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Blood Anatomy and Physiology PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Blood Anatomy and Physiology” by Dr Nishant Verma.

This medical PowerPoint presentation is about blood, a fluid connective tissue that circulates throughout the body, carrying nutrients, oxygen, and waste products to and from the cells. It is composed of cells and plasma, a liquid portion that contains dissolved substances such as electrolytes, hormones, and proteins.

Anatomy: There are three types of cells found in blood: red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes). Red blood cells are the most abundant, and they transport oxygen from the lungs to the body tissues. White blood cells are involved in the immune response and help fight infections. Platelets are important for blood clotting and prevent excessive bleeding.

Physiology: Blood carries oxygen from the lungs to the body tissues and carbon dioxide from the tissues to the lungs. It also carries nutrients such as glucose, amino acids, and fatty acids from the digestive system to the cells and removes waste products such as urea and lactic acid from the cells to be eliminated from the body.

Tags : Blood Anatomy and Physiology, blood, red blood cells, erythrocytes, white blood cells, leukocytes, platelets, thrombocytes, Hematology, Hematology PowerPoint presentation

Published on : May 29, 2023 | Views : 3332 | Downloads : 6

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Slide 1-

19 Blood
Slide 2-

An Introduction to Blood and the Cardiovascular System Learning Outcomes 19-1 Describe the components and major functions of blood, identify blood collection sites, and list the physical characteristics of blood. 19-2 Specify the composition and functions of plasma. 19-3 List the characteristics and functions of red blood cells, describe the structure and functions of hemoglobin, describe how red blood cell components are recycled, and explain erythropoiesis.
Slide 3-

An Introduction to Blood and the Cardiovascular System Learning Outcomes 19-4 Explain the importance of blood typing, and the basis for ABO and Rh incompatibilities. 19-5 Categorize white blood cell types based on their structures and functions, and discuss the factors that regulate the production of each type. 19-6 Describe the structure, function, and production of platelets. 19-7 Discuss the mechanisms that control blood loss after an injury, and describe the reaction sequences responsible for blood clotting.
Slide 4-

An Introduction to Blood and the Cardiovascular System The Cardiovascular System consists of: A pump (the heart) A conducting system (blood vessels) A fluid medium (blood) Is specialized fluid of connective tissue Contains cells suspended in a fluid matrix
Slide 5-

An Introduction to Blood and the Cardiovascular System Blood Transports materials to and from cells Oxygen and carbon dioxide Nutrients Hormones Immune system components Waste products
Slide 6-

19-1 Physical Characteristics of Blood Important Functions of Blood Transportation of dissolved substances Regulation of pH and ions Restriction of fluid losses at injury sites Defense against toxins and pathogens Stabilization of body temperature
Slide 7-

19-1 Physical Characteristics of Blood Whole Blood Plasma Fluid consisting of: Water Dissolved plasma proteins Other solutes Formed elements All cells and solids
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Figure 19-1 The Composition of Whole Blood Plasma Proteins Other Solutes Water Platelets White Blood Cells Red Blood Cells Plasma Formed Elements 46–63% 37–54% 7% 1% 92% < .1% < .1% 99.9%
Slide 9-

19-1 Physical Characteristics of Blood Three Types of Formed Elements Red blood cells (RBCs) or erythrocytes Transport oxygen White blood cells (WBCs) or leukocytes Part of the immune system Platelets Cell fragments involved in clotting
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19-1 Physical Characteristics of Blood Hemopoiesis Process of producing formed elements By myeloid and lymphoid stem cells Fractionation Process of separating whole blood for clinical analysis Into plasma and formed elements
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19-1 Physical Characteristics of Blood Three General Characteristics of Blood 38C (100.4F) is normal temperature High viscosity Slightly alkaline pH (7.35–7.45)
Slide 12-

19-1 Physical Characteristics of Blood Characteristics of Blood Blood volume (liters) = 7% of body weight (kilograms) Adult male 5 to 6 liters Adult female 4 to 5 liters
Slide 13-

19-2 Plasma The Composition of Plasma Makes up 50–60% of blood volume More than 90% of plasma is water Extracellular fluids Interstitial fluid (IF) and plasma Materials plasma and IF exchange across capillary walls Water Ions Small solutes
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19-2 Plasma Plasma Proteins Albumins (60%) Globulins (35%) Fibrinogen (4%)
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19-2 Plasma Albumins (60%) Transport substances such as fatty acids, thyroid hormones, and steroid hormones Globulins (35%) Antibodies, also called immunoglobulins Transport globulins (small molecules): hormone-binding proteins, metalloproteins, apolipoproteins (lipoproteins), and steroid-binding proteins Fibrinogen (4%) Molecules that form clots and produce long, insoluble strands of fibrin
Slide 16-

