Chapter 19 The Cardiovascular System: The Blood

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Chapter 19 The Cardiovascular System: The Blood . Fluids of the Body . Cells of the body are serviced by 2 fluids blood composed of plasma and a variety of cells transports nutrients and wastes interstitial fluid bathes the cells of the body
Chapter 19 The Cardiovascular System: The Blood

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Chapter 19 the cardiovascular system the blood l.jpgSlide 1

Chapter 19The Cardiovascular System: The Blood

Tortora & Grabowski 9/e 2000 JWS

Fluids of the body l.jpgSlide 2

Fluids of the Body

  • Cells of the body are serviced by 2 fluids

    • blood

      • composed of plasma and a variety of cells

      • transports nutrients and wastes

    • interstitial fluid

      • bathes the cells of the body

  • Nutrients and oxygen diffuse from the blood into the interstitial fluid & then into the cells

  • Wastes move in the reverse direction

  • Hematology is study of blood and blood disorders

Tortora & Grabowski 9/e 2000 JWS

Functions of blood l.jpgSlide 3

Functions of Blood

  • Transportation

    • O2, CO2, metabolic wastes, nutrients, heat & hormones

  • Regulation

    • helps regulate pH through buffers

    • helps regulate body temperature

      • coolant properties of water

      • vasodilatation of surface vessels dump heat

    • helps regulate water content of cells by interactions with dissolved ions and proteins

  • Protection from disease & loss of blood

Tortora & Grabowski 9/e 2000 JWS

Physical characteristics of blood l.jpgSlide 4

Physical Characteristics of Blood

  • Thicker (more viscous) than water and flows more slowly than water

  • Temperature of 100.4 degrees F

  • pH 7.4 (7.35-7.45)

  • 8 % of total body weight

  • Blood volume

    • 5 to 6 liters in average male

    • 4 to 5 liters in average female

    • hormonal negative feedback systems maintain constant blood volume and osmotic pressure

Tortora & Grabowski 9/e 2000 JWS

Techniques of blood sampling l.jpgSlide 5

Techniques of Blood Sampling

  • Venipuncture

    • sample taken from vein with hypodermic needle & syringe

    • median cubital vein (see page 717)

    • why not stick an artery?

      • less pressure

      • closer to the surface

  • Finger or heel stick

    • common technique for diabetics to monitor daily blood sugar

    • method used for infants

Tortora & Grabowski 9/e 2000 JWS

Components of blood l.jpgSlide 6

Components of Blood

  • Hematocrit

    • 55% plasma

    • 45% cells

      • 99% RBCs

      • < 1% WBCs and platelets

Tortora & Grabowski 9/e 2000 JWS

Blood plasma l.jpgSlide 7

Blood Plasma

  • 0ver 90% water

  • 7% plasma proteins

    • created in liver

    • confined to bloodstream

  • albumin

    • maintain blood osmotic pressure

  • globulins (immunoglobulins)

    • antibodies bind to foreignsubstances called antigens

    • form antigen-antibody complexes

  • fibrinogen

    • for clotting

  • 2% other substances

    • electrolytes, nutrients, hormones, gases, waste products

  • Tortora & Grabowski 9/e 2000 JWS

    Formed elements of blood l.jpgSlide 8

    Formed Elements of Blood

    • Red blood cells ( erythrocytes )

    • White blood cells ( leukocytes )

      • granular leukocytes

        • neutrophils

        • eosinophils

        • basophils

      • agranular leukocytes

        • lymphocytes = T cells, B cells, and natural killer cells

        • monocytes

    • Platelets (special cell fragments)

    Tortora & Grabowski 9/e 2000 JWS

    Hematocrit l.jpgSlide 9


    • Percentage of blood occupied by cells

      • female normal range

        • 38 - 46% (average of 42%)

      • male normal range

        • 40 - 54% (average of 46%)

        • testosterone

    • Anemia

      • not enough RBCs or not enough hemoglobin

    • Polycythemia

      • too many RBCs (over 65%)

