Hemostasis and Blood Coagulation Events in Hemostasis
The term hemostasis means prevention of blood loss. Whenever a
vessel is severed or ruptured,
hemostasis is achieved by several mechanisms: (1) vascular
constriction, (2) formation of a platelet plug, (3) formation of a blood
clot as a result of blood coagulation, and (4) eventual growth of
fibrous tissue into the blood clot to close the hole in the vessel
permanently.
Vascular Constriction
Immediately after a blood vessel has been cut or ruptured, the trauma
to the vessel wall itself causes the smooth muscle in the wall to
contract; this instantaneously reduces the flow of blood from the
ruptured vessel. The contraction results from
(1) local myogenic spasm, (2) local autacoid factors from the
traumatized tissues and blood platelets, and (3) nervous reflexes
Mechanism of the Platelet Plug. When platelets come in contact with a
damaged vascular surface, especially with collagen fibers in the
vascular wall, the platelets themselves immediately change their own
characteristics drastically. They begin to swell; they assume irregular
forms with numerous irradiating pseudopods protruding from their
surfaces; their contractile proteins contract forcefully and cause
the release of granules that contain multiple active factors; they
become sticky so that they adhere to collagen on the tissues and to a
protein called von Willebrand factor that leaks into the traumatized
tissue from the plasma; they secrete large quantities of ADP; and their
enzymes form thromboxane A2. The ADP and thromboxane in turn act
on nearby platelets to activate them as well, and the stickiness of
these additional platelets causes them to adhere to the original
activated platelets.
Therefore, at the site of any opening in a blood vessel wall, the
damaged vascular wall activates successively increasing numbers of
platelets that themselves attract more and more additional platelets,
thus forming a platelet plug. This is at first a loose plug, but
it is usually successful in blocking blood loss if the vascular
opening is small. Then, during the subsequent process of blood
coagulation, fibrin threads form. These attach tightly to the platelets,
thus constructing an unyielding plug
Blood clotting ;
Normally the blood remaine in its liquid form, as long as it
remain in the vesseles .if drawn outside the body ,it thicken&
form a gel. ,the gel eventually separates from the liquid .
The straw – colored liquid called serum (it is blood plasmsa
minus clotting protens. The gel is called a clot , it contain
network of insoluble proteins fiber called fibrin in which the
formed elements of blood are trapped .
The process of gel formation called clotting or coagulation
process. < is a series of chemical reactions that culminates in
formation of fibrin threads. If clotting involve undamged
vesseles the result is thrombosis. If blood takes long time to
clot, haemorrage can occure.
Clotting involve many factores called ,clotting (coagulation
factors).
.
Clotting can be devided into 3 stages.;
1- intrinsic & exrinsic pathways.
2- prothrombinase convert prthrombine to thrombine .
3- thrombine converts fibringen to fibrin which form thread of
clot.
Extrinsic pathway;
it occurs within seconds if the trauma is sever , tissue
facter(TF) known as thromboplastin leaks from the cells of
damaged tissue to the blood ( that’s why called (extrinsic).it
intiate formation of prothrombinase . TF is mixture of
lipoproteins & phospholipids , in the presence of Ca , TF ,
begins a sequences of reactions that ultimatly activate facter
X , once activated it combimne with facter V & presence of Ca
To form prothrombinase .
Extrinsic pathway ;
Intrinsic pathway :So called because its activatores are either in direct
contact with blood or or contained within the blood . If endothelial cells
become roughened or damaged , blood come in contactr with collagen
fibers in the connective tissue.around the endotheium of the blood vessels,
in addition trauma causes damage to the platelates( result in release of
phospholipids), , contact with collagen fibers activate factor XII which
begin asquences of reactions that eventually activate facter X..then it
combine facter Vto form prothrombinase
Common pathway :
Prthrombinase with Ca catalyze the conversion
of prothrombin to thrombin . Which inturn
with Ca activate the conversion of fibrinogen
to fibrin ( insoluble, thrombin also activate
facter XIII whch strengthen & stabilizethe
fibrin thread
Thrombine has 2 +ve feed back :
1)Involve facter V , it accelerate the formation o
prothrombinase which accelerate the
production of more thrombin.
2) Activate platelateswhich reinforce their
aggrigation & release of phopholipids.
Common pathway
Clot retraction ;
Is the consolidation or lightening of fibrin clot , the fibrin
thread attach to the damaged surface of blood
cvessels,gradually contract as platelate pull on them.
Normal contraction depend on numberr of platlate in the clot..
Role of vitamine K in clotting :
It is required in synthesis of clotting facters , it is fat soluble &
absorbed through the intestinal linnig , in people suffering
from disorder in absorption of lipid , for eg. Due to iadequate
release of bile will experience uncontrloed bleeding.
Hemostatic control mechanism:
The fibrinolytic system dissolves clots at a site of damage once
the damage is repaired , dissolution of clot is called
fibrinolysis when clot is formed , an inactive enzyme (
plasminogens) is incorporated in to the clot, both body tissue
& blood contain substances that activate plasminogen to
plasmin (fibrinolysin), it can dissolve clot by digesting fibrin
thread .
The clott is localised to the damaged tissue because of
1- fibrin absorbe thrombin to the clot.,
2- the disperasal of clotting facter by blood.
3- release of prostocyclin by endothelial cell , which inhibit
platelat adhesion & release.
4- anticoagulants : antithrombin, heparin , activated proteins.
Intravascularv clotting :
Sometimes , clot formed within CVS , such clot may be
intiated by roughened endothelial surface (due to trauma,
infection , atherosclerosis), these conditions induces adhesion
of platelates , or when blood flows slowly allowing clotting
factores to accumelate locally in high concntration to intiate
coagulatiobn . Clotting in unbroken blood vessel called
thrombosis., if the thrombus remain intact it may disloged &
sweptaway in the blood , ablood clot , bubbes of air , fat from
broken bone or a piece or debris transported by the blood
stream called embolus , when emblus lodges in the lung calle
pulmnary embolism.