GOR Gastritis PDF

REFLUX OESOPHAGITIS, GASTRITIS & PEPTIC ULCER DISEASE One of the most common problems related to the gastrointestinal tract. There is reflux of gastric acid and pepsin into the lower oesophagus. This will cause irritation, inflammation and damage to the lower oesophageal mucosa. Can progres...

REFLUX OESOPHAGITIS, GASTRITIS & PEPTIC ULCER DISEASE One of the most common problems related to the gastrointestinal tract. There is reflux of gastric acid and pepsin into the lower oesophagus. This will cause irritation, inflammation and damage to the lower oesophageal mucosa. Can progress to columnar cell (intestinal) metaplasia (Barrett oesophagus). BARRETT OESOPHAGUS Complication of chronic GERD characterized by intestinal metaplasia of the oesophageal squamous mucosa Endoscopy: Tongues of red, velvety mucosa extending upwards PATHOGENESIS OF GERD Pathogenesis is multifactorial  Transient lower esophageal sphincter relaxation: major cause  Increase in intra-abdominal pressure  Pregnancy  Old age, alcohol, tobacco  Hiatus hernia  Delayed gastric emptying  Defective oesophageal mucosal resistance  Increased gastric volume  CNS depressants Symptoms  Regurgitation  Heartburn Complications  Ulceration/ erosions  Bleeding  Stricture formation  Barrett oesophagus (columnar cell metaplasia) GASTRITIS  Gastritis is defined as inflammation of the gastric mucosa.  Inflammation may be predominantly Types 1. Acute (Neutrophils) 2. Chronic (Lymphocytes and Plasma cells) 3. Mixed (Both acute and chronic) ACUTE GASTRITIS  Acute gastritis is an acute mucosal inflammatory process usually of a transient nature.  Severe erosive form of the disease is an important cause of acute gastrointestinal bleeding. Clinical features  Asymptomatic  Epigastric pain  Nausea, vomiting  Hematemesis  Melena Pathogenesis of acute gastritis  NSAIDs , chemotherapeutic agents  Excessive alcohol & smoking  Irradiation  Stress  Ischaemia & shock  Severe systemic infections (salmonellosis)  Uraemia  Acids & alkali  Mechanical trauma (nasogastric intubation)  After distal gastrectomy MORPHOLOGY  Mucosal oedema  Vascular congestion  Neutrophilic infiltrate (neutrophils within the epithelial cells signifies active inflammation)  Severe form – mucosal erosion (loss of superficial epithelium) with hemorrhage. HISTOLOGY Neutrophils within the epithelial cells CHRONIC GASTRITIS  Chronic gastritis is defined as chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia.  The epithelial changes may become dysplastic and constitute a background for the development of carcinoma. Etiology  Chronic infection by Helicobacter pylori-most common  Autoimmune (immunologic)  Toxins – alcohol, smoking  Radiation  Chronic bile reflux (after gastroenterostomy)  Mechanical HELICOBACTER PYLORI ASSOCIATED CHRONIC GASTRITIS  The most common cause of chronic gastritis (90%) is infection with the bacillus H. pylori.  H. pylori is a motile, spiral shaped or curved, gram-negative rod.  Transmission is primarily by the fecal-oral route. H. pylori infection is associated with poverty & overcrowding.  Infection is usually acquired in childhood. Colonization rate increases with age. Pathogenesis of h. pylori associated chronic gastritis There are several factors that are involved in the pathogenesis: 1. Bacterial virulence − Flagella (motile in thick mucus) − Urease (produces ammonia from endogenous urea and increases the local pH and hence bacterial survival − Adhesins − Toxins (cytotoxin- associated gene Cag A) 2. Host factors − Genetic polymorphism that leads to the increased expression of proinflammatory cytokines (TNF, IL -1β) or reduced expression of anti-inflammatory cytokines (IL-10). 3. Breakdown of gastric mucosal defense mechanisms normal defense mechanisms include − Surface mucus secretion (protective) − Bicarbonate secretion − Rich mucosal blood flow − Apical surface membrane transport − Epithelial regenerative capacity Prostaglandins Pathogenesis (h. Pylori infection) Morphology (h.pylori associated chronic gastritis )  Predominantly involves the antrum.  Patients present with increased or normal acid production.  Organisms concentrate within the surface mucus overlying epithelial cells (easily seen with special stains – Giemsa, Warthin -Starry silver stain)  Inflammation – neutrophils, plasma cells, lymphoid aggregates……  Can progress to patchy mucosal atrophy and intestinal metaplasia.  Sequelae – − Peptic ulcer − Gastric adenocarcinoma − Lymphoma(MALT)  Active, chronic inflammation with lymphoid follicles Special Stain (H. pylori) AUTOIMMUNE GASTRITIS  Accounts for less than 10% of cases of chronic gastritis.  Involves the body & fundus of the stomach and typically spares the antrum and cardia  Autoimmune destruction of parietal cells.  Characterized by: − antibodies to parietal cells & intrinsic factor. − decreased acid production (achlorhydria) & increased gastrin release. − vitamin B12 deficiency (pernicious anaemia). − reduced serum pepsinogen I  Can be associated with other autoimmune diseases.  Histology − Involves the body & fundus of the stomach and typically spares the antrum and cardia − Diffuse atrophy, oxyntic mucosa thinned out and rugal folds lost − Cells- lymphocytes, plasma cells, macrophages, lymphoid follicles. − Loss of parietal cells & chief cells can be extensive − Atrophy and metaplasia. UNCOMMON TYPES OF GASTRITIS 1. Eosinophilic gastritis 2. Lymphocytic gastritis 3. Granulomatous gastritis (mycobacteria, sarcoidosis, Crohn’s, idiopathic…) PEPTIC ULCER DISEASE o Peptic ulcer disease (PUD) refers to chronic mucosal ulceration affecting the duodenum or stomach. o Almost always associated with H.pylori, NSAIDs or cigarette smoking o Ulcer – is a breach in the mucosa o Peptic ulcers are relapsing lesions that are most often diagnosed in middle-aged to older adults. Pathogenesis of peptic ulcer disease  Peptic ulcers are produced due to an imbalance between the gastroduodenal mucosal defense mechanisms and the damaging forces.  PUD generally develops on a background of chronic gastritis.  Risk factors − Helicobacter pylori − Cigarette smoking (Synergizes with H Pylori) − Alcohol − NSAIDs, steroids − Psychological stress − Drugs - Cocaine − Zollinger-Ellison syndrome − Endocrine cell hyperplasia − Viral infection (CMV, HSV) − COPD Pathogenesis Macroscopic features  Usually solitary lesions.  Site- first part of duodenum, lesser curvature of stomach near the interface of the body and antrum.  Shallow or deep, size is variable (mm to cm)  Round to oval, sharply, punched- out lesion with relatively straight walls.  Mucosal margin may overhang the base.  Base is smooth and clean (due to peptic digestion).  Later there is scarring and puckering of the surrounding mucosa ( with mucosal folds that radiate from the crater). CHRONIC GASTRIC ULCER (MICROSCOPY)  There are four zones 1. Superficial thin layer of necrotic debris and fibrin. 2. Beneath this zone there are inflammatory cells predominantly consisting of neutrophils. 3. Granulation tissue in the deeper layers. 4. Collagenous/ fibrous scar with thick walled, thrombosed vessels. Complications  Bleeding  Perforation  Obstruction – due to oedema or scarring  Malignant transformation – very rare