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[[Ficheiro:Thrombocyteaggregation.jpg|miniatura|Agregación de [[trombocito]]s (plaquetas). O plasma humano rico en plaquetas (vial esquerdo) é un líquido túrbido. Coa adición de [[Adenosín difosfato|ADP]], as plaquetas son activadas e empezan a agregarse, formando unha especie de folerpas brancas (vial da dereita)]]
A hemostase ocorre cando o sangue sae fóra dos vasos sanguíneos. É unha resposta do corpo pra deter a perda de sngue. Durante a hemostase sucédense rapidamente tres etapas. A primeira resposta é o espasmo muscular na que os vasos se constrinxen pasrsa diminuír o fluxo de sangue. No segundo paso prodúcese a formación do tapón, no cal as plaquetas se pegan uns a outras para formar un selo temporal para cubrir a rotura da parede do vaso. O terceiro e último paso denomínase coagulación. A coagulación reforza o tapón plaquetario con febras de [[fibrina]] que actúa como "pegamento molecular".<ref name=marieb/> As plaquetas son fundamentais no proceso da hemostase. Permiten a creación do "tapón plaquetario" que se forma case inmediatamente despois da rotura do vaso. Poucos segundos despois de que se produce a rotura do vaso snguíneo as plaquetas emoezan a adherirse á superficie do sub[[endotelio]]. Tarda aproximadamente sesenta segundos ata que as primeiras febras de fibrina empezan a entretecerse entre a ferida. Pasados varios minutos o tapón plaquetario está completamente formado por fibrina.<ref>Boon, G. D. "An Overview of Hemostasis." Toxicologic Pathology 21.2 (1993): 170-79.</ref> A hemostase mantense no corpo por tres mecanismos:
#'''[[Espasmo vascular]] (vasoconstrición) -''' A vasoconstrición é causada polas [[músculo liso|células musculares lisas]] vasculares, e é a primeira resposta do vaso sanguíneo ante a lesión. As células do músculo liso son controladas polo endotelio vascular, que libera sinais intravasculares para controlar as propiedades contráctiles do músculo. Cano o vaso está danado, prodúcese un reflexo inmediato, iniciado polos receptores da dor simpáticos locais, que axuda a promover a vasoconstrición. Os vasos danados contráense (vasoconstrición), que reduce a cantidade de fluxo sanguíneo na zona e limita a perda de sangue. O [[coláxeno]] queda exposto no sitio da lesión, o coláxeno promove que as plaquetas se adhiran ao sitio do dano. As plaquetas liberan [[gránulo (bioloxía)|gránulos]] citoplasmáticos que conteñen [[serotonina]], [[ADP]] e [[tromboxano A2]], todos os cales incrementan o efecto vasoconstritor. A resposta do espasmo é máis efectiva a medida que a cantidade de danos aumenta. O espasmo vascular é moito máis efectivo nos vasos sanguíneos pequenos.<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|isbn=|location=Philadelphia|pages=300}}</ref><ref>{{Cite book|title=Essentials of pathophysiology for pharmacy|last=Zdanowicz|first=M|publisher=CRC Press|year=2003|isbn=|location=Florida|pages=23}}</ref>
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#'''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|url=|journal=Arteriosclerosis, Thrombosis, and Vascular Biology|doi=10.1161/ATVBAHA.110.207522|pmid=|access-date=|volume=30|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 [[Fibrin]] from inactive fibrinogen plasma protein. Thus, a [[Fibrin]] mesh is produced all around the platelet plug to hold it in place; this step is called "Secondary Hemostasis". During this process some red and white blood cells are trapped in the mesh which causes the primary hemostasis plug to become harder: the resultant plug is called as 'thrombus' or 'Clot'. Therefore 'blood clot' contains secondary hemostasis plug with blood cells trapped in it. Though this is often a good step for [[wound healing]], it has the ability to cause severe health problems if the thrombus becomes detached from the vessel wall and travels through the circulatory system; If it reaches the brain, heart or lungs it could lead to [[stroke]], [[heart attack]], or [[pulmonary embolism]] respectively. However, without this process the healing of a wound would not be possible.<ref name="marieb" />
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