Blood PPT PDF

The Cardiovascular System (Blood)  Some Latin Prefixes & Suffixes You Should Know! Hemo/a-: blood -penia: poverty, Anti-: against not enough Erythros-: red -osis: too many Leukos-: white Thrombos-: -cyte: cell clot -stasis: halt,...

The Cardiovascular System (Blood)  Some Latin Prefixes & Suffixes You Should Know! Hemo/a-: blood -penia: poverty, Anti-: against not enough Erythros-: red -osis: too many Leukos-: white Thrombos-: -cyte: cell clot -stasis: halt, stop Blood… The Fluid Of The Cardiovascular System Provides to cells/tissues: – Nutrients – Oxygen (O2) – Hormones/enzymes – Removal of wastes – Special cells to protect against disease & infection (WBCs & antibodies) Regulates: – pH & ion composition of cellular fluids – Clotting capabilities to restrict blood loss – Body temperature  What kind of tissue is blood? – Connective Tissue What makes blood fluid? – Plasma What are the 3 “formed elements” of blood? – Platelets – White blood cells – leukocytes (WBCs) – Red blood cells - erythrocytes (RBCs) Components Of Blood Video Clip Components of Blood  Functions Of Blood Components Formed elements made RBCs – through hemopoiesis (hematopoiesis) – Most abundant Blood… – Transport of O2 – Temperature = ~38°C (100.4°F) WBCs – – 5x more viscous than water – Body’s defense – Slightly alkaline; pH 7.35-7.45 – Adult male = 5-6 L mechanism against – Adult female = 4-5 L disease & infection Platelets – – Contain enzymes important for clotting What Do You Get With A Complete Blood Count?  Hemopoiesis (All Blood Cells) Adult produces 400 billion platelets, 200 billion RBCs and 10 billion WBCs every day Hemopoietic tissues produce blood cells – yolk sac produces stem cells colonize fetal bone marrow, liver, spleen and thymus – liver stops producing blood cells at birth – spleen remains involved with WBC production lymphoid hemopoiesis occurs in widely distributed lymphoid tissues (thymus, tonsils, lymph nodes, spleen and peyers patches in intestines) – red bone marrow pluripotent stem cells myeloid hemopoiesis produces RBCs, WBCs and platelets  Composition Of Plasma – Water – Proteins Albumin: most abundant – Viscosity and osmolarity (blood volume, pressure, flow) Globulins: transport, clotting, immunity Fibrinogen: framework of blood clot – Nutrients – Electrolytes – Nitrogenous wastes Urea: AA breakdown – Hormones – Gasses What The Heck Are Albumin & Globulin Proteins? Albumins help transport substances: – Fatty acids – Thyroid hormones – Steroid hormones *Hormones that are not attached to a carrier protein are called what? Globulins – Antibodies, also called immunoglobulins (more on this in a few weeks) – Transport globulins (small molecules): Hormone-binding proteins Metalloproteins – Metals Apolipoproteins (lipoproteins) – I.E. Triglycerides Steroid-binding proteins – I.E. Testosterone  Origins Of Plasma Proteins 90% made in liver (albumin, fibrinogen, etc) – What could happen in a patient with liver disease? – What does fibrinogen do? – i.e. Uncontrollable bleeding due to reduced fibrinogen Antibodies made by plasma cells – Plasma cells are derived from lymphocytes Peptide hormones made by endocrine organs  What Exactly Is Hematocrit? The hematocrit, also known as the "Hct", "crit" or PCV (packed cell volume) determines the percentage of red blood cells in the plasma. The term hematocrit means "to separate blood." When the patient's blood sample is spun in a centrifuge, the white blood cells and platelets rise to the top in what is known as the "buffy coat." The heavier red blood cells sink to the bottom, where they can be calculated as a percentage of the total blood sample. Newborn: up to 60% Adults: (males): 40- 54% (Females): 36 – 46% Pregnancy: decreased hematocrit, especially in the last trimester as plasma volume increases Children: varies with age  Red Blood Cells Most numerous Biconcave disc shaped – The 'dent' in each side of a red blood cell, like its small size, increases the amount of surface area in relation to