The hemostasis of the human body is mainly composed of three parts:

1. Tension of the blood vessel itself 2. Platelets form an embolus 3. Initiation of coagulation factors

When we get injured, we damage the blood vessels beneath the skin, which can cause blood to seep into our tissues, forming a bruise if the skin is intact, or bleeding if the skin is broken. At this time, the body will start the hemostatic mechanism.

First, blood vessels constrict, reducing blood flow

Second, platelets begin to aggregate. When a blood vessel is damaged, collagen is exposed. Collagen attracts platelets to the injured area, and the platelets stick together to form a plug. They quickly build a barrier that prevents us from bleeding too much.

Fibrin continues to attach, allowing the platelets to connect more tightly. Eventually a blood clot forms, preventing more blood from leaving the body and also preventing nasty pathogens from entering our body from the outside. At the same time, the coagulation pathway in the body is also activated.

There are two types of external and internal channels.

Extrinsic coagulation pathway: Initiated by exposure of damaged tissue to blood contact with factor III. When tissue damage and blood vessel rupture, the exposed factor III forms a complex with Ca2+ and VII in plasma to activate factor X. Because the factor III that initiates this process comes from tissues outside the blood vessels, it is called the extrinsic coagulation pathway.

Intrinsic coagulation pathway: initiated by the activation of factor XII. When the blood vessel is damaged and the subintimal collagen fibers are exposed, it can activate Ⅻ to Ⅻa, and then activate Ⅺ to Ⅺa. Ⅺa activates Ⅸa in the presence of Ca2+, and then Ⅸa forms a complex with activated Ⅷa, PF3, and Ca2+ to further activate X. The factors involved in blood coagulation in the above-mentioned process are all present in the blood plasma in blood vessels, so they are named as intrinsic blood coagulation pathway.

This factor has a key role in the coagulation cascade due to the merger of the two pathways at the level of factor X Factor X and factor V activate inactive factor II (prothrombin) in plasma to active factor IIa, (thrombin) . These large amounts of thrombin lead to further activation of platelets and formation of fibers. Under the action of thrombin, fibrinogen dissolved in plasma is converted into fibrin monomers; at the same time, thrombin activates XIII to XIIIa, making fibrin monomers The fibrin bodies connect with each other to form water-insoluble fibrin polymers, and interweave each other into a network to enclose blood cells, form blood clots, and complete the blood coagulation process. This thrombus eventually forms a scab that protects the wound as it rises and forms a new layer of skin underneath Platelets and fibrin are only activated when the blood vessel is ruptured and exposed, meaning that in normal healthy blood vessels they don't randomly lead to clots.

But it also indicates that if your blood vessels rupture due to plaque deposition, it will cause a large number of platelets to gather, and finally form a large number of thrombus to block the blood vessels. This is also the pathophysiological mechanism of coronary heart disease, myocardial infarction, and stroke.