Education, Inc. Figure 17.10d, e (d) Small lymphocyte; large spherical nucleus (e) Monocyte; kidney-shaped nucleus

59 Copyright © 2010 Pearson Education, Inc. Table 17.2 (1 of 2)

60 Copyright © 2010 Pearson Education, Inc. Leukopoiesis Production of WBCs Stimulated by chemical messengers from bone marrow and mature WBCs Interleukins (e.g., IL-1, IL-2) All leukocytes originate from hemocytoblasts

61 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

62 Copyright © 2010 Pearson Education, Inc. Leukocyte Disorders Leukopenia Abnormally low WBC count—drug/toxin 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

63 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

64 Copyright © 2010 Pearson Education, Inc. Platelets

65 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 (nitric oxide) and prostacyclin from endothelial cells of blood vessels

66 Copyright © 2010 Pearson Education, Inc. Figure Stem cellDevelopmental pathway Hemocyto- blast Megakaryoblast Promegakaryocyte MegakaryocytePlatelets

67 Copyright © 2010 Pearson Education, Inc. Hemostasis

68 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)

69 Copyright © 2010 Pearson Education, Inc. Vascular Spasm Vasoconstriction of damaged blood vessel Triggers Direct injury Chemicals released by endothelial cells and platelets Pain reflexes

70 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

71 Copyright © 2010 Pearson Education, Inc. Coagulation A set of reactions in which blood is transformed from a liquid to a gel Reinforces the platelet plug with fibrin threads

72 Copyright © 2010 Pearson Education, Inc. Coagulation

73 Copyright © 2010 Pearson Education, Inc. Coagulation Three phases of coagulation 1.Prothrombin activator is formed (intrinsic and extrinsic pathways) 2.Prothrombin is converted into thrombin 3.Thrombin catalyzes the joining of fibrinogen to form a fibrin mesh

74 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

75 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

76 Copyright © 2010 Pearson Education, Inc. CLOTTING PATHWAYS Measured by: PTT Drugs: Heparin Measured by PT/INR Drugs: Warfarin, ASA, Vitamin-E, EFA’s Factors PROTHROMBIN ACTIVATOR made up of V&X: Started by X alone and V becomes active with + feedback Extrinsic Pathway: Damage outside of blood vessels. Intrinsic Pathway: Blood trauma (turbulence and viscosity) or collagen and blood contact.

77 Copyright © 2010 Pearson Education, Inc. Figure 17.15

78 Copyright © 2010 Pearson Education, Inc. Clot Retraction Actin and myosin in platelets contract within 30–60 minutes Platelets pull on the fibrin strands, squeezing serum from the clot

79 Copyright © 2010 Pearson Education, Inc. Clot Repair Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore the endothelial lining

80 Copyright © 2010 Pearson Education, Inc. Fibrinolysis Begins within two days Plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA), factor XII and thrombin Plasmin is a fibrin-digesting enzyme

81 Copyright © 2010 Pearson Education, Inc. Factors Preventing Undesirable Clotting Platelet adhesion is prevented by Smooth endothelial lining of blood vessels Antithrombic substances nitric oxide and prostacyclin secreted by endothelial cells Vitamin E quinine, which acts as a potent anticoagulant

82 Copyright © 2010 Pearson Education, Inc. Disorders of Hemostasis Thromboembolytic disorders: undesirable clot formation Bleeding disorders: abnormalities that prevent normal clot formation

83 Copyright © 2010 Pearson Education, Inc. Thromboembolytic Conditions Thrombus: clot that develops and persists in an unbroken blood vessel May block circulation, leading to tissue death Embolus: a thrombus freely floating in the blood stream Pulmonary emboli impair the ability of the body to obtain oxygen Cerebral emboli can cause strokes

84 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

85 Copyright © 2010 Pearson Education, Inc. Disseminated Intravascular Coagulation (DIC) Widespread clotting blocks intact blood vessels Severe bleeding occurs because residual blood unable to clot Most common in pregnancy, septicemia, or incompatible blood transfusions

86 Copyright © 2010 Pearson Education, Inc. Bleeding Disorders Thrombocytopenia: deficient number of circulating platelets Petechiae appear due to spontaneous, widespread hemorrhage Due to suppression or destruction of bone marrow (e.g., malignancy, radiation) Platelet count <50,000/mm 3 is diagnostic Treated with transfusion of concentrated platelets

87 Copyright © 2010 Pearson Education, Inc. Bleeding Disorders Impaired liver function Inability to synthesize procoagulants Causes include vitamin K deficiency, hepatitis, and cirrhosis Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption

