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Blood Functions of Blood Transportation Regulation Delivery of nutrients, hormones Removal of wastes Body temperature pH Fluid volume Protection Prevent blood loss Prevent infection Physical Characteristics of Blood A liquid connective tissue A mixture Heavier, thicker, more viscous than water Formed elements - living blood cells Plasma - fluid matrix Due to ions, plasma proteins, blood cells Composition and volume regulated by hormones Temp - 38° C, higher than body temperature pH - 7.4 (ranges from 7.35-7.45) Volume differs between sexes, conditional Female - average 4-5 L Male - average 5-6 L Components of Blood Blood sample Spin it Separates into 2 parts plasma • • formed elements • straw colored liquid on top 55% of the volume solid portion on bottom – red blood cells – buffy coat - white blood cells and platelets 45% of the volume Hematocrit percentage of formed element in a volume of blood about 45% (higher in males than females) Components of Blood Blood Plasma Plasma 92% water 7% proteins 1% other solutes Blood Plasma Proteins important (I ) for osmotic balance Albumin Fibrinogen (blood clotting) Globulins Regulatory proteins Blood Plasma Other solutes Waste products Nutrients Regulatory substances Gases Electrolytes Formed Elements Formed elements 99% red blood cells 1% white blood cells and thrombocytes (platelets) Formed Elements Erythrocytes - Red Blood Cell's (RBC’s) IMPORTANT! Note the differences in relative size and appearance! Formed Elements Leukocytes - White Blood Cells Granular leukocytes (granulocytes) Agranular leukocytes (agranulocytes) neutrophils eosinophils basophils lymphocytes - T cells, B cells Monocytes Thrombocytes platelets Blood Components Formation of Blood Cells Hematopoiesis - blood cell formation All blood cells come from pluripotent hematopoietic stem cells (hemocytoblasts) Reside in red bone marrow Give rise to precursor cells which develop into RBC’s, WBC’s and thrombocytes Formation of Blood Cells Erythropoiesis RBC production, specifically Hormonally controlled Three phases production of ribosomes synthesis of hemoglobin ejection of the nucleus and organelles Leave bone marrow as reticulocyte Mature in blood to a erythrocyte Formation of Blood Cells Regulation of RBC production Regulated by negative feedback O2 levels monitored in kidneys hypoxia increases RBC production Production stimulated by erythropoietin (EPO) from kidneys Numbers M - 5.4 million RBC’s/L (Testosterone stimulates EPO) F - 4.8 million RBC's/L 2 million cells released into blood/second Anemia - Low O2 carrying capacity of blood Insufficient # of RBC’s hemorrhage - loss of RBC’s hemolytic anemia - premature RBC rupture due to transfusion, disease, genetic problems aplastic anemia • • destruction or inhibition of hematopoietic components in bond marrow toxins, drugs or irradiation Decreased hemoglobin content iron (heme) deficiency insufficient iron due to diet or poor absorption Formation of Blood Cells Hematocrit % of blood that is RBC’s M 40-54% (47%), F 38-46% (42%), Why? Indicates RBC production and hydration state Abnormal Hct? altitude – hypoxia, increased RBC’s athletes - blood doping anemia – decreased RBC’s dehydration Red Blood Cells (Erythrocytes) RBC’s 99% of formed elements Function to carry O2 Anatomy Biconcave disks, 8µm in diameter No nucleus or metabolic machinery Filled with hemoglobin (Hgb) O2 carrying protein synthesized in cytosol before nucleus lost 33% of cell weight Red Blood Cells (Erythrocytes) Normal Hgb in blood Infants 14-20g Hgb/100ml Adult Male 14-15g Hgb /100ml Female 12-15g Hgb /100 ml 1.3 ml O2/g Hgb RBC’s (Light Microscopy) RBC Physiology RBC specialized for O2 carrying 280 million Hgb molecules/cell All internal space available for O2 carrying - no metabolism Concave shape Allows higher surface area/volume ratio increases gas diffusion Allows passage through capillaries, very flexible RBC Physiology RBC Physiology O2 combines with Hgb in lungs Hemoglobin O2 not very soluble in H2O Need something to carry it 4 globin (protein) chains - 2 chains, 2 chains 4 non-protein heme pigments Heme pigment has iron ion (Fe²+) that carries 1 O2 Each RBC can carry about 1 billion O2 molecules RBC's carry ¼ CO2 bound to hgb - forms carbaminohemoglobin RBC Life Cycle Life span Only 100-120 days Cells cannot repair damage due to loss of nucleus, ribosomes Old RBC’s