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These three conditions are collectively known as [[Virchow's triad]] and lead to intravascular [[coagulation]], forming a mass of [[red blood cell]]s, [[leukocyte]]s, and [[fibrin]]. | These three conditions are collectively known as [[Virchow's triad]] and lead to intravascular [[coagulation]], forming a mass of [[red blood cell]]s, [[leukocyte]]s, and [[fibrin]]. | ||
Shown below is a table depicting the elements of Virchow's triad and their modern counterparts. | |||
{| class="wikitable" | |||
|- | |||
! Virchow's<ref name="isbn1-4020-6649-X">{{cite book |author=Agutter, Paul S. |title=The Aetiology of Deep Venous Thrombosis: A Critical, Historical and Epistemological Survey |publisher=Springer |location=Berlin |year=2008 |pages=84 |isbn=1-4020-6649-X |oclc= |doi= |accessdate=}}</ref> | |||
! Modern | |||
! Notes | |||
|- | |||
| Phenomena of interrupted [[blood]]-flow | |||
| "Stasis" or "[[venous stasis]]"<ref name="pmid15692260">{{cite journal |author=Lowe GD |title=Virchow's triad revisited: abnormal flow |journal=Pathophysiol. Haemost. Thromb. |volume=33 |issue=5-6 |pages=455–7 |year=2003 |pmid=15692260 |doi=10.1159/000083845 |url=http://content.karger.com/produktedb/produkte.asp?doi=10.1159/000083845&typ=pdf}}</ref> | |||
| The first category, alterations in normal [[blood]] flow, refers to several situations. These include [[turbulence]], [[stasis (medicine)|stasis]], [[mitral stenosis]], and [[varicose veins]]. The equivalence of [[Virchow's triad|Virchow's]] version and the modern version has been disputed.<ref name="urlFurther reflections on Virchows triad. - Free Online Library">{{cite web |url=http://www.thefreelibrary.com/Further+reflections+on+Virchow%27s+triad.(Letter+to+the+Editor)-a0128075135 |title=Further reflections on Virchow's triad. - Free Online Library |format= |work= |accessdate=2009-02-10}}</ref> | |||
|- | |||
| 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,<ref name="pmid15692259">{{cite journal |author=Chung I, Lip GY |title=Virchow's triad revisited: blood constituents |journal=Pathophysiol. Haemost. Thromb. |volume=33 |issue=5-6 |pages=449–54 |year=2003 |pmid=15692259 |doi=10.1159/000083844 |url=http://content.karger.com/produktedb/produkte.asp?doi=10.1159/000083844&typ=pdf}}</ref> has numerous possible [[risk factors]] such as [[hyperviscosity]], deficiency of [[antithrombin]] III, [[nephrotic syndrome]], changes after severe [[Physical trauma|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=== | |||
* Normal [[homeostasis]] is maintained by the balance between the [[coagulation]] and [[fibrinolysis]] systems of the body. A [[homeostatic]] imbalance leads to the formation of a [[thrombus]] or [[hemorrhage]]. | |||
* 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 cell|red blood cells]], [[leukocyte|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 DVT can extend well into the [[iliac vein|iliac veins]] or [[inferior vena cava|the inferior vena cava]]. | |||
'''This video explains the process of thrombosis:''' | '''This video explains the process of thrombosis:''' | ||
Revision as of 15:38, 25 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Formation of the blood clot is called thrombosis. This process can happen in the artery and vein.
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[1] | Modern | Notes |
|---|---|---|
| Phenomena of interrupted blood-flow | "Stasis" or "venous stasis"[2] | 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.[3] |
| 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,[4] 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
- Normal homeostasis is maintained by the balance between the coagulation and fibrinolysis systems of the body. A homeostatic imbalance leads to the formation of a thrombus or hemorrhage.
- 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 DVT can extend well into the iliac veins or the inferior vena cava.
This video explains the process of thrombosis:
{{#ev:youtube|X_POCRsy7i4}}
References
- ↑ 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.