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Hemostasis: Basic Overview Online Training

Hemostasis is the process of maintaining blood in its fluid state as well as the ability to stop bleeding in the case of trauma or disease. Maintaining this balance requires several different systems to work together to prevent excessive bleeding or clotting. Effective treatment of bleeding and clotting disorders depends on the proper identification of the abnormality. The hemostasis laboratory plays an important role in diagnosing, monitoring and treatment of bleeding and clotting disorders.

Continue Continue Hemostasis Master Template HOOD05162003052540 | Effective Date: 26-Nov-2019 ? Hemostasis: Basic Overview Online Training The body’s ability to maintain the delicate balance between blood in a liquid and solid form is called hemostasis. The hemostasis laboratory therefore plays an important role in diagnosing, monitoring and in the treatment of bleeding and clotting disorders. Process of hemostasis 1 Common tests performed in hemostasis 4 Hemostasis disease states and anticoagulant therapies 3 Different pathways of the coagulation cascade 2 Welcome Filename: hemostasis_olt_welcome Welcome to the Hemostasis: Basic Overview Online Training. Hemostasis is the process of maintaining blood in its fluid state as well as the ability to stop bleeding in the case of trauma or disease. Maintaining this balance requires several different systems to work together to prevent excessive bleeding or clotting. Effective treatment of bleeding and clotting disorders depends on the proper identification of the abnormality. The hemostasis laboratory plays an important role in diagnosing, monitoring and treatment of bleeding and clotting disorders. This course will cover the following four learning objectives. For navigation help, select the question mark button located in the lower right corner of each slide. ? Hemostasis Process Hemostasis is the process of maintaining a balance between keeping blood in its fluid state and stopping bleeding in cases of trauma or disease. Select the numbered steps below to learn more about the hemostasis process. 1 1 1 2 2 2 3 3 3 4 4 4 5 5 5 Hemostasis Process Filename: hemostasis_olt_hemostasisprocess_baselayer Hemostasis is the process of maintaining a balance between keeping blood in its fluid state and stopping bleeding in cases of trauma or disease. Select the numbered steps below to learn more about the hemostasis process. Filename: hemostasis_olt_hemostasisprocess_normalhemostasis Normal hemostasis involves a balance between two processes: the formation of blood clots to stop bleeding from injured vessels and the natural anticoagulant and fibrinolytic systems to prevent clot formation beyond the site of injury. In most patients, these processes work together to form a clot to stop bleeding, and to prevent unwanted clot formation so that blood flows freely through arteries, veins, and capillaries. Filename: hemostasis_olt_hemostasisprocess_vascularsystem Under normal conditions, blood remains liquid and flows freely through the body’s blood vessels. The blood vessels are lined with a thin layer of endothelial cells that prevents the blood from adhering to the vessel walls and prevents clot formation. During vessel injury or in some disease states, this endothelial cell lining is disrupted. This initiates vasoconstriction in which the vessel narrows to restrict the blood flow to the site of the injury. When the endothelial cells are disrupted, they also expose the flowing blood to the sub layer of the vessel lining called the collagen layer. The exposure of the collagen layer and release of other substances from the damaged tissue begins a series of events that quickly seal the damaged area of the vessel and prevent excessive blood loss. Filename: hemostasis_olt_hemostasisprocess_plateletsrole Platelets that are circulating in the blood, are the first to respond to the collagen exposure. Very quickly, the platelets begin to adhere to the site of the injury and activate. Activated platelets change shape and become sticky. They also release a series of chemicals that cause additional platelets to activate and aggregate or stick together in the damaged area. Platelet aggregation causes a fragile plug to form that stops blood from escaping through the damaged vessel lining. This platelet plug formation is called primary hemostasis. Contact with exposed collagen causes platelet activation and adhesion at the site of the injury. Activated platelets release various substances and initiate platelet aggregation in the damaged area. Platelet aggregation causes the formation of a platelet plug to stop bleeding in the damaged area. Filename: hemostasis_olt_hemostasisprocess_coagulationfactors The platelet plug is extremely fragile and needs to be stabilized to effectively prevent bleeding. This involves interactions of coagulation proteins resulting in formation of fibrin which stabilizes the platelet plug. Platelets play a role by secreting phospholipid materials which serve as the basis for the activation of the coagulation cascade. The coagulation cascade is a series of sequential reactions involving the coagulation factors that eventually create a stable fibrin clot at the site of injury.  