destroyed in liver, spleen Macrophages eat old RBC's Breakdown products recycled Different pathways for each part of Hgb molecule globin - AA's used for other protein synthesis heme • • iron portion - Fe2+ recycled non-iron portion - bilirubin – released in bile, secreted into blood – bile enters intestine converted to urobilinogen by bacteria – gives urine/feces color RBC Life Cycle Granular Leukocytes Eosinophil Neutrophil Basophil Neutrophil 60-70% of all WBC’s Anatomy 10-12 µm diameter 2-5 connected nuclear lobes Fine, pale lilac granules Physiology Respond first to bacteria damage by chemotaxis Phagocytosis After engulfing pathogen release several chemicals lysozymes strong oxidants defensins Eosinophil 2-4% of all WBC’s Anatomy 10-12 µm diameter 2-3 connected nuclear lobes red/orange large, uniform granules, do not block nucleus Physiology Exit capillaries, enter tissue fluid Combat parasites histamine Phagocytize antigenantibody complexes Basophil 0.5-1% of all WBC’s Anatomy 8-10 µm diameter Bilobed nucleus Large granules round, blueblack, block nucleus Physiology Exit caps enter tissue fluids Release heparin, histamine, serotonin – stimulate inflammation Hypersensitivity (allergic) reactions Agranular Leukocytes Lymphocyte Monocyte Lymphocytes 20-25% of all WBC’s Anatomy 7-15µm Nucleus dark stained, round or indented Cytoplasm sky blue rim around nucleus Lymphocytes - Physiology Immune response through lymphocytes responding to antigen An antigen is: Any chemical substance recognized as foreign when in body Substance (mainly proteins) that stimulate immune response Lymphocytes - Physiology Two types of lymphocytes B-cells particularly active in killing bacteria develop into plasma cells to form antibodies • antigen blockers that create antibody-antigen complex • complex prevents interactions w/ other body cells T-cells kill viruses, fungi, transplants, cancer, some bacteria 3 types of cells • cytotoxic (killer) T cells - destroy foreign invaders • helper T cells - assist B cells and cytotoxic T cells • memory T cells - immune response memory Monocytes 3-8% of all WBC’s Anatomy 12-20 µm Indented or kidney-shaped nucleus (not smooth) cytoplasm foamy Physiology Slow to respond but arrive in larger numbers Enlarge, differentiate into wandering macrophages Clean up cellular debris, microbes following infection Leukocyte Life Span and Number Life span determined by foreign invaders! Ingesting foreign bodies toxic, shortens cell life Healthy WBC's - months/years, generally days During infection may only live hours fill with toxins may die or burst Leukocyte Life Span and Number 5,000 - 10,000 WBC’s/mm3 blood RBC/WBC ratio 700/1 Differential WBC count (We have seen these before!) Neutrophils 60-70% Lymphocytes 20-25% Monocytes 3-8% Eosinophils 2-4% Basophils 0.5-1% Leukocyte Disorders Leukopenia Insufficient WBC production Induced by drugs - glucocorticoids, anti-cancer drugs Leukemia Cancer (excess production) of the leukocytes Bone marrow fills with cancerous (nonfunctional) leukocytes Crowds out other cells types anemia bleeding Leukocyte Disorders Generally a descendent of a single cell Different types of cells myelocytic leukemia lymphocytic leukemia Under different cancerous conditions acute - if derived from -blast type cells chronic - if derived from later stages QUIZ! Identify the marked cells! 1. 3. 2. Answers 1. 2. 3. 4. 5. Neutrophil Basophil Monocyte Lymphocyte Eosinophil 5. 4. Platelets - Thrombocytes Development Megakaryoblasts shed small fragments Each fragment has plasma membrane Anatomy 250,000400,000/mm3 No nucleus, disc shaped 2-4 µm diameter w/ many granules Platelets Physiology Short life span (5-9 days) Help plug small holes in vessels Granules several important functions alpha granules • • clotting factors platelet derived growth factor (PDGF) dense granules - Ca++, ADP, ATP, etc. Also Thromboxane A2, vasoconstrictors, clot promoting enzymes Hemostasis 3 mechanisms in stopping bleeding First - Vascular Spasm Blood vessel constricts when damaged wall smooth muscle contracts immediately slows flow through vessel reflexive? Hemostasis Second - Platelet Plug Formation 1) Platelet adhesion platelets stick to exposed collagen activates platelets 2) Platelet release reaction platelets attach to other platelets release granule contents (thromboxane A2) promote vasoconstriction, platelet activation and aggregation 3) Platelet aggregation