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Chapter 19

Chapter 19. Cardiovascular System: The Blood. Cardiovascular System: The Blood. Functions of the Blood Plasma Formed Elements Hemostasis Blood Grouping Diagnostic Blood Tests. Cardiovascular System. Fig. 1.3 pg 8.

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Chapter 19

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  1. Chapter 19 Cardiovascular System: The Blood AP2 Chap. 19: Cardiovascular Syst

  2. Cardiovascular System: The Blood • Functions of the Blood • Plasma • Formed Elements • Hemostasis • Blood Grouping • Diagnostic Blood Tests AP2 Chap. 19: Cardiovascular Syst

  3. Cardiovascular System Fig. 1.3 pg 8 • Cells req. constant nutrition & waste removal b/c they are metabolically active • This system made up of the heart, the blood vessels, & the blood: connects the various tissues of the body. The heart pumps blood thru the blood vessels & the blood delivers nutrients & picks up waste products. AP2 Chap. 19: Cardiovascular Syst

  4. Blood: Facts & Figures • Blood: Type of CT • Formed Elements: • 45% make-up • Cells • Cell Fragments • Plasma • 55% bld vol. • Liquid Matrix • Total Bld Vol. • ♀ 4-5 Liters • ♂ 5-6 Liters • 8% of total body Weight Figure 19.1 pg 651 AP2 Chap. 19: Cardiovascular Syst

  5. I. Fxns of the blood AP2 Chap. 19: Cardiovascular Syst

  6. I. Fxns of the blood The blood helps maintain homeostasis in several ways: 1. Transport of gases, nutrients, & waste products. 2. Transport of processed molecules 3. Transport of regulatory molecules 4. Regulation of pH & Osmosis 5. Maintenance of Body Temperature 6. Protection against foreign substances 7. Clot formation AP2 Chap. 19: Cardiovascular Syst

  7. The blood helps maintain homeostasis in several ways: I. Fxns of the blood 1. Transport of gases, nutrients, & waste products. 2. Transport of processed molecules Many things are made in one place in the body. They are then carried via the blood to another part for modification & finalization. Ex\ Skin prod’s Vit D Transferred to liver & kidney to modify into its active form Finalized form travels to the small intestine to promote Ca2+ uptake • O2: • lungs cells • CO2: • cells  lungs for exhalation • Ingested nutrients, ions, & H2O: • Digestive system  cells • Waste products: • Cells  kidneys for elimination 3. Transport of regulatory molecules • Carries hormones & enz’s that regulate body processes from 1 body part to another

  8. The blood helps maintain homeostasis in several ways: I. Fxns of the blood 6. Protection against foreign substances 4. Regulation of pH & Osmosis Buffers maintain blood pH Homeostasis=7.35-7.45 Osmotic composition: Bld is critical for maintaining normal fluid &ion balance • An important part of the immune system is located w/in the blood & helps fight foreign substances such as toxins or microorganisms 5. Maintenance of Body Temp. 7. Clot formation • Warm bld is transferred from the body core to the body surface where heat is released • Protects against XSV bld loss when bld vessels are damaged • 1st step in tissue repair & return to fxn when tissues are damaged AP2 Chap. 19: Cardiovascular Syst

  9. II. Plasma AP2 Chap. 19: Cardiovascular Syst

  10. II. Plasma Figure 19.1 pg 651 • 91% water & 9% other • Proteins, ions, nutrients, gases, wastes • Colloid • Plasma Proteins: • Pro’d by liver or bld cells • Globulins • Albumins • Fibrinogen • Ions: Na, K, Ca, Mg, Cl, Fe, PO4, H, OH-, HCO3- • Nutrients: • Vitamins • Glucose, AA’s, Cholesterol, & triglycerides (aka triacylglycerol ) • Gases: O2, CO2, & N2 • Waste: Urea, Uric Acid, Creatinine, Ammonia Salts, Bilirubin, & lactic acid • Regulatory Substances

  11. Functions in the plasma: II. Plasma • Water: • Acts as a solvent & suspending medium • Ions: • Involved in osmosis, membrane potential, & acid-base balance • Nutrients: • Vitamins: promote enz activity • Rest: energy & building blocks • Regulatory Substances: • Enz’s catalyze chem rxns • Hormones stimulate/inhibit body fxns • Gases • O2 • Req’d for aerobic respiration • CO2 • Waste product of aerobic respiration that can be used as bicarbonate helping buffer bld • N2 • Inert

