Coagulation test is a process that causes blood clotting. This process, from both internal and external pathways, converts fibrinogen to fibrin, activates coagulation factors and aggregates platelets. Blood coagulation, although blood clots, stop bleeding, and the defect in the process is noticeable in diseases such as lethargic hemophilia, but involuntary coagulation of the bloodstream also affects the development of myocardial infarction and cerebral ischemia.
The mechanisms of clotting begin by damaging the vessel or surrounding tissues, or blood contact with damaged endothelial cells and collagen. In each case, these factors lead to the formation of prothrombin activator, which causes the conversion of prothrombin to thrombin and subsequent coagulation. Typically, the prothrombin activator is generated from two paths.
- External route
- Internal route
Due to damages to the arterial wall, the tissue factor is introduced into the vascular system. The tissue factor is capable of producing a stable, protein-rich protein called Factor VII, which requires phospholipid and calcium ion. Finally, the complex will activate the factor X and IX.
Fibrinogen (factor I)
Plasma proteins that coagulate in the pathway of coagulation and, when the blood is released, activates the thrombin enzyme into insoluble fibrin fibers and plays an important role in coagulation of blood. Fibrinogen is produced in the liver and its blood levels increase in conditions such as pregnancy and inflammation.
Prothrombin (Factor II)
Peru is an enzyme that acts on a coagulation pathway. Its biosynthesis is in the liver and is one of the important factors in coagulation of the blood. Prothrombin is in normal plasma at a concentration of about 15 mg / dL.
- Testing of prothrombin time (PT), sometimes called the INR, is a selective test for evaluating the external pathway and coagulation pathway and factors X, VII, V, II and I.
- ts natural value is 14-10 seconds.
- Blood coagulation time in liver disease, intake of blood-thinning drugs, vitamin K deficiency, decreased coagulation proteins. It also reduces the intake of vitamin K supplements or foods containing vitamin K and estrogen-containing drugs.
- The use of the International Normalized Ratio (INR) with PT Test is recommended for patients who are taking warfarin (Coumadine) diluent drugs.
The factor of factor (factor III, thromboplastin) accelerates the coagulation of the blood. This factor acts in the coagulation phenomenon by interacting with the factor VII in the outer coagulation pathway.
factor V, Proaccelerin
Factor V is required to activate prothrombin in the coagulation pathway. This factor is made in the liver and inaccessible in calcium-free plasma and quickly deactivated by EDTA and oxalate.
factor VII, Proconvertin
Factor VII is a serum protease that is linked to vitamin K synthesized in the liver and is part of the pathway of coagulation, which is measured by the time of prothrombin (PT). The bioavailable plasma of factor VII is about 3 to 6 hours. Lack of this factor leads to bleeding in susceptible individuals.
- Detection of congenital defect of coagulation factor VII
- Evaluation of Acquired Impairment with Hepatic Diseases, Oral Anticoagulation and Vitamin K Deficiency
- Determine the amount of warfarin antagonist associated with protein C levels.
- Prolonged prothrombin time study.
- Liver disease, vitamin K deficiency, and anticoagulant warfarin can reduce the activity of factor VII.
- In general, in heterozygous individuals, the activity level is> 50%. Homozygous individuals typically have activity levels of 20% and infants with a 25% activity level.
- In Factor VII deficiency, abnormal PT test and normal PTT test.
Factor VIII Activity Assay, Antihemophilic Factor
Factor VIII is a protein that is made in the liver and other tissues and has a half-life of 18-9 hours and is required on the internal coagulation pathway. In the internal pathway of complex coagulation, factors VIII and IX associated with calcium ions and platelet phospholipid ultimately activate the x-factor. The lack of this coagulation factor causes hemophilia A to occur.
- Diagnosis of von Willebrand disease, when the antigen and von Willebrand factor factor activity are measured with factor eight.
- Diagnosis of acquired factor VIII deficiency such as liver function disorders, diffuse intravascular coagulation (DIC).
- Investigate prolonged active thromboplastin time.
- Factor VIII specific antibodies are the most common coagulant inhibitors that can lead to severe bleeding.
- Typically, a liver patient will increase the level of factor VIII.
- Congenital deficiency of factor VIII may occur with factor 5 deficiency (V).
- Measuring factor 8 is not helpful in inferring carrier status in suspected female carriers of the Hemophilia gene. Unless the percentage of activity is less than 50% normal.
- Factor VIII decreases in von Willebrand’s disease.
In the absence of factor VIII, the normal prothrombin time and relative thromoblastin time are abnormal.
Von Willebrand factor
It is one of the acute phase proteins that plays an important role in hemostasis in the blood. This protein, which is essential for platelet adhesion, is produced by the intraperitoneal layer and megakaryocytes and vascular layers. This factor acts as a carrier protein for coagulation factor VII. Deficiency of this protein (VWF) in von Willebrand disease causes blood coagulation disorder. The von Willebrand disease is the most common hereditary bleeding disorder.
IX (Antihemophilic factor B or Christmas factor)
Factor IX, or a Christmas factor, is a serum protease with a molecular weight of about 57 kDa, which is made in the liver. The vitamin IX requires vitamin K to activate. Its half-life is 24-18 hours and operates on the internal co-ordination path.
- Diagnosis of coagulation factor IX, especially hemophilia B
- Evaluation of the effect of liver disease on homeostasis
- Investigate Long-Term Relative Thromboplastin Time.
The severity of hemophilia B depends on the activity of the factor IX.
PTT test (Relative Activated Thromboplastin Time)
- PTT is used to monitor heparin treatment.
- Selective test is to assess the internal and common pathway and factors I, II, V, VIII, IX, X, XI and XII.
