Hemostasis Case Studies

1.HEMOSTASIS

OVERVIEW

Hemostasis is the normal physiological response that prevents significant blood loss after vascular injury which is essential in survival.

Hemostasis is a complex process helps close off damaged blood vessels, keep blood in a fluid state and dissolve blood clots following restoration of vascular integrity. Hemostasis is now also known to play an important role in wound healing and endothelial barrier protection and function. (1)

The process consists of a complex regulated system mediated by enzymes, activators, inhibitors, platelets, neutrophils, and endothelial cells, which is dependent on a delicate balance among several systems. work together when the blood vessel endothelial cells is injured by mechanical trauma, physical

Platelet adhesion is mediated by von Willebrand factor(vWF), which sticks circulating platelets to the area of damaged vessel wall by binding to its receptors located in platelet membrane glycoprotein Ib. The adherent platelets then undergo a “release reaction,” adenosine diphosphate(ADP), thromboxane A2(TXA2), and other components which act in concert to recruit and activate additional platelets from the circulation to the site of vascular injury. In the process of platelet aggregation (platelet-platelet interactions), fibrinogen (or vWF under conditions of high shear stress) mediates the final formation of an occlusive platelet plug, If the plug contains only platelets it is termed a white thrombus; if red blood cells (RBCs) are present it is called a red thrombus.(2) Negative feedback of the plug formation is controlled by prostacyclin released by the endothelium and this reduces platelet aggregation. White blood cells(WBCs) in the area also release proteins that prevent the clot getting out of control. Plasma enzymes will also break down adenosine triphosphate(ATP) that is found circulating near the plug, and thus reduce the amount of energy available to the

through the activation of intrinsic and extrinsic pathways (Figure-1.1), Current evidence supports the understanding that intrinsic pathway is not a parallel pathway but indeed it augments thrombin generation primarily initiated by the extrinsic pathway. Newer model describes coagulation with following steps: Initiation > Amplification > propagation > stabilization.

The coagulation proteins also called clotting factors (Table-1) reactions are the core components of the coagulation system that lead to the conversion of fibrinogen into fibrin strands helping to stabilize a platelet plug, as well as isolating it from the normal circulation, thus acting as a further feedback mechanism.

Activated fibrin will basically entangle platelets, and RBCs in a big blood clot, the anticoagulant system exerts a regulatory role over the procoagulant activity thus localizing the thrombus formation. The main anticoagulant mechanisms naturally present in the body include the following: Antithrombin, Tissue factor plasminogen inhibitor(TFPI), protein C, protein S, protein Z dependent protease inhibitor(PZI).(3), However,