Fibrin is a very sticky mesh that adheres to the damaged vessel trapping platelets and other blood cells in a solid form. The formation of the fibrin clot is called secondary hemostasis. The coagulation factors consist of plasma proteins, calcium and a material released by the vessel when damaged called thromboplastin. Most coagulation factors are made in the liver and circulate freely in the blood stream in an inactive form. Filename: hemostasis_olt_hemostasisprocess_fibrinolyticsystem After the injury is repaired, the fibrin clot is dissolved by a process called fibrinolysis. During fibrinolysis the stable fibrin clot is broken down into smaller pieces by fibrinolytic factors. The fibrinolytic system is also very important in keeping clots from forming beyond the site of the injury once the platelets and coagulation factors are activated. The two main components of the fibrinolytic system are: - Plasminogen, a plasma protein circulating in the blood.  When the initial vessel damage occurs, plasminogen is activated to its enzymatic form, Plasmin. - Plasmin breaks down both fibrinogen that circulates freely in the blood stream and the stable fibrin clot created during the coagulation cascade. The products of Fibrinolysis are fibrinogen degradation products, fibrin degradation products and D-dimer. Fibrinogen degradation products are created when plasmin breaks down fibrinogen molecules, the precursors of fibrin that circulate freely in the blood stream. Fibrin degradation products are created when plasmin breaks down stable fibrin clots.  Both products are referred to as FDPs. D-dimer is a specific type of degradation product that is created strictly when plasmin breaks down a stable fibrin clot, not by the breakdown of fibrinogen. Therefore, the presence of D-dimer molecules in a patient’s blood indicate that a stable fibrin clot was formed and broken down by plasmin. Fibrinolytic System 5 Clot lysis The two main components of the Fibrinolytic system are: Plasminogen, a plasma protein circulating in the blood. When the initial vessel damage occurs, plasminogen is activated to its enzymatic form, plasmin Plasmin breaks down both fibrinogen that circulates freely in the blood stream and the stable fibrin clot created during the coagulation cascade The products of Fibrinolysis are: Fibrinogen Degradation Products Fibrin Degradation Products D-dimer Coagulation Factors Coagulation factors are: Made up of plasma proteins, calcium and thromboplastin Produced in the liver, except for Factor VIII Circulated in plasma in an inactive form as enzyme precursors, or as catalysts for other enzymatic reactions 4 Clot formation Platelet's Role Contact with exposed collagen causes platelet activation and adhesion at the site of the injury. Activated platelets release various substances and initiate platelet aggregation in the damaged area. Platelet aggregation causes the formation of a platelet plug to stop bleeding in the damaged area. 3 Platelet activation Vasoconstriction Vascular Response When a blood vessel is damaged, the following vascular reactions can occur: Vasoconstriction: blood vessels narrow to reduce blood flow to a damaged area Collagen exposure: the collagen layer is part of the sub-endothelium of blood vessels. Platelets and clotting factors activate when they come in contact with exposed collagen of damaged blood vessels 2 Injured Vessel Vasoconstriction Normal Hemostasis 1 During normal hemostasis, the following systems work together: Vascular system Platelets Blood coagulation factors Fibrinolytic system ? Coagulation Cascade The coagulation cascade is a series of enzymatic reactions that result in the formation of a fibrin clot to stop bleeding. There are three pathways that constitute the coagulation cascade: Intrinsic pathway Extrinsic pathway Common pathway Select the tab arrows to learn more about the coagulation cascade. Intrinsic Pathway Extrinsic Pathway Common Pathway Cascade Coagulation Cascade Filename: hemostasis_olt_coagulationcascade_baselayer The coagulation cascade is a series of enzymatic reactions that result in the formation of a fibrin clot to stop bleeding. Fibrin can be formed through two pathways that eventually converge into a common pathway. All the pathways involve a series of cascading enzymatic reactions. Select the tab arrows to learn more about the coagulation cascade. hemostasis_coagulation_cascade_intrinsic_pathway.mp4 The intrinsic pathway is named because all of the factors required to complete the enzymatic reactions in this pathway are naturally present in circulating blood. The intrinsic pathway begins when circulating factor XII comes in contact with and is bound to a negatively charged surface, such as collagen. The change in structure of factor