Haemostasis Flashcards
How long does it take for a clot to disappear
1 week
Clot formation elements
Platelets, vWF, coagulation factors all of which are unactivated under normal circumstances
What allows the clot to remain confined to the site of injury
Natural Anticoagulants
What makes the clot disappear
Fibrinolytic System
Prevention of blood sticking to the wall of the vessel
Endothelial surface of blood vessels produces Heparis, TFPO, thrombomodulin, nitric oxide, prostacyclin
Vessel Damage: Platelet Adhesion
Platelets become activated and stick to the subendothelial collagen, Von Willebrand Factor is also introduced
Platelets Glycoproteins
Presence of receptors on the platelets which bind to other coagulation factors
Platelet Cell Surface Receptors
ADP receptor, Epineprhine, Thrombin, signalling inside the platelet and tells it what to do
Dense Granules and Alpha Granules
Dense (ADP/ATP, Calium, serotonin) and alpha granules (VWF and thrombin) contain key molecules which have a significant role in improving clot formation. Degranulation into the open canalicular system.
GP Ia/IIa
Bind to collagen
GP IIb/IIIa
Fibrinogen
GPIb
Von Willebrand Factor
Activation of platelet
Via ADP and Epinephrine Receptors resulting in Arachdonic Acid to Thromboxane A2 by Cycloxidase
Scramblase
enzyme which flips the membranes to allow aggregrates on the surface
Definitive Haemostasis
The formation of a definitive fibrin clot. Small platelet plug with fibrin plug on top of it.
Haemophilia B
Factor IX would be deficient
Haemophilia A
Factor VIII is deficient
Coagulation Cascade
Tissue factor released at the site of injury, VIIa activates factor 10, results in the conversion of prothrombin to thrombin (resulting in the conversion of fibrinogen to fibrin) and the clot forms.
Natural Anticogulants TFPI
Switches off Xa and VIIa
Natural Anticoagulants Protein C and S
Switches off factor 5a
Natural Anticoagulants Antithrombin
Switches off XIa, IXa, VIIIa, Xa and thrombin
Fibrinolysis
Endothelial cells produce t-PA and u-PA (plasminogen activator). Cleaves plasminogen into plasmin. The plasmin breaks the clot down and re-distributes it.
Fibrin Degradation Products
Formed after the breakdown of the fibrin clot
Inhibitors of plasmic
Antiplasmin and macroglobulin
Aspirin
Prevents the enzyme of COX from converting Arachadonic Acid to Thromboxane A2 (prevents platelet aggregration)
Clopidegral, Prasugrel, Ticagrelor
These prevent activation of the platelet through the ADP receptor. Used in the prevention of stent occlusion.
Tibrofibran, Abciximab, Eptifibatide
Prevent the binding of fibrinogen to the platelet
Warfarin
Inhibits the action of vitamin K which is required for the production of factors IX, Prothrombin, X, VII. Produces an anticoagulated state. Useful in AF.
Heparins (Rivaroxaban, Edoxaban, Apixiban)
Prevents the formation of Xa preventing the formation of thrombin therefore less fibrin is made. Also indirectly inhibit thrombin
Dabigatran
Thrombin Inhibitors