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Chapter 18 Lecture PowerPoint
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The Circulatory System: Blood
Introduction Erythrocytes Blood types Leukocytes Platelets and Hemostasis – The Control of Bleeding 18-2
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Circulatory System functions of circulatory system transport
O2, CO2, nutrients, wastes, hormones, stem cells protection inflammation, limit spread of infection, destroy microorganisms and cancer cells, neutralize toxins, initiates clotting regulation fluid balance, stabilizes pH of ECF, temperature control 18-3
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Components and General Properties of Blood
adults have 4-6 L of blood a liquid connective tissue consisting of cells and extracellular matrix plasma – matrix of blood a clear, light yellow fluid formed elements - blood cells and cell fragments red blood cells, white blood cells, and platelets 18-4
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Components and General Properties of Blood
seven kinds of formed elements erythrocytes - red blood cells (RBCs) platelets cell fragments from special cell in bone marrow leukocytes - white blood cells (WBCs) – 5 types 18-5
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Formed Elements of Blood
Monocyte Small lymphocyte Neutrophil Platelets Eosinophil Small lymphocyte Erythrocyte Young (band) neutrophil Neutrophil Monocyte Large lymphocyte Neutrophil Basophil Figure 18.1 18-6
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Separating Plasma From Formed Elements of Blood
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Withdraw blood hematocrit - centrifuge blood to separate components erythrocytes heaviest - settle first 37% to 52% total volume white blood cells and platelets 1% total volume buffy coat plasma 47% - 63% complex mix of water, proteins, nutrients, electrolytes, nitrogenous wastes, hormones, and gases Centrifuge Plasma Buffy coat: leukocytes and platelets Erythrocytes Formed elements Figure 18.2 18-7
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Plasma and Plasma Proteins
plasma – liquid portion of blood 3 major categories of plasma proteins albumins – smallest and most abundant contributes to viscosity and osmolarity, influences blood pressure, flow and fluid balance globulins (antibodies) provide immune system functions fibrinogen helps form blood clots Other substances in blood – glucose, waste, electrolytes 18-8
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Properties of Blood osmolarity of blood - the total molarity of those dissolved particles that cannot pass through the blood vessel wall if too high, blood absorbs too much water, increasing the blood pressure if too low, too much water stays in tissue, blood pressure drops and edema occurs optimum osmolarity is achieved by body’s regulation of sodium ions, proteins, and red blood cells. 18-9
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Starvation and Plasma Proteins
Blood Tissue hypoproteinemia deficiency of plasma proteins extreme starvation liver or kidney disease severe burns kwashiorkor children with severe protein deficiency fed on cereals once weaned thin arms and legs swollen abdomen protein Water flows into tissue by osmosis 18-10
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Erythrocytes two principal functions:
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Capillary wall Erythrocytes Figure 18.4c (c) 7 µm two principal functions: carry oxygen from lungs to cell tissues pick up CO2 from tissues and bring to lungs Not enough RBC’s not enough O2 rapid death 18-12
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Erythrocytes (RBCs) disc-shaped cell with thick rim
lose nearly all organelles blood type determined by surface molecules cytoskeletal proteins give membrane durability and resilience stretch and bend through small capillaries Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Surfaceview 7.5 µm 2.0 µm (a) Sectional view Figure 18.4a 18-13
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Hemoglobin (Hb) Structure
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. each Hb molecule consists of: four protein chains – globins four heme groups heme groups nonprotein moiety that binds O2 to ferrous ion (Fe2+) Beta Alpha Heme groups (a) Alpha Beta CH3 CH CH2 C C HC C C CH C N C CH3 C C CH3 N Fe2+ N CH2 C C CH CH2 C N C CH2 HC C C CH COOH C C CH2 CH3 CH2 COOH (b) Figure 18.5 a-b 18-14 14
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Erythrocyte Production (Erythropoiesis)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pluripotent stem cell Colony-forming unit (CFU) Precursor cells Mature cell Erythrocyte CFU Erythroblast Reticulocyte Erythrocyte Figure 18.6 Produced in red bone marrow 2.5 million RBCs produced per second average lifespan of about 120 days development takes 3-5 days first committed cell - erythrocyte colony forming unit has receptors for erythropoietin (EPO) from kidneys 18-15
