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

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

4 AP2 Chap. 19: Cardiovascular SystBlood: 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 AP2 Chap. 19: Cardiovascular SystI. 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 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 O2: lungs cells CO2: cells  lungs for exhalation Ingested nutrients, ions, & H2O: Digestive system  cells Waste products: Cells  kidneys for elimination 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 3. Transport of regulatory molecules Carries hormones & enz’s that regulate body processes from 1 body part to another

8 I. Fxns of the blood The blood helps maintain homeostasis in several ways: 4. Regulation of pH & Osmosis 6. Protection against foreign substances Buffers maintain blood pH Homeostasis= 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 AP2 Chap. 19: Cardiovascular SystII. Plasma AP2 Chap. 19: Cardiovascular Syst

10 II. Plasma 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 Figure 19.1 pg 651 Waste: Urea, Uric Acid, Creatinine, Ammonia Salts, Bilirubin, & lactic acid Regulatory Substances

11 Functions in the 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 II. Plasma Functions in the plasma:

12 II. Plasma Fxn of plasma proteins1. 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 AP2 Chap. 19: Cardiovascular SystII. 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 AP2 Chap. 19: Cardiovascular SystIII. Formed Elements Production of Formed Elements Red Blood Cells White Blood Cells Platelets AP2 Chap. 19: Cardiovascular Syst

15 III. Formed Elements: 3 major classesRed 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 III. Formed Elements Prod’n of formed elementsHematopoiesis (Hemopoiesis) 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) III. Formed Elements Prod’n of formed elements Figure 19.2 pg 655

17 III. Formed Elements RBC’s: StructureBiconcave 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 ’ing its 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 Elements RBC’s: FXNPrimary 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 Elements RBC’s: HemoglobinFigure 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 3rd mo fetal replaces embryonic hemoglobin Adult: by birth 60-90% is adult by 2 to 4 almost nothing but adult Each RBC contains 270 million hemoglobin proteins (each carrying 4 oxygen) And we have trillion RBC’s at any given time….Try the math on that!! (~25% of all of the body’s cells we have ~ 100 trillion in total.) AP2 Chap. 19: Cardiovascular Syst

20 III. Formed Elements RBC’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’s Life History of RBC’sRBC 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’s Life History of RBC’sRBC 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’sRBC 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’sFigure 19.3 pg 656 Figure 19.7 pg 661 Figure 19.8 pg 662 AP2 Chap. 19: Cardiovascular Syst

25 III. Formed Elements: WBC’sLack 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’s 3 major classesRed 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 GranulocytesBasophil Eosinophil Neutrophil Nucleus w/ 2 indistinct lobes; cytoplasmic granules stain blue-purple; mm in diameter Fxn: Releases: Histamine promotes inflammation Heparin prevents clot formation Nucleus often bilobed; cytoplasmic granules stain orange-red to bright red; 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; mm diameter Fxn Phagocytizes microorganisms, Ag-Ab complexes & other substances Lysozyme 0.5-1% WBC 2-4% WBC 60-70% WBC AP2 Chap. 19: Cardiovascular Syst

28 III. Formed Elements: WBC’s AgranulocytesLymphocytes Monocytes 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 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 20-25% WBC 3-8% WBC AP2 Chap. 19: Cardiovascular Syst

29 III. Formed Elements: PlateletsCell 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 AP2 Chap. 19: Cardiovascular SystIV. Hemostasis Vascular Spasm Platelet plug formation Coagulation Control of Clot formation Clot retraction & Dissolution AP2 Chap. 19: Cardiovascular Syst

31 AP2 Chap. 19: Cardiovascular SystIV. 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 SpasmImmediate 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 FormationPlatelet 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: CoagulationWhen 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 formation Extrinsic PathwayFor 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 formation Intrinsic PathwayIntrinsic 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 formation Common PathwayExtrinsic 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 formationIf 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. @ 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. 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

39 IV. Hemostasis: Clot Retraction & DissolutionClot 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 bld flw, reduces infection, & enhances healing. AP2 Chap. 19: Cardiovascular Syst

40 IV. Hemostasis: Clot Retraction & DissolutionFibrinolysis: 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 ABO Blood Group Rh Blood GroupV. 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 bld vol 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 Type A Type B Type AB Type O Rh+ Rh-ABO-Blood Group Variants on Chromosome 9 Type A Type B Type AB Type O Surface displays A-Ag’s only Surface displays B-Ag’s only Surface displays No Ags Surface displays A & B-Ag’s Codominance Rh-Factor Blood Group on Chromosome 1 Rh+ Rh- Surface displays Rh-Fator Surface displays No antigens

45 Most common blood types that existType 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 B blood…his body makes Ab’s against the B-Ag and his blood agglutinates & hemolysis and Frank dies from massive clot formation   Transfused with Type A blood…lives happily every after 

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

48 Agglutination reactionFigure 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.