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Related Concept Videos

Coagulation01:09

Coagulation

11.9K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
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Coagulation01:06

Coagulation

1.7K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
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Introduction to Hemostasis01:05

Introduction to Hemostasis

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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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Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

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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...
15.3K
Disorders of Hemostasis01:24

Disorders of Hemostasis

2.7K
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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Formation of the Platelet Plug01:22

Formation of the Platelet Plug

10.7K
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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Related Experiment Video

Updated: Mar 31, 2026

A Precision Medicine Tool for Measurement and Monitoring of Hemoglobin S in Sickle Cell Disease Patients Receiving Transfusion Therapy
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Coagulation activation in sickle cell trait: an exploratory study.

Chirag Amin1, Soheir Adam1, Micah J Mooberry1

  • 1Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, USA.

British Journal of Haematology
|October 30, 2015
PubMed
Summary
This summary is machine-generated.

Sickle cell trait (HbAS) may increase venous thromboembolism risk. Healthy HbAS individuals show elevated markers of coagulation activation, suggesting a potential prothrombotic state.

Keywords:
coagulationsicklethrombintissue factorvenous thrombosis

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Area of Science:

  • Hematology
  • Thrombosis Research
  • Genetics

Background:

  • Epidemiologic studies link sickle cell trait (HbAS) to increased venous thromboembolism (VTE) risk.
  • The underlying mechanisms for this association in healthy individuals remain unclear.
  • Investigating basal coagulation status in HbAS is crucial for understanding VTE risk.

Purpose of the Study:

  • To explore whether healthy individuals with sickle cell trait exhibit chronic basal hyperactivation of coagulation.
  • To identify potential mechanisms contributing to a prothrombotic state in sickle cell trait.
  • To compare coagulation markers in HbAS individuals with healthy controls (HbAA) and sickle cell disease patients (HbSS).

Main Methods:

  • Comparative study involving healthy HbAS individuals, healthy HbAA controls, and HbSS patients.
  • Measurement of plasma thrombin-antithrombin complexes and D-dimer levels.
  • Assessment of thrombin generation in platelet-poor plasma and whole blood tissue factor activity.
  • Evaluation of plasma microparticle tissue factor activity.

Main Results:

  • Elevated plasma thrombin-antithrombin complexes and D-dimer levels were observed in HbAS individuals compared to HbAA controls.
  • Thrombin generation in platelet-poor plasma was similar between HbAS and HbAA groups.
  • Plasma microparticle tissue factor activity showed a non-significant trend toward elevation in HbAS.

Conclusions:

  • Preliminary findings suggest a basal procoagulant state in healthy individuals with sickle cell trait.
  • Elevated markers of coagulation activation may contribute to the increased VTE risk associated with HbAS.
  • Further research in larger cohorts is warranted to confirm these findings and elucidate mechanisms.