1 / 53

BLOOD - PowerPoint PPT Presentation

  • Uploaded on

BLOOD. Blood. fluid connective tissue contains specialized cells- formed elements suspended in matrix- plasma containing-collagen & elastic fibers protein fibers are in solution-visible during clotting process. Functions.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'BLOOD' - tamber

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript


  • fluid connective tissue

  • contains specialized cells-formed elements

  • suspended in matrix-plasma

  • containing-collagen & elastic fibers

    • protein fibers are in solution-visibleduring clotting process


  • transports &distributes nutrients, gases, hormones & waste products

  • regulates pH & ion composition of interstitial fluids

  • restricts fluid loss at injury sites

  • defends against toxins & pathogens

  • helps to maintain bodytemperature


  • 8% of total body weight

    • 5-6 liters in males

    • 4-5L in females

  • Temperature-38oC

    • just above body temperature

  • Viscosity5X more viscous than water

  • pH between7.35-7.45


  • Whole blood = plasma + formed elements

  • red blood cells (RBCs)

  • white blood cells (WBCs)

  • platelets

  • Centrifuged-separates into three parts

  • Bottom-erythrocytes (RBCs)

  • top-plasma

  • junction of RBC & plasma-buffy coat

    • contains WBCs & platelets

Plasma composition
Plasma Composition

  • 46-63% of blood volume

  • 92% water

  • plasma proteins-made by liver

  • Albumin-60%

    • major contributor to osmotic pressure

    • transports fatty acids, steroid & thyroid hormones

  • Globulins-35%

    • from smallest to largest in molecular weights-alpha, beta & gamma globulins

    • used to transport hormones, metal ions, triglycerides and lipids

    • includes antibodies orimmunoglobins

      • defend against infections and foreign materials

  • Fibrinogen-4%

    • blood clotting

    • fibrinogen is cleaved into fibrin-basic framework of clot


  • most numerous of formed elements

  • number varies with health & altitude

    • Peruvians who live 18,000 feet above sea level may have as many as 8.3 x 106 RBCs/µl

  • contain hemoblobin (Hb)

    • red pigment which transports O2 & CO2

    • gives blood its color

  • Ratio of RBC/plasma is hematocrit

    • % of whole blood occupied by cellular elements: 40-45%-women; 37-48%-men

    • almost entirely due to volume of RBCs

    • provides estimate of packed cell volume (PCV)

    • PCV increases with dehydration & with erythropoietin-protein which stimulates RBC production

  • RBCs are a major contributor to blood viscosity

    • as numbers increaseviscosity increasesblood flow slowsblood thinsflows more rapidly

Rbc structure
RBC Structure

  • simple-small, biconcave disc

  • plasma membrane-no nucleus & no organelles

  • bag of Hb

  • no nucleuscannot divide or make proteins

    • can’t repair its self and has a short life span-120 days

  • shape is directly related to function-most important transport of O2

    • large surface area, relative to volume

    • 30% more surface area than spherical cells

    • larger surface area makes for faster gas exchange

  • shape allows them to stack like dinner plates

    • allows for smoother flow of blood through vessels

  • Flexible

    • able to pass through small capillaries

  • Modify shape in response to osmotic changes

    • Hypotonic solutionswellsforms sphere without disrupting integrity of membrane

    • Hypertonic solutionshrinksforms spikey surface

  • No mitochondria

    • generate ATP anaerobically via glycolysis

    • do not need O2- makes them very efficient O2 transporters

Hemoglobin hb structure
Hemoglobin (HB) Structure

  • red pigment

  • formed by 4 globular polypeptide chains

  • 2 & 2

  • each chain has a molecule of heme

  • each heme has iron (Fe) molecule

  • each Fe can carry one molecule of oxygentherefore each HB molecule can carry 4 molecules of oxygen

