Blood

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Overview of Blood Circulation : 

Overview of Blood Circulation Blood leaves the heart via arteries that branch repeatedly until they become capillaries Oxygen (O2) and nutrients diffuse across capillary walls and enter tissues Carbon dioxide (CO2) and wastes move from tissues into the blood

Overview of Blood Circulation : 

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 CO2 and picks up O2 The oxygen-rich blood returns to the heart

Composition of Blood : 

Composition of Blood Blood is the body’s only fluid tissue It is composed of liquid plasma and formed elements Formed elements include: Erythrocytes, or red blood cells (RBCs) Leukocytes, or white blood cells (WBCs) Platelets Hematocrit – the percentage of RBCs out of the total blood volume

Components of Whole Blood : 

Components of Whole Blood Figure 17.1

Physical Characteristics and Volume : 

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

Functions of Blood : 

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

Distribution : 

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

Regulation : 

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

Protection : 

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

Blood Plasma : 

Blood Plasma Blood plasma contains over 100 solutes, including: Proteins – albumin, globulins, clotting proteins, and others Lactic acid, urea, creatinine Organic nutrients – glucose, carbohydrates, amino acids Electrolytes – sodium, potassium, calcium, chloride, bicarbonate Respiratory gases – oxygen and carbon dioxide

Formed Elements : 

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 formed elements survive in the bloodstream for only a few days Most blood cells do not divide but are renewed by cells in bone marrow

Erythrocytes (RBCs) : 

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

Erythrocytes (RBCs) : 

Erythrocytes (RBCs) Figure 17.3

Components of Whole Blood : 

Components of Whole Blood Figure 17.2

Erythrocytes (RBCs) : 

Erythrocytes (RBCs) Erythrocytes are an example of the complementarity of structure and function 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

Erythrocyte Function : 

Erythrocyte Function RBCs are dedicated to respiratory gas transport 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

Structure of Hemoglobin : 

Structure of Hemoglobin Figure 17.4

Hemoglobin (Hb) : 

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 Carbon dioxide loading takes place in the tissues PLAY InterActive Physiology ®: Respiratory System: Gas Transport, pages 3–13

Production of Erythrocytes : 

Production of Erythrocytes Hematopoiesis – blood cell formation Hematopoiesis occurs in the red bone marrow of the: Axial skeleton and girdles Epiphyses of the humerus and femur Hemocytoblasts give rise to all formed elements

Production of Erythrocytes: Erythropoiesis : 

Production of Erythrocytes: Erythropoiesis A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts The developmental pathway consists of three phases 1 – ribosome synthesis in early erythroblasts 2 – Hb accumulation in late erythroblasts and normoblasts 3 – ejection of the nucleus from normoblasts and formation of reticulocytes Reticulocytes then become mature erythrocytes

Production of Erythrocytes: Erythropoiesis : 

Production of Erythrocytes: Erythropoiesis A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts

Production of Erythrocytes: Erythropoiesis : 

Production of Erythrocytes: Erythropoiesis The developmental pathway consists of three phases 1 – ribosome synthesis in early erythroblasts 2 – Hb accumulation in late erythroblasts and normoblasts 3 – ejection of the nucleus from normoblasts and formation of reticulocytes Reticulocytes then become mature erythrocytes

Production of Erythrocytes: Erythropoiesis : 

Production of Erythrocytes: Erythropoiesis Figure 17.5

Regulation and Requirements for Erythropoiesis : 

Regulation and Requirements for Erythropoiesis Circulating erythrocytes – the number remains constant and reflects a balance between RBC production and destruction Too few RBCs leads to tissue hypoxia Too many RBCs causes undesirable blood viscosity Erythropoiesis is hormonally controlled and depends on adequate supplies of iron, amino acids, and B vitamins

Hormonal Control of Erythropoiesis : 

Hormonal Control of Erythropoiesis Erythropoietin (EPO) release by the kidneys is triggered by: Hypoxia due to decreased RBCs Decreased oxygen availability Increased tissue demand for oxygen Enhanced erythropoiesis increases the: RBC count in circulating blood Oxygen carrying ability of the blood

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Increases O2-carrying ability of blood Erythropoietin stimulates red bone marrow Reduces O2 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 O2 Start Imbalance Imbalance Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Start Imbalance Imbalance Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Reduces O2 levels in blood Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Start Imbalance Imbalance Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Reduces O2 levels in blood Kidney (and liver to a smaller extent) releases erythropoietin Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Start Imbalance Imbalance Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Erythropoietin stimulates red bone marrow Reduces O2 levels in blood Kidney (and liver to a smaller extent) releases erythropoietin Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Start Imbalance Imbalance Erythropoietin Mechanism Figure 17.6

