Tumours of the Gastrointestinal Tract — Notes OmpathStudy

Oesophageal Tumours 1. Oesophageal Adenocarcinoma Demographics: White males; 7× more common in men; highest in developed Western countries. Risk Factors: Barrett oesophagus, chronic GERD, documented dysplasia, tobacco, obesity, radiation. Protective Factors: Fruits and vegetables. Pathogenesis: Accumulation of genetic and epigenetic changes (TP53, chromosomal abnormalities). Morphology: Location: Distal 1/3 of oesophagus; may invade gastric cardia. Gross: Early flat/raised patches; late exophytic mass or ulcerated. Microscopy: Mucin-producing, gland-forming tumour; Barrett oesophagus adjacent to tumour. 2. Oesophageal Squamous Cell Carcinoma (SCC) Demographics: Adults 45 yrs; males 4× more; higher incidence in African Americans. Risk Factors: Alcohol and tobacco (synergistic), poverty, nutritional deficiencies, caustic injury, achalasia, Plummer-Vinson syndrome, hot beverages, HPV (high-risk regions). Morphology: Location: Middle 1/3 of oesophagus. Gross: Grey-white plaque-like thickenings; later polypoid/obstructing or ulcerated. Microscopy: Moderately to well differentiated; variants include verrucous and spindle cell. Spread: Rich submucosal lymphatics lead to circumferential and longitudinal spread (skip lesions). Lymph Node Metastases: Upper 1/3: Cervical nodes. Middle 1/3: Mediastinal, paratracheal, tracheobronchial. Lower 1/3: Gastric and coeliac nodes. Gastric Tumours 1. Gastric Polyps Inflammatory & Hyperplastic Polyps: Associated with chronic gastritis; risk of dysplasia increases with size. Gastric Adenomas: Arise in background of chronic gastritis with intestinal metaplasia; premalignant; require complete excision. 2. Gastric Adenocarcinoma Aetiology: H. pylori (most common), chronic atrophic gastritis, EBV infection. Histologic Types: Intestinal Type: Bulky, discrete, gland-forming cells. Diffuse Type: Signet ring cells; diffuse infiltration leading to Linitis Plastica ("leather bottle stomach"). 3. Gastric MALT Lymphoma Derived from mucosa-associated lymphoid tissue (MALT) induced by chronic H. pylori gastritis. H. pylori eradication can lead to tumour regression in early stages. 4. Gastrointestinal Stromal Tumour (GIST) Most common mesenchymal tumour of the abdomen; arises from Interstitial Cells of Cajal. Mutations: Activating mutations in c-KIT or PDGFRA tyrosine kinases. Treatment: Tyrosine kinase inhibitors (e.g., Imatinib). Colorectal Tumours 1. Colorectal Polyps Non-Neoplastic: Inflammatory, Hamartomatous (Peutz-Jeghers), and Hyperplastic (no malignant potential). Neoplastic (Adenomas): Characterized by cytologic dysplasia; precursors to adenocarcinoma. Sessile Serrated Adenomas: Lack cytologic dysplasia but carry malignant potential. 2. Genetic Syndromes Familial Adenomatous Polyposis (FAP): APC mutation (Chr 5); 100 polyps; cancer risk 100% by age 30; Chromosomal Instability (CIN) pathway. Hereditary Non-Polyposis Colorectal Cancer (HNPCC/Lynch): DNA mismatch repair gene mutations (MLH1, MSH2); Microsatellite Instability (MSI) pathway. 3. Colorectal Adenocarcinoma Prognostic Factors: 1. Depth of invasion (T stage) 2. Lymph node metastases (N stage). Appendix Tumours Carcinoid: Most common; usually incidental at distal tip; almost always benign. Adenocarcinoma: Can lead to intraperitoneal seeding; mimics mucinous ovarian tumours in women. Pseudomyxoma Peritonei: Advanced complication where the abdomen fills with mucin; managed by debulking but often fatal. Summary Table Tumour Location Key Feature --- --- --- Oesophageal Adenocarcinoma Distal 1/3 Barrett oesophagus; TP53 mutation Oesophageal SCC Middle 1/3 Alcohol/Tobacco; HPV (some regions) Gastric Adenocarcinoma Stomach H. pylori; Signet ring cells GIST Stomach c-KIT mutation; Cajal cells Carcinoid Small Intestine Most aggressive site for carcinoids FAP Colon APC mutation; 100 polyps HNPCC Colon Mismatch repair defect; MSI