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28 Cards in this Set

  • Front
  • Back
primary hemostasis
platelet plug formation
damaged endothelial cells interact w/ platelets via von Willebrand's factor (vWF)
von willebrand factor
mediates platelet adhesion to exposed extracellular matrix
by binding to platelet membrane and collagen fibers in tissue
thrombin and thromboxane increase Ca concentration of platelets
secondary hemostasis
formation of crosslinked fibrin clot through activated clotting factors
takes place on plateles surface
forming a clot
tightly controlled-abnormal clotting produces thrombus which causes vascular inclusion/infarction
1. endothelial cells
2. subendothelial tissue
3. platelets
4. clotting factors
inhibit blood clotting
form prostacyclin (inhibitor of platelet adhesion/aggregation)
endothelial cells
not normally exposed to blood
bound by platelets and clotting factors
subendothelial tissue
release proteins/vasoactive amines after binding to subendothelial tissue
plasma proteins that create proteolytic cascase that produces insoluble fibrin from soluble fibrinogen
clotting factors
platelet aggregation
caused by fibrinogen binding to platelet receptors
the postcursor of fibrinogen
form a soft gel
transglutaminase triggers crosslinking
converts fibrinogen into fibrin
cleaves 2 bonds b/t Aa and BB chains, releasing fibrinopeptides A and B
remaining peptide is fibrin monomer
thrombin formation
limited to site of injury
produced from prothrombin by factor Xa
inactive fragment also produced, contains 10 residues of g-carboxyglutamate (produced by hepatocytes in vit. K mediated reaction)
can be activated by extrnsic and intrinsic pathways
factor X
extrinsic pathway
stab wound, GSW
factor VIIa-protease active only in presence of tissue factor
intrinsic pathway
endothelial lining still intact or microdamaged
requires negatively charged surface to activate (i.e. glass)
contact phase activation
iniating reactions of intrinsic pathway
requires kallikrein and factor XIIa (proteases) and kininogen (HMWK-activator protein)
contact activation steps
factor XIIa activates factor XI
XI activates factor IX
IX activates factor X
factor VIII needed for last step
inhibition of clotting
Antithrombin III (protease inhibitors) is activated by heparin (both intrinsic and extrinsic pathways)
degrades fibrin clot
formed from plasminogen which bind fibrin clot
used w/in 1 hour of acute MI
plasmin activation
tissue type plasminogen activator (tPA)-serine protease that also binds to fibrin (needs both plasmin and fibrin to activate)
streptokinase (allosterically)
1. heparin
2. coumadin
remove Ca ions
all g-carboxyglutamate factors (prothrombin, VII, IX, X) depend on Ca
assessing blood clotting
1. bleeding time
2. activated partial (aPTT) thromboplastin time
3. prothrombin time
prolong in platelet disorders
bleeding time (most important assessment)
measures efficacy of heparin
tests intrinsic and final common pathways
prolonged in extrinsic and final common pathways
measures coumadin therapy
intrinsic pathway summary
initiated by KKK (kaolin, prekallikrein, high molecular wt kininogen)
measured by aPTT
longer pathway and activation time
order-TENET (XII, XI, IX, VIII, X)
amplification phase of coagulation (big thrombin amounts)
extrinsic pathway summary
VIIa activates X
measured by PT
shorter pathway and activation time
activation phase of coagulation (little thrombin amounts)
common pathway summary
convergence of intrinsic and extrinsic pathways
Va cofactor for Xa
VIIIa cofactor for IXa (8 follows 9)