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Erythropoietin stimulates red bone marrow Reduces O2 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 O2 Start Imbalance Imbalance Erythropoietin Mechanism

Erythropoietin Mechanism : 

Homeostasis: Normal blood oxygen levels Increases O2-carrying ability of blood Erythropoietin stimulates red bone marrow Reduces O2 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 O2 Start Erythropoietin Mechanism Figure 17.6

Dietary Requirements of Erythropoiesis : 

Erythropoiesis requires: Proteins, lipids, and carbohydrates Iron, vitamin B12, and folic acid The body stores iron in Hb (65%), the liver, spleen, and bone marrow Intracellular iron is stored in protein-iron complexes such as ferritin and hemosiderin Circulating iron is loosely bound to the transport protein transferrin Dietary Requirements of Erythropoiesis

Fate and Destruction of Erythrocytes : 

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

Fate and Destruction of Erythrocytes : 

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

Fate and Destruction of Erythrocytes : 

Fate and Destruction of Erythrocytes Globin is metabolized into amino acids and is released into the circulation Hb released into the blood is captured by haptoglobin and phgocytized

Slide 38: 

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, 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 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 O2 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. 1 2 3 4 5 6 Figure 17.7

Slide 39: 

Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 Figure 17.7

Slide 40: 

Erythropoietin levels rise in blood. Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 Figure 17.7

Slide 41: 

Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 3 Figure 17.7

Slide 42: 

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 O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 3 4 Figure 17.7

Slide 43: 

Hemoglobin 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 O2 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. 1 2 3 4 5 Figure 17.7

Slide 44: 

Hemoglobin Globin Heme Figure 17.7

Slide 45: 

Hemoglobin Amino acids Globin Heme Figure 17.7

Slide 46: 

Hemoglobin Amino acids Globin Heme Iron stored as ferritin, hemosiderin Bilirubin Figure 17.7

Slide 47: 

Hemoglobin Amino acids Globin Heme Iron stored as ferritin, hemosiderin Bilirubin Figure 17.7

Slide 48: 

Hemoglobin Amino acids Globin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Heme Iron stored as ferritin, hemosiderin Bilirubin Figure 17.7

Slide 49: 

Hemoglobin Amino acids Globin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Heme 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 Figure 17.7

Slide 50: 

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 Figure 17.7

Slide 51: 

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, 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 6 Figure 17.7

Slide 52: 

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, 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 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 O2 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. 1 2 3 4 5 6 Figure 17.7

Erythrocyte Disorders : 

Anemia – blood has abnormally low oxygen-carrying capacity It is a symptom rather than a disease itself Blood oxygen levels cannot support normal metabolism Signs/symptoms include fatigue, paleness, shortness of breath, and chills Erythrocyte Disorders

Anemia: Insufficient Erythrocytes : 

Anemia: Insufficient Erythrocytes Hemorrhagic anemia – result of acute or chronic loss of blood Hemolytic anemia – prematurely ruptured RBCs Aplastic anemia – destruction or inhibition of red bone marrow

Anemia: Decreased Hemoglobin Content : 

Iron-deficiency anemia results from: A secondary result of hemorrhagic anemia Inadequate intake of iron-containing foods Impaired iron absorption Pernicious anemia results from: Deficiency of vitamin B12 Lack of intrinsic factor needed for absorption of B12 Treatment is intramuscular injection of B12; application of Nascobal Anemia: Decreased Hemoglobin Content

Anemia: Abnormal Hemoglobin : 

Anemia: Abnormal Hemoglobin Thalassemias – absent or faulty globin chain in Hb RBCs are thin, delicate, and deficient in Hb Sickle-cell anemia – results from a defective gene coding for an abnormal Hb called hemoglobin S (HbS) HbS has a single amino acid substitution in the beta chain This defect causes RBCs to become sickle-shaped in low oxygen situations

Polycythemia : 

Polycythemia Polycythemia – excess RBCs that increase blood viscosity Three main polycythemias are: Polycythemia vera Secondary polycythemia Blood doping

Leukocytes (WBCs) : 

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 / mm3 Normal response to bacterial or viral invasion

Percentages of Leukocytes : 

Percentages of Leukocytes Figure 17.9

Granulocytes : 