XII, along with Kallikrein and High Molecular Weight Kininogen activates factor XII to factor XIIa. Activated Factor XII activates factor XI. Activated Factor XI plus calcium activate factor IX. Activated factor IX, Calcium and the activated Factor VIII form a complex on the platelet surface. The activated factor IXa-factor VIIIa complex is needed to convert factor X to Xa in the common pathway. hemostasis_coagulation_cascade_extrinsic_pathway.mp4 The extrinsic pathway is so named because NOT all of the factors required to complete the enzymatic reactions in this pathway are naturally present in circulating blood. To initiate this pathway, tissue thromboplastin, (also called tissue factor or factor III), must be released into the circulatory system, such as when there is blood vessel damage. This activates factor VII and in the presence of calcium, the Thromboplastin / Factor VIIa complex is created. The factor VII-thromboplastin complex rapidly converts factor X to the enzyme Xa in the common pathway. hemostasis_coagulation_cascade_common_pathway.mp4 The enzymatic reactions that take place in the intrinsic and extrinsic pathways converge as they enter the common pathway. Via the intrinsic pathway, the factor IXa-factor VIIIa complex slowly converts factor X to the enzyme Xa. Via the extrinsic pathway, the factor VII-thromboplastin complex rapidly converts factor X to the enzyme Xa. Factor Xa creates a complex with factor Va and Calcium in the presence of Platelet Factor 3. This complex activates Prothrombin or Factor II to create Thrombin or Factor IIa. Thrombin converts fibrinogen to fibrin to form an unstable clot. The fibrin strands in the unstable clot begin to gel and are acted upon by factor XIIIa to form a stable insoluble clot in which the fibrin strands become cross linked to each other in their D-dimer region. hemostasis_coagulation_cascade_common_pathway.mp4 When the coagulation cascade is activated, both the intrinsic and extrinsic pathways can progress simultaneously. Both pathways converge into the common pathway by activating factor X finally resulting in the formation of a fibrin clot. Cascade The intrinsic pathway and extrinsic pathway occur simultaneously activating the common pathway. ? Common Pathway Factors involved: Factor V Factor X Prothrombin (Factor II) Fibrinogen (Factor I) ? Extrinsic Pathway Factor involved:  Factor VII ? Intrinsic Pathway Factors involved: Factor XII Factor XI Factor IX Factor VIII ? ? Hemostasis Disorders In the following section, you will learn about hemorrhagic disorders and thrombotic events, both of which can be congential or acquired. Anticoagulant therapies will also be discussed. Hemostasis Disorders Filename: hemostasis_olt_hemostasisdisorders Hemostasis disorders have a variety of causes that can accelerate clot formation or lead to bleeding. These abnormalities require clinical examination, lab testing, and investigation into family medical history for diagnosis. In the following section, you will learn about bleeding and clotting disorders along with anticoagulant therapies. ? Bleeding Disorders Bleeding disorders can occur for various reasons and can lead to hemorrhage. Select the tab arrows to learn about common bleeding disorders. Specific Factor Deficiencies Vitamin K Deficiency Hemophilia Von Willebrand Bleeding Disorders Filename: hemostasis_olt_bleedingdisorders_baselayer Hemorrhaging , or excessive bleeding, can occur for various reasons such as vitamin deficiencies or inherited conditions. Select the tab arrows to learn about common bleeding disorders. The following slides do not have audio. Von Willebrand Von Willebrand disease is the most commonly inherited coagulation disorder. This is a result of a deficiency or functional abnormality in Factor VIII - von Willebrand factor causing interference with platelet adhesion. Clinical signs are variable from prolonged bleeding to massive bleeding. ? Hemophilia Hemophilia is an inherited bleeding disorder caused by a Factor VIII or Factor IX deficiency and can be present in one of several forms. The most severe hereditary hemophilic disorder is a deficiency of Factor VIII. Hemophilia A, an X-linked recessive gene, affecting male offspring of females who carry the gene. Signs can vary from mild (trauma results in prolonged bleeding) to severe (spontaneous excessive bleeding in the tissues). ? Vitamin K Deficiency Vitamin K is essential for the production of many coagulation factors. Depending on the extent of deficiency, this can lead to bleeding problems in the patient. ? Specific Factor Deficiencies Many patients have individual factor deficiencies that can cause lifelong bleeding disorders. Some factor deficiencies are prevalent in certain ethnic groups i.e., Factor XI is found in Ashkenazi Jews. Patients may also develop inhibitors (antibodies) to factors, which can also cause life threatening bleeding. These are the result of the formation of IgG antibodies. ? ? Clotting Disorders Thrombosis or clotting events are more common