Copyright 2009, John Wiley & Sons, Inc. Chapter 19: The Cardiovascular System: The Blood.
Transcript of Copyright 2009, John Wiley & Sons, Inc. Chapter 19: The Cardiovascular System: The Blood.
Copyright 2009, John Wiley & Sons, Inc.
Chapter 19: The Cardiovascular System: The Blood
Copyright 2009, John Wiley & Sons, Inc.
Blood
Liquid connective tissue 3 general functions
1. Transportation Gases, nutrients, hormones, waste products
2. Regulation pH, body temperature, osmotic pressure
3. Protection Clotting, white blood cells, proteins
Copyright 2009, John Wiley & Sons, Inc.
Components of Blood
Blood plasma – water liquid extracellular matrix 91.5% water, 8.5% solutes (primarily proteins) Hepatocytes synthesize most plasma proteins
Albumins, fibrinogen, antibodies Other solutes include electrolytes, nutrients, enzymes,
hormones, gases and waste products Formed elements – cells and cell fragments
Red blood cells (RBCs) White blood cells (WBCs) Platelets
Copyright 2009, John Wiley & Sons, Inc.
Copyright 2009, John Wiley & Sons, Inc.
Formed Elements of Blood
Copyright 2009, John Wiley & Sons, Inc.
Formation of Blood Cells
Negative feedback systems regulate the total number of RBCs and platelets in circulation
Abundance of WBC types based of response to invading pathogens or foreign antigens
Hemopoiesis or hematopoiesis Red bone marrow primary site Pluripotent stem cells have the ability to
develop into many different types of cells
Copyright 2009, John Wiley & Sons, Inc.
Copyright 2009, John Wiley & Sons, Inc.
Formation of Blood Cells
Stem cells in bone marrow Reproduce themselves Proliferate and differentiate
Cells enter blood stream through sinusoids Formed elements do not divide once they
leave red bone marrow Exception is lymphocytes
Copyright 2009, John Wiley & Sons, Inc.
Formation of Blood Cells
Pluripotent stem cells produce Myeloid stem cells
Give rise to red blood cells, platelets, monocytes, neutrophils, eosinophils and basophils
Lymphoid stem cells give rise to Lymphocytes
Hemopoietic growth factors regulate differentiation and proliferation Erythropoietin – RBCs Thrombopoietin – platelets Colony-stimulating factors (CSFs) and interleukins – WBCs
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Red Blood Cells/ Erythrocytes Contain oxygen-carrying protein hemoglobin Production = destruction with at least 2
million new RBCs per second Biconcave disc – increases surface area Strong, flexible plasma membrane Glycolipids in plasma membrane responsible
for ABO and Rh blood groups Lack nucleus and other organelles
No mitochondria – doesn’t use oxygen
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Hemoglobin
Globin – 4 polypeptide chains Heme in each of 4 chains Iron ion can combine reversibly with one oxygen
molecule Also transports 23% of total carbon dioxide
Combines with amino acids of globin Nitric oxide (NO) binds to hemoglobin
Releases NO causing vasodilation to improve blood flow and oxygen delivery
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Shapes of RBC and Hemoglobin
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Red Blood Cells
RBC life cycle Live only about 120 days Cannot synthesize new components – no nucleus Ruptured red blood cells removed from circulation
and destroyed by fixed phagocytic macrophages in spleen,liver & red bone marrow
Breakdown products recycled Globin’s amino acids reused Iron reused Non-iron heme ends as yellow pigment urobilin in urine
or brown pigment stercobilin in feces
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Formation and Destruction of RBC’s
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
1
Globin
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
Heme
4
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Liver
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
54
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Macrophage inspleen, liver, orred bone marrow
FerritinHeme Fe3+
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme Fe3+
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Circulation for about120 days
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
10
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Stercobilin
Bilirubin
Urobilinogen
Feces
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Macrophage inspleen, liver, orred bone marrow
FerritinHeme
Biliverdin Bilirubin
Fe3+
12
1110
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Urine
Stercobilin
Bilirubin
Urobilinogen
Feces
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Kidney
Macrophage inspleen, liver, orred bone marrow
Ferritin
Urobilin
Heme
Biliverdin Bilirubin
Fe3+
13 12
1110
9
8
7
654
3
2
1
Aminoacids
Reused forprotein synthesisGlobin
Urine
Stercobilin
Bilirubin
Urobilinogen
Feces
Largeintestine
Smallintestine
Circulation for about120 days
Bacteria
Bilirubin
Red blood celldeath andphagocytosis
Transferrin
Fe3+
Fe3+ Transferrin
Liver
+Globin
+Vitamin B12
+Erythopoietin