88 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

89 Copyright © 2010 Pearson Education, Inc. Transfusions Whole-blood transfusions are used when blood loss is substantial Packed red cells (plasma removed) are used to restore oxygen-carrying capacity Transfusion of incompatible blood can be fatal

90 Copyright © 2010 Pearson Education, Inc. Blood Types

91 Copyright © 2010 Pearson Education, Inc. Blood Groups Humans have 30 varieties of naturally occurring RBC antigens Antigens of the ABO and Rh blood groups cause vigorous transfusion reactions Other blood groups (MNS, Duffy, Kell, and Lewis) are usually weak agglutinogens

92 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 the surface of the RBCs Blood may contain anti-A or anti-B antibodies (agglutinins) that act against transfused RBCs with ABO antigens not normally present Anti-A or anti-B form in the blood at about 2 months of age

93 Copyright © 2010 Pearson Education, Inc. Table 17.4

94 Copyright © 2010 Pearson Education, Inc. Rh Blood Groups There are 45 different Rh agglutinogens (Rh factors) C, D, and E are most common Rh + indicates presence of D Rh + = 85% of the population Rh - = 15% of the population

95 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

96 Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalance: Hemolytic Disease of the Newborn Also called erythroblastosis fetalis Rh – mother becomes sensitized when exposure to Rh + blood causes her body to synthesize anti-Rh antibodies Anti-Rh antibodies cross the placenta and destroy the RBCs of an Rh + baby

97 Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalance: Hemolytic Disease of the Newborn The baby can be treated with prebirth transfusions and exchange transfusions after birth RhoGAM serum containing anti-Rh can prevent the Rh– mother from becoming sensitized

98 Copyright © 2010 Pearson Education, Inc. ABO Blood Typing

99 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)

100 Copyright © 2010 Pearson Education, Inc. Restoring Blood Volume Death from shock may result from low blood volume Volume must be replaced immediately with Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition Plasma expanders (e.g., purified human serum albumin, hetastarch, and dextran) Mimic osmotic properties of albumin More expensive and may cause significant complications

101 Copyright © 2010 Pearson Education, Inc. Diagnostic Blood Tests Hematocrit Blood glucose tests Microscopic examination reveals variations in size and shape of RBCs, indications of anemias RBCs too big = macrocytic anemia (B12/folic acid deficiency, etc.) RBCs too small = microcytic anemia (iron deficiency, thalassemia, etc.)

102 Copyright © 2010 Pearson Education, Inc. Diagnostic Blood Tests Differential WBC count Prothrombin time (PTT) and platelet counts assess hemostasis SMAC (or CMP), a blood chemistry profile Complete blood count (CBC)

103 Copyright © 2010 Pearson Education, Inc. Developmental Aspects Fetal blood cells form in the fetal yolk sac, liver, and spleen Red bone marrow is the primary hematopoietic area by the seventh month Blood cells develop from mesenchymal cells called blood islands The fetus forms HbF, which has a higher affinity for O 2 than hemoglobin A formed after birth

104 Copyright © 2010 Pearson Education, Inc. Developmental Aspects Blood diseases of aging Chronic leukemias, anemias, clotting disorders Usually precipitated by disorders of the heart, blood vessels, and immune system

105 Copyright © 2010 Pearson Education, Inc. QUESTIONS TO TEST WHAT YOU NOW KNOW!!!

106 Copyright © 2010 Pearson Education, Inc. Which of the following comprise a logical sequence of vessels as blood exits the heart? A.Capillaries, arteries, veins B.Veins, capillaries, arteries C.Arteries, capillaries, veins D.Arteries, veins, capillaries

107 Copyright © 2010 Pearson Education, Inc. After centrifuging, of the listed blood components, which contains the components of immune function? A.Plasma B.Buffy coat C.Erythrocytes D.Hematocrit

108 Copyright © 2010 Pearson Education, Inc. The major function of the most common plasma protein, albumin, is __________. A.maintenance of plasma osmotic pressure B.buffering changes in plasma pH C.fighting foreign invaders D.both a and b

109 Copyright © 2010 Pearson Education, Inc. Red blood cells are efficient oxygen transport cells. Of the following characteristics, which is the major contributor to the significant oxygen- carrying capacity of a red blood cell? A.Red blood cells lack mitochondria. B.Red blood cells don’t divide. C.Red blood cells are biconcave discs. D.Red blood cells contain myoglobin.

