13..the gastrointestinal tract pathology

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  • 1. THE GASTROINTESTINAL TRACT ESOPHAGUS
  • 2. ESOPHAGUS  Fibromuscular tube, 25 cm long ; connects pharynx and stomach  Extends from cricopharyngeal sphincter in pharynx (level of C6) to lower esophageal sphinchter at GE junction (T11/T12), 2 cm of this tube lies below the diaphragm.  Main purpose is to propel food from pharynx to stomach via peristalsis
  • 3. Regions     Cervical (cricoid cartilage to suprasternal notch, 3 cm long, 15 cm from incisors) Upper thoracic (suprasternal notch to tracheal bifurcation, 6 cm long, 18 cm from incisors) Mid-thoracic (tracheal bifurcation to diaphragmatic hiatus, 8 cm long, 24 cm from incisors) Lower thoracic and abdominal (8 cm long, 32 cm from incisors)
  • 4. Three physiological constrictions
  • 5. Normal histology of esophagus      Mucosa: nonkeratinized stratified squamous epithelium lamina propria: fibrovascular connective tissue between epithelium and muscularis mucosae Submucosa: submucosal glands lined by mucinous cells that produce acid mucin Muscularis propria: inner circular and outer longitudinal layers Adventitia: loose connective tissue
  • 6. Esophagitis  Defined as epithelial damage and inflammation of the esophagus.  Most common cause – Gastroesophageal reflux disease (reflux of gastric contents into lower esophagus)  Infectious- less common cause
  • 7. Type of ESOPHAGITIS  Chemical (corrosive) esophagitis – alcohol, corrosive acids or alkalis, excessively hot fluids, and heavy smoking, medicinal pills, cytotoxic drugs  Infections esophagitis – Viral: CMV, herpetic, HPV, HIV – Fungal: Candida, aspergilus – Bacterial: rare, tuberculosis Eosinophilic esophagitis 
  • 8. Morphology  The morphology of chemical and infectious esophagitis varies with etiology.  Dense infiltrates of neutrophils are present in most cases but may be absent following injury induced by chemicals, which may result in necrosis of the esophageal wall.  Pill-induced esophagitis frequently occurs at the site of strictures that impede passage of luminal contents.
  • 9. CMV - cytomegalovirus esophagitis  Usually immunocompromised patients  Up to 30% of AIDS patients have CMV  Gross: punched out mucosal ulcers with normal surrounding mucosa  Micro: Basophilic cytoplasm often has coarse intracytoplasmic granules  Prominent intranuclear basophilic inclusions surrounded by clear halo  Macrophage aggregates in perivascular distribution
  • 10. Herpes simplex esophagitis  Usually an opportunistic infection in immunosuppressed / AIDS patients  Gross: shallow vesicles and ulcers  Micro: Ulcers contain necrotic debris and exudate with neutrophils; viral inclusions are present in multinucleated squamous cells (Cowdry type A) 
  • 11. Morphology, viral esophagitis
  • 12. Herpes esophagitis
  • 13. REFLUX ESOPHAGITIS  Reflux of gastric contents into the lower esophagus is the most frequent cause of esophagitis  The associated clinical condition is termed gastroesophageal reflux disease (GERD).
  • 14. Pathogenesis  Reflux of gastric juices is central to the development of mucosal injury in GERD.  In severe cases, reflux of bile from the duodenum may exacerbate the damage.  Conditions that decrease LES tone or increase abdominal pressure contribute to GERD: – alcohol and tobacco use – obesity, CNS depressants, pregnancy, hiatal hernia, delayed gastric emptying.
  • 15. Morphology  Endoscopy: linear ulcers at distal esophagus, often with exudate; also erythema or edema.  Gross: severe cases have hyperemic mucosa with focal hemorrhage  Micro: inflammatory cells in epithelial layer (eosinophils, neutrophils, lymphocytes); basal cell hyperplasia, elongation of lamina propria papillae; ballooned squamous cells, vascular dilatation
  • 16. REFLUX ESOPHAGITIS
  • 17. Clinical Features     The most common clinical symptoms are heartburn, dysphagia,nausea vomitting. Severity of symptoms is NOT related to histology; pain may be mistaken for myocardial infarction. Treatment: proton pump inhibitors or H2 receptor antagonists. Complications: esophageal ulceration, hematemesis, melena, stricture development, and Barrett esophagus.
