Table of Contents
There are several groups of anticoagulants, and each has a different mechanism of action! Some of the most commonly used are drugs such as heparin and coumarin.
This group of medications is usually administered to patients with myocardial infarction, venous thrombosis, peripheral arterial emboli and pulmonary emboli. Therefore, anticoagulants are not only extremely useful, but lifesaving because they are used to prevent transient ischemic attacks and to reduce the risk of recurrent myocardial infarction.
Overview of coagulation
Coagulation is an extremely complex, the simplest definition of which would be “a process by which blood forms solid clots”. It is part of a larger process called hemostasis, which prevents over-bleeding and death. That’s why disorders of coagulation can lead to an increased risk of bleeding, clotting, embolism and death. Therefore coagulation can be seen as a vital process.
Coagulation is a fast process, initiated almost instantly after an injury to the blood vessel’s endothelium. Hemostasis, on the other hand, can be primary and secondary. Primary is done by hemostatic plug at the site of injury, and secondary hemostasis occurs simultaneously via coagulation factors which form fibrin.
Mechanism of clotting
A blood clot forms as a result of concerted action of some 20 different substances, mostly plasma glycoproteins. This extremely complex process can be divided into two different pathways, although their end result is the same:
- the intrinsic pathway
- the extrinsic pathway
The difference between these two pathways is in the composition of the proteins and their origin. The intrinsic pathway uses only factors that are soluble in plasma, while the extrinsic pathway consists of some factors that are insoluble in plasma.
Both pathways, after the initiation of coagulation, proceed through a common pathway by forming activated factor X. Factor II or Prothrombin is cleaved at two sites by factor Xa to yied thrombin which directly cleaves fibrinogen. There is a lot of fibrinogen in the blood, about 2-3% of plasma protein. Thrombin is important because it chemically changes arg-X peptide bond in fibrinogen to form soluble fibrin monomers. These monomers are the key of coagulation because they spontaneously aggregate to form a polymeric structure called "soft clot" which later turns into a more stable "hard clot" by the covalent cross-linking of neighboring fibrin molecules.
Below are listed most blood coagulation factors along with their most important function in the chain of coagulation:
Forms clot (fibrin)
Its active form (IIa) activates I, V, VII, XIII, protein C, platelets
Tissue Factor or thromboplastin
Co-factor of VIIa (formerly known as factor III)
Required for coagulation factors to bind to phospholipid (formerly known as factor IV)
Co-factor of X with which it forms the prothrombinase complex
Activates IX, X
Antihemophilic A factor
Co-factor of IX with which it forms the tenase complex
Antihemophilic B factor or Christmas factor
Activates X: forms tenase complex with factor VIII
Stuart or Stuart-Prower factor
Activates II: froms prothrombinase complex with factor V
Plasma thomboplastin antecedent
Activates XII, IX and prekallikrein
Hageman factor, contact factor
Activates prekallikrein and fibrinolysis
Fibrin stabilizing factor
Activates XII and prekallikrein; cleaves HMWK
Supports reciprocal activation of XII, XI, and prekallikrein