HAEMOSTASIS
Haemostasis is cessation of blood loss from a damaged vessel. Loss of blood is
stopped by series of overlapping processes, inn which platelets play a vital role.
Primary haemostasis:
Local vasoconstriction and soft platelet plug formation occur within seconds of
injury. It successfully stops hundreds of small hemorrhages everyday & partly
because it triggers blood clotting mechanism.
Secondary haemostasis:
Coagulation system & results in formation of fibrin soft platelet plug is stabilized and
strengthed. It needs several minutes to complete.
Vasoconstriction:
Platelets come in contact with damaged blood vessels and become sticky and get
adhere to the damaged wall.
They release serotonin and thromboxanes which constricted blood vessels and
reduce blood flow.
Endoothelins are released by damaged blood vessels itself.
Vascular spasm is immediately but temporary closure of blood vessels resulting
from contraction of smooth muscle within wall of blood vessel.
Vasoconstriction only lasts for few minutes.
Platelet plug formation:
, It is accumulateion of platelets that can seal up small breaks in blood vessels.
Sticky platelets clump and release other substance including ADP which attract other
platelets.
Passing platelets attract to already sticked platelets and they also release their
chemicals.
This is positive feedback mechanism by which paltelets rapidly gather at the vascular
damage site and quickly form a temporary seal.
It is formed within 6 minutes however it is soft and easily damaged it is precursor to
more durable blood clot.
Coagulation:
Positive feedback system, complex process in which clotting factors are activated in
a specific order which results in formation of prothrombin activator.
Coagulation factors are proteins found within plasma[ they are synthesized in liver
and released in blood plasma] normally they are in inactive form and do not cause
clotting. After injury they become active.
STAGE 1: formation of prothrombin activator
a. Intrinsic pathway
b. Extrinsic pathway
Extrinsic pathway
1. Is initiated with material outside to blood. This material, tissue thromboplastin
[factor3] is released by damaged tissue cells.
2. Factor3 permits the clotting process to take a chemical shortcut. As a result, it
is very rapid process within 12 to 15 seconds.
Haemostasis is cessation of blood loss from a damaged vessel. Loss of blood is
stopped by series of overlapping processes, inn which platelets play a vital role.
Primary haemostasis:
Local vasoconstriction and soft platelet plug formation occur within seconds of
injury. It successfully stops hundreds of small hemorrhages everyday & partly
because it triggers blood clotting mechanism.
Secondary haemostasis:
Coagulation system & results in formation of fibrin soft platelet plug is stabilized and
strengthed. It needs several minutes to complete.
Vasoconstriction:
Platelets come in contact with damaged blood vessels and become sticky and get
adhere to the damaged wall.
They release serotonin and thromboxanes which constricted blood vessels and
reduce blood flow.
Endoothelins are released by damaged blood vessels itself.
Vascular spasm is immediately but temporary closure of blood vessels resulting
from contraction of smooth muscle within wall of blood vessel.
Vasoconstriction only lasts for few minutes.
Platelet plug formation:
, It is accumulateion of platelets that can seal up small breaks in blood vessels.
Sticky platelets clump and release other substance including ADP which attract other
platelets.
Passing platelets attract to already sticked platelets and they also release their
chemicals.
This is positive feedback mechanism by which paltelets rapidly gather at the vascular
damage site and quickly form a temporary seal.
It is formed within 6 minutes however it is soft and easily damaged it is precursor to
more durable blood clot.
Coagulation:
Positive feedback system, complex process in which clotting factors are activated in
a specific order which results in formation of prothrombin activator.
Coagulation factors are proteins found within plasma[ they are synthesized in liver
and released in blood plasma] normally they are in inactive form and do not cause
clotting. After injury they become active.
STAGE 1: formation of prothrombin activator
a. Intrinsic pathway
b. Extrinsic pathway
Extrinsic pathway
1. Is initiated with material outside to blood. This material, tissue thromboplastin
[factor3] is released by damaged tissue cells.
2. Factor3 permits the clotting process to take a chemical shortcut. As a result, it
is very rapid process within 12 to 15 seconds.
