Hemostasis is the process that occurs when a blood vessel ruptures and large amounts of plasma and formed elements are allowed to escape (Bostwick and Wingerd, 2013). It can be divided into primary and secondary hemostasis. Primary hemostasis includes a platelet and vascular response activated by small injuries to blood vessels or damaged endothelial cells (Rodak, Fritsma, & Doig, 2007). Shortly after primary hemostasis begins, secondary hemostasis is activated with the aim of stabilizing the blood clot to prevent its dislodgement. The process involves attracting additional platelets to the clot and using the clotting factor fibrin to provide a firm, insoluble fiber matrix within the clot. Secondary hemostasis begins with the activation of the coagulation cascade, a series of clotting factors or proteins that change shape, thereby activating the next step in the cascade. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay The end product of this cascade is the cross-linked fibrin that forms the solid matrix that stabilizes the clot (Beebe and Myers, 2011). The coagulation cascade is divided into intrinsic and extrinsic pathways, which converge toward a common pathway. The coagulation cascade is generally assessed by measuring prothrombin time (PT) and activated partial thromboplastin time (aPTT). These tests can quickly detect significant deficiencies in the extrinsic, intrinsic and common pathway. PT is a simple test that measures the time required to generate fibrin after factor VII activation. It measures the integrity of the extrinsic and common pathway. The aPTT measures the time required to generate fibrin from the start of the intrinsic pathway. It measures the integrity of the intrinsic and common pathway. Both of these tests are capable of detecting a single factor deficiency, but they should be interpreted as a matched pair to further clarify any clotting defect. When used together, they can detect approximately 95% of clotting defects (Fischbach, 2009). A normal PT with an abnormal aPTT would suggest that the defect is in the first step 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 PT and aPTT are prolonged, it may be due to severe liver disease, vitamin K deficiency, or disseminated intravascular coagulation (DIC). Other individual tests may be performed to determine a particular factor that is deficient. Abnormal PT and aPTT can be completely corrected when mixed with normal plasma, unless an inhibitor is present (Fischbach, 2009). As shown in Table 1 below the readings obtained, the aPTT value for patient A was prolonged because it exceeded the normal range. A more in-depth investigation therefore had to be carried out. To correct these abnormal coagulation test results, coagulation corrections are performed. This correction is generally done via a mixing study. The goal of a mixture study is to determine whether a prolonged PT or aPTT is due to factor deficiency or 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 factor deficiency while failure to correct indicates the presence of inhibitors. However, due to a lack of reagents, further investigation results could not be obtained for patient B. Therefore, the, 1990).