  • Fe binds with O2 oxyhemoglobin bright red

  • Fe-O2 bond is weak

  • can separate easily without damage to Fe or O2

  • Hb from which O2 has separated is deoxyhemoglobindark red

Hemoglobin functions
Hemoglobin Functions

  • Transport gases-O2 & CO2

    • there are 280X106 Hb molecules in eachRBC

    • each contain 4 heme groups

    • gives blood capacity to carry a billion O2 molecules

  • amount of O2 bound depends on O2 content of plasma

Leukocytes white blood cells
Leukocytes-White Blood Cells

  • less numerous than RBCS

  • 1% of total blood volume

  • provide protection against infections

  • complete cells

    • typically have lobed nuclei, organelles & no Hb

  • two groups based on appearance after staining

  • Granulocytes

    • contain cytoplasmicinclusions

    • Basophils

    • Eosinophils

    • Neutrophils

  • Agranulocytes

    • contain only a very few stained granules

    • Lymphocytes

    • Monocytes


  • 60-70% of circulating WBC population

  • live only about 10 hours

  • twice size of RBC

  • Nucleus-polymorphonuclear

    • varied nuclear shapes

    • mature have 3-5 lobes connected by slender nuclear strands

  • cytoplasmic granules in cytoplasm are packedwith lysosomal enzymes & bacteria killing compounds

  • produced in response to acute body stress

    • infection, infarction, trauma, emotional distress

  • can double inafew hours

  • highly mobile

    • first WBC to arrive at injury site

  • specialize in attacking & digesting bacteria

  • when binds to bacteriummetabolic rate increases H2O2 -hydrogen peroxide & O2- superoxide anions are produced which kill bacteria

  • neutrophil + bacterium will fuse with a lysosome which contains digestive enzymes & defensins

  • defensins kill bacteria & lysozymes digest them

  • makes prostaglandins & leukotrienes during this process

    • restricts spread of infection & attracts other phagocytotic cells

  • cell kills its self in the process

  • Neutrophils + other waste = pus


  • 2-4% of WBCs

  • bilobed nuclei

  • contain deep redgranules

  • population increases sharply during parasitic infections & allergic responses

  • release histaminases which combat the effects of histamine


  • smallest part of WBC population-0.5-1%

  • large, deep purple granules in cytoplasm

    • hides nucleus

  • increase in number during infections

  • leave blood & develop into mast cells

  • granules contain histamine, serotonin & heparin

  • histamine increases blood flow to area which dilates blood vessels

  • heparin prevents blood clotting


  • largest agranulocytes

  • 3-8% of WBC population

  • nucleus is large

    • clearly visible

    • ovoid or kidney shaped

  • cytoplasm contains sparse, fine granules

  • arrive in large numbers at the site of an infection

  • enlarge & differentiate into wandering macrophages


  • second most numerous circulating leukocyte-25-33%

  • Nucleus-large, round or slightly dimpled on one side

  • continually migrates from blood stream through peripheral tissues & back to blood stream

  • life span varies from several days to years

  • B cells or B lymphocytes

    • bone marrow derived

    • make antibodies which attack foreign antigens

  • T lymphocytes or T cells

    • thymus dependent cells

    • provide cell mediated immunity

    • attack foreign cells

  • Natural Killer Cells

    • immune surveillance cells

    • detect &destroy abnormal tissue cells

    • may help prevent cancer

Differential cell count
Differential Cell Count

  • determines number of each type of WBC in a sample

  • gives valuable information

  • pathogens, infections, inflammation & allergic reactions change WBC numbers

  • count of different types can help to diagnose disease and illness

  • Leukopenia

    • inadequate number

  • Leuocytosis

    • Excessive number

Blood cell formation
Blood Cell Formation

  • all formed elements arise from a single cell type: pluripotent stem cell

  • Hemocytoblast

  • hematopoietic stem cellor hemocytoblast

  • rare-one in 10,000 bone marrow cells

  • cell differentiates along maturation pathwhich leads to different kinds of blood cells

  • each type produced in different numbers in response to needs & regulatory factors-cytokines or hormones

Hemopoietic tissues
Hemopoietic Tissues

  • Tissues producing blood cells

  • first-yolk sac

    • makes stem cells that migrate into embryo populate bone marrow, liver, spleen & thymus stem cells multiply & give rise to blood cells throughout fetal development

