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CORNELL NS 3410 - Blood Part 2
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NS 3410 1st Edition Lecture 14Outline of Last LectureI. BloodII. Erythrocytes (RBCs)III. ErythropoiesisIV. AnemiaOutline of Current LectureI. LeukocytesII. Platelets III. HemostasisIV. PlasmaV. Blood TypingCurrent LectureI. Leukocytes- Leukocytes are white blood cells- Mobile units of body’s immune defense system- Functions:-Recognize and destroy or neutralize materials within body that are foreign to normal self-Defends against invading pathogens-Identifies and destroys cancer cells that arise in body-Functions as a “cleanup crew” that removes worn-out cells and tissue debris- 2 Categories: These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.-Granulocytes (small granules present): 1) neutrophil- phagocytize bacteria, 2) eosinophil- attack parasitic worms, lack digestive enzymes to digest bacteria, 3) basophil-release histamine, contains heparin-Agranulocytes: 1) lymphyocytes- T and B lymphocytes, natural killers, 2) monocyte: phagocytosis, develop into macrophages- Leukocytes make up less than 1% of total blood volume; can double the number within only a few hours if an infectionII. Platelets- Cell fragments: lack nuclei, have organelles and cytosolic enzymes for generating energy and synthesizing secretory products- Lifespan is 10 days- Removed from circulation by tissue macrophages- Thrombocytopoiesis is the formation of platelets and it occurs in the red bone marrow. Megakaryoctes make structural proteins, enzymes and membranes. Shed cytoplasm in small membrane-enclosed packets= platelets- Thrombopoietin: hormone produced by kidneys increases platelet productionIII. Hemostasis- Prevents blood loss from a broken blood vessel- Involves three major steps:-Vascular spasm: reduces blood flow through a damaged vessel, endothelial cells contract and expose underlying basement membrane and collagen-Formation of a platelet plug: platelets aggregate on contact with exposed collagen in damaged wall of the vessel. Platelets release chemicals ADP and thromboxane A2 which causes surface of nearby circulating platelets to become sticky in order to adhere to first layer of aggregated platelets-Blood Coagulation: transformation of blood from liquid into a solid gel- Clot formation: reinforces platelet plug and converts blood in the vicinity of vessel injury into a nonflowing gel. Clotting factors are always present in blood plasma in inactive precursor form. Prothrombin and fibrinogen are produced by the liver. They are inactive until the clotting cascade is initiated. A series of steps involving 12 plasma clotting factors lead to final conversion of fibrinogen into a stabilized fibrin mesh- Clotting Cascade: two pathways initiate the clotting process1) Extrinsic pathway: forms a clot very quickly, activated by factors from outside the blood, happens when tissue damage occurs2) Intrinsic pathway: slower, initiated by factors found within the blood, activated by damage to lining of vessel-Common pathway: both extrinsic and intrinsic start with activation of Factor X- Thrombus- stationary clot- Embolus- clot free-floating; problematic- Causes of clots: slow flow-veins, hypertension, atherosclerosis- Anticoagulants prevent coagulation-Aspirin inhibits production of thromboxane A2-Heparin interferes with thrombin, action in minutes-Coumadin interferes with liver production of clotting factors, action in days- Clot Busters: tPA-Tissue Plasminogen Activator; leads to production of the enzyme plasmin which can digest fibrin strands and dissolve clotIV. Plasma- 90% water- Abundance of dissolved elements- Plasma proteins: albumins, globulins, fibrinogens- Balance acidosis and alkalosis- Compare 6% to 8% of plasma’s total weight- Albumins transport substances and account for plasma colloid osmotic pressure- Globulins are antibodies that attack foreign proteins that transport water insoluble substances and act as clotting factors- Fibrinogen is the inactive precursor of the fibrin meshwork of a blood clotV. Blood Typing- AB O blood groups-Type A: donor has A antigen, antibodies against B-Type B: donor has B antigen, antibodies against A-Type AB: donor has both A and B antigens, but neither antibody; the universal blood recipient-Type O: donor has neither A nor B antigen, but both antibodies; the universal blood donor- Testing blood type before transfusion is a life-saving requirement- Rh blood groups: Rh+ means that you have Rh antigen and Rh- means that you don’t have Rh antigen. Antibodies not automatically formed against Rh antigens- Blood Doping: boost RBC in circulation to enhance athletic


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CORNELL NS 3410 - Blood Part 2

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