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Physiology of Blood coagulation Animation Extrinsic and intrinsic pathway

Coagulation Overview

Platelet plug formation is primary hemostasis
Endothelial injury → collagen exposed → platelets adhere to vWF in the subendothelium (adhesion)
Binding of platelets also activates them to release their granules which contain key molecules: TXA2 (thromboxane A2), ADP, Ca2+, and serotonin
Role of ADP in platelet activation: ADP binds receptors on platelet surface, causing insertion of GpIIb/IIIa (fibrinogen receptor) → allows aggregation of platelets
Aggregation is mediated by fibrinogen, which binds GpIIb/IIIa on adjacent platelets
Aggregation is inhibited by endothelial cells that release PGI2 (prostacyclin) and NO
The goal of secondary hemostasis is generation of the fibrin clot
Many reactions in the cascade require Ca2+ and platelet phospholipid as cofactors
Factors X, IX, VII, II (mnemonic "1972") are vitamin Kdependent
Inhibition of the clotting cascade occurs via activated Protein C (APC) and Antithrombin III. tPA (tissue plasminogen activator) disrupts existing clots.
Prothrombin Time (PT) evaluates the extrinsic system: Factors VII, X, V, II and I
The normal PT is between 1012 seconds.
INR (International Normalized Ratio) is a standardized value for PT that is often quoted when following warfarin therapy. The normal value is set at 1.
An elevated INR indicates relative increase in anticoagulation (i.e. INR = 23)
↑ PT can be seen with warfarin therapy, or any process affecting the synthesis or consumption of coagulation factors (i.e. liver disease and DIC; respectively).
PTT (Partial Thromboplastin Time) evaluates the intrinsic system: Factors XII, XI, IX, VIII, X, V, II and I.
The normal PTT is between 2540 seconds.
PTT is used to follow heparin but not LMWH (i.e. enoxaparin) therapy.
↑ PTT is seen with factor deficiencies, DIC, vWD and antiphospholipid syndrome (associated with SLE).

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