platelet plug blocks blood loss in small vessels not as good in larger vessels Hemostasis Third - Coagulation Gel formation (clotting) in blood traps formed elements Thrombosis clotting in a normal vessel Hemorrhage slow clotting leading to a bleed Hemostasis - Coagulation A complicated process that works in a positive feedback cascade 3 pathways - extrinsic, intrinsic and common Pathways involve 12 factors in clot formation Hemostasis Coagulation Overview Hemostasis - Coagulation Stage 1: Prothrombinase formation Extrinsic Pathway Intrinsic Pathway Prothrombinase catalyzes Thrombin formation from Prothrombin Stage 1 has 2 parts Part 1: Extrinsic Pathway • • • Rapid (seconds) Tissue factor (TF) enters blood from tissue Ultimately activates prothrombinase Prothrombinase Hemostasis - Coagulation Stage 1: Prothrombinase formation (cont.) Intrinsic Pathway Part 2: Intrinsic Pathway Extrinsic Pathway Slower (minutes) Activators in blood damaged red blood or endothelial cells activate clotting Extrinsic pathway also activates Intrinsic pathway Ultimately activates prothrombinase Ca2+ required for activation of both paths! Prothrombinase Hemostasis - Coagulation Stage 2 - Common Pathway Thrombin Formation requires enzyme Prothrombinase w/ Ca++ catalyzes prothrombin conversion to thrombin Thrombin accelerates formation of prothrombinase (positive feedback) Thrombin accelerates platelet activation (positive feedback) + + Prothrombinase 2. Common Pathway Hemostasis Coagulation Stage 3 - Common Pathway Fibrin formation activated enzyme thrombin w/ Ca++ catalyzes fibrinogen fibrin • • fibrinogen (soluble) fibrin (insoluble) Fibrin Protein threads attach to vessel surface Absorbs/inactivates 90% of thrombin, limits clot formation 3. Hemostasis - Coagulation Overview Hemostasis - Coagulation Clot retraction and repair Clot retraction also known as syneresis Platelets continue to pull on fibrin threads closing wound Formed elements trapped in fibrin threads, some serum may leak out Hemostatic control mechanisms Important that clot formation remains local, not systemic Several mechanisms work together: fibrin absorbing thrombin removal of local clotting factors - washed away endothelial cells inhibit platelet aggregation Hemostasis - Coagulation Fibrinolysis - dissolution of a clot, begins within 2 days Plasminogen trapped in clot Many factors convert plasminogen into plasmin (fibrinolysin) thrombin activated factor XII tissue plasminogen activator (tPA) Plasmin Digests fibrin threads Inactivates fibrinogen, prothrombin, and several clotting factors Hemostasis - Coagulation Thrombolytic (clot-dissolving) agents that can be used clinically Chemical substances that activate plasminogen Streptokinase, tissue plasminogen activator (t-PA) Anticoagulants present in blood - heparin Produced by mast cells, basophils Used clinically to prevent blood clotting in blood samples Inhibits thrombin and intrinsic pathway Hemostasis - Coagulation Other anticoagulants Warfarin (coumadin) - Vitamin K antagonist slow acting, takes days to start and stop rat poison Vitamin K • produced by gut bacteria • required for synthesis of factors II (prothrombin), VII, IX, X Aspirin blocks platelet aggregation prevents formation of thromboxane A2 CPD (citrate phosphate dextrose) removes Ca2+ Used in blood banks Hemostasis - Coagulation Intravascular Clotting Roughened endothelium (atherosclerosis, trauma, infection) or slow blood flow may result in spontaneous clot (thrombus) formation, thrombosis Thrombus released into blood becomes embolus pulmonary embolus also may be air or debris Angioplasty - may trigger thrombus Blood Types • RBC surface has genetically determined antigens, agglutinogens Agglutinins • ABO blood typing – 2 glycolipid agglutinogens, A + B – one gene from each parent, A, B or O – 6 combinations - AA, AB, AO, BB, BO, OO (no agglutinogens) Naturally occurring antibodies produced in response to the agglutinogens not present in your blood React in antigen-antibody response to blood not of your type AB - universal recipients O - universal donors Blood Types Blood Types Rh typing - Rhesus monkey With Rh antigens are Rh+ Without Rh agglutinogens Rh normally blood does not contain Rh agglutinins body only makes agglutinins in response to exposure Rh sensitivity does not occur until second transfusion hemolytic disease of the newborn Blood Types Hemolytic disease of the newborn
