change from a liquid to a thickened or solid state; "coagulated blood" (同)coagulate
a lump of material formed from the content of a liquid (同)coagulum
cause to change from a liquid to a solid or thickened state (同)coagulate
make solid or more solid; cause to solidify
become solid; "The metal solidified when it cooled"
transformed from a liquid into a soft semisolid or solid mass; "coagulated blood"; "curdled milk"; "grumous blood" (同)coagulated, curdled, grumous, grumose
a cord on which clothes are hung to dry
ordinary clothing suitable for public appearances (as opposed to costumes or sports apparel or work clothes etc.)
"Clot" redirects here. For other uses, see Clot (disambiguation).
Not to be confused with Embolism or Thrombosis.
Thrombus
Other names
Blood clot
Diagram of a thrombus (blood clot) that has blocked a blood vessel valve
Specialty
Vascular surgery
A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis. There are two components to a thrombus: aggregated platelets and red blood cells that form a plug, and a mesh of cross-linked fibrin protein. The substance making up a thrombus is sometimes called cruor. A thrombus is a healthy response to injury intended to prevent bleeding, but can be harmful in thrombosis, when clots obstruct blood flow through healthy blood vessels.
Mural thrombi are thrombi that adhere to the wall of a blood vessel. They occur in large vessels such as the heart and aorta, and can restrict blood flow but usually do not block it entirely. They appear grey-red with alternating light and dark lines (known as lines of Zahn) which represent bands of entrapped white blood cells and red blood cells (darker).
Contents
1Cause
2Classification
3Pathophysiology
3.1Formation
4Prevention and treatment
5Prognosis
6See also
7References
8External links
Cause
Virchow's triad describes the pathogenesis of thrombus formation:[1][2]
Endothelial injury: Injury to the endothelial causing platelet activation and aggregation
Common causes include: trauma, smoking, hypertension, atheroma
Stasis: Blood stasis promotes greater contact between platelets/coagulative factors with vascular endothelium.
Common causes of stasis include anything that leads to prolonged immobility and reduced blood flow such as: trauma/broken bones and extended air travel
Hypercoagulability (also called thrombophilia; any disorder of the blood that predisposes to thrombosis)
Common causes include: cancer (leukaemia), Factor V mutation (Leiden) - prevents Factor V inactivation leading to increased coagulability.
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 subsequent activation of fibrinolysis using all of the body's available platelets and clotting factors. The end result is hemorrhaging and ischaemic necrosis of tissue/organs. Causes are septicaemia, acute leukaemia, shock, snake bites, fat emboli from broken bones, or other severe traumas. DIC may also be seen in pregnant females. Treatment involves the use of fresh frozen plasma to restore the level of clotting factors in the blood, as well as platelets and heparin to prevent further thrombi formation.
Classification
Thrombi are classified in three major groups depending on the relative amount of platelets and red blood cells (RBCs).[3]
The three major groups are:
White thrombi (characterized by predominance of platelets)
Red thrombi (characterized by predominance of red blood cells)
Mixed thrombi (with features of both white and red thrombi - an intermediate).
Pathophysiology
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 embolus.
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 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.
Formation
Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption.[clarification needed] The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.[4] This process is regulated through thromboregulation.
Illustration Comparing Normal Artery vs Diseased Artery with a Blood Clot
Micrograph showing a thrombus (center of image) within a blood vessel of the placenta. H&E stain.
Illustration depicting thrombus formation over arterial plaque.
Prevention and treatment
Main articles: Thrombolysis, Thrombosis prophylaxis, and Reperfusion therapy
This section needs more medical references for verification or relies too heavily on primary sources. Please review the contents of the section and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed.(November 2018)
Blood clot prevention and treatment reduce the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation.[2] The mechanism of action of heparin and warfarin are different as they work on different pathways of the coagulation cascade.[5] Heparin works by binding to and activating the enzyme inhibitor antithrombin III, an enzyme that acts by inactivating thrombin and factor Xa.[5] In contrast, warfarin works by inhibiting vitamin K epoxide reductase, an enzyme needed to synthesize vitamin K dependent clotting factors II, VII, IX, and X.[5][6] Bleeding time with heparin and warfarin therapy can be measured with the partial thromboplastin time (PTT) and prothrombin time (PT), respectively.[6]
Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria.[7] This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is tissue plasminogen activator (tPA).[7] This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme, plasmin.[8] There are also some anticoagulants that come from animals that work by dissolving fibrin. For example, Haementeria ghilianii, an Amazon leech, produces an enzyme called hementin from its salivary glands.[9] As of 2012[update], this enzyme has been successfully produced by genetically engineered bacteria and is administered to cardiac patients.
