Chapter 18- the Circulatory System: Blood
Chapter 18- the Circulatory System: Blood BIOL 20214
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This 0 page Study Guide was uploaded by Marlee Porter on Sunday January 31, 2016. The Study Guide belongs to BIOL 20214 at Texas Christian University taught by Mrs. Crenshaw in Spring 2016. Since its upload, it has received 31 views. For similar materials see Anatomy and Physiology in Biology at Texas Christian University.
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Date Created: 01/31/16
Chapter 18 The Circulatory System Blood Functions Distribution Transport nutrients waste and hormones Regulation Maintain body temp pH and uid volume Protection Prevents blood loss following trauma and infection with leukocytes antibodies and complement proteins Components Plasma 55 of blood Formed Elements Erythrocytes 45 of blood Leukocytes lt1 Neutrophils Eosinophils Basophils Lymphocytes and Monocytes Platelets lt1 gt Hemopoiesis production of all blood cells all arise from a common stem cell General Properties Volume in an adult Female 4 5 L Male 5 6 L pH 735 745 Osmolarity 280 296 mOsM Salinity 09 Hematocrit Female 37 48 Male 45 52 Hemoglobin Female 12 16 gdL Male 13 18 gdL RBC count Female 42 54 millionuL Male 46 62 millior uL Platelet count 130000 360000uL WBC count 5 00 10000 uL Blood Plasma Straw colored sticky Contains hormones blood proteins electrolytes waste gases and nutrients 90 water Constant production due to homeostatic mechanisms Serum the components of plasma minus fibrinogen Osmolarity total molarity of dissolved particles that cannot pass through the blood vessel wall Colloid Osmotic Pressure COP the contribution of proteins to blood osmotic pressure Ensures balance of uid between the blood and the tissues Proteins Albumin 60 COP major contributor to blood viscosity transport lipids hormones calcium and other solutes buffers blood pH Alpha Globulins Transports hemoglobin copper lipids fat soluble vitamins and hormones and promotes blood clotting Beta Globulins Transports iron and lipids aids in destruction of toxins and microorganisms Gamma Globulins Antibodies combat pathogens Fibrinogen 4 Becomes fibrin the major component of blood clots Erythrocytes Functi0n transport respiratory gases Pick up 02 from the lungs and transport to body tissues Pick of C02 from body tissues and transport to the lungs Contributes to blood viscosity Hematocrit percentage of erythrocytes in a blood sample Stmcture at biconcave discs ideal for transport and gas exchange Spectrin and Actin maintain the shape Very exible Short lifespan due to no nucleus Hemoglobin protein that makes up 97 of contents Lack a nucleus Lack mitochondria generate ATP by anaerobic mechanisms to prevent metabolism of 02 Carbonic Anhvdrase enzyme that catalyzes the metabolism of C02 Hemoglobin Made up of 4 globin chains and heme red pigment 2 alpha globins and 2 beta globins Globins are the site of C02 binding Heme iron containing molecule site of 02 binding Carries most of the body s 02 and 20 of the body s C02 Each molecule can bind to 4 molecules of 02 250 million moleculesRBC 1 billion molecules of 02 per RBC Changes shapecolor when it bindsunbinds to respiratory gases Oxygen loading 02 is picked up by Hb in the lungs Oxygen unloading when 02 is released by Hb in body tissues 0xvhemoglobin Hb02 bound to oxygen appears ruby red colored Highest levels in pulmonary veins and systemic arteries Deoxvhemoglobin HHb unbound to oxygen appears dark red colored Highest levels in pulmonary arteries and systemic veins arbaminohemoglobin gHbC021 bound to carbon dioxide Highest levels in pulmonary arteries and systemic veins Iron Metabolism Ir0n nutritional requirement for erythropoiesis Ingested iron Ferric Fe3 and Ferrous Fe2 ions Stomach acid converts Fe3 into Fe2 Gastroferritin binds F62 in the stomach and transports it to the small intestine At the small intestine gastroferritin F62 complex is absorbed into the blood F62 is unbound from gastroferritin and binds to Transferrin Transferrin binds to F62 and transports it through the blood to Liver where it is stored as ferritin Hepatic Portal System Muscle cells for myoglobin synthesis Bone marrow for erythrocyte synthesis Most body cells formation of cytochromes for ATP production Copyright e Mc rawHill Educstigma iF39erm39iassinn required Juli repmduetnen cw display it Fiernaining tianstetriin is distributed to either ergans where Feta is used tat matte hemegiebing mysgle ein eta iiiiiatuire ei Fe2 and Fe3 is ingested F39e3 binds te apetenritin Ferritm Sternasn acid it be stated sensetts Fe3 as territin in F9 Apeierritin Gastre territin in liven seine transteriin 39 Fez binds in gestrnteriritin releases Fe2 fer stnrage II 39 Bluest aliasima at 51 39 39 V 39 i a a in bland piasi