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Erythrocyte Homeostasis
negative feedback control drop in RBC count causes kidney hypoxemia kidney production of erythropoietin stimulates bone marrow RBC count increases in days stimuli for increasing erythropoiesis low levels O2 (hypoxemia) high altitude increase in exercise loss of lung tissue in emphysema Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Hypoxemia (inadequate O2 transport) Increased O2 transport Sensed by liver and kidneys leaves Increased RBC count Accelerated erythropoiesis Secretion of erythropoietin Stimulation of red bone marrow Figure 18.8 18-16
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Erythrocyte Disorders
polycythemia - an excess of RBCs primary polycythemia cancer of erythropoietic cell line in red bone marrow secondary polycythemia from dehydration, emphysema, high altitude, or physical conditioning dangers of polycythemia increased blood volume, pressure, viscosity can lead to embolism, stroke or heart failure 18-17
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Anemia causes of anemia fall into three categories:
inadequate erythropoiesis or hemoglobin synthesis kidney failure and insufficient erythropoietin iron-deficiency anemia inadequate vitamin B12 from poor nutrition or lack of intrinsic factor (pernicious anemia) hemorrhagic anemias from bleeding hemolytic anemias from RBC destruction 18-18
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Anemia anemia has three potential consequences:
tissue hypoxia and necrosis patient is lethargic shortness of breath upon exertion life-threatening necrosis of brain, heart, or kidney blood osmolarity is reduced, producing tissue edema blood viscosity is low heart races and pressure drops cardiac failure may ensue 18-19
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© Meckes/Ottawa/Photo Researchers, Inc.
Sickle-Cell Disease Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. hereditary hemoglobin defect -mostly among people of African descent recessive allele that modifies the structure of the hemoglobin molecule (HbS) HbS does not bind oxygen well RBCs become rigid, sticky, pointed at ends clump together and block small blood vessels: intense pain can lead to kidney or heart failure, stroke, rheumatism or paralysis 7 µm © Meckes/Ottawa/Photo Researchers, Inc. Figure 18.10 18-20
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Blood Types RBC antigens called agglutinogens
called antigen A and B determined by molecules found on RBC surface antibodies called agglutinins found in plasma anti-A and anti-B Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Type O Type B leaves Type A Type AB Key Galactose Fucose N-acetylgalactosamine Figure 18.12 18-21
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ABO Group your ABO blood type is determined by presence or absence of antigens (agglutinogens) on RBCs blood type A person has A antigens blood type B person has B antigens blood type AB has both A and B antigens blood type O person has neither antigen most common - type O rarest - type AB 18-22
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Plasma Antibodies antibodies (agglutinins); anti-A and anti-B
we have antibodies to the antigens we don’t have (if you are type A, you have anti-B; if you are type O, you have anti-A and anti-B, etc.) agglutination each antibody can attach to several foreign antigens on several different RBCs at the same time - clumps the blood 18-23
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Agglutination of Erythrocytes
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Antibodies (agglutinins) Figure 18.13 18-24
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Transfusion Reaction Figure 18.15 Blood from type A donor Type B
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Blood from type A donor leaves Type B (anti-A) recipient Donor RBCs agglutinated by recipient plasma Agglutinated RBCs block small vessels Figure 18.15 18-25
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Leukocytes (WBCs) least abundant formed element
protect against infectious microorganisms and other pathogens conspicuous nucleus spend only a few hours in the blood stream before migrating to connective tissue retain their organelles for protein synthesis 18-27
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Types of Leukocytes granulocytes agranulocytes neutrophils (60-70%)-
eosinophils (2-4%) basophils (<1%) agranulocytes lymphocytes (25-33%) monocytes (3-8%) 18-28
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Granulocytes Figure TA 18.1 Figure TA 18.2 Figure TA 18.3 Neutrophils
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Neutrophils 10 µm Eosinophil 10 µm Basophil 10 µm all: © Ed Reschke Figure TA 18.1 Figure TA 18.2 Figure TA 18.3 18-29
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both: Michael Ross/Photo Researchers, Inc.