the volume of the cell, giving it a large surface area to volume ratio. This large surface area means that oxygen can diffuse quickly into or out of the cell Smaller than white blood cells, larger than platelets No nucleus when mature Produced in the red marrow of long bones Destroyed in the liver and spleen Contain the iron protein compound HEMOGLOBIN whose chief function is to combine with oxygen and carry it to the cells Importance Of RBC Biconcave Disc Shape 1. High surface-to-volume ratio: – quickly absorbs and releases oxygen 2. Discs form stacks: - Rouleau – smoothes flow through narrow blood vessels 3. Discs bend and flex entering small capillaries: – 7.8 µm RBC passes through 4 µm capillary *folded pizza to get into mouth – MMMMM PIZZA!  Structure & Function Of RBC’s Each RBC has ~280 thousand Hb molecules Hemoglobin (Hb) molecule responsible for transporting O2 & CO2 to & away from tissues – Single pigment molecule of heme Iron (Fe) ion that interacts with O2 molecule = oxyhemoglobin – Bright red Fe not bound to O2 = deoxyhemoglobin – Dark red/burgundy 4 oxygen molecules can bind to one 1 molecule of Hb  Hemoglobin (Hb) Structure Globins - 4 protein chains 2 alpha chains 2 beta chains – fetal Hb - gamma replace beta chains; binds O2 better REMEMBER: 4 oxygen molecules can bind to one 1 molecule of Hb Oxygen Loading And Unloading From Hemoglobin  Carbon monoxide has 40x the affinity of oxygen for hemoglobin -- breathing it may lead to death  Erythrocyte Homeostasis Negative feedback control – drop in RBC count causes kidney hypoxemia – EPO production stimulates bone marrow – RBC count  in 3 - 4 days Stimulus for erythropoiesis – low levels O2 – increase in exercise – loss of lung tissue in emphysema  Stimulating Hormones Erythropoietin (EPO) Also called erythropoiesis- stimulating hormone: – secreted when oxygen in peripheral tissues is low (hypoxia) – due to disease or high altitude Where have you seen this stuff in the news?  Recycling RBCs 1% of circulating RBCs wear out per day: – about 3 million RBCs per second Macrophages of liver, spleen, and bone marrow: – monitor RBCs – engulf RBCs before membranes rupture (hemolyze)  Hemoglobin Recycling Phagocytes break hemoglobin into components: – globular proteins to amino acids – heme to biliverdin (due to iron being stripped away) Green color Then converted to bilirubin – Has orange-yellow color – Liver removes bilirubin – Jaundice if liver damage – iron  Iron Recycling To transport proteins (transferrin) – Taken back to bone marrow to be used in new hemoglobin To storage proteins (ferritin and hemosiderin) – Stored in the liver if excess transferrin Recycling RBCs What does a person look like if this can’t be broken down by the liver? Figure 19–4  Anemia - Causes Inadequate erythropoiesis or hemoglobin synthesis – inadequate vitamin B12 from poor nutrition or lack of intrinsic factor (pernicious anemia) – iron-deficiency anemia – kidney failure and insufficient erythropoietin – aplastic anemia - complete cessation of RBC production Hemolytic anemias Hemorrhagic anemias  Anemia - Effects Tissue hypoxia and necrosis (short of breath and lethargic) Low blood osmolarity (tissue edema) Low blood viscosity (heart races and pressure drops)  Sickle-Cell Disease Hereditary Hb ‘defect recessive allele modifies hemoglobin structure – sickle-cell trait - heterozygous for HbS individual has resistance to malaria – HbS indigestible to malaria parasites – sickle-cell disease - homozygous for HbS individual has shortened life – in low O2 concentrations HbS causes cell elongation and sickle shape – cell stickiness causes agglutination and blocked vessels – intense pain; kidney and heart failure; paralysis; stroke – chronic hypoxemia reactivates hemopoietic tissue » enlarging spleen and bones of cranium Sickle-Cell Disease  Pernicious Anemia Building red blood cells requires: – amino acids – iron – vitamins B12, B6, and folic acid Low RBC production due to unavailability of vitamin B12 What type