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Fibrin Information and Courses from MediaLab, Inc.

These are the MediaLab courses that cover Fibrin and links to relevant pages within the course.

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Authentic and Spurious Causes of Thrombocytopenia
Increased platelet destruction

The most common cause of thrombocytopenia is increased destruction of platelets. Platelets are eliminated from peripheral circulation faster than the bone marrow can produce new platelets.Increased platelet destruction may be the result of immune or nonimmune mechanisms. Immune platelet destruction begins when antibodies coat platelets. These sensitized platelets are then destroyed by macrophages, mostly from the spleen but also from the liver. Disorders that are associated with immune mechanisms of destruction include: Idiopathic (or immune) thrombocytopenic purpura (ITP) Heparin-induced thrombocytopenia (HIT) Neonatal alloimmune thrombocytopenia (NAIT)Increased destruction of platelets is not always caused by the immune system. Platelet destruction can occur as a result of abnormal platelet aggregation or endothelial cell injury. Both of these occurrences can cause fibrin to form in arterioles and capillaries. This leads to platelet activation and consumption. Conditions associated with nonimmune destruction and consumptive thrombocytopenia include: Thrombotic thrombocytopenic purpura (TTP) Hemolytic uremic syndrome (HUS) Disseminated intravascular coagulation (DIC) All of these conditions are associated with significantly decreased platelet counts that may become life threatening. Restoration of platelet numbers is essential to promote clotting and vascular patency.

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Laboratory Findings

These laboratory findings are associated with TTP and HUS:Thrombocytopenia -- Platelet count is often less than 20 x 109/L in TTP, but may not be as low in HUS. Schistocytes (red blood cell fragments, as indicated by the arrows in the image to the right) may be observed on the peripheral blood smear. Schistocytes are the result of erythrocytic membrane damage caused by sheering of red blood cells as they pass through a fibrin mesh of clot formation occurring in the blood vessels. LDH, serum bilirubin, and reticulocyte counts are elevated. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) are usually normal. Proteinuria and hematuria may be present.

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Case Studies in Clinical Microbiology
Review 1

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.

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Decreasing the risk of staphylococcal colonization of indwelling catheters in the future may involve:View Page

Fundamentals of Hemostasis
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 is the term that describes the process by which fibrin strands are broken down and then removed from an established clot?View Page
Which of the following mechanisms involve a series of interrelated chemical processes that lead to the formation of durable fibrin strands?View Page
Which of the following processes does NOT occur during primary hemostasis?View Page
Primary Hemostasis: Platelet Function

Platelets have four primary functions: Maintain vascular integrity-- Platelets contain chemicals within their granules that are vital to the normal growth and maintenance of the vascular system.Form a platelet plug-- Platelets are the fundamental components of the physical barrier that initially fills the breach in the compromised vessel.Provide the surface for creation of fibrin-- Fibrin strands, created during secondary hemostsis will weave in amongst the bound platelets that make up the platelet plug, solidifying the structure and creating a fibrin clotStimulate healing of the damaged tissues-- Platelet growth factors actually stimulate the production of new cells to replace those that were damaged, particularly smooth muscle cells and fibroblasts.

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Kinetic Processes Specific to Platelets

Adhesion When platelets adhere to exposed collagen, they take on a characteristic "spiny" shape. Their inherent stickiness, and the aforementioned spiny shape serve to compliment each other during this process. Von Willebrands Factor (vWF) is absorbed by surface receptors on both the platelet and exposed subendothelial tissue, thereby linking the platelets to the tissue.Shape change In response to chemical changes, platelets undergo shape changes from discs to spiny spheres.Release This process occurs prior to or concurrently with aggregation. Platelets dump the contents of their granules (ADP, serotonin, and calcium), which aids the upcoming aggregation process by acting as a chemical signal.Aggregation Platelets physically bind to each other, not just to the exposed subendothelial walls and collagen of the breached vessel. Platelet aggregation requires sufficient chemical signal stimulation.

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All of the following are activities associated with platelets except:View Page
Summary of Primary Hemostasis

In summation, we have covered the following sequence of events, which comprise primary hemostasis. The process begins with damage to a vessel wall, as blood flows outside the vasculature. The body responds with vasoconstriction, decreasing blood flow to the affected area. Platelets begin sticking to the damaged vessel walls (platelet adhesion). As the platelets stick, they change their shape (platelet activation) and release chemicals which signal other platelets to respond (platelet secretion). As other platelets arrive, they begin sticking to one another, clumping together, forming a plug to fill in the breach (platelet aggregation). This plug, while strong, is a temporary fix, and must be reinforced with fibrin strands to effectively fill the breach during the vessel repair process (secondary hemostasis).