19-2 Plasma Serum Liquid part of a blood sample In which dissolved fibrinogen has converted to solid fibrin
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19-2 Plasma Other Plasma Proteins 1% of plasma Changing quantities of specialized plasma proteins Peptide hormones normally present in circulating blood Insulin, prolactin (PRL), and the glycoproteins thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH)
Slide 18-

19-2 Plasma Origins of Plasma Proteins More than 90% made in liver Antibodies made by plasma cells Peptide hormones made by endocrine organs
Slide 19-

19-3 Red Blood Cells Red blood cells (RBCs) Make up 99.9% of blood’s formed elements Hemoglobin The red pigment that gives whole blood its color Binds and transports oxygen and carbon dioxide
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19-3 Red Blood Cells Abundance of RBCs Red blood cell count - the number of RBCs in 1 microliter of whole blood Male: 4.5–6.3 million Female: 4.2–5.5 million
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19-3 Red Blood Cells Abundance of RBCs Hematocrit - (packed cell volume, PCV) percentage of RBCs in centrifuged whole blood Male: 40–54 Female: 37–47
Slide 22-

19-3 Red Blood Cells Structure of RBCs Small and highly specialized discs Thin in middle and thicker at edge
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19-3 Red Blood Cells Three Important Effects of RBC Shape on Function High surface-to-volume ratio Quickly absorbs and releases oxygen Discs form stacks called rouleaux Smooth the flow through narrow blood vessels Discs bend and flex entering small capillaries 7.8-µm RBC passes through 4-µm capillary
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Figure 19-2a The Anatomy of Red Blood Cells Blood smear When viewed in a standard blood smear, RBCs appear as two-dimensional objects, because they are flattened against the surface of the slide. LM  477
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Figure 19-2b The Anatomy of Red Blood Cells Red blood cells The three-dimensional shape of RBCs SEM  1838
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Figure 19-2c The Anatomy of Red Blood Cells A sectional view of a mature RBC, showing the normal ranges for its dimensions 0.45–1.16 μm 2.31–2.85 μm 7.2–8.4 μm
Slide 27-

Figure 19-2d The Anatomy of Red Blood Cells Sectioned capillaries Red blood cell (RBC) Rouleau (stacked RBCs) Nucleus of endothelial cell Blood vessels (viewed in longitudinal section) When traveling through relatively narrow capillaries, RBCs may stack like dinner plates. LM  1430
Slide 28-

19-3 Red Blood Cells Life Span of RBCs Lack nuclei, mitochondria, and ribosomes Means no repair and anaerobic metabolism Live about 120 days
Slide 29-

19-3 Red Blood Cells Hemoglobin (Hb) Protein molecule that transports respiratory gases Normal hemoglobin (adult male) 14–18 g/dL whole blood Normal hemoglobin (adult female) 12–16 g/dL whole blood
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19-3 Red Blood Cells Hemoglobin Structure Complex quaternary structure Four globular protein subunits Each with one molecule of heme Each heme contains one iron ion
Slide 31-

19-3 Red Blood Cells Hemoglobin Structure Iron ions Associate easily with oxygen (oxyhemoglobin, HbO2) Dissociate easily from oxygen (deoxyhemoglobin)
Slide 32-

Figure 19-3 The Structure of Hemoglobin Hemoglobin molecule Heme Heme  chain 2  chain 2  chain 1  chain 1
Slide 33-

19-3 Red Blood Cells Fetal Hemoglobin Strong form of hemoglobin found in embryos Takes oxygen from mother’s hemoglobin
Slide 34-

19-3 Red Blood Cells Hemoglobin Function Carries oxygen With low oxygen (peripheral capillaries) Hemoglobin releases oxygen Binds carbon dioxide and carries it to lungs Forms carbaminohemoglobin
Slide 35-

Figure 19-4 “Sickling” in Red Blood Cells
Slide 36-

19-3 Red Blood Cells RBC Formation and Turnover 1% of circulating RBCs wear out per day About 3 million RBCs per second Hemoglobin Conversion and Recycling Macrophages of liver, spleen, and bone marrow Monitor RBCs Engulf RBCs before membranes rupture (hemolyze)
Slide 37-