More recent research indicates that tPA could have toxic effects in the central nervous system. In cases of severe stroke, tPA can cross the blood-brain barrier and enter interstitial fluid, where it then increases excitotoxicity, potentially affecting permeability of the blood-brain barrier,[10] and may even cause cerebral hemorrhaging.[11]
Prognosis
Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.[12]
Propagation of a thrombus occurs towards the direction of the heart and involves the accumulation of additional platelets and fibrin. This means that it is anterograde in veins or retrograde in arteries.
Embolization occurs when the thrombus breaks free from the vascular wall and becomes mobile, thereby traveling to other sites in the vasculature. A venous embolus (mostly from deep vein thrombosis in the lower limbs) will travel through the systemic circulation, reach the right side of the heart, and travel through the pulmonary artery resulting in a pulmonary embolism. Arterial thrombosis resulting from hypertension or atherosclerosis can become mobile and the resulting emboli can occlude any artery or arteriole downstream of the thrombus formation. This means that cerebral stroke, myocardial infarction, or any other organ can be affected.
Dissolution occurs when the fibrinolytic mechanisms break up the thrombus and blood flow is restored to the vessel. This may be aided by fibrinolytic drugs such as Tissue Plasminogen Activator (tPA) in instances of coronary artery occlusion. The best response to fibrinolytic drugs is within a couple of hours, before the fibrin meshwork of the thrombus has been fully developed.
Organization and recanalization involves the ingrowth of smooth muscle cells, fibroblasts and endothelium into the fibrin-rich thrombus. If recanalization proceeds it provides capillary-sized channels through the thrombus for continuity of blood flow through the entire thrombus but may not restore sufficient blood flow for the metabolic needs of the downstream tissue.[1]
See also
Embolism
Thrombolysis ("destruction of clot")
Thrombogenicity (the tendency to clot)
National Blood Clot Alliance
Prothrombin time
References
^ abRobbins and Cotran pathologic basis of disease. Kumar, Vinay, 1944-, Abbas, Abul K.,, Aster, Jon C.,, Perkins, James A., (Ninth ed.). Philadelphia, PA. ISBN 9781455726134. OCLC 879416939.CS1 maint: others (link)
^"White Thrombi". Bayer. Retrieved 27 October 2015.
^Furie, Bruce; Furie, Barbara (2008). "Mechanisms of Thrombus Formation". The New England Journal of Medicine. 359 (9): 938–49. doi:10.1056/NEJMra0801082. PMID 18753650.
^ abcHarter, K.; Levine, M.; Henderson, S. O. (2015). "Anticoagulation Drug Therapy: A Review". The Western Journal of Emergency Medicine. 16 (1): 11–17. doi:10.5811/westjem.2014.12.22933. PMC 4307693. PMID 25671002.
^ abWhalen, Karen; Finkel, Richard S.; Panavelil, Thomas A. (2014). Pharmacology. Whalen, Karen,, Finkel, Richard (Richard S.),, Panavelil, Thomas A. (Sixth ed.). Philadelphia. ISBN 9781451191776. OCLC 881019575.
^ abGurewich, V. (2016). "Therapeutic Fibrinolysis: How Efficacy and Safety Can be Improved". Journal of the American College of Cardiology. 68 (19): 2099–2106. doi:10.1016/j.jacc.2016.07.780. PMID 27810050.
^Saladin, Kenneth S. (2012). Anatomy & Physiology: The Unity of Form and Function (6th ed.). New York, NY: McGraw-Hill. p. 710. ISBN 978-0-07-337825-1.
^Budzynski, A. Z. (1991). "Interaction of hementin with fibrinogen and fibrin". Blood Coagulation & Fibrinolysis : An International Journal in Haemostasis and Thrombosis. 2 (1): 149–52. PMID 1772982.
^Fredriksson, L.; Lawrence, D. A.; Medcalf, R. L. (2016). "TPA modulation of the blood-brain barrier: A unifying explanation for the pleiotropic effects of tPA in the CNS?". Seminars in Thrombosis and Hemostasis. 43 (2): 154–168. doi:10.1055/s-0036-1586229. PMC 5848490. PMID 27677179.
^Medcalf, R. (2011). "Plasminogen activation-based thrombolysis for ischaemic stroke: the diversity of targets may demand new approaches". Current Drug Targets. 12 (12): 1772–1781. doi:10.2174/138945011797635885.
^Kumar, Vinay; et al. (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders/Elsevier. ISBN 978-1-4160-2973-1.
External links
Look up thrombus or clot in Wiktionary, the free dictionary.
Treatment and Symptoms of Blood Clots -- MDhealthnetwork.org, Medical Information Resource, 1999
North American Thrombosis Forum - NATF is a nonprofit organization dedicated to promoting thrombosis research, prevention and education, public policy, and advocacy outreach.
Muscle Relaxing Drugs Can Reduce Lethal Blood Clots
Air Pollution Triggers Blood Clots - US Study.