  12. II. PlasmaFxn of plasma proteins 1. Globulins: • a • Protects tissues via inflammation • Fxns as a transport protein • Converts Fe2+ to Fe3+ for transport in transferrin • Transports hemoglobin from damaged RBC’s • b • Acts as a transport protein • Involved in immunity • Prevents blood loss • g • Most antibodies are g globulins involved in immunity 2. Albumin: • Partly responsible for bld viscosity & osmotic pressure • Acts as a buffer • Acts as a transport protein 3. Fibrinogen • Fxns in bld clotting

  13. II. Plasma Composition Waste: • Urea, Uric Acid, Creatinine, Ammonia Salts: • Byproducts of protein metabolism that are excreted by the kidneys • Bilirubin • Byproduct of RBC breakdown that is excreted by the liver as part of the bile into the intestine • Lactic Acid • Byproduct of anaerobic respiration that is converted into glucose by the liver AP2 Chap. 19: Cardiovascular Syst

  14. III. Formed Elements Production of Formed Elements Red Blood Cells White Blood Cells Platelets AP2 Chap. 19: Cardiovascular Syst

  15. III. Formed Elements:3 major classes Red Blood Cells (Erythrocytes) RBC’s 700X more than WBC 17X more than platelets White Blood Cells (Leukocytes) WBC’s Platelets (Thrombocytes) Granulocytes Agranulocytes Basophil Monocyte Eosinophil Lymphocyte Neutrophil

  16. Hematopoiesis (Hemopoiesis) III. Formed ElementsProd’n of formed elements • Embryo: • Tissues like the yoke sac, liver, thymus, spleen, lymph nodes, & red bone marrow (RBM) • After Birth: • Confined to RBM with some lymphoid tissue aiding in prod’n of lymphocytes • Young children almost all bone marrow is RBM • Adults RBM confined to ribs, sternum, vertebrae, pelvis, proximal femur & humerus (rest replaced by Yellow bone marrow) Figure 19.2 pg 655

  17. III. Formed ElementsRBC’s: Structure • Biconcave disk with thicker edges than in the center • Allows for greater surface area & makes movement of gases into the cell more rapid • Allows for easier bending & folding ’ingits size to allow it to pass more easily thru small bld vessels • Original cell looses its nucleus & almost all organelles when mature. • Main Component w/in RBC: • Hemoglobin red pigmented protein filling 1/3 of the RBC vol. • Minor Components: • Lipids, ATP & the enz: carbonic anhydrase Figure 19.3 pg 656 AP2 Chap. 19: Cardiovascular Syst

  18. III. Formed ElementsRBC’s: FXN Primary Fxn O2 transport • Take O2 from the lungs to the body tissues • 98.5% of O2 in bld linked to hemoglobin • 1.5% dissolved in plasma • Take CO2 from body tissues to the lungs • RBC rupturehemolysis • Hemoglobin must be in cell if not denatures & no longer fxnal • CO2 Transport in blood • 3 major ways: • 7% dissolved in plasma • 23% attached to Hemoglobin • 70% transported as bicarbonate ion (HCO3-) • Carbonic anhydrase is the enzyme responsible for converting CO2 & H2O into Carbonic Acid wh/dissociates into a H+ & HCO3- AP2 Chap. 19: Cardiovascular Syst

  19. III. Formed ElementsRBC’s: Hemoglobin Figure 19.4 pg 656 • 4 PP-Chain + 4 Heme-groups • Each polypeptide chain (globin) is bound to 1 heme. • 9 hemoglobin types based on aa sequence (a, b, g, d & embryonic) • Most adult is a combo of 2 a and 2 b • Heme is a red pigment molecule containing an iron atom • 3 types of Hemoglobin exist w/ diff’s in their affinity for O2 • Embryonic: pro’d up to 3rd mo. of development • Fetal: @ 3rd mo fetal replaces embryonic hemoglobin • Adult: by birth 60-90% is adult by 2 to 4 almost nothing but adult AP2 Chap. 19: Cardiovascular Syst

  20. III. Formed ElementsRBC’s: Hemoglobin Iron (Fe) • Fe is req’d for normal hemoglobin fxn b/c O2 binds to the Fe molecule w/in the heme • It is usually ingested in diet. • Exposure to O2, binds 1 O2 to each Heme (oxyhemoglobin) w/o (deoxyhemoglobin) • AA’s of the globin bind to CO2 : • Carbaminohemoglobin • Also bind to NO, which fxns as a chemical signal in the body (hormone) & induces the relaxation of smooth muscle • Thus Hemoglobin may play a role in blood pressure via NO involvement. AP2 Chap. 19: Cardiovascular Syst

