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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.

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  • 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