Clot retraction is dependent on the release of multiple coagulation factors released at the end of the coagulation cascade, most notably factor XIIIa crosslinks.
These factors cause the fibrin mesh to contract by forming twists and knots that condense the size of the clot. Following clot retraction, a separate process called fibrinolysis occurs which degrades the fibrin of the clot while macrophages consume the expended platelets, thus preventing possible thromboembolism.
While the clot retracts, the wound begins to heal. The first step of wound healing is epithelial cell migration, which forms a scab before the clot retracts. This occurs due to the stimulus of platelet-derived growth factor PDGF. After clot retraction, true repair begins as tissue proliferation starts and collagen from the extracellular matrix is deposited in the wound while granulation tissue forms.
Then new blood vessels grow into the healing tissue in a process called angiogenesis, which is stimulated by vascular endothelial growth factor VEGF. The wound itself contracts, reducing in size. After these steps occur, new epithelial cells grow to cover the wound. If the wound was severe or unevenly shaped, or if healing takes too long, scarring may occur from collagen deposition. Most scarring on the skin is benign, but scarring inside the tissues of organs such as the heart or the lungs can cause health problems.
Fibrinolysis is a process of breaking down clots in order to prevent them from growing and becoming problematic. Fibrinolysis is a process that removes clots following hemostasis and clot retraction, preventing uncontrolled thrombosis and embolism. There are two types of fibrinolysis: primary fibrinolysis and secondary fibrinolysis.
Primary fibrinolysis is a normal body process, whereas secondary fibrinolysis is the breakdown of clots due to a medication, medical disorder, or other cause. Primary fibrinolysis normally occurs following clot retraction, in which the clot has already condensed considerably in size. The main enzyme in primary fibrinolysis is plasmin, a proteolytic enzyme that degrades fibrin mesh.
Plasmin cleaves fibrin at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidneys and liver. Plasmin is produced in an inactive form, plasminogen, in the liver. Plasminogen cannot cleave fibrin and circulates in the bloodstream. Instead, it is incorporated into the clot when it is formed and then activated into plasmin later. Plasminogen is activated to plasmin by tissue plasminogen activator t-PA and urokinase, an enzyme found in the urine.
Fibrinolysis : Blue arrows denote stimulation and red arrows inhibition. T-PA is released into the blood very slowly by the damaged endothelium of the blood vessels.
In contrast, plasmin further stimulates plasmin generation by producing more active forms of both tissue plasminogen activator tPA and urokinase. Following fibrin degradation by plasmin, old activated platelets from the platelet plug are phagocytized and destroyed by macrophages. Alpha 2-antiplasmin and alpha 2-macroglobulin inactivate plasmin. Plasmin activity is also reduced by thrombin -activatable fibrinolysis inhibitor TAFI , which modifies fibrin to make it more resistant to the tPA-mediated plasminogen.
Plasmin operates on a negative feedback process because it is reduced when the fibrin clot is fully degraded. Secondary fibrinolysis generally refers to treatment of pathological thromboembolism.
If blood clots embolize to different parts of the body, they can cause tissue death by blocking off blood flow to those tissues. This is a common cause of heart attacks, pulmonary embolism, and strokes. Several medications exist to help treat and prevent these conditions. Fibrinolytic drugs include synthesized tissue plasminogen activator and streptokinase, a bacterial enzyme that has degrades fibrin directly. Clots may also be prevented or kept from worsening through the use of blood thinners anticoagulants.
Aspirin has anticoagulant properties because it inhibits cyoclo-oxygenase dependent pathways of platelet activation, which can prevent clotting from worsening. Heparin is a fast-acting anticoagulant produced by the body and used as a drug which inhibits the activity of thrombin.
Warfarin inhibits vitamin K cofactor activation during the coagulation cascade, and citrates chelate calcium to prevent prothrombin activation into thrombin. All of these treatments have been shown to have tremendous therapeutic benefit in treating those with thromboembolic diseases; however, they can make injury much more difficult to treat by disrupting the clotting process.
For example, patients thought to be suffering from a stroke obstructed artery in the brain must be screened through imaging before given aspirin or a fibrinolytic drug, because if they have an aneurysm or hemorrhage burst blood vessel or bleeding in the brain , administering fibrinolytic treatment would make their condition worse and possibly fatal by inhibiting the clotting that could save their lives.
Privacy Policy. Skip to main content. Cardiovascular System: Blood. Search for:. Overview of Hemostasis Hemostasis is the natural process that stops blood loss when an injury occurs. Learning Objectives Explain the steps involved in hemostasis. Key Takeaways Key Points Hemostasis is the natural process that stops blood loss when an injury occurs. It involves three steps: 1 vascular spasm vasoconstriction ; 2 platelet plug formation; and 3 coagulation.