than bleeding disorders and can be very severe. Select the tab arrows to learn about common clotting events. Deep Vein Thrombosis (DVT) Pulmonary Embolism (PE) Thrombotic Strokes Disseminated Intravascular Coagulation (DIC) Clotting Disorders Filename: hemostasis_olt_clottingdisorders_baselayer Thrombosis or clotting disorders are much more common than bleeding disorders. Thrombosis can be very severe and lead to death in some cases without proper diagnosis and treatment. Select the tab arrows to learn more about the common clotting disorders. The following slides do not have audio. Disseminated Intravascular Coagulation (DIC) Disseminated intravascular coagulation (DIC) is a serious condition in which widespread thromboses lead to massive internal bleeding when all of the coagulation factors become consumed. Bleeding and clotting occurs due to the simultaneous formation of thrombin and plasmin. Patients can develop DIC which causes widespread damage to the vascular system from injuries such as those incurred from an automobile accident. Certain bacterial and viral infections and drug reactions also can lead to DIC. ? Thrombotic Strokes When a thrombus in the deep veins dislodges, it can travel throughout the body, following normal blood flow. When that clot travels far enough to reach the brain, a thrombotic stroke occurs. ? Pulmonary Embolism (PE) When a thrombus in the deep veins dislodges, it can travel to the heart where the veins are larger and the emboli do not get lodged. The clot can travel through the heart and to the lungs, following the normal blood flow pathway. In the lungs, the vessels are smaller. The clot may finally get lodged there. This is called pulmonary embolism (PE). If the blockage is large or a result of many clots and goes un-detected, it can be fatal. ? Deep Vein Thrombosis (DVT) Most commonly, clots develop in the deep veins of the legs, pelvis or upper extremities. If they remain in the leg, they create problems such as phlebitis which can be mild to severe. If the clot is dislodged, it may travel towards the heart, lungs or brain. ? ? Anticoagulant Therapy In cases of an inappropriate clot formation, patients can be treated with anticoagulants to prevent additional clots from forming. Select the tab arrows to learn more about each type of anticoagulant therapy. Heparin Therapy Oral Anticoagulant Therapy Aspirin Therapy Anticoagulant Therapy Filename: hemostasis_olt_anticoagulanttherapy_baselayer In cases of an inappropriate clot formation, patients can be treated with anticoagulants to prevent additional clots from forming. Select the tab arrows to learn more about each type of anticoagulant therapy. The following slides do not have audio. Aspirin Therapy Aspirin, along with its pain relieving properties, has the ability to interfere with platelet activation. In coronary heart disease, the blood vessels become lined with cholesterol.  These “plaques” of cholesterol can initiate platelet adhesion and aggregation. Aspirin reduces the platelets ability to activate and adhere to the vessel walls, reducing the risk of clot formation, heart attack and stroke. ? Oral Anticoagulant Therapy Oral anticoagulants are used as a long term therapy to prevent reoccurrences of a thrombotic episode. They inhibit the patient’s ability to form clots by reducing the function of Vitamin K, rendering the Vitamin K dependent factors (II, VII, IX and X) non-functional. ? Heparin Therapy In patients with serious clotting disorders such as acute coronary syndrome, pulmonary embolism and deep vein thrombosis, heparin therapy typically is the first response to prevent further clot formation. Heparin, administered intravenously, is fast acting, but cannot dissolve clots that already exist. However, by preventing the activation of Factor X and thrombin, heparin stops additional clots from developing. ? ? Hemostasis Tests During Hemostasis testing, the patient’s ability to form a clot is evaluated. When the specimen is collected, a light blue top tube containing 3.2% sodium citrate anticoagulant is used. Note: A 9:1 ratio of blood to citrate must be maintained. If the tube is not properly filled or has the incorrect blood:citrate ratio, it may affect test results. Most hemostasis testing is performed on platelet poor plasma. Select the button below to learn more about the types of tests performed in the Hemostasis Lab. Hemostasis Lab Plasma Cells Cells separate from plasma Hemostasis Tests Filename: hemostasis_olt_hemostasistests Just as there are a vast number of hemostatic diseases, disorders, and associated problems, there also are many tests of different types available to assist in the diagnosis of the disorders and complications. During Hemostasis testing, the patient’s ability to form a clot is evaluated. When the specimen is collected, tube containing 3.2 percent sodium citrate anticoagulant is used. Sodium citrate prevents the patient’s blood from clotting in the tube. A 9 to 1 ratio of blood to citrate must be maintained. If the tube is not properly filled or has the incorrect blood to citrate ratio, it may affect test results. Most hemostasis testing is performed on platelet poor plasma. Platelets are a source of phospholipids and the reagents used for testing contain phospholipids, thus, if platelets are present in the plasma they may falsely shorten results. Normal plasma contains all coagulation factors. Most hemostasis analyzers detect clot formation optically. When the sample and reagent are added to a reaction vessel, the solution begins as a liquid and light passes easily through the solution.  