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Chapter 17 Blood. Overview of Blood Circulation Blood leaves the heart via arteries that branch repeatedly until they become capillaries Oxygen (O 2 )

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Presentation on theme: "Chapter 17 Blood. Overview of Blood Circulation Blood leaves the heart via arteries that branch repeatedly until they become capillaries Oxygen (O 2 )"— Presentation transcript:

1 Chapter 17 Blood

2 Overview of Blood Circulation Blood leaves the heart via arteries that branch repeatedly until they become capillaries Oxygen (O 2 ) and nutrients diffuse across capillary walls and enter tissues Carbon dioxide (CO 2 ) and wastes move from tissues into the blood Blood Circulation Review

3 Overview of Blood Circulation Oxygen-deficient blood leaves the capillaries and flows in veins to the heart This blood flows to the lungs where it releases CO 2 and picks up O 2 The oxygen-rich blood returns to the heart

4 Composition of Blood Blood is the bodys only fluid tissue It is considered a connective tissue Contains cells: formed elements Extracellular matrix: plasma + dissolved fibrous proteins Formed elements include: Erythrocytes, or red blood cells (RBCs) Leukocytes, or white blood cells (WBCs) Platelets

5 Components of Whole Blood Figure 17.1 Hematocrit – the percentage of RBCs out of the total blood volume

6 Physical Characteristics and Volume Blood is a sticky, opaque fluid with a metallic taste Color varies from scarlet (oxygen- rish) to dark red (oxygen-poor) The pH of blood is 7.35–7.45 Temperature is 38C Blood accounts for approximately 8% of body weight Average volume: 5–6 L for males, and 4–5 L for females

7 Functions of Blood Blood performs a number of functions dealing with: Substance distribution Regulation of blood levels of particular substances Body protection

8 Distribution Blood transports: Oxygen from the lungs and nutrients from the digestive tract Metabolic wastes from cells to the lungs and kidneys for elimination Hormones from endocrine glands to target organs

9 Regulation Blood maintains: Appropriate body temperature by absorbing and distributing heat Normal pH in body tissues using buffer systems Adequate fluid volume in the circulatory system

10 Protection Blood prevents blood loss by: Activating plasma proteins and platelets Initiating clot formation when a vessel is broken Blood prevents infection by: Synthesizing and utilizing antibodies Activating complement proteins Activating WBCs to defend the body against foreign invaders

11 Blood Plasma Blood plasma contains over 100 solutes, including: Proteins – albumin, globulins, clotting proteins, and others (8% by weight) Metabolic wastes - Lactic acid, urea, creatinine Organic nutrients – glucose, carbohydrates, amino acids Electrolytes – sodium, potassium, calcium, chloride, bicarbonate Respiratory gases – oxygen and carbon dioxide Hormones

12 Formed Elements Erythrocytes, leukocytes, and platelets make up the formed elements Only WBCs are complete cells RBCs have no nuclei or organelles, and platelets are just cell fragments Most blood cells do not divide but are renewed by cells in bone marrow

13 Components of Whole Blood Figure 17.2

14 Erythrocytes (RBCs) Biconcave discs, anucleate, essentially no organelles Filled with hemoglobin (Hb), a protein that functions in gas transport Contain the plasma membrane protein SPECTRIN and other proteins that: Give erythrocytes their flexibility Allow them to change shape as necessary

15 Erythrocytes (RBCs) Figure 17.3

16 Erythrocytes (RBCs) Structural characteristics contribute to its gas transport function Biconcave shape has a huge surface area relative to volume Erythrocytes are more than 97% hemoglobin ATP is generated ANAEROBICALLY, so the erythrocytes do not consume the oxygen they transport

17 Erythrocyte Function RBCs are dedicated to respiratory gas transport Hemoglobin (Hb) reversibly binds with oxygen and most oxygen in the blood is bound to Hb Hb is composed of the protein globin, made up of two alpha and two beta chains, each bound to a heme group Each heme group bears an atom of iron, which can bind to one oxygen molecule Each Hb molecule can transport four molecules of oxygen

18 Structure of Hemoglobin Figure 17.4

19 Hemoglobin (Hb) Oxyhemoglobin – Hb bound to oxygen Oxygen loading takes place in the lungs Deoxyhemoglobin – Hb after oxygen diffuses into tissues (reduced Hb) Carbaminohemoglobin – Hb bound to carbon dioxide (globin part) ~20% of carbon dioxide Carbon dioxide loading takes place in the tissues

