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 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 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