Clotting factors: Clinical biochemistry and their roles as plasma enzymes.

The purpose of this review is to describe structure and function of the multiple proteins of the coagulation system and their subcomponent domains. Coagulation is the process by which flowing liquid blood plasma is converted to a soft, viscous gel entrapping the cellular components of blood including red cells and platelets and thereby preventing extravasation of blood. This process is triggered by the minimal proteolysis of plasma fibrinogen. This transforms the latter to sticky fibrin monomers which polymerize into a network. The proteolysis of fibrinogen is a function of the trypsin-like enzyme termed thrombin. Thrombin in turn is activated by a cascade of trypsin-like enzymes that we term coagulation factors. In this review we examine the mechanics of the coagulation cascade with a view to the structure-function relationships of the proteins. We also note that two of the factors have no trypsin like protease domain but are essential cofactors or catalysts for the proteases. This review does not discuss the major role of platelets except to highlight their membrane function with respect to the factors. Coagulation testing is a major part of routine diagnostic clinical pathology. Testing is performed on specimens from individuals either with bleeding or with thrombotic disorders and those on anticoagulant medications. We examine the basic in-vitro laboratory coagulation tests and review the literature comparing the in vitro and in vivo processes. In vitro clinical testing typically utilizes plasma specimens and non-physiological or supraphysiological activators. Because the review focuses on coagulation factor structure, a brief overview of the evolutionary origins of the coagulation system is included.

Process Improvements to Reduce Cardiac Troponin Turnaround Time in the Emergency Department.

BACKGROUND: An efficient testing process is a key to a timely diagnosis of acute myocardial infarction in the emergency department (ED). This includes a rapid evaluation cardiac biomarkers. METHODS: We conducted a quality and process improvement project to reduce troponin-T turnaround time (TAT) in the central laboratory at our facility. An interdisciplinary team, including front-line staff members, reviewed each step of troponin-T processing in both the ED and the central laboratory. A series of improvements were implemented during 2013, including changes to specimen labeling, elimination of duplicate test ordering, and efficiencies within the laboratory. Data from January 2013 to December 2014 on 31,496 patients with troponin tests were included in the analysis. RESULTS: Over the 2-year period of the projects, median troponin-T TAT decreased from 74 minutes to consistently less than 60 minutes. CONCLUSIONS: With an interdisciplinary team of health care professionals, we successfully reduced troponin-T TAT for possible acute coronary syndrome patients in our ED by 19%, consistently achieving laboratory results in less than 60 minutes.

Steps to diagnosis of a case of surreptitious intake of one of the newer direct oral anticoagulants: a case report and literature review.

Little is known about the effects of newer oral anticoagulants on various coagulation factors. When presented with a case of intentional or suspected overdose with an abnormal coagulation profile, it is imperative to have a working diagnostic algorithm to narrow the cause to a specific drug or drug class. This may become more crucial and time sensitive when dealing with a case of acute hemorrhage. Here we discuss the first reported case of what appears to be a surreptitious intake of newer oral anticoagulants and the steps leading to the diagnosis.