110 Copyright © 2010 Pearson Education, Inc. Each hemoglobin can transport ________ oxygen atoms. A.4 B.40 C.400 D.4000

111 Copyright © 2010 Pearson Education, Inc. Oxygen binds to the _______ portion of hemoglobin. A.globin B.oxyhemoglobin C.iron atom D.amino acid

112 Copyright © 2010 Pearson Education, Inc. A patient with low iron levels would experience which of the following symptoms? A.An increased white blood cell count B.An increase in energy level C.An increase in fatigue D.A decreased white blood cell count

113 Copyright © 2010 Pearson Education, Inc. A hematopoietic stem cell will give rise to __________. A.erythrocytes B.leukocytes C.platelets D.all of the above

114 Copyright © 2010 Pearson Education, Inc. Predict the outcome of an overdose of the hormone erythropoietin. A.The blood viscosity increases to levels that may induce heart attacks or strokes. B.The oxygen-carrying capacity remains unchanged despite elevated red blood cell counts. C.Red blood cell counts remain unchanged, but the number of reticulocytes increases. D.Blood viscosity levels decrease while oxygen-carrying capacity increases.

115 Copyright © 2010 Pearson Education, Inc. What response would you expect after traveling to high altitude for two weeks? A.Blood levels of oxygen would remain depressed for the duration. B.A surge in iron release from the liver would occur. C.The kidneys would secrete elevated amounts of erythropoietin. D.There would be no change in blood composition.

116 Copyright © 2010 Pearson Education, Inc. If a patient has pernicious anemia, the inability of the body to absorb vitamin B 12, the patient __________. A.would have reduced blood iron levels B.would have a decreased number of red blood cells C.would have increased levels of hemoglobin D.would not experience any effects on red blood cells

117 Copyright © 2010 Pearson Education, Inc. Which of the following statements is true regarding the mechanism controlling movement of white blood cells into damaged areas? A.White blood cells exit the capillary and move through the tissue spaces with cytoplasmic extensions by following a trail of chemicals produced by other white blood cells. B.Capillaries break open, flooding a damaged area with white blood cells. C.The damaged tissues synthesize their own white blood cells. D.None of the statements are true.

118 Copyright © 2010 Pearson Education, Inc. An elevated neutrophil count would be indicative of ________. A.an allergic reaction B.a cancer C.an acute bacterial infection D.a parasitic infection

119 Copyright © 2010 Pearson Education, Inc. Antihistamines counter the actions of which white blood cells? A.Neutrophils B.Lymphocytes C.Basophils D.Eosinophils

120 Copyright © 2010 Pearson Education, Inc. Leukemia is a general descriptor for which of the following disorders? A.An abnormally low white blood cell count B.Overproduction of abnormal leukocytes C.Elevated counts of normal neutrophils D.Overproduction of abnormal erythrocytes

121 Copyright © 2010 Pearson Education, Inc. A __________ is the progenitor of platelets. A.thrombopoietin B.thrombocyte C.megakaryocyte D.thrombocytoblast

122 Copyright © 2010 Pearson Education, Inc. Why don’t platelets form plugs in undamaged vessels? A.Platelets aren’t formed until vessel damage occurs. B.Only contact of platelets with exposed collagen fibers and von Willebrand factor causes them to be sticky and form plugs. C.Plugs do form, but are removed by macrophages. D.Platelets don’t form plugs, it is the megakaryocytes that form the plugs.

123 Copyright © 2010 Pearson Education, Inc. Activation of the extrinsic pathway of coagulation requires exposure of the blood to _________. A.collagen B.tissue factor III C.prothrombin activator D.serotonin

124 Copyright © 2010 Pearson Education, Inc. Why doesn’t a clot fill the entire vasculature system once it has started forming? A.Rapid blood flow washes away and dilutes activated clotting factors. B.Thrombin is inactivated by antithrombin III if it enters the general circulation. C.Both a and b occur. D.Neither a nor b occurs.

125 Copyright © 2010 Pearson Education, Inc. An oral heparin medication might be prescribed for a patient who: A.is at risk for embolism (clots that spontaneously form and wedge in blood vessels). B.has thrombocytopenia. C.is a hemophiliac. D.has a deficiency in a clotting factor.

126 Copyright © 2010 Pearson Education, Inc. Why is it possible for a person with type A negative blood to have a negative reaction when receiving a transfusion of whole type O negative blood? A.Some type O cells possess B agglutinogens on their surface. B.The Rh factor would cross-react. C.Blood transfusions can only occur within the same blood group. D.The type O blood may have high enough levels of anti-A antibodies that could cross-react with the recipient’s cells.


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