  21. III. Formed Elements: RBC’sLife History of RBC’s RBC Production • Lowered bld O2 induced the kidney to release erythropoietin wh/goes to bone marrow & increases RBC prod’n thus increasing bld O2 levels Figure 19.5 pg 659 AP2 Chap. 19: Cardiovascular Syst

  22. III. Formed Elements: RBC’sLife History of RBC’s RBC death and Hemoglobin recycling • RBC’s only live for 110(♀)-120(♂) days • W/O nuclei they have no way to prod. new proteins or divide thus existing proteins, enz’s, PM components & other structures begin to degenerate & the RBC becomes less able to transport O2 & the PM b/c’s more fragile over time. They can rupture releasing hemoglobin. • What to do???? Figure 19.6 pg 660 Aged, damaged, or abnormal RBC’s are taken to the spleen, liver & other lymphatic tissue. Here macrophages isolate hemoglobin.

  23. III. Formed Elements: RBC’s: Life History of RBC’s RBC death and Hemoglobin recycling • Hemoglobin is separated into Heme & Globin • Globin is broken down into it’s component AA’s that can be used to make new proteins or metabolized. • Heme- Fe is released and the rest is converted 1st into biliverdin then to bilirubin • Bilirubin via bld goes to the liver & excreted w/in bile to the small intestine (colors both feces & urine & reabsorbed bilirubin derivatives) • Fe: bound to transferrin & carried in bld to: • Various tissues for storage • Bone marrow to be used in the production of new hemoglobin. Figure 19.6 pg 660

  24. III. Formed Elements: WBC’s Figure 19.3 pg 656 Figure 19.7 pg 661 Figure 19.8 pg 662 AP2 Chap. 19: Cardiovascular Syst

  25. III. Formed Elements: WBC’s • Lack hemoglobin • Have a nucleus • Protect the body against invading microorganisms & remove dead cells & debris from the body • Most are motile exhibiting ameboid movement. • Leave the bld stream & enter the tissue via diapedesis • b/c thin & elongated & slip btwn or thru the cells of the blood vessel walls • Chemotaxis: WBC attraction to foreign materials or dead cells w/in the tissue • At the site of infections WBC’s accumulate & phagocytize bacteria, dirt, & dead cells; then they die: • Pus buildup of dead WBC’s+ bacteria + fluid + cell debris AP2 Chap. 19: Cardiovascular Syst

  26. III. Formed Elements: WBC’s3 major classes Red Blood Cells (Erythrocytes) RBC’s 700X more than WBC 17X more than platelets White Blood Cells (Leukocytes) WBC’s Platelets (Thrombocytes) Granulocytes Agranulocytes Basophil Monocyte Eosinophil Lymphocyte Neutrophil

  27. III. Formed Elements: WBC’s Granulocytes Eosinophil Neutrophil Basophil • Nucleus often bilobed; cytoplasmic granules stain orange-red to bright red; 11-14 mm diameter • Fxn: • Releases chemicals that reduce inflammation • Attacks certain worm parasites • Nucleus has 2 to 4 lobes connected by thin filaments; cytoplasmic granules stain light pink to reddish purple; 10-12 mm diameter • Fxn • Phagocytizes microorganisms, Ag-Ab complexes & other substances • Lysozyme • Nucleus w/ 2 indistinct lobes; cytoplasmic granules stain blue-purple; 10-12 mm in diameter • Fxn: • Releases: • Histamine promotes inflammation • Heparin prevents clot formation 0.5-1% WBC 2-4% WBC 60-70% WBC AP2 Chap. 19: Cardiovascular Syst

  28. III. Formed Elements: WBC’s Agranulocytes Lymphocytes Monocytes Nucleus can be round, kidney shaped, or horse shoe shaped; contains more cytoplasm than lymphocyte; 12-20mm diameter Phagocytic cell in the bld; leaves the bld & becomes a macrophage, wh/ phagocytizes bacteria, dead cells, cell fragments, & other debris w/in tissue • Round nucleus; cytoplasm forms a halo around the nucleus; 6-14 mm diameter • Produces antibodies (Ab’s) & other chemicals responsible for destroying microorganisms; contributes to allergic rxns, graft rejection, tumor control, & reg’n of the immune system 20-25% WBC 3-8% WBC AP2 Chap. 19: Cardiovascular Syst

