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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

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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...
508
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

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

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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...
554
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

437
In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
437
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

128
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...
128
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

515
Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
515
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

566
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
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The Dyspepsia Educational Tool As a Novel Aid in Dyspepsia Management
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Deprescribing proton pump inhibitors.

Justin P Turner1, Wade Thompson2, Emily Reeve3

  • 1BPharm, MClinPharm, PhD, Senior Lecturer, Centre for Medicine Use and Safety, Faculty of Pharmacy and Pharmaceutical Sciences, Monash University, Vic; Faculty of Pharmacy, University of Montreal, Quebec, Canada.

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Summary

This article provides evidence-based strategies for deprescribing proton pump inhibitors (PPIs). It emphasizes a patient-centered approach, including dose reduction and gradual tapering, to minimize rebound effects and ensure safe discontinuation of PPI therapy.

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Area of Science:

  • Pharmacology
  • Evidence-Based Medicine
  • Patient Safety

Background:

  • Proton pump inhibitors (PPIs) are frequently overused beyond recommended durations and indications.
  • Long-term PPI use, especially beyond eight weeks, increases the risk of adverse events.
  • Many PPI prescriptions lack current evidence-based support.

Purpose of the Study:

  • To outline evidence-based approaches for the deprescription of proton pump inhibitors (PPIs).
  • To guide healthcare professionals in safely reducing or discontinuing PPI therapy.

Main Methods:

  • Review of evidence supporting PPI deprescribing strategies.
  • Emphasis on patient-centered care in the deprescribing process.
  • Description of dose-reduction and gradual tapering methods.

Main Results:

  • A patient-centered approach involving dose reduction or switching to pro re nata (PRN) use is supported by evidence.
  • Gradual dose tapering can minimize short-term rebound acid hypersecretion.
  • Collaborative planning between prescribers and patients is crucial.

Conclusions:

  • PPI deprescribing should be considered when long-term therapy is not indicated.
  • A structured, gradual approach is recommended to manage potential rebound symptoms.
  • Involving patients in the deprescribing plan enhances adherence and safety.