      • dehydration, tissue hypoxia, blood doping in athletes

    Tortora & Grabowski 9/e 2000 JWS

    Blood doping l.jpgSlide 10

    Blood Doping

    • Injecting previously stored RBC’s before an athletic event

      • more cells available to deliver oxygen to tissues

    • Dangerous

      • increases blood viscosity

      • forces heart to work harder

    • Banned by Olympic committee

    Tortora & Grabowski 9/e 2000 JWS

    Formation of blood cells l.jpgSlide 11

    Formation of Blood Cells

    • Most blood cells types need to be continually replaced

      • die within hours, days or weeks

      • process of blood cells formation is hematopoiesis or hemopoiesis

    • In the embryo

      • occurs in yolk sac, liver, spleen, thymus, lymph nodes & red bone marrow

    • In adult

      • occurs only in red marrow of flat bones like sternum, ribs, skull & pelvis and ends of long bones

    Tortora & Grabowski 9/e 2000 JWS

    Hematopoiesis l.jpgSlide 12


    Tortora & Grabowski 9/e 2000 JWS

    Stages of blood cell formation l.jpgSlide 13

    Stages of Blood Cell Formation

    • Pluripotent stem cells

      • .1% of red marrow cells

      • replenish themselves as they differentiate into either myeloid or lymphoid stem cells

    • Myeloid stem cell line of development continues:

      • progenitor cells(colony-forming units) no longer can divide and are specialized to form specific cell types

        • example: CFU-E develops eventually into only red blood cells

      • next generation is blast cells

        • have recognizable histological characteristics

        • develop within several divisions into mature cell types

    • Lymphoid stem cell line of development

      • pre-B cells & prothymocytes finish their develop into B & T lymphocytes in the lymphatic tissue after leaving the red marrow

    Tortora & Grabowski 9/e 2000 JWS

    Hemopoietic growth factors l.jpgSlide 14

    Hemopoietic Growth Factors

    • Regulate differentiation & proliferation

    • Erythropoietin (EPO)

      • produced by the kidneys increase RBC precursors

    • Thrombopoietin (TPO)

      • hormone from liver stimulates platelet formation

    • Cytokines are local hormones of bone marrow

      • produced by some marrow cells to stimulate proliferation in other marrow cells

      • colony-stimulating factor (CSF) & interleukin stimulate WBC production

    Tortora & Grabowski 9/e 2000 JWS

    Medical uses of growth factors l.jpgSlide 15

    Medical Uses of Growth Factors

    • Available through recombinant DNA technology

      • recombinant erythropoietin (EPO) very effective in treating decreased RBC production of end-stage kidney disease

      • other products given to stimulate WBC formation in cancer patients receiving chemotherapy which kills bone marrow

        • granulocyte-macrophage colony-stimulating factor

        • granulocyte colony stimulating factor

      • thrombopoietin helps prevent platelet depletion during chemotherapy

    Tortora & Grabowski 9/e 2000 JWS

    Red blood cells or erythrocytes l.jpgSlide 16

    Red Blood Cells or Erythrocytes

    • Contain oxygen-carrying protein hemoglobin that gives blood its red color

      • 1/3 of cell’s weight is hemoglobin

    • Biconcave disk 8 microns in diameter

      • increased surface area/volume ratio

      • flexible shape for narrow passages

      • no nucleus or other organelles

        • no cell division or mitochondrial ATP formation

    • Normal RBC count

      • male 5.4 million/drop ---- female 4.8 million/drop

      • new RBCs enter circulation at 2 million/second

    Tortora & Grabowski 9/e 2000 JWS

    Hemoglobin l.jpgSlide 17


    • Globin protein consisting of 4 polypeptide chains

    • One heme pigment attached to each polypeptide chain

      • each heme contains an iron ion (Fe+2) that can combine reversibly with one oxygen molecule

    Tortora & Grabowski 9/e 2000 JWS

    Transport of o2 co2 and nitric oxide l.jpgSlide 18

    Transport of O2, CO2 and Nitric Oxide

    • Each hemoglobin molecule can carry 4 oxygen molecules from lungs to tissue cells

    • Hemoglobin transports 23% of total CO2 waste from tissue cells to lungs for release

      • combines with amino acids in globin portion of Hb

    • Hemoglobin transports nitric oxide & super nitric oxide helping to regulate BP

      • iron ions pick up nitric oxide (NO) & super nitric oxide (SNO)& transport it to & from the lungs