  • 18. Barrett Esophagus, IMP     Definition: condition where distal squamous mucosa of esophagus is replaced by metaplastic columnar epithelium as a response to chronic injury Appears to be irreversible Barrett esophagus is a complication of chronic GERD Barrett esophagus is a pre-malignant condition for esophageal adenocarcinoma.
  • 19. Barrett Esophagus   Causes: usually chronic GERD Almost always associated with – sliding hiatal hernia – esophageal stricture – Chemotherapy – bile/pancreatic juice reflux – peptic ulceration, decreased resting pressure of lower esophageal sphincter
  • 20. Morphology    Gross: patches of red, velvety mucosa extending upward from the GE junction. This metaplastic mucosa alternates with residual smooth, pale squamous (esophageal) mucosa and interfaces with light-brown columnar (gastric) mucosa distally. Subclassification : – Long-segment: Barrett’s mucosa extends 3 cm or more – Short-segment: Barrett’s mucosa extends less than 3 cm
  • 21. Morphology  Micro: esophageal squamous epithelium is replaced by columnar epithelium of intestinal type (stomach, small bowel, colon) with goblet cells  Lamina propria is fibrotic with mild chronic inflammation  Muscularis mucosae may be thickened
  • 22. Morphology  When dysplasia is present, it is classified as low grade or high grade.  High grade dysplasia: 15-50% risk of invasive adenocarcinoma  Low grade dysplasia: may progress to high grade dysplasia or carcinoma for up to 10 years
  • 23. Barrett’s esophagus, endoscopy
  • 24. Barrett’s esophagus
  • 25. Gross
  • 26. Esophageal tumors  BENIGN    LEIOMYOMAS FIBROVASCULAR POLYPS LIPOMAS  MALIGNANT – – Squamous cell carcinoma Adenocarcinoma
  • 27. Squamous cell carcinoma  Half of squamous cell carcinomas occur in the middle third of the esophagus  Highest incidence in northern Iran, northern China, and other developing countries  Usually men (75%) age 50+ years; more common in blacks (4:1) in US  Mutations of several tumor suppressor genes, including p53 and p16,EGFR gene.
  • 28. Risk factors for SQC  Long-standing esophagitis, achalasia  Plummer-Vinson syndrome- triad of esophageal webs, microcytic hypochromic anemia,dysphagia, atrophic glossitis Alcohol consumption, tobacco abuse Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine) Deficiency of trace metals (zinc, molybdenum) Fungal contamination of foodstuffs High content of nitrites/nitrosamines Genetic Predisposition      
  • 29. Morphology  Squamous cell carcinomas are usually preceded by a long prodrome of mucosal epithelial dysplasia followed by carcinoma in situ and, ultimately, by the emergence of invasive cancer.
  • 30. Morphology    Gross: Early lesions: small, gray-white, plaque-like thickenings Advanced lesion: – Fungating/exophytic lesions – Ulcerative lesions – Infiltrative lesions- causing thick, rigid esophageal wall
  • 31. Gross
  • 32. Microscopy  Sheets or islands of large polygonal malignant cells with pink cytoplasm and distinct cell borders.  Presence of keratinization and/or intercellular bridges in the form of squamous pearls or individual cells with markedly eosinophilic dense cytoplasm  Lymphoid stroma  Desmoplasia present
  • 33. Microscopy
  • 34. Superficial squamous cell carcinoma  Tumor confined to mucosa and submucosa regardless of lymph node status  Intramucosal tumors have 5% lymph node involvement vs. 35% for submucosal tumors  5 year survival is 85% without vs. 40% with nodal involvement
  • 35. Clinical Features  Progressive dysphagia  Odynophagia (pain on swallowing).  Extreme weight loss and debilitation result from both impaired nutrition and effects of the tumor itself.