As the fibrin clot begins to form the solution changes from a liquid to a solid which decreases the amount of light that can pass through the reaction vessel.  An algorithm is then used to determine the clot time based on the pattern of light transmittance or absorbance. Select the button below to learn more about the types of tests performed in the Hemostasis Lab. ? Hemostasis Lab Just as there are many interdependent systems to maintain hemostasis within the body, there are many different tests used to monitor the effectiveness of these systems. The hemostasis laboratory plays an important role in the diagnoses, monitoring and treatment of bleeding and clotting disorders. Select the tab arrows to learn more about some of the most common tests performed in the hemostasis laboratory. Prothrombin Time (PT) Activated Partial Thromboplastin Time (aPTT) Fibrinogen Assay D-dimer Assay Coagulation Factor Assays Platelet Function Assay (PFA) Hemostasis Lab Filename: hemostasis_olt_virtuallaboratory_baselayer The hemostasis laboratory plays an important role in the diagnoses, monitoring and treatment of bleeding and clotting disorders. Select the tab arrows to learn more about some of the most common tests performed in the hemostasis laboratory. Filename: hemostasis_olt_virtuallaboratory_pt The Prothrombin Time or PT is used to evaluate the effectiveness of the Extrinsic and Common Pathways of the Coagulation Cascade. It does not test for a specific factor or analyte, but for the ability of all factors involved in the extrinsic pathway and common pathway to work together to form a fibrin clot. The test is performed by adding thromboplastin and calcium to the patient’s plasma sample and measuring the amount of time required to form a fibrin clot. The PT and a-PTT together are common screening tests when evaluating a patient’s ability to clot especially prior to surgery or other medical procedures. It also is a good starting point when a patient is bleeding for an unknown reason. The PT also is the test used to monitor oral anticoagulant therapy. The physician uses the result to determine if the patient is taking the appropriate amount of warfarin. Since the PT result in seconds can vary depending on the instrument or reagents used, the PT also is reported out as an I-N-R or International Normalized Ratio. This value is a way to standardize the patient’s PT result, regardless of what laboratory performs the testing. Filename: hemostasis_olt_virtuallaboratory_aptt The activated Partial Thromboplastin Time or a-PTT is used to evaluate the effectiveness of the Intrinsic and Common Pathways of the Coagulation Cascade. It does not test for a specific factor or analyte, but for the ability of all of the factors involved in the intrinsic pathway and common pathway to work together to form a fibrin clot. During the a-PTT test procedure, several reagents are added to the patient’s sample. An activator is used to simulate the surface contact that initiates the intrinsic pathway. Partial Thromboplastin is used as a platelet substitute and calcium is added. The time until the fibrin clot is formed is reported in seconds. The PT and a-PTT together are common screening tests when evaluating a patient’s ability to clot especially prior to surgery or other medical procedures. It is also good starting point when a patient is bleeding for an unknown reason. The activated Partial Thromboplastin time also is utilized when monitoring heparin therapy. The physician determines the appropriate amount of heparin to give a patient based on the increase in the patient’s a-PTT result. Filename: hemostasis_olt_virtuallaboratory_fibrinogen Fibrinogen is the direct precursor to fibrin. When evaluating a patient’s ability to clot, it is important to know how much fibrinogen the patient has available to convert to fibrin. Unlike the PT and a-PTT assays, the fibrinogen assay specifically measures the amount of active fibrinogen in a sample. The test is performed by adding thrombin to the patient’s sample. Thrombin converts fibrinogen to fibrin and the amount of time required to form a fibrin clot is measured in seconds. Since the physician needs to know the amount of fibrinogen in the sample, the seconds are converted to a concentration. The fibrinogen assay is critical when evaluating the severity of a patient in D-I-C. During D-I-C, the patient is clotting uncontrollably and consuming all coagulation factors, including