Key:
in blood
in bile
Erythropoiesis inred bone marrow
Kidney
Macrophage inspleen, liver, orred bone marrow
Ferritin
Urobilin
Heme
Biliverdin Bilirubin
Fe3+
14
13 12
1110
9
8
7
654
3
2
1
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Erythropoiesis
Starts in red bone marrow with proerythroblast
Cell near the end of development ejects nucleus and becomes a reticulocyte
Develop into mature RBC within 1-2 days
Negative feedback balances production with destruction
Controlled condition is amount of oxygen delivery to tissues
Hypoxia stimulates release of erythropoietin
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White Blood Cells/ Leukocytes Have nuclei Do not contain hemoglobin Granular or agranular based on staining
highlighting large conspicuous granules Granular leukocytes
Neutrophils, eosinophils, basophils Agranular leukocytes
Lymphocytes and monocytes
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Types of White Blood Cells
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Functions of WBCs
Usually live a few days Except for lymphocytes – live for months or years Far less numerous than RBCs Leukocytosis is a normal protective response to
invaders, strenuous exercise, anesthesia and surgery
Leukopenia is never beneficial General function to combat invaders by
phagocytosis or immune responses
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Emigration of WBCs
Many WBCs leave the bloodstream
Emigration (formerly diapedesis)
Roll along endothelium Stick to and then
squeeze between endothelial cells
Precise signals vary for different types of WBCs
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WBCs
Neutrophils and macrophages are active phagocytes Attracted by chemotaxis
Neutrophils respond most quickly to tissue damage by bacteria Uses lysozymes, strong oxidants, defensins
Monocytes take longer to arrive but arrive in larger numbers and destroy more microbes Enlarge and differentiate into macrophages
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WBCs
Basophila leave capillaries and release granules containing heparin, histamine and serotonin, at sites of inflammation Intensify inflammatory reaction Involved in hypersensitivity reactions (allergies)
Eosinophils leave capillaries and enter tissue fluid Release histaminase, phagocytize antigen-
antibody complexes and effective against certain parasitic worms
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Lymphocytes
Lymphocytes are the major soldiers of the immune system B cells – destroying bacteria and inactivating their
toxins T cells – attack viruses, fungi, transplanted cells,
cancer cells and some bacteria Natural Killer (NK) cells – attack a wide variety of
infectious microbes and certain tumor cells
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Platelets/ Thrombocytes
Myeloid stem cells develop eventually into a megakaryocyte
Splinters into 2000-3000 fragments Each fragment enclosed in a piece of plasma
membrane Disc-shaped with many vesicles but no nucleus Help stop blood loss by forming platelet plug Granules contain blood clot promoting chemicals Short life span – 5-9 days
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Stem cell transplants
Bone marrow transplant Recipient's red bone marrow replaced entirely by healthy,
noncancerous cells to establish normal blood cell counts Takes 2-3 weeks to begin producing enough WBCs to fight
off infections Graft-versus-host-disease – transplanted red bone marrow
may produce T cells that attack host tissues Cord-blood transplant
Stem cells obtained from umbilical cord shortly before birth Easily collected and can be stored indefinitely Less likely to cause graft-versus-host-disease
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Hemostasis
Sequence of responses that stops bleeding 3 mechanisms reduce blood loss1. Vascular spasm
Smooth muscle in artery or arteriole walls contracts
2. Platelet plug formation Platelets stick to parts of damaged blood vessel,
become activated and accumulate large numbers
3. Blood clotting (coagulation)
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Platelet Plug Formation
1
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Platelet adhesion11
2
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Liberated ADP,serotonin, andthromboxane A2
Platelet adhesion1
Platelet release reaction2
1
2
3
Red blood cell
Platelet
Collagen fibersand damagedendothelium
Liberated ADP,serotonin, andthromboxane A2
Platelet plug
Platelet adhesion1
Platelet release reaction2
Platelet aggregation3
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Blood Clotting
3. Blood clotting Serum is blood plasma
minus clotting proteins Clotting – series of
chemical reactions culminating in formation of fibrin threads
Clotting (coagulation) factors – Ca2+, several inactive enzymes, various molecules associated with platelets or released by damaged tissues
Copyright 2009, John Wiley & Sons, Inc.
