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Hemostasis is the arrest of bleeding from a broken blood vesselthat is, the
stopping of hemorrhage (hemo means blood; stasis means standing). For bleeding
to take place from a vessel, there must be a break in the vessel wall and the pressure
inside the vessel must be greater than the pressure outside it to force blood out through
the defect
Hemostasis involves three major steps: (1) vascular spasm, (2) formation of a
platelet plug, and (3) blood coagulation (clotting). Platelets play a pivotal role in
hemostasis. They obviously play a major part in forming a platelet plug, but they also
contribute significantly to the other two steps.
Clot formation results from a triggered chain reaction involving plasma clotting
factors.
CLOT FORMATION The ultimate step in clot formation is the conversion of
fibrinogen, a large, soluble plasma protein produced by the liver and normally always
present in the plasma, into fibrin, an insoluble, threadlike molecule. This conversion into
f brin is catalyzed by the enzyme thrombin at the site of the injury. Fibrin molecules
adhere to the damaged vessel surface, forming a loose, netlike meshwork that traps
blood cells, including aggregating platelets. The resulting mass, or clot, typically appears
red because of the abundance of trapped RBCs, but the foundation of the clot is formed
of fi brin derived from the plasma. Except for platelets, which play an important role in
ultimately bringing about the conversion of fibrinogen to fibrin, clotting can take place
in the absence of all other blood cells. The original fibrin web is rather weak, because
the fi brin strands are only loosely interlaced. However, chemical linkages rapidly form
between adjacent strands to strengthen and stabilize the clot meshwork. This cross-
linkage process is catalyzed by a clotting factor known as factor XIII (fibrin-stabilizing
factor), which normally is present in the plasma in inactive form
THE CLOTTING CASCADE Yet another activated plasma clotting factor, factor X,
converts prothrombin to thrombin; factor X itself is normally present in the blood in
inactive form and must be converted into its active form by still another activated
factor, and so on. Altogether, 12 plasma clotting factors participate in essential steps
that lead to the final conversion of fibrinogen into a stabilized fibrin mesh.
INTRINSIC AND EXTRINSIC PATHWAYS The clotting cascade may be triggered by the intrinsic
pathway or the extrinsic pathway:
Most of these clotting factors are plasma proteins synthesized by the liver. Normally,
they are always present in the plasma in an inactive form, such as fibrinogen and prothrombin.
Sorces :
Sources :
b. Hemophilia
X link-resesive
There is two classification of hemophilia, that is Hemophilia A and
Hemophilia B
Hemophilia A caused by F. VIII deficiency
Hemophilia B caused by F. IX deficiency
Hemophilia A is 85%, while hemophilia B is 15% of hemophilia cases.
Hemophilia is foun in men, and women mostly carier