View source for Thrombus

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{{SI}}
{{CMG}}; {{AE}} {{VC}}

{{SK}} Thrombosis

==Overview==
A '''thrombus''', or '''blood clot''', is the final product of the [[blood coagulation]] step in [[hemostasis]]. It is achieved via the aggregation of [[platelets]] that form a platelet plug, and the activation of the humoral [[coagulation]] system (i.e. clotting factors). A thrombus is [[physiology|physiologic]] in cases of [[injury]], but [[pathology|pathologic]] in case of [[thrombosis]].

==Causes==
*Drugs
**[[Desogestrel and Ethinyl Estradiol]]
**[[Tranexamic acid]]

==Pathophysiology==
Specifically, a thrombus is a blood clot in an intact blood vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel.  In a small blood vessel, blood flow may be completely cut-off resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is an [[embolus]]. 

Some of the conditions which elevate risk of blood clots developing include [[atrial fibrillation]] (a form of [[cardiac arrhythmia]]), heart valve replacement, a recent [[myocardial infarction|heart attack]], extended periods of inactivity (see [[deep venous thrombosis]]), and genetic or disease-related deficiencies in the blood's clotting abilities. 

Preventing blood clots reduces the risk of stroke, heart attack and [[pulmonary embolism]]. [[Heparin]] and [[warfarin]] are often used to inhibit the formation and growth of existing blood clots, thereby allowing the body to shrink and dissolve the blood clots through normal methods (see [[anticoagulant]]).

A thrombus differs from a [[hematoma]] by:
*Having high [[hematocrit]]
*Being non-laminar
*Being soft and friable
*Having an absence of circulation

====Virchow's Triad====
[[Rudolf Virchow|Virchow's]] [[Virchow's triad|Triad]] describes the conditions necessary for thrombus formation:

# Changes in vessel wall morphology (e.g. trauma, [[atheroma]])
# Changes in blood flow through the vessel (e.g. [[valvulitis]], [[aneurysm]])
# Changes in blood composition (e.g. [[leukaemia]], hypercoagulability disorders)

Disseminated intravascular coagulation ([[DIC]]) involves widespread microthrombi formation throughout the majority of the blood vessels. This is due to excessive consumption of coagulation factors and [[fibrinolysis]] using all of the body's available [[platelets]] and clotting factors. The end result is ischaemic necrosis of the affected tissue/organs and spontaneous bleeding due to the lack of clotting factors. Causes are [[septicaemia]], acute [[leukaemia]], [[Shock (medical)|shock]], snake bites or severe trauma. Treatment involves the use of fresh, frozen plasma to restore the level of clotting factors in the blood.

====Thrombogenecity====
Thrombogenicity refers to the tendency of a material in contact with the blood to produce a thrombus, or clot. It not only refers to fixed thrombi but also to [[embolus|emboli]], thrombi which have become detached and travel through the bloodstream. Thrombogenicity can also encompass events such as the activation of [[immunity|immune]] pathways and the [[complement system]]. All materials are considered to be thrombogenic with the exception of the [[endothelial cells]] which line the vasculature. Certain medical implants appear non-thrombogenic due to high flow rates of blood past the implant, but in reality all are thrombogenic to a degree.

A thrombogenic implant will eventually be covered by a fibrous capsule, the thickness of this capsule can be considered one measure of thrombogenicity, and if extreme can lead to the failure of the implant.

====Arterial thrombus====
The pathogenic process of arterial thrombosis involves the formation of platelet-rich “white clots” after the rupture of [[atherosclerosis|atherosclerotic plaques]] and exposure of procoagulant material such as [[foam cell|lipid-rich macrophages (foam cells)]], [[collagen]], [[tissue factor]], and/or endothelial breach, in a high shear environment. The exposed material come from within the plaque and also from the activation and aggregation of [[platelet]]s. Platelet accumulation and fibrin deposition cause an occlusive platelet-rich intravascular thrombus. The growing thrombus increases the degree of narrowing, which may result in extremely high shear rates within the [[stenosis|stenotic]] region. This phenomenon is responsible for a [[turbulent flow]] which is developed downstream of the stenosis depending on stenosis geometry and location in the vasculature.<ref name="Bark-2010">{{Cite journal | last1 = Bark | first1 = DL. | last2 = Ku | first2 = DN. | title = Wall shear over high degree stenoses pertinent to atherothrombosis. | journal = J Biomech | volume = 43 | issue = 15 | pages = 2970-7 | month = Nov | year = 2010 | doi = 10.1016/j.jbiomech.2010.07.011 | PMID = 20728892 }}</ref><ref name="Wolberg-2012">{{Cite journal | last1 = Wolberg | first1 = AS. | last2 = Aleman | first2 = MM. | last3 = Leiderman | first3 = K. | last4 = Machlus | first4 = KR. | title = Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited. | journal = Anesth Analg | volume = 114 | issue = 2 | pages = 275-85 | month = Feb | year = 2012 | doi = 10.1213/ANE.0b013e31823a088c | PMID = 22104070 }}</ref>