- PTT is used to identify coagulation inhibitors of the internal and common pathway, such as lupus anticoagulant, and specific and non-specific factor inhibitors such as antiphospholipids.
Activated Clotting Time (ACT) and Total Clotting Time (CT)
ACT is used to measure the effect of heparin as an anticoagulant during cardiac angioplasty, hemodialysis, and cardiopulmonary bypass surgery. This test, like the aPPT, measures the ability of the internal pathway to initiate clot formation by activating factor XII. The use of ACT in detecting the appropriate amount of protamine sulfate needed to neutralize the effect of heparin after surgery and hemodialysis is very important.
Factor X or Stuart-Prowr Factor
Serum vitamin X is a vitamin K-linked protease factor that is produced in the liver. Its half-life is 48-24 hours. This factor is activated by products of both internal and external coagulation pathways. It plays a key role as a progeny for the formation of prothrombinase in a common way.
- Diagnosis of congenital and acquired coagulation factor X
- Evaluation of hemostatic activity in liver disease
- Investigate the active partial thromboplastin time and prolonged prothrombin time
- Congenital Factor X deficiency is rare.
- Acquired Factor X deficiency is associated with liver disease, warfarin therapy and vitamin K deficiency.
- Lack of factor X prolongs PT and PTT
- Acquired defect is more common than congenital defects.
Factor XI or precursor factor of thromoblastin, an anti-hemophilic factor C
Coagulation factor XI is synthesized in the liver and its half-life is 60 to 80 hours. The XI factor is a component of the internal coagulation pathway. It activates the inactive factor IX when activated. In the absence of factor XI, the timing of thromboplastin may be prolonged. Lack of this factor leads to a mild bleeding disorder. But there is a weak link between the level of activity of this factor and the amount of bleeding. Congenital deficiency of factor XI has a relatively high incidence of Jewish ascension (Hemophilia C) populations.
- Assessing the shortage of factor XI
- Hepatitis C diagnosis
- Study of the prolonged time of active thromboplastin time
- Reducing the amount of factor XI does not have a significant relationship with the risk of bleeding.
- Acquired deficiency of factor XI is associated with liver disease and rarely coagulation inhibitors.
- The deficiency of factor XI is the natural prothrombin time (PT) and the abnormal relative thromoblastin (PTT) time.
Factor XII or Hageman factor
The XII factor is made in the liver and has a half-50 to 40 hours. This factor is activated by contact with the external surface. Factor XII plays a role in the coagulation pathway and fibrinolysis system.
- Assessing the shortage of Factor XII
- Study of the prolonged time of active thromboplastin time
The factors of the quinine system
Two compositions of the Kinine Plasma System, called Prekallikrein, and High Molecular Weight Kininogen, play a vital role in the internal coagulation pathway. The quinine system is an enzymatic cascade and begins when a coagulation factor called XII factor is followed by vascular endothelium and vascular injury. Activating this system increases vascular permeability, inflammation, vascular dilation and pain.
Protein C and S (Protein C, S)
Protein C is an anticoagulant of vitamin K, which is made in the liver and has a half-life of 10-6 hours. Protein C is activated in the presence of endothelial cell cofactor (thrombomudolin), and the active protein C makes enzyme activity. Protein S is a glycoprotein, a protein bound to vitamin K, which is synthesized in the liver and acts as a protein factor C cofactor.
- As a preliminary test to evaluate suspected patients with congenital proteinuria deficiency, such as those with a history of a person or family history of vascular thrombosis.
- Detection and confirmation of congenital defects of C-type heterozygote protein (activity and protein C decreases) and type II (activity decreased, but normal).
- Diagnosis and confirmation of congenital homozygote protein C deficiency
- Lack of vitamin K, septic shock, intravascular coagulation, pulmonary embolism, liver disease, preterm labor, acute inflammation, autoimmune disease, acute thrombosis, and warfarin administration cause deficiency of these proteins.
- Protein-C and protein-S activity testing should be checked at the same time, because the protein C deficiency may be the cause of proteinuria deficiency.
- The anticoagulant activity of protein C, which is activated with protein S, is increased.
- Protein C deficiency is seen in hepatitis anticoagulant therapy.
- Pregnancy or the use of exogenous sex hormones is associated with lowering the protein C and S.
A group of plasma proteins that are coagulant-inhibitors of the blood. These proteins are produced by the liver and enter the bloodstream, and there are three types. Antithrombin III, by binding to the thrombin, inhibits thrombin and prevents fibrinogen conversion to fibrin. The half-life of antithrombin in plasma is three days. Antitrombin abnormalities that occur in both inherited and acquired forms cause intravascular thrombosis.
BT test (Bleeding time)
To evaluate platelet function. This test is often performed before surgery to ensure that the hemostasis is adequately controlled on patients. BT tests in von Willebrand disease and other inherited platelet function disorders, as well as in uremia and macroglobulinemia. In general, this test is not intended to diagnose or predict the risk of bleeding properly and reliably.
- PT (Prothrombin time)
- APTT (Activated Partial Thromboplastin Time)
- CT (Clotting time)
- BT (Bleeding time)
- Plasma Protein-C assay
- Plasma protein-S assay
- Plasma anti-thrombin III
- Factor V Leiden (APC-R)
- Plasma fibrinogen level
- Lupus Anticoagulant (Circulating Anticoagulant, CAC)
- dRVVT (Dilute Russell’s Viper Venom Time) mixing study
- Anti-Prothrombin (screen)
- Anti-β۲ glycoprotein-I (IgG & IgM)
- FDP plasma(Fibrin Degradation Products)
- Fibrin D-Dimer assay(Fibrin Degradation Fragment)
- Anti-Phospholipid (IgG & IgM)
- Anti-Cardiolipin (IgG & IgM)