: : 7
begin to adhere to each other. They release PROSTOGLANDINS, CALCIUM, PLATELET PROTEINS and ENZYMES that promote chemotaxis, attracting more platelets to collect in injured area. PLATELET ADHESION occurs, when platelets stick to each other and to the exposed collagen within the walls of the injured blood vessels. Most of this adhesion occurs because of von WILLEBRAND FACTOR (vWF), a protein produced and secreted by the blood vessel, forming bridges between the platelets and the collagen found within the vessel wall. Due to a series of reactions, more platelets collect at the site, release chemicals by exocytosis. These activated platelets change shape, form FIBRINOGEN RECEPTOR that will be able to bind with FIBRINOGEN, a plasma protein that is crucial to hemostasis. Within 1 minute a PLATELET PLUG is formed. ASA( aspirin) will inhibit the prostaglandins from being released and therefore can inhibit PP formation. A person before surgery is told not to use ASA. What might be a problem with this advice in relation to the digestive system? 3. COAGULATION Vascular spasm and platelet plugs are not enough to stop bleeding from larger cuts. Coagulation is also necessary for more extensive damage. During coagulation, a clot is formed in the injured area. A BLOOD CLOT is a network of threadlike protein fibers (FIBRIN) that traps blood cells, platelets and fluid. The formation of a clot is dependent upon the existence of COAGULATION FACTORS circulating within the blood plasma. When not needed, these factors are in an INACTIVE state and won’t trigger clotting. In response to an injury however, the clotting factors are activated and a clot is
You've reached the end of your free preview.
Want to read all 34 pages?
- Fall '16
- Lambrini Nicopoulos