Test 3 Study Guide Part 3 Flashcards
Von Willebrand’s factor:
Von Willebrand’s factor which are bound to collagen, they then bind thrombocytes and anchor them so blood flow does not move them away.
What is within the granules of thrombocytes?
When is it released?
Serotonin
Thromboxane A2 (promotes binding/clotting of thrombocytes)
ADP (promotes binding/clotting of thrombocytes)
Platelet release reaction
The release of Thromboxane A2, ADP, and Seratonin is called what?
A platelet release reaction.
Describe the complete arc of platelet plug formation, starting from the normal state.
endothelial cells produce: NO-, prostacyclin. (which act as vasodilators and inhibit clotting)
Endothelial cells also have CD39 on their plasma membrane surface, which ADP -> AMP (ADP promotes clotting so this is important)
Wounding exposes the collagen of the tissue behind the endothelium, which results in clotting. Thrombocytes bind to Von Willebrands factor, which in turn binds to collagen.
There are two signalling changes which have occurred. Death of endothelium has likely resulted in decreased production of prostacyclin two, and decreased production of NO (and a little less CD39 activity). Additionally a platelet release reaction has occurred, and the platelets have released granules of ADP, thrombaxane A2, and serotonin.
The platelet plug will form, and can stop bleeding, but requires fibrin reinforcement to be able to hold.
Platelets also help produce what change in fibrinogen?
It converts it fibrin, which is insoluble, and helps form the clot.
What does the color of a clot tell you?
Fibrin forms a mesh which traps other cells within it, if it traps a great deal of RBCs, it will form a red clot. If it is in an artery, it will not trap as many and the clot will be white.
Clot retraction can occur because:
Contractile actin myosin system, as is seen elsewhere in the body.
- Step called clot retraction
Serum redefined:
Plasma without fibrinogen (as it has been used in clot formation)
Extrinsic pathway:
Tissue Factor (thromboplastin, factor III) -> factor VII -> VII complex (tissue factor, factor VII, and Ca2+) -> Common Pathway (factor X)
Intrinsic Pathway:
Activator (collagen) -> Factor XII -> Factor XI -> Factor IX -> VIII complex (factor IX activated, factor VIII, Ca2+)
Common Pathway:
X -> V complex (factor five V, X activated, Ca2+) -> factor II (Prothrombin) which becomes thrombin -> fibrinogen -> fibrin
How is the clotting pathway stopped in plasma tubes?
Ca2+ is chelated, which stops it from participating in clotting complexes
Aim of coagulation:
Create fibrin from fibrinogen (factor 1)
Fibrin stabilizing factor (factor VIII)
Common Pathway pneumonic:
1 * 2 * 5 = 10
Factor ten forms complex five (X activated, factor V, Ca2+) activates prothrombin into thrombin (thrombin/prothrombin is factor II) -> fibrinogen (factor I) -> fibrin
Extrinsic pathway pneumonic:
3 + 7 = 10 factor III (tissue factor, thromboplastin), complexes with factor VII, and Ca2+
Intrinsic pathway pneumonic:
Factors 12 to 8 are involved in the intrinsic pathway, excluding factor X which is the common.
XII -> XI -> IX -> VIII complex (VIII, IX, Ca2+)
(plasminogen is the inactive precursor) Plasmin:
Decays blood clots (like fibrin)
How is the extrinsic pathway started?
Tissue is damaged, and cell innards are revealed, including thromboplastin (Factor III), which can now bind with factor 7, calcium and phospholipids to start activate factor 10