====Venous thrombus====
The pathophysiology of venous thrombosis or thromboembolism is associated to plasma [[hypercoagulability]] triggered by the expression of procoagulant activity, in intact [[endothelium]],  from inflammation or reduced/static [[blood flow]] resulting in prolonged immobility. Therefore the venous clots are slowly formed involving the formation of fibrin-rich “red clots” which have regions or layers showing substantial [[erythrocyte]] incorporation. Finally, the venous thrombi may initiate behind valve pockets, in which the reduced or static flow decreases wall shear stress that normally regulates endothelial cell phenotype.<ref name="Wolberg-2012">{{Cite journal | last1 = Wolberg | first1 = AS. | last2 = Aleman | first2 = MM. | last3 = Leiderman | first3 = K. | last4 = Machlus | first4 = KR. | title = Procoagulant activity in hemostasis and thrombosis: Virchow's triad revisited. | journal = Anesth Analg | volume = 114 | issue = 2 | pages = 275-85 | month = Feb | year = 2012 | doi = 10.1213/ANE.0b013e31823a088c | PMID = 22104070 }}</ref> Thus, this phenomenum makes the venous endotelium more likely to develop inappropriate expression of intravascular procoagulant activity and so to trigger [[venous thromboembolism]].<ref name="Machlus-2011">{{Cite journal | last1 = Machlus | first1 = KR. | last2 = Cardenas | first2 = JC. | last3 = Church | first3 = FC. | last4 = Wolberg | first4 = AS. | title = Causal relationship between hyperfibrinogenemia, thrombosis, and resistance to thrombolysis in mice. | journal = Blood | volume = 117 | issue = 18 | pages = 4953-63 | month = May | year = 2011 | doi = 10.1182/blood-2010-11-316885 | PMID = 21355090 }}</ref><ref name="Campbell-2009">{{Cite journal | last1 = Campbell | first1 = RA. | last2 = Overmyer | first2 = KA. | last3 = Selzman | first3 = CH. | last4 = Sheridan | first4 = BC. | last5 = Wolberg | first5 = AS. | title = Contributions of extravascular and intravascular cells to fibrin network formation, structure, and stability. | journal = Blood | volume = 114 | issue = 23 | pages = 4886-96 | month = Nov | year = 2009 | doi = 10.1182/blood-2009-06-228940 | PMID = 19797520 }}</ref>
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| [[Image:Blood clot diagram.png|thumb|350px|Venous thrombus]]
| [[Image:Venous thrombus 01.jpeg|thumb|300px|Venous thrombus]]
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==Clinical Significance==
====Arterial Thrombosis====
* [[Acute ischemic stroke]]
* [[Myocardial infarction]]

====Venous Thrombosis====
* [[Atrial fibrillation]]
* [[Budd-Chiari syndrome]]
* [[Cerebral venous sinus thrombosis]]
* [[Deep vein thrombosis]]
* Jugular vein thrombosis
* [[Mesenteric ischemia]]
* [[Paget-Schroetter disease]]
* [[Portal vein thrombosis]]
* [[Pulmonary embolism]]
* [[Renal vein thrombosis]]

==Treatment==
{{Main article|Thrombolysis|Percutaneous coronary intervention}}

Thrombolysis is the breakdown of blood clots. It is colloquially referred to as clot busting for this reason. It works by stimulating [[fibrinolysis]] by [[plasmin]] through infusion of analogs of tissue plasminogen activator, the protein that normally activates plasmin.

==References==
{{Reflist|2}}

{{Electrocardiography}}
{{Circulatory system pathology}}

[[Category:Hematology]]
[[Category:Cardiology]]

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