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Blood Physiology

Blood Physiology. Dr. Meg- angela Christi Amores. RBC (Red Blood Cells) Erythrocytes Transport hemoglobin Contain carbonic anhydrase. Erythrocytes (RBC). Biconcave discs, diameter of 7.8 um Shape changes remarkably as they squeeze through capillaries Normal blood levels: average:

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Blood Physiology

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  1. Blood Physiology Dr. Meg-angela Christi Amores

  2. RBC (Red Blood Cells) • Erythrocytes • Transport hemoglobin • Contain carbonic anhydrase

  3. Erythrocytes (RBC) • Biconcave discs, diameter of 7.8 um • Shape changes remarkably as they squeeze through capillaries • Normal blood levels: average: • Men : 5,200 / um • Women: 4,700 /um • Hemoglobin: Men: 15 g/dL; Women: 14 g/dL

  4. WBC (White Blood Cells) • Leukocytes • Work to prevent disease by: • (1) by actually destroying invading bacteria or viruses by phagocytosis, • (2) by forming antibodies and sensitized lymphocytes • mobile units of the body's protective system

  5. Leukocytes (WBC) • Types: • polymorphonuclearneutrophils (62%), polymorphonucleareosinophils (2.3%), polymorphonuclearbasophils (0.4%), monocytes(5.3%) , lymphocytes (30%) • Normal blood levels: ave: 7,000/uL

  6. Blood Types • What is your blood type?

  7. ABO and Rh system • Two antigens-type A and type B-occur on the surfaces of the red blood cells • also called agglutinogens because they often cause blood cell agglutination • people may have neither of them on their cells, they may have one, or they may have both simultaneously

  8. ABO Blood types with agglutinins

  9. Rh System • also important when transfusing blood • In the O-A-B system, the plasma agglutinins responsible for causing transfusion reactions develop spontaneously • in the Rh system, spontaneous agglutinins almost never occur

  10. Rh System • Rh antigens • D antigen is widely prevalent • Rh positive : with D antigen • ErythroblastosisFetalis • ("Hemolytic Disease of the Newborn") • disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetus's red blood cells

  11. ErythroblastosisFetalis • mother is Rh negative and the father Rh positive • baby has inherited the Rh-positive antigen from the father, and the mother develops anti-Rh agglutinins from exposure to the fetus'sRh antigen • the mother's agglutinins diffuse through the placenta into the fetus and cause red blood cell agglutination

  12. ErythroblastosisFetalis • jaundiced, erythroblastotic newborn baby is usually anemic at birth • liver and spleen become greatly enlarged • permanent mental impairment or damage to motor areas of the brain • Treatment: replace the neonate's blood with Rh-negative blood

  13. Blood Transfusion • Immediate/ Acute Hemolysis • Delayed Hemolysis • When blood are mismatched, red cells agglutinate as a result of the agglutinins' attaching themselves to the red blood cell • Cells clump (agglutinate) and hemolyze (destroyed by WBC, releasing hemoglobin)

  14. Hemolysis • antibodies cause lysis of the red blood cells by activating the complement system, which releases proteolytic enzymes (the lytic complex) that rupture the cell membranes

  15. Hemostasis • hemostasis means prevention of blood loss • (1) vascular constriction • (2) formation of a platelet plug • (3) formation of a blood clot as a result of blood coagulation • (4) eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently

  16. Blood Coagulation • Vascular Constriction • trauma to the vessel wall itself causes the smooth muscle in the wall to contract • (1) local myogenic spasm, (2) local autacoid factors from the traumatized tissues and blood platelets, and (3) nervous reflexes

  17. Blood Coagulation • Formation of Platelet Plug • platelets come in contact with a damaged vascular surface they change their own characteristics • begin to swell; assume irregular forms with numerous irradiating pseudopods protruding from their surfaces • become sticky ,adhere to collagen in the tissues and to a protein called von Willebrand factor • The ADP and thromboxane in turn act on nearby platelets to activate them as well

  18. Blood Coagulation • Formation of the blood clot • begins to develop in 15 to 20 seconds if the trauma to the vascular wall has been severe, and in 1 to 2 minutes if the trauma has been minor • Within 3-6 mins, entire opening filled with clot • After 20 mins to 1 hour – clot retracts

  19. Blood Coagulation • Fibrous Organization • Clot: • (1) It can become invaded by fibroblasts, which subsequently form connective tissue all through the clot, or (2) it can dissolve • Fibroblasts: continues to complete organization of the clot into fibrous tissue within about 1 to 2 weeks.

  20. Mechanism of blood coagulation • Basic Theory • Balance between procoagulant and anticoagulant • Normal blood vessel: anticoagulant dominate • Rupture blood vessel: procoagulant

  21. Mechanism of blood coagulation • General Mechanism • (1) ruptured vessel: a complex cascade of chemical reactions occurs for formation of prothrombin activator • (2) The prothrombin activator catalyzes conversion of prothrombin into thrombin • (3) The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that enmesh platelets, blood cells, and plasma to form the clot.

  22. Vicious Circle of Clot Formation • the clot itself initiates a vicious circle to promote more clotting • the proteolytic action of thrombin allows it to act on many of the other blood-clotting factors in addition to fibrinogen

  23. Fibrinolysis • Lysis of fibrin clots • plasminogen (or profibrinolysin) • becomes a substance called plasmin (or fibrinolysin). • Plasmin digests fibrin fibers and some other protein coagulants such as fibrinogen, Factor V, Factor VIII, prothrombin, and Factor XII

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