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==Pathophysiology== [[File:Thrombosis formation.gif|thumb|Animation of the formation of an occlusive thrombus in a vein. A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to aggregate and coagulate. Coagulation of unmoving blood on both sides of the blockage may propagate a clot in both directions.]] A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an [[Embolism|embolus]].{{citation needed|date=February 2021}} If an embolus becomes trapped within a blood vessel, it blocks blood flow and is termed as an embolism. Embolisms, depending on their specific location, can cause more significant effects like strokes, heart attacks, or even death.<ref>{{cite book |last1=Marieb |first1=Elaina N. |title=Human Anatomy and Physiology |publisher=Pearson |edition=11th}}</ref> [[File:1909 Blood Clotting.jpg|thumb|Mechanism of blood clotting]] Some of the conditions which increase the risk of blood clots developing include [[atrial fibrillation]] (a form of [[cardiac arrhythmia]]), heart valve replacement, a recent [[myocardial infarction|heart attack]] (also known as a [[myocardial infarction]]), extended periods of inactivity (see [[deep venous thrombosis]]), and genetic or disease-related deficiencies in the blood's clotting abilities.{{citation needed|date=February 2021}} ===Formation=== Platelet activation occurs through injuries that damage the [[endothelium]] of the blood vessels, exposing the enzyme called [[factor VII]], a protein normally circulating within the vessels, to the [[tissue factor]], which is a protein encoded by the F3 gene. The platelet activation can potentially cause a cascade, eventually leading to the formation of the thrombus.<ref>{{cite journal |last1=Furie |first1=Bruce |last2=Furie |first2=Barbara |year=2008 |title=Mechanisms of Thrombus Formation |journal=The New England Journal of Medicine |volume=359 |issue=9 |doi=10.1056/NEJMra0801082 |pmid=18753650 |pages=938β49}}</ref> This process is regulated through [[thromboregulation]]. <gallery> File:Fetal thrombotic vasculopathy - very high mag.jpg|[[Micrograph]] showing a thrombus (center of image) within a blood vessel of the [[placenta]]. [[H&E stain]]. File:Blausen 0088 BloodClot.png|Illustration depicting thrombus formation over arterial plaque. File:Composition of a fresh thrombus.jpg|Composition of a fresh thrombus at microscopy, showing nuclear debris in a background of [[fibrin]] and [[red blood cell]]s. </gallery>
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