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: – polymorphonuclear neutrophils (62%), polymorphonuclear eosinophils (2.3%), polymorphonuclear basophils (0.4%), monocytes(5.3%), lymphocytes (30%) Normal blood levels: ave: 7,000/uL

7. Blood Types What is your blood type?

8. 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

9. ABO Blood types with agglutinins GenotypeBlood TypeAgglutinogensAgglutininFrequency OOO-Anti A and Anti B47% OA or AAAAAnti B41% OB or BBBBAnti A9% AB A and B-3%

10. 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

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

12. Erythroblastosis Fetalis – 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's Rh antigen – the mother's agglutinins diffuse through the placenta into the fetus and cause red blood cell agglutination

14. Erythroblastosis Fetalis 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

15. 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)

16. 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

17. 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

18. 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

19. 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

20. 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

22. 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.

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

25. 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 thrombinthrombin – (3) The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that enmesh platelets, blood cells, and plasma to form the clot.thrombin

27. FibrinogenFactor I ProthrombinFactor II Tissue factorFactor III; tissue thromboplastin CalciumFactor IV Factor VProaccelerin; labile factor; Ac-globulin (Ac- G) Factor VIISerum prothrombin conversion accelerator (SPCA); proconvertin; stable factor Factor VIIIAntihemophilic factor (AHF); Factor IXPlasma thromboplastin component (PTC); Christmas factor; antihemophilic factor B Factor XStuart factor; Stuart-Prower factor Factor XIPlasma thromboplastin antecedent (PTA); antihemophilic factor C Factor XIIHageman factor Factor XIIIFibrin-stabilizing factor PrekallikreinFletcher factor High-molecular-weight kininogenFitzgerald factor; HMWK (high-molecular- weight) kininogen

28. 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 fibrinogenthrombin

29. 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