  29. III. Formed Elements: Platelets • Cell fragments surrounded by plasma membrane & containing granules • ~ 3mm diameter • Surface displays proteins that allow platelets to stick to other molecules (glycoproteins) • These surface molecules & internal granules help control bld loss • Also contains actin & myosin to cause platelet contraction • Life 5-7 days • Essential Functional Roles: • Forming platelet plugs, which seal holes in small vessels • Promoting the formation & contraction of clots; wh/help seal off larger wounds in bld vessels AP2 Chap. 19: Cardiovascular Syst

  30. IV. Hemostasis Vascular Spasm Platelet plug formation Coagulation Control of Clot formation Clot retraction & Dissolution AP2 Chap. 19: Cardiovascular Syst

  31. IV. Hemostasis • The stoppage of bleeding to maintain homeostasis. • 3 major steps to achieve hemostasis  • Vascular Spasm • Platelet plug formation • Coagulation AP2 Chap. 19: Cardiovascular Syst

  32. IV. Hemostasis: 1. Vascular Spasm • Immediate but temporary constriction of blood vessel resultant from vessel wall smooth muscle contraction. • Can close small vessels completely to stop bleeding • Produced by: • Nervous System Reflexes • Damage can cause reflexive contraction • Chemical Signals • Ex/ platelets release thromboxanes & damaged endothelial cells release endothelian both of wh/ induce contraction AP2 Chap. 19: Cardiovascular Syst

  33. IV. Hemostasis:2. Platelet Plug Formation • Platelet Adhesion: • von Willebrand factor (vWF) binds platelets to collagen in damaged tissue attaching platelets to damaged surface • Platelet release rxn: • Bound platelets release ADP, thromboxanes, & other chemicals that activate other platelets • Platelet aggregation • Activated platelets express fibrinogen receptors that bind fibrinogen (a plasma protein) wh/ is used to link platelet to platelet with an interlinking fibrinogen. • Activated platelets also express platelet factor III & coagulation factor V wh/ are imp. to clot formation • Accumulation of platelets that can seal-up small breaks in blood vessels • Described in steps that actually occur simultaneously Figure 19.9 pg 663

  34. IV. Hemostasis: Coagulation • When a bld vessel is severely damaged blood clotting (coagulation) results in the formation of a clot. • Blood clot network of threadlike protein fibers called fibrin that trap blood cells, platelets, & fluid. • Formation of a blood clot depends on a number of proteins called coagulation factors. • These factors only fxn after activation wh/is a complex process involving multiple chemical rxns. • Activation begins with 1. Extrinsic & 2. Intrinsic pathways that converge into the Common Pathway Figure 19.10 pg 664 AP2 Chap. 19: Cardiovascular Syst

  35. IV. Hemostasis: Coagulation: Clot formationExtrinsic Pathway For simplicity Factor will be abbreviated as F and roman numerals will be numbers • Extrinsic is so called b/c chemicals being released come from damaged tissue and not w/in the blood. • Tissues release thromboplastin/tissue factor(TF)/F3 (combo of lipoproteins & phospholipids) • TF in the presence of Ca2+ forms a complex with F7  • This complex activates F10 • This is the beginning of the common pathway Figure 19.11 pg 665 AP2 Chap. 19: Cardiovascular Syst

  36. IV. Hemostasis: Coagulation: Clot formationIntrinsic Pathway • Intrinsic is so called b/c chemicals being released come directly from the blood. • Plasma F12 contacts collagen from damaged tissue  F12 activation • Active F12 stimulation F11 activates F9 • Activated F9 joins with F13, platelet phospholipids & Ca2+ to activate F10 • This is the beginning of the common pathway Figure 19.11 pg 665 AP2 Chap. 19: Cardiovascular Syst

  37. IV. Hemostasis: Coagulation: Clot formationCommon Pathway • Extrinsic pathway may influence the fxn of the intrinsic thus they are not exclusive • On the platelet surface activated F10, F5, platelet phospholipids, & Ca2+ complex to form Prothrombinase (PT). • PT converts soluble plasma protein prothrombin into the enz  Thrombin (Tn) • Tn: • Converts soluble plasma protein fibrinogen into insoluble fibrin wh/ forms the fibrous network of the clot • Stimulate F13 activation necessary to stabilize the clot • Also part of + fdbk that stimulates the production of more Tn & platelet activation Figure 19.11 pg 665 AP2 Chap. 19: Cardiovascular Syst

  38. IV.Hemostasis:Control of clot formation • If clotting got out of control…homeostasis wouldn’t be maintained and it would lead to death. • Bld has several anticoagulants to prevent unwanted clotting via inhibition of clotting factors. • Examples: • Antithrombin • Plasma protein from liver that slowly inactivates thrombin • Heparin • w/antithrombin inactivates thrombin • Prostacyclin • Counteracts prothrombin by causing vasodilatation & inhibiting coagulation factor release from platelets • @ site of injury anticoagulants are outnumbered and thus unable to prevent clotting • Away from site of injury clotting factors are so dilute that anticoagulants can fxn properly.

