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 the platelet and vascular response that is 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 goal of stabilizing the blood clot to prevent dislodgement. The process involves attracting additional platelets into the clot and using the clotting factor fibrin to provide a solid, insoluble fiber matrix in the clot. Secondary hemostasis begins with the activation of the coagulation cascade, a series of clotting factors or proteins that change shape, thus activating the next step of the cascade. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay The final 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 into a common pathway. The coagulation cascade is typically assessed by measurement of prothrombin time (PT) and activated thromboplastin time (aPTT). These tests provide a rapid way to detect significant deficiencies in the extrinsic, intrinsic, and common pathways. PT is a simple test that measures the time it takes to generate fibrin after factor VII activation. 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. Measures intrinsic and common pathway integrity. These two tests can detect single factor deficiency, but must be interpreted as a matched pair to further clarify any clotting 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 is in 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 possible factor VII deficiency. If both PT and aPTT are prolonged, it may be caused by severe liver disease, vitamin K deficiency, or disseminated intravascular coagulation (DIC). Further individual analysis can be carried out to determine a particular deficient factor. Both abnormal PT and aPTT can be completely corrected when mixed with normal plasma unless an inhibitor is present (Fischbach, 2009). As seen in Table 1 below the readings obtained, the aPTT value for Patient A was prolonged as it exceeded the normal range. Therefore, further investigations were necessary. To correct these abnormal clotting test results, coagulation corrections are performed. This correction is typically done via a blending study. The goal of a mixing study is to determine whether the prolonged PT or aPTT is due to a factor deficiency or the presence of an inhibitor. In this test, the patient's plasma is mixed with an equal volume of normal plasma. PT and aPTT are then measured immediately after incubation. Complete correction suggests a deficiency of factors while failure to correct indicates the presence of inhibitors. Due to the shortage of reagents, however, it was not possible to obtain the values ​​of the further investigation for patient B. Therefore, the expected values ​​were also included in the, 1990).