nai Transferrin i d G agtr f mtm ltransp rtg Fest bind m transferrin Fe t in email intestine and i reieases it far abserpti Erythropoiesis Negative feedback Erythrocyte production begins as the hemocytoblast and is committed as proerythroblast Takes 15 days Reticulocyte counts provide rough indeX of rate of RBC formation Homeostasis is maintained by oxygen content of the blood n Hymnalf y quotUy J39L39I39l39e39tKI Cl llUmeqtm39 391 oxemiagh m h deficiency in quotbd HEW Er th 9 ietin EPO glycoprotein hormone that stimulates red bone marrow to Ef e 39 i quot r r V 39i 39 i 39 A V i i quot v39 iEimnmswe CitquotLi Emh rsbiast Hstieiilseirts Exist in red bane marrew Exist in sirsLiiatien Polycythemia Abnormal excess of erythrocytes Increases blood Viscosity which slows blood ow Primary Polycythemia gVera bone marrow cancer resulting in polycythemia Can reach up to 80 hematocrit SecondarV PochVthemia polycythemia from all other causes High Altitude Dehydration Emphysema Use of recombinant EPO treatment Excessive aerobic exercise Erythrocyte Elimination RBC lifespan lOO 120 days Due to anucleate condition Old RBCs lose exibility as Spectrin is broke down Most are lost in the spleen RBC graveyard Hemolysis rupture of RBC Fragments eliminated by macrophages Heme groups are separated from globins Iron is bound to Transferrina d ntgegfpr fur reruse39r rtnebeuy The Heme group is con verted to Biliverdilnatchden conV 9 o Bilirubin will be bound to albump 39g ieeaairbemtranspo aged two Bilirubin can be seciii39iii it ser a A Can be metabolii ilin in the intestine Ue e in the yellow bone marrow 39 quoth H I quot ye e liver Erythrocytes r Circular2 Em m clays Expired EWI IFDE WE39E Weak EJIE I EI39I litEr and when le gme l c z Emil HE H39i39lg i bal39l degrade7 a 7 7 I H zemge letin 2 l I E that 539 Pen Hyrimiyiaeul to Free El ii is ammo acids I39M Savage FEE use Loss Ergr ELMh mE ag ima ih n j Irmunf Etc Feelarm Anemia Blood has abnormally low oxygen carrying capacity Causes Insufficient number of RBCs Hemorrhagic anemia blood loss Hemolytic anemia lysis of RBCs due to parasitic or bacterial infection bad blood transfusion or hemoglobin abnormalities Aplastic Anemia destruction of red marrow Renal Anemia results from renal disease insufficient production of EPO Low hemoglobin content Iron deficiency anemia production of small pale erythrocytes called Microcytes Pernicious anemia autoimmune disorder which causes stomach mucosa to cease production of Intrinsic factor forms Macrocytes Abnormal hemoglobin Thalassemias hereditary group of diseases Absent or faulty globin chain often seen in Mediterranean ancestry Symptoms fatigue shortness of breath stunted growth in children and jaundice Sickle Cell anemia abnormal hemoglobin gene 14OO African American newborns in the US Crescent shaped erythrocyte Can cause extreme pain in muscles and bones Erythrocytes rupture easily and can block blood ow in blood vessels causing stroke Human Blood Groups Antigens glycoproteins and glycolipids on RBC plasma membranes Aka Agglutinogens promote agglutination clumping when missed with an incorrect blood type Determines ABO blood groups The Rh blood group is determined by the presence of the D antigen denotes or gglutinins antibodies that include agglutination of RBCs wit foreign antigens Alpha Agglutinin Antifl reacts to antigen A to induce agglutination Beta Agglutinin AntiB reacts to antigen B to induce agglutination AB blood type A and B antigens no antibodies will accept A B AB or 0 blood universal acceptor A blood type A antigens Anti B antibody will accept A or 0 blood B blood type B antigens Anti A antibody will accept B or 0 blood 0 blood type no antigens Anti A and Anti B antibodies will accept 0 blood universal donor Rh Factor Rh individuals do not produce anti Rh antibodies unless they encounter Rh blood Rh mothers who are pregnant with Rh babies will produce anti Rh antibodies during bleeding which occurs with placental attachment RhoGAM shot is given after giving birth to prevent antibody formation If this does not happen in later pregnancies with Rh babies this will result in Hemolytic Disease of the Newborn erythroblastosis fetalis and the baby will become anemic and hypoxic Transfusions Transfusion Reaction induces clumping and destruction of RBCs Reduced oxygen carrying capacity Hindered blood ow Autologous Transfusions patients pre donate their own blood in the case that they need a transfusion Plasmapheresis Blood is removed plasma is separated from formed elements and the formed elements are returned to the patient or donor Antibodies from the blood of individuals with autoimmune disorders are removed during the process Plasma can be used for burn victims Plasma proteins and factors can be used for research and other therapies Restoring blood volume