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Digestive Disorders and Their Clinical Features

Gastroesophageal reflux disease (GERD) or gastro-oesophageal reflux disease (GORD) is a chronic upper gastrointestinal disease in which stomach content persistently and regularly flows up into the esophagus, resulting in symptoms and/or complications. Symptoms include dental corrosion, dysphagia, heartburn, odynophagia, regurgitation, non-cardiac chest pain, extraesophageal symptoms such as chronic cough, hoarseness, reflux-induced laryngitis, or asthma. In the long term, and when not treated, complications such as esophagitis, esophageal stricture, and Barrett's esophagus may arise. Risk factors include obesity, pregnancy, smoking, hiatal hernia, and taking certain medications. Medications that may cause or worsen the disease include benzodiazepines, calcium channel blockers, tricyclic antidepressants, NSAIDs, and certain asthma medicines.

Figures (10)

EsophagusStomachUlcersDuodenumMucosaSubmucosaMuscle
Deaths from peptic ulcer disease per million persons in 2012 .mw-parser-output .legend{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .legend-color{display:inline-block;min-width:1.25em;height:1.25em;line-height:1.25;margin:1px 0;text-align:center;border:1px solid black;background-color:transparent;color:black}.mw-parser-output .legend-text{} 0–7 8–11 12–16 17–19 20–25 26–32 33–40 41–53 54–72 73–132
Disability-adjusted life year for peptic ulcer disease per 100,000 inhabitants in 2004 (WHO, 2009). no data less than 20 20–40 40–60 60–80 80–100 100–120 120–140 140–160 160–180 180–200 200–220 more than 220
Dysfunctional bone metabolism in coeliac disease
Factors involved in the pathogenesis of coeliac disease
Antigen-presenting cells bind peptides and "present" them to T cells, which detect HLA–peptide complexes through T-cell receptors. In coeliac disease, T cells respond to gluten peptides bound to HLA-DQ2 or HLA-DQ8. Gluten-derived peptides (red diamond) bind only with low affinity to HLA-DQ2 and HLA-DQ8, but TG2 can modify such peptides, turning them into high-affinity binders. Consequently, the HLA–gluten peptide complexes are more stable, which facilitates and enhances T-cell responses.
Small-bowel mucosal TG2 (red)-specific IgA deposits (green). A) Positive staining (arrow) in the mucosal villous of a short-term treated coeliac disease patient (gluten-free diet for three years). B) Negative IgA deposits (arrow) in the small-bowel mucosa of a long-term treated coeliac disease patient (gluten-free diet for eight years). Co-localisation of IgA deposits with TG2 is shown in yellow.
Schematic representation of intestinal mucosal events involved in coeliac disease pathogenesis
Immunofluorescence staining pattern of endomysial antibodies on a monkey oesophagus tissue sample
Endoscopic still of duodenum of a person with coeliac disease showing scalloping of folds and "cracked-mud" appearance to mucosa

Key Points

  • An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer.
  • The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating.
  • Coeliac disease (Commonwealth English) or celiac disease (American English) is a chronic autoimmune disease, mainly affecting the small intestine.
  • Crohn's disease and ulcerative colitis are both common differential diagnoses for the other, and confidently diagnosing a patient with one of the two diseases may sometimes not be possible.
  • Ulcerative colitis, in contrast, is restricted to the colon and the rectum.

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