      • NO causing vasoconstriction is released in the lungs

      • SNO causing vasodilation is picked up in the lungs

    Tortora & Grabowski 9/e 2000 JWS

    Rbc life cycle l.jpgSlide 19

    RBC Life Cycle

    • RBCs live only 120 days

      • wear out from bending to fit through capillaries

      • no repair possible due to lack of organelles

    • Worn out cells removed by fixed macrophages in spleen & liver

    • Breakdown products are recycled

    Tortora & Grabowski 9/e 2000 JWS

    Recycling of hemoglobin components l.jpgSlide 20

    Recycling of Hemoglobin Components

    • In macrophages of liver or spleen

      • globin portion broken down into amino acids & recycled

      • heme portion split into iron (Fe+3) and biliverdin (green pigment)

    Tortora & Grabowski 9/e 2000 JWS

    Fate of components of heme l.jpgSlide 21

    Fate of Components of Heme

    • Iron(Fe+3)

      • transported in blood attached to transferrin protein

      • stored in liver, muscle or spleen

        • attached to ferritin or hemosiderin protein

      • in bone marrow being used for hemoglobin synthesis

    • Biliverdin (green) converted to bilirubin (yellow)

      • bilirubin secreted by liver into bile

        • converted to urobilinogen then stercobilin (brown pigment in feces) by bacteria of large intestine

        • if reabsorbed from intestines into blood is converted to a yellow pigment, urobilin and excreted in urine

    Tortora & Grabowski 9/e 2000 JWS

    Erythropoiesis production of rbcs l.jpgSlide 22

    Erythropoiesis: Production of RBCs

    • Proerythroblast starts to produce hemoglobin

    • Many steps later, nucleus is ejected & a reticulocyte is formed

      • orange in color with traces of visible rough ER

    • Reticulocytes escape from bone marrow into the blood

    • In 1-2 days, they eject the remaining organelles to become a mature RBC

    Tortora & Grabowski 9/e 2000 JWS

    Feedback control of rbc production l.jpgSlide 23

    Feedback Control of RBC Production

    • Tissue hypoxia (cells not getting enough O2)

      • high altitude since air has less O2

      • anemia

        • RBC production falls below RBC destruction

      • circulatory problems

    • Kidney response to hypoxia

      • release erythropoietin

      • speeds up development of proerythroblasts into reticulocytes

    Tortora & Grabowski 9/e 2000 JWS

    Normal reticulocyte count l.jpgSlide 24

    Normal Reticulocyte Count

    • Should be .5 to 1.5% of the circulating RBC’s

    • Low count in an anemic person might indicate bone marrow problem

      • leukemia, nutritional deficiency or failure of red bone marrow to respond to erythropoietin stimulation

    • High count might indicate recent blood loss or successful iron therapy

    Tortora & Grabowski 9/e 2000 JWS

    Wbc anatomy and types l.jpgSlide 25

    WBC Anatomy and Types

    • All WBCs (leukocytes) have a nucleus and no hemoglobin

    • Granular or agranular classification based on presence of cytoplasmic granules made visible by staining

      • granulocytes are neutrophils, eosinophils or basophils

      • agranulocytes are monocyes or lymphocytes

    Tortora & Grabowski 9/e 2000 JWS

    Neutrophils granulocyte l.jpgSlide 26

    Neutrophils (Granulocyte)

    • Polymorphonuclear Leukocytes or Polys

    • Nuclei = 2 to 5 lobes connected by thin strands

      • older cells have more lobes

      • young cells called band cells because of horseshoe shaped nucleus (band)

    • Fine, pale lilac practically invisible granules

    • Diameter is 10-12 microns

    • 60 to 70% of circulating WBCs

    Tortora & Grabowski 9/e 2000 JWS

    Eosinophils granulocyte l.jpgSlide 27

    Eosinophils (Granulocyte)

    • Nucleus with 2 or 3 lobes connected by a thin strand

    • Large, uniform-sized granules stain orange-red with acidic dyes

      • do not obscure the nucleus

    • Diameter is 10 to 12 microns

    • 2 to 4% of circulating WBCs

    Tortora & Grabowski 9/e 2000 JWS

    Basophils granulocyte l.jpgSlide 28

    Basophils (Granulocyte)

