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Related Concept Videos

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

353
Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
353
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

349
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.
349
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

535
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...
535
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

126
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...
126
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

66
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...
66
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

402
Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
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Related Experiment Video

Updated: May 31, 2025

Author Spotlight: Point-of-Care Ultrasound for Gastric Content Assessment and Risk Stratification in Perioperative Care
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Predictive Factors Associated with Inappropriate Intravenous Proton Pump Inhibitors Use in Hospitalized Patients: A

Niveen Khoury1, David Stepensky2, Naim Abu Freha3

  • 1Pharmacy Department, EMMS Nazareth Hospital, Nazareth 16100, Israel.

Medicina (Kaunas, Lithuania)
|January 25, 2025
PubMed
Summary

Inappropriate use of intravenous Proton Pump Inhibitors (PPIs) remains common. Factors like congestive heart failure and surgeon prescription increase risks, highlighting a need for better IV PPI stewardship.

Keywords:
clinical outcomeshospitalinappropriate prescriptionintravenousproton pump inhibitors

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Area of Science:

  • Gastroenterology
  • Clinical Pharmacy
  • Hospital Medicine

Background:

  • Proton Pump Inhibitors (PPIs) are primary treatments for acid-related gastrointestinal disorders.
  • Intravenous (IV) PPI formulation use has significantly increased in hospital settings.

Purpose of the Study:

  • To evaluate the appropriateness of IV PPI prescribing.
  • To identify risk factors and clinical outcomes linked to inappropriate IV PPI use.

Main Methods:

  • A retrospective case-control study analyzed 540 hospitalized patients receiving IV PPIs.
  • Data collection included patient records from admission through a 3-month post-discharge period.
  • Appropriateness of IV PPI use and clinical outcomes were assessed.

Main Results:

  • 24% of patients (130/540) exhibited inappropriate IV PPI use regarding indication, dosage, or duration.
  • Inappropriate use was associated with congestive heart failure (OR 1.77) and prescription by surgeons (OR 1.53).

Conclusions:

  • Inappropriate IV PPI administration is prevalent in clinical practice.
  • Predictors of inappropriate use include congestive heart failure, advanced age, anticoagulant/antithrombotic use, and surgical management.