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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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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...
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Introduction to Hemostasis01:05

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Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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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...
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Disorders of Hemostasis01:24

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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.
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Rh Blood Group01:19

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The Rhesus (Rh) antigen is crucial in determining blood groups and ensuring compatibility during blood transfusions.
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Factor IX inhibitors and anaphylaxis in haemophilia B.

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Factor IX inhibitors and anaphylaxis in hemophilia B.

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Related Experiment Video

Updated: May 5, 2026

Live-cell Imaging of Platelet Degranulation and Secretion Under Flow
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Von Willebrand's disease

B M Ewenstein1

  • 1Hematology-Oncology Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. bmewenstei@bics.bwh.harvard.edu

Annual Review of Medicine
|January 1, 1997
PubMed
Summary

Von Willebrand

Area of Science:

  • Hematology
  • Molecular Biology
  • Genetics

Background:

  • Von Willebrand's disease (vWD) is a bleeding disorder caused by abnormalities in von Willebrand factor (vWF).
  • vWF is crucial for primary and secondary hemostasis.
  • vWD classification includes types 1 (partial deficiency), 3 (complete deficiency), and 2 (qualitative defects).

Purpose of the Study:

  • To review the classification, molecular basis, diagnosis, and treatment of von Willebrand's disease.
  • To highlight the distinct subtypes of type 2 vWD and their underlying genetic causes.

Main Methods:

  • Review of existing literature on vWD.
  • Description of diagnostic methods including immunologic and functional studies of vWF, factor VIII levels, and multimer gel electrophoresis.

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In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
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  • Discussion of therapeutic strategies.

    • Main Results:

    • Type 2 vWD is subdivided into four subtypes (2A, 2B, 2N, 2M) based on functional abnormalities, often caused by missense mutations.
    • Type 3 vWD results from major disruptions in the vWF gene.
    • The molecular basis for type 1 vWD remains largely undefined.

    Conclusions:

    • Accurate diagnosis of vWD subtypes relies on comprehensive laboratory testing.
    • Desmopressin is the primary treatment, stimulating endogenous vWF release.
    • Alternative therapies like cryoprecipitate and factor VIII concentrates are used for desmopressin-unresponsive patients.