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Research on the Coagulation Cascade

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Hemostasis is the process that occurs when a blood vessel ruptures and large amounts of plasma and formed elements may escape (Bostwick and Wingerd, 2013). It can be divided into primary and secondary hemostasis. Primary hemostasis includes platelet and vascular response that is activated by small injuries to blood vessels or damaged endothelial cells (Rodak, Fritsma and Doig, 2007). Shortly after the initiation of primary hemostasis, secondary hemostasis is activated with the aim of stabilizing the blood clot to prevent dislodgement. The process involves attracting additional platelets to the clot and using clotting factor fibrin to provide a firm and insoluble matrix of fibers in the clot. Secondary hemostasis begins with the activation of the coagulation cascade, a series of clotting factors or protein that change form, thereby activating the next step in the cascade.

The final product in this cascade is the cross-linked fibrin that forms the solid matrix which stabilizes the clot (Beebe and Myers, 2011).

The coagulation cascade is divided into the intrinsic and extrinsic pathway, that converges in a common pathway.

The coagulation cascade is typically assessed by measurement of the prothrombin time (PT) and activated thromboplastin time (aPTT). These tests provide a rapid way of detecting significant deficiencies in the extrinsic, intrinsic and common pathway. The PT is a simple test that measures the time necessary to generate fibrin after activation of factor VII. It measures the integrity of the extrinsic and common pathway. The aPTT measures the time necessary to generate fibrin from initiation of the intrinsic pathway. It measures the integrity of intrinsic and common pathway. These two tests are capable of detecting a single factor deficiency, but they must be interpreted as a matched pair to further clarify any coagulation defects. They can detect approximately 95%of coagulation defects when used together (Fischbach, 2009).

A normal PT with an abnormal aPTT would suggest that the defect lies within the first stage of the coagulation cascade in the extrinsic pathway (factors VIII, IX, XI or XII). A normal aPTT with an abnormal PT suggests a possible factor VII deficiency. If both PT and aPTT are prolonged, it might be caused by severe hepatic disease, vitamin K deficiency or disseminated intravascular coagulation (DIC). Further individual assays may be held to determine a particular factor that is deficient. Both abnormal PT and aPTT are able to be completely corrected when mixed with normal plasma unless an inhibitor is present (Fischbach, 2009). As seen in table 1 under readings obtained, the aPTT value for patient A was prolonged as it exceeded the normal range. Thus, further investigation had to be carried out. To correct these abnormal coagulation test results, coagulation corrections are done. This correction is typically done through a mixing study. The objective of a mixing study is to determine if prolonged PT or aPTT is due to a factor deficiency or due to the presence of an inhibitor. In this test, the patient’s plasma is mixed with an equal volume of normal plasma. After which PT and aPTT are measured immediately after incubation, Complete correction suggests a factor deficiency while, failure to correct indicates the presence of inhibitors. Due to a shortage of reagents, however, readings from the further investigation were unable to be obtained for patient B. Therefore, the expected readings have been included in table 1 as well. These expected readings will be discussed in the discussion section.

Discussion: Unexplained prolonged timings are a common problem in the PT and PTT. Referring to the expected results from table 1, patient A has both a prolonged PT and PTT. After doing coagulation correction, the results were as such: upon addition of normal plasma, both PT and aPTT were normalized, upon addition of adsorbed plasma, neither of the values were corrected. The normal plasma contains all coagulation factors, while the adsorbed plasma only contains coagulation factors: I, V, VIII, XI, XII. However, since PT and aPTT of patient A remain prolonged after addition of adsorbed plasma, it can be concluded that the factor(s) having a deficiency are absent in the adsorbed plasma. Since PT and aPTT measure extrinsic, intrinsic and common pathway, there could be a deficiency in all the factors of the three pathways excluding I, V, VIII, XI, and XII.

Based on this, it can be reasoned that patient A is deficient in either all or one of factors II, VII, IX and X. So, patient A either has a deficiency in factor II, VII, IX or X, or all. Individual factor assays may be conducted to deduce specific factor that might be deficient. Since factor II, VII, IX, and X are vitamin K-dependent, Patient A might have a combined deficiency vitamin K- dependent clotting factors. It is typically an acquired clinical problem, often resulting from liver disease, malabsorption or warfarin overdose. The liver is required for the synthesis of many coagulation factors, many of which require a vitamin K cofactor for their activation. Thus, a hepatic impairment may lead to a deficiency in coagulation factors. Also, since vitamin K is a fat-soluble vitamin, fat malabsorption may cause hypovitaminosis. This lead to inactive coagulation factors. Anticoagulant agents like warfarin interfere directly with vitamin K dependent activation of coagulation factors. Therefore, an overdose of such agents will cause a deficiency in coagulation factors. These problems will lead to subsequent prolongation of PT and aPTT (Lee, 2009). Patient B has a normal PT and an abnormal aPTT. After doing coagulation correction, aPTT normalized upon addition of normal plasma but remained prolonged upon addition of adsorbed plasma. Since aPTT measures the integrity of intrinsic and common pathway, it can be reasoned that patient B is deficient in either factor II, IX or X, or all. However, patient B cannot be deficient in factor II and X as they have a normal PT level.

Therefore, it can be presumed that patient B is deficient in coagulation factor IX. This deficiency is named hemophilia B, also known as the Christmas disease. However, after adding normal plasma, it was only prolonged by one second and was almost corrected. Therefore, further investigation has to be done to confirm if it there really is a defect in factor IX. This can be done through a retest or checking for the presence of inhibitors. The inhibitors can be either physiological or acquired but are almost always acquired. An example of a physiological inhibitor is anti-thrombin. It inhibits the activity of thrombin in the conversion of fibrinogen to fibrin. The acquired inhibitors, also known as circulating anticoagulants, are antibodies that neutralize specific clotting proteins, thereby interfering with their normal function. These inhibitors prevent the prolonged PT and aPTT from completely correcting despite adding normal plasma (Raber, 1990).

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