fibrinogen. The concentration of fibrinogen left in a patient’s sample allows the physician to assess the severity of the patient’s condition. Filename: hemostasis_olt_virtuallaboratory_d-dimer When plasmin breaks down a stable fibrin clot during fibrinolysis, D-dimers are formed. A quantitative D-dimer such as the INNOVANCE D-Dimer assay can measure the concentration of these molecules. The reagent used during the D-dimer assay contains latex beads coated with antibodies specific to D-dimer. When D-dimer is present in the patient sample, the latex beads stick together, and the turbidity of the solution is measured and converted to a concentration. Since D-dimers are only formed from the cross-linkage fibrin strands when the fibrin clot is stabilized, the detection of D-dimer in the patient sample indicates that a clot has formed and been broken down. This helps the physician diagnose clotting disorders such as Deep Vein Thrombosis or Pulmonary Embolism. Filename: hemostasis_olt_virtuallaboratory_coagulationfactor Coagulation factor assays test for specific factors in the coagulation cascade. The patient sample is mixed with a reagent plasma that is deficient in the factor being tested for, such as Factor VIII. This factor VIII deficient plasma contains all coagulation factors except factor VIII. Since factor VIII is part of the intrinsic pathway, an a-PTT is then measured. The time until a fibrin clot is formed is measured and converted to a percent activity level for factor VIII. Factor assays are used to determine factor deficiencies such as the Factor VIII deficiency of Hemophilia patients. Filename: hemostasis_olt_virtuallaboratory_plateletfunction The Platelet Function Assay or PFA determines the ability of a patient’s platelets to aggregate during primary hemostasis. During the PFA assay the patient’s whole blood is added to a cartridge coated with reagents. The time required for the platelets to plug a small aperture is measured and reported in seconds. The PFA is used to determine if the patient has a platelet dysfunction such as Von Willebrand Disease or Aspirin Ingestion. Platelet Function Assay (PFA) Evaluates the ability of platelets to adhere and aggregate Time required to plug an aperture is measured and reported in seconds Determines platelet dysfunction such as von Willebrands Disease or Aspirin ingestion Injured Vessel Platelet Activation ? Coagulation Factor Assays Evaluates specific factors in the coagulation cascade Sample is added to a reagent plasma deficient in the factor being tested for and either a PT or aPTT is measured. The time required to form the fibrin clot is converted to a % activity Factor assays can be used to determine factor deficiencies such as Hemophilia ? D-dimer Assay Evaluates the presence of D-dimers in the patient sample Turbidity of the test solution is measured and converted to a concentration Concentration of D-dimer in a patient sample can help rule out deep vein thrombosis and pulmonary embolism ? Fibrinogen Assay Evaluates the amount of fibrinogen capable of converting to fibrin Measures time in seconds required to form a fibrin clot then converts the seconds to a concentration Critical test for determining the severity of DIC (Disseminated Intravascular Coagulation) ? Activated Partial Thromboplastin Time (aPTT) Evaluates the intrinsic and common pathways Measures the time in seconds to create a fibrin clot Screening test for evaluating a patient's ability or inability to clot Used to monitor heparin therapy ? Prothrombin Time (PT) Evaluates the extrinsic and common pathways Measures the time in seconds to create a fibrin clot Screening test for evaluating a patient's ability or inability to clot International Normalized Ratio (INR) Used to monitor oral anticoagulant therapy Standardized result regardless of instrument or reagent system used ? ? Course Review Congratulations. You have completed the Hemostasis: Basic Overview Online Training course. Select the numbered buttons below to review the material before proceeding to the final assessment. Common tests performed in hemostasis 4 4 4 Hemostasis disease states and anticoagulant therapies Different pathways of the coagulation cascade 2 2 2 The process of hemostasis 1 1 3 3 3 Course Review Common tests performed in hemostasis The Prothrombin Time (PT) evaluates the effectiveness of the extrinsic and common pathways of the coagulation cascade. The PT is used as a screening test to evaluate a patient’s ability to clot and to monitor Oral Anticoagulant Therapy such as warfarin therapy The activated Partial Thromboplastin Time (aPTT) evaluates the effectiveness of the intrinsic and common pathways of the coagulation cascade. The aPTT is used as a screening test to evaluate a patient’s ability to clot and to monitor heparin therapy The Fibrinogen assay evaluates the amount of fibrinogen available to convert into fibrin and create a fibrin clot. The Fibrinogen assay can help determine the severity of Disseminated Intravascular Coagulation (DIC) where a patient clots uncontrollably consuming all of his coagulation factors Assay (PFA) evaluates the platelets ability to adhere and aggregate, creating a platelet plug during primary hemostasis.  