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This powerpoint presentation has been adapted from Life 4e-Lewis, Gaffin, Hoefnagels and Parker. Publishers-McGraw-Hill

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This powerpoint presentation has been adapted from Life 4e-Lewis, Gaffin, Hoefnagels and Parker. Publishers-McGraw-Hill

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    1. Tortora & Grabowski 9/e ?2000 JWS 19-1 This powerpoint presentation has been adapted from Life 4e-Lewis, Gaffin, Hoefnagels and Parker. Publishers-McGraw-Hill 1998 and Principles of Anatomy and Physiology,Tortora and Grabowski. Publishers- John Wiley & sons, Inc. 2000

    2. Tortora & Grabowski 9/e ?2000 JWS 19-2 Chapter 19 The Cardiovascular System: The Blood

    3. Tortora & Grabowski 9/e ?2000 JWS 19-3 Cells of the body are serviced by 3 closely related fluids Blood composed of plasma and a variety of cells transports nutrients, gases and wastes Interstitial fluid bathes the cells of the body Lymph Interstitial fluid that does not directly return to blood vessels but first passes thru lymph nodes and then back to blood Nutrients and oxygen diffuse from the blood into the interstitial fluid & then into the cells Wastes and carbon dioxide move in the reverse direction Hematology is study of blood and blood disorders Fluids of the Body

    4. Tortora & Grabowski 9/e ?2000 JWS 19-4 Functions of Blood Transportation O2, C O2, metabolic wastes, nutrients, heat & hormones Regulation helps regulate pH through buffers helps regulate body temperature High heat capacity and heat of vaporization for water Vasodilation of surface vessels allow heat to radiate to environment. Vasoconstriction of surface vessels reduces heat radiation to environment. helps regulate water content of cells by interactions with dissolved ions and proteins Protection from disease & loss of blood

    5. Tortora & Grabowski 9/e ?2000 JWS 19-5 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

    6. Tortora & Grabowski 9/e ?2000 JWS 19-6 Techniques of Blood Sampling Venipuncture sample taken from vein with hypodermic needle & syringe median cubital vein (see page 803) Why stick an vein? less pressure closer to the surface Finger or heel stick common technique for diabetics to monitor daily blood sugar method used for infants

    7. Tortora & Grabowski 9/e ?2000 JWS 19-7 Components of Blood Hematocrit 55% plasma 45% cells 99% RBCs < 1% WBCs and platelets

    8. Tortora & Grabowski 9/e ?2000 JWS 19-8 Blood Plasma 0ver 90% water 7% plasma proteins created in liver confined to bloodstream albumin maintain blood osmotic pressure globulins (immunoglobulins) antibodies bind to foreign substances called antigens form antigen-antibody complexes fibrinogen for clotting 2% other substances electrolytes, nutrients, hormones, gases, waste products

    9. Tortora & Grabowski 9/e ?2000 JWS 19-9

    10. Tortora & Grabowski 9/e ?2000 JWS 19-10

    11. Tortora & Grabowski 9/e ?2000 JWS 19-11 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)

    12. Tortora & Grabowski 9/e ?2000 JWS 19-12 Hematocrit Percentage of blood occupied by red blood 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

    13. Tortora & Grabowski 9/e ?2000 JWS 19-13 Blood Doping EPO 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

    14. Tortora & Grabowski 9/e ?2000 JWS 19-14 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, vertebra, pelvis and proximal epiphysis of femur and humerus

    15. Tortora & Grabowski 9/e ?2000 JWS 19-15 Hematopoiesis

    16. Tortora & Grabowski 9/e ?2000 JWS 19-16 Stages of Blood Cell Formation Pluripotent stem cells .1% of red marrow cells (indistinguishable from other 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

    17. Tortora & Grabowski 9/e ?2000 JWS 19-17 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

    18. Tortora & Grabowski 9/e ?2000 JWS 19-18 Medical Uses of Growth Factors Available through recombinant DNA technology recombinant erythropoietin (EPO) very effective in treating decreased RBC production because of end-stage kidney disease as well as treating anemias 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

    19. Tortora & Grabowski 9/e ?2000 JWS 19-19 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 (250 million Hb/cell!!) 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/leave circulation at 2 million/second Red Blood Cells or Erythrocytes

    20. Tortora & Grabowski 9/e ?2000 JWS 19-20 Hemoglobin Globin protein consisting of 4 polypeptide chains One heme pigment attached to each polypeptide chain each heme contains an iron ion (Fe2+) that can combine reversibly with one oxygen molecule

    21. Tortora & Grabowski 9/e ?2000 JWS 19-21 Transport of O2, CO2 and Nitric Oxide Each hemoglobin molecule can carry 4 oxygen(O2) 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

    22. Tortora & Grabowski 9/e ?2000 JWS 19-22 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/attached macrophages in spleen & liver Breakdown products are recycled Blood cells are replaced w/in 5-7 days after donation -uses up Fe3+ supplies Blood bank makes you wait 8 weeks