3 Stages of Clotting
1. Extrinsic or intrinsic pathways lead to formation of prothrombinase
2. Prothrombinase converts prothrombin into thrombin
3. Thrombin converts fibrinogen (soluble) into fibrin (insoluble) forming the threads of the clot
Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
V
1
Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
Prothrombin(II)
Ca2+
THROMBIN
(c) Common pathway
V
1
2
+
+
Tissue trauma
Tissuefactor(TF)
Blood trauma
Damagedendothelial cellsexpose collagenfibers
(a) Extrinsic pathway (b) Intrinsic pathway
Activated XII
Ca2+
Damagedplatelets
Ca2+
Plateletphospholipids
Activated X
Activatedplatelets
Activated X
PROTHROMBINASECa2+
VCa2+
Prothrombin(II)
Ca2+
THROMBIN
Ca2+
Loose fibrinthreads
STRENGTHENEDFIBRIN THREADS
Activated XIIIFibrinogen(I)
XIII
(c) Common pathway
V
1
2
3
+
+
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Blood Clotting
Extrinsic pathway Fewer steps then intrinsic and occurs rapidly Tissue factor (TF) or thromboplastin leaks into the blood
from cells outside (extrinsic to) blood vessels and initiates formation of prothrombinase
Intrinsic pathway More complex and slower than extrinsic Activators are either in direct contact with blood or
contained within (intrinsic to) the blood Outside tissue damage not needed Also forms prothrombinase
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Blood Clotting: Common pathway
Marked by formation of prothrombinase Prothrombinase with Ca2+ catalyzes conversion of
prothrombin to thrombin Thrombin with Ca2+ converts soluble fibrinogen
into insoluble fibrin Thrombin has 2 positive feedback effects
Accelerates formation of prothrombinase Thrombin activates platelets Clot formation remains localized because fibrin absorbs
thrombin and clotting factor concentrations are low
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Blood Groups and Blood Types Agglutinogens – surface of RBCs contain
genetically determined assortment of antigens
Blood group – based on presence or absence of various antigens
At least 24 blood groups and more than 100 antigens ABO and Rh
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ABO Blood Group
Based on A and B antigens Type A blood has only antigen A Type B blood has only antigen B Type AB blood has antigens A and B
Universal recipients – neither anti-A or anti-B antibodies Type O blood has neither antigen
Universal donor Reason for antibodies presence not clear
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Antigens and Antibodies of ABO Blood Types
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Hemolytic Disease
Rh blood group People whose RBCs have
the Rh antigen are Rh+
People who lack the Rh antigen are Rh-
Normally, blood plasma does not contain anti-RH antibodies
Hemolytic disease of the newborn (HDN) – if blood from Rh+ fetus contacts Rh-
mother during birth, anti-Rh antibodies made Affect is on second Rh+
baby
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Typing Blood
Single drops of blood are mixed with different antisera
Agglutination with an antisera indicates the presence of that antigen on the RBC
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End of Chapter 19
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