Vasoconstriction is a reflex in which blood vessels narrow to increase blood pressure. Next, platelet plug formation involves the activation, aggregation, and adherence of platelets into a plug that serves as a barrier against blood flow. Coagulation involves a complex cascade in which a fibrin mesh is cleaved from fibrinogen. Key Terms hemostasis : The process of slowing and stopping the flow of blood to initiate wound healing. It prevents activation of platelets and clotting factors.
Vascular Spasm Vasoconstriction is the narrowing of the blood vessels, which reduces blood loss during injury. Learning Objectives Describe vascular spasms in hemostasis. Key Takeaways Key Points Vasoconstriction is the narrowing of the blood vessels, which increases blood pressure but can decrease blood flow and loss. Vasoconstriction is mediated by contraction of the smooth muscles lining a blood vessel.
Vasoconstriction is caused by thromboxane A 2 from activated platelets and injured epithelial cells, nervous system reflexes from pain, and direct injury to vascular smooth muscle. The Blood Coagulation Process. Coagulation can be initiated by either of two distinct pathways.
Regardless of whether the Extrinsic or Intrinsic pathway starts coagulation, completion of the process follows a common pathway. Both pathways are required for normal hemostasis and there are positive feedback loops between the two pathways that amplify reactions to produce enough fibrin to form a lifesaving plug.
The Rh blood group was first discovered in Rhesus monkeys. The first exposure does not usually cause a reaction; however, at the second exposure, enough antibodies have built up in the blood to produce a reaction that causes agglutination and breakdown of red blood cells. An injection can prevent this reaction. Play a blood typing game on the Nobel Prize website to solidify your understanding of blood types. Specific components of the blood include red blood cells, white blood cells, platelets, and the plasma, which contains coagulation factors and serum.
Red blood cells are specialized cells that contain hemoglobin and circulate through the body delivering oxygen to cells. White blood cells are involved in the immune response to identify and target invading bacteria, viruses, and other foreign organisms; they also recycle waste components, such as old red blood cells.
Platelets and blood clotting factors cause the change of the soluble protein fibrinogen to the insoluble protein fibrin at a wound site forming a plug. Plasma consists of 90 percent water along with various substances, such as coagulation factors and antibodies. The serum is the plasma component of the blood without the coagulation factors. Skip to content Chapter The Circulatory System. Learning Objectives By the end of this section, you will be able to: List the basic components of the blood Compare red and white blood cells Describe blood plasma and serum.
The Role of Blood in the Body. Red Blood Cells. White Blood Cells. Platelets and Coagulation Factors. Plasma and Serum. Human red blood cells may have either type A or B glycoproteins on their surface, both glycoproteins combined AB , or neither O.
The glycoproteins serve as antigens and can elicit an immune response in a person who receives a transfusion containing unfamiliar antigens. Type O blood, which has no A or B antigens, does not elicit an immune response when injected into a person of any blood type.
Thus, O is considered the universal donor. Persons with type AB blood can accept blood from any blood type, and type AB is considered the universal acceptor. Exercises White blood cells can be classified as granulocytes or agranulocytes defend the body against bacteria and viruses are also called leucocytes All of the above Platelet plug formation occurs at which point?
List some of the functions of blood in the body. How does the lymphatic system work with blood flow? Answers D C B C Red blood cells are coated with proteins called antigens made of glycolipids and glycoproteins.
When type A and type B blood are mixed, the blood agglutinates because of antibodies in the plasma that bind with the opposing antigen. Type O blood has no antigens. Blood also transports clotting factors and disease-fighting agents. Thrombolytic drugs, which include streptokinase and tissue plasminogen activators, are sometimes used to treat heart attacks and strokes caused by blood clots.
These drugs may save lives, but they can also put the person at risk of severe bleeding. Heparin , a drug given to reduce the risk of clot formation, sometimes has an unintended, paradoxical activating effect on platelets that increases the risk of clotting heparin -induced thrombocytopenia-thrombosis. Estrogen , alone or in oral contraceptives, can have the unintended effect of causing excessive clot formation.
Certain drugs used to treat cancer chemotherapy drugs , such as asparaginase , can also increase the risk of clotting. Merck and Co.
From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Manual was first published in as a service to the community. Learn more about our commitment to Global Medical Knowledge. This site complies with the HONcode standard for trustworthy health information: verify here. Common Health Topics. Blood vessel factors. Platelet factors. Blood clotting factors.
Stopping clotting. Drugs and blood clots. Blood Clotting Process. Test your knowledge. What is the medical term for the procedure in which a person donates his or her own blood to be used if needed during or after a surgical procedure?
More Content. Click here for the Professional Version. Too little clotting can cause excessive bleeding from minor injury.
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