19-3 Red Blood Cells Hemoglobin Conversion and Recycling Phagocytes break hemoglobin into components Globular proteins to amino acids Heme to biliverdin Iron
Slide 38-

19-3 Red Blood Cells Hemoglobin Conversion and Recycling Hemoglobinuria Hemoglobin breakdown products in urine due to excess hemolysis in bloodstream Hematuria Whole red blood cells in urine due to kidney or tissue damage
Slide 39-

19-3 Red Blood Cells Breakdown of Biliverdin Biliverdin (green) is converted to bilirubin (yellow) Bilirubin Is excreted by liver (bile) Jaundice is caused by bilirubin buildup Converted by intestinal bacteria to urobilins and stercobilins
Slide 40-

19-3 Red Blood Cells Iron Recycling Iron removed from heme leaving biliverdin To transport proteins (transferrin) To storage proteins (ferritin and hemosiderin)
Slide 41-

Figure 19-5 Recycling of Red Blood Cell Components Events Occurring in Macrophages Macrophages in liver, spleen, and bone marrow Heme Biliverdin Bilirubin Bilirubin bound to albumin in bloodstream Amino acids Liver Bilirubin Bilirubin Excreted in bile Urobilins, stercobilins Events Occurring in the Liver Events Occurring in the Large Intestine Eliminated in feces Absorbed into the circulation Events Occurring in the Kidney Eliminated in urine Urobilins Kidney Hb Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Fe2+ Fe2+ transported in circulation by transferrin 90% 10% Old and damaged RBCs Average life span of RBC is 120 days In the bloodstream, the rupture of RBCs is called hemolysis. New RBCs released into circulation RBC formation Events Occurring in the Red Bone Marrow
Slide 42-

Figure 19-5 Recycling of Red Blood Cell Components Events Occurring in Macrophages Macrophages in liver, spleen, and bone marrow Heme Biliverdin Bilirubin Bilirubin bound to albumin in bloodstream Amino acids Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Fe2+ Fe2+ transported in circulation by transferrin 90% 10% Old and damaged RBCs Average life span of RBC is 120 days In the bloodstream, the rupture of RBCs is called hemolysis.
Slide 43-

Figure 19-5 Recycling of Red Blood Cell Components Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Fe2+ transported in circulation by transferrin Average life span of RBC is 120 days In the bloodstream, the rupture of RBCs is called hemolysis. New RBCs released into circulation RBC formation Events Occurring in the Red Bone Marrow
Slide 44-

Figure 19-5 Recycling of Red Blood Cell Components Liver Bilirubin Bilirubin Excreted in bile Urobilins, stercobilins Events Occurring in the Liver Absorbed into the circulation Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Bilirubin bound to albumin in bloodstream
Slide 45-

Figure 19-5 Recycling of Red Blood Cell Components Urobilins, stercobilins Eliminated in feces Absorbed into the circulation Events Occurring in the Kidney Eliminated in urine Urobilins Kidney Hb Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Bilirubin Events Occurring in the Large Intestine
Slide 46-

19-3 Red Blood Cells RBC Production Erythropoiesis Occurs only in myeloid tissue (red bone marrow) in adults Stem cells mature to become RBCs
Slide 47-

19-3 Red Blood Cells Hemocytoblasts Stem cells in myeloid tissue divide to produce: Myeloid stem cells become RBCs, some WBCs Lymphoid stem cells become lymphocytes
Slide 48-

19-3 Red Blood Cells Stages of RBC Maturation Myeloid stem cell Proerythroblast Erythroblasts Reticulocyte Mature RBC
Slide 49-

Figure 19-6 Stages of RBC Maturation Day 1: Proerythroblast Day 2: Basophilic erythroblast Day 3: Polychromatophilic erythroblast Day 4: Normoblast Days 5–7: Reticulocyte Ejection of nucleus Erythroblasts RED BONE MARROW Enters circulation Mature red blood cell
Slide 50-

19-3 Red Blood Cells Regulation of Erythropoiesis Building red blood cells requires: Amino acids Iron Vitamins B12, B6, and folic acid Pernicious anemia Low RBC production Due to unavailability of vitamin B12
Slide 51-

19-3 Red Blood Cells Stimulating Hormones Erythropoietin (EPO) Also called erythropoiesis-stimulating hormone Secreted when oxygen in peripheral tissues is low (hypoxia) Due to disease or high altitude
Slide 52-