20 Production of Erythrocytes Hematopoiesis – blood cell formation Hematopoiesis occurs in the red bone marrow of the: Axial skeleton and girdles Proximal epiphyses of the humerus and femur Hematopoietic stem cells (hemocytoblasts) give rise to all formed elements

21 Production of Erythrocytes: Erythropoiesis Figure 17.5

22 Regulation & Requirements for Erythropoiesis Maintain homeostasis – produces 2 million cells per second Hormonal Controls Erythropoietin = hormone produced by kidneys Production stimulated by; Reduced # of RBCs Insufficient hemoglobin per RBC Reduced availability of oxygen Dietary Requirements Amino acids, lipids, & carbohydrates. IRON

23 Regulation & Requirements for Erythropoiesis Dietary Requirements Amino acids, lipids, & carbohydrates. IRON 65% is in hemoglobin Free iron ions are toxic Inside cells: ferritin, hemosiderin Blood transportation: transferrin

24 Homeostasis: Normal blood oxygen levels Increases O 2 -carrying ability of blood Erythropoietin stimulates red bone marrow Reduces O 2 levels in blood Kidney (and liver to a smaller extent) releases erythropoietin Enhanced erythropoiesis increases RBC count Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O 2 Start Imbalance Erythropoietin Mechanism Figure 17.6

25 Fate and Destruction of Erythrocytes The life span of an erythrocyte is 100–120 days Old RBCs become rigid and fragile, and their Hb begins to degenerate Dying RBCs are engulfed by macrophages Heme and globin are separated and the iron is salvaged for reuse

26 Fate and Destruction of Erythrocytes Globin is metabolized into amino acids and is released into the circulation Hb released into the blood is phagocytized

27 Fate and Destruction of Erythrocytes Heme is degraded to a yellow pigment called bilirubin The liver secretes bilirubin into the intestines as bile The intestines metabolize it into urobilinogen This degraded pigment leaves the body in feces, in a pigment called stercobilin (makes feces brown)

28 Hemoglobin Amino acids Globin Raw materials are made available in blood for erythrocyte synthesis. 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 Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. New erythrocytes enter bloodstream; function about 120 days. Low O 2 levels in blood stimulate kidneys to produce erythropoietin. Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down Figure 17.7

29 Erythrocyte Disorders Anemias = blood has abnormally low oxygen-carrying capacity Insufficient number of RBCs E.g. hemorrhagic anemias Low hemoglobin content E.g. Iron-deficiency anemia Abnormal hemoglobin E.g. Sickle-cell anemia

30 Leukocytes (WBCs) Leukocytes, the only blood components that are complete cells: Are less numerous than RBCs Make up 1% of the total blood volume Can leave capillaries via diapedesis Move through tissue spaces Leukocytosis – WBC count over 11,000 / mm 3 Normal response to bacterial or viral invasion

31 Percentages of Leukocytes Figure 17.9

32 WBCs - Granulocytes Granulocytes 1.neutrophils, 2.eosinophils, and 3.basophils Are larger and usually shorter-lived than RBCs Have lobed nuclei Are all phagocytic cells

33 Neutrophils Neutrophils are our bodys bacteria slayers Granules contain antimicrobial proteins (defensins) YouTube - neutrophils in action

34 Eosinophils account for 1–4% of WBCs Lead the bodys counterattack against parasitic worms Lessen the severity of allergies Eosinophils

35 Account for 0.5% of WBCs and: Have U- or S-shaped nuclei with two or three conspicuous constrictions Contain histamine Histamine – inflammatory chemical that acts as a vasodilator and attracts other WBCs (antihistamines counter this effect) Basophils Explanation of Allergies

36 WBCs - Agranulocytes Two Types; Lymphocytes Monocytes Lack visible granules Nuclei typically spherical or kidney shaped

37 Account for 25% or more of WBCs and: Have large, circular nuclei Are found mostly in lymphoid tissue Two types: T cells and B cells T cells function in the immune response against virus infected cells and tumor cells B cells give rise to plasma cells, which produce antibodies (like gamma globulin) Lymphocytes

38 Monocytes account for 4–8% of leukocytes Largest leukocytes Purple-staining, kidney-shaped nuclei They leave the circulation, enter tissue, and differentiate into macrophages Bodys defense against viruses, some intracellular bacterial parasites, and chronic infections e.g. tuberculosis Activate lymphocytes to mount an immune response Monocytes

39 Leukocytes Figure 17.10

40 Production & Lifespan WBCs Leukopoiesis – production of white blood cells Stimulated by chemical messengers Interleukins Numbered (e.g. IL-3) Colony-stimulating factors (CSFs) Named for leukocyte them stimulate (e.g. granulocyte-CSF = G-CSF) Released by supporting cells of bone marrow and mature WBCs

