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Paper-MZ-202(Animal Physiology) - Blood Coagulation
Blood coagulation, or clotting, is the transformation of blood from a liquid into a solid gel
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Furthermore, as blood in the vicinity of the vessel defect solidifies,
it can no longer flow
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It is required
to stop bleeding from all but the most minute defects
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This conversion
into fibrin is catalyzed by the enzyme thrombin at the site of the injury
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The resulting mass, or clot, typically appears red because of the
abundance of trapped RBCs, but the foundation of the clot is formed of fibrin derived from the
plasma (❯ Figure 10-12)
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The original fibrin web is rather weak, because the fibrin strands are only
loosely interlaced
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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 an inactive form
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Thrombin converts the
ever-present fibrinogen molecules in the
plasma into a blood-staunching clot, so it
must normally be absent from the plasma, except in the vicinity of vessel damage
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How can thrombin
normally be absent from the plasma, yet be readily available to trigger fibrin formation when a
vessel is injured? The solution lies in thrombin’s existence in the plasma in the form of an
inactive precursor called prothrombin
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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 an inactive form and must be converted into its
active form by still another activated factor, and so on
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These factors are designated by Roman numerals in the order they were discovered, not in the
order they participate in the clotting process
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One consequence of liver disease is that clotting time is prolonged due
to a reduced production of clotting factors
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In contrast to fibrinogen, which is converted
into insoluble fibrin strands, prothrombin and the other precursors act as proteolytic
(proteinsplitting) enzymes when converted to their active form
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Once the first factor in the sequence is activated, it
activates the next factor, and so on, in a series of sequential reactions known as the clotting
cascade; this continues until thrombin catalyzes the final conversion of fibrinogen into fibrin
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Thus, platelets also contribute to clot
formation
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All elements necessary to bring about clotting by means of the intrinsic
pathway are present in the blood
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Remember that exposed collagen also initiates platelet aggregation
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Furthermore, these complementary haemostatic
mechanisms reinforce each other
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• The extrinsic pathway takes a shortcut and requires only four steps (shown in
grey in Figure 10-14)
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When a tissue is traumatized, it
releases a protein complex known as tissue thromboplastin
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From this point
on, the two pathways are identical
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Typically, clots are fully formed in three to six
minutes
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During clot retraction, fluid is squeezed
from the clot
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AMPLIFICATION DURING CLOTTING PROCESS
Although a clotting process that involves so many steps may seem inefficient, its advantage is
the amplification accomplished during many of the steps
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In this way, large numbers of the
final factors involved in clotting are rapidly activated as a result of the initial activation of only a
few molecules in the beginning step of the sequence
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Fortunately, after participating in the local clotting process, the massive
number of factors activated in the vicinity of vessel injury is rapidly inactivated by enzymes and
other factors present in the plasma or tissue
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It is a transient device to stop
bleeding until the vessel can be repaired
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Fibroblasts
form a scar at the vessel defect
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If
clots were not removed after they performed their haemostatic function, the vessels, especially
the small ones that endure tiny ruptures on a regular basis, would eventually become obstructed
by clots
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Plasmin is activated in a fast cascade
of reactions involving many factors, among them factor XII (Hageman factor), which also
triggers the chain reaction leading to clot formation (❯ Figure 10-16)
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Phagocytic white blood cells gradually remove the products
of clot dissolution
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The coloration results from the slow removal of the deoxygenated clotted blood
that escaped into the tissue layers of your skin
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PREVENTING INAPPROPRIATE CLOT FORMATION
In addition to removing clots that are no longer needed, plasmin functions continually to prevent
clots from forming inappropriately
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Clots do not develop,
however, because plasmin, activated by tissue plasminogen activator (tPA), quickly gets rid of
the fibrin from the tissues, especially the lungs
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Only when a vessel is damaged do additional factors precipitate the explosive chain reaction that
leads to more extensive fibrin formation and results in local clotting at the site of injury
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Administering a clotbusting drug within the first hours after a clot has blocked a coronary (heart) vessel often
dissolves the clot in time to restore blood flow to the cardiac muscle that is supplied by the
blocked vessel before the muscle dies of oxygen deprivation
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