The ability to control bleeding hinges primarily on the availability of both platelets and coagulation factors, as well as their adequate functionality. It is important to note, however, that there are limits in the size, or the degree of damage that can be controlled and repaired without outside (medical) intervention. As one may expect, and the image on the previous page illustrates, damage to a larger vessel yields a more substantial bleed, and in turn consumes a greater quantity of coagulation components. These variables can radically alter the effectiveness of hemostatic control mechanisms.
As we will discover later in the course, there are other variables that impact the effectiveness of hemostatic mechanisms as well, such as acquired disease states, and inborn metabolic pathway defects. For now, our focus will be on the mechanisms, processes, and components that work together to achieve coagulation, or the cessation of blood flow from a damaged vessel.
Note: The terms "coagulation" and "hemostasis" are used interchangeably throughout this course.