    • Large, dark purple, variable-sized granules stain with basic dyes

      • obscure the nucleus

    • Irregular, s-shaped, bilobed nuclei

    • Diameter is 8 to 10 microns

    • Less than 1% of circulating WBCs

    Tortora & Grabowski 9/e 2000 JWS

    Lymphocyte agranulocyte l.jpgSlide 29

    Lymphocyte (Agranulocyte)

    • Dark, oval to round nucleus

    • Cytoplasm sky blue in color

      • amount varies from rim of blue to normal amount

    • Small cells 6 - 9 microns in diameter

    • Large cells 10 - 14 microns in diameter

      • increase in number during viral infections

    • 20 to 25% of circulating WBCs

    Tortora & Grabowski 9/e 2000 JWS

    Monocyte agranulocyte l.jpgSlide 30

    Monocyte (Agranulocyte)

    • Nucleus is kidney or horse-shoe shaped

    • Largest WBC in circulating blood

      • does not remain in blood long before migrating to the tissues

      • differentiate into macrophages

        • fixed group found in specific tissues

          • alveolar macrophages in lungs

          • kupffer cells in liver

        • wandering group gathers at sites of infection

    • Diameter is 12 - 20 microns

    • Cytoplasm is a foamy blue-gray

    • 3 to 8% o circulating WBCs

    Tortora & Grabowski 9/e 2000 JWS

    Wbc physiology l.jpgSlide 31

    WBC Physiology

    • Less numerous than RBCs

      • 5000 to 10,000 cells per drop of blood

      • 1 WBC for every 700 RBC

    • Leukocytosis is a high white blood cell count

      • microbes, strenuous exercise, anesthesia or surgery

    • Leukopenia is low white blood cell count

      • radiation, shock or chemotherapy

    • Only 2% of total WBC population is in circulating blood at any given time

      • rest is in lymphatic fluid, skin, lungs, lymph nodes & spleen

    Tortora & Grabowski 9/e 2000 JWS

    Emigration phagocytosis in wbcs l.jpgSlide 32

    Emigration & Phagocytosis in WBCs

    • WBCs roll along endothelium, stick to it & squeeze between cells.

      • adhesion molecules (selectins) help WBCs stick to endothelium

        • displayed near site of injury

      • molecules (integrins) found on neutrophils assist in movement through wall

    • Neutrophils & macrophages phagocytize bacteria & debris

      • chemotaxis of both

        • kinins from injury site & toxins

    Tortora & Grabowski 9/e 2000 JWS

    Neutrophil function l.jpgSlide 33

    Neutrophil Function

    • Fastest response of all WBC to bacteria

    • Direct actions against bacteria

      • release lysozymes which destroy/digest bacteria

      • release defensin proteins that act like antibiotics & poke holes in bacterial cell walls destroying them

      • release strong oxidants (bleach-like, strong chemicals ) that destroy bacteria

    Tortora & Grabowski 9/e 2000 JWS

    Monocyte function l.jpgSlide 34

    Monocyte Function

    • Take longer to get to site of infection, but arrive in larger numbers

    • Become wandering macrophages, once they leave the capillaries

    • Destroy microbes and clean up dead tissue following an infection

    Tortora & Grabowski 9/e 2000 JWS

    Basophil function l.jpgSlide 35

    Basophil Function

    • Involved in inflammatory and allergy reactions

    • Leave capillaries & enter connective tissue as mast cells

    • Release heparin, histamine & serotonin

      • heighten the inflammatory response and account for hypersensitivity (allergic) reaction

