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{{Short description|Process of preventing and stopping bleeding}}{{Distinguish|homeostasis}}
In [[biology]], '''hemostasis''' [[American and British English spelling differences#ae and oe|or]] '''haemostasis''' is a process to prevent and stop [[bleeding]], meaning to keep [[blood]] within a damaged [[blood vessel]] (the opposite of hemostasis is [[Bleeding|hemorrhage]]). It is the first stage of [[wound healing]].
* [[vasoconstriction]]
* temporary blockage of a hole in a damaged blood vessel by a [[platelet plug]]
* [[coagulation|blood coagulation]] (formation of [[fibrin]] clots)
Coagulation, the changing of blood from a liquid to a [[gel]] which forms the fibrin clots, is essential to hemostasis. Intact blood vessels moderate blood's tendency to form [[thrombus|clots]]. The [[endothelium|endothelial]] cells of intact vessels prevent blood clotting with a heparin-like molecule and [[thrombomodulin]], and prevent platelet aggregation with [[nitric oxide]] and [[prostacyclin]]. When endothelium of a blood vessel is damaged, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete [[von Willebrand factor]], which initiates the maintenance of hemostasis after injury. These processes seal the injury or hole until tissues are healed.
==Etymology and pronunciation==
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# '''[[Vascular spasm]]:''' Vasoconstriction is produced by vascular smooth muscle cells, and is the blood vessel's first response to injury. The smooth muscle cells are controlled by vascular endothelium, which releases intravascular signals to control the contracting properties. When a blood vessel is damaged, there is an immediate reflex, initiated by local sympathetic [[pain receptors]], which helps promote vasoconstriction. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss. Collagen is exposed at the site of injury, the collagen promotes platelets to adhere to the injury site. Platelets release cytoplasmic granules which contain serotonin, ADP and thromboxane A2, all of which increase the effect of vasoconstriction. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective in smaller blood vessels.<ref name=":0">{{Cite book|title=The Surgical Review: An Integrated Basic and Clinical Science Study Guide|last=Alturi|first=Pavan|publisher=Lippincott Williams & Wilkins.|year=2005|location=Philadelphia|pages=300}}</ref><ref>{{Cite book|title=Essentials of pathophysiology for pharmacy|url=https://archive.org/details/essentialspathop00zdan|url-access=limited|last=Zdanowicz|first=M|publisher=CRC Press|year=2003|location=Florida|page=[https://archive.org/details/essentialspathop00zdan/page/n41 23]|isbn=9781587160363 }}</ref>
# '''Platelet plug formation:''' [[Platelet]]s adhere to damaged endothelium to form a platelet plug (''primary hemostasis'') and then degranulate. This process is regulated through [[thromboregulation]]. Plug formation is activated by a [[glycoprotein]] called [[von Willebrand factor]] (vWF), which is found in [[Blood plasma|plasma]]. Platelets play one of major roles in the hemostatic process. When platelets come across the injured endothelium cells, they change shape, release granules and ultimately become ‘sticky’. Platelets express certain receptors, some of which are used for the adhesion of platelets to collagen. When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and adhesion. Platelets release cytoplasmic granules such as [[adenosine diphosphate]] (ADP), [[serotonin]] and [[thromboxane A2]]. Adenosine diphosphate (ADP) attracts more platelets to the affected area, serotonin is a vasoconstrictor and thromboxane A2 assists in platelet aggregation, vasoconstriction and degranulation. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process in a [[positive feedback]] loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis. This is referred to as primary hemostasis.<ref name=":0" /><ref>{{Cite journal|last=Li|first=Zhenyu|date=11 Nov 2010|title=Signaling during platelet adhesion and activation|journal=Arteriosclerosis, Thrombosis, and Vascular Biology|doi=10.1161/ATVBAHA.110.207522|pmid=21071698|volume=30|issue=12|pages=2341–2349|pmc=3085271}}</ref>
# '''Clot formation:''' Once the platelet plug has been formed by the platelets, the [[clotting factors]] (a dozen proteins that travel along the blood plasma in an inactive state) are activated in a sequence of events known as 'coagulation cascade' which leads to the formation of [[
==Types==
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