Gerinnungssystem/en: Unterschied zwischen den Versionen
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The [[Blut/en|blood]] taken from the [[Blutgefäße/en|blood vessels]] "coagulates" spontaneously in the test tube within a few minutes. The blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to coagulate outside the [[Gefäßsystem/en|vascular system]] is an extremely vital process whose importance lies in protecting the body from loss of its blood fluid. | The [[Blut/en|blood]] taken from the [[Blutgefäße/en|blood vessels]] "coagulates" spontaneously in the test tube within a few minutes. The blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to coagulate outside the [[Gefäßsystem/en|vascular system]] is an extremely vital process whose importance lies in protecting the body from loss of its blood fluid. | ||
| + | [[Blood/en|blood]] taken from [[Blutgefäße/en|blood vessels]] "coagulates" spontaneously within a few minutes in the test tube. During this process, the blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to clot outside the [[Gefäßsystem/en|vascular system]] is an extremely vital process, the importance of which lies in protecting the body from losing its blood fluid. | ||
| + | Blood clotting has several phases | ||
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| + | <div class="mw-translate-fuzzy"> | ||
The wound plug, initially composed solely of [[Thrombozyten/en|thrombocytes]], is not capable of permanently closing the injured vascular site. This is also a good thing, because otherwise such grafts could sometimes be formed too quickly. The complex coagulation system ensures that coagulation only takes place when it is really needed. | The wound plug, initially composed solely of [[Thrombozyten/en|thrombocytes]], is not capable of permanently closing the injured vascular site. This is also a good thing, because otherwise such grafts could sometimes be formed too quickly. The complex coagulation system ensures that coagulation only takes place when it is really needed. | ||
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| + | It is activated at the site of the injury at the same time as the complex platelet processes take place. Its clearly slower process ends in the formation of [[Fibrin/en|fibrin]] threads, which spin through the wound graft in a net-like manner and usually also deposit in the immediate vicinity of the graft, whereby abundant [[Erythrozyt/en|erythrocytes]] are included. | ||
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| − | + | Dazu werden sie durch wandständige Kollagenfasern, die in den Verletzungsbereich hineinragen, aktiviert. Die Aktivierung bedeutet, dass sie größer werden, dass sich aus ihrer Wand Ausläufer entwickeln und dass sie sich mit Hilfe einer Art Kleber an die Kollagenfasern anheften. Dabei aktivieren sie wiederum andere nahe Thrombozyten und entwickeln so einen Thrombozytenpropf, den sogenannte Primärthrombus. | |
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The final strength of the closure plug is achieved by the contraction of the platelets, which are "felted" with their pseudopodia and fibrin threads. | The final strength of the closure plug is achieved by the contraction of the platelets, which are "felted" with their pseudopodia and fibrin threads. | ||
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This process, which normally takes 5 - 7 minutes (coagulation time), involves platelets as well as a large number of plasmatic factors. | This process, which normally takes 5 - 7 minutes (coagulation time), involves platelets as well as a large number of plasmatic factors. | ||
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The actual coagulation process - like primary haemostasis - is triggered by the vessel and tissue injury and activated in two different ways: | The actual coagulation process - like primary haemostasis - is triggered by the vessel and tissue injury and activated in two different ways: | ||
* exogenous or extravascular way ([[Extrinsic-System/en|Extrinsic System]]) | * exogenous or extravascular way ([[Extrinsic-System/en|Extrinsic System]]) | ||
* endogenous or intravascular way ([[Intrinsic-System/en|Intrinsic System]]) | * endogenous or intravascular way ([[Intrinsic-System/en|Intrinsic System]]) | ||
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On the exogenous path, activation takes place very quickly (within seconds), while on the endogenous path, activation takes place over a larger number of intermediate stages and takes longer (minutes). As a rule, both systems are involved in the normal coagulation process. The common final stage of the two activating systems finally makes [[Prothrombin/en|prothrombin]] (factor II) and [[Vitamin_K/en|vitamin K]] formed in the liver is converted into [[Thrombin/en|thrombin]]. The thrombin thus formed is an [[Enzym/en|enzyme]], which also synthesizes the [[Fibrinogen/en|fibrinogen]] (factor I) and thus initiates the formation of [[Fibrin/en|fibrin]]. | On the exogenous path, activation takes place very quickly (within seconds), while on the endogenous path, activation takes place over a larger number of intermediate stages and takes longer (minutes). As a rule, both systems are involved in the normal coagulation process. The common final stage of the two activating systems finally makes [[Prothrombin/en|prothrombin]] (factor II) and [[Vitamin_K/en|vitamin K]] formed in the liver is converted into [[Thrombin/en|thrombin]]. The thrombin thus formed is an [[Enzym/en|enzyme]], which also synthesizes the [[Fibrinogen/en|fibrinogen]] (factor I) and thus initiates the formation of [[Fibrin/en|fibrin]]. | ||
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https://en.wikipedia.org/wiki/Coagulation | https://en.wikipedia.org/wiki/Coagulation | ||
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| + | === Gerinnungskaskade === | ||
| + | Der eigentliche Gerinnungsprozess wird - wie die primäre Hämostase - durch die Gefäß- und Gewebsverletzung ausgelöst und auf zwei verschiedenen Wegen aktiviert: | ||
| + | *exogener oder extravaskulärer Weg ([[Extrinsic-System]]) - bei Gewebsverletzungen, schnelle Reaktion | ||
| + | *endogener oder intravasaler Weg ([[Intrinsic-System]]) - bei Verletzungen im Gefäß selbst, zum Beispiel [[Endothel]]veränderungen ([[Entzündung]]en, [[Arteriosklerose]]), langsame Reaktion | ||
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| + | Auf dem exogenen Weg erfolgt die Aktivierung also sehr schnell (innerhalb von Sekunden), während der Aktivierungsprozess auf dem endogenen Weg über eine größere Zahl von Zwischenstufen abläuft und längere Zeit (Minuten) benötigt. An dem normalen Gerinnungsablauf sind in der Regel beide Systeme ineinandergreifend beteiligt. Durch die gemeinsame Endstufe der beiden aktivierenden Systeme wird schließlich [[Prothrombin]] (Faktor II) und unter Mitwirkung von [[Vitamin K]] das in der Leber gebildet wird, in [[Thrombin]] umgewandelt. Das so entstandene Thrombin ist ein [[Enzym]], welches das gleichfalls in der Leber synthetisierte [[Fibrinogen]] (Faktor I) spaltet und damit die Bildung von [[Fibrin]] einleitet. | ||
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| + | Die Gerinnungskaskade sieht graphisch folgendermaßen aus: | ||
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| + | [[Datei:Gerinnungskaskade_neu.png]] | ||
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| + | Weitere Informationen: | ||
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| + | https://de.wikipedia.org/wiki/Hämostase | ||
Version vom 22. Februar 2022, 13:32 Uhr
The arrest of bleeding, also called blood clotting or hemostasis, is the ability of blood to provide closure to a wound.
