blood hemostasis - Blood: functions Blood: •...

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Unformatted text preview: Blood: functions Blood: • Transportation of dissolved gases, nutrients, Transportation hormones, and metabolic wastes hormones, • Regulation of pH and ion composition of Regulation interstitial fluids interstitial • Restriction of fluid loss at injury sites • Defense against toxins and pathogens • Stabilization of body temperature Blood: composition Blood: • Blood is 5 times more viscous than water-why? • Formed cellular elements (37-54%) – RBCs (erythrocytes): 99% – WBCs (leukocytes) and platelets (0.1%) • Plasma (46-63%) – Water (92%) – Proteins (7%): source, liver • _albumins_ (60%): osmotic pressure • __globulins_(35%): transport proteins __globulins_(35%): and immunoglobulins • fibrinogen (~4%): blood clotting Formed elements Formed • Red blood cells • 1/3 of all cells in human body – structure • biconcave shape – provides higher surface area to volume ratio – allows cells to stack, preventing clumping of cells – allows cells to bend and flex • lack organelles, nucleus, mitochondria contains hemoglobin; allows O and CO transport • RBCs development eliminates all aspects of cell RBCs function except that pertaining to transport of gases function – takes ~_7days takes • RBCs contain hemoglobin – 95% of RBC intracellular protein – 2 α chains, 2 β chains • contains heme, a pigment complex containing iron each heme can bind to O : results in bright red color Relationship of heme group to hemoglobin tetramer Fig. 17-13, Martini • RBC life span-circulation – single trip from heart and back-less than 1 minute! – 1% of RBCs replaced each day 1% each • Fig. 19-4, Martini – phagocytes (liver, spleen, bone marrow) normally phagocytes engulf RBCs before hemolysis occurs engulf –In macrophages: •heme converted to biliverdin (green color) •biliverdin converted to bilirubin (yellow color) biliverdin in macrophage in –binds to albumin, transported to liver, excreted binds in bile in –accumulation of bilirubin causes yellow skin, or accumulation jaundice jaundice –many liver dysfunctions result in this skin color – in intestine, bilirubin converted to urobilinogens and stercobilinogens and –provides darker color to fecal material Fig. 17-4, Martini • RBC production – ‘erythropoiesis urs in bone marrow erythropoiesis urs – regulation of _erythropoiesis • stimulated by androgens, thyroxin, erythropoietin • erythropoietin (EPO) produced in response to: – anemia – decreased kidney blood flow – low oxygen content in lungs (high altitude) – damage to respiratory surfaces of lung Other formed elements of blood • white blood cells – capable of amoeboid movement • migrate out of bloodstream – attracted to specific stimuli • positive chemotaxis – neutrophils, eosinophils, monocytes capable of neutrophils, phagocytosis phagocytosis • What do WBCs do in the blood? • neutrophils, eosinophils, basophils, neutrophils, monocytes monocytes – _________________________ defenses • lymphocytes – _______________________ defenses • mediates attack toward a specific protein or cell • differentiation of blood cells – all but lymphocytes share the same common all progenitor cell type with RBCs progenitor • _____________________ stem cells – lymphocytes • _____________________ stem cells – similar steps to RBC differentiation • these cells retain nuclei, many organelles • platelets – non-nucleated, “cell fragments” – functions (primarily “clotting”): • transport of chemicals to the clotting process • forms a temporary patch in damaged blood vessel – “platelet plug” • causes active contraction after clotting has completed – platelets contain __________________________ – differentiate from megakaryocytes • myeloid stem cells • alterations in the cellular elements of blood – anemia • severe ____________________ of RBCs severe ____________________ – leukemia • large increase in WBCs; “white blood” large increase – leukopenia • severe _____________________ in WBCs severe _____________________ – thrombocytopenia • excessive platelet destruction/lack of production • causes excessive bleeding – thrombocytosis • excessive platelet formation – in response to infection, inflammation, cancer Hemostasis Hemostasis • the “cessation of bleeding” • 3 phases – – – vascular phase platelet phase coagulation phase Vascular phase Vascular • vascular spasm (Fig. 17-11, Martini) – endothelial cells contract • expose the basement membrane to bloodstream – endothelial cells release substances • ADP, tissue factor, prostacyclin • ‘endothelians’ (peptide hormones) – stimulates smooth muscles contraction – stimulates cell division – endothelial cells become “sticky” Fig. 17-11, Martini Platelet phase Platelet Fig. 17-11 • platelet adhesion to sticky endothelial cells • leads to platelet aggregation, releasing: – ADP – thromboxane A2 and serotonin • enhances vascular spasms – clotting factors – platelet derived growth factor – Ca++ • “positive feedback loop” Platelet phase Platelet Fig. 17-11 • platelet plug – formed from aggregation and activation of platelets – growth limited by • • • • • prostacyclin (released by endothelial cells) compounds released by WBCs plasma enzymes that break down ADP blood clot formation, which surrounds platelet plug high concentration of factors Coagulation phase of hemostasis Coagulation Fig. 17-12 (overview) • causes conversion of fibrinogen (plasma causes protein) into fibrin protein) • fibrin traps more platelets and cells • blood clot formed as a result • What are some of the events leading to What production of fibrin? production Fig. 17-12, Martini • ____________________ pathway – faster acting than intrinsic pathway – release of tissue factor (Factor III) release – causes eventual production of Factor VII Ca dependent • _______________________ pathway – platelet mediated – activating proenzymes (factor XII) released • by endothelial cells – combines with platelet factors (PF-3) Ca dependent • regulation of hemostasis – hemostasis is a positive feedback loop – factors that inhibit clotting (anticoagulants) • heparin reduction of Ca levels ...
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This note was uploaded on 05/29/2011 for the course BMS 290 taught by Professor Tba during the Spring '08 term at Grand Valley State University.

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