13 Clotting Factors| 3 Pathways Blood Coagulation |Hemostasis

                                                 Blood Coagulation

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In this article, I will discuss blood coagulation, the factors responsible for coagulation, the coagulation mechanism, and more.

Keywords: Blood coagulation| Platelets| kallikrein| fibrinogen| Clot retraction| von-Willebrand| thrombosthein| primary |secondary|hemostasis

Table of contents

1.	Definition
2	Hemostasis
3.	Clotting factors
4.	Mechanism
5.	Pathways

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Introduction: 

Blood coagulation is the process of blood clotting in which liquid blood is transformed into a gel-forming blood clot.  It is very effective in hemostasis-preventing bleeding. Platelets are the primary cells in hemostasis. The mechanism of coagulation involves:

At cellular levels:

1.  activation of Platelets

2.  adhesion of Platelets

3.  aggregation of Platelets

At the biochemical level:

4. and deposition of Fibrin by the process of blood coagulation.

Coagulation

When a blood vessel is injured, coagulation begins instantly.  he endothelium is damaged, and subendothelial tissues are exposed.  lood contacts the subendothelial tissues of the vessel wall and initiates two mechanisms: cellular and chemical.

1.  Cellular -> Platelets are activated, and

2.  Chemical: changes in clotting factors.

Immediately after an injury, a platelet plug is formed at the injury site, known as primary hemostasis.  This temporary blockage is vital for hemostasis, and platelets play an essential role.

When there is a breach in the continuity of the blood vessel wall, platelets begin to adhere to the subendothelial surface. Platelets bind to collagen with collagen-specific Glycoprotein Ia /IIa surface receptors. The endothelium and platelets release the von Willebrand factor.  The GP1b receptors on the platelet surface interact with the von Willebrand factor A1 domain. Von-Willebrand factor forms additional links between glycoprotein 1b/IX/V and the A1 domain.

Adding platelet glycoprotein V1 to collagen activates platelet integrins, which mediate the tight binding of platelets to extracellular tissues.

The von Willebrand factor is released from

1.  The exposed endothelium of the blood vessels and

2.  The platelets.

 This adherence is due to the von Willebrand factor in the blood.  This factor binds the platelet to the subendothelial surface of the blood vessel.  As a result, platelets liberate many chemicals present in platelet granules.  ADP, serotonin, platelet-activating factor (PAF), platelet factor 4, and thromboxane A2 (TXA2) attract and aggregate other platelets.

In addition, these chemicals activate a Gq-linked protein receptor, which increases calcium ions in the platelet.  The calcium activates protein kinase  C, which activates phospholipase A2.

The platelet integrin membrane glycoprotein IIb/IIIa affinity to fibrinogen increases.

There is a difference between adherence and aggregation. Adherence is between platelet and subendothelial tissue. Aggregation occurs between the platelets.

The platelets liberate thrombosthein, an actin-myosin-like protein.  In addition, many platelets aggregate and are joined by Fibrin in the blood.  The fibrin threads act as a molecular glue.  This forms a soft white platelet plug and provides temporary blockage at the damaged site. This is also known as the white plug.  In one minute, the first Fibrin appears among the platelets. After several minutes, the platelet plug is entirely formed by Fibrin. Their blood cells, especially red blood cells, adhere to this white platelet plug, which converts to red.

2.  The clot formation chemical starts simultaneously to form Fibrin, which strengthens the white plug.

Arbitrarily, the coagulation process is divided into two pathways based on laboratory tests.   The intrinsic pathway starts with clotting using glass, and the extrinsic pathway begins with mixing thromboplastin, a mixture of tissue factors and phospholipids.

The coagulation process begins with two pathways, leading to a common path of fibrin formation.

   J Intrinsic pathway or contact activation pathway: activated by contact.

  J  Extrinsic pathway or tissue factor pathway: The primary main pathway activated by tissue factors and

 J Common pathway.