Agranulocytes Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lymphocyte 10 µm Monocyte 10 µm both: Michael Ross/Photo Researchers, Inc. Figure TA 18.4 Figure TA 18.5 18-30
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Leukopoiesis Figure 18.18 Eosinophil Basophil Neutrophil Monocyte
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Pluripotent stem cell Colony-forming units (CFUs) Precursor cells Mature cells Eosinophil leaves Eosinophilic CFU Eosinophilic myeloblast Eosinophilic promyelocyte Eosinophilic myelocyte Basophil Basophilic CFU Basophilic myeloblast Basophilic promyelocyte Basophilic myelocyte Neutrophil Neutrophilic CFU Neutrophilic myeloblast Neutrophilic promyelocyte Neutrophilic myelocyte Monocyte Monocytic CFU Monoblast Promonocyte B lymphocyte B prolymphocyte T lymphocyte T prolymphocyte Lymphocytic CFU Lymphoblast Figure 18.18 NK cell 18-31 NK prolymphocyte
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Leukocyte Disorders leukopenia - low WBC count below 5000/L
causes: radiation, poisons, infectious disease effects: elevated risk of infection leukocytosis - high WBC count above 10,000/L causes: infection, allergy and disease differential WBC count – identifies what percentage of the total WBC count consists of each type of leukocyte patient subject to opportunistic infection, anemia 18-32 32
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Leukocyte Disorders leukemia - cancer of hemopoietic tissue - produces an extremely high number of circulating leukocytes and their precursors myeloid leukemia – uncontrolled granulocyte production lymphoid leukemia - uncontrolled lymphocyte or monocyte production acute leukemia – appears suddenly, progresses rapidly, death within months chronic leukemia –undetected for months, survival time three years effects - impaired clotting; opportunistic infections patient subject to opportunistic infection, anemia 18-33 33
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Normal and Leukemic Blood
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Platelets Monocyte Neutrophils Lymphocyte Erythrocytes (a) Figure a-b (b) 75 µm 18-34 © Ed Reschke
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Hemostasis hemostasis – the cessation of bleeding
stopping potentially fatal leaks hemorrhage – excessive bleeding three hemostatic mechanisms vascular spasm platelet plug formation blood clotting (coagulation) platelets play an important role in all three 18-36
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Platelets platelets - small fragments of megakaryocyte cells functions
secrete vasoconstrictors that help reduce blood loss stick together to form platelet plugs to seal small breaks secrete procoagulants or clotting factors promote clotting chemically attract neutrophils and monocytes to sites of inflammation phagocytize and destroy bacteria 18-37
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all 3 pathways involve platelets
Hemostasis Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Vasoconstriction Platelet plug Blood clot Platelet Vessel injury Collagen fibers Endothelial cells (a) Vascular spasm (b) Platelet plug formation (c) Coagulation Figure a-c all 3 pathways involve platelets 18-38
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Hemostasis - Vascular Spasm
vascular spasm - prompt constriction of a broken vessel most immediate protection against blood loss causes: pain receptors some directly innervate blood vessels to constrict smooth muscle injury platelets release serotonin (vasoconstrictor) effects: prompt constriction of a broken vessel provides time for other two clotting pathways 18-39
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Hemostasis -Platelet Plug Formation
broken vessel exposes collagen platelet pseudopods stick to damaged collagen and other platelets - pseudopods contract and draw walls of vessel together platelet plug platelets degranulate releasing a variety of substances positive feedback cycle is active until break in small vessel is sealed 18-40
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Hemostasis - Coagulation
coagulation (clotting) – last and most effective defense against bleeding conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot procoagulants (clotting factors), usually produced by the liver, are present in plasma activate one factor and it will activate the next to form a reaction cascade 18-41
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© P. Motta/SPL/Photo Researchers, Inc.
SEM of Blood Clot Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 18.22 © P. Motta/SPL/Photo Researchers, Inc. 18-42
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Enzyme Amplification in Clotting
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Factor XII Factor XI Factor IX Figure 18.24 Factor VIII Reaction cascade (time) Factor X Prothrombin activator Thrombin Fibrin rapid clotting - each activated cofactor activates many more molecules in next step of sequence 18-43
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Clotting Disorders - Hemophilia
deficiency of any clotting factor can shut down the coagulation cascade hemophilia – family of hereditary diseases characterized by deficiencies of one factor or another sex-linked recessive (on X chromosome) physical exertion causes bleeding and severe pain Treatment transfusion of plasma or purified clotting factors factor VIII produced by transgenic bacteria 18-44
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Coagulation Disorders
thrombosis - abnormal clotting in unbroken vessel thrombus - clot most likely to occur in leg veins of inactive people pulmonary embolism - clot may break free, travel from veins to lungs embolus – anything that can travel in the blood and block blood vessels infarction (tissue death) may occur if clot blocks blood supply to an organ (MI or stroke) 650,000 Americans die annually of thromboembolism – traveling blood clots 18-45
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