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Overview of Secondary Hemostasis

Secondary hemostasis is the series of interrelated chemical processes that lead to the formation of durable fibrin strands, as well as being involved in their incorporation into the existing platelet plug, creating a fibrin clot. The fibrin strands themselves are manufactured through the interaction of various coagulation factors via a process known as the coagulation cascade. After fibrin strand construction, fibrin monomers are woven into the framework of the platelet plug, adding greater strength and stability. Once woven into the platelet plug and further stabilized with covalent cross-linking, a fibrin clot (the end goal of secondary hemostasis) is achieved. The fibrin clot is more durable and can withstand the blood shear stress caused by passing cells and plasma. This fibrin clot is more of a long term fix, allowing time for continued vascular repair.

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Secondary Hemostasis: Fibrin Formation via the Coagulation Cascade

The formation of fibrin involves three interconnected biochemical pathways; the intrinsic, extrinsic, and common pathways. These pathways allow for the interaction of coagulation factors via a finely tuned sequence of chemical processes, where the factors themselves control the activity of the pathway. Most coagulation factors are stimulated and activated by the preceding factor, hence the term, "coagulation cascade." Since factor activation requires the activation of a preceding factor, a deficiency in the functionality or availability of any factor would seriously impact the effectiveness of the coagulation process. Factor deficiencies do occur, however, and often lead to impaired vascular repair and depressed hemostatic activity. The image to the right shows a fibrin clot containing red cells (red) and platelets (blue). The fibrin strands, which are created through the process of secondary hemostasis via the coagulation cascade, are shown in yellow.

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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.

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The Fibrinolytic System

There is a very close relationship between the formation of fibrin, and its eventual degradation, or lysis. A fibrin clot serves as a temporary seal, intended to prevent continued blood loss from the damaged vessel while repair activities are performed. The breakdown of the clot begins almost as soon as the clot is formed! The process by which fibrin is broken down and removed from the clot, ultimately leading to complete dissolution of the clot, is called fibrinolysis.

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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.

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Which of the following statements is NOT correct?View Page
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.

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Hematology / Hemostasis Question Bank - Review Mode (no CE)
Match 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
Which changes Fibrinogen into Fibrin Monomer:View Page

Histology Special Stains: Connective Tissue
Masson's Trichrome Staining - Chemistry

Using acid-base chemistry, three dyes are employed to selectively stain muscle, collagen fibers, fibrin, and erythrocytes. Bouin’s solution is used first as a mordant to link the dye to the targeted tissue components. Nuclei are stained with Weigert’s hematoxylin, an iron hematoxylin, which is resistant to decolorization by the subsequent acidic staining solutions. Biebrich scarlet acid fuchsin stains all acidophilic tissue elements such as cytoplasm, muscle, and collagen. Subsequent application of phosphomolybdic/phosphotungstic acid is used as a decolorizer causing the Biebrich scarlet acid fuchsin to diffuse out of the collagen fibers while leaving the muscle cells red. Application of aniline blue will stain the collagen after which, 1% acetic acid is applied to differentiate the tissue section.

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Metabolic Syndrome

PAI-1 is a cytokine responsible for much of the prothrombotic state associated with metabolic syndrome. PAI-1 regulates the formation of thrombi by promoting formation of thrombin, platelet aggregation, and fibrin. PAI-1 inhibits fibrinolysis by blocking the activity of tissue-type plasminogen activator. PAI-1 is synthesized and released from the liver and adipocytes.PAI-1 is increased in obesity, is associated with insulin resistance, and is an early inflammatory predictor of type 2 diabetes.

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Red Cell Disorders: Peripheral Blood Clues to Nonneoplastic Conditions
The presence of erythrocytes with altered morphology (as indicated by the arrows in the image to the right) has a close association with each of the following conditions EXCEPT:View Page
The cells marked by blue arrows in the image below are associated with all of the following conditions except:View Page

Red Cell Morphology
Match the forms of poikilocytosis listed below with the physiological/environmental condition associated with their formation from the drop-down box.View Page
Match the forms of poikilocytosis on the left with the physiological/environmental condition associated with their formation on the right:View Page
Fragmented Red Blood Cells

Red cell fragments are formed when fibrin strands come in contact with circulating red cells. The strands cut a small piece from the original cell. Several descriptive names have been used for fragmented red cells, depending on the resulting shape of the fragment. These include pre-keratocyte (blister cell), keratocyte (horn cell or helmet cell), and schistocyte (more of a catch-all term). Schistocytes can be seen in disseminated intravascular coagulation (DIC), micropathic hemolytic anemia, glomerulonephritis, and hemolytic anemia resulting from mechanical trauma to the red blood cells (such as severe burns).

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Prekeratocytes or Blister Cells

The red cell fragment in the center of this slide is sometimes referred to as a prekeratocyte or blister cell. Notice the cell appears to have a blister or pseudo-vacuole extending around the flat edge. This cell has freed itself from a fibrin strand, and when the vacuole bursts, one or more projections may be visible. Survival time in circulation for these cells is very short.

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The prekeratocyte becomes a keratocyte when the vacuole ruptures, leaving a damaged cell that resembles a 'helmet' as seen in this image. Keratocytes are also referred to as 'horn' cells because they resemble a red cell with two horns.

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