Definition.docx

Definition Venous thromboembolism (VTE) can manifest as Deep Vein Thrombosis (DVT), Ischemic Stroke, and Pulmonary Embolism (PE) that they are coming from the same pathological entity (Wong and Chaudhry, 2013, Koupenova et al., 2016, A. Caprini, 2005). Thromboembolism might stem from the words Thrombus and Embolus. Embolus can be defined as an intravascular material that moves from its origin which allows occlusion in a more distal part of the blood vessel. Although embolus generally can be blood clot, fat, water, amniotic fluid or tumor, PE is often caused by thrombus originating from the deep veins of the legs (Wong and Chaudhry, 2013). Etiology The etiology of VTE can be explained by Virchow's triad theorem which explains the predisposition of thrombus, namely Hypercoagulability, Stasis, and endothelial damage (Wong and Chaudhry, 2013). Firstly, this hypercoagulability can be either hereditary or acquired. Hereditary hypercoagulability can be as factor V leiden (mutations that cause factor Va to be resistantly inactivated, prothrombin G20210A (mutations that cause increased prothrombin production), and difficiency antithrombin, protein S and C, and plasminogen. Meanwhile, acquired hypercoagulability can be caused by cancer chemotheraphy, oral contraceptives and hormone replacement therapy, pregnancy and postpartum period, central obesity, and heparin-induced thrombocytopenia (Wong and Chaudhry, 2013). Secondly, VTE can also be caused by stasis which can cause endothelial injury directly by reducing natural fibrinolysis. Decreased mobility, polycythemia, and congestive heart failure can cause stasis to occur (Wong and Chaudhry, 2013). Thirdly, VTE can be caused by endothelial damage and dysfunction. Endothelial dysfunction can lead to decreased synthesis of NO and prostacyclin and increased endothelin-1. Meanwhile, endothelial damage can cause exposure to subendothelial tissue and collagen with platelets (Wong and Chaudhry, 2013). Both of them can lead to blood clotting formation. Pathophysiology of Deep vein thrombosis (Wong and Chaudhry, 2013 Deep venous thrombosis is used as a common cause of extremity, which is commonly from calf veins, specifically in the soleus sinusoids and cusps of the valves. Venous valve is avascular so that the decrease of oxygenated blood flow causes exposure to endothelial conditions with hypoxemia. The endothelium responds by exposing the adhesion molecule that invites leukocytes. This cell moves tissue factor to the endothelium, which can be complex with VIIa to begin the coagulation cascade via extrinsic pathway. The main components of this venous thrombi are over fibrin and trapped in the clot. Platelets also contribute, but only slightly (Wong and Chaudhry, 2013). Meanwhile, skeletal muscle pumps the venous to prevent DVT so that activated clotting factors spread and cause new thrombus formation. When the clot doesn’t resolve, it will spread proximally and can colonize the condition of the blood vessels that are suitable (Wong and Chaudhry, 2013). Pathophysiology of Pulmonary embolism (Swaroop and Tarbox, 2013) PE is a condition in which DVT releases and embolizes the pulmonary circulation resulting in occlusion and disrupting gas exchange and circulation. Pulmonary artery obstruction results in dead space

ventilation because capillary ventilation exceeds capillary blood flow. this causes ventilation-perfusion mismatch and induces the release of serotonin and thromboxane from activated platelets. As a result, vasoconstriction is very likely to occur in the unaffected areas of lung and cause increased pulmonary pressure resulting in the occurrence of right heart failure. This can result in impaired left ventricular filling and can cause hypoxemia and tissue hypoxia.

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