    23. Tortora & Grabowski 9/e ?2000 JWS 19-23 Recycling of Hemoglobin Components pg. 697 In macrophages of liver, spleen and/or red bone marrow globin portion broken down into amino acids & recycled heme portion split into iron (Fe3+) and biliverdin (green pigment)

    24. Tortora & Grabowski 9/e ?2000 JWS 19-24 Erythropoiesis: Production of RBCs Requires Fe3+, vit B12, intrinsic factor, Erythropoetin, dietary protein Proerythroblast starts to produce hemoglobin Many steps later, nucleus is ejected & a reticulocyte is formed Reticulocytes escape from bone marrow into the blood In 1-2 days, they eject the remaining organelles to become a mature RBC

    25. Tortora & Grabowski 9/e ?2000 JWS 19-25 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

    26. Tortora & Grabowski 9/e ?2000 JWS 19-26 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

    27. Tortora & Grabowski 9/e ?2000 JWS 19-27 Pg. 694

    28. Tortora & Grabowski 9/e ?2000 JWS 19-28 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 monocytes or lymphocytes

    29. Tortora & Grabowski 9/e ?2000 JWS 19-29 WBC Physiology Less numerous than RBCs 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, lymph nodes, skin, lungs& spleen

    30. Tortora & Grabowski 9/e ?2000 JWS 19-30 Emigration & Phagocytosis in WBCs WBCs roll along endothelium, stick to it & squeeze between cells. Neutrophils & macrophages phagocytize bacteria & debris chemotaxis of both kinins from injury site & toxins

    31. Tortora & Grabowski 9/e ?2000 JWS 19-31 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

    32. Tortora & Grabowski 9/e ?2000 JWS 19-32 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

    33. Tortora & Grabowski 9/e ?2000 JWS 19-33 Basophil Function Involved in inflammatory and allergy reactions Leave capillaries & enter connective tissue as mast cells Release heparin & histamine heighten the inflammatory response and account for hypersensitivity (allergic) reaction

    34. Tortora & Grabowski 9/e ?2000 JWS 19-34 Eosinophil Function Leave capillaries to enter tissue fluid Release histaminase slows down inflammation caused by basophils Attack parasitic worms Phagocytize antibody-antigen complexes

    35. Tortora & Grabowski 9/e ?2000 JWS 19-35 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

    36. Tortora & Grabowski 9/e ?2000 JWS 19-36 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)

    37. Tortora & Grabowski 9/e ?2000 JWS 19-37 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, testicular cancer, lymphoma or aplastic anemia

    38. Tortora & Grabowski 9/e ?2000 JWS 19-38 Platelets A cubic milliliter contains ~ 250,000 platelets. Thrombocytes are small, nucleated cells that are involved in clotting of blood. A cubic milliliter contains ~ 250,000 platelets. Thrombocytes are small, nucleated cells that are involved in clotting of blood.

    39. Tortora & Grabowski 9/e ?2000 JWS 19-39 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

    40. Tortora & Grabowski 9/e ?2000 JWS 19-40 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

    41. Tortora & Grabowski 9/e ?2000 JWS 19-41 Complete Blood Count Screens for anemia and infection

    42. Tortora & Grabowski 9/e ?2000 JWS 19-42 Hemostasis 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)

    43. Tortora & Grabowski 9/e ?2000 JWS 19-43 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

    44. Tortora & Grabowski 9/e ?2000 JWS 19-44 Platelet Plug Formation Platelets store a lot of chemicals in granules needed for platelet plug formation Some cause proliferation of vascular endothelial cells, smooth muscle & fibroblasts to repair damaged vessels Steps in the process (1) platelet adhesion (2) platelet release reaction (3) platelet aggregation

    45. Tortora & Grabowski 9/e ?2000 JWS 19-45 Platelet Adhesion Platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall

    46. Tortora & Grabowski 9/e ?2000 JWS 19-46 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

    47. Tortora & Grabowski 9/e ?2000 JWS 19-47 Blood Clotting

    48. Tortora & Grabowski 9/e ?2000 JWS 19-48 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 Ca2+, 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 & Ca2+ convert prothrombin into thrombin thrombin converts fibrinogen into fibrin threads

    49. Tortora & Grabowski 9/e ?2000 JWS 19-49 Overview of the Clotting Cascade pg. 683 Prothrombinase is formed by either the intrinsic or extrinsic pathway Final common pathway produces fibrin threads

    50. Tortora & Grabowski 9/e ?2000 JWS 19-50 ? Platelet plug forms There are at least 15 clotting factors that are required for blood to clot. Lack of vitamins C & K will slow clotting, because these vitamins are required to synthesize clotting factors. Fibrin threads form a meshwork that entraps red blood cells & more platelets, forming a clot.There are at least 15 clotting factors that are required for blood to clot. Lack of vitamins C & K will slow clotting, because these vitamins are required to synthesize clotting factors. Fibrin threads form a meshwork that entraps red blood cells & more platelets, forming a clot.

