PowerPoint Lecture Slides prepared by Vince Austin, Bluegrass Technical and Community College CHAPTER Elaine N. Marieb Katja Hoehn Human Anatomy & Physiology SEVENTH EDITION Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 17 Blood 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Composition of Blood Blood is the bodys 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Components of Whole Blood Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.1 Constituent Plasma 55% Major Functions 90% of plasma volume; solvent
for carrying other substances; absorbs heat Salts (electrolytes) Sodium Osmotic balance, pH buffering, Potassium regulation of membrane Calcium permeability Magnesium Chloride Bicarbonate Water Plasma proteins Albumin Fibrinogen Globulins Formed elements (cells) 45% Cell Type Number (per mm3 of blood)
Erythrocytes (red blood cells) Leukocytes (white blood cells) 46 million Transport oxygen and help transport carbon dioxide 4,80010,800 Osmotic balance, pH buffering Clotting of blood Defense (antibodies) and lipid transport Substances transported by blood Nutrients (glucose, fatty acids, amino acids, vitamins) Waste products of metabolism (urea, uric acid) Respiratory gases (O2 and CO2) Hormones (steroids and thyroid hormone are carried by plasma proteins)
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Functions Defense and immunity Platelets 250,000400,000 Blood clotting 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 7.357.45
Temperature is 38C Blood accounts for approximately 8% of body weight Average volume: 56 L for males, and 45 L for females Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Functions of Blood Blood performs a number of functions dealing with: Substance distribution
Regulation of blood levels of particular substances Body protection Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Erythrocytes (RBCs) Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.3 Components of Whole Blood Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.2 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Structure of Hemoglobin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.4 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
PLAY Carbon dioxide loading takes place in the tissues InterActive Physiology : Respiratory System: Gas Transport, pages 313 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Production of Erythrocytes: Erythropoiesis A hemocytoblast is transformed into a proerythroblast Proerythroblasts develop into early erythroblasts
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Production of Erythrocytes: Erythropoiesis Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.5 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Erythropoietin Mechanism I mb ala nce Start Homeostasis: Normal blood oxygen levels Im b ala n ce
Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Increases O2-carrying ability of blood Reduces O2 levels in blood Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Kidney (and liver to a smaller extent) releases erythropoietin Figure 17.6 Erythropoietin Mechanism Homeostasis: Normal blood oxygen levels Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.6 Erythropoietin Mechanism I mb ala nce Start Homeostasis: Normal blood oxygen levels Im b ala n Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
ce Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Figure 17.6 Erythropoietin Mechanism I mb ala nce Start Homeostasis: Normal blood oxygen levels Im b ala n ce
Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Reduces O2 levels in blood Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.6 Erythropoietin Mechanism I mb ala nce Start Homeostasis: Normal blood oxygen levels Im b ala n
ce Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Reduces O2 levels in blood Kidney (and liver to a smaller extent) releases erythropoietin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.6 Erythropoietin Mechanism I mb ala nce Start
Homeostasis: Normal blood oxygen levels Im b ala n ce Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Reduces O2 levels in blood Erythropoietin stimulates red bone marrow Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Kidney (and liver to a smaller extent) releases erythropoietin
Figure 17.6 Erythropoietin Mechanism I mb ala nce Start Homeostasis: Normal blood oxygen levels Im b ala n ce Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Reduces O2 levels in blood
Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Kidney (and liver to a smaller extent) releases erythropoietin Erythropoietin Mechanism Start Homeostasis: Normal blood oxygen levels Stimulus: Hypoxia due to decreased RBC count, decreased amount of hemoglobin, or decreased availability of O2 Increases
O2-carrying ability of blood Reduces O2 levels in blood Enhanced erythropoiesis increases RBC count Erythropoietin stimulates red bone marrow Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Kidney (and liver to a smaller extent) releases erythropoietin 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Fate and Destruction of Erythrocytes The life span of an erythrocyte is 100120 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 2 Erythropoietin levels rise in blood. 3 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 4 New erythrocytes enter bloodstream; function about 120 days. 5 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. Hemoglobin
Heme Globin Bilirubin Amino acids Iron stored as ferritin, hemosiderin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria and excreted in feces Circulation
Food nutrients, including amino acids, Fe, B12, and folic acid are absorbed from intestine and enter blood 6 Raw materials are made available in blood for erythrocyte synthesis. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7
1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 2 Erythropoietin levels rise in blood. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 3 Erythropoietin levels rise in blood.
Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 3 Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 4 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
New erythrocytes enter bloodstream; function about 120 days. Figure 17.7 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 1 2 3 Erythropoietin levels rise in blood. Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 4 5
Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. New erythrocytes enter bloodstream; function about 120 days. Hemoglobin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Hemoglobin Heme Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Globin
Figure 17.7 Hemoglobin Heme Globin Amino acids Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Amino acids Figure 17.7 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Amino acids Figure 17.7 Hemoglobin Heme
Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Hemoglobin Heme Globin
Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria and excreted in feces Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Hemoglobin Heme
Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria and excreted in feces Circulation Food nutrients,
including amino acids, Fe, B12, and folic acid are absorbed from intestine and enter blood Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Hemoglobin Heme Globin Bilirubin Iron stored as ferritin, hemosiderin Amino acids Iron is bound to
transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria and excreted in feces Circulation Food nutrients, including amino acids, Fe, B12, and folic acid are absorbed from intestine and enter blood Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 6 Raw materials are made available in
blood for erythrocyte synthesis. Figure 17.7 1 Low O2 levels in blood stimulate kidneys to produce erythropoietin. 2 Erythropoietin levels rise in blood. 3 Erythropoietin and necessary raw materials in blood promote erythropoiesis in red bone marrow. 4 New erythrocytes enter bloodstream; function about 120 days. 5 Aged and damaged red blood cells are engulfed by macrophages of liver, spleen, and bone marrow; the hemoglobin is broken down. Hemoglobin Heme
Globin Bilirubin Amino acids Iron stored as ferritin, hemosiderin Iron is bound to transferrin and released to blood from liver as needed for erythropoiesis Bilirubin is picked up from blood by liver, secreted into intestine in bile, metabolized to stercobilin by bacteria and excreted in feces Circulation Food nutrients,
including amino acids, Fe, B12, and folic acid are absorbed from intestine and enter blood 6 Raw materials are made available in blood for erythrocyte synthesis. Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.7 Erythrocyte Disorders Anemia blood has abnormally low oxygencarrying 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Anemia: Insufficient Erythrocytes Normal RBC Population Hemolytic anemia Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Polycythemia Polycythemia excess RBCs that increase blood viscosity Three main polycythemias are: Polycythemia vera Secondary polycythemia Blood doping Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Percentages of Leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.9 Granulocytes Granulocytes neutrophils, eosinophils, and basophils Contain cytoplasmic granules Are larger and usually shorter-lived than RBCs Have lobed nuclei
Are all phagocytic cells Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Neutrophils Neutrophils have two types of granules that: Give the cytoplasm a lilac color Contain peroxidases, hydrolytic enzymes, and defensins (antibiotic-like proteins) Neutrophils are our bodys bacteria
slayers Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Eosinophils Eosinophils account for 14% of WBCs Have U-shaped nuclei Have red to crimson, large, coarse, lysosome-like granules Lead the bodys counterattack against parasitic worms
Lessen the severity of allergies by phagocytizing immune complexes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Basophils Account for 0.5% of WBCs and: Have U- or S-shaped nuclei with two or three conspicuous constrictions Function in response to inflammation 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) Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 clumped 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Antibody
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Monocytes Monocytes account for 48% of leukocytes They are the largest leukocytes They have purple-staining, U- or kidney-shaped nuclei They leave the circulation, enter tissue, and differentiate into macrophages Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Macrophages Macrophages: Are highly mobile and actively phagocytic Activate lymphocytes to mount an immune response Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.10
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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Summary of Formed Elements Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 17.2.1 Summary of Formed Elements Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 17.2.2 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic
myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte Prolymphocyte
Monocytes Lymphocytes (e) (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues) Some become Plasma cells Figure 17.11 Stem cells
Hemocytoblast Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells
Myeloblast Myeloblast Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental
pathway Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Promonocyte Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway
Eosinophilic myelocyte Basophilic myelocyte Promonocyte Neutrophilic myelocyte Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells
Myeloblast Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic
band cells Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Promonocyte Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway
Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c)
Promonocyte Monocytes (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Myeloblast
DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils
(a) (b) (c) Promonocyte Monocytes (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues) Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell
Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells
Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Promonocyte Monocytes (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues)
Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte
Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte
Monocytes (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues) Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast
Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic
band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte Prolymphocyte Monocytes (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues)
Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte
Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte
Prolymphocyte Monocytes Lymphocytes (e) (d) Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues) Figure 17.11 Stem cells Hemocytoblast Myeloid stem cell
Committed Myeloblast cells Myeloblast Lymphoid stem cell Myeloblast DevelopPromyelocyte Promyelocyte Promyelocyte mental pathway Eosinophilic myelocyte Basophilic myelocyte Neutrophilic myelocyte Eosinophilic band cells
Basophilic band cells Neutrophilic band cells Eosinophils Basophils Neutrophils (a) (b) (c) Lymphoblast Promonocyte Prolymphocyte Monocytes Lymphocytes (e) (d)
Agranular leukocytes Granular leukocytes Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Some become Macrophages (tissues) Some become Plasma cells Figure 17.11 Platelets Platelets are fragments of megakaryocytes with a bluestaining 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell Hemocytoblast
Developmental pathway Megakaryoblast Promegakaryocyte Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Megakaryocyte Platelets Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell
Hemocytoblast Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell Hemocytoblast Developmental pathway Megakaryoblast Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 17.12 Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell Hemocytoblast Developmental pathway Megakaryoblast Promegakaryocyte Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.12
Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell Hemocytoblast Developmental pathway Megakaryoblast Promegakaryocyte Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Megakaryocyte Figure 17.12
Genesis of Platelets The stem cell for platelets is the hemocytoblast The sequential developmental pathway is as shown. Stem cell Hemocytoblast Developmental pathway Megakaryoblast Promegakaryocyte Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Megakaryocyte Platelets
Figure 17.12 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)
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coagulation Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 17.13a Detailed Events of Coagulation Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 17.13b 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Coagulation Phase 2: Pathway to Thrombin Prothrombin activator catalyzes the transformation of prothrombin to the active enzyme thrombin Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Factors Limiting Clot Growth or Formation Two homeostatic mechanisms prevent clots from becoming large Swift removal of clotting factors Inhibition of activated clotting factors
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Inhibition of Clotting Factors
Thrombin not absorbed to fibrin is inactivated by antithrombin III Heparin, another anticoagulant, also inhibits thrombin activity Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Prevention of Undesirable Clots Substances used to prevent undesirable clots:
Aspirin an antiprostaglandin that inhibits thromboxane A2 Heparin an anticoagulant used clinically for preand postoperative cardiac care Warfarin used for those prone to atrial fibrillation Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Hemostasis Disorders: Bleeding Disorders Symptoms include prolonged bleeding and painful and disabled joints Treatment is with blood transfusions and the injection of missing factors
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings ABO Blood Groups
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 17.4 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Blood Typing Blood type being tested RBC agglutinogens Serum Reaction
Anti-A Anti-B AB A and B + + B B + A A +
O None Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Transfusion Reactions 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Transfusion Reactions Circulating hemoglobin precipitates in the kidneys and causes renal failure
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Plasma Volume Expanders When shock is imminent from low blood volume, volume must be replaced Plasma or plasma expanders can be administered Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings Diagnostic Blood Tests Laboratory examination of blood can assess an individuals 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 ones general health status in relation to normal values Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings 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 Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
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