blood physiology
DESCRIPTION
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: - PowerPoint PPT PresentationTRANSCRIPT
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/dL; Women: 14 g/dL
• 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/uL
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 agglutininsGenotype 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 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.
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-molecular-weight) 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 V, Factor VIII, prothrombin, and Factor XII