L3 esophagitis


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L3 esophagitis

  1. 1. EsophagitisLecture3
  2. 2. Esophagitis• Inflammation of esophagus (after injury toesophageal mucosa).Predisposing factors/Origins/Causes:• Prolonged gastric intubation,• Ureamia• Ingestion of corrosive or Irritant substances• Radiation• Chemotherapy
  3. 3. Epidemiology• In Iran (more than80%) and China the prevalence isextremely high due to unknown reason.• In Western countries high prevalence is due toreflux of gastric contents (reflux esophagitis).• In USA o.5% due to gastro esophageal disease
  4. 4. Types/causes of esophagitisReflux esophagitisCHEMICAL AND INFECTIOUS ESOPHAGITISEOSINOPHILIC ESOPHAGITISHerpes simplex esophagitisCytomegalovirus (CMV) esophagitisCandida esophagitisCrohn’s diseaseIdiopathic eosinophilic esophagitisOther types of esophagitis include those caused by tuberculosis,blastomycosis, drugs, allergic reactions, irradiation and ingestion ofcorrosive chemicals.
  5. 5. The stratified squamous epithelium ofthe esophagus is resistant toabrasion from foods but is sensitiveto acid.Submucosal glands, which are mostabundant in the proximal and distalesophagus, contribute to mucosalprotection by secreting mucin andbicarbonate.
  6. 6. GERD• constant lower esophageal sphincter toneprevents reflux of acidic gastric contents,which are under positive pressure and wouldotherwise enter the esophagus. Reflux ofgastric contents into the lower esophagus isthe most frequent cause of esophagitis .Theassociated clinical condition is termedgastroesophageal reflux disease (GERD).
  7. 7. Pathogenesis.• Reflux of gastric juices is central to thedevelopment of mucosal injury in GERD.• In severe cases, reflux of bile from the duodenummay exacerbate the damage.
  8. 8. • Conditions that decrease lower esophagealsphincter tone or increase abdominalpressure contribute to GERD and includealcohol and tobacco use, obesity, centralnervous system depressants, pregnancy,hiatal hernia ,delayed gastric emptying, andincreased gastric volume.• In many cases, no definitive cause isidentified.
  9. 9. Morphology.•Simple hyperemia, evident to the endoscopistas redness, may be the only alteration.• In mild GERD the mucosal histology is oftenunremarkable. t.
  10. 10. • With more significant disease,eosinophilsare recruited into thesquamous mucosa followed by neutrophils,which are usually associated with moresevere injury.
  11. 11. • Basal zone hyperplasia exceeding 20% of thetotal epithelial thickness and elongation oflamina propria papillae, such that theyextend into the upper third of theepithelium, may also be present.
  12. 12. Clinical Features• GERD is most common in adults over age 40but also occurs in infants and children. Themost common clinical symptoms aredysphagia, heartburn, and, less frequently,noticeable regurgitation of sour-tastinggastric contents.• Rarely, chronic GERD is punctuated byattacks of severe chest pain that may bemistaken for heart disease.
  13. 13. Treatment• Treatment with proton pump inhibitors or H2histamine receptor antagonists, which reducegastric acidity, typically providessymptomatic relief.
  14. 14. Complications• esophageal ulceration,• hematemesis,• melena,• stricture development, and• Barrett esophagus.
  15. 15. Barrett’s Esophagus• Defined as occurrence of aspecialized columnar epitheliumlining a segment of distalesophagus above the level oflower esophageal sphincter.
  16. 16. MOTOR DISORDERS• Achalasia• Hiatal Hernia (sliding [95%],paraesophageal)• “ZENKER” diverticulum (pharyngoesophageal diverticulum)• Esophagophrenic diverticulum• Mallory-Weiss tear
  17. 17. Hiatal hernia• is characterized by separation of thediaphragmatic crura and protrusion of thestomach into the thorax through the resulting gap.Congenital hiatal hernias are recognized in infantsand children, but many are acquired in later life.Hiatal hernia is symptomatic in fewer than 10% ofadults, and these cases are generally associatedwith other causes of LES incompetence.Symptoms, including heartburn and regurgitationof gastric juices, are similar to GERD.
  18. 18. ACHALASIA• Increased tone of the lower esophagealsphincter (LES), as a result of impairedsmooth muscle relaxation, is an importantcause of esophageal obstruction. Achalasia ischaracterized by the triad of incomplete LESrelaxation, increased LES tone, andaperistalsis of the esophagus.
  19. 19. Mallory-Weiss tears• Longitudinal tears in the esophagus near thegastroesophageal junction are termedMallory-Weiss tears, and are most oftenassociated with severe retching or vomitingsecondary to acute alcohol intoxication.
  20. 20. Esophagus• Normal Anatomy– Muscular tube, 25 cm inlength in adults.– Extending from the upperesophageal sphincter at 15-18 cm from the incisors tolower esophageal sphincterat 40 cm (variable).
  21. 21. • Histology– Lined by stratifiedsquamous non-keratinizedepithelium.– Basal layer 4 cell thick; notmore than 15% of totalepithelial thickness.Melanocytes &neuroendocrine cellsmaybe found.
  22. 22. ESOPHAGUS– Lamina propria: Loose connective tissue, mucous glands indistal portion (cardiac glands)– Muscularis Mucosae: Thicker than other parts of GI tract.– Submucosa: Submucosal glands.– Muscularis propria: Admixture of striated & smooth muscle inthe upper quarter, only smooth muscle in the rest of the organ.– No serosal layer, except for the most distal portion.– Autonomic nervous system: Meissner’s plexus in submucosa(sparse); Auerbach (Myenteric) plexus in muscularis propria(denser in the distal portion).– Lymphatics: Upper third drains into the cervical nodes, themiddle third into the paraesophageal and paratracheal nodes,and lower third into nodes around aorta and celiac axis.