The National Alliance for Thrombosis and Thrombophilia - has extensive stories from patients and family members on living with Thrombosis and Thrombophilia, assembled frequently asked questions and created publications addressing specific blood clot issues.
Classification
D
ICD-10: Xxx.x
ICD-9-CM: xxx
v
t
e
Disorders of blood flow
Decreases
Clots
Thrombus
Thrombosis
Renal vein thrombosis
Ischemia
Brain ischemia
Ischaemic heart disease
large intestine: Ischemic colitis
small intestine: Mesenteric ischemia
Infarction
Types
Anemic
Hemorrhagic
Location
Heart
Brain
Spleen
Limb
Increases
Hemorrhage
Bruise/Hematoma
Petechia
Purpura
Ecchymosis
head
Epistaxis
Hemoptysis
Intracranial hemorrhage
Hyphema
Subconjunctival hemorrhage
torso
Hemothorax
Hemopericardium
Pulmonary hematoma
abdomen
Gastrointestinal bleeding
Haemobilia
Hemoperitoneum
Hematocele
Hematosalpinx
joint
Hemarthrosis
Edema
Anasarca
Angioedema/Lymphedema
Exudate/Transudate
Cerebral edema
Pulmonary edema
Hydrothorax
Ascites/hydroperitoneum
Hydrosalpinx
Other
Hyperemia
UpToDate Contents
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
Dynamics of pathologic clot formation: A mathematical model.
Shavlyugin EA, Hanin LG, Khanin MA.SourceMathematical Modeling Laboratory, Center for Theoretical Problems of Physicochemical Pharmacology, Russian Academy of Sciences, Kosygina Street 4, Moscow 119991, Russia. Electronic address: eshavlyugin@gmail.com.
Journal of theoretical biology.J Theor Biol.2014 Jan 7;340:96-104. doi: 10.1016/j.jtbi.2013.08.007. Epub 2013 Aug 23.
Recent studies have provided evidence of a significant role of the Hageman factor in pathologic clot formation. Since auto-activation of the Hageman factor triggers the intrinsic coagulation pathway, we study the dynamics of pathologic clot formation considering the intrinsic pathway as the predomin
Functional characterization of a slow and tight-binding inhibitor of plasmin isolated from Russell's viper venom.
Cheng AC, Tsai IH.SourceInstitute of Biological Chemistry, Academia Sinica, Taipei 11529, Taiwan. Electronic address: adamcheng@gate.sinica.edu.tw.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jan;1840(1):153-9. doi: 10.1016/j.bbagen.2013.08.019. Epub 2013 Aug 30.
BACKGROUND: Snake venoms are rich in Kunitz-type protease inhibitors that may have therapeutic applications. However, apart from trypsin or chymotrypsin inhibition, the functions of most of these inhibitors have not been elucidated. A detailed functional characterization of these inhibitors may lead
Lack of functional information explains the poor performance of 'clot load scores' at predicting outcome in acute pulmonary embolism.
Clark AR, Milne D, Wilsher M, Burrowes KS, Bajaj M, Tawhai MH.SourceAuckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand. Electronic address: alys.clark@auckland.ac.nz.
Clot load scores have previously been developed with the goal of improving prognosis in acute pulmonary embolism (PE). These scores provide a simple estimate of pulmonary vascular bed obstruction, however they have not been adopted clinically as they have poor correlation with mortality and right ve
3-d transcranial ultrasound imaging with bilateral phase aberration correction of multiple isoplanatic patches: a pilot human study with microbubble contrast enhancement.
Lindsey BD, Nicoletto HA, Bennett ER, Laskowitz DT, Smith SW.SourceDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, USA; Joint Department of Biomedical Engineering, University of North Carolina and North Carolina State University, Chapel Hill, North Carolina, USA. Electronic address: brooks.lindsey@unc.edu.
Ultrasound in medicine & biology.Ultrasound Med Biol.2014 Jan;40(1):90-101. doi: 10.1016/j.ultrasmedbio.2013.09.006. Epub 2013 Nov 14.
With stroke currently the second-leading cause of death globally, and 87% of all strokes classified as ischemic, the development of a fast, accessible, cost-effective approach for imaging occlusive stroke could have a significant impact on health care outcomes and costs. Although clinical examinatio
… In this study we improved the prescription of fibrin clot embedded human leukemia cells for murine subrenal capsule grafting. … In conclusion nude mice and immunosuppressed mice were right animals for antitumor activity assay by subrenal capsule grafting using fibrin-cancer cell clot. …
… Emergent decompressive craniotomy revealed an encapsulated solid fresh clot in the subdural space and a bleeding small cortical artery under the clot. … The red blood cells constituting the clot in the capsule maintained their cell structure. …