Granulocytes Granulocytes – neutrophils, eosinophils, and basophils Contain cytoplasmic granules that stain specifically (acidic, basic, or both) with Wright’s stain Are larger and usually shorter-lived than RBCs Have lobed nuclei Are all phagocytic cells

Neutrophils : 

Neutrophils Neutrophils have two types of granules that: Take up both acidic and basic dyes Give the cytoplasm a lilac color Contain peroxidases, hydrolytic enzymes, and defensins (antibiotic-like proteins) Neutrophils are our body’s bacteria slayers

Eosinophils : 

Eosinophils account for 1–4% of WBCs Have red-staining, bilobed nuclei connected via a broad band of nuclear material Have red to crimson (acidophilic) large, coarse, lysosome-like granules Lead the body’s counterattack against parasitic worms Lessen the severity of allergies by phagocytizing immune complexes Eosinophils

Basophils : 

Account for 0.5% of WBCs and: Have U- or S-shaped nuclei with two or three conspicuous constrictions Are functionally similar to mast cells Have large, purplish-black (basophilic) granules that contain histamine Histamine – inflammatory chemical that acts as a vasodilator and attracts other WBCs (antihistamines counter this effect) Basophils

Agranulocytes : 

Agranulocytes – lymphocytes and monocytes: Lack visible cytoplasmic granules Are similar structurally, but are functionally distinct and unrelated cell types Have spherical (lymphocytes) or kidney-shaped (monocytes) nuclei Agranulocytes

Lymphocytes : 

Account for 25% or more of WBCs and: Have large, dark-purple, circular nuclei with a thin rim of blue cytoplasm Are found mostly enmeshed in lymphoid tissue (some circulate in the blood) There are two types of lymphocytes: T cells and B cells T cells function in the immune response B cells give rise to plasma cells, which produce antibodies Lymphocytes

Monocytes : 

Monocytes account for 4–8% of leukocytes They are the largest leukocytes They have abundant pale-blue cytoplasms They have purple-staining, U- or kidney-shaped nuclei They leave the circulation, enter tissue, and differentiate into macrophages Monocytes

Macrophages : 

Macrophages: Are highly mobile and actively phagocytic Activate lymphocytes to mount an immune response Macrophages

Leukocytes : 

Leukocytes Figure 17.10

Summary of Formed Elements : 

Summary of Formed Elements Table 17.2.1

Summary of Formed Elements : 

Summary of Formed Elements Table 17.2.2

Production of Leukocytes : 

Leukopoiesis is stimulated by interleukins and colony-stimulating factors (CSFs) Interleukins are numbered (e.g., IL-1, IL-2), whereas CSFs are named for the WBCs they stimulate (e.g., granulocyte-CSF stimulates granulocytes) Macrophages and T cells are the most important sources of cytokines Many hematopoietic hormones are used clinically to stimulate bone marrow Production of Leukocytes

Formation of Leukocytes : 

Formation of Leukocytes All leukocytes originate from hemocytoblasts Hemocytoblasts differentiate into myeloid stem cells and lymphoid stem cells Myeloid stem cells become myeloblasts or monoblasts Lymphoid stem cells become lymphoblasts Myeloblasts develop into eosinophils, neutrophils, and basophils Monoblasts develop into monocytes Lymphoblasts develop into lymphocytes

Slide 73: 

(a) (b) (c) (d) (e) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Plasma cells Some become Monocytes Lymphocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 74: 

Hemocytoblast Stem cells Figure 17.11

Slide 75: 

Hemocytoblast Myeloid stem cell Stem cells Figure 17.11

Slide 76: 

Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Figure 17.11

Slide 77: 

Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Develop- mental pathway Figure 17.11

Slide 78: 

Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Develop- mental pathway Figure 17.11

Slide 79: 

Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Figure 17.11

Slide 80: 

(a) (b) (c) (d) Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Agranular leukocytes Figure 17.11

Slide 81: 

(a) (b) (c) (d) Hemocytoblast Myeloid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 82: 

(a) (b) (c) (d) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 83: 

(a) (b) (c) (d) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 84: 

(a) (b) (c) (d) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 85: 

(a) (b) (c) (d) (e) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Monocytes Lymphocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Slide 86: 

(a) (b) (c) (d) (e) Hemocytoblast Myeloid stem cell Lymphoid stem cell Myeloblast Myeloblast Myeloblast Lymphoblast Stem cells Committed cells Promyelocyte Promyelocyte Promyelocyte Promonocyte Prolymphocyte Eosinophilic myelocyte Neutrophilic myelocyte Basophilic myelocyte Eosinophilic band cells Neutrophilic band cells Basophilic band cells Develop- mental pathway Eosinophils Neutrophils Basophils Granular leukocytes Plasma cells Some become Monocytes Lymphocytes Macrophages (tissues) Agranular leukocytes Some become Figure 17.11

Leukocytes Disorders: Leukemias : 

Leukocytes Disorders: Leukemias Leukemia refers to cancerous conditions involving WBCs Leukemias are named according to the abnormal WBCs 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

Leukemia : 

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

Platelets : 

Platelets are fragments of megakaryocytes with a blue-staining outer region and a purple granular center Their granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF) Platelets function in the clotting mechanism by forming a temporary plug that helps seal breaks in blood vessels Platelets not involved in clotting are kept inactive by NO and prostacyclin Platelets

Genesis of Platelets : 

Stem cell Developmental pathway Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown.

Genesis of Platelets : 

Stem cell Hemocytoblast Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown.

Genesis of Platelets : 

Stem cell Developmental pathway Hemocytoblast Megakaryoblast Figure 17.12 The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Genesis of Platelets

Genesis of Platelets : 

Stem cell Developmental pathway Hemocytoblast Megakaryoblast Promegakaryocyte Figure 17.12 The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Genesis of Platelets

Genesis of Platelets : 

Stem cell Developmental pathway Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Figure 17.12 The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Genesis of Platelets

Genesis of Platelets : 

Stem cell Developmental pathway Hemocytoblast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown.

Hemostasis : 

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)

Platelet Plug Formation : 

Platelet Plug Formation Platelets do not stick to each other or to blood vessels Upon damage to blood vessel endothelium platelets: With the help of von Willebrand factor (VWF) adhere to collagen Are stimulated by thromboxane A2 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 by prostacyclin

Coagulation : 

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

Coagulation : 

Coagulation Figure 17.13a

Detailed Events of Coagulation : 

Detailed Events of Coagulation Figure 17.13b

Coagulation Phase 1: Two Pathways to Prothrombin Activator : 

Coagulation Phase 1: Two Pathways to Prothrombin Activator May be initiated by either the intrinsic or extrinsic pathway Triggered by tissue-damaging events Involves a series of procoagulants Each pathway cascades toward factor X Once factor X has been activated, it complexes with calcium ions, PF3, and factor V to form prothrombin activator

Coagulation Phase 2: Pathway to Thrombin : 

Coagulation Phase 2: Pathway to Thrombin Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin

Coagulation Phase 3: Common Pathways to the Fibrin Mesh : 

Coagulation Phase 3: Common Pathways to the Fibrin Mesh Thrombin catalyzes the polymerization of fibrinogen into fibrin Insoluble fibrin strands form the structural basis of a clot Fibrin causes plasma to become a gel-like trap Fibrin in the presence of calcium ions activates factor XIII that: Cross-links fibrin Strengthens and stabilizes the clot

Clot Retraction and Repair : 

Clot Retraction and Repair Clot retraction – stabilization of the clot by squeezing serum from the fibrin strands Repair Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall Fibroblasts form a connective tissue patch Stimulated by vascular endothelial growth factor (VEGF), endothelial cells multiply and restore the endothelial lining

Factors Limiting Clot Growth or Formation : 

Factors Limiting Clot Growth or Formation Two homeostatic mechanisms prevent clots from becoming large Swift removal of clotting factors Inhibition of activated clotting factors

Inhibition of Clotting Factors : 

Inhibition of Clotting Factors Fibrin acts as an anticoagulant by binding thrombin and preventing its: Positive feedback effects of coagulation Ability to speed up the production of prothrombin activator via factor V Acceleration of the intrinsic pathway by activating platelets

Inhibition of Clotting Factors : 

Inhibition of Clotting Factors Thrombin not absorbed to fibrin is inactivated by antithrombin III Heparin, another anticoagulant, also inhibits thrombin activity

Factors Preventing Undesirable Clotting : 

Unnecessary clotting is prevented by endothelial lining the blood vessels Platelet adhesion is prevented by: The smooth endothelial lining of blood vessels Heparin and PGI2 secreted by endothelial cells Vitamin E quinone, a potent anticoagulant Factors Preventing Undesirable Clotting

Hemostasis Disorders:Thromboembolytic Conditions : 

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

Hemostasis Disorders:Thromboembolytic Conditions : 

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

Prevention of Undesirable Clots : 

