{{Short description|Process of preventing and stopping bleeding}}{{Distinguish|homeostasis}}

In [[biology]], '''Hemostasishemostasis''' [[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]]. This involves [[coagulation]], blood changing from a liquid to a gel. Intact blood vessels are central to moderating 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 endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete [[von Willebrand factor]], which initiate the maintenance of hemostasis after injury. Hemostasis hasinvolves three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a [[platelet plug]], and 3) blood coagulation, or formation of a fibrin clot. These processes seal the hole until tissues are repaired.

The word ''hemostasis'' ({{IPAc-en|ˌ|h|iː|m|oʊ-|ˈ|s|t|eɪ|s|ᵻ|s|}},{{refn|{{MerriamWebsterDictionary|accessdateaccess-date=2016-01-21|hemostasis}}}}{{refn|{{OxfordDictionariesCite dictionary |url=http://www.lexico.com/definition/hemostasis |accessdatearchive-url=2016https://web.archive.org/web/20200322184242/https://www.lexico.com/definition/haemostasis |url-01status=dead |archive-21date=2020-03-22 |title=hemostasis |dictionary=[[Lexico]] UK English Dictionary |publisher=[[Oxford University Press]]}} }} ''sometimes'' {{IPAc-en|ˌ|h|iː|ˈ|m|ɒ|s|t|ə|s|ᵻ|s}}) uses the [[classical compound|combining forms]] ''{{nowrap|[[wikt:hemo-#Prefix|''hemo-]]'']]}} and ''{{nowrap|[[wikt:-stasis#Suffix|''-stasis]]'']]}}, [[New Neo-Latin]] from [[Ancient Greek]] {{lang|grc|αἱμο-}} ''{{lang|grc-Latn|haimo-''}} (akinsimilar to {{lang|grc|αἷμα}} ''{{lang|grc-Latn|haîma''}}), meaning "blood", and {{lang|grc|στάσις}} {{lang|grc-Latn|stásis}}, meaning "[[wikt:stasis#Noun|stasis]]", yielding "motionlessness or stopping of blood".

[[File:Thrombocyteaggregation.jpg|thumb|Aggregation of [[thrombocytesthrombocyte]]s (platelets). Platelet-rich human blood plasma (left vial) is a turbid liquid. Upon addition of [[Adenosine diphosphate|ADP]], platelets are activated and start to aggregate, forming white flakes (right vial)]]

Hemostasis occurs when blood is present outside of the body or blood vessels. It is the innate response for the body to stop bleeding and loss of blood. During hemostasis three steps occur in a rapid sequence. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. In the second step, platelet plug formation, [[platelets]] stick together to form a temporary seal to cover the break in the vessel wall. The third and last step is called coagulation or blood clotting. Coagulation reinforces the platelet plug with fibrin threads that act as a "molecular glue".<ref name=marieb/> Platelets are a large factor in the hemostatic process. They allow for the creation of the "platelet plug" that forms almost directly after a blood vessel has been ruptured. Within seconds of a blood vessel's epithelial wall being disrupted, platelets begin to adhere to the sub-[[endothelium]] surface. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes the platelet plug is completely formed by fibrin.<ref>Boon, G. D. "An Overview of Hemostasis." Toxicologic Pathology 21.2 (1993): 170-79170–179.</ref> Hemostasis is maintained in the body via three mechanisms:

# '''[[Vascular spasm]] (Vasoconstriction) -:''' 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|isbn=|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|isbn=|location=Florida|pagespage=[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 [[Vonvon 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=21071698|access-date=|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 [[Fibrinfibrin]] from inactive fibrinogen plasma protein. Thus, a [[Fibrin]]fibrin mesh is produced all around the platelet plug to hold it in place; this step is called "Secondary''secondary Hemostasis"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 asa '[[thrombus']] or 'Clot'blood clot. Therefore,The 'blood clot' contains the secondary hemostasis plug with blood cells trapped in it. Though thisThis is often a goodnecessary step for [[wound healing]], but 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" />

