Hemostasis: Mechanisms of Blood Coagulation
Hemostasis: Mechanisms of Blood Coagulation
Hemostasis is the body's normal physiological response for the prevention and stopping of
bleeding/hemorrhage. It results in the blocking of any vascular rupture. Generally speaking, it
helps ensure blood fluidity and blood vessel integrity. Abnormalities in hemostasis can result in
bleeding (hemorrhage) or blood clots (thrombosis).
2. Platelet plug. Platelets aggregate to the site of the injury. They stick together acting as a
"plug." Platelets also activate the process which causes a fibrin clot to form, known as secondary
hemostasis.
B. Secondary hemostasis.
Platelets alone are not enough to secure the damage in the vessel wall. A clot must form at the
site of injury. The formation of a clot depends upon several substances called clotting
factors. These factors are designated by roman numerals I through XIII. These factors activate
each other in what as known as the clotting cascade. The end result of this cascade is that
fibrinogen, a soluble plasma protein, is cleaved into fibrin, a nonsoluble plasma protein. The
fibrin proteins stick together forming a clot.
The clotting cascade occurs through two separate pathways that interact, the intrinsic and the
extrinsic pathway.
1. Extrinsic Pathway:
The extrinsic pathway is activated by external trauma that causes blood to escape from the
vascular system. This pathway is quicker than the intrinsic pathway. It involves factor VII.
2. Intrinsic Pathway:
The intrinsic pathway is activated by trauma inside the vascular system, and is activated by
platelets, exposed endothelium, chemicals, or collagen. This pathway is slower than the extrinsic
pathway, but more important. It involves factors XII, XI, IX, VIII.
3. Common Pathway:
Both pathways meet and finish the pathway of clot production in what is known as the common
pathway. The common pathway involves factors I, II, V, and X.
4. Fibrinolytic Pathway:
Fibrinolytic System. The fibrinolytic system functions to remove the clot after the vasculature
is repaired, as well as to degrade clots that form in the bloodstream. The final step in
this pathway is the plasmin-mediated cleavage of fibrin, creating fibrin degradation products.
Clotting Factors
Factor Name
number Type of molecule Source Pathway(s)
I Common; converted
Fibrinogen Plasma protein Liver
into fibrin
II Common; converted
Prothrombin Plasma protein Liver*
into thrombin
III Tissue thromboplastin or Damaged cells
Lipoprotein mixture Extrinsic
tissue factor and platelets
IV Diet, platelets,
Calcium ions Inorganic ions in plasma Entire process
bone matrix
V Proaccelerin Plasma protein Liver, platelets Extrinsic and intrinsic
VI Not used Not used Not used Not used
VII Proconvertin Plasma protein Liver * Extrinsic
VIII Intrinsic; deficiency
Platelets and
Antihemolytic factor A Plasma protein factor results in hemophilia
endothelial cells
A
IX Antihemolytic factor B Intrinsic; deficiency
(plasma thromboplastin Plasma protein Liver* results in hemophilia
component) B
X Stuart–Prower factor
Protein Liver* Extrinsic and intrinsic
(thrombokinase)
XI Antihemolytic factor C Intrinsic; deficiency
(plasma thromboplastin Plasma protein Liver results in hemophilia
antecedent) C
XII Intrinsic; initiates
Hageman factor Plasma protein Liver clotting in vitro also
activates plasmin
XIII Stabilizes fibrin; slows
Fibrin-stabilizing factor Plasma protein Liver, platelets
fibrinolysis