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The Cardiovascular System (Introduction)
The body’s internal transport network Includes the heart, blood, and blood vessels Transports Nutrients Oxygen Waste products Chemical messengers
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Functions of Blood (11-1) Transports dissolved gases, nutrients, hormones, and metabolic wastes Regulates interstitial fluid pH and ion composition Restricts fluid loss at injury sites Defends against toxins and pathogens Stabilizes body temperature
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Composition of Blood (11-1)
Liquid connective tissue Contains cells (formed elements) suspended in a fluid matrix (plasma) Formed elements include red blood cells, white blood cells, and platelets Blood volume varies by average body size Adult males average 5–6 liters Adult females average 4–5 liters
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Characteristics of Blood (11-1)
Temperature is 38ºC, slightly above body temperature Blood is five times more viscous than water Viscosity refers to thickness, stickiness, and resistance to flow More viscous due to plasma proteins and formed elements pH is slightly alkaline in a range of 7.35–7.45
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Plasma (11-2) Along with interstitial fluid, accounts for most of the volume of extracellular fluid (ECF) Makes up about 55 percent of volume of whole blood Contains: Water (92%) Plasma proteins (7%) Other solutes (1%) which include hormones, nutrients, and gases
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Erythrocytes or Red Blood Cells (11-3)
RBCs Account for 99.9 percent of formed elements Contain red pigment molecule hemoglobin Transports oxygen and carbon dioxide Hematocrit Percentage of RBCs in whole blood Hematocrit in men is 46 percent Hematocrit in women is 42 percent
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Structure of RBCs (11-3) Specialized to transport oxygen and carbon dioxide Unique biconcave shape provides advantages Increased rate of diffusion Increased flexibility to squeeze through narrow capillaries During RBC formation organelles are lost Cannot go through cell division since they lack a nucleus For energy, rely on anaerobic metabolism of glucose absorbed from plasma
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Figure 11-2 The Anatomy of Red Blood Cells.
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Hemoglobin Structure (11-3)
Hemoglobin (Hb) structure Accounts for over 95 percent of all RBC intracellular proteins Composed of two pairs of globular proteins, called subunits Each subunit contains a heme, with an iron atom Transports oxygen and carbon dioxide Oxygen binds to heme Carbon dioxide binds to the globin subunits
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Anemia (11-3) Reduction in the blood’s oxygen-carrying capacity
Caused by: Low hematocrit Reduced hemoglobin content in RBCs Symptoms include: Muscle fatigue and weakness General lack of energy
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RBC Life Span and Circulation (11-3)
RBCs are exposed to stresses of friction and wear and tear Bounce against walls of blood vessels Squeeze through small capillaries Life span is about 120 days About 1 percent of all RBCs are replaced each day About 3 million new RBCs enter circulation per second
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Gender and Iron Reserves (11-3)
Men have about 3.5 g of iron (in the ionic form of Fe2+) 2.5 g of that is bound to Hb Reserve of 1 g stored in liver and bone marrow Women have 2.4 g of Fe2+ 1.9 g in Hb Reserve of only 0.5 g Women often require dietary supplements If inadequate, iron deficiency anemia may appear
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RBC Formation (11-3) Also called erythropoiesis
In adults, occurs in red bone marrow Requires amino acids, iron, and vitamins
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Stages in RBC Maturation (11-3)
Embryonic cells differentiate into multipotent stem cells, called hemocytoblasts Hemocytoblasts, or hematopoietic stem cells (HSCs), produce myeloid stem cells Erythroblasts are immature and are synthesizing Hb When nucleus is shed they become reticulocytes Reticulocytes enter bloodstream to mature into RBCs
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Figure 11-4 The Origins and Differentiation of Red Blood Cells, Platelets, and White Blood Cells.
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Regulation of Erythropoiesis (11-3)
Stimulated by low tissue oxygen, called hypoxia Kidney hypoxia triggers release of erythropoietin (EPO) When anemia occurs When blood flow to kidney decreases When oxygen content of air in the lungs declines When damage to respiratory surfaces occur Speeds up rate of maturation of RBCs
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Figure 11-5 The Role of EPO in the Stimulation of Erythropoiesis.
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ABO Blood Types and Rh System (11-4)
Based on antigen–antibody responses Antigens are substances that can trigger an immune response Surface antigens on your body’s cells are considered normal, not foreign Presence or absence of antigens on membrane of RBC determines blood type Three major antigens are A, B, and Rh (or D)
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Blood Types (11-4) Type A blood has antigen A only
Type B blood has antigen B only Type AB blood had both A and B Type O blood has neither A nor B Rh antigen indicated by presence (Rh positive, or Rh+) or absence (Rh negative, or Rh–) Blood types reported with positive or negative signs Examples: O– or AB+
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Figure 11-6a Blood Types and Cross-Reactions.
