Chapter 19

1

Chapter 19Cardiovascular System:

The Blood

AP2 Chap. 19: Cardiovascular Syst

AP2 Chap. 19: Cardiovascular Syst 2

Cardiovascular System: The Blood

I. Functions of the Blood

II. Plasma

III. Formed Elements

IV. Hemostasis

V. Blood Grouping

VI. Diagnostic Blood Tests


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


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


I. Fxns of the blood


I. Fxns of the bloodThe 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

7


1. Transport of gases, nutrients, & waste products.

• O2:– lungs cells

• CO2:– cells lungs for exhalation

• Ingested nutrients, ions, & H2O: – Digestive system cells

• Waste products:– Cells kidneys for elimination

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

The blood helps maintain homeostasis in several ways:

3. Transport of regulatory molecules

• Carries hormones & enz’s that regulate body processes from 1 body part to another

8


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


The blood helps maintain homeostasis in several ways:

5. Maintenance of Body Temp.

6. Protection against foreign substances

• Warm bld is transferred from the body core to the body surface where heat is released

• 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

• Protects against XSV bld loss when bld vessels are damaged

• 1st step in tissue repair & return to fxn when tissues are damaged


II. Plasma

II. Plasma• 91% water & 9% other

– 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, PO4, H, OH-, HCO3

-

• Nutrients: – Vitamins – Glucose, AA’s, Cholesterol,

& triglycerides (aka triacylglycerol )

• Gases: O2, CO2, & N2 10

Figure 19.1 pg 651

• Waste: Urea, Uric Acid, Creatinine, Ammonia Salts, Bilirubin, & lactic acid

• Regulatory Substances

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II. Plasm

a• 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

Functions in the plasm

a:

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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


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



A. Production of Formed Elements

B. Red Blood Cells

C. White Blood Cells

D. Platelets

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III. Formed Elements:3 major classes

Red Blood Cells(Erythrocytes)

RBC’s700X more than WBC

17X more than platelets

White Blood Cells(Leukocytes)

WBC’s

Platelets(Thrombocytes)

Granulocytes Agranulocytes

Basophil

Eosinophil

Neutrophil

Monocyte

Lymphocyte

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III. F

orm

ed E

lem

ents

Pro

d’n

of fo

rmed

ele

men

ts

• 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)

Hematopoiesis(Hemopoiesis)

Figure 19.2 pg 655



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

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RBC’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 rupturehemolysis• 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 (HCO3

-)• Carbonic anhydrase is the

enzyme responsible for converting CO2 & H2O into Carbonic Acid wh/dissociates into a H+ & HCO3

-



III. Formed ElementsRBC’s: Hemoglobin

• 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

1. Embryonic: pro’d up to 3rd mo. of development

2. Fetal: @ 3rd mo fetal replaces embryonic hemoglobin

3. Adult: by birth 60-90% is adult by 2 to 4 almost nothing but adult

Figure 19.4 pg 656



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.


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

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????22

Fig

ure

19.6

pg

660

Aged, damaged, or abnormal RBC’s are taken to the spleen, liver & other lymphatic tissue. Here macrophages isolate hemoglobin.

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. 23Figure 19.6 pg 660


III. Formed Elements: WBC’s

Figure 19.7 pg 661

Figure 19.8 pg 662

Figure 19.3 pg 656


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

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III. Formed Elements: WBC’s3 major classes

Red Blood Cells(Erythrocytes)

RBC’s700X more than WBC

17X more than platelets

White Blood Cells(Leukocytes)

WBC’s

Platelets(Thrombocytes)

Granulocytes Agranulocytes

Basophil

Eosinophil

Neutrophil

Monocyte

Lymphocyte



Granulocytes

Basophil• Nucleus w/ 2 indistinct

lobes; cytoplasmic granules stain blue-purple; 10-12 mm in diameter

• Fxn:– Releases:– Histamine

promotes inflammation

– Heparin prevents clot formation

Eosinophil• 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

Neutrophil• 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

60-70% WBC

2-4% WBC

0.5-1% WBC



AgranulocytesLymphocytes

• 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

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

20-25% WBC

3-8% WBC


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:

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


IV. HemostasisA. Vascular Spasm

B. Platelet plug formation

C. Coagulation

D. Control of Clot formation

E. Clot retraction & Dissolution


IV. Hemostasis

• The stoppage of bleeding to maintain homeostasis.

• 3 major steps to achieve hemostasis

1. Vascular Spasm

2. Platelet plug formation

3. Coagulation


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

IV. Hemostasis:

2. Platelet Plug Formation

• Accumulation of platelets that can seal-up small breaks in blood vessels

• Described in steps that actually occur simultaneously

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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


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

IV. Hemostasis: Coagulation: Clot formationExtrinsic 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 Ca2+ forms a complex with F7

• This complex activates F10• This is the beginning of the

common pathway


Figure 19.11 pg 665

For simplicity Factor will be abbreviated as F and roman numerals will be numbers

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

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

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

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• @ 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.


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.


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


V. Blood Grouping

ABO Blood Group

Rh Blood Group

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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.

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

ABO-Blood Group Variants on Chromosome 9

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Type BType A Type AB Type OSurface displays

A-Ag’s only

Surface displays

B-Ag’s onlySurface displays

A & B-Ag’s

Codominance

Surface displays

No Ags

Rh-Factor Blood Group on Chromosome 1

Rh+Surface displays

Rh-Fator

Rh-Surface displays

No antigens

Most common blood types that exist

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Type B-Type A- Type AB- Type O-

Type B+Type A+ Type AB+ Type O+

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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


V. Blood Grouping: Ag’s & Ab’s

What would happen to the type AB if an A-Ab was introduced??

Fig

ure

19.

13

pg

668


Agglutination reaction

Figure 19.14 pg 669

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.


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

Chapter 19

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