Fibrinogen Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Fibrinogen and links to relevant pages within the course.
Learn more about laboratory continuing education for medical technologists to earn CE credit for AMT, ASCP, NCA, and state license renewal and recertification. Or get information about laboratory safety and compliance courses that deliver cost-effective OSHA safety training and continuing education to your laboratory's employees.
|Idiopathic Thrombocytopenic Purpura|
Idiopathic thrombocytopenic purpura (ITP) is an immune-mediated disorder in which platelets are coated with autoantibodies; the antibody-coated platelets are subsequently removed by the spleen. The autoantibodies are directed against glycoproteins IIb/IIIa (fibrinogen receptor) and the complex GPIb/IX (von Willebrand factor receptor). These glycoproteins are located on the platelet membrane and play an important role in platelet aggregation, in creating a bridge with fibrinogen, and in platelet adhesion. The pathophysiology for this disorder is unclear. There is speculation that the autoantibodies arise as a result of a common viral or bacterial infection. Another speculation is that there may be a failure of T-regulatory cells. In addition to increased platelet destruction, platelet production may also be impaired or disrupted to some extent, possibly as a result of megakaryocyte injury by the autoantibodies. ITP can be acute or chronic.
Laboratory findings include: Thrombocytopenia Prolonged PT, aPTT, thrombin time Decreased fibrinogen Elevated D-dimers Schistocytes on the peripheral blood smearThrombocytopenia and schistocytes are also associated with TTP and HUS; it is the abnormal coagulation tests that distinguish DIC from these other conditions.
|Which of the following laboratory results would you find with disseminated intravascular coagulation (DIC) but NOT with thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS)?||View Page|
|Which of the following blood components will provide the best source of fibrinogen for a patient with hypofibrinogenemia:||View Page|
Francois P. Vaudaux P. Foster TJ. Lew DP.: Host-bacteria interactions in foreign body infections. Infection Control & Hospital Epidemiology. 17:514-20, 1996 Persistent staphylococcal infections are a major medical problem, especially when they occur on implanted materials or intravascular catheters. This review describes some of the recently discovered molecular mechanisms of Staphylococcus aureus attachment to host proteins coating biomedical implants. These interactions involve specific surface proteins, called bacterial adhesins, that recognize specific domains of host proteins deposited on indwelling devices, such as fibronectin, fibrinogen, or fibrin. Elucidation of molecular mechanisms of S. aureus adhesion to the different host proteins may lead to the development of specific inhibitors blocking attachment of S. aureus, which may decrease the risk of bacterial colonization of indwelling devices.
Cunningham MW.: Pathogenesis of group A streptococcal infections. Clinical Microbiology Reviews. 13):470-511, 2000 Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. A resurgence of invasive streptococcal diseases and rheumatic fever has appeared in outbreaks over the past 10 years, with a predominant M1 serotype as well as others identified with the outbreaks. Emm (M protein) gene sequencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expanded to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features. At least nine superantigens have been characterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup. Eleven adhesions have been reported, and surface plasmin-binding proteins have been defined. The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies have focused on recombinant M protein and C5a peptidase vaccines, and mucosal vaccine delivery systems are under investigation.
|What are the factors related to the strong resistance of certain strains of group A streptococci to phagocytosis? (Choose all that apply)||View Page|
|Which of the following characteristics of cerebrospinal fluid are considered abnormal?||View Page|
Clot formation is always abnormal and is often due to increased levels of protein, especially fibrinogen. When the protein level is 1000 mg/dL, clot formation will most likely occur but clots may also form at lower levels of protein. Some clots may be very fine and appear as a thin membrane or "scum" on the surface of the CSF specimen. This type of clot is referred to as a pellicle. Pellicles are composed of fibrinogen and white blood cells. The type of clot formed may give some specific information about the disease state. Some examples are provided in the following table: Example of ConditionType of Clotbacterial meningitis pellicle forms in a short time; large clot formation followsTB meningitis web-like clot (pellicle) after 12-24 hours (enhanced by refrigeration)paresis (type of neurosyphilis) incomplete clotblockage of CSF circulation completely clotted due to protein
|Macroscopic abnormalities may include which of the following?||View Page|
|What additional fraction would be seen if plasma rather than serum was subjected to electrophoresis:||View Page|
|Which of the following is found in plasma but absent in serum:||View Page|
|Label these SPE scans.||View Page|
|Coagulation Factors Involved in the aPTT Test|
The aPTT test measures the adequacy/functionality of factors that comprise the intrinsic and common pathways including: Factor I (fibrinogen) Factor II Factor V Factor VIII Factor IX Factor X Factor XI Factor XII If the level of one or more of the factors above is deficient, the aPTT will be prolonged. An aPTT mixing study may be ordered in this case.Since heparin inhibits the activity of multiple coagulation factors in the aPTT test, it is advisable to perform a thrombin time (TT) to rule out heparin contamination prior to performing a mixing study. A deficiency in any factor that is a component of the common pathway in the coagulation cascade will cause both a prolonged PT and aPTT. This includes factors I, II, V, and X.