    Tortora & Grabowski 9/e 2000 JWS

    Eosinophil function l.jpgSlide 36

    Eosinophil Function

    • Leave capillaries to enter tissue fluid

    • Release histaminase

      • slows down inflammation caused by basophils

    • Attack parasitic worms

    • Phagocytize antibody-antigen complexes

    Tortora & Grabowski 9/e 2000 JWS

    Lymphocyte functions l.jpgSlide 37

    Lymphocyte Functions

    • B cells

      • destroy bacteria and their toxins

      • turn into plasma cells that produces antibodies

    • T cells

      • attack viruses, fungi, transplanted organs, cancer cells & some bacteria

    • Natural killer cells

      • attack many different microbes & some tumor cells

      • destroy foreign invaders by direct attack

    Tortora & Grabowski 9/e 2000 JWS

    Differential wbc count l.jpgSlide 38

    Differential WBC Count

    • Detection of changes in numbers of circulating WBCs (percentages of each type)

      • indicates infection, poisoning, leukemia, chemotherapy, parasites or allergy reaction

    • Normal WBC counts

      • neutrophils 60-70% (up if bacterial infection)

      • lymphocyte 20-25% (up if viral infection)

      • monocytes 3 -- 8 % (up if fungal/viral infection)

      • eosinophil 2 -- 4 % (up if parasite or allergy reaction)

      • basophil <1% (up if allergy reaction or hypothyroid)

    Tortora & Grabowski 9/e 2000 JWS

    Bone marrow transplant l.jpgSlide 39

    Bone Marrow Transplant

    • Intravenous transfer of healthy bone marrow

    • Procedure

      • destroy sick bone marrow with radiation & chemotherapy

      • donor matches surface antigens on WBC

      • put sample of donor marrow into patient's vein for reseeding of bone marrow

      • success depends on histocompatibility of donor & recipient

    • Treatment for leukemia, sickle-cell, breast, ovarian or testicular cancer, lymphoma or aplastic anemia

    Tortora & Grabowski 9/e 2000 JWS

    Platelet thrombocyte anatomy l.jpgSlide 40

    Platelet (Thrombocyte) Anatomy

    • Disc-shaped, 2 - 4 micron cell fragment with no nucleus

    • Normal platelet count is 150,000-400,000/drop of blood

    • Other blood cell counts

      • 5 million red & 5-10,000 white blood cells

    Tortora & Grabowski 9/e 2000 JWS

    Platelets life history l.jpgSlide 41

    Platelets--Life History

    • Platelets form in bone marrow by following steps:

      • myeloid stem cells to megakaryocyte-colony forming cells to megakaryoblast to megakaryocytes whose cell fragments form platelets

    • Short life span (5 to 9 days in bloodstream)

      • formed in bone marrow

      • few days in circulating blood

      • aged ones removed by fixed macrophages in liver and spleen

    Tortora & Grabowski 9/e 2000 JWS

    Complete blood count l.jpgSlide 42

    Complete Blood Count

    • Screens for anemia and infection

    • Total RBC, WBC & platelet counts; differential WBC; hematocrit and hemoglobin measurements

    • Normal hemoglobin range

      • infants have 14 to 20 g/100mL of blood

      • adult females have 12 to 16 g/100mL of blood

      • adult males have 13.5 to 18g/100mL of blood

    Tortora & Grabowski 9/e 2000 JWS

    Hemostasis l.jpgSlide 43


    • Stoppage of bleeding in a quick & localized fashion when blood vessels are damaged

    • Prevents hemorrhage (loss of a large amount of blood)

    • Methods utilized

      • vascular spasm

      • platelet plug formation

      • blood clotting (coagulation = formation of fibrin threads)

    Tortora & Grabowski 9/e 2000 JWS

    Vascular spasm l.jpgSlide 44

    Vascular Spasm

    • Damage to blood vessel produces stimulates pain receptors

    • Reflex contraction of smooth muscle of small blood vessels

    • Can reduce blood loss for several hours until other mechanisms can take over

    • Only for small blood vessel or arteriole

    Tortora & Grabowski 9/e 2000 JWS

    Platelet plug formation l.jpgSlide 45

    Platelet Plug Formation

    • Platelets store a lot of chemicals in granules needed for platelet plug formation

      • alpha granules

        • clotting factors

        • platelet-derived growth factor

          • cause proliferation of vascular endothelial cells, smooth muscle & fibroblasts to repair damaged vessels

      • dense granules

        • ADP, ATP, Ca+2, serotonin, fibrin-stabilizing factor, & enzymes that produce thromboxane A2