  • Liver

    • primary site of RBC production during 2-5th month neonatally is liver & spleen

    • stops making blood cells at time of birth

  • Spleen

    • stops soon after but continues to make white blood cells throughout life

  • red bone marrow produces all formed elements from infancy onward


  • inadequate oxygen (hypoxia)kidney EPO (erythopoietin) stimulates production of RBCs

  • Hemoblasts myeloid stem cellsproethryoblastearly erythroblasts

  • early erhtyhroblasts multiply & make hemoglobinlate erythroblast normoblast

  • once normoblast accoulates 34% Hborganelles are ejected, nucleus degeneratescell collapses inwardreticulocyte

  • still has ribosomes & rough ER; leaves bone marrow

  • matures in two daysmature erythrocyte

Rbc lifecycle
RBC LifeCycle

  • RBC is terminally differentiated

  • cannot synthesize proteins, enzymes or renew membranes

  • life span-about 120 days

  • engulfed & destroyed by phagocytotic cells in liver, spleen and bone marrow

  • process is hemolysis

  • once hemolyzed-parts are broken down

  • globular proteins are disassembled into amino acids

  • Heme splits from globin of HB molecule

  • Iron is stripped from hemebiliverdin (green, organic compound)bilirubin (orange/yellow pigment)released into blood binds albumin transported to liver for excretion in bile

    • If circulating levels cannot be handled by liverhyperbilirubinemia-condition which turnsperipheral tissues yellowjaundice

  • Fe salvaged for reuse

  • toxic to body-must be stored & transported bound to a protein

  • Tranferrin used for iron transport

  • hemosiderin for iron storage

  • in bone marrow Fe is taken into the mitochondria of developing RBCs and is used to make heme

Wbc production leukopoiesis
WBC Production-Leukopoiesis

  • begins with same pluripotent stem used in erythropoiesis-hemocytoblast

  • differentiate into distinct types of CFUs-colony forming units

  • CFUs go on to produce 3 cell lines committed to a certain outcome

  • Myleoblasts

  • Monoblasts

  • Lymphoblasts

Platelets thrombocytes

  • not cells in strictest sense

    • Fragments

  • continuously replaced

  • always present-not active unless damage has occurred

  • Thrombocytosis

    • too many

  • Throbocytopenia

    • Too few

  • if numbers drop below 50 X 103/ul there is danger of uncontrolled bleeding

  • Functions

    • contain chemicals for clotting

    • form temporary platelet plug needed in clotting

    • secrete growth factors

    • secrete chemical to attract neutrophils and monocytes to site of inflammation


  • occurs in bone marrow

  • thrombopoieten-secreted by liverstimulate growth & maturation of hemocytoblastsrepeated mitosis (up to 7X) without nuclear or cytoplasmicdivisionvery large polypoloid cell-megakaryocyte

  • presses against sinusoid wallruptureplatelet fragments

  • life span-about 5 – 9 days


  • cut or damaged blood vessels bleed

  • outflow must be stopped before shock & death occur

  • accomplished by solidification of blood or coagulation

  • also called clotting or hemostasis

  • clotting is

  • fast

  • localized

  • carefully controlled

  • three phases

    • vascular spasm

    • platelet plug formation

    • coagulation phase

Vascular spasm phase
Vascular Spasm Phase

  • blood vessels vasoconstrict

    • diameter decreases at injury site

  • immediate & most effective in small vessels

  • contraction exposes underlying basement membrane to bloodstream

Platelet plug formation
Platelet Plug Formation

  • endothelial cell membranes become sticky

  • sticky membranes allow platelets to adhere to injury site

  • forms temporary plug within 1 minute of injury

  • as platelets keep arriving continue sticking to each otherplatelet aggregationplatelet plug

  • plug seals break in vessel

  • as arrive become activatedchange shape

  • become more spherical & develop cytoplasmic processes that extend toward other platelets

