V-Coagulation Flashcards
vascular system function
constriction of damaged vessels
healthy vessels will reduce unnecessary clot formation
platelet system function
temporary platelet plug
primary hemostasis
coagulation factor cascade function
make insoluble clot with fibrin
secondary hemostasis
anticoagulation system function
inhibit coagulation
fibrinolytic system function
degrade clots
GPIb binds to
from platelet
vWF (von willebrand factor) from subendothelial matrix
for platelet adhesion
GPVI binds to
from platelet
collagen from subendothelial matrix
for platelet adhesion
protease activated receptor binds
thrombin to inc platelet activation and aggregation
P2Y12 receptors bind
on platelets
ADP that gets released from platelet granules
for activation of nearby platelets and enhance plates already adhered
TXA2 receptors bind
TXA2 secreted from platelets AFTER vWF and ADP bind
for platelet activation and enhance plates already adhered
same function as ADP/P2Y12
GPIIb/IIIa bind
fibrinogen from plasma
for platelet aggregation
function of NO and PGI2
released by healthy endothelium to inhibit platelet aggregation + act on smooth muscle to vasodilate
how do platelets connect to coagulation cascade
activated platelets release pro-coagulant cofactors (Ca and neg charged phospholipids) to accelerate thrombin formation by coag cascade
intrinsic pathway starts with
factor XII contacts collagen exposed by injury or phospholipids on platelets
extrinsic pathway start with
factor VII contacts tissue factor exposed by injury
intrinsic pathway steps
- XII to XIIa
- XI to XIa
- IX to IXa
- X to Xa (trace amounts)
- prothrombin to thrombin in small amounts
extrinsic pathway steps
- tissue factor converts VII to VIIa
- X to Xa (trace amounts)
- prothrombin to thrombin in small amounts
common pathway steps
- Xa from both extrinsic and intrinsic convert prothrombin to thrombin in large amounts via complex with Va + phospholipids + Ca
how coagulation gets amplified
the little amount of thrombin will activate
1. V to Va
2. VIII to VIIIa > will make complex with IXa to activate more Xa to be produced for the prothrombin complex
thrombin affect on platelets
binds protease activated receptors on platelets to cleave fibrinogen to fibrin monomers > fibers > cross link via XIII activation
cause of hemophilia A
factor VIII deficiency, x linked recessive
no complex is made with IXa to amplify Xa production for prothrombin complex
cause of factor V leiden thrombophilia
mutation in factor V so prevents it from being inactivated by activated protein C (APC)
-aka always on so induces hypercoagulable state
function of antithrombin
from the liver to bind heparan sulfate @ endo cells to degrade thrombin and Xa
function of tissue factor pathway inhibitor
secreted from endo cells to reduce thrombin by inhibiting VIIa/TF complex and Xa
function of thrombomodulin
on endo cells binds thrombin to activate APC
-APC and protein S complex will degrade Va and VIIIa
tPA and uPA function
tissue plasminogen activator and urokinase plasminogen activator
-secreted by endo cells to convert plasminogen to plasmin so that plasmin can digest fibrin fibers/clots
plasmin is protease
how fibrinolytic system is regulated
- plasminogen activator inhibitor from platelets and endo cells so no degradation
- a-2 plasmin inhibitor from liver so no degradation