Table 19-1 RBC Tests and Related Terminology
Slide 53-

Table 19-3 Formed Elements of the Blood
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19-4 Blood Typing Surface Antigens Are cell surface proteins that identify cells to immune system Normal cells are ignored and foreign cells attacked Blood Types Are genetically determined By presence or absence of RBC surface antigens A, B, Rh (or D)
Slide 55-

19-4 Blood Typing Four Basic Blood Types A (surface antigen A) B (surface antigen B) AB (antigens A and B) O (neither A nor B)
Slide 56-

19-4 Blood Typing Agglutinogens Antigens on surface of RBCs Screened by immune system Plasma antibodies attack and agglutinate (clump) foreign antigens
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19-4 Blood Typing Blood Plasma Antibodies Type A Type B antibodies Type B Type A antibodies Type O Both A and B antibodies Type AB Neither A nor B antibodies
Slide 58-

Figure 19-7a Blood Types and Cross-Reactions Type A Type B Type A blood has RBCs with surface antigen A only. Type B blood has RBCs with surface antigen B only. Surface antigen A Surface antigen B If you have Type A blood, your plasma contains anti-B antibodies, which will attack Type B surface antigens. If you have Type B blood, your plasma contains anti-A antibodies, which will attack Type A surface antigens.
Slide 59-

Figure 19-7a Blood Types and Cross-Reactions Type AB Type O Type AB blood has RBCs with both A and B surface antigens. Type O blood has RBCs lacking both A and B surface antigens. If you have Type AB blood, your plasma has neither anti-A nor anti-B antibodies. If you have Type O blood, your plasma contains both anti-A and anti-B antibodies.
Slide 60-

19-4 Blood Typing The Rh Factor Also called D antigen Either Rh positive (Rh) or Rh negative (Rh) Only sensitized Rh blood has anti-Rh antibodies
Slide 61-

Figure 19-9 Hemolytic Disease of the Newborn Problems seldom develop during a first pregnancy, because very few fetal cells enter the maternal circulation then, and thus the mother’s immune system is not stimulated to produce anti-Rh antibodies. Fetal blood supply and tissue Maternal blood supply and tissue During First Pregnancy Placenta The most common form of hemolytic disease of the newborn develops after an Rh– woman has carried an Rh+ fetus. Rh+ fetus Rh– mother
Slide 62-

Figure 19-9 Hemolytic Disease of the Newborn Exposure to fetal red blood cell antigens generally occurs during delivery, when bleeding takes place at the placenta and uterus. Such mixing of fetal and maternal blood can stimulate the mother’s immune system to produce anti-Rh antibodies, leading to sensitization. Hemorrhaging at Delivery Maternal blood supply and tissue Fetal blood supply and tissue Rh antigen on fetal red blood cells
Slide 63-

Figure 19-9 Hemolytic Disease of the Newborn Roughly 20% of Rh– mothers who carried Rh+ children become sensitized within 6 months of delivery. Because the anti-Rh antibodies are not produced in significant amounts until after delivery, a woman’s first infant is not affected. Maternal antibodies to Rh antigen Maternal blood supply and tissue Maternal Antibody Production
Slide 64-

Figure 19-9 Hemolytic Disease of the Newborn In a subsequent pregnancy, the mother is sensitized to the Rh+ fetus. Therefore, the mother’s anti-Rh antibodies cross the placenta and attack the fetal red blood cells. During Second Pregnancy Fetal blood supply and tissue Maternal blood supply and tissue Maternal anti-Rh antibodies Rh+ fetus Rh– mother Hemolysis of fetal RBCs
Slide 65-

19-4 Blood Typing Cross-Reactions in Transfusions Also called transfusion reaction Plasma antibody meets its specific surface antigen Blood will agglutinate and hemolyze Occur if donor and recipient blood types not compatible
Slide 66-

Figure 19-7b Blood Types and Cross-Reactions In a cross-reaction, antibodies react with their target antigens causing agglutination and hemolysis of the affected RBCs. Surface antigens Opposing antibodies RBC Agglutination (clumping) Hemolysis
Slide 67-

19-4 Blood Typing Testing for Transfusion Compatibility Performed on donor and recipient blood for compatibility Without cross-match, type O is universal donor
Slide 68-

Figure 19-8 Blood Type Testing Anti-A Anti-B Anti-D Blood type B+ AB+ O– A+
Slide 69-