The blood taken from the blood vessels "coagulates" spontaneously in the test tube within a few minutes. The blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to coagulate outside the vascular system is an extremely vital process whose importance lies in protecting the body from loss of its blood fluid.
blood taken from blood vessels "coagulates" spontaneously within a few minutes in the test tube. During this process, the blood changes from a liquid state to a gelatinous state with the participation of formed elements. The property of blood to clot outside the vascular system is an extremely vital process, the importance of which lies in protecting the body from losing its blood fluid. Blood clotting has several phases
The wound plug, initially composed solely of thrombocytes, is not capable of permanently closing the injured vascular site. This is also a good thing, because otherwise such grafts could sometimes be formed too quickly. The complex coagulation system ensures that coagulation only takes place when it is really needed.
It is activated at the site of the injury at the same time as the complex platelet processes take place. Its clearly slower process ends in the formation of fibrin threads, which spin through the wound graft in a net-like manner and usually also deposit in the immediate vicinity of the graft, whereby abundant erythrocytes are included.
Dazu werden sie durch wandständige Kollagenfasern, die in den Verletzungsbereich hineinragen, aktiviert. Die Aktivierung bedeutet, dass sie größer werden, dass sich aus ihrer Wand Ausläufer entwickeln und dass sie sich mit Hilfe einer Art Kleber an die Kollagenfasern anheften. Dabei aktivieren sie wiederum andere nahe Thrombozyten und entwickeln so einen Thrombozytenpropf, den sogenannte Primärthrombus.
The final strength of the closure plug is achieved by the contraction of the platelets, which are "felted" with their pseudopodia and fibrin threads.
This process, which normally takes 5 - 7 minutes (coagulation time), involves platelets as well as a large number of plasmatic factors.
The actual coagulation process - like primary haemostasis - is triggered by the vessel and tissue injury and activated in two different ways:
- exogenous or extravascular way (Extrinsic System)
- endogenous or intravascular way (Intrinsic System)
On the exogenous path, activation takes place very quickly (within seconds), while on the endogenous path, activation takes place over a larger number of intermediate stages and takes longer (minutes). As a rule, both systems are involved in the normal coagulation process. The common final stage of the two activating systems finally makes prothrombin (factor II) and vitamin K formed in the liver is converted into thrombin. The thrombin thus formed is an enzyme, which also synthesizes the fibrinogen (factor I) and thus initiates the formation of fibrin.
Gerinnungskaskade
Der eigentliche Gerinnungsprozess wird - wie die primäre Hämostase - durch die Gefäß- und Gewebsverletzung ausgelöst und auf zwei verschiedenen Wegen aktiviert:
- exogener oder extravaskulärer Weg (Extrinsic-System) - bei Gewebsverletzungen, schnelle Reaktion
- endogener oder intravasaler Weg (Intrinsic-System) - bei Verletzungen im Gefäß selbst, zum Beispiel Endothelveränderungen (Entzündungen, Arteriosklerose), langsame Reaktion
Auf dem exogenen Weg erfolgt die Aktivierung also sehr schnell (innerhalb von Sekunden), während der Aktivierungsprozess auf dem endogenen Weg über eine größere Zahl von Zwischenstufen abläuft und längere Zeit (Minuten) benötigt. An dem normalen Gerinnungsablauf sind in der Regel beide Systeme ineinandergreifend beteiligt. Durch die gemeinsame Endstufe der beiden aktivierenden Systeme wird schließlich Prothrombin (Faktor II) und unter Mitwirkung von Vitamin K das in der Leber gebildet wird, in Thrombin umgewandelt. Das so entstandene Thrombin ist ein Enzym, welches das gleichfalls in der Leber synthetisierte Fibrinogen (Faktor I) spaltet und damit die Bildung von Fibrin einleitet.
Die Gerinnungskaskade sieht graphisch folgendermaßen aus:
Weitere Informationen: