PATH EXAM 2

• Oesophagitis

  Chemical or infectious causes of inflammation within the oesophagus
• Oesophagus

  • Stratified squamous
• Causes of oesophagitis

  • Reflux (most common, GORD)
  • Infectious (immunocomp, HSV, CMV, candida → more chronic)
  • Iatrogenic (Tetracyclines, iron tablets, strong acids, batteries)
• Macroscopic findings in oesophagitis

  Linear ulcers, erythema and oedema
• Microscopic findings in oesophagitis


  • Eosinophils + neutrophils
  • Basal cell hyperplasia
  • Elongation of lamina propria
• Complications of oesophagitis

  • Bleeding
  • Ulceration
  • Penetration
  • Strictures
  • Malignancy (adenocarcinoma)
• Oesophageal varices

  Dilated vessels within the submucosa of the distal oesophagus and proximal stomach due to portal hypertension
• Mallory-Weiss Tear


  Longitudinal tears in the oesophagus from several episodes of vomiting
• Boerhaave Syndrome


  Complication of Mallory-Weiss Tear and continued severe vomiting → transmural perforation of oesophagus
• Oesophageal adenocarcinoma


  Arises from areas of Barrett's oesophagus in the distal 1/3 of the oesophagus
• Oesophageal squamous cell carcinoma

  Arises in the middle 1/3 of the oesophagus
• Risk factors for oesophageal squamous cell carcinoma


  • Alcohol
  • Smoking
  • Plummer-Vinson (Paterson-Brown-Kelly) syndrome
  • Achalasia
• Acute gastritis


  Acute mucosal inflammation of the stomach lining
• Macroscopic findings in acute gastritis


  • Focal damage, erythema, bleeding
• Microscopic findings in acute gastritis


  • Neutrophils present in the mucosa of the stomach
• Causes of acute gastritis


  • NSAIDs
  • EtOH
  • Smoking
  • Stress
  • Trauma (NGT)
  • Chemotherapy
• Mechanisms to protect the stomach


  • Mucus secretion
  • Bicarbonate secretion
  • Tight junctions
  • Rapid turnover of cells
  • Blood flow
• Prostaglandins


  Stimulate the protective mechanisms in the stomach
• NSAIDs


  Inhibit COX 1/2 and hence block prostaglandin synthesis, reducing the protective factors
• Type A chronic gastritis


  Autoimmune, associated with pernicious anaemia
• Microscopic findings in type A chronic gastritis


  • Presence of lymphocytes, macrophages, plasma cells and large lymphoid follicles
  • Parietal cell pseudohypertrophy
  • Mucosal atrophy
• Type B chronic gastritis


  Caused by H. pylori, can progress to intestinal metaplasia and gastric adenocarcinoma
• Microscopic findings in type B chronic gastritis


  • Intraepithelial neutrophils, atrophy, intestinal metaplasia
• Progression of gastritis


  Acute gastritis (H. pylori) → chronic generalised gastritis → chronic atrophic gastritis → intestinal metaplasia → cancer
• Benign gastric lesions


  • Hyperplastic polyp
  • Adenomatous polyp
• Hyperplastic polyp


  Small (<1cm), often multiple, in chronic gastritis, with irregular, cystically dilated foveolar glands
• Adenomatous polyp


  Usually single, ~2cm, made of epithelium with intestinal metaplasia and dysplasia
• Types of gastric adenocarcinoma


  • Intestinal type
  • Diffuse type
• Intestinal type gastric adenocarcinoma


  • Elderly and males, solid, polypoid, ulcerated mass with crowded glandular structure and cellular atypia
• Diffuse type gastric adenocarcinoma

  • Young and females, spread throughout the stomach wall, firm and thick appearance of entire wall (linitis plastica), discohesive sheets of cells with large intracytoplasmic mucin vacuoles (signet ring cells)
• MALToma


  Mucosal associated lymphoid tissue tumour, dense lymphocytic infiltrate and lymphoid cells within the gastric glands, mainly caused by H. pylori
• Gastrointestinal stromal tumour (GIST)


  Mesenchymal tumour forming a mass with mass effect symptoms, composed of spindle epithelial cells
• Inflammatory bowel disease


  Chronic autoimmune condition leading to inflammation within the bowel, includes Crohn's disease and ulcerative colitis
• Epidemiology of inflammatory bowel disease


  • More common in teens/early 20s, Caucasians, and Western world
• Pathogenesis of inflammatory bowel disease


  Not fully understood, involves genetics, environment, defects in epithelial structure, impaired mucosal response, and microbes
• Crohn's disease


  Can occur anywhere in the gastrointestinal tract, most commonly in the terminal ileum, caecum, and ileocecal valve
• Macroscopic findings in Crohn's disease


  • Deep fissures and ulcers interspersed with normal mucosa (cobblestone appearance with skip lesions), entire wall affected leading to strictures and scarring with a thickened bowel wall, mesenteric fat wrapping
• Microscopic findings in Crohn's disease


  • Crypt abscesses, non-caseating granulomas, transmural inflammation, distortion of mucosal architecture, Paneth cell metaplasia
• Ulcerative colitis


  Mainly limited to the rectum with proximal continuation, high chance of developing colorectal cancer
• Macroscopic findings in ulcerative colitis


  • Superficial (limited to mucosa) broad-based ulcers, no skip lesions, pseudopolyps (regenerating tissue), mucosal atrophy, diffuse loss of haustral folds