    • Steps in the process

      • (1) platelet adhesion (2) platelet release reaction (3) platelet aggregation

    Tortora & Grabowski 9/e 2000 JWS

    Platelet adhesion l.jpgSlide 46

    Platelet Adhesion

    • Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall

    Tortora & Grabowski 9/e 2000 JWS

    Platelet release reaction l.jpgSlide 47

    Platelet Release Reaction

    • Platelets activated by adhesion

    • Extend projections to make contact with each other

    • Release thromboxane A2 & ADP activating other platelets

    • Serotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel

    Tortora & Grabowski 9/e 2000 JWS

    Platelet aggregation l.jpgSlide 48

    Platelet Aggregation

    • Activated platelets stick together and activate new platelets to form a mass called a platelet plug

    • Plug reinforced by fibrin threads formed during clotting process

    Tortora & Grabowski 9/e 2000 JWS

    Blood clotting l.jpgSlide 49

    Blood Clotting

    • Blood drawn from the body thickens into a gel

      • gel separates into liquid (serum) and a clot of insoluble fibers (fibrin) in which the cells are trapped

    • If clotting occurs in an unbroken vessel is called a thrombosis

    • Substances required for clotting are Ca+2, enzymes synthesized by liver cells and substances released by platelets or damaged tissues

    • Clotting is a cascade of reactions in which each clotting factor activates the next in a fixed sequence resulting in the formation of fibrin threads

      • prothrombinase & Ca+2 convert prothrombin into thrombin

      • thrombin converts fibrinogen into fibrin threads

    Tortora & Grabowski 9/e 2000 JWS

    Overview of the clotting cascade l.jpgSlide 50

    Overview of the Clotting Cascade

    • Prothrombinase is formed by either the intrinsic or extrinsic pathway

    • Final common pathway produces fibrin threads

    Tortora & Grabowski 9/e 2000 JWS

    Extrinsic pathway l.jpgSlide 51

    Extrinsic Pathway

    • Damaged tissues leak tissue factor (thromboplastin) into bloodstream

    • Prothrombinase forms in seconds

    • In the presence of Ca+2, clotting factor X combines with V to form prothrombinase

    Tortora & Grabowski 9/e 2000 JWS

    Intrinsic pathway l.jpgSlide 52

    Intrinsic Pathway

    • Activation occurs

      • endothelium is damaged & platelets come in contact with collagen of blood vessel wall

      • platelets damaged & release phospholipids

    • Requires several minutes for reaction to occur

    • Substances involved: Ca+2 and clotting factors XII, X and V

    Tortora & Grabowski 9/e 2000 JWS

    Final common pathway l.jpgSlide 53

    Final Common Pathway

    • Prothrombinase and Ca+2

      • catalyze the conversion of prothrombin to thrombin

    • Thrombin

      • in the presence of Ca+2 converts soluble fibrinogen to insoluble fibrin threads

      • activates fibrin stabilizing factor XIII

      • positive feedback effects of thrombin

        • accelerates formation of prothrombinase

        • activates platelets to release phospholipids

    Tortora & Grabowski 9/e 2000 JWS

    Clot retraction blood vessel repair l.jpgSlide 54

    Clot Retraction & Blood Vessel Repair

    • Clot plugs ruptured area of blood vessel

    • Platelets pull on fibrin threads causing clot retraction

      • trapped platelets release factor XIII stabilizing the fibrin threads

    • Edges of damaged vessel are pulled together

    • Fibroblasts & endothelial cells repair the blood vessel

    Tortora & Grabowski 9/e 2000 JWS

    Role of vitamin k in clotting l.jpgSlide 55

    Role of Vitamin K in Clotting

    • Normal clotting requires adequate vitamin K

      • fat soluble vitamin absorbed if lipids are present

      • absorption slowed if bile release is insufficient

    • Required for synthesis of 4 clotting factors by hepatocytes

      • factors II (prothrombin), VII, IX and X

    • Produced by bacteria in large intestine

    Tortora & Grabowski 9/e 2000 JWS

    Hemostatic control mechanisms l.jpgSlide 56

    Hemostatic Control Mechanisms

    • Fibrinolytic system dissolves small, inappropriate clots & clots at a site of a completed repair

