Thrombosis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Irreversible formation of the [[blood clot]] is called thrombosis. This process can happen in the [[artery]] and [[vein]] <ref name="pmid25163306">{{cite journal |vauthors=Asakura H |title=[Pathophysiology and classification of thrombosis] |language=Japanese |journal=Nippon Rinsho |volume=72 |issue=7 |pages=1184–90 |date=July 2014 |pmid=25163306 |doi= |url=}}</ref>. | |||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 15:55, 25 July 2018
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Thrombosis Microchapters |
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Site of Thrombosis |
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Differentiating Thrombosis from other Diseases |
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Diagnosis |
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Treatment |
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Thrombosis pathophysiology On the Web |
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Risk calculators and risk factors for Thrombosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-In-Chief: Aida Javanbakht, M.D.
Overview
Irreversible formation of the blood clot is called thrombosis. This process can happen in the artery and vein [1].
Pathophysiology
Rudolf Virchow noted several factors affecting the clot formation, which are as follows:
1) Alterations in blood flow (stasis): Blood flows throughout the circulatory system, without significantly stopping or slowing any where. In certain pathological conditions where the blood flow slows down or stops, it causes:
- Increase in platelet to endothelium contact
- Decrease the dilution of clotting factors
This increases the risk of clot formation and form microthrombi, which further grow and propagate.
2) Injury to the vascular endothelium: Intrinsic or secondary to external trauma (eg, catheterization) can cause intimal damage and stimulates clot formation. See Coagulation.
3) Alterations in the constitution of blood (hypercoagulability): It is the propensity to develop thrombosis due to an abnormality in the system of coagulation.
These three conditions are collectively known as Virchow's triad and lead to intravascular coagulation, forming a mass of red blood cells, leukocytes, and fibrin.
Shown below is a table depicting the elements of Virchow's triad and their modern counterparts.
| Virchow's[2] | Modern | Notes |
|---|---|---|
| Phenomena of interrupted blood-flow | "Stasis" or "venous stasis"[3] | The first category, alterations in normal blood flow, refers to several situations. These include turbulence, stasis, mitral stenosis, and varicose veins. The equivalence of Virchow's version and the modern version has been disputed.[4] |
| Phenomena associated with irritation of the vessel and its vicinity | "Endothelial injury" or "vessel wall injury" | The second category, injuries and/or trauma to endothelium includes damage to the veins arising from shear stress or hypertension. |
| Phenomena of blood-coagulation | "Hypercoagulability" | The last category, alterations in the constitution of blood,[5] has numerous possible risk factors such as hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, disseminated cancer, late pregnancy and delivery, race, age, whether the patient is a smoker, and obesity. All of these risk factors lead to hypercoagulability. |
Thrombus Formation
- Usually there is a balance between the coagulation and fibrinolysis systems in order to not having abnormal thrombosis in the body.
- Factors that increase the risk for a homeostatic imbalance include:
- Thrombophilia
- Immobilization
- Trauma
- An insult to homeostatic balance can expose the sub-endothelium and lead to the collection of various coagulation factors. Accumulation of coagulation factors can lead to the formation of a thrombus of red blood cells, leukocytes, and fibrin.
- A thrombus is characteristically found to first develop in the calf veins and progressively grow in the direction of blood flow (leading to the heart).
- An exceedingly extensive thrombosis in deep veins can extend well into the iliac veins or the inferior vena cava.
- Atherosclerosis is a miss balance between lipids and the hemostasis system which caused clot in arteries. By occluding the artery myocardial infarction, stroke could happen [6].
This video explains the process of thrombosis:
{{#ev:youtube|X_POCRsy7i4}}
References
- ↑ Asakura H (July 2014). "[Pathophysiology and classification of thrombosis]". Nippon Rinsho (in Japanese). 72 (7): 1184–90. PMID 25163306.
- ↑ Agutter, Paul S. (2008). The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey. Berlin: Springer. p. 84. ISBN 1-4020-6649-X.
- ↑ Lowe GD (2003). "Virchow's triad revisited: abnormal flow". Pathophysiol. Haemost. Thromb. 33 (5–6): 455–7. doi:10.1159/000083845. PMID 15692260.
- ↑ "Further reflections on Virchow's triad. - Free Online Library". Retrieved 2009-02-10.
- ↑ Chung I, Lip GY (2003). "Virchow's triad revisited: blood constituents". Pathophysiol. Haemost. Thromb. 33 (5–6): 449–54. doi:10.1159/000083844. PMID 15692259.
- ↑ Prentice CR (1990). "Pathogenesis of thrombosis". Haemostasis. 20 Suppl 1: 50–9. doi:10.1159/000216161. PMID 2083873.