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

Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

325
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...
325
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

1.0K
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
1.0K
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

777
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
777
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

654
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
654
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

791
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
791
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

161
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
161

You might also read

Related Articles

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

Sort by
Same author

Quality Assurance in Platelet Function Testing.

Clinics in laboratory medicine·2026
Same author

Pathogenic PF4/Polyanion ELISA-Negative Antibodies in HIT.

American journal of hematology·2026
Same author

Platelet factor 4 antibody persistence and long-term pathogenicity in vaccine-induced immune thrombotic thrombocytopenia.

Journal of thrombosis and haemostasis : JTH·2026
Same author

A Diagnostic Journey through a Rare Hemostatic Disorder.

The journal of applied laboratory medicine·2026
Same author

Platelet Factor 4 Antibody Persistence and Long-term Pathogenicity in Vaccine-induced Immune Thrombotic Thrombocytopenia.

medRxiv : the preprint server for health sciences·2025
Same author

Pathogenic PF4/Polyvinylsulfonate ELISA-negative Antibodies in HIT.

medRxiv : the preprint server for health sciences·2025
Same journal

Nze C, Flowers CR. Barriers to accessing cellular therapy for patients receiving care in community practices. Hematology Am Soc Hematol Educ Program. 2023;2023(1):382-385.

Hematology. American Society of Hematology. Education Program·2025
Same journal

CAR T-cell therapy and bispecific antibodies in the management of multiple myeloma.

Hematology. American Society of Hematology. Education Program·2025
Same journal

Emerging immunotherapy advances for non-Hodgkin lymphomas: engaging T cells in the fight.

Hematology. American Society of Hematology. Education Program·2025
Same journal

Anticoagulants in hematologic malignancies: what is the data?

Hematology. American Society of Hematology. Education Program·2025
Same journal

Diagnosis and management of cold agglutinin disease.

Hematology. American Society of Hematology. Education Program·2025
Same journal

What to know about rare B-cell malignancies in 2025.

Hematology. American Society of Hematology. Education Program·2025
See all related articles

Related Experiment Video

Updated: Oct 10, 2025

Mouse Model of Pressure Ulcers After Spinal Cord Injury
06:51

Mouse Model of Pressure Ulcers After Spinal Cord Injury

Published on: March 9, 2019

9.7K

Cryptogenic oozers and bruisers.

Kristi J Smock1, Karen A Moser2

  • 1Department of Pathology, University of Utah, Salt Lake City, UT.

Hematology. American Society of Hematology. Education Program
|December 10, 2021
PubMed
Summary
This summary is machine-generated.

Diagnosing bleeding disorders with unclear coagulation tests is challenging. Advanced platelet function tests, genetic panels, and expert interpretation are key to identifying these conditions.

More Related Videos

Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
03:05

Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors

Published on: February 16, 2024

1.2K
A Simplified Technique for Producing an Ischemic Wound Model
12:00

A Simplified Technique for Producing an Ischemic Wound Model

Published on: May 2, 2012

17.5K

Related Experiment Videos

Last Updated: Oct 10, 2025

Mouse Model of Pressure Ulcers After Spinal Cord Injury
06:51

Mouse Model of Pressure Ulcers After Spinal Cord Injury

Published on: March 9, 2019

9.7K
Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors
03:05

Author Spotlight: Advancing Early Detection and Treatment of Gastrointestinal Tumors

Published on: February 16, 2024

1.2K
A Simplified Technique for Producing an Ischemic Wound Model
12:00

A Simplified Technique for Producing an Ischemic Wound Model

Published on: May 2, 2012

17.5K

Area of Science:

  • Hematology
  • Clinical Diagnostics
  • Genetics

Background:

  • Bleeding disorders with non-diagnostic coagulation tests pose significant diagnostic challenges.
  • Primary hemostasis disorders require advanced platelet function testing and specialized von Willebrand factor assays.
  • Secondary hemostasis and fibrinolytic disorders also present diagnostic difficulties with current methods.

Observation:

  • A substantial number of patients remain undiagnosed after comprehensive testing.
  • Many undiagnosed patients exhibit mild bleeding phenotypes and may have undiagnosed platelet function disorders.
  • Current diagnostic options for fibrinolytic disorders are limited.

Findings:

  • Specialized testing, including platelet electron microscopy and advanced von Willebrand factor assays, aids in diagnosing primary hemostasis disorders.
  • Coagulation factor assays and factor XIII assays are crucial for evaluating secondary hemostasis.
  • High-throughput genetic testing holds promise for diagnosing a larger proportion of patients in the future.

Implications:

  • A logical, expert-guided laboratory workup is essential for maximizing diagnostic yield.
  • Future research should focus on improving diagnostic tools for fibrinolytic disorders and undiagnosed platelet function disorders.
  • Genetic testing panels may significantly improve the diagnosis of rare bleeding disorders.