Ulcer PDF - General Pathology Lecture 08

General pathology Lecture 08 Ulcer 03.09.2024  ULCERATION Apparent loss of surface epithelium When surface covering of an organ or tissue is lost >>> loss of an important defence mechanism >> expose underlying tissue from acid and enzymes. Once the submucosa is exposed to...

General pathology Lecture 08 Ulcer 03.09.2024  ULCERATION Apparent loss of surface epithelium When surface covering of an organ or tissue is lost >>> loss of an important defence mechanism >> expose underlying tissue from acid and enzymes. Once the submucosa is exposed to these agents, large vessel walls can be digested >> massive bleeding Most common sites >> Alimentary tract & the skin.  STOMACH The stomach is divided into four major anatomic regions: 1. Cardia, 2. Fundus, 3. Body, & 4. Antrum. 3-forms of mucosa are seen The cardia is lined mainly by mucin- secreting foveolar cells that form shallow glands.  The well- developed glands of the body and fundus also contain chief cells Chief cells produce & secrete digestive enzymes such as pepsin.  The antral glands are similar but also contain endocrine cells( G cells), that release gastrin to stimulate luminal acid secretion by parietal cells.  Peptic Ulcers Open sores that develop on the inside lining of stomach and the duodenum Types of peptic ulcers >> based on their location: 1. Gastric ulcers inside of the stomach. 2. Duodenal ulcers inside of the upper portion of the small intestine (duodenum) 3. Esophageal ulcers at the bottom of the esophagus and are associated with gastroesophageal reflux disease (GERD). Progression from more mild forms of injury to ulceration that occur with acute or chronic gastritis. Ulcers include layers of necrotic debris  INCIDENCE Peptic ulcers are more frequent in middle-aged adults. The peak incidence for duodenal ulcer >> 5th decade Gastric ulcer >> 6th decade Duodenal as well as gastric ulcers are more common in males than in females. Duodenal ulcer is almost four times more common than gastric ulcer MORPHOLOGIC FEATURES Gastric ulcers predominantly along the lesser curvature in the region of pyloric antrum, more commonly on the posterior than the anterior wall. Duodenal ulcers in the first part of the duodenum, usually immediate post-pyloric, more commonly on the anterior than the posterior wall.  Benign ulcers >> flat margins in level with the surrounding mucosa. The mucosal folds converge towards the ulcer. May vary in depth from being superficial (confined to mucosa) to deep ulcers (penetrating into the muscular layer). 10-20% of cases, gastric & duodenal ulcers >> coexist Vast majority of the peptic ulcers are benign. Chronic duodenal ulcer never turns malignant, Chronic gastric ulcer may develop carcinoma in less than 1% of cases. Malignant gastric ulcers are larger, bowl-shaped with elevated and indurated mucosa at the margin.  ACUTE PEPTIC ULCER Acute peptic ulcer Lesions range in depth 1. shallow erosions caused by superficial epithelial damage 2. deeper lesions that penetrate the mucosa. Healing with complete re-epithelialization occurs days or weeks after the injurious factors are removed. 3- Cushing ulcers 1- Stress ulcers, 2- Curling ulcers Brain trauma, shock, sepsis, or severe burns CNS injury, brain severe trauma (> 30% TBSA) or injury, increased Stomach, duodenum trauma intracranial pressure Stomach, duodenum Stomach, duodenum or esophagus  CHRONIC PEPTIC ULCERS (Gastric & Duodenal Ulcers) Chronic peptic ulcers >> Gastric and Duodenal ulcers, Morphological findings in both are similar and quite diagnostic.  PEPTIC ULCERATION When acid-containing gastric juices breach the mucosa of the gut  GASTRIC ULCER Impaired gastric mucosal defenses against acid-pepsin secretions. Some other features in the pathogenesis of gastric ulcer are as follows: 1. Hyperacidity may occur >> due to increased serum gastrin levels in response to ingested food in an atonic stomach. 2 However, many patients of gastric ulcer have low-to normal gastric acid levels. 3. Damaged protective gastric mucus ‘barrier’ against acid-pepsin 4. There is depletion in the quantity as well as quality of gastric mucus. 5. One of the mechanisms for its depletion is colonisation of the gastric mucosa by H. pylori >> in 75-80% patients of gastric ulcer.  DUODENAL ULCER The role of high acid-pepsin secretions in the causation of duodenal ulcers. Features in the pathogenesis of duodenal ulcers are as follows: 1. There is generally hypersecretion of gastric acid into the fasting stomach at night >> under the influence of vagal stimulation. There is high basal as well as maximal acid output (BAO and MAO) 2. Patients of duodenal ulcer have rapid emptying of the stomach so that the food which normally buffers and neutralises the gastric acid, passes down into the small intestine, leaving the duodenal mucosa exposed to the aggressive action of gastric acid. 3. Helicobacter gastritis caused by H. pylori is seen in 95-100% cases of duodenal ulcers. Microscopically Chronic peptic ulcers have 4 histological zones. From within outside, these are as under: 1. Necrotic zone ❖ lies in the floor of the ulcer ❖ Composed of fibrinous exudate containing necrotic debris & a few leukocytes. 2. Superficial exudative zone ❖ lies underneath the necrotic zone ❖ tissue elements here show coagulative necrosis giving eosinophilic, smudgy appearance with nuclear debris. Microscopically 3. Granulation tissue zone ❖ seen merging into the necrotic zone. ❖ composed of nonspecific inflammatory infiltrate and proliferating capillaries. 4. Zone of cicatrisation ❖ seen merging into thick layer of granulation tissue. ❖ composed of dense fibrocollagenic scar tissue over which granulation tissue rests.  ETIOLOGY Normally gastric mucosal damage is prevented by a balance between the damaging agents and the mucosal defenses  Although the mechanism in gastric and duodenal ulcers differ, in both HELICOBACTER PYLORI infection is important SEQUELS AND COMPLICATIONS