Injury- because of injury blood leaks
through the blood vessels and it leads to two changes- changes in platelets and
exposure of sub endothelial tissue factor II to plasma factor VII. When a blood
vessel is injured the walls of the blood vessels contract to reduce the flow of
the blood to the injured area. Platelets stick to the side of injury around a collagen
part of the blood vessel and spread along the surface of the blood vessel to
stop the bleeding.
Release of chemicals from platelets-
chemical signals are being released from small sacks inside the platelets that
attract other cells to the area and make them clamp together to form a platelet
plug. Platelets will release thromboplastins and then this will turn inactive
thrombin with the help of calcium ions and vitamin K.
Clumping of platelets at wound site- When a person is healing from an injury, the wound must be closed to prevent blood loss and the entry
of pathogens so the blood begins to clot because of the action of platelets (cells circulating in blood that clump together to prevent excessive bleeding) by arising
a small and temporary plug. Platelets cause clotting at injury sites, and are helpful there so the patient does not
lose too much blood. Formation of fibrin clot- An essential
part of the process to stop blood loss after vascular injury is the formation
of a fibrin clot at the site of an injury to the wall of a normal blood vessel.
Cascade is group of process that leads to fibrin clot formation. In those
processes the product of each step is an enzyme or cofactor which is essential
for following reactions to begin a course of action efficiently. The clotting
cascade can be divided into three main processes: the extrinsic pathway, the
intrinsic pathway, and the common pathway. During the process of extrinsic
pathway tissue factor at the site of vascular injury is being released which
results in the activation of factor X. The intrinsic pathway provides an
alternative mechanism for activation of factor X, starting from the activation
of factor XII. The common pathway consists of the steps which are linked to the
activation of factor X and the formation of a multimeric, cross-linked fibrin
clot. Each of these pathways includes numerous positive and negative regulatory
events and a cascade of events that generate the catalytic activities needed
for clot formation.
5. Explain the role of clotting factors in the
blood in the formation of the blood clot.
Fibrinogen is a soluble protein that is produced by the liver
and found in blood plasma. Fibrinogen
can bind with platelets thus linking platelets together also called platelet
aggregation. It does this by forming glycoprotein IIb-IIIa complex. When tissue is being damaged it results in
bleeding, fibrinogen is
converted at the wound into fibrin by the action of a clotting enzyme (thrombin).
Prothrombin is transformed into thrombin by a clotting
factor known as factor X or prothrombinase. Afterwards thrombin transforms fibrinogen into fibrin, which, in combination
with platelets from the blood is
forming a clot (coagulation).
Thromboplastin is a complex enzyme that can be found in brain,
lungs, and in blood platelets. Its
main function is the conversion of prothrombin to thrombin in the process of blood clotting (thrombokinase). Thromboplastin by itself can activate
the extrinsic coagulation
processes -platelet aggregation and fibrin formation require the proteolytic
enzyme thrombin. The platelets produce a substance that
combines with calcium ions in the blood to form thromboplastin, which in turn
converts the protein prothrombin into thrombin in a complex series of
of calcium in blood is to circulate
and be available to tissues. Heart cells, muscle cells and neurons are dependent
on calcium for their function. Calcium is required for these excitable cells to
contract or send impulses.
6. Clotting factors are biochemical molecules which are working
together with platelets to clot
blood. Clotting factors are required for
people’s blood to successfully clot. Blood plasma does not contain active
clotting factors itself. Clotting factors such as thromboplastins are released
by injured cells which lead to the conversion of prothrombin to thrombin. Without
injury there will be no active clotting factors as you would not want blood
clots to be formed in blood vessels.