      • fibrinolysis is dissolution of a clot

    • Inactive plasminogen is incorporated into the clot

      • activation occurs because of factor XII and thrombin

      • plasminogen becomes plasmin (fibrinolysin) which digests fibrin threads

    • Clot formation remains localized

      • fibrin absorbs thrombin

      • blood disperses clotting factors

      • endothelial cells & WBC produce prostacyclin that opposes thromboxane A2 (platelet adhesion & release)

    • Anticoagulants present in blood & produced by mast cells

    Tortora & Grabowski 9/e 2000 JWS

    Intravascular clotting l.jpgSlide 57

    Intravascular Clotting

    • Thrombosis

      • clot (thrombus) forming in an unbroken blood vessel

        • forms on rough inner lining of BV

        • if blood flows too slowly (stasis) allowing clotting factors to build up locally & cause coagulation

      • may dissolve spontaneously or dislodge & travel

    • Embolus

      • clot, air bubble or fat from broken bone in the blood

        • pulmonary embolus is found in lungs

    • Low dose aspirin blocks synthesis of thromboxane A2 & reduces inappropriate clot formation

      • strokes, TIAs and myocardial infarctions

    Tortora & Grabowski 9/e 2000 JWS

    Anticoagulants and thrombolytic agents l.jpgSlide 58

    Anticoagulants and Thrombolytic Agents

    • Anticoagulants suppress or prevent blood clotting

      • heparin

        • administered during hemodialysis and surgery

      • warfarin (Coumadin)

        • antagonist to vitamin K so blocks synthesis of clotting factors

        • slower than heparin

      • stored blood in blood banks treated with citrate phosphate dextrose (CPD) that removes Ca+2

    • Thrombolytic agents are injected to dissolve clots

      • directly or indirectly activate plasminogen

      • streptokinase or tissue plasminogen activator (t-PA)

    Tortora & Grabowski 9/e 2000 JWS

    Blood groups and blood types l.jpgSlide 59

    Blood Groups and Blood Types

    • RBC surfaces are marked by genetically determined glycoproteins & glycolipids

      • agglutinogens or isoantigens

      • distinguishes at least 24 different blood groups

        • ABO, Rh, Lewis, Kell, Kidd and Duffy systems

    Tortora & Grabowski 9/e 2000 JWS

    Abo blood groups l.jpgSlide 60

    ABO Blood Groups

    • Based on 2 glycolipid isoantigens called A and B found on the surface of RBCs

      • display only antigen A -- blood type A

      • display only antigen B -- blood type B

      • display both antigens A & B -- blood type AB

      • display neither antigen -- blood type O

    • Plasma contains isoantibodies or agglutinins to the A or B antigens not found in your blood

      • anti-A antibody reacts with antigen A

      • anti-B antibody reacts with antigen B

    Tortora & Grabowski 9/e 2000 JWS

    Rh blood groups l.jpgSlide 61

    RH blood groups

    • Antigen was discovered in blood of Rhesus monkey

    • People with Rh agglutinogens on RBC surface are Rh+. Normal plasma contains no anti-Rh antibodies

    • Antibodies develop only in Rh- blood type & only with exposure to the antigen

      • transfusion of positive blood

      • during a pregnancy with a positive blood type fetus

    • Transfusion reaction upon 2nd exposure to the antigen results in hemolysis of the RBCs in the donated blood

    Tortora & Grabowski 9/e 2000 JWS

    Hemolytic disease of newborn l.jpgSlide 62

    Hemolytic Disease of Newborn

    • Rh negative mom and Rh+ fetus will have mixing of blood at birth

    • Mom's body creates Rh antibodies unless she receives a RhoGam shot soon after first delivery, miscarriage or abortion

      • RhoGam binds to loose fetal blood and removes it from body before she reacts

    • In 2nd child, hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs

    Tortora & Grabowski 9/e 2000 JWS

    Transfusion and transfusion reactions l.jpgSlide 63

    Transfusion and Transfusion Reactions

    • Transfer of whole blood, cells or plasma into the bloodstream of recipient

      • used to treat anemia or severe blood loss

    • Incompatible blood transfusions

      • antigen-antibody complexes form between plasma antibodies & “foreign proteins” on donated RBC's (agglutination)

