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

Transcription

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

2 Cardiovascular System: The Blood I. Functions of the Blood II. Plasma III. Formed Elements IV. Hemostasis V. Blood Grouping VI. Diagnostic Blood Tests AP2 Chap. 19: Cardiovascular Syst 2

3 Cardiovascular System 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. Fig. 1.3 pg 8 AP2 Chap. 19: Cardiovascular Syst 3

4 Blood: Facts & Figures Figure 19.1 pg 651 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 AP2 Chap. 19: Cardiovascular Syst 4

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

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 6

7 O2: 1. Transport of gases, nutrients, & waste products. lungs cells CO2: cells lungs for exhalation Ingested nutrients, ions, & H2O: Digestive system cells Waste products: Cells kidneys for elimination I. Fxns of the blood The blood helps maintain homeostasis in several ways: 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 3. Transport of regulatory molecules Carries hormones & enz s that regulate body processes from 1 body part to another 7

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

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

10 II. Plasma 91% water & 9% other Figure 19.1 pg 651 Proteins, ions, nutrients, gases, wastes Colloid Plasma Proteins: Pro d by liver or bld cells 1. Globulins 2. Albumins 3. Fibrinogen Ions: Na, K, Ca, Mg, Cl, Fe, PO 4, H, OH -, HCO - 3 Waste: Urea, Uric Acid, Nutrients: Creatinine, Ammonia Vitamins Salts, Bilirubin, & lactic Glucose, AA s, Cholesterol, & triglycerides (aka triacylglycerol ) acid Gases: O 2, CO 2, & N 2 Regulatory Substances 10

11 Water: Acts as a solvent & suspending medium Ions: Involved in osmosis, membrane potential, & acidbase balance Nutrients: Vitamins: promote enz activity Rest: energy & building blocks Regulatory Substances: Enz s catalyze chem rxns Hormones stimulate/inhibit body fxns Gases O 2 Req d for aerobic respiration CO 2 Waste product of aerobic respiration that can be used as bicarbonate helping buffer bld N 2 Inert II. Plasma Functions in the plasma: 11

12 II. Plasma Fxn of plasma proteins 1. Globulins: α Protects tissues via inflammation Fxns as a transport protein Converts Fe2+ to Fe3+ for transport in transferrin Transports hemoglobin from damaged RBC s β Acts as a transport protein Involved in immunity Prevents blood loss γ Most antibodies are γ 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 12

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 13

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

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 15

16 III. Formed Elements Prod n of formed elements Hematopoiesis (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) Figure 19.2 pg

17 III. Formed Elements RBC 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 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 17

18 III. Formed Elements RBC s: FXN Primary Fxn O 2 transport Take O 2 from the lungs to the body tissues 98.5% of O 2 in bld linked to hemoglobin 1.5% dissolved in plasma Take CO 2 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: 1. 7% dissolved in plasma 2. 23% attached to Hemoglobin 3. 70% transported as bicarbonate ion (HCO 3- ) Carbonic anhydrase is the enzyme responsible for converting CO 2 & H 2 O into Carbonic Acid wh/ dissociates into a H + & HCO 3 - AP2 Chap. 19: Cardiovascular Syst 18

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

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 O 2, binds 1 O 2 to each Heme (oxyhemoglobin) w/o (deoxyhemoglobin) AA s of the globin bind to CO 2 : 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 20

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

22 III. Formed Elements: RBC s Life 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 O 2 & 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. 22

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 1 st 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

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 24

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 25

26 III. Formed Elements: WBC s 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 26

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

28 III. Formed Elements: WBC s Agranulocytes Lymphocytes Round nucleus; cytoplasm forms a halo around the nucleus; 6-14 µm 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 Monocytes Nucleus can be round, kidney shaped, or horse shoe shaped; contains more cytoplasm than lymphocyte; 12-20µm 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 28

29 III. Formed Elements: Platelets Cell fragments surrounded by plasma membrane & containing granules ~ 3µm 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: 1. Forming platelet plugs, which seal holes in small vessels 2. Promoting the formation & contraction of clots; wh/help seal off larger wounds in bld vessels AP2 Chap. 19: Cardiovascular Syst 29

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

31 IV. Hemostasis The stoppage of bleeding to maintain homeostasis. 3 major steps to achieve hemostasis 1. Vascular Spasm 2. Platelet plug formation 3. Coagulation AP2 Chap. 19: Cardiovascular Syst 31

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: 1. Nervous System Reflexes Damage can cause reflexive contraction 2. Chemical Signals Ex/ platelets release thromboxanes & damaged endothelial cells release endothelian both of wh/ induce contraction AP2 Chap. 19: Cardiovascular Syst 32

33 Accumulation of platelets that can seal-up small breaks in blood vessels Described in steps that actually occur simultaneously IV. Hemostasis: 2. Platelet Plug Formation Figure 19.9 pg 663 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 33

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 pg 664 AP2 Chap. 19: Cardiovascular Syst 34

35 IV. Hemostasis: Coagulation: Clot formation Extrinsic Pathway 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 Ca 2+ forms a complex with F7 This complex activates F10 This is the beginning of the common pathway For simplicity Factor will be abbreviated as F and roman numerals will be numbers Figure pg 665 AP2 Chap. 19: Cardiovascular Syst 35

36 IV. Hemostasis: Coagulation: Clot formation Intrinsic 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 & Ca 2+ to activate F10 This is the beginning of the common pathway Figure pg 665 AP2 Chap. 19: Cardiovascular Syst 36

37 IV. Hemostasis: Coagulation: Clot formation Common Pathway Extrinsic pathway may influence the fxn of the intrinsic thus they are not exclusive On the platelet surface activated F10, F5, platelet phospholipids, & Ca 2+ 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 pg 665 AP2 Chap. 19: Cardiovascular Syst 37

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 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 38

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 bld flw, reduces infection, & enhances healing. AP2 Chap. 19: Cardiovascular Syst 39

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 pg 667 AP2 Chap. 19: Cardiovascular Syst 40

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

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. 42

43 V. Blood Grouping 43 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 Type A Type B Type AB Type O Surface displays Surface displays Surface displays Surface displays A-Ag s only B-Ag s only A & B-Ag s Codominance No Ags Rh+ Surface displays Rh-Fator Rh-Factor Blood Group on Chromosome 1 Rh- Surface displays No antigens 44

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

46 Issues w/blood donation & necessity of blood typing: Ab s do not develop unless they are exposed to a foreign Ag. Thus: Transfused with Type A blood lives happily every after 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 46

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

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

49 Hemolytic Disease of a Newborn (HDN) Rh - mother gives birth to an Rh + fetus 1 st birth: Everything is okay. Baby is born with out incident. During birth mother is exposed to babies blood and can form antibodies 2 nd 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 Clinical Focus: pg AP2 Chap. 19: Cardiovascular Syst 50