Table 19-2 Differences in Blood Group Distribution
Slide 70-

19-5 White Blood Cells White Blood Cells (WBCs) Also called leukocytes Do not have hemoglobin Have nuclei and other organelles WBC functions: Defend against pathogens Remove toxins and wastes Attack abnormal cells
Slide 71-

19-5 White Blood Cells WBC Circulation and Movement Most WBCs in: Connective tissue proper Lymphatic system organs Small numbers in blood 5000 to 10,000 per microliter
Slide 72-

19-5 White Blood Cells WBC Circulation and Movement Four Characteristics of Circulating WBCs Can migrate out of bloodstream Have amoeboid movement Attracted to chemical stimuli (positive chemotaxis) Some are phagocytic Neutrophils, eosinophils, and monocytes
Slide 73-

19-5 White Blood Cells Types of WBCs Neutrophils Eosinophils Basophils Monocytes Lymphocytes
Slide 74-

Figure 19-10 White Blood Cells LM  1500 Neutrophil LM  1500 LM  1500 LM  1500 LM  1500 Eosinophil Basophil Monocyte Lymphocyte RBC RBC RBC RBC RBC
Slide 75-

19-5 White Blood Cells Neutrophils Also called polymorphonuclear leukocytes 50–70% of circulating WBCs Pale cytoplasm granules with: Lysosomal enzymes Bactericides (hydrogen peroxide and superoxide)
Slide 76-

19-5 White Blood Cells Neutrophil Action Very active, first to attack bacteria Engulf and digest pathogens Degranulation Removing granules from cytoplasm Defensins (peptides from lysosomes) attack pathogen membranes Release prostaglandins and leukotrienes Form pus
Slide 77-

Figure 19-10a White Blood Cells Neutrophil LM  1500 RBC
Slide 78-

19-5 White Blood Cells Eosinophils (Acidophils) 2–4% of circulating WBCs Attack large parasites Excrete toxic compounds Nitric oxide Cytotoxic enzymes Are sensitive to allergens Control inflammation with enzymes that counteract inflammatory effects of neutrophils and mast cells
Slide 79-

Figure 19-10b White Blood Cells LM  1500 Eosinophil RBC
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19-5 White Blood Cells Basophils Are less than 1% of circulating WBCs Accumulate in damaged tissue Release histamine Dilates blood vessels Release heparin Prevents blood clotting
Slide 81-

Figure 19-10c White Blood Cells LM  1500 Basophil RBC
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19-5 White Blood Cells Monocytes 2–8% of circulating WBCs Are large and spherical Enter peripheral tissues and become macrophages Engulf large particles and pathogens Secrete substances that attract immune system cells and fibrocytes to injured area
Slide 83-

Figure 19-10d White Blood Cells LM  1500 Monocyte RBC
Slide 84-

19-5 White Blood Cells Lymphocytes 20–30% of circulating WBCs Are larger than RBCs Migrate in and out of blood Mostly in connective tissues and lymphoid organs Are part of the body’s specific defense system
Slide 85-

Figure 19-10e White Blood Cells LM  1500 Lymphocyte RBC
Slide 86-

19-5 White Blood Cells Three Classes of Lymphocytes T cells Cell-mediated immunity Attack foreign cells directly
Slide 87-

19-5 White Blood Cells Three Classes of Lymphocytes B cells Humoral immunity Differentiate into plasma cells Synthesize antibodies Natural killer (NK) cells Detect and destroy abnormal tissue cells (cancers)
Slide 88-

19-5 White Blood Cells The Differential Count and Changes in WBC Profiles Detects changes in WBC populations Infections, inflammation, and allergic reactions
Slide 89-

19-5 White Blood Cells WBC Disorders Leukopenia Abnormally low WBC count Leukocytosis Abnormally high WBC count Leukemia Extremely high WBC count
Slide 90-

19-5 White Blood Cells WBC Production All blood cells originate from hemocytoblasts Which produce progenitor cells called myeloid stem cells and lymphoid stem cells
Slide 91-

19-5 White Blood Cells WBC Production Myeloid Stem Cells Produce all WBCs except lymphocytes Lymphoid Stem Cells Lymphopoiesis - the production of lymphocytes
Slide 92-

19-5 White Blood Cells WBC Development WBCs, except monocytes Develop in bone marrow Monocytes Develop into macrophages in peripheral tissues
Slide 93-