  • Release

    • ADP-adenosine diphosphate

      • aggregating agent

    • Serotonin

      • enhances vascular spasms

    • Enzymes that help make Thromboxane A2

      • recruits & activates more platelets & stimulates vascular spasms

    • PDGF

      • platelet derived growth factor

      • promotes vessel repair

    • Calcium

      • required for platelet aggregation

Coagulation phase
Coagulation Phase

  • occurs in asequence of steps

  • requires 13 clotting factors called procoagulants

  • designated by Roman numerals

    • many circulate as proenzymes- inactive precursors

  • converted to active forms during clotting process

  • activated by proteolytic cleavage & active proteases

  • all but 3 are made & released by the liver (III, IV, VIII)

  • all but 2 (III & VIII) are always present in blood

  • activated platelets release 5 during platelet phase (III, IV, V, VIII & XIII)

Coagulation cascade
Coagulation Cascade

  • activation of one proenzymeactivates another proenzyme

  • chain reaction or reaction cascade

  • 2 reaction pathways to coagulation:

  • extrinsic

  • Intrinsic

  • Both lead to the formation of prothrombinase

  • at this point the two unite- common pathway

Extrinsic pathway
Extrinsic Pathway

  • shorter & faster-fewer steps

  • TF-tissue factor or thromboplastin or clotting factor III is released by damaged blood vessels

  • leaks into blood (extrinsic to it)

  • TF binds Ca++ & Factor VII forming an enzyme complex

  • complex cleaves Factor X (prothrombinase) active factor X

  • first step in common pathway of coagulation

Intrinsic pathway
Intrinsic Pathway

  • more complex & slower

  • activators are in blood or in direct contact with it (intrinsic to it)

  • contact with collagen fibers or even glass of a collecting vialactivates Factor XII

  • Begins a series of reactions

  • activated factors VIII & IX combine to form enzyme complex which activates Factor X

Common coagulation pathway
Common Coagulation Pathway

  • the two paths unite at a common pathwaythrombin synthesis

  • begins when activated Factor X or prothombinase converts prothombin or Factor IIthrombin

  • Thrombin cleaves fibrinogen or Factor I (soluble)insoluble fibrin

The clot
The Clot

  • fibrin glues platelets together forming intertwined web

    • structural basis of a clot

  • thrombin & Ca++ activate Factor XIII-fibrin stabilizing factor

  • cross linking enzyme

  • forms covalent bonds between fibrin molecules converting them into insoluble meshwork

  • stabilizes clot

Clot retraction
Clot Retraction

  • further stabilizes clot

  • occurs minutes after initial clot formation

  • platelets contain contractile proteins-actin & myosin

  • these contract pull fibrin strands together

  • squeezing out serum compacts clot

  • functions to:

  • pull torn edges of broken vessel together

  • reduce size of damaged area


  • begins with clot formation

  • PDGFstimulates smooth muscle cells & fibroblast division to rebuild vessel wall

    • angiogenesis

  • Thrombin, factors VII & X promote healing by stimulating growth of new blood vessels at site of damage


  • hemostasis is not complete until clot has been dissolved

  • plasminogen is incorporated into clot as it forms

  • nearby cells release TPA-tissue pasminogen activator

  • binds to fibren and activates plasimnogen converting it to plasmin

  • plasmin digests fibrindissolving clot

Control of clotting
Control of Clotting

  • clotting must be carefully regulated

  • inappropriate formation-life-threatening

    • too much-thrombus

  • clotting-restricted by several mechanisms

  • 1. Platelets do not adhere to normal endothelium

    • intact endothelial cells convert membrane lipids into prostacyclin

      • blocks platelet adhesion & aggregation

      • limits platelet plug to area of damage

Control of clotting1
Control of Clotting

  • Plasma contains anticoagulants

    • Antithrombin III inactivates thrombin

    • Heparin accelerates activation of antithrombin III enhances inhibition of thrombin synthesis

Control of clotting2
Control of Clotting

  • 3. Endothelial cells release thrombomodulin-binds to thrombin converts it into enzyme that activates protein c

