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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...

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Evidence for covalent linkage between some plasma α2-antiplasmin molecules and Aα chains of circulating fibrinogen.

Journal of thrombosis and haemostasis : JTH·2013
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Short by one mechanism: a rebuttal.

Journal of thrombosis and haemostasis : JTH·2010
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Human fibrinogen heterogeneities: determination of the major Aalpha chain derivatives in blood.

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Thrombosis risk modification in transgenic mice containing the human fibrinogen thrombin-binding gamma' chain sequence.

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Evidence that alpha2-antiplasmin becomes covalently ligated to plasma fibrinogen in the circulation: a new role for plasma factor XIII in fibrinolysis regulation.

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Related Experiment Video

Updated: Jun 25, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Dysfibrinogenemia and thrombosis.

M W Mosesson1

  • 1Sinai Samaritan Medical Center, University of Wisconsin Medical School, Milwaukee 53233, USA.

Seminars in Thrombosis and Hemostasis
|August 12, 1999
PubMed
Summary

Congenital fibrinogen defects (dysfibrinogenemias) arise from structural issues, potentially causing bleeding or clotting disorders. This review details molecular defects linked to thrombosis in these rare fibrinogen abnormalities.

Area of Science:

  • Hematology
  • Molecular Biology
  • Genetics

Background:

  • Congenital abnormal fibrinogen molecules, or dysfibrinogenemias, result from structural defects.
  • While often asymptomatic, dysfibrinogenemias can manifest as bleeding disorders, thrombophilia, or both.
  • Understanding fibrinogen's molecular structure aids in identifying these abnormalities.

Purpose of the Study:

  • To review identified dysfibrinogenemias associated with thrombosis.
  • To describe the molecular defects underlying these fibrinogen abnormalities.
  • To highlight potential co-existing hemostasis defects in affected patients.

Main Methods:

  • Literature review of dysfibrinogenemias associated with thrombosis.
  • Analysis of molecular defects in abnormal fibrinogen molecules.

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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
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The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

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Related Experiment Videos

Last Updated: Jun 25, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
07:09

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

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The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

Published on: February 27, 2026

  • Examination of associated hemostasis defects and clinical presentations.

    • Main Results:

    • Dysfibrinogenemias can stem from impaired fibrinopeptide release, defective fibrin polymerization, or abnormal factor XIIIa cross-linking.
    • Thrombophilia is linked to abnormal fibrinopeptide release or polymerization defects.
    • Other described defects include abnormal platelet interactions, fibrinolysis, fibrinolytic system assembly, and calcium binding.

    Conclusions:

    • Dysfibrinogenemias represent a spectrum of molecular defects with varied clinical outcomes, including bleeding and thrombosis.
    • Molecular characterization is crucial for understanding the pathophysiology of dysfibrinogenemias.
    • Co-existing hemostatic defects can influence the clinical presentation and management of dysfibrinogenemias.