Thromboembolism is a dangerous disease especially in the United States; the major cause of death in the United States is abnormal-blood-clotting (thrombosis). Many researches are published to improve our understanding of the etiology and causes of the abnormal blood clotting, and many reports talk about improvement of clinical diagnosis and therapy. There are major classification of thrombosis; arterial thrombosis, develop of blood clot in the arterial circulation, it’s usually due to arteries disease such as atherosclerosis, and venous thrombosis, develop of blood clot in the venous circulation, it may be due to injury or inactivity to the vein.
Thrombosis which develops in the circulation may be fragmented and these fragments (emboli) flow to other parts of the circulation, these emboli may cause severe damage to the organ and then death. Strokes may cause by these emboli and heart attack also. Pulmonary emboli may cause rapidly death. So we can say that: – thrombosis” A blood clot that forms abnormally within the vessels” and – embolus: A blood clot that breaks free from its site of formation”, so the disease called thromboembolism since two thrombosis and embolism occurred together.
Patents whose have thromboembolism must be have one or more risk factors either acquired or genetic risk factor. Genetic risk factors increase the person risk to develop thromboembolic disease. Actually genetic factors act with acquired risk factors and involve the blood vessels, and blood flow through blood vessels, and platelets, and chemicals that are part of the hemostatic system. The person who has the tendency to develop thrombosis, due to either acquires risk factor or genetic one, called thrombophilia case. There is a great interest in avoiding acquired risk factors and early discover and treatment of patients. Many laboratory tests and drugs are available now for this purpose.
Introduction to Hemostasis:
Hemostasis is a physiological condition that keeps the blood in the vessels, maintain fluidity, and stop bleeding when the vessel injured. Hemostasis can defined as “The natural process to prevent blood loss from blood vessels and wounds by the formation of blood clots. It’s a complicated process depends on reactions between vessels and tissues, endothelial cells, platelets, plasma coagulation proteins, and fibrinolytic system. Any change in the hemostatic system leading to pathologic bleeding or clotting.
What help bleeding to stop is:
- Extra vascular forces ” pressure exerted by the skin and supporting tissue”
- Physical resistance provided by the blood vessels.
- Substances present in the blood( platelets and coagulation factors)
Vessels constrict when injured, limiting the blood flow to the injured site. Collagen fibers exposed by the vascular damage then platelets adhere to collagen and aggregate to form loose and temporary plug (primary plug). Platelet aggregation stimulated by plasma protein fibrinogen. The primary plug of platelets submission to medical and biomedical changes, called activation. Platelets which activated release chemical substances that activate others and initiate the coagulation cascade. Coagulation produces a fibrin mesh which stabilizes the platelet plug. To return the normal function, the process of healing and recovery is initiated. The endothelium heals and blood clot is dissolved through the action of plasmin and other components of the fibrinolytic system. So, the stages of coagulation include:
- Vessel constriction
- Formation of platelet plug ( primary hemostasis)
- Coagulation and fibrin generation (secondary hemostasis)
- Fibrinolysis, healing and repair
The body has an efficient system to assure that unneeded blood clotting does not occur. For example, active coagulation substances are effective for only very short periods of time (milliseconds to seconds) and are rapidly diluted by normal blood flow. The liver and other parts of the body remove activated coagulation factors and an elaborate system of chemical substances destroys them. Lastly, the walls of the vessels throughout the body (vascular endothelium) release chemical substances (i.e., anti-thrombin, protein C pathway, etc.) that prevent platelet activation and the activation of chemical mediators.
Normally, these systems work together to assure that bleeding does not occur, but also to prevent thromboembolic disease. Unfortunately, defects in the blood vessels (vascular defects), or in any of the processes leading to defective formation of the hemostatic plug (platelet dysfunction, coagulation defects) may result in a bleeding disorder, while thromboembolic disease may be caused by vascular injury or arterial disease, blood stasis, inappropriate activation of hemostasis, or defective modulation of the mechanisms that normally regulate blood clotting.
Risk Factors for Thromboembolic Disease:
The major types of venous thromboembolism, deep venous thrombosis (DVT) and pulmonary embolism are a leading cause of morbidity and mortality in hospitalized patients. They are being seen with increasing frequency in outpatients as well. The discovery of a number of acquired and genetic risk factors for thromboembolic disease has provided a means to predict the risk of these diseases and institute preventive therapy.
Acquired Risk Factors:
Acquired risk factors for venous thromboembolism include
- Immobilization or venous stasis
- Inflammatory diseases
- The use of oral contraceptives containing synthetic estrogens
- Congestive heart failure and other diseases.
Venous stasis in the extremities, venous obstruction, increased blood viscosity and direct venous damage may cause or contribute to the development of venous thromboembolism. The increasing tendency to early hospital discharge of postsurgical patients may be responsible for the increasing incidence of venous thromboembolism in outpatients. Venous thromboembolism usually involves the deep or superficial veins of the legs. Blood clots in the superficial veins (superficial thrombophlebitis) leads to localized tenderness, surrounded by an area of redness (erythema), heat and edema. A thrombus can often be palpated in the affected vein. Although usually benign and self-limiting, superficial thromboemboli can cause serious complications if they extend into the other veins. Deep thrombi confined to calf veins rarely cause clinical problems but can lead to pulmonary emboli (PE).The antiphospholipid syndrome (APS) is another common acquired cause of thrombosis. APS is caused by autoantibodies that form against certain components of the coagulation system. In addition to venous and arterial thrombosis, including strokes, APS is associated with cause bleeding, miscarriages and other medical problems. The long-term use of certain drugs, including chlorpromazine and phenothiazine, may result in APS. Generally, patients with APS have a six to 10 times risk of developing venous thrombosis than normal individuals; the risk of atrial thrombosis is increased as well.
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