Blood Physiology Dr Megangela Christi Amores RBC Red

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: • Men : 5, 200 / um • Women: 4, 700 /um – Hemoglobin: Men: 15 g/d. L; Women: 14 g/d. L

• 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

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/u. L

Blood Types • What is your blood type?

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

ABO Blood types with agglutinins Genotype Blood Type Agglutinogens Agglutinin Frequency OO O - Anti A and Anti B 47% OA or AA A A Anti B 41% OB or BB B B Anti A 9% AB AB A and B - 3%

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

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

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

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

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)

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

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 • •

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

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

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

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.

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

Mechanism of blood coagulation • General Mechanism – (1) ruptured vessel: a complex cascade of chemical reactions occurs 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.

Fibrinogen Factor I Prothrombin Factor II Tissue factor Factor III; tissue thromboplastin Calcium Factor IV Factor V Proaccelerin; labile factor; Ac-globulin (Ac. G) Factor VII Serum prothrombin conversion accelerator (SPCA); proconvertin; stable factor Factor VIII Antihemophilic factor (AHF); Factor IX Plasma thromboplastin component (PTC); Christmas factor; antihemophilic factor B Factor X Stuart factor; Stuart-Prower factor Factor XI Plasma thromboplastin antecedent (PTA); antihemophilic factor C Factor XII Hageman factor Factor XIII Fibrin-stabilizing factor Prekallikrein Fletcher factor High-molecular-weight kininogen Fitzgerald factor; HMWK (high-molecularweight) kininogen

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

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 VIII, prothrombin, and Factor XII