Back To CourseHuman Anatomy & Physiology: Help and Review
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Dr. Gillaspy has taught health science at University of Phoenix and Ashford University and has a degree from Palmer College of Chiropractic.
We previously learned that the body works hard to regulate and control blood flow. But if a blood vessel gets injured, the body must jump into action to avoid the loss of too much blood. In this lesson, you will learn about the events that happen immediately after a wound to control bleeding.
Almost immediately after you suffer a cut, your body reacts by initiating a series of events that happen one after another until the bleeding stops. Hemostasis is a term used to describe the stoppage of bleeding. This is an easy term to recall if you remember that 'heme' is the Greek word for 'blood' and 'stasis' is the Greek word for 'halt.' So hemostasis can be literally thought of as the halting of blood or the stoppage of bleeding.
This series of events depends on specific proteins called clotting factors. Clotting factors are substances in your blood that act in sequence to stop bleeding by forming a clot. There are many clotting factors, and they often interact with each other. Many of them are named using Roman numerals, such as factor XII, factor XI, factor X, and so on, while others go by more common names, such as fibrinogen (factor I), prothrombin (factor II), or tissue factor (factor III). We'll learn more about these clotting factors later in the lesson.
These clotting factors depend on vitamin K to function properly. Vitamin K is required for the synthesis of clotting factors, and it's so important to the blood-clotting process that it sometimes goes by the nickname 'the clotting vitamin.' Without it, you could experience excessive bleeding, so vitamin K is important to get in your diet, and it's found in such foods as green leafy vegetables, broccoli, cauliflower, and cabbage. So there's another good reason for you to eat your vegetables.
When a blood vessel wall is damaged, collagen fibers from within the wall are exposed. These exposed fibers become a place for platelets to cling to. Platelets are irregular-shaped bodies that help the clotting process by sticking to the lining of the blood vessels. These odd-shaped fragments of cells are normally found floating around your blood along with your red blood cells, kind of minding their own business. But when the cells that line the blood vessels get injured, they release chemicals that cause the platelets to kick into action and become sticky. What we see is layer upon layer of platelets laying down over the wound, somewhat like dirty 'plates' piling up in a sink.
Platelets are like the first responder to a site of an emergency, but platelets can't plug the hole alone. They need some help. This is where we start to see some of the clotting factors that we talked about earlier. One in particular, called fibrinogen, is an inactive clotting factor that helps bind the platelets to form a clot. These inactive clotting factors act as little cross-links, attaching the adjacent platelets to each other. So, in wound healing, platelets take a lot of the glory for being the first ones to the scene, but without their support team, fibrinogen, they would not be able to properly hold together.
So we're starting to see how a wound can get plugged up with platelets. But the thing is, there are not enough platelets in the immediate area of the wound to properly plug the hole. So platelets solve this problem by calling for help. How do platelets call for help? They do this by releasing tiny granules that send out chemical signals. These chemicals attract more platelets to the wound site, which helps build the plug. But these chemicals do more than just recruit more platelets. For instance, one important chemical in this process is called thromboxane A2. Thromboxane A2 is a product of activated platelets that promotes the collection of more platelets and vasoconstriction. Vasoconstriction is an important component of wound-healing, and it's one of the very first steps in healing a damaged blood vessel. It's this vasoconstriction that initially slows the flow of blood through the vessels and decreases the amount of blood lost.
So thromboxane A2 is a platelet-recruiter and a vasoconstrictor, making it an important player in blood clotting. Interestingly, though, aspirin is an antithrombotic agent. We know that 'anti' means 'against' and 'thrombo' means 'blood clot,' so aspirin is a drug that is against the formation of a blood clot because it blocks the synthesis of thromboxane A2. Without the thromboxane A2, the platelets can't keep coming to the injured site as quickly, so aspirin can lead to more or prolonged bleeding.
We already see that wound healing is a series of events that picks up momentum as it goes. The activated platelets start plugging the wound and send out chemicals to attract more platelets. We previously learned that this is known as a positive feedback loop because it is the type of feedback that results in an increase, or amplification, of the effect by its own influence on the process. In other words, we can say that the process of healing promotes more healing. This positive feedback accelerates blood clotting and speeds the overall healing process.
At this point, the wound has a temporary plug to stem the bleeding, but it needs something more permanent. Tissue factor or factor III is a clotting factor that is activated due to damage of a blood vessel wall. This starts a cascade of events that causes one clotting factor after another to activate, somewhat like a waterfall. This waterfall of events is known as the coagulation cascade and is defined as a series of reactions involving clotting factors that stop bleeding by forming a clot.
Now, if you have ever stood beside a powerful waterfall, you realize that the water is going to fall no matter what you do. The same goes for the coagulation cascade. The clotting factors continue to activate each other, one after another, until they reach the bottom of the waterfall. While it's not important to learn each of these clotting factors, we can focus on the clotting factors at the bottom. Here we notice that we have the inactive clotting factor prothrombin (factor II) that changes to its active form, thrombin. Thrombin, then in turn, catalyzes the conversion of fibrinogen to fibrin. Fibrin is at the bottom of our coagulation cascade, and indeed, it can be thought of as the last step because it is fibrin that's the biological glue that seals the damaged vessel and ensures hemostasis. It does this by forming long strands of fibrin threads that crisscross heavily and form a fibrin mesh over the original wound site.
Let's review: Hemostasis is the term used to describe the stoppage of bleeding. Hemostasis is really a series of events that depends on the specific proteins called clotting factors, which are substances in the blood that act in sequence to stop bleeding by forming a clot. Vitamin K is required for the synthesis of clotting factors.
When a blood vessel wall is damaged, one of the first things to happen is vasoconstriction. This slows blood flow to the damaged area. The damaged blood vessel also releases chemicals that cause platelets to become sticky. Platelets are defined as irregular-shaped bodies that help the clotting process by sticking to the lining of the blood vessels. These platelets get a little help to hold themselves together from fibrinogen, which helps bind the platelets to form a clot. Activated platelets also send out for help by releasing chemicals to pull more platelets into the area. Because of this, we can say that blood clotting is accelerated by a positive feedback loop. Thromboxane A2 is one of these chemicals released by the activated platelets that promotes the collection of more platelets and vasoconstriction. Aspirin can block thromboxane A2 and may lead to increased bleeding.
Now that the wound is temporarily sealed, the body can start work on a more permanent healing through the coagulation cascade. This is a series of reactions involving clotting factors. The cascade continues until we see the activation of fibrin. It is fibrin that is the biological glue that seals the damaged vessel and ensures hemostasis. It does this by forming long fibrin threads that crisscross heavily and form a fibrin mesh over the original wound site.
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Back To CourseHuman Anatomy & Physiology: Help and Review
20 chapters | 736 lessons