  • 36. Adenocarcinoma of esophagus  40-50%% of primary esophageal cancers  increasing incidence over past 20 years for unknown reasons  Age 50+ years; 80% men  95% arise in setting of Barrett’s esophagus Risk factors: alcohol or tobacco use, positive family history 
  • 37. Pathogenesis.  Molecular studies suggest that the progression of Barrett esophagus to adenocarcinoma occurs over an extended period through the stepwise acquisition of genetic and epigenetic changes.  Barrett metaplasia- progression to dysplasia and invasive carcinoma.  Mutation of p53 and retinoblastoma gene are present  Alterations in HER-2/NEU gene.
  • 38. ADENOCARCINOMA
  • 39. Morphology  Usually occurs in the distal third of the esophagus.  Gross: Initially appearing as flat or raised patches on an otherwise intact mucosa, they may develop into large nodular masses or show deeply ulcerative or diffusely infiltrative features.
  • 40. Morphology  Micro: most tumors are mucin-producing glandular tumors showing intestinal-type features. Barrett esophagus is frequently present adjacent to the tumor  Less frequently tumors are composed of diffusely infiltrative signet-ring cells.
  • 41. Gross
  • 42. Adenocarcinoma
  • 43. STOMACH
  • 44. STOMACH
  • 45. STOMACH
  • 46. Mucosal defense      (a) Mucus secretion: mucus is relatively impermeable to H+ (b) Bicarbonate secretion creates pH neutral microenvironment adjacent to cell surface (c) Intercellular tight junctions prevent backdiffusion of H+; disruptions are quickly repaired (d) Mucosal blood flow supplies bicarbonate and nutrients and removes acid (e) Elaboration of prostaglandins
  • 47. Mucosal injury           NSAID, aspirin Alcohol Stress H.pylori Ischemia Shock Smoking, steroid Autoimmune Duodenal-gastric reflux Delayed gastric emptying
  • 48. Mechanisms of gastric injury and protection
  • 49. GASTRITIS     ACUTE gastritis CHRONIC gastritis AUTOIMMUNE gastritis OTHER – EOSINOPHILIC – ALLERGIC – LYMPHOCYTIC – GRANULOMATOUS – GVH
  • 50. Acute Gastritis/ Active gastritis  Acute gastritis is a transient inflammatory process of gastric mucosa.  It may be asymptomatic or cause variable degrees of epigastric pain, nausea, and vomiting.  May be accompanied by local hemorrhage or mucosal sloughing
  • 51. Acute gastritis           Associated with (NSAIDs), particularly aspirin Excessive alcohol consumption Heavy smoking CHEMO Uremia Severe stress (e.g., trauma, burns, surgery) Ischemia and shock Suicidal attempts, as with acids and alkali Mechanical (e.g., nasogastric intubation)
  • 52. Pathogenesis  Increased acid production with back diffusion  Decreased bicarbonate production and direct mucosal damage
  • 53. Morphology  Gross: Edema and hyperemia with occasional hemorrhage.  Micro: Scattered intraepithelial neutrophils or neutrophils within mucosal glands.  With more severe mucosal damage, erosions and hemorrhage develop.  An erosion: loss of the superficial epithelium (epithelial sloughing), generating a defect in the mucosa that is limited to the lamina propria.
  • 54. Erosions and hemorrhage
  • 55. Acute gastritis
  • 56. ACUTE GASTRIC ULCERATION  Stress ulcers are most common in patients in ICU with shock, sepsis, or severe trauma.  Curling ulcers: Ulcers occurring in the proximal duodenum and associated with severe burns or trauma .  Cushing ulcers: Gastric, duodenal, and esophageal ulcers arising in persons with intracranial disease. It carry a high incidence of perforation.
  • 57. Morphology  Acute ulcers are shallow and punched out, size: up to 1 cm in diameter.  The ulcer base is frequently stained brown to black by acid digestion of extravasated blood  The gastric rugal folds are essentially normal, and the margins and base of the ulcers are not indurated.
  • 58. Morphology  Micro: sharply demarcated, with essentially normal adjacent mucosa, blood into the mucosa and submucosa.  Healing with complete re-epithelialization (without scar) occurs after the injurious factors are removed.
  • 59. Complications of Gastric Ulcers    Acute ulcer: – Bleeding (hematemesis and or malena) – Perforation Chronic ulcer: Pyloric stenosis, secondary to edema or scarring – Penetration into neighboring viscera – Malignant ulcer