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Table 11.1
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Antibodies (11-4) Found in plasma
Will not attack your own surface antigens on your RBCs Will attack foreign antigens on RBCs of different blood type Type A blood contains anti-B antibodies Type B blood contains anti-A antibodies Type AB blood contains neither antibody Type O blood contains both antibodies
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Cross-Reactions in Transfusions (11-4)
Occur when antibodies in recipient react with their specific surface antigen on donor’s RBCs Causes clumping of RBCs Checking blood types before transfusions ensures the types are compatible
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The Difference between ABO and Rh (11-4)
Anti-A or anti-B antibodies Spontaneously develop during first six months of life No exposure to foreign antigens needed Anti-Rh antibodies in Rh-negative person Do not develop unless individual is exposed to Rh- positive blood Exposure can occur accidentally during a transfusion or during childbirth
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Leukocytes, or White Blood Cells (11-5)
WBCs Larger than RBCs Help defend the body against invasion by pathogens Remove toxins, wastes, and abnormal or damaged cells Contain nucleus and other organelles Lack hemoglobin Number about 5000–10,000 per microliter of blood
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Two Categories of White Blood Cells (11-5)
Granulocytes Neutrophils, eosinophils, basophils Agranulocytes Lymphocytes and monocytes
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WBC Circulation and Movement (11-5)
Four characteristics of circulating WBCs All are capable of amoeboid movement All can migrate outside of bloodstream through process called diapedesis All are attracted to specific chemical stimuli, which guide them to pathogens; process is called positive chemotaxis Neutrophils, eosinophils, and monocytes are phagocytes
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Types of WBCs (11-5) Neutrophils, eosinophils, basophils, and monocytes Part of the body’s nonspecific defenses Respond to any threat Lymphocytes Responsible for specific defenses Respond to specific, individual pathogens
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Neutrophils (11-5) Make up 50–70 percent of circulating WBCs
Have a dense, contorted multilobular nucleus Usually first WBC to arrive at injury site Very active phagocytes, attacking and digesting bacteria
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Eosinophils (11-5) Make up 2–4 percent of circulating WBCs
Have granules that stain deep red and a two-lobed nucleus Are phagocytic, but also attack through exocytosis of toxic compounds Numbers increase during parasitic infection or allergic reactions Release enzymes that reduce inflammation
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Basophils (11-5) Somewhat smaller than neutrophils and eosinophils
Rare, less than 1 percent of circulating WBCs Granules stain deep purple or blue Release: Heparin which prevents blood clotting Histamine which dilates blood vessels
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Monocytes (11-5) About twice the size of a typical RBC with a large, kidney bean–shaped nucleus Usually 2–8 percent of circulating WBCs Migrate into tissues and become macrophages Aggressive phagocytes Figure 11-8d White Blood Cells.
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Lymphocytes (11-5) Slightly larger than typical RBC with nucleus taking up most of cell About 20–40 percent of circulating WBCs Large numbers migrate in and out of peripheral tissues Some attack foreign cells, others secrete antibodies into circulation Figure 11-8e White Blood Cells.
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The Differential WBC Count (11-5)
Indicates the number of each type of cell in a sample of 100 WBCs Provides information about type of disorder, infection, inflammation, or allergic reaction Reduced numbers of WBCs is called leukopenia Excessive numbers of WBCs is called leukocytosis Leukemia Cancer of blood-forming tissues Indicated by extreme leukocytosis or by presence of abnormal or immature WBCs
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Platelets versus Thrombocytes (11-6)
In nonmammalian vertebrates Platelets exist as nucleated cells called thrombocytes In humans Platelets exist as cell fragments of enormous cells called megakaryocytes
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Platelets (11-6) Initiate clotting process and help close injured blood vessels Circulate for 9–12 days Normal count is 150,000–500,000/µL Low count is called thrombocytopenia High count is called thrombocytosis Figure 11-1 The Composition of Whole Blood.
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Three Phases of Hemostasis (11-7)
Hemostasis, or the stopping of bleeding Halts the loss of blood through damaged vessels Establishes framework for tissue repair Three steps Vascular phase Platelet phase Coagulation phase
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The Vascular Phase (11-7) Blood vessels contain smooth muscle lined with endothelium Damage triggers contraction in smooth muscle fibers (called vascular spasm) Decreases vessel diameter Slows or stops loss of blood through wall of small vessel Endothelial cells at the site become “sticky”
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The Platelet Phase (11-7) Occurs within 15 seconds of injury
Platelets attach to sticky endothelium and exposed collagen More platelets arrive and stick to each other forming a platelet plug May be enough to close a small break Figure 11-9 The Vascular, Platelet, and Coagulation Phases of Hemostasis.
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The Coagulation Phase (11-7)
Begins 30 seconds or more after damage Involves complex sequence of steps, or cascade End result is conversion of protein fibrinogen to insoluble fibrin Fibrin mesh grows Traps cells and more platelets Forms a blood clot Seals damaged portion of blood vessel
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The Clotting Process (11-7)
Requires clotting factors Calcium ions, vitamin K, and 11 different plasma proteins Proteins are converted from inactive proenzymes to active enzymes involved in reactions Liver synthesizes most of these clotting proteins Clotting factors interact in a sequence, or cascade Product of first reaction is enzyme that activates second reaction, etc.
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The Extrinsic Pathway of Blood Clotting (11-7)
Begins outside the bloodstream in the vessel wall Starts when damaged tissues release tissue factor More damage = more tissue factor = faster clotting Tissue factor combines with calcium and Factor VII That combination forms an enzyme that can activate Factor X
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The Intrinsic Pathway of Blood Clotting (11-7)
Begins in the bloodstream Starts with activation of proenzymes exposed to collagen fibers at injury site Proceeds with help from platelet factor released from aggregating platelets Several reactions occur, forming an enzyme that can activate Factor X
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The Common Pathway of Blood Clotting (11-7)
Begins when enzymes from either extrinsic or intrinsic pathway activate Factor X Factor X activates prothrombin activator Which converts prothrombin into thrombin Which converts fibrinogen into fibrin And stimulates tissue factor and platelet factors Positive feedback loop accelerates clot formation and rapidly prevents blood loss
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Figure 11-10 The Structure of a Blood Clot.
Platelets Trapped RBC Fibrin network Blood clot containing trapped RBCs SEM × 1850
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Clot Retraction and Removal (11-7)
Fibrin network traps platelets and RBCs Platelets contract, pulling torn edges of vessel closer together in process called clot retraction During repair of tissue, clot dissolves through fibrinolysis Plasminogen is activated by thrombin and tissue plasminogen activator (t-PA) Plasminogen produces plasmin, which digests fibrin strands, breaking down clot
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