  • Protein Cinactivates clotting factors & stimulates plasmin formation

Thromboembolytic disorders
Thromboembolytic Disorders

  • Undesirable clottingthrombus

    • blood clots in unbroken vessels

  • gets into coronary circulationheart attack

  • thrombus that breaks away & floats freeembolus

  • Cerebral embolusstroke

  • Pulmonary emboluslung

  • Conditions that roughen endothelium encourage clot formation-

    • Arteriosclerosis

Bleeding disorders
Bleeding Disorders

  • Thrombocytopenia

    • deficient platelet number

    • can result in spontaneous bleeding from small vessels

  • Impaired liver function

    • liver makes procoagulants & when unable to do so result is severe bleeding

  • Deficiency of Vitamin K

    • may be a cause of liver dysfunction

    • cofactor needed for synthesis of factors II, VII, IX, X & proteins C & S

    • blocking action of vitamin K helps prevent inappropriate clotting

      • Warfarin-vitamin K antagonist

  • Deficiency of clotting factors

    • not enough produced or mutant version fails to perform properly

    • von Willebrand disease-most common

    • Hemophilia A-classic-factor VIII deficiency

    • antihemophilic factor-hemophilia B

    • factor XI deficiency-hemophilia C-

    • actor XI deficiency-in both sexes

  • Lowered Calcium

    • affects nearly all clotting pathways

    • any lowering of Ca impairs blood clotting

Abo blood types
ABO Blood Types

  • blood type-determined by presence or absence of antigens-A and B

  • Presence of A-blood type A

  • Presence of B-blood type B

  • Presense of both-blood type AB

  • Absence of both-blood type O

Abo blood types1
ABO Blood Types

  • antibodies begin to appear in plasma 2 to 8 months after birth

  • person produces antibodies against antigens that are notpresent on his or her RBCs

  • Blood type A-makes antibody B

  • Blood type B-makes antibody A

  • Blood type O-makes antibodies A & B

  • Blood type AB-does not make antibodies

Blood type
Blood Type

  • Antigens are often referred to as agglutinogens

  • Antibodies-immunoglobulins are made by immune system in response to foreign material-agglutinins

  • antibody adheres to foreign material & eliminates it

  • presence of antigens on cells is a way for immune system to decide whether substance is foreign or not

  • immune system ignores surface antigens on your RBCs

  • when blood-type antigen senses foreign antigen has entered system alerts immune system to create antibodies to that antigen

    • antibodies attach themselves to foreign antigens destroy them

  • when attack foreign cellsclump together-agglutinate- termed agglutination


  • Antibodies react against A or B antigen except those of one’s own RBCs

  • person with antigen A produces anti-B antibodiesattack type B antigens

  • person with antigen B produces anti-A antibodiesattack type A antigens

  • person with neither A or B antigens produces both anti-A & anti-B antibodies

  • person with both antigens A & B will produce no antibodies

  • When antibody meets specific surface antigenRBCs agglutinate & may hemolyze

    • Cross reaction or transfusion reaction

    • can be dangerous to receive wrong blood type during a transfusion

  • Compatibility can be verified with blood typing

    • mix small sample of blood with anti-A or anti-B antibodies-called antiserum

    • presence or absence of clumping is determined for each type of antiserum

    • clumping only with anti-A serum blood type A

    • clumping only with anti-B serumblood type B

    • clumping with both antigensblood type AB

    • Absence of clumping with either antigenblood type O

Universal donor recipient
Universal Donor & Recipient

  • Type O-universal donor

    • no surface antigensrecipient’s blood can have antibodies but there will be no clumping

  • Type AB-universal receiver

    • holdsno antibodies to react with antigens

Antigen d rh factor
Antigen D-Rh Factor

  • rhesus antigen

  • in Rh negative individuals D antigen is missing

  • 84% of humans are Rh positive

  • Blood Type A+ carries A & Rh antigens

  • shouldn't mix A+ with A- blood

  • blood must also be typed for Rh factor

  • Anti-D antibodies are not normally found in blood as anti a and b antibodies are

  • form only in Rh negative individuals who are exposed to Rh positive blood

  • Rh negative person receives Rh positive transfusionrecipient produces anti-d antibodies

  • Anti-d does not appear instantaneously

  • presents little danger

  • if person gets another Rh positive transfusion, his or her anti-D could agglutinate donor’s RBCs