Coagulation

blood clottingblood coagulationclottingclotting factorscoagulation cascadecoagulatecoagulation factorclotting factorcoagulation factorscoagulant
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot.wikipedia
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Thrombus

blood clotblood clotsclot
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot.
A thrombus, colloquially called a blood clot, is the final product of the blood coagulation step in hemostasis.

Blood

human bloodhematologicaloxygen consumption
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot.
Platelets are important in the clotting of blood.

Hemostasis

haemostasishemostaticstop bleeding
It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair.
This involves coagulation, blood changing from a liquid to a gel.

Factor VII

factor VIIaVIIcoagulation factor VII
Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma factor VII, which ultimately leads to cross-linked fibrin formation.
Factor VII (, blood-coagulation factor VIIa, activated blood coagulation factor VII, formerly known as proconvertin) is one of the proteins that causes blood to clot in the coagulation cascade.

Integrin

integrinsintegrin receptorintegrin alpha1
PLA 2 then modifies the integrin membrane glycoprotein IIb/IIIa, increasing its affinity to bind fibrinogen.
signal platelets to initiate an interaction with coagulation factors).

Bruise

bruisingcontusionbruises
Disorders of coagulation are disease states which can result in hemorrhage, bruising, or thrombosis.
Disease states such as insufficient or malfunctioning platelets, other coagulation deficiencies, or vascular disorders, such as venous blockage associated with severe allergies can lead to the formation of purpura which is not to be confused with trauma-related bruising/contusion.

Thrombin

prothrombinIIFactor II
The main role of the tissue factor pathway is to generate a "thrombin burst", a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly.
Prothrombin (coagulation factor II) is proteolytically cleaved to form thrombin in the clotting process.

Platelet factor 4

CXCL4PF4platelet factor-4
The granules include ADP, serotonin, platelet-activating factor (PAF), vWF, platelet factor 4, and thromboxane A 2 (TXA 2 ), which, in turn, activate additional platelets.
This chemokine is released from alpha-granules of activated platelets during platelet aggregation, and promotes blood coagulation by moderating the effects of heparin-like molecules.

Fibrin

defibrinatedfibrin modulating agentsfibrins
The mechanism of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of fibrin.
Excessive generation of fibrin due to activation of the coagulation cascade leads to thrombosis, the blockage of a vessel by an agglutination of red blood cells, platelets, polymerized fibrin and other components.

Tenase

tenase" complex
Factor XIa activates FIX, which with its co-factor FVIIIa form the tenase complex, which activates FX to FXa.
In coagulation, the procoagulant protein factor X can be activated into factor Xa two ways; extrinsically or intrinsically.

Contact activation system

contact activation pathway
The contact activation pathway begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor).
In the contact activation system or CAS, three proteins in the blood, factor XII (FXII), prekallikrein (PK) and high molecular weight kininogen (HK), bind to a surface and cause blood coagulation and inflammation.

High-molecular-weight kininogen

kininogen, high-molecular-weightHMWKFitzgerald factor
The contact activation pathway begins with formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and FXII (Hageman factor).
High-molecular-weight kininogen (HMWK or HK) is a circulating plasma protein which participates in the initiation of blood coagulation, and in the generation of the vasodilator bradykinin via the kallikrein-kinin system.

Tissue factor

CD142coagulation factor IIIF3
Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma factor VII, which ultimately leads to cross-linked fibrin formation. The main role of the tissue factor pathway is to generate a "thrombin burst", a process by which thrombin, the most important constituent of the coagulation cascade in terms of its feedback activation roles, is released very rapidly.
The best known function of tissue factor is its role in blood coagulation.

Endothelium

endothelialendothelial cellsendothelial cell
Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the blood vessel.

Vitamin K

KMenaquinoneVitamin K 1
Vitamin K is an essential factor to a hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z.
The human body requires vitamin K for complete synthesis of certain proteins that are needed for blood coagulation (K from Koagulation, Danish for "coagulation") or for controlling binding of calcium in bones and other tissues.

Glycoprotein IIb/IIIa

GPIIb/IIIaplatelet glycoprotein gpiib-iiia complexglycoprotein IIb/IIIa (GpIIb/IIIa)
PLA 2 then modifies the integrin membrane glycoprotein IIb/IIIa, increasing its affinity to bind fibrinogen.
It is a receptor for fibrinogen and von Willebrand factor and aids platelet activation.

Thrombophilia

hypercoagulabilityhypercoagulable statehypercoagulable
Quantitative or qualitative deficiency of either (protein C or protein S) may lead to thrombophilia (a tendency to develop thrombosis).
Thrombophilia (sometimes hypercoagulability or a prothrombotic state) is an abnormality of blood coagulation that increases the risk of thrombosis (blood clots in blood vessels).

Prothrombinase

prothrombinase complexfragment 1+2Prothrombin fragment 1+2
The activation of thrombin is a critical reaction in the coagulation cascade, which functions to regulate hemostasis in the body.

Antithrombin

antithrombin IIIantithrombin III deficiencySERPINC1
Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa.
Antithrombin (AT) is a small protein molecule that inactivates several enzymes of the coagulation system.

Warfarin

CoumadinAthrombinAthrombin-K
Vitamin K epoxide reductase is pharmacologically important as a target of anticoagulant drugs warfarin and related coumarins such as acenocoumarol, phenprocoumon, and dicumarol.
Warfarin decreases blood clotting by blocking an enzyme called vitamin K epoxide reductase that reactivates vitamin K 1.

Protein Z

PROZZ
Vitamin K is an essential factor to a hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z.
Protein Z is a member of the coagulation cascade, the group of blood proteins that leads to the formation of blood clots.

Thrombomodulin

CD141THBDBDCA-3
Thrombin functions not only to convert fibrinogen to fibrin, it also activates Factors VIII and V and their inhibitor protein C (in the presence of thrombomodulin); and it activates Factor XIII, which forms covalent bonds that crosslink the fibrin polymers that form from activated monomers.
It reduces blood coagulation by converting thrombin to an anticoagulant enzyme from a procoagulant enzyme.

Transglutaminase

transglutaminasesTGMtransglutaminases (TGs
Tissue factor, FV and FVIII are glycoproteins, and Factor XIII is a transglutaminase.
The exact biochemical activity of transglutaminases was discovered in blood coagulation protein factor XIII in 1968.

Serpin

serine protease inhibitorSerpinsserine protease inhibitors
Antithrombin is a serine protease inhibitor (serpin) that degrades the serine proteases: thrombin, FIXa, FXa, FXIa, and FXIIa.
Protease inhibition by serpins controls an array of biological processes, including coagulation and inflammation, and consequently these proteins are the target of medical research.

Heparan sulfate

heparan sulfate proteoglycanheparan sulphateheparin sulfate
It is constantly active, but its adhesion to these factors is increased by the presence of heparan sulfate (a glycosaminoglycan) or the administration of heparins (different heparinoids increase affinity to FXa, thrombin, or both).
It is in this form that HS binds to a variety of protein ligands, including Wnt, and regulates a wide range of biological activities, including developmental processes, angiogenesis, blood coagulation, abolishing detachment activity by GrB (Granzyme B), and tumour metastasis.