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Related Concept Videos

Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

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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.
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Peptic ulcers can also be...
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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.
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Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
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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.
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Enteral Nutrition II: Nasointestinal and Gastrostomy Feeding01:15

Enteral Nutrition II: Nasointestinal and Gastrostomy Feeding

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Enteral nutrition encompasses various methods of delivering nutrition directly to the gastrointestinal (GI) tract, bypassing traditional oral intake. It is particularly beneficial for patients who cannot eat by mouth but have a functioning digestive system. Key methods include nasointestinal feeding, gastrostomy, and jejunostomy, each suited to different clinical scenarios based on the patient's needs and condition.
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Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis
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Formula Feeding Predisposes Gut to NSAID-Induced Small Intestinal Injury.

A Schuck-Phan1, T Phan2, P A Dawson3

  • 1Department of Pediatrics, Division of Pediatric Gastroenterology, University of Texas Health Science Center, Houston, TX, USA.

Clinical & Experimental Pharmacology
|October 1, 2019
PubMed
Summary
This summary is machine-generated.

Maternal separation and formula feeding sensitize rat intestines to Non-Steroidal Anti-Inflammatory Drugs (NSAID)-induced injury. This stress response alters intestinal maturation, increasing vulnerability to injury in newborns.

Keywords:
Formula feedingIndomethacinIntestinal injuryIntestinal maturationPremature infants

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Area of Science:

  • Neonatal physiology
  • Gastrointestinal development
  • Pharmacology

Background:

  • Breastfeeding offers protection against infant diseases like necrotizing enterocolitis.
  • Maternal separation and NSAIDs can cause intestinal injury and bleeding in infants.
  • Early life stress and feeding practices may impact intestinal vulnerability.

Purpose of the Study:

  • To investigate if maternal separation and formula feeding increase intestinal sensitivity to indomethacin (NSAID)-induced injury in suckling rats.
  • To explore the underlying mechanisms of this increased sensitivity.

Main Methods:

  • Suckling rats were either dam-fed or separated and formula-fed for 6 days.
  • Indomethacin or saline was administered for 3 days.
  • Intestinal injury, bleeding, and maturation markers (bile acids, sucrase, corticosterone, ASBT mRNA) were assessed.

Main Results:

  • Formula-fed rats treated with indomethacin showed a 2-fold increase in intestinal bleeding and mucosal injury compared to controls.
  • Indomethacin did not affect dam-fed rats.
  • Formula-fed rats exhibited increased luminal bile acids, sucrase activity, corticosterone, and ASBT mRNA expression.

Conclusions:

  • Maternal separation stress induces early intestinal maturational changes via corticosteroid release.
  • These changes increase epithelial exposure to bile acids, sensitizing the intestine to NSAID-induced injury.
  • Early life stress may compromise intestinal defense mechanisms in newborns.