Hemostasis can be achieved in various other ways if the body cannot do it naturally (or needs help) during surgery or medical treatment. When the body is under shock and stress, hemostasis is harder to achieve. Though natural hemostasis is most desired, having other means of achieving this is vital for survival in many emergency settings. Without the ability to stimulate hemostasis the risk of [[hemorrhaging]] is great. During surgical procedures, the types of hemostasis listed below can be used to control bleeding while avoiding and reducing the risk of tissue destruction. Hemostasis can be achieved by [[chemical agents|chemical agent]] as well as mechanical or physical agents. Which hemostasis type used is determined based on the situation.<ref name=roshni>{{cite journal | author = Kulkarni Roshni | year = 2004 | title = Alternative and Topical Approaches to Treating the Massicely Bleeding Patient | url = httphttps://www.clinicaladvances.com/article_pdfs/ho-article-200407-hem.pdf | format = PDF | journal = Advances in Hematology | volume = 2 | issue = 7 | pages = 428–31428–431 | access-date = 2012-04-26 | archive-url = https://web.archive.org/web/20090106061129/httphttps://www.clinicaladvances.com/article_pdfs/ho-article-200407-hem.pdf | archive-date = 2009-01-06 | url-status = dead }}</ref>

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The body's hemostasis system requires careful regulation in order to work properly. If the blood does not clot sufficiently, it may be due to bleeding disorders such as [[hemophilia]] or [[immune thrombocytopenia]]; this requires careful investigation. Over-active clotting can also cause problems; [[thrombosis]], where blood clots form abnormally, can potentially cause [[embolisms]], where blood clots break off and subsequently become lodged in a vein or artery.{{cn|date=November 2021}}

The process of preventing blood loss from a vessel or organ of the body is referred to as hemostasis. The term comes from the [[Ancient Greek]] roots "heme" meaning blood, and "stasis" meaning halting; Put together means the "halting of the blood".<ref name=marieb>{{cite book|last1=Marieb|first1=Elaine Nicpon|first2=Katja|last2=Hoehn|title=Human Anatomy & Physiology|edition=8th|location=San Francisco|publisher=Benjamin Cummings|year=2010|pages=649–50649–650}}</ref>

The origin of hemostasis dates back as far as ancient Greece; first referenced to being used in the [[Battle of Troy]]. It started with the realization that excessive bleeding inevitably equaled death. Vegetable and mineral styptics were used on large wounds by the Greeks and Romans until the takeover of Egypt around 332BC by Greece. At this time many more advances in the general medical field were developed through the study of Egyptian [[mummification]] practice, which led to greater knowledge of the hemostatic process. It was during this time that many of the veins and arteries running throughout the human body were found and the directions in which they traveled. Doctors of this time realized if these were plugged, blood could not continue to flow out of the body. Nevertheless, it took until the invention of the printing press during the fifteenth century for medical notes and ideas to travel westward, allowing for the idea and practice of hemostasis to be expanded.<ref name=weis>{{Cite journal|title=Wies, C. H. "The History of Hemostasis." Yale Journal of Biology and Medicine 2|year=1929|pages=167–68167–168|pmc=2606227|last1=Wies|first1=C. H.|journal=The Yale Journal of Biology and Medicine|volume=2|issue=2}}</ref>

There is currently a great deal of research being conducted on hemostasis. The most current research is based on genetic factors of hemostasis and how it can be altered to reduce the cause of [[genetic disorders]] that alter the natural process hemostasis.<ref>{{cite journal |last1=Rosen |first1=Elliot D. |last2=Xuei |first2=Xiaoling |last3=Suckow |first3=Mark |last4=Edenberg |first4=Howard |date=2006 |title=Searching for hemostatic modifier genes affecting the phenotype of mice with very low levels of FVII |journal=Blood Cells, Molecules and Diseases |volume=36 |issue=2 |pages=131–134 |doi=10.1016/j.bcmd.2005.12.037|pmid=16524747 }}</ref>

[[Von Willebrand disease]] is associated with a defect in the ability of the body to create the platelet plug and the fibrin mesh that ultimately stops the bleeding. New research is concluding that the von Willebrand disease is much more common in adolescence. This disease negatively hinders the natural process of Hemostasis causing excessive bleeding to be a concern in patients with this disease. There are complex treatments that can be done including a combination of therapies, [[estrogen]]-[[progesterone]] preparations, [[desmopressin]], and Von Willebrand factor concentrates. Current research is trying to find better ways to deal with this disease; however, much more research is needed in order to find out the effectiveness of the current treatments and if there are more operative ways to treat this disease.<ref name="mikhail">{{cite journal |last1=Mikhail |first1=Sameh |last2=Kouides |first2=Peter |date=December 2010 |title=von Willebrand Disease in the Pediatric and Adolescent Population |journal=Journal of Pediatric &and Adolescent Gynecology |volume=23 |issue=6 |pages=S3–S10 |doi=10.1016/j.jpag.2010.08.005|pmid=20934894 }}</ref>

* Blood tests:

* [[Prothrombin time]]

* [[Partial thromboplastin time]]