The process of coagulation is an oversimplification of a highly complex mechanism.

The pathways are a series of reactions.  First, an inactive enzyme precursor (the zymogen of a serine protease and its glycoprotein co-factor ) is converted into an active form. This stimulates the subsequent response in the cascade, ultimately forming Fibrin.

One point worth recitation is that a few factors produce many following factors. A small amount of a factor is activated, which activates a large quantity of subsequent inactive factors.  This is a cascade of amplification reactions.

Coagulation Factors

Thirteen factors responsible for blood coagulation are designated by Roman numerals according to the recommendations of an International committee, which indicates their historical sequence.

Blood clotting factors.

International Nomenclature	Name
Factor  I	Fibrinogen
Factor II	Prothrombin
Factor III	Thromboplastin or tissue factor
Factor IV	Ionic calcium
Factor V	Labile factor
Factor VI
Factor VII	Proconvertin or autoprothrombin I
Factor VIII	Antihemophilic factors
Factor IX	Christmas factor or autoprothrombin II
Factor X	Stuart Prower factor/ autoprothrombin C
Factor XI	Plasma thromboplastin antecedent (PTA)
Factor XII	Hageman factor or contact factor
Factor XIII	Fibrin stabilizing factor or Laki-Lorand factor

Two other factors have been added recently

1. Fletcher factor =prekallikrein

2. Fitzegerald factor

All factors are produced in the liver except for Ca++ and Tissue factor III, so advanced liver diseases have a bleeding tendency.

Tissue factors V and VIII are glycoproteins and factor XIII is a transglutaminase.

 Clot retraction occurs due to the contraction of thrombosthenin present in platelets. Therefore, the compacted clot is the more effective hemostatic plug.

Extrinsic pathway =Tissue factor pathway

When a blood vessel is damaged, factor VII comes in contact with the Tissue factor and forms activated complex TF-VIIa.This activates factors IX and X.

Factor Xa and factor Va form Prothrmbinase complex or prothrombin activator, which converts prothrombin II  to its active form –Thrombin.   

The thrombin-a proteolytic enzyme converts soluble plasma protein fibrin into insoluble Fibrin.

Intrinsic pathway=Contact activation pathway

The contact pathway begins with the formation of the kallikrein. First, Prekallikerin is converted into kallikrein, and then factor XII gets converted into its active form XIIa.

Finally, XIIa converts XI into XIa.

XIa converts IX into IXa with VIIIa activating factor X to Xa.

Common Pathway

Mode of action

Thrombin cleavages the‘  'vinyl-glycine’ 'and in fibrinogen molecules, removing two polypeptides and forming a fibrin monomer.

       Main reactions are

1)          1) Fibronegen          to      Fibrin monomer.

2)          2) Fibrin monomer to       Fibrin polymer.

  3)  Fibrin polymer to insoluble Fibrin clot.

Clotting Mechanism

Functions of thrombin: 1.     Converts fibrinogen to fibrin 2.     Activates factors V, VIII, and XIII 3.     Inhibits protein C. Hey, let's connect on Twitter, Instagram, and Linkedin.  Follow me on Instagram @ bijaykprasad  Follow us on Twitter @BijayPr60250287   Follow me on YouTube: www.youtube.com/@dr bijayprasad4475                                                           @drbijaykvideo Please remember to follow and share this post.  lease follow me on learn-and-fly.co.in I am more enthusiastic, and you can get new insights from my articles later. Learn More : 1.  About us 2.  Contact us 3.  Disclaimer 4.  Privacy Policy 5.  DMCA 6.  About Author andAdmin. Please submit your comments about this article.  The team will work hard to evaluate the statement and make appropriate corrections. Our help will improve the content. Thank you very much for reading. Appreciate your time with us.  If you enjoyed it, please leave a review or a comment.  our comments will encourage others to read.

Hashtag: Blood coagulation# Platelets#  kallikrein# fibrinogen# Clot retraction # von-Willebrand#  thrombosthein

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