30. Hemostasis and hemocoagulation. Vascular -trombocyte and coagulation hemostasis. Fibri-nolysis and anticoagulational mechanisms. Control of hemostasis.

Overview

Hemostasis stops bleeding from an injured vessel and keeps blood fluid elsewhere, through the vessel wall, platelets, the plasma coagulation system, and the anticoagulant and fibrinolytic mechanisms that limit and remove the clot.

Hemostasis is the set of mechanisms that stops bleeding from an injured vessel while keeping blood fluid elsewhere. This topic covers the vascular reaction, the formation of the platelet plug (primary hemostasis), the plasma coagulation factors and the cascade that produces a stable fibrin clot (secondary hemostasis), clot retraction, and the basic laboratory tests. Fibrinolysis and the natural anticoagulants are described in the later sections.

Vascular phase

Hemostasis runs as overlapping stages rather than strictly one after another:

1. Vascular spasm: immediate local vasoconstriction.
2. Platelet plug formation: adhesion, activation and aggregation of platelets.
3. Blood coagulation: conversion of soluble fibrinogen to an insoluble fibrin network.
4. Clot retraction, followed by fibrinolysis and tissue repair.

Vasoconstriction results from direct myogenic response of the injured smooth muscle, local axon reflexes, and vasoactive substances released by platelets and endothelium, especially thromboxane A₂, serotonin and endothelin. It is most effective in small vessels. Intact endothelium normally prevents clotting by producing prostacyclin (PGI₂) and nitric oxide, which inhibit platelets; injury exposes subendothelial collagen and tissue factor, which trigger hemostasis.