The PFA can help diagnose platelet dysfunction such as von Willebrands Disease or Aspirin Ingestion Hemostasis disease states and anticoagulant therapies Hemostasis disorders can cause excessive bleeding or excessive clotting and can range from mild to life threatening. Bleeding disorders such as von Willebrands Disease, factor deficiencies (Hemophilia) or Vitamin K deficiencies reduce the patient's ability to clot and can result in excessive bleeding. Inherited or acquired clotting disorders increase the patient's ability to form clots and can cause Deep Vein Thrombosis or Pulmonary Embolism. Heparin therapy or Oral Anticoagulant therapy is used to reduce the patient’s risk of a thrombotic (clotting) event and must be monitored carefully. Different pathways of the coagulation cascade The coagulation cascade is a series of enzymatic reactions that result in a stable fibrin clot to stop bleeding and consists of three pathways. The intrinsic pathway involves factors XII, XI, IX, and VIII and is initiated by contact with the surface of the injured blood vessel The extrinsic pathway involves factor VII and is initiated by tissue thromboplastin released into the blood stream when there is vessel damage The intrinsic and extrinsic pathways converge into the common pathway which includes factors V, X, II (prothrombin) and I (fibrinogen) The Process of Hemostasis The process of hemostasis involves 4 systems: the vascular system, platelets, coagulation factors and the fibrinolytic system. The vascular response includes collagen exposure at the site of injury and vasoconstriction to reduce blood loss. Platelets are activated and aggregate at the site of injury, creating a platelet plug. This process is called primary hemostasis. The coagulation cascade is activated resulting in a stable fibrin clot at the site of the injury.  This process is called secondary hemostasis. Once the injured vessel is healed the fibrinolytic system breaks down the clot and prevents clot formation beyond the site of injury. Disclaimer Please note that the learning material is for training purposes only. For the proper use of the software or hardware, please always use the Operator Manual or Instructions for Use (hereinafter collectively “Operator Manual”) issued by Siemens Healthineers. This material is to be used as training material only and shall by no means substitute the Operator Manual. Any material used in this training will not be updated on a regular basis and does not necessarily reflect the latest version of the software and hardware available at the time of the training. The Operator Manual shall be used as your main reference, in particular for relevant safety information like warnings and cautions. Please note: Some functions shown in this material are optional and might not be part of your system. 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Disclaimer Assessment This assessment will test your retention of the presented content. A passing score of 80% or higher is required to complete the course and earn your certificate. You may repeat the assessment as many times as needed. Start ? Assessment Select the best answer. ? Question 1 of 10 The Prothrombin Time (PT) evaluates what process? The extrinsic and common pathways of the coagulation cascade Platelet Aggregation The intrinsic and common pathways of the coagulation cascade  Fibrinolysis Multiple Choice Incorrect Active Fibrinolysis can be detected by a positive D-dimer assay. Incorrect The intrinsic and common pathways of the coagulation cascade are evaluated by the Activated Partial Thromboplastin Time (APTT). Incorrect Platelet Aggregation is evaluated by the Platelet Function Assay (PFA). Incorrect Select the best answer. ? Question 2 of 10 The vascular response in hemostasis includes: Vasoconstriction Formation of a fibrin clot Formation of a platelet plug Multiple Choice Incorrect The formation of a platelet plug is the result of platelet activation or primary hemostasis. Incorrect The formation of a fibrin clot is the end result of the coagulation cascade or secondary hemostasis. Incorrect Select the best answer. ? Question 3 of 10 A patient is experiencing frequent nose bleeds and the physician suspects a platelet dysfunction. What test would help the physician with this diagnosis? Platelet Function Assay (PFA) Factor VIII Assay INNOVANCE® D-dimer Assay Activated Partial Thomboplastin Time (aPTT) Multiple Choice Incorrect The Activated Partial Thromboplastin Time (APTT) evaluates the intrinsic and common pathways of the coagulation cascade. Incorrect The INNOVANCE® D-Dimer assay would help rule out DVT or PE. Incorrect A Factor VIII Assay would help diagnose or monitor a factor VIII deficiency (hemophilia). Incorrect Select the best answer. ? Question 4 of 10 Most Siemens Healthcare Diagnostics hemostasis analyzers utilize what methodology when detecting a fibrin clot? Optical Mechanical LOCI Multiple Choice Incorrect LOCI is a technology used on the Dimension® Vista System. Incorrect The only Siemens hemostasis analyzer that utilizes a mechanical method is the BFT™II Analyzer. Incorrect Select the best answer. ? Question 5 of 10 During which pathway of the coagulation cascade is fibrinogen (Factor I) converted to fibrin (Factor Ia)?  