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

Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

203
Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
203
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

84
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...
84
Mitral Valve Prolapse III: Nursing Management01:19

Mitral Valve Prolapse III: Nursing Management

86
The nursing management of Mitral Valve Prolapse, or MVP, centers around patient education, symptom monitoring, and lifestyle modifications.Patient Education on MVP Diagnosis and Heredity: Nurses should provide comprehensive education about MVP, a condition where the mitral valve does not close appropriately during heartbeats. This education often includes the condition's pathophysiology, symptoms, and potential complications, like arrhythmias or mitral regurgitation. Though not fully...
86
Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

77
Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
77
Disorders of Hemostasis01:24

Disorders of Hemostasis

1.4K
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.
1.4K
Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

127
Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...
127

You might also read

Related Articles

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

Sort by
Same author

Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

First-trimester plasma targeted metabolomics for eicosanoids reveals predictive potential and preventive targets for severe preeclampsia: a nested case-control study.

BMC pregnancy and childbirth·2026
Same author

Trajectories of Maternal Placental Growth Factor Levels from Early to Late Pregnancy: Prenatal Factors and Adverse Perinatal Outcomes.

International journal of women's health·2026
Same author

Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

A Component Analysis of Endotheliopathy of Trauma.

Research square·2026
Same author

OmicGlaze: Spatial Multi-Omic Mapping of Traumatic Brain Injury.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Oct 28, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
05:31

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

1.0K

Prothrombotic state associated with preeclampsia.

Cha Han1, Yuan-Yuan Chen1, Jing-Fei Dong2,3

  • 1Department of Obstetrics and Gynecology, Tianjin Medical University General Hospital, Tianjin, China.

Current Opinion in Hematology
|July 16, 2021
PubMed
Summary
This summary is machine-generated.

Preeclampsia, a pregnancy complication, shifts the blood towards a prothrombotic state due to placental issues and maternal factors. Understanding this transition is key to preventing severe maternal and fetal complications.

More Related Videos

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

11.5K
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

781

Related Experiment Videos

Last Updated: Oct 28, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
05:31

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

1.0K
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

11.5K
Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

781

Area of Science:

  • Obstetrics and Gynecology
  • Maternal-Fetal Medicine
  • Hematology

Background:

  • Preeclampsia is a significant cause of maternal and fetal morbidity and mortality.
  • Pregnancy normally involves a hypercoagulable state, which can become prothrombotic in preeclampsia.
  • The mechanisms driving this transition from hypercoagulable to prothrombotic are not fully understood.

Purpose of the Study:

  • To review recent advancements in understanding the pathophysiology of preeclampsia.
  • To elucidate the mechanisms behind the prothrombotic state associated with preeclampsia.
  • To discuss the factors contributing to the transition from a normal pregnancy hypercoagulable state to a prothrombotic state in preeclampsia.

Main Methods:

  • Review of current literature on preeclampsia pathophysiology.
  • Analysis of factors contributing to the prothrombotic state in preeclampsia.
  • Discussion of the role of placental factors and maternal conditions.

Main Results:

  • The prothrombotic state in preeclampsia is initiated by placental factors, exacerbated by ischemic and oxidative injuries.
  • It is multifactorial, involving placental issues, genetic predisposition, pre-existing conditions, and acquired conditions.
  • Endotheliopathy is central to preeclampsia, driving dysregulation of coagulation, platelets, and adhesive ligands, thus promoting the prothrombotic state.

Conclusions:

  • Preeclampsia patients frequently develop a severe prothrombotic state, increasing risks of thrombosis and thromboembolism.
  • This state poses life-threatening risks during and after pregnancy.
  • Early identification and management of the prothrombotic state are crucial for improving outcomes.