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

Disorders of Hemostasis01:24

Disorders of Hemostasis

696
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.
696
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

607
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...
607
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

5.3K
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...
5.3K
Coagulation01:09

Coagulation

4.5K
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...
4.5K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

131
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
131
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

4.2K
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...
4.2K

You might also read

Related Articles

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

Sort by
Same author

Optimizing Extraction and HPLC-ESI-QTOF-MS/MS Analysis of Bound Phenolics From Okra (<i>Abelmoschus esculentus</i>) and Their Biological Activity.

Food science & nutrition·2026
Same author

Reprogramming macrophage immunometabolism via glutamine antagonism potentiates colorectal cancer therapy in mice.

Nature communications·2026
Same author

Mucosal Involvement in Bullous Pemphigoid: Severity Indicator and Associated Clinical Features from a Retrospective Cohort Study.

Journal of inflammation research·2026
Same author

Comparative study on the wound healing effects of local versus systemic application of Polymyxin B in mice infected with multidrug-resistant <i>Pseudomonas aeruginosa</i>.

Frontiers in microbiology·2026
Same author

Safety, Pharmacokinetics, and Efficacy of 1.5% Ruxolitinib Gel (HDM3010) in Adult Patients with Prurigo Nodularis: A Phase I/II, Randomized, Double-Blind, Vehicle-Controlled Multicenter Clinical Trial.

Dermatology and therapy·2026
Same author

Efficient Photocatalytic Elimination of Imidazolinone Herbicides by Bismuth-Based Photocatalyst BiOIO<sub>3</sub>.

Molecules (Basel, Switzerland)·2026

Related Experiment Video

Updated: Jun 3, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.5K

Bullous pemphigoid and hypercoagulability: a review.

Bingjie Zhang1, Nan Yang2, Li Li1

  • 1Department of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, China.

Expert Review of Clinical Immunology
|January 8, 2025
PubMed
Summary

Bullous pemphigoid (BP) is an autoimmune disease linked to increased clotting risk. Monitoring coagulation markers like D-dimer is vital for managing BP patients with thrombotic events.

Keywords:
Bullous pemphigoidcoagulation parameterhypercoagulabilitythrombo-prophylaxisthrombosis

More Related Videos

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

481
Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
04:56

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients

Published on: August 4, 2023

687

Related Experiment Videos

Last Updated: Jun 3, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.5K
Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

481
Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients
04:56

Author Spotlight: Deciphering Coagulation Disorders in Traumatic Brain Injury Patients

Published on: August 4, 2023

687

Area of Science:

  • Dermatology
  • Hematology
  • Immunology

Background:

  • Bullous pemphigoid (BP) is an autoimmune blistering disease.
  • BP is associated with a high incidence of thrombotic events, indicating a hypercoagulable state.

Purpose of the Study:

  • To review the interplay between coagulation and immune-inflammatory responses in BP.
  • To highlight characteristic coagulation parameter changes in BP patients.

Main Methods:

  • Literature review up to August 2024.
  • Selective search in the PubMed database.

Main Results:

  • The hypercoagulable state and BP have a mutually reinforcing effect.
  • Key coagulation markers to monitor include D-dimer, fibrinogen, and fibrin degradation products (FDP).

Conclusions:

  • Close monitoring of coagulation markers is crucial for BP patients.
  • Targeting shared pathways in treatment may benefit patients with both BP and hypercoagulability.