    51. Tortora & Grabowski 9/e ?2000 JWS 19-51

    52. Tortora & Grabowski 9/e ?2000 JWS 19-52

    53. Tortora & Grabowski 9/e ?2000 JWS 19-53

    54. Tortora & Grabowski 9/e ?2000 JWS 19-54

    55. Tortora & Grabowski 9/e ?2000 JWS 19-55 Extrinsic Pathway Damaged tissues leak tissue factor (thromboplastin) into bloodstream Prothrombinase forms in seconds In the presence of Ca2+ , clotting factor X combines with V to form prothrombinase

    56. Tortora & Grabowski 9/e ?2000 JWS 19-56 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: Ca2+ and clotting factors XII, X and V

    57. Tortora & Grabowski 9/e ?2000 JWS 19-57 Final Common Pathway Prothrombinase and Ca2+ catalyze the conversion of prothrombin to thrombin Thrombin in the presence of Ca2+ 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

    58. Tortora & Grabowski 9/e ?2000 JWS 19-58 Clot Retraction & Blood Vessel Repair Clot plugs ruptured area of blood vessel Platelets pull on fibrin threads causing clot retraction trapped platelets release factors that stabilize the fibrin threads Edges of damaged vessel are pulled together Fibroblasts & endothelial cells repair the blood vessel

    59. Tortora & Grabowski 9/e ?2000 JWS 19-59 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 Produced by bacteria in large intestine

    60. Tortora & Grabowski 9/e ?2000 JWS 19-60 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 which digests fibrin threads Clot formation remains localized fibrin absorbs thrombin blood disperses clotting factors Anticoagulants present in blood & produced by mast cells

    61. Tortora & Grabowski 9/e ?2000 JWS 19-61 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 reduces inappropriate clot formation strokes, TIAs and myocardial infarctions

    62. Tortora & Grabowski 9/e ?2000 JWS 19-62 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 Ca2+ Thrombolytic agents are injected to dissolve clots directly or indirectly activate plasminogen streptokinase or tissue plasminogen activator (t-PA)

    63. Tortora & Grabowski 9/e ?2000 JWS 19-63 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

    64. Tortora & Grabowski 9/e ?2000 JWS 19-64 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

    65. Tortora & Grabowski 9/e ?2000 JWS 19-65 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

    66. Tortora & Grabowski 9/e ?2000 JWS 19-66 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

    67. Tortora & Grabowski 9/e ?2000 JWS 19-67 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, still have A & B agglutinins theoretically can be given to anyone

    68. Tortora & Grabowski 9/e ?2000 JWS 19-68 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

    69. Tortora & Grabowski 9/e ?2000 JWS 19-69

    70. Tortora & Grabowski 9/e ?2000 JWS 19-70

    71. Tortora & Grabowski 9/e ?2000 JWS 19-71

    72. Tortora & Grabowski 9/e ?2000 JWS 19-72 Umbilical Cord Contents 2 arteries that carry blood to the placenta 1 umbilical vein that carries oxygenated blood to the fetus primitive connective tissue Stub drops off in 2 weeks leaving a scar called the umbilicus

    73. Tortora & Grabowski 9/e ?2000 JWS 19-73

    74. Tortora & Grabowski 9/e ?2000 JWS 19-74 Hemolytic Disease of Newborn (erythroblastois fetalis) Rh negative mom and Rh+ fetus will have mixing of blood at birth. Anti-Rh antibodies are 5x smaller than the A, B antibodies. These small antibodies will cross the placental barrier Mom's body creates Rh antibodies unless she receives a RhoGam shot at 28 weeks (greatest risk of maternal-fetal exchange) and w/in 72 hours after delivery, miscarriage or abortion. RhoGam binds to loose fetal blood and removes it from body before her immune system reacts In 2nd + child, if mom had no RhoGam, hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs

    75. Tortora & Grabowski 9/e ?2000 JWS 19-75 Stages of Labor Dilation 6 to 12 hours rupture of amniotic sac & dilation of cervix Expulsion 10 minutes to several hours baby moves through birth canal Placental 30 minutes afterbirth is expelled by muscular contractions

    76. Tortora & Grabowski 9/e ?2000 JWS 19-76 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)

    77. Tortora & Grabowski 9/e ?2000 JWS 19-77 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

    78. Tortora & Grabowski 9/e ?2000 JWS 19-78 Hemophilia 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 (primarily males) most common Hemophilia B lacks factor IX (primarily males) Hemophilia C (males & females) less severe because alternate clotting activator exists Treatment is transfusions of fresh plasma or concentrates of the missing clotting factor

    79. Tortora & Grabowski 9/e ?2000 JWS 19-79 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

    80. Tortora & Grabowski 9/e ?2000 JWS 19-80 Leukemia 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.

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