|Which of the following tests could be used to determine whether an abnormal screening coagulation test result (PT or aPTT) is caused by a factor deficiency or an inhibitor?.||View Page|
|What laboratory test result is commonly used to monitor oral anticoagulant therapy?||View Page|
|Secondary Hemostasis: The Common Pathway, continued|
Thrombin, after its conversion from prothrombin, catalyzes the conversion of fibrinogen into a fibrin monomer. Additionally, thrombin triggers the conversion of factor XIII into factor XIIIa, which forms covalent bonds that crosslink and stabilize the fibrin monomers. Finally, thrombin feeds back into the intrinsic and common pathways, accelerating the action of factors XI, V, and VIII.
|The Fibrinolytic System, continued|
Fibrin strands woven into the clot structure are cleaved into soluble fibrin fragments and then removed by macrophages. The action of fibrinolysis also serves to restore blood flow into the area that had been sealed off, helping to promote further healing. Fibrinolysis is mediated by a proteolytic enzyme called plasmin (plasminogen is the inactive precursor form of plasmin that is found in plasma). Plasmin takes on fibrinolytic properties after activation, digesting both fibrin and fibrinogen. Inhibitors act to control the process, serving as a check and balance system for fibrinolytic activities.
The fibrinogen assay performed in the clinical laboratory is a quantitative measure of factor I. This assay is used to determine whether there is enough fibrinogen present to allow for normal clotting. It is performed in cases of an unexpected, prolonged bleeding event, or an unexpected abnormal PT and/or aPTT. Additionally, it is also used to aid in the diagnosis of disseminated intravascular coagulation (DIC).The fibrinogen reference range is typically around 200-400 mg/dL. Fibrinogen levels <100 mg/dL are often associated with free bleeding, or impaired hemostatic function.
|Fibrin/Fibrinogen Degradation Products and D-Dimers|
The presence of D-dimers in plasma or whole blood indicates that fibrin has been formed and degraded (fibrinolysis). Plasmin can also degrade intact fibrinogen, generating fibrinogen degradation products that are detected in fibrin/fibrinogen degradation products (FDP) assays. D-dimers and FDP can become elevated whenever the coagulation and fibrinolytic systems are activated. The presence of D-dimer confirms that both thrombin and plasmin have been generated, since it can only be produced as the result of the plasmin degradation of fibrin. D-dimer is a sensitive, but non-specific marker of fibrin formation and fibrinolysis that occurs with the formation of blood clots.The D-dimer test can be useful in the diagnosis of deep venous thrombosis (DVT) or pulmonary embolism (PE), two forms of venous thromboembolism (VTE). When the test is being used for this purpose, it is important that the D-dimer method has been validated by medical literature and D-dimer levels are accurately measured and accurately reported because of the serious nature of this clinical decision. If the test is positive in a patient suspected to have DVT or PE, clinicians proceed with further diagnostic tests. If the test is negative, depending on the clinical situation and the sensitivity of the D-dimer assay, DVT or PE is considered unlikely and further diagnostic tests for DVT or PE might not be pursued. D-dimer is also a sensitive, but non-specific diagnostic test for disseminated intravascular coagulation, and an indicator of increased risk of future myocardial infarction in patients evaluated for chest pain.
|Which of the following statements regarding D-dimer are true?||View Page|
|Coagulation Disorders and Liver Disease|
The liver is the site of production for the vast majority of our clotting factors. Therefore, impaired liver function could adversely affect these hemostatic proteins. Some early indicators of a potential liver problem include:An increase in factor VIII. It is not produced in the liver and will be present in elevated numbers as the body attempts to compensate. The PT is sensitive to liver function, so an unexpected, prolonged PT should be evaluated. A lack of fibrinogen is often indicative of severe liver disease. It is difficult to treat liver disease, so therapy typically centers around replacing the missing factors by way of administration of fresh frozen plasma.
|Which of the following is most responsible for increasing the erythrocyte sedimentation rate (ESR):||View Page|
|The RBCs found in this illustration are the result of:||View Page|
|Match the clotting factor with its commonly associated name:||View Page|
|Which of the following is not a likely cause of an abnormal thrombin time (TT):||View Page|
|Match Factors with the assays used to monitor them||View Page|
|Which changes Fibrinogen into Fibrin Monomer:||View Page|
According to the American Heart Association, the risk factors for metabolic syndrome include:Abdominal obesity (excessive fat tissue in and around the abdomen) Atherogenic dyslipidemia (blood fat disorders – high triglycerides, low HDL cholesterol and high LDL cholesterol – that foster plaque buildups in artery walls) Elevated blood pressure Insulin resistance or glucose intolerance (the body can't properly use insulin or blood sugar) Prothrombotic state (e.g., high fibrinogen or plasminogen activator inhibitor–1 in the blood) Proinflammatory state (e.g., elevated high sensitivity C-reactive protein in the blood) Reference: Metabolic syndrome.The American Heart Association website. Available at:http://www.heart.org/HEARTORG/Conditions/More/MetabolicSyndrome/Metabolic-Syndrome_UCM_002080_SubHomePage.jsp#. Accessed December 5, 2011.
Liver synthesis of fibrinogen and other coagulation factors is often increased in metabolic syndrome and these elevated factor levels along with PAI-1 increase the risk of clot formation.
|Which condition is caused by the increased PAI-1 and fibrinogen often present in metabolic syndrome?||View Page|
|The arrangement of erythrocytes on this peripheral blood smear can be associated with each of the following conditions except:||View Page|
|The arrangement of the erythrocytes in this peripheral smear should be reported out as rouleaux formation.||View Page|