41 Formation of Leukocytes All leukocytes originate from hemocytoblasts Hemocytoblasts differentiate into; lymphoid stem cells myeloid stem cells

42 (a) (b)(c) (d) (e) Hemocytoblast Myeloid stem cellLymphoid stem cell Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte PromonocyteProlymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway EosinophilsNeutrophilsBasophils Granular leukocytes Plasma cells Some become Monocytes Lymphocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

43 Leukocytes Disorders: Leukemias Leukemia refers to cancerous conditions involving WBCs Leukemias are named according to the abnormal WBCs involved Pictured: Acute lymphocytic leukemia

44 Leukemia Immature WBCs are found in the bloodstream in all leukemias Bone marrow becomes totally occupied with cancerous leukocytes The WBCs produced, though numerous, are not functional Death is caused by internal hemorrhage and overwhelming infections Treatments include irradiation, antileukemic drugs, and bone marrow transplants

45 Bone Marrow Removal for Transplant

46 Platelets are fragments of megakaryocytes (found in bone marrow) Platelets function in the clotting mechanism by forming a temporary plug that helps seal breaks in blood vessels The stem cell for platelets is the hemocytoblast Platelets

47 Stem cellDevelopmental pathway HemocytoblastMegakaryoblastPromegakaryocyteMegakaryocytePlatelets Figure Genesis of Platelets The sequential developmental pathway is as shown.

48 Same stem cell for RBCs Figure 17.5

49 (a) (b)(c) (d) (e) Hemocytoblast Myeloid stem cellLymphoid stem cell Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte PromonocyteProlymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway EosinophilsNeutrophilsBasophils Granular leukocytes Plasma cells Some become Monocytes Lymphocytes Macrophages (tissues) Agranular leukocytes Some become Figure Same stem cell for WBCs

50 Hemostasis A series of reactions for stoppage of bleeding During hemostasis, three phases occur in rapid sequence Vascular spasms – immediate vasoconstriction in response to injury Platelet plug formation Coagulation (blood clotting)

51 Vascular Spasm Immediate response to injury is vasoconstriction Factors that trigger the spasm are damaged cells, platelets and pain reflexes As damage increases, vascular spasm increases

52 Platelet Plug Formation Platelets do not stick to each other or to blood vessels when there is no damage Upon damage to blood vessel endothelium platelets: Adhere to collagen Stick to exposed collagen fibers and form a platelet plug Release serotonin and ADP, which attract still more platelets The platelet plug is limited to the immediate area of injury

53 A set of reactions in which blood is transformed from a liquid to a gel Coagulation follows intrinsic and extrinsic pathways to thromboplastin The final three steps of this series of reactions are: Prothrombin activator is formed Prothrombin is converted into thrombin Thrombin starts the joining of fibrinogen (plasma protein) into a fibrin mesh Coagulation

54 Fibrin mesh forming in wound

55 Clot Retraction and Repair Clot retraction – stabilization of the clot by squeezing serum from the fibrin strands Repair Fibroblasts form a connective tissue patch Endothelial cells multiply and restore the endothelial lining of blood vessel

56 Cross section of healing wound- dont pick at it!!!

57 Factors Limiting Clot Growth or Formation Two homeostatic mechanisms prevent clots from becoming large Swift removal of clotting factors Stop formation of further clotting factors

58 Hemostasis Disorders: Thromboembolytic Conditions Thrombus – a clot that develops and persists in an unbroken blood vessel Thrombi can block circulation, resulting in tissue death Coronary thrombosis – thrombus in blood vessel of the heart

59 Thrombus/Embolus

60 Hemostasis Disorders: Thromboembolytic Conditions Embolus – a thrombus freely floating in the blood stream Pulmonary emboli can impair the ability of the body to obtain oxygen Cerebral emboli can cause strokes

61 Substances used to prevent undesirable clots: Aspirin Heparin – an anticoagulant used clinically for pre- and postoperative cardiac care Warfarin – used for those prone to atrial fibrillation Prevention of Undesirable Clots

62 Hemophilias – hereditary bleeding disorders caused by lack of clotting factors Hemophilia A – most common type (83% of all cases) due to a deficiency of factor VIII Hemophilia B – due to a deficiency of factor IX Hemophilia C – mild type, due to a deficiency of factor XI Hemostasis Disorders: Bleeding Disorders