When there is not enough time for blood typing blood volume may increase to prevent shock Does not increase oxygen carrying capacity Normal Saline or Multiple Electrolyte Solutions Ringer s Solution can increase plasma Plasma expanders mimic the osmotic properties of albumin but may involve other complications Leukocytes lt1 of total blood volume Protect the body from damage due to bacteria toxins viruses parasites and tumors Circulate through blood and exit capillaries through tiny pores diapedesis Attracted to target sitesmolecules via Chemotaxis Leulltocytosis increase WBC number due to infection Two Categories Gmnulocytes contain granules Agmnulocytes no granules Granulocytes Neutrophils Most common Phagocytize bacteria Release antimicrobial chemicals Eosinophils Phagocytize antigen antibody complexes allergens and in ammatory chemicals Release enzymes that weaken or destroy parasites B asophils Secrete histamine vasodilator and heparin anticoagulant Agranulocytes Lymphocytes Destroy cancer cells cells infected with Viruses and foreign cells Secrete antibodies Immune memory T cell or B cell Monocytes Differentiate into macrophages Phagocytize pathogens dead neutrophils and debris of dead cells Present antigens to activate other cells of the immune system Leukopoiesis Production of white blood cells All derived from Hematopoietic Stem Cells HSC HSCs differentiate into colony forming units CFUs and then into more specific cell lines Myeloblasts CFUs that differentiate into neutrophils eosinophils and basophils Monoblasts CFUs that differentiate into monocytes Lymphoblasts CFUs that differentiate into lymphocytes Red bone marrow stores granulocytes and monocytes until they are needed Most circulating leukocytes have a shelf life in the blood Lymphocytes are responsible for immune memory that can eXist for decades Leukocyte Disorders Leuk0penia WBC count is below 5000 Causes Anticancer treatments and radiation Lead arsenic and mercury poisoning Measles mumps chickenpox polio in uenza and AIDS Can result in opportunistic infections that are not normally seen in healthy individuals LeukocytoSiS WBC count above 10000 Analysis of WBC types can indicate allergies infection or cancer Can also be seen during dehydration Diagnostic Blood Tests Complete Blood Count CBC Count different types of formed elements hematocrit hemoglobin content and size of RBCs Differential WBC count indicating number of each type of leukocyte Bone Marrow Aspiration and Biopsy Small amount of bone marrow aspirated to test blood cell formation Biopsy of bone marrow itself provides analysis of entire sections of tissue Leukemia Overproduction of unspecialized leukocytes WBCs are large amorphous and non functional Causes Destruction of red bone marrow viral infection and genetics Irradiation and antileukemic drugs destroy cancerous cells and stem cell transplants increase WBC production Characterized as Myeloid uncontrolled granulocyte production Lymphoid uncontrolled lymphocyte or monocyte production AND Acute quickly advancing leukocytes are undifferentiated common in children Chronic slowly advancing derived from cells later than myelocytes common in elderly Symptoms Anemia Vulnerability to infection Impaired blood clotting Frequent metastasis Acute Lymphoblastic Leukemia is most common type of childhood cancer Greatest success in treatment and rate of cure Treatments Chemotherapy Marrow transplants Controlling side affects like anemia hemorrhage and infection Platelets Anucleate fragments that arise from larger marrow Megakaryocytes Intemal granules secrete chemicals that Induce vasodilation Promote blood clotting Attract neutrophils and monocytes to in ammation sites Initiate the formation of clot dissolving enzymes Aggregate to form platelet plugs to prevent blood loss from broken blood vessels Secrete growth factors to stimulate repair of broken blood vessels Intemalize and destroy bacteria 1 ts2m gem if I 4 F Hmm n Fmrm nknmm Thmopoesis Wk r y l t Emink rg eym liltalni roduction of platelets Thr0b0p0ietin produced by the liver and induces production of large megakaryocytes in red bone marrow Megakaryocytes rupture into tiny inactive platelets that are released into the blood stream Platelets circulate for about 10 days Thrombosvtopenia platelet deficiency Hemostasis Cessation of bleeding by the use of platelets 1 Vascular Spasm Damaged blood vessels induce vasoconstriction to slow blood ow Smooth muscle injury triggers the chemical release of platelets or endothelial cells and by refluX induced by local pain receptors Constricted vessels stop blood loss for 20 30 minutes and is most effective in smaller vessels 2 Platelet Plug Formation Prostacyclin prevents platelets from adhering to the endothelium that lines the blood vessels Broken blood vessels eXpose collagen