Pathogenesis The main causes of<unk>  are given in Virchow's triad which lists<unk> ophilia, endothelial cell injury, and disturbed blood flow. Generally speaking the risk for<unk>  increases over the life course of individuals, depending on life style factors like smoking, diet, and physical activity, the presence of other diseases like cancer or autoimmune disease, while also platelet properties change in aging individuals which is an important consideration as well. Hypercoagulability Hypercoagulability or<unk> ophilia, is caused by, for example, genetic deficiencies or autoimmune disorders. Recent studies indicate that white blood cells play a pivotal role in deep vein<unk> , mediating numerous pro-thrombotic actions. Endothelial cell injury Any inflammatory process, such as trauma, surgery or infection, can cause damage to the endothelial lining of the vessel's wall. The main mechanism is exposure of tissue factor to the blood coagulation system. Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state. When this occurs, endothelial cells downregulate substances such as<unk> omodulin, which is a key modulator of<unk> in activity. The end result is a sustained activation of<unk> in and reduced production of protein C and tissue factor inhibitor, which furthers the pro-thrombotic state. Endothelial injury is almost invariably involved in the formation of<unk> i in arteries, as high rates of blood flow normally hinder clot formation. In addition, arterial and cardiac clots are normally rich in platelets–which are required for clot formation in areas under high stress due to blood flow. Disturbed blood flow Cancer-associated<unk>  can result from: (1) stasis, i.e., direct pressure on blood vessels by the tumor mass, poor performance status, and bed rest following surgical procedures; (2) iatrogenic, due to treatment with antineoplastic medications; and (3) secretion of heparanase from malignant tumors that results in degradation of endogenous heparin. Source: Potential Mechanisms of Cancer-Related Hypercoagulability. Nasser NJ, Fox J, Agbarya A. Cancers (Basel). 2020 Feb 29;12(3):566. https://doi.org/10.3390/cancers12030566 Causes of disturbed blood flow include stagnation of blood flow past the point of injury, or venous stasis which may occur in heart failure, or after long periods of sedentary behaviour, such as sitting on a long airplane flight. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA), or left atrial appendage (LAA), and can lead to a<unk> oembolism. Cancers or malignancies such as leukemia may cause increased risk of<unk>  by possible activation of the coagulation system by cancer cells or secretion of procoagulant substances (paraneoplastic syndrome), by external compression on a blood vessel when a solid tumor is present, or (more rarely) extension into the vasculature (for example, renal cell cancers extending into the renal veins). Also, treatments for cancer (radiation, chemotherapy) often cause additional hypercoagulability. There are scores that correlate different aspects of patient data (comorbidities, vital signs, and others) to risk of<unk> , such as the POMPE-C, which stratifies risk of mortality due to pulmonary embolism in patients with cancer, who typically have higher rates of<unk> . Also, there are several predictive scores for<unk> oembolic events, such as Padua, Khorana, and ThroLy score. Pathophysiology Natural history Fibrinolysis is the physiological breakdown of blood clots by enzymes such as plasmin. Organisation: following the<unk> otic event, residual vascular<unk> us will be re-organised histologically with several possible outcomes. For an occlusive<unk> us (defined as<unk>  within a small vessel that leads to complete occlusion), wound healing will reorganise the occlusive<unk> us into collagenous scar tissue, where the scar tissue will either permanently obstruct the vessel, or contract down with myofibroblastic activity to unblock the lumen. For a mural<unk> us (defined as a<unk> us in a large vessel that restricts the blood flow but does not occlude completely), histological reorganisation of the<unk> us does not occur via the classic wound healing mechanism. Instead, the platelet-derived growth factor degranulated by the clotted platelets will attract a layer of smooth muscle cells to cover the clot, and this layer of mural smooth muscle will be vascularised by the blood inside the vessel lumen rather than by the vasa vasorum. Ischemia/infarction: if an arterial<unk> us cannot be lysed by the body and it does not embolise, and if the<unk> us is large enough to impair or occlude blood flow in the involved artery, then local ischemia or infarction will result. A venous<unk> us may or may not be ischemic, since veins distribute deoxygenated blood that is less vital for cellular metabolism. Nevertheless, non-ischemic venous<unk>  may still be problematic, due to the swelling caused by blockage to venous drainage. In deep vein<unk>  this manifests as pain, redness, and swelling; in retinal vein occlusion this may result in macular oedema and visual acuity impairment, which if severe enough can lead to blindness. Embolization A<unk> us may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel, which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. Venous<unk>  can lead to pulmonary embolism when the migrated embolus becomes lodged in the lung. In people with a "shunt" (a connection between the pulmonary and systemic circulation), either in the heart or in the lung, a venous clot can also end up in the arteries and cause arterial embolism. Arterial embolism can lead to obstruction of blood flow through the blood vessel that is obstructed by it, and a lack of oxygen and nutrients (ischemia) of the downstream tissue. The tissue can become irreversibly damaged, a process known as necrosis. This can affect any organ; for instance, arterial embolism of the brain is one of the causes of stroke.
Thrombosis
Thrombus
Angiopathy
Sclerosis 
Calcification
Infarction
Adhesion 
Abscess