63 Hemophilia bleeding into joint

64 Transfusion & Blood Replacement Cardiovascular system minimizes blood loss by 1.Vasoconstriction 2.Increased RBC production Whole blood transfusions vs. Packed red cells Blood bank collects blood and adds anticoagulant, usually separates into components Shelf life at 4ºC about 35 days

65 RBC membranes have glycoprotein antigens on their external surfaces These antigens are: Unique to the individual Recognized as foreign if transfused into another individual RBC antigens promote agglutination, thus referred to as agglutinogens Presence or absence of these antigens is used to classify blood groups Human Blood Groups

66 Plasma Membrane

67 Humans have 30 varieties of naturally occurring RBC antigens The antigens of the ABO and Rh blood groups cause vigorous transfusion reactions when they are improperly transfused Other blood groups (M, N, Dufy, Kell, and Lewis) are mainly used for legalities Blood Groups

68 The ABO blood groups consists of: Two antigens (A and B) on the surface of the RBCs = agglutinogens Two antibodies in the plasma (anti-A and anti-B) = agglutinins ABO Blood Groups

69 Table 17.4

70 There are 45 different types of Rh agglutinogens (only 3 common – C, D, E) Rh + = presence of the D antigen Rh- (D)= RBCs do not carry D antigen Anti-Rh antibodies are not spontaneously formed in Rh – individuals However, if an Rh – individual receives Rh + blood, anti-Rh antibodies form A second exposure to Rh + blood will result in a typical transfusion reaction Rh Blood Groups

71 The blood type of the mother and the blood type of her baby can have a significant effect on the health of the fetus or newborn baby. Usually in discussions on this topic we are concerned when a mother has Rh- blood and her husband has Rh+ blood. This combination can lead to a baby with Rh+ blood. If the mother is already sensitized to Rh+ blood cells, the Rh+ baby she is carrying will be affected to some degree by Rh hemolytic disease. If the mother becomes sensitized after delivery, every future Rh+ baby is at risk. There is a difference between these blood antigens and the A and B antigens. We are not born with antibodies against these blood antigens. For example, an Rh- person is not born with anti-D (anti-Rh) antibodies. However, if we are exposed to blood with one of these unfamiliar antigens, we can develop antibodies against blood with those antigens. We can get exposed to these blood antigens by getting a transfusion with a foreign type of blood or carrying a child with a different blood type from our own. When a woman is pregnant, a few of the babys blood cells will often leak through the placenta and show up in her blood system. We do not develop the antibodies immediately. We use the blood cells that are circulating in our system, as if they were our own. When these cells get old they are processed through our spleen to reuse all the spare parts. At this point, antibody production may be started. Pregnant women do not always develop antibodies against new foreign blood cells during pregnancy. A pregnant womans immune system is somewhat suppressed when it finds new antigens. If it was not, her body would be more likely to reject the pregnancy. This immune suppression does not always afford protection from Rh sensitization, however.

72 Hemolytic Disease of the Newborn Hemolytic disease of the newborn – Rh + antibodies of a sensitized Rh – mother cross the placenta and attack and destroy the RBCs of an Rh + baby Rh – mother becomes sensitized when exposure to Rh + blood causes her body to synthesize Rh + antibodies

73 Hemolytic Disease of the Newborn The drug RhoGAM can prevent the Rh – mother from becoming sensitized Treatment of hemolytic disease of the newborn involves pre-birth transfusions and exchange transfusions after birth

74 Transfusion reactions occur when mismatched blood is infused Donors cells are attacked by the recipients plasma agglutinins causing: Diminished oxygen-carrying capacity Clumped cells that impede blood flow Ruptured RBCs that release free hemoglobin into the bloodstream that causes kidney failure Transfusion Reactions

75 Blood type being tested RBC agglutinogens Serum Reaction Anti-AAnti-B ABA and B++ BB–+ AA+– ONone–– Blood Typing


77 Diagnostic Blood Tests Color (high fat – lipidemia) Hematocrit (anemia) Blood glucose (diabetes) Differential White Blood Cell Count E.g. high eosinophil -> parasitic infection Prothrombin time & Platelet count (hemostasis system) SMAC (chemistry profile) & Complete blood count (CBC) are routine before hospital admissions

78 Developmental Aspects Early fetal development – blood formation sites Yolk sac, liver, spleen 7 th month -> red marrow becomes primary area Hemoglobin F has a higher affinity for oxygen than adult hemoglobin After birth, rapidly destroyed by liver

79 Developmental Aspects Most common blood diseases; Chronic leukemias, Anemias, Clotting disorders Usually disorders of the heart, blood vessels, or immune system precede blood diseases

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