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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

521
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...
521
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

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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...
141
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

515
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.
515
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

442
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...
442
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

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

565
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...
565
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

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

588
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...
588

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Simultaneous Laryngopharyngeal and Conventional Esophageal pH Monitoring
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SAFETY OF LONG-TERM PROTON PUMP INHIBITORS: FACTS AND MYTHS.

Decio Chinzon1, Gerson Domingues2, Nivia Tosetto3

  • 1Faculdade de Medicina da Universidade de São Paulo, Departamento de Gastroenterologia, São Paulo, SP, Brasil.

Arquivos De Gastroenterologia
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Summary

Proton pump inhibitors (PPIs) are widely used, but long-term use may increase risks for fractures, infections, and kidney disease. Rational PPI use at the lowest effective dose is key to mitigating potential adverse effects.

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Area of Science:

  • Gastroenterology
  • Pharmacology
  • Internal Medicine

Background:

  • Proton pump inhibitors (PPIs) are among the most frequently prescribed medications globally.
  • Concerns regarding potential adverse effects have arisen due to their widespread and long-term use.

Purpose of the Study:

  • To review and discuss the available data and causality of adverse events associated with proton pump inhibitors (PPIs).

Main Methods:

  • A narrative review of safety and adverse events related to PPIs from 2015 to 2020.
  • Systematic search on PubMed for systematic reviews and meta-analyses on gastric cancer, micronutrient deficiency, acid rebound, infections, fractures, dementia, kidney disease, and cardiovascular changes.

Main Results:

  • Potential associations found between PPI use and osteoporosis-related fractures, intestinal infections (e.g., Clostridium difficile), and deficiencies in vitamins B12, magnesium, and iron.
  • Reports link PPIs to dementia, pneumonia, kidney disease, myocardial infarction, and stroke, with consistent evidence suggesting increased kidney event risk in elderly, long-term users, or those with pre-existing kidney disease.
  • Acid rebound, characterized by increased gastric acid production upon abrupt discontinuation, is a noted phenomenon.

Conclusions:

  • Rational use of PPIs, including the lowest effective dose and shortest duration, is crucial for mitigating adverse effects.
  • While potential clinical impacts exist, the causal association of these adverse effects with PPIs requires further validation.