  39. IV. Hemostasis: Clot Retraction & Dissolution • Clot retraction: formed clot begins condenses into denser compact structure. • Actin & myosin w/in platelets are like smooth muscle & begin to contract causing retraction • Serum will also be squeezed out of the clot. • Plasma minus fibrinogen & clotting factors • Consolidation of the clot pulls edges of damaged bld vessel together helps stop bldflw, reduces infection, & enhances healing. AP2 Chap. 19: Cardiovascular Syst

  40. IV. Hemostasis: Clot Retraction & Dissolution • Fibrinolysis: process by which a clot is dissolved w/in a few days of its formation. • Norm bld protein plasminogen is converted into plasmin: once active it is an enz that hydrolyzes fibrin. • It b/c part of the clot as it is forming. • Activated by: thrombin, F12, tissue plasminogen activator, urokinase, & lysosomal enz’s released from damaged tissues Figure 19.12 pg 667 AP2 Chap. 19: Cardiovascular Syst

  41. V. Blood Grouping ABO Blood Group Rh Blood Group AP2 Chap. 19: Cardiovascular Syst

  42. V. Blood Grouping • Transfusion: transfer of blood or blood components from one individual to another • Infusion: introduction of fluid other than blood (Saline/Glucose sol’n) into the blood. • Used in cases when bldvol needs to be restored to prevent shock. • Antigen (Ag): Surface protein • Antibody (Ab): protein from the blood plasma that binds to an antigen and marks that cell for death. • Ab’s are specific to a certain Ag. When Ab’s bind Ag’s on RBC’s they form molecular bridges attaching multiple RBC’s together. This “clumping” is called Agglutination. • This complex may also cause hemolysis.

  43. V. Blood Grouping Red Blood Cell Antigen (Ag) Antibody (Ab) In the human there have been 35 blood groups identified, but there are 2 primary groups of antigens that are displayed on RBC’s

  44. ABO-Blood Group Variants on Chromosome 9 Rh-Factor Blood Group on Chromosome 1 Type B Type A Type AB Type O Surface displays A-Ag’s only Surface displays B-Ag’s only Surface displays A & B-Ag’s Codominance Surface displays No Ags Rh+ Surface displays Rh-Fator Rh- Surface displays No antigens

  45. Most common blood types that exist Type A- Type B- Type AB- Type O- Type A+ Type B+ Type AB+ Type O+

  46. Issues w/blood donation & necessity of blood typing: • Ab’s do not develop unless they are exposed to a foreign Ag. Thus:  Frank A-type Blood Shot   Needs a blood transfusion  • Transfused with Type A blood…lives happily every after  • Transfused with Type B blood…his body makes Ab’s against the B-Ag and his blood agglutinates & hemolysis and Frank dies from massive clot formation  

  47. V. Blood Grouping: Ag’s & Ab’s Figure 19.13 pg 668 What would happen to the type AB if an A-Ab was introduced?? AP2 Chap. 19: Cardiovascular Syst

  48. Agglutination reaction Figure 19.14 pg 669 AP2 Chap. 19: Cardiovascular Syst

  49. Hemolytic Disease of a Newborn(HDN) • Rh- mother gives birth to an Rh+ fetus • 1st birth: • Everything is okay. Baby is born with out incident. • During birth mother is exposed to babies blood and can form antibodies… • 2nd birth: • Antibodies in the mothers body attack the baby as a foreign object and can kill it. • Prevention: • Injection of mother with RhoGAM soon after each birth. • It takes care of babies blood before the immune system can respond.

  50. Your responsibility for the exam! Pg 654: Stem cells & cancer therapy Pg 658: Effect of carbon monoxide on oxygen transport Pg 658: Hemoglobin-based Oxygen carriers Pg 663 Clinical importance of activating platelets Pg 666 How vitamin K helps prevent bleeding Pg 666 Danger of unwanted clots Diagnostic Blood Tests: pg 671-2 Clinical Focus: pg 673-4 AP2 Chap. 19: Cardiovascular Syst

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