of person has a lack of B12 in their diet? – Gastrointestinal disease which causes absorption problems – Strict vegetarians (a small percentage of people that get pericious anemia) – B12 supplements – found in fortified foods  Other Conditions Associated With Blood Thalassemia – Inherited disorder resulting in mutation of hemoglobin gene and malformed hemoglobin molecule – Bone marrow transplants & blood transfusions are methods used to combat the disorder Jaundice – Yellowish-brownish staining of skin & sclerae (whites of eyes) caused by high levels of chemical called bilirubin in blood – Bilirubin is a waste product that comes from old, destroyed RBCs & is removed from blood by liver (eliminated in the feces, giving it its brown color)  Quick Immunology Lesson Before We Cover Blood Types Antigens – unique molecules on cell surface used to distinguish self from foreign foreign antigens generate immune response Antibodies – secreted by plasma cells as part of immune response to foreign matter Agglutination – antibody molecule binding to antigens – causes clumping  Antigens – – Your Blood type surface antigens (A, B & Rh) – Rh antigen (Rh factor) Plasma contains antibodies that will attack antigens on “foreign” RBCs – Causes agglutination (clumping together of RBCs) & hemolysis (breaking apart of RBCs) = cross-reaction Blood type determined by presence or absence of surface antigens (agglutinognes) – Type A (~40%) Antigen A present Anti-B antibodies – Type B (~10%) Antigen B present Anti-A antibodies  Blood Types – Type AB (~4%) = universal recipients Both Antigens A & B present – Type O (~46%) = universal donors Neither Antigens A & B present Both Anti-A & Anti-B antibodies  Transfusion Reaction Agglutinated RBCs block blood vessels and hemolyze (rutpure) – free Hb blocks kidney tubules, causes death   Rh Group Rh (D) antigens discovered in rhesus monkey in 1940 – Rh+ blood type has D agglutinogens on RBCs – Rh frequencies vary among ethnic groups Anti - D antibodies (agglutinins) not normally present in plasma – form in Rh- individuals exposed to Rh+ blood Rh- woman with an Rh+ fetus or transfusion of Rh+ blood no problems with first transfusion or pregnancy Maternal – Fetal Rh Group Incompatability  Hemolytic Disease Of The Newborn RhoGAM to the rescue! Anti-RhD) antibodies that suppresses the mother's immune system from attacking Rh-positive blood cells which have entered the maternal blood stream from fetal circulation.  White Blood Cells (Leukocytes) Structure – – No hemoglobin Functions – – Defend body against pathogens – Remove toxins, waste & damaged cells Location & Movement – – Most WBCs in body in Connective Tissue Proper or lymphathic organs – Circulating WBCs only small fraction of total population – Use bloodstream as mode of transportation to area of Macrophage Attac infection/injury k Video Clip  Granulocyte Functions Neutrophils ( in bacterial infections) – phagocytosis of bacteria Eosinophils ( in parasitic infections or allergies) – phagocytosis of antigen-antibody complexes, allergens and inflammatory chemicals – release enzymes to destroy parasites Basophils ( in chicken pox, sinusitis, diabetes) – secrete histamine (vasodilator) – secrete heparin (anticoagulant)  Agranulocyte Functions Lymphocytes (T-cells, B-cells, NK cells)   in diverse infections and immune responses – destroy cells (cancer, foreign, and virally infected cells) – “present” antigens to activate other immune cells – coordinate actions of other immune cells – secrete antibodies and provide immune memory Monocytes ( in viral infections and inflammation) – differentiate into macrophages – phagocytize pathogens and debris – “present” antigens to activate other immune cells  Leukocyte Life Cycle Leukopoiesis – pluripotent stem cells – myeloblasts – form neutrophils, eosinophils, basophils monoblasts form monocytes lymphoblasts form B and T lymphocytes and NK cells – T lymphocytes complete development in thymus Red bone marrow stores and releases granulocytes