The Cardiovascular System (Blood) PDF

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

The Cardiovascular System (Blood)  Some Latin Prefixes & Suffixes You Should Know! Hemo/a-: -penia: blood poverty, not Anti-: enough against -osis: too Erythros-: many red Thrombos-: Leukos-: clot white -stasis: halt, 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 Three formed elements” – Platelets Clotting – White blood cells – leukocytes (WBCs) Immune defense – Red blood cells - erythrocytes Components Of Blood Video Cl (RBCs) ip  Hemopoiesis Hemopoiesis refers to the productions of ALL blood cells Adult produces 400 billion platelets, 200 billion RBCs and 10 billion WBCs every day Hemopoietic tissues produce blood cells – Liver produces RBCs until birth – Red bone marrow – where most hemopoeisis takes place (RBCs, WBCs, and platelets) – Spleen remains involved with WBC production lymphoid hemopoiesis occurs in widely distributed lymphoid tissues (thymus, tonsils, lymph nodes, spleen and peyers patches in intestines)  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 – 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 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? "Hct", "crit" or PCV (packed cell volume)- determines the percentage of red blood cells in the plasma – Means "to separate blood." Blood sample is spun in a centrifuge – White blood cells and platelets rise to the top- "buffy coat." – Heavier red blood cells sink to the bottom, where they can be calculated as a percentage of the total blood sample. Percent refers to how much of the sample is RBCs. – Newborn: up to 60%, children vary with age – Adults: (males): 40- 54% – (Females): 36 – 46% – Pregnancy: decreased hematocrit, especially in the last trimester as plasma volume increases  Red Blood Cells Most numerous Biconcave disc shaped – The 'dent' increases the amount of surface area – Large surface to volume area means oxygen diffuses 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 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  Structure & Function Of Each RBC has ~280 RBC’s thousand hemoglobin molecules Hb transports O2 & CO2 – 2 parts: heme and globin Heme- pigment molecule – Made of porphyrin & iron -Fe ion bound to O2 is oxyhemoglobin – Bright red -Fe not bound to O2 is deoxyhemoglobin – Dark red/burgundy  Hemoglobin (Hb) Structure Globins - 4 protein chains 2 alpha chains 2 beta chains – fetal Hb - gamma replace beta chains; binds O2 better  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 Lance Armstrong  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: 1. globular proteins amino acids 2. heme biliverdin (due to iron being stripped away) – Green color Then converted to bilirubin – orange-yellow color – Liver removes bilirubin » Bilirubin gets converted to Red Blood Cell Recycling Video stercobilins & urobilins in the intestines » Stercobilin gets pooped out » Urobilin is excreted in urine – Jaundice if liver damage 3. Iron  Iron Recycling To transport proteins (transferrin) – Taken back to bone marrow to be used in new hemoglobin To storage proteins (feritin and hemosiderin) – Stored in the liver if excess transferrin  Anemia - Causes Only 3 Causes of Anemia - symptoms are all generally the same no matter the cause. 1. 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 2. Hemolytic anemias- something is causing the RBCs to hemolyze 3. Hemorrhagic anemias- blood loss through bleeding (internal or external)  Anemia – General Effects Tissue hypoxia and necrosis (short of breath and lethargic) Low blood osmolarity (tissue edema) Low blood viscosity (heart races and pressure drops)  Other Conditions Jaundice – Yellowish-brownish staining of skin & sclerae (whites of eyes) caused by high levels of chemical called bilirubin in blood – Bilirubin- Waste product that comes from old, destroyed RBCs Removed from blood by liver (eliminated in the feces, giving it its brown color) Sickle-Cell Disease  Sickle-Cell Disease Recessive allele modifies hemoglobin structure – hereditary – Sickle-cell trait - heterozygous for HbS individual has resistance to malaria – HbS indigestible to malaria parasites -Sickle-cell disease - homozygous for HbS, 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  Pernicious Anemia Building red blood cells requires: – amino acids – iron – vitamins B12, B6, and folic acid Low RBC production due to lack of vitamin B12 Why no B12? – Gastrointestinal disease which causes absorption problems – Diet, i.e. Strict vegans (a small percentage of people that get pernicious anemia) – Insufficient B12 supplements – found in fortified foods Found in meat, dairy, eggs etc.  