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Related Concept Videos

Gastroesophageal Reflux Disease II: Clinical Features and Management01:29

Gastroesophageal Reflux Disease II: Clinical Features and Management

Gastroesophageal reflux disease, or GERD, is a persistent medical condition that affects many individuals worldwide. Its clinical manifestations can vary greatly, making diagnosis and management challenging for healthcare professionals. The following is a comprehensive overview of the clinical manifestations, assessment, and management strategies for GERD.
Clinical Manifestations
GERD presents itself in a multitude of ways, with symptoms varying from person to person. The hallmark symptoms are...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

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

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...
Gastroesophageal Reflux Disease01:25

Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is the backward flow of stomach contents (acid, pepsin, or bile) into the esophagus, causing mucosal inflammation known as esophagitis. It results from failure of antireflux mechanisms, mainly the lower esophageal sphincter (LES), influenced by mechanical and physiological factors.Etiology and Risk FactorsGERD develops when LES function is weakened or when intra-abdominal pressure increases. Risk factors include aging, obesity, and sliding hiatal hernia,...
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

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...
Gastroesophageal Reflux Disease I: Meaning and Pathophysiology01:29

Gastroesophageal Reflux Disease I: Meaning and Pathophysiology

Gastroesophageal Reflux Disease (GERD) involves the recurrent backflow of the stomach or duodenal contents into the esophagus, leading to troublesome symptoms and potential esophageal mucosal damage. Although GERD is often referred to as a disease, it is more accurately described as a syndrome, as it encompasses a range of symptoms and complications rather than a singular pathological entity, impacting a large number of individuals as the most prevalent upper gastrointestinal problem. Roughly...
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

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...

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Updated: May 28, 2026

Cooling or Warming the Esophagus to Reduce Esophageal Injury During Left Atrial Ablation in the Treatment of Atrial Fibrillation
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Extinguish holiday heartburn

Marvin Lipman1

  • 1New York Medical College and Consumer Reports, USA.

Consumer Reports
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PubMed
Summary

No abstract available in PubMed .

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