Substances used to prevent undesirable clots: Aspirin – an antiprostaglandin that inhibits thromboxane A2 Heparin – an anticoagulant used clinically for pre- and postoperative cardiac care Warfarin – used for those prone to atrial fibrillation Prevention of Undesirable Clots

Hemostasis Disorders : 

Disseminated Intravascular Coagulation (DIC): widespread clotting in intact blood vessels Residual blood cannot clot Blockage of blood flow and severe bleeding follows Most common as: A complication of pregnancy A result of septicemia or incompatible blood transfusions Hemostasis Disorders

Hemostasis Disorders: Bleeding Disorders : 

Thrombocytopenia – condition where the number of circulating platelets is deficient Patients show petechiae due to spontaneous, widespread hemorrhage Caused by suppression or destruction of bone marrow (e.g., malignancy, radiation) Platelet counts less than 50,000/mm3 is diagnostic for this condition Treated with whole blood transfusions Hemostasis Disorders: Bleeding Disorders

Hemostasis Disorders: Bleeding Disorders : 

Inability to synthesize procoagulants by the liver results in severe bleeding disorders Causes can range from vitamin K deficiency to hepatitis and cirrhosis Inability to absorb fat can lead to vitamin K deficiencies as it is a fat-soluble substance and is absorbed along with fat Liver disease can also prevent the liver from producing bile, which is required for fat and vitamin K absorption Hemostasis Disorders: Bleeding Disorders

Hemostasis Disorders: Bleeding Disorders : 

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

Hemostasis Disorders: Bleeding Disorders : 

Hemostasis Disorders: Bleeding Disorders Symptoms include prolonged bleeding and painful and disabled joints Treatment is with blood transfusions and the injection of missing factors

Blood Transfusions : 

Blood Transfusions Whole blood transfusions are used: When blood loss is substantial In treating thrombocytopenia Packed red cells (cells with plasma removed) are used to treat anemia

Human Blood Groups : 

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

Blood Groups : 

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

ABO Blood Groups : 

The ABO blood groups consists of: Two antigens (A and B) on the surface of the RBCs Two antibodies in the plasma (anti-A and anti-B) ABO blood groups may have various types of antigens and preformed antibodies Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactions ABO Blood Groups

ABO Blood Groups : 

ABO Blood Groups Table 17.4

Rh Blood Groups : 

There are eight different Rh agglutinogens, three of which (C, D, and E) are common Presence of the Rh agglutinogens on RBCs is indicated as Rh+ 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

Hemolytic Disease of the Newborn : 

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

Hemolytic Disease of the Newborn : 

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

Transfusion Reactions : 

Transfusion reactions occur when mismatched blood is infused Donor’s cells are attacked by the recipient’s plasma agglutinins causing: Diminished oxygen-carrying capacity Clumped cells that impede blood flow Ruptured RBCs that release free hemoglobin into the bloodstream Transfusion Reactions

Transfusion Reactions : 

Transfusion Reactions Circulating hemoglobin precipitates in the kidneys and causes renal failure

Blood Typing : 

Blood Typing When serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens Positive reactions indicate agglutination

Blood Typing : 

Blood Typing

Plasma Volume Expanders : 

Plasma Volume Expanders When shock is imminent from low blood volume, volume must be replaced Plasma or plasma expanders can be administered

Plasma Volume Expanders : 

Plasma Volume Expanders Plasma expanders Have osmotic properties that directly increase fluid volume Are used when plasma is not available Examples: purified human serum albumin, plasminate, and dextran Isotonic saline can also be used to replace lost blood volume

Diagnostic Blood Tests : 

Diagnostic Blood Tests Laboratory examination of blood can assess an individual’s state of health Microscopic examination: Variations in size and shape of RBCs – predictions of anemias Type and number of WBCs – diagnostic of various diseases Chemical analysis can provide a comprehensive picture of one’s general health status in relation to normal values

Developmental Aspects : 

Developmental Aspects Before birth, blood cell formation takes place in the fetal yolk sac, liver, and spleen By the seventh month, red bone marrow is the primary hematopoietic area Blood cells develop from mesenchymal cells called blood islands The fetus forms HbF, which has a higher affinity for oxygen than adult hemoglobin

Developmental Aspects : 

Developmental Aspects Age-related blood problems result from disorders of the heart, blood vessels, and the immune system Increased leukemias are thought to be due to the waning deficiency of the immune system Abnormal thrombus and embolus formation reflects the progress of atherosclerosis