19-5 White Blood Cells Regulation of WBC Production Colony-stimulating factors (CSFs) Hormones that regulate blood cell populations M-CSF stimulates monocyte production G-CSF stimulates production of granulocytes (neutrophils, eosinophils, and basophils) GM-CSF stimulates granulocyte and monocyte production Multi-CSF accelerates production of granulocytes, monocytes, platelets, and RBCs
Slide 94-

Table 19-3 Formed Elements of the Blood
Slide 95-

Table 19-3 Formed Elements of the Blood
Slide 96-

Figure 19-11 The Origins and Differentiation of Formed Elements Blast Cells Progenitor Cells Lymphoid Stem Cells Myeloid Stem Cells Hemocytoblasts Red bone marrow Proerythroblast Erythroblast stages Ejection of nucleus Reticulocyte Erythrocyte Red Blood Cells (RBCs) Megakaryocyte Platelets Myelocytes Band Cells Agranulocytes Monoblast Promonocyte Monocyte Lymphoblast Prolymphocyte Lymphocyte Myeloblast Basophil Eosinophil Neutrophil Granulocytes White Blood Cells (WBCs)
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Figure 19-11 The Origins and Differentiation of Formed Elements Progenitor Cells Lymphoid Stem Cells Myeloid Stem Cells Hemocytoblasts Red bone marrow
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Figure 19-11 The Origins and Differentiation of Formed Elements Blast Cells Proerythroblast Monoblast Lymphoblast Myeloblast
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Figure 19-11 The Origins and Differentiation of Formed Elements Erythroblast stages Ejection of nucleus Reticulocyte Megakaryocyte Myelocytes Band Cells Promonocyte Prolymphocyte
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Figure 19-11 The Origins and Differentiation of Formed Elements Erythrocyte Red Blood Cells (RBCs) Platelets Agranulocytes Monocyte Lymphocyte Basophil Eosinophil Neutrophil Granulocytes White Blood Cells (WBCs)
Slide 101-

19-6 Platelets Platelets Cell fragments involved in human clotting system Nonmammalian vertebrates have thrombocytes (nucleated cells) Circulate for 9–12 days Are removed by spleen 2/3 are reserved for emergencies
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19-6 Platelets Platelet Counts 150,000 to 500,000 per microliter Thrombocytopenia Abnormally low platelet count Thrombocytosis Abnormally high platelet count
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19-6 Platelets Three Functions of Platelets Release important clotting chemicals Temporarily patch damaged vessel walls Reduce size of a break in vessel wall
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19-6 Platelets Platelet Production Also called thrombocytopoiesis Occurs in bone marrow Megakaryocytes Giant cells in bone marrow Manufacture platelets from cytoplasm
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19-6 Platelets Platelet Production Hormonal controls Thrombopoietin (TPO) Interleukin-6 (IL-6) Multi-CSF
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Table 19-3 Formed Elements of the Blood
Slide 107-

19-7 Hemostasis Hemostasis Is the cessation of bleeding Consists of three phases Vascular phase Platelet phase Coagulation phase
Slide 108-

19-7 Hemostasis The Vascular Phase A cut triggers vascular spasm that lasts 30 minutes Three Steps of the Vascular Phase Endothelial cells contract and expose basement membrane to bloodstream
Slide 109-

19-7 Hemostasis Three Steps of the Vascular Phase Endothelial cells Release chemical factors ADP, tissue factor, and prostacyclin Release local hormones, endothelins Stimulate smooth muscle contraction and cell division Endothelial plasma membranes become “sticky” Seal off blood flow
Slide 110-

Figure 19-12 The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 1) Vascular Phase The vascular phase of hemostasis lasts for roughly 30 minutes after the injury occurs. The endothelial cells contract and release endothelins which stimulate smooth muscle contraction and endothelial division. The endothelial cells become “sticky” and adhere to platelets and each other. Knife blade Blood vessel injury Vascular spasm
Slide 111-

19-7 Hemostasis The Platelet Phase Begins within 15 seconds after injury Platelet adhesion (attachment) To sticky endothelial surfaces To basement membranes To exposed collagen fibers Platelet aggregation (stick together) Forms platelet plug which closes small breaks
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19-7 Hemostasis Platelet Phase Activated platelets release clotting compounds Adenosine diphosphate (ADP) Thromboxane A2 and serotonin Clotting factors Platelet-derived growth factor (PDGF) Calcium ions
Slide 113-