Intrinsic Pathway Common Pathway Extrinsic Pathway Multiple Choice Incorrect The extrinsic pathway involves Factor VII. Incorrect Incorrect The intrinsic pathway involves Factors XII, XI, IX and VIII. Select the best answer. ? Question 6 of 10 A patient with an acute coronary episode just presented to the emergency room. What anticoagulant therapy would be most appropriate to quickly prevent this patient from forming more clots?  Heparin Therapy Oral Anticoagulant Therapy Aspirin Therapy Multiple Choice Incorrect Aspirin therapy is for long term prevention of clot formation. Incorrect Oral anticoagulant therapy is for long term prevention of future episodes but is not fast acting. Correct Select the best answer. ? Question 7 of 10 A patient presenting to the emergency room with leg pain and swelling has a positive D-dimer test. What does this likely indicate for the patient? They have Deep Vein Thrombosis They have a platelet dysfunction They have a factor deficiency They received aspirin therapy Multiple Choice Incorrect Aspirin therapy reduces the platelets’ ability to aggregate and would be indicated by an abnormal Platelet Function Assay (PFA). Incorrect An abnormal factor assay would indicate a factor deficiency. Incorrect Platelet dysfunction would be indicated by an abnormal Platelet Function Assay (PFA). Correct Select the best answer. ? Question 8 of 10 Which of the following best describes platelet aggregation?  When the platelets change shape and release chemicals  When the platelets stick to the site of the vessel injury When the platelets begin to stick together and create the platelet plug When the fibrin clot is dissolved  Multiple Choice Incorrect The fibrin clot is dissolved during fibrinolysis. Incorrect Incorrect Platelet adhesion occurs when the platelets begin to stick to the site of vessel injury. Correct Platelet activation causes the platelets to change shape and release chemicals. Select the best answer. ? Question 9 of 10 When are D-dimers formed? When a stable fibrin clot is broken down by plasmin When fibrinogen is broken down by plasmin During vasoconstriction During vessel injury Multiple Choice Incorrect Tissue thromboplastin is released and collagen is exposed when the blood vessel is injured. Incorrect Vasoconstriction is the narrowing of the blood vessel after injury to restrict blood flow to the site of the injury. Incorrect Plasmin breaks down fibrinogen into fibrinogen degradation products (FDP). Correct Select the best answer. ? Question 10 of 10 A patient has Hemophilia A and the physician needs to determine the severity of his deficiency. What test would you perform? Factor VIII assay Fibrinogen assay D-dimer assay Multiple Choice Incorrect D-dimer assay test should not be used to determine the severity of this patient’s deficiency. Incorrect Fibrinogen assay test should not be used to determine the severity of this patient’s deficiency. Correct Assessment Results YOUR SCORE: PASSING SCORE: Review Retry Retry Continue Continue Continue %Results.ScorePercent%% %Results.PassPercent%% ? Assessment Results You did not pass the course. Take time to review the assessment then select Retry to continue. Congratulations. You passed the course.. Exit To access your Certificate of Completion, select the Launch button drop down on the course overview page. You can also access the certificate from your PEPconnect transcript. ? You have completed the Hemostasis: Basic Overview Online Training. Completion Navigation Help Select the icon above to open the table of contents. Click Next to continue. Next Welcome Slide The timeline displays the slide progression. Slide the orange bar backwards to rewind the timeline. Click Next to continue. Next Timeline Select the CC icon to display closed captioning (subtitles). Click Next to continue. Next Caption Icon add subtitles Select the buttons to learn more about a topic. Be sure to review all topics before navigating to the next slide. Click Next to continue. Next Tab Arrow Slide Select the X to close the pop-up. Click Next to continue. Next Layer Slide Select Submit to record your response. Click the X in the upper right corner to exit the navigation help. Assessment Slide Question Bank 1 HILS2240 | Effective Date: 20 DEC 2021 1.1 Welcome 1.2 Hemostasis Process 1.3 Coagulation Cascade 1.4 Hemostasis Disorders 1.5 Bleeding Disorders 1.6 Clotting Disorders 1.7 Anticoagulant Therapy 1.8 Hemostasis Tests 1.9 Hemostasis Lab 1.10 Course Review 1.11 Disclaimer 1.12 Assessment 1.24 Completion

  • heme
  • hemostasis
  • coag
  • platelet
  • blood