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Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

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Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
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Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid...
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Intestinal Obstruction I: Introduction01:29

Intestinal Obstruction I: Introduction

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Intestinal obstruction is a partial or complete blockage of the small or large intestine that disrupts the normal flow of intestinal contents through the lumen. This interruption impairs digestion, absorption, and fluid balance, and may lead to serious complications if not treated promptly.Mechanical ObstructionMechanical obstruction occurs when a physical blockage prevents intestinal contents from passing, arising from within the lumen or the bowel wall, or from external compression.Adhesions,...
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Inflammatory Bowel Disease V: Surgical Management01:21

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Inflammatory Bowel Disease I: Introduction01:26

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Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows...
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Author Spotlight: Enhancing Understanding and Treatment Strategies with the NEC-on-a-Chip Model
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Necrotizing enterocolitis: the road to zero.

Jae H Kim1

  • 1Divisions of Neonatology & Pediatric Gastroenterology, Hepatology and Nutrition, University of California San Diego, Rady Children's Hospital of San Diego, 200 West Arbor Dr MPF 1140, San Diego, CA 92103-8774, USA.

Seminars in Fetal & Neonatal Medicine
|November 26, 2013
PubMed
Summary
This summary is machine-generated.

Necrotizing enterocolitis (NEC) is a severe condition in preterm infants. This review summarizes optimal prevention and programmatic strategies to eliminate NEC in healthcare settings.

Keywords:
Necrotizing enterocolitisNeonatePreventionStrategies

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Area of Science:

  • Neonatal Medicine
  • Gastroenterology
  • Pediatric Surgery

Background:

  • Necrotizing enterocolitis (NEC) remains a critical gastrointestinal emergency for preterm neonates.
  • The complex pathogenesis of NEC involves enteral feeding, gut immunity, and microbiota.
  • Current early diagnosis and treatment of NEC are suboptimal, highlighting the need for prevention.

Purpose of the Study:

  • To review and summarize the most effective strategies for NEC prevention.
  • To discuss the importance of programmatic changes in reducing NEC rates.
  • To identify optimal approaches for eliminating NEC within an institution.

Main Methods:

  • Literature review of current NEC prevention and management strategies.
  • Analysis of the role of enteral feeding, gut immunity, and microbiota in NEC pathogenesis.
  • Synthesis of evidence-based recommendations for institutional NEC elimination programs.

Main Results:

  • Prevention strategies are paramount due to limitations in early diagnosis and treatment of NEC.
  • Understanding the interplay of feeding, immunity, and microbiota offers new avenues for NEC reduction.
  • Integrated programmatic changes are crucial alongside individual prevention tactics.

Conclusions:

  • Implementing comprehensive prevention strategies is the most effective approach to reducing NEC.
  • A multi-faceted approach, including programmatic changes, is essential for NEC elimination.
  • Further research into NEC pathogenesis may yield novel preventive measures.