fibers which adhere to circulating platelets Positive feedback cycle Platelets swell and release granules containing thromboxane A2 ADP serotonin and PF3 These chemicals attract more platelets to the site New platelets swell secrete these chemicals and attract more platelets 3 Coagulation Triggered by clotting factors Mostly produced by the liver Synthesis of clotting factors require Vitamin K A cascade of events leads to the activation of each clotting factor When activated most clotting factors undergo conformational change and become enzymes Calcium and Fibrinogen are the exception End goal is the formation of a Fibrin Polymer Mesh Initiation of Coagulation 2 ways Extrinsic Pathway Fast initiated by clotting factors released by damaged blood vessel walls Damaged tissue initiates the cascade by releasing Thromboplastin Thromboplastin combines with Factor VII in the presence of Ca2 to from Thrombokinase Intrinsic Pathway Slow requires factors that circulate in blood Platelets release Factor XII which initiates a cascade to activate XI IX and VIII in the presence of Thromboplastin and Ca2 Ends with the formation of Thrombokinase Completion of Coagulation Once Thrombokinase is activated it combines with factors III and V with Ca2 and PF3 to form Prothrombin Activator Prothrombin activator enzymatically catalyzes the transformation of Prothrombin into Thrombin Thrombin converts inactive F ibrinogen into Fibrin strands Fibrirz threads are linked with factor XIII and Ca2 to form a Fibrin Polymer Fibrin Polymer mesh traps platelets and RBCs forming a blood clot Clot is usually formed 3 6 minutes after Fieauz39tiin cascade time damage occurs The activation cascade becomes amplified through positive feedback Post Coagulation Fibrous pseudopods of platelets adhere to fibrin strands and contract clot retraction This shrinks the clot within 30 min Chemical signals begin the process of tissue repair for the damaged vessel during and after coagulation Platelet Derived Growth Factor PDGF Released by platelets to stimulate smooth muscle and fibroblast restoration Vascalar Endothelial Growth Factor VEGF Stimulates endothelial restoration Fibrinolysi dissolution of a clot Factor XII catalyzes the formation of Kallikrein Kallikrein and Thrombin convert the inactive plasminogen into plasmin Plasmin catalyzes the break down of the fibrin mesh Plasmin activates Kallikrein positive feedback cycle Endothelial cells also being to release Tissue Plasminogen Activator tPA in the presence of a clot Converts plasminogen to plasmin reha liiIir in Helm Jill Fmitin Feedback iiip Fiaemin E i Fibrin a39agm a nn Elm l l jli l l lili39 i l l I Anticoagulants Inhibit blood clotting dominant when there is no vessel damage Most anticoagulants inhibit the intrinsic pathway Plasmirz Prostacyclin and Nitric Oxide NO circulate through blood to prevent platelets from aggregating at the wrong time Antithrombin III inhibit activation of all thrombin enzymes not bound to fibrin Heparin released by basophils and mast cells found on the surface of endothelial cells Pharmaceutical Heparin is the most used anticoagulant in the hospital Warfarin Coumadin most used in outpatient treatment to reduce clotting associated with atrial fibrillation which might lead to strokes Vitamin K green foods can decrease effectiveness of Warfarin tPA prevent ischemic strokes and heart attacks Thromboembolic Disorders Caused by atherosclerosis and in ammation that can roughen vessel walls stimulating the aggregation of platelets Thrombus clot that develops and persists in an unbroken vessel Embolus a thrombus that becomes dislodged and oats through the blood stream Embolism an embolus that becomes wedged and obstructs a blood vessel Pulmonary embolism impairs oxygen supply Cerebral Embolism can cause stroke Disseminated Intravascular Coagulation DIC widespread blood clotting prevents residual blood from being able to clot Blockages and severe bleeding Common pregnancy complication septicemia or bad blood transfusions Hemat0ma accumulated clotted blood in the tissues Results from injury Eventually absorbed naturally unless infection develops Thr0mbocyt0penia platelet count under 50000 Hemorrhage in small vessels in body resulting in petechial on skin Seen during cancer infection autoimmune disorders and drug reactions Transfusions provide temporary relief Impaired liver function Due to vitamin K deficiency hepatitis cirrhosis or cancer Hemophili deficient clotting factors Hemophilia A and B are X linked traits and are more common in males Hemophilia C occurs equally among the sexes Minor tissue damage can be lethal joints are often disabled due to repeated bleeding following exercise or trauma Rely on transfusions of blood plasma or clotting factors
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