LEC3- PRIMARY HEMOSTASIS Flashcards
what are the coag factors that are inactivated by the anti thrombin III
activated factor II, IX, X
factor X is also known as
Stuart- prower factor
it helps by activating protein C, while being binded to thrombin
thrombomodulin
the activated protein C will inhibits what factors
factor V and VIII (labile factors )
summarize how blood are being maintained not to clot unless there’s an injury
endothelial cells will produce PROSTACYCLIN and NITRIC OXIDE they both will inactivate the platelet to prevent it to adhere in endothelial cells
endothelial cell will release an another substance that is the Heparin sulfate. It will then bind to anti-thrombin III, anti-thrombin III will inhibit thrombin. Anti-thrombin III together with Heparin sulfate will inhibit or shutdown the activated Factor II, IX, and X
Lastly, it will produce thrombomodulin, will will bind to thrombin. Once protein C pass by, it will be enhanced and activated by thrombomodulin and will then bind with thrombin. They will then inhibit the labile factors which are the Factor V and VIII
it present a smooth contiguous surface
rhomboid cell of vascular epithelium
eicosanoid platelet inhibitor
prostacyclin
a vascular “relaxing” factor
nitric oxide
an anticoagulant that regulates thrombin generation
glycosaminoglycan heparin sulfate
a regulator of the extrinsic pathway of coagulation
TFPI - tissue factor pathway inhibitor
an integral component of the protein C control system
endothelial cell protein C receptor (EPCR)
a protein C coagulation control system activator
thrombomodulin
activated fibrinolysis
Tissue plasminogen activator (tPA)
what are the responses or mechanism that will occur once there’s a blood vessel damage
vascular response
platelet response
clotting system
fibrinolytic system
when there’s blood vessel damage, what are the responses under primary hemostasis>
vascular response - vasoconstriction
platelet response - adhesion and aggregation
is the primary response reversible?
yes, reversible and unstable
when there’s blood vessel damage, what are the responses under secondary hemostasis>
clotting system - through coagulation factors
when there’s blood vessel damage, what are the responses under tertiary hemostasis>
fibrinolytic system
are secondary hemostasis reversible?
nope, it’s irreversible and stable
what are needed to activate plasminogen to become plasmin and destroy the clot made during 2ndary hemostasis
fibrinolytic proteins
what are the platelet receptors needed
Gp Ib-IX-V
Gp IIb-IIIa
P2y12
TPa
Gp Ia
Gp VI
what is the receptor used for von willebrand factor?
Gp Ib-IX-V
receptor used for fibrinogen and vWF
Gp IIb-IIIa
receptor used for ADP
p2Y12
receptor used for Thromboxane A2
Tissue plasminogen activator
Receptor used for collagen
Gp Ia
Gp VI
Basic Sequence of Events in Primary and
Secondary Hemostasis after Vessel Injury
vasoconstriction
platelet adhesion
platelet aggregation
fibrin-platelet plug formation
fibrin stabilization
what factor can stabilize the fibrin clot?
factor XIII
refers to the role of blood vessels and
platelets in the initial response to a
vascular injury or to the commonplace
desquamation of dying or damaged
endothelial cells
Primary Hemostasis
they are the one responsible in primary hemostasis
blood vessels and
platelets
Primary Hemostasis
Activated by desquamation and small injuries to blood vessels
true or false
true the fire
Primary Hemostasis
➢Role of blood vessel and platelets in response to vascular injury
what is the products of primary hemostasis
➢Formation of platelet plug
SUBSTANCESRELEASED in primarry hemostasis
Prostacyclin
Adenosine
Thrombomodulin
Heparin sulfate
tPA
Von Willebrand Factor
13-HODE ( 3-Hydroxyoctadecadienoic acid )
13 HODE means
( 13-Hydroxyoctadecadienoic acid )
how do vasoconstriction occurs during the vessel injury
endothelial cell will release a component called endothelin
this endothelin will bind to the smooth muscle receptor causing contraction and will cause vasoconstriction
the binding of endothelin and smoothmuscle will inactivate ______ causing contraction
inactivates intracellular mechanism
aside from the release of endothelin, we have another way of activating constriction, what are the 2nd and 3rd reason
myogenic reaction
pain receptor or noisy reaction
what are the 3 causes of vasoconstriction
release of endothelin
myogenic reaction
nocireceptor/pain receptor
this type of reaction leading to vasoconstriction in which there’s a direct damage or contact to the smooth muscle making it to contract
myogenic action
this type of reaction leading to vasoconstriction in which where there’s inflammation, smooth muscle will release inflammatory chemicals leading to contraction
pain receptor
o Converts plasminogen to qplasmin
tPA
responsible in dissolution of clot
plasmin
oEnhances activity of anti-thrombin III
*Heparan sulfate
PARTS OF PLATELET PLUG FORMATION
*Primary hemostasis
* Secondary hemostasis
* Fibrinolytic system
2 types of adhesion
direct
indirect
a type of adhesion when there’s injury, the collagen explode
(there’s strong attraction between platelet and
collagen.
Direct
the type of adhesion where the Von Willebrand factor will stick to the collagen when there’s injury and help
the platelet, to bind to it
Indirect
platelets undergo shape changes with the intrusion of numerous pseudopods due to the _____
contraction of
microtubules.
platelet release reaction is Stimulated by
o Collagen
o Thrombin
o Epinephrine
o Thromboxane A2
Caused by the release of granules
and ADP from the adhering platelet
Initial Aggregation
Platelets form a link or bridge Gp
IIb/IIa
secondary Aggregation
Mediates ADP induced aggregation:
Gp IIb/IIIa with calcium and fibrinogen
o Deficiency in aggregation results to what syndrome
Glanzmann’s
Thrombasthenia
Thrombasthenia means
weak platelets
vasoconstrictor and stimulates platelet
aggregation
Thromboxane
Enables the vascular tissues or
vessels to close in order to conserve the
blood from getting out of the blood vessel.
Thromboxane A2
Counterpart of prostacyclin
Thromboxane