and monocytes Circulating WBCs do not stay in bloodstream – granulocytes leave in 8 hours and live 5 days longer – monocytes leave in 20 hours, transform into macrophages and live for several years – WBCs provide long-term immunity (decades) Leukopoiesis.. Are We Having Fun Yet? Here’s Another One That You Might Like Better…  Leukocyte Disorders Leukopenia - low WBC count (10,000/L) – causes: infection, allergy and disease Leukemia = cancer of hemopoietic tissue – myeloid and lymphoid - uncontrolled WBC production – acute and chronic - death in months or  3 years – effects - normal cell % disrupted; impaired clotting Leukocyte Histology Normal Blood Leukemia Smear  Platelets Functions: – Cell fragments that play major role in clotting system Release chemicals important to clotting process Formation of temporary patch in walls of damaged blood vessels Active contraction after clot has formed Important Facts: – Continuously removed & replaced every 9-12 days by phagocytes in spleen – Thrombocytopoiesis (platelet production) occurs in bone marrow – Thrombocytopenia – Abnormally low platelet count – Thrombocytosis – Abnormally high platelet count Thrombocytopoiesis A typical megakaryocyte is seen with platelets budding off the periphery. The granular cytoplasm fragments from separate regions of the massive cell, resulting in the formation of platelets.  Hemostasis Hemostasis – stopping of bleeding through damaged vessels (clotting) 3 Phases: – Vascular Phase – Local blood vessels constrict to stop loss of blood – “vascular spasm” Lasts ~30 mins. – Platelet Phase – Platelets activate, aggragate (clump together) & stick to damaged surface to form “platelet plug” Release ADP, thromboxane A2, serotonin, clotting factors, platelet-derived growth factors, Ca2+ ions Begins within ~15 secs. Clotting Video Clip 1 – Coagulation Phase – Begins 30 secs. or more after injury Conversion of fibrinogen to insoluble protein fibrin – Clot retraction: platelets contract & pull torn edges of vessel closer – Fibrinolysis: clot dissolves Clotting Video Clip 2  Hemostasis All 3 pathways involve platelets This phase gets complicated   Coagulation Pathways Extrinsic Pathway: Begins In The Vessel Wall Outside Blood Stream Intrinsic Pathway: Begins With Circulating Proenzymes Within Bloodstream Common Pathway: Where Intrinsic And Extrinsic Pathways Converge Calcium Required For Either Pathway The Common Pathway Up Close Both pathways converge at Factor X Factor X forms the enzyme prothrombinase Converts prothrombin to thrombin Thrombin converts fibrinogen to fibrin Fibrin is the goal of all of this! Prothrombinase  Fibrinolysis & Anticoagulants Fibrinolysis = breaking a clot apart Thrombin and Tissue Plasminogen Activator (tPA): – Activate Plasminogen Thrombin Plasminogen Produces Plasmin: or tPA – Digests Fibrin Strands Anticoagulants = clot busters – Antithrombin III (From Liver) Deactivates Thrombin Before It Can Act On Fibrinogen – Heparin (From Basophils And Mast Cells) Activates Antithrombin III – Warfarin (Coumadin) – tPA activates plasmin to degrade clot  Hemophilia Rare inherited (genetic) bleeding disorder in which your blood doesn’t clot normally Almost always occurs in males –XY, no back up copy to make clotting factor Certain clotting factors in the blood are either insufficient or missing – Type A: 80% - clotting factor VIII – Type B: 15% - clotting factor IX Hemophiliacs bleed longer not faster Seen when born, umbilical cord bleeds excessively Infant stage - more bruising with mild irritation Older - Nose bleeds, easily bruised, blood in urine, severe joint pain brought upon by blood in the joint cavities  Coagulation Disorders Thrombosis - abnormal clotting in unbroken vessel – most likely to occur in leg veins of inactive people (DVT) – pulmonary embolism (PE) - clot may break free, travel from veins to lungs Infarction (blockage) may occur if clot blocks blood supply to an organ (MI or stroke) – 650,000 Americans die annually of thromboembolism