Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Coagulation01:06

Coagulation

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...
Coagulation01:09

Coagulation

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...
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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Oxidative damage in age-related macular degeneration.

Histology and histopathology·2007
Same author

H-Ras oncogene counteracts the growth-inhibitory effect of genistein in T24 bladder carcinoma cells.

British journal of cancer·2004
Same author

Potential clozapine target sites on peripheral hematopoietic cells and stromal cells of the bone marrow.

The pharmacogenomics journal·2003
Same author

Role of splenectomy in immune (idiopathic) thrombocytopenic purpura.

Blood reviews·2002
Same author

Thrombotic thrombocytopenic purpura associated with clopidogrel.

The New England journal of medicine·2000
Same author

Megakaryocyte-targeted synthesis of the integrin beta(3)-subunit results in the phenotypic correction of Glanzmann thrombasthenia.

Blood·2000
Same journal

An approach to the management of dementia syndromes.

The Johns Hopkins medical journal·1982
Same journal

Torsion dystonia.

The Johns Hopkins medical journal·1982
Same journal

The Rieger syndrome: a heritable disorder associated with glaucoma.

The Johns Hopkins medical journal·1982
Same journal

Cerebro-hepato-renal (Zellweger) syndrome and neonatal adrenoleukodystrophy: similarities in phenotype and accumulation of very long chain fatty acids.

The Johns Hopkins medical journal·1982
Same journal

Surgical therapy of complex partial epilepsy.

The Johns Hopkins medical journal·1982
Same journal

Toxic epidermal necrolysis.

The Johns Hopkins medical journal·1982
See all related articles

Related Experiment Video

Updated: Jun 30, 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

Disseminated intravascular coagulation

W R Bell

    The Johns Hopkins Medical Journal
    |June 1, 1980
    PubMed
    Summary
    This summary is machine-generated.

    Disseminated intravascular coagulation (DIC) is a complex syndrome caused by simultaneous activation of clotting and fibrinolysis. Identifying and controlling the underlying cause is crucial for managing patients with DIC.

    More Related Videos

    In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
    09:19

    In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

    Published on: May 24, 2020

    Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
    04:56

    Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

    Published on: August 4, 2023

    Related Experiment Videos

    Last Updated: Jun 30, 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

    In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
    09:19

    In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time

    Published on: May 24, 2020

    Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
    04:56

    Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

    Published on: August 4, 2023

    Area of Science:

    • Hematology
    • Pathophysiology

    Background:

    • Disseminated intravascular coagulation (DIC) is a serious condition characterized by the simultaneous activation of coagulation and fibrinolytic systems.
    • DIC presents with diverse clinical manifestations and can be triggered by various underlying conditions.

    Purpose of the Study:

    • To explore the multifaceted nature of DIC.
    • To highlight the need for further research into the mechanisms initiating DIC, including endothelial damage, hemodynamic changes, and the role of natural inhibitors.
    • To emphasize the importance of understanding DIC's pathophysiology for improved therapeutic strategies.

    Main Methods:

    • Review of existing literature on DIC pathophysiology.
    • Analysis of factors contributing to DIC initiation.
    • Discussion of diagnostic and therapeutic challenges.

    Main Results:

    • DIC results from uncontrolled activation of both coagulation and fibrinolysis.
    • Multiple pathways can initiate DIC, involving vascular endothelium and hemostasis inhibitors.
    • Effective management hinges on identifying and addressing the primary underlying disease.

    Conclusions:

    • Further research is essential to elucidate the precise mechanisms driving DIC.
    • A comprehensive understanding of DIC's triggers will enhance treatment protocols.
    • Prompt identification and management of the underlying pathology are paramount for successful patient outcomes.