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


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


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


Formed Elements of Blood


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



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



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


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


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


Shapes of RBC and Hemoglobin


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


Formation and Destruction of RBC’s

Red blood celldeath andphagocytosis

Key:

in blood

in bile

Macrophage inspleen, liver, orred bone marrow

1

Globin


Key:

in blood

in bile


Heme2

1

Aminoacids

Reused forprotein synthesisGlobin


Key:

in blood

in bile


Heme

3

2

1

Aminoacids



Transferrin

Fe3+

Key:

in blood

in bile


Heme

4

3

2

1

Aminoacids



Transferrin

Fe3+

Liver

Key:

in blood

in bile


FerritinHeme

54

3

2

1

Aminoacids



Transferrin

Fe3+

Fe3+ Transferrin

Liver

Key:

in blood

in bile


FerritinHeme

654

3

2

1

Aminoacids



Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile


FerritinHeme Fe3+

7

654

3

2

1

Aminoacids


Circulation for about120 days


Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile

Erythropoiesis inred bone marrow


FerritinHeme Fe3+

8

7

654

3

2

1

Aminoacids




Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile



FerritinHeme

Biliverdin Bilirubin

Fe3+

9

8

7

654

3

2

1

Aminoacids



Bilirubin


Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile



FerritinHeme


Fe3+

10

9

8

7

654

3

2

1

Aminoacids


Stercobilin

Bilirubin

Urobilinogen

Feces

Smallintestine


Bacteria

Bilirubin


Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile



FerritinHeme


Fe3+

12

1110

9

8

7

654

3

2

1

Aminoacids


Urine

Stercobilin

Bilirubin

Urobilinogen

Feces

Smallintestine


Bacteria

Bilirubin


Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile


Kidney


Ferritin

Urobilin

Heme


Fe3+

13 12

1110

9

8

7

654

3

2

1

Aminoacids


Urine

Stercobilin

Bilirubin

Urobilinogen

Feces

Largeintestine

Smallintestine


Bacteria

Bilirubin


Transferrin

Fe3+

Fe3+ Transferrin

Liver

+Globin

+Vitamin B12

+Erythopoietin

Key:

in blood

in bile


Kidney


Ferritin

Urobilin

Heme


Fe3+

14

13 12

1110

9

8

7

654

3

2

1


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


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


Types of White Blood Cells


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


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


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


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


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


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


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


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)


Platelet Plug Formation

1

Red blood cell

Platelet

Collagen fibersand damagedendothelium

Platelet adhesion11

2

Red blood cell

Platelet


Liberated ADP,serotonin, andthromboxane A2

Platelet adhesion1

Platelet release reaction2

1

2

3

Red blood cell

Platelet


Liberated ADP,serotonin, andthromboxane A2

Platelet plug

Platelet adhesion1

Platelet release reaction2

Platelet aggregation3


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


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



Activated XII

Ca2+

Damagedplatelets

Ca2+


Activated X

Activatedplatelets

Activated X

PROTHROMBINASECa2+

VCa2+

Prothrombin(II)

Ca2+

THROMBIN

(c) Common pathway

V

1

2

+

+

Tissue trauma

Tissuefactor(TF)

Blood trauma



Activated XII

Ca2+

Damagedplatelets

Ca2+


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

+

+


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


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


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


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


Antigens and Antibodies of ABO Blood Types


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


Typing Blood

Single drops of blood are mixed with different antisera

Agglutination with an antisera indicates the presence of that antigen on the RBC


End of Chapter 19

Copyright 2009 John Wiley & Sons, Inc.All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein.

Copyright 2009, John Wiley & Sons, Inc. Chapter 19: The Cardiovascular System: The Blood.

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Transcript of Copyright 2009, John Wiley & Sons, Inc. Chapter 19: The Cardiovascular System: The Blood.