Platelets and hemostasis Flashcards
Platelets aka
thrombocytes
platelets dervied from
cytoplasm fragmentation of megakaryocytic (goat multinucleate cells)
promote blood clotting and help repair gaps in walls of blood vessels, prevent blood loss
Platelets
small, disc shaped, non-nucleated cell fragments
Hyalomere
peripheral light blue stained zone
Granulomere
darker zone with purple granules
Platelet structure
alpha granules: largest. Vessel repair, blood coagulation, platelet aggregation
Delta granules: facilitate platelet adhesion, vasoconstriction. Contain ATP, ADP, histamine, serotonin
Lamda granules: clot resorption
Stages of hemostasis **need to know
1) Vascular wall injury and exposure of sub-endothelial collagen
2) Vasconstriction
3) Formation of platelet plug
4) Coagulation cascade
5) Formation of fibrin clot (plug)
6) Healing and fibrinolysis
Platelet functions in hemostasis
***need to know
1) Adhesion to the injured surface
2) Shape change
3) Release of granule contents
4) Aggregation
Mechanism of Hemostasis
She will test
1) Blood vessel wall injured, collagen fibers exposed at damaged site
2) release of endothelia (vasoconstrictor) and von Willebrand factor (vWF) which binds exposed collagen fibers
3) Platelets adhere to exposed collagen by binding to vWF and they get activated (platelet activation)
4) Conversion of fibrinogen to fibrin
5) clot shrinks
6) Vessel wall repaired
Coagulation pathway
Calcium-dependent pathway
Vitamin K dependent factors II, VII, IX, X
Instrinsic pathways
Begins with activation of F XII -> XI-> IX (calcium required) -> IX a (activated) -> F IX + VIII = F X
12 -> 11-> 9 + calcium -> 9 +8 -> 10
Calcium and phospholipid are required
Extrincitic pathway
1st to kick in
Depends on release of tissue factor (TF) thromboplastin (F III)
TF binds to F VII
F III aka thromboplastin complex converts F X -> F Xa
calcium converted
VII + TF = X –> Xa
Prothrombrin (F II) —> Thrombin (II a)
In presence of calcium, phospholipid and F V is converted
Thrombin converts
Factor XIII —> XIII active (clot formation)
Essential Thrombocythemia
increased platelet count
Genetic JAK2 mutation