Hemostasis

Both coagulation promoting factor and anticoagulant factor can regulate hemostasis. Activation of the coagulation cascade is divided into extrinsic and intrinsic pathways (Figure 11.3). Factors involved in these cascades amplify the clotting response and together produce thrombi. The extrinsic pathway accounts for the majority of coagulation in the body, but destruction of endothelial integrity by both coagulation pathways is much slower than platelet aggregation. Simplifies the following description of the pathway for determining important steps in drug-controlled coagulation

The extrinsic coagulation pathway is caused by exposure of blood to tissue factor (TF) on the endothelial cell surface after vascular injury and is rapidly activated within minutes of endothelial destruction. Formation of a complex of TF and Factor VIIa in the presence of phospholipid and Ca 2+ results in the conversion of inactive factor X into activity Xa

Contact between the negatively charged surface such as subendothelial collagen and the blood initiates an intrinsic coagulation pathway whose activation is delayed more than 10 minutes after tissue destruction. The unique coagulation pathway involves a series of enzyme-mediated responses, including sequential activation of several coagulation factors and final activation of factor X.

The two coagulation pathways converge with activation of Factor X that mediates the hydrolysis of prothrombin to thrombin (FIG. 11a; see Figure 11.3). Thrombin converts soluble protein fibrinogen to insoluble fibrin gel. Thrombin also activates Factor XIII that cross-links the fibrin polymer and forms a fibrin network that captures circulating platelets, leukocytes and erythrocytes.

The effects of thrombin and several other activated coagulation factors (see Figure 11.3) are inhibited by circulating antithrombin. Antithrombin inhibits clotting factors after forming complexes with heparin-like molecules produced by intact endothelial cells and with heparin released from mast cells. When it produces enough thrombin to overcome the effects of circulating antithrombin, it can cause blood clotting

Each activated coagulation factor is very rapidly inactivated and continues to limit the coagulation process to the site of the initial event. However, aggregates of platelets bound to fibrin clots may embolize and occlude more distal parts of the circulation.

The composition of arterial thrombosis or venous thrombosis is different. Arterial thrombosis occurs under conditions of high flow and high shear stress and platelets play an important role in thrombus development and growth. In contrast, venous thrombosis is formed in low flow velocity, low shear stress environment. Venous thrombosis usually begins with a quiescent state of the deep venous valve lumen, which consists mainly of fibrin and red blood cells and has few platelets.

Hemostasis may be primary or secondary. Primary hemostasis refers to the formation of platelet embolism that forms primary thrombus. Secondary hemostasis refers to a coagulation cascade that produces a fibrin network to enhance platelet embolism. Secondary hemostasis occurs concurrently with primary hemostasis, but usually it is completed thereafter. Coagulation factors circulate as inactive enzyme precursors involved in a series of reactions that constitute the coagulation cascade upon activation. Serine protease (enzyme)

Haemorrhagic diseases are characterized by increased bleeding sensitivity (also known as bleeding sensitivity). They are caused by platelet disease (primary hemostatic failure), coagulopathy (secondary haemostasis), or in some cases a combination of the two. Coagulopathy can be classified as general or even endogenous or extrinsic defects, depending on the particular pathway of the diseased coagulation cascade. Hemorrhagic disease is hereditary or acquired. Although clinical features of hereditary and acquired diseases may overlap, mucosal cutaneous bleeding (eg, nasal bleeding, ecchymosis bleeding, gastrointestinal bleeding) is more related to platelet disease, and potential space Infiltration (eg articular bleeding). Muscle hemorrhage) is a characteristic of coagulopathy.