19-7 Hemostasis Factors That Limit the Growth of the Platelet Plug Prostacyclin, released by endothelial cells, inhibits platelet aggregation Inhibitory compounds released by other WBCs Circulating enzymes break down ADP Negative (inhibitory) feedback from serotonin Development of blood clot isolates area
Slide 114-

Figure 19-12 The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 2) Platelet Phase The platelet phase of hemostasis begins with the attachment of platelets to sticky endothelial surfaces, to the basement membrane, to exposed collagen fibers, and to each other. As they become activated, platelets release a variety of chemicals that promote aggregation, vascular spasm, clotting, and vessel repair. Release of chemicals (ADP, PDGF, Ca2+, platelet factors) Plasma in vessel lumen Platelet adhesion to damaged vessel Platelet aggregation Endothelium Basement membrane Vessel wall Contracted smooth muscle cells Platelet plug may form Interstitial fluid Cut edge of vessel wall
Slide 115-

19-7 Hemostasis The Coagulation Phase Begins 30 seconds or more after the injury Blood clotting (coagulation) Cascade reactions Chain reactions of enzymes and proenzymes Form three pathways Convert circulating fibrinogen into insoluble fibrin
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19-7 Hemostasis Clotting Factors Also called procoagulants Proteins or ions in plasma Required for normal clotting
Slide 117-

Table 19-4 Clotting Factors
Slide 118-

19-7 Hemostasis Three Coagulation Pathways Extrinsic pathway Intrinsic pathway Common pathway
Slide 119-

19-7 Hemostasis The Extrinsic Pathway Begins in the vessel wall Outside bloodstream Damaged cells release tissue factor (TF) TF + other compounds = enzyme complex Activates Factor X
Slide 120-

19-7 Hemostasis The Intrinsic Pathway Begins with circulating proenzymes Within bloodstream Activation of enzymes by collagen Platelets release factors (e.g., PF-3) Series of reactions activates Factor X
Slide 121-

19-7 Hemostasis The Common Pathway Where intrinsic and extrinsic pathways converge Forms enzyme prothrombinase Converts prothrombin to thrombin Thrombin converts fibrinogen to fibrin
Slide 122-

Figure 19-12 The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 3) Coagulation Phase Coagulation, or blood clotting, involves a complex sequence of steps leading to the conversion of circulating fibrinogen into the insoluble protein fibrin. As the fibrin network grows, blood cells and additional platelets are trapped in the fibrous tangle, forming a blood clot that seals off the damaged portion of the vessel. Prothrombin Prothrombinase Factor X Tissue factor complex Tissue factor (Factor III) Tissue damage Contracted smooth muscle cells Platelet factor (PF-3) Fibrinogen Fibrin Thrombin Clotting factor (VII) Common Pathway Extrinsic Pathway Ca2+ Intrinsic Pathway Factor X activator complex Clotting factors (VIII, IX) Activated proenzymes (usually Factor XII) Blood clot containing trapped RBCs SEM  1200 Ca2+
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19-7 Hemostasis Feedback Control of Blood Clotting Stimulates formation of tissue factor Stimulates release of PF-3 Forms positive feedback loop (intrinsic and extrinsic) Accelerates clotting
Slide 124-

19-7 Hemostasis Feedback Control of Blood Clotting Anticoagulants (plasma proteins) Antithrombin-III Alpha-2-macroglobulin Heparin Aspirin Protein C (activated by thrombomodulin) Prostacyclin
Slide 125-

19-7 Hemostasis Calcium Ions, Vitamin K, and Blood Clotting Calcium ions (Ca2+) and vitamin K are both essential to the clotting process
Slide 126-

19-7 Hemostasis Clot Retraction Pulls torn edges of vessel closer together Reducing residual bleeding and stabilizing injury site Reduces size of damaged area Making it easier for fibrocytes, smooth muscle cells, and endothelial cells to complete repairs
Slide 127-

Figure 19-12 The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 4) Clot Retraction Once the fibrin meshwork has formed, platelets and red blood cells stick to the fibrin strands. The platelets then contract, and the entire clot begins to undergo clot retraction, a process that continues over 30–60 minutes.
Slide 128-

19-7 Hemostasis Fibrinolysis Slow process of dissolving clot Thrombin and tissue plasminogen activator (t-PA) Activate plasminogen Plasminogen produces plasmin Digests fibrin strands