      • donated RBCs become leaky (complement proteins) & burst

      • loose hemoglobin causes kidney damage

    • Problems caused by incompatibility between donor’s cells and recipient’s plasma

    • Donor plasma is too diluted to cause problems

    Tortora & Grabowski 9/e 2000 JWS

    Universal donors and recipients l.jpgSlide 64

    Universal Donors and Recipients

    • People with type AB blood called “universal recipients” since have no antibodies in plasma

      • only true if cross match the blood for other antigens

    • People with type O blood cell called “universal donors” since have no antigens on their cells

      • theoretically can be given to anyone

    Tortora & Grabowski 9/e 2000 JWS

    Typing and cross matching blood l.jpgSlide 65

    Typing and Cross-Matching Blood

    • Mixing of incompatible blood causes agglutination (visible clumping)

      • formation of antigen-antibody complex that sticks cells together

      • not the same as blood clotting

    • Typing involves testing blood with known antisera that contain antibodies A, B or Rh+

    • Cross-matching is to test by mixing donor cells with recipient’s serum

    • Screening is to test recipient’s serum against known RBC’s having known antigens

    Tortora & Grabowski 9/e 2000 JWS

    Anemia not enough rbcs l.jpgSlide 66

    Anemia = Not Enough RBCs

    • Symptoms

      • oxygen-carrying capacity of blood is reduced

      • fatigue, cold intolerance & paleness

        • lack of O2 for ATP & heat production

    • Types of anemia

      • iron-deficiency =lack of absorption or loss of iron

      • pernicious = lack of intrinsic factor for B12 absorption

      • hemorrhagic = loss of RBCs due to bleeding (ulcer)

      • hemolytic = defects in cell membranes cause rupture

      • thalassemia = hereditary deficiency of hemoglobin

      • aplastic = destruction of bone marrow (radiation/toxins)

    Tortora & Grabowski 9/e 2000 JWS

    Sickle cell anemia sca l.jpgSlide 67

    Sickle-cell Anemia (SCA)

    • Genetic defect in hemoglobin molecule (Hb-S) that changes 2 amino acids

      • at low very O2 levels, RBC is deformed by changes in hemoglobin molecule within the RBC

        • sickle-shaped cells rupture easily = causing anemia & clots

    • Found among populations in malaria belt

      • Mediterranean Europe, sub-Saharan Africa & Asia

    • Person with only one sickle cell gene

      • increased resistance to malaria because RBC membranes leak K+ & lowered levels of K+ kill the parasite infecting the red blood cells

    Tortora & Grabowski 9/e 2000 JWS

    Hemophilia l.jpgSlide 68


    • Inherited deficiency of clotting factors

      • bleeding spontaneously or after minor trauma

      • subcutaneous & intramuscular hemorrhaging

      • nosebleeds, blood in urine, articular bleeding & pain

    • Hemophilia A lacks factor VIII (males only)

      • most common

    • Hemophilia B lacks factor IX (males only)

    • Hemophilia C (males & females)

      • less severe because alternate clotting activator exists

    • Treatment is transfusions of fresh plasma or concentrates of the missing clotting factor

    Tortora & Grabowski 9/e 2000 JWS

    Disseminated intravascular clotting l.jpgSlide 69

    Disseminated Intravascular Clotting

    • Life threatening paradoxical presence of blood clotting and bleeding at the same time throughout the whole body

      • so many clotting factors are removed by widespread clotting that too few remain to permit normal clotting

    • Associated with infections, hypoxia, low blood flow rates, trauma, hypotension & hemolysis

    • Clots cause ischemia and necrosis leading to multisystem organ failure

    Tortora & Grabowski 9/e 2000 JWS

    Leukemia l.jpgSlide 70


    • Acute leukemia

      • uncontrolled production of immature leukocytes

      • crowding out of normal red bone marrow cells by production of immature WBC

      • prevents production of RBC & platelets

    • Chronic leukemia

      • accumulation of mature WBC in bloodstream because they do not die

      • classified by type of WBC that is predominant---monocytic, lymphocytic.

    Tortora & Grabowski 9/e 2000 JWS

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