Thalassemia Inherited disorder Rare in U.S. – Most common in people of Italian, Greek, Turkish, Middle Eastern, South Asian, and African descent Caused by mutations in hemoglobin, so it binds into a tetramer, creating misshapen RBCs.  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 Your Blood type- surface antigens (A, B & Rh antigen (Rh factor) Antibodies – secreted by plasma cells as part of immune response to foreign matter Agglutination – antibody molecule binding to antigens – causes clumping  Plasma contains antibodies that will attack antigens on “foreign” RBCs – Causes agglutination (clumping together of RBCs) – Hemolysis- breaking apart of RBCs = cross-reaction – Type A (~40%) Antigen A present Anti-B antibodies – Type B (~10%) Antigen B present Anti-A antibodies Blood Types 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 (rupture) – free hemoglobin molecules blocks kidney tubules,  Rh Group Separate antigens from A & B. Rh (D) antigens discovered in rhesus monkey in 1940 – Rh+ blood type has D agglutinogens (antigen) 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 Comparing Maternal – Fetal Rh Group Incompatability Maternal – Fetal Rh Group Incompatibility Read on your own. Maternal – Fetal Rh Group Incompatibility Read on your own.  Read on your own. Maternal – Fetal Rh Group Incompatab ility Maternal – Fetal Rh Group Incompatability  Hemolytic Disease Of The Newborn RhoGAM Suppresses the mother's immune system from producing antibodies against Rh- positive blood cells which MAY have entered the maternal blood stream from fetal circulation Destroys any fetal blood cells which may have made it into maternal circulation before mom can begin making her own antibodies Given at 28 weeks gestation and 72 hours after birth to prevent mom from making Rh antibodies 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 Macrophage Att transportation to area of ack Video Clip Granulocyt e 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 Agranulocyte Functions  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) Origins of Formed Elements You need to know the ones circled in Lymphoblast  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 Normal Blood Leukemia Smear Platelets aka Thrombocytes 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.  Hemostasis Hemostasis – stopping of bleeding (clotting) 3 Phases: 1. Vascular Phase – Lasts ~30 mins. Local blood vessels constrict– “vascular spasm” 2. Platelet Phase – Begins within ~15 secs. Platelets activate, aggregate (clump together) & stick to damaged surface to form “platelet plug” Release ADP, thromboxane A2, serotonin, clotting factors, platelet-derived growth factors, Ca2+ ions 3. 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 Hemostasis This phase gets complicated  Coagulation- 2 Beginnings, 1 End Coagulation can begin 2 ways – Extrinsic pathway activated by damaged tissue – Intrinsic pathway activated by exposed collagen inside blood vessels Both activate the Common Pathway – Common pathway begins at Factor X X = 10 in roman numerals. – Goal of the common pathway is to make fibrin, a net of proteins to stop bleeding. Coagulati on Pathways Extrinsic Pathway: Is initiated outside by chemicals of or "extrinsic" to the blood. Tissue Thromboplastin (Factor III) released by damaged tissue cells. Extrinsic pathway is a very rapid process, i.e., within 12 to 15 seconds. Production of Thrombin is low and the resulting clot is small. This pathway is most effective as a "quick patch" process.  Coagulation Pathways Intrinsic Pathway: Is initiated by the blood coming in contact with exposed collagen in the blood vessel wall due to endothelial damage. – Think damage due to atherosclerosis Considerably slower (5 to 10 minutes) than extrinsic but results in the formation of larger amounts of thrombin. – Allows the formation of larger clots. Coagulati on Pathways 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 & Fibrinolysis =Anticoagulants breaking a clot apart Thrombin and Tissue Plasminogen Activator (tPA): – Activate Plasminogen Plasminogen Produces Plasmin: – 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) prevent factor X activation. – tPA activates plasmin to  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 – Stroke can be caused by clots going to the brain Thrombus: A blood clot within a vessel Embolus: A blood clot that has broken free and travels through vessels. Infarction (blockage) may occur if clot blocks blood supply to an organ (MI or stroke) – 650,000 Americans die annually of thromboembolism