Pathology of the Stomach PDF

Pathology of the stomach BY DR. HUSAMELDIN OMER Stomach diseases include:  Congenital abnormalities: e.g. pyloric stenosis.  Gastritis.  Hypertrophic gastropathy  Peptic ulcer.  Gastric polyps (non neoplastic).  Tumors of the stomach.  Congenital abnormalities Co...

Pathology of the stomach BY DR. HUSAMELDIN OMER Stomach diseases include:  Congenital abnormalities: e.g. pyloric stenosis.  Gastritis.  Hypertrophic gastropathy  Peptic ulcer.  Gastric polyps (non neoplastic).  Tumors of the stomach.  Congenital abnormalities Congenital pyloric stenosis: An abnormal thickening of pylorus muscles that results in stenosis of the pyloric valve between the infant's stomach and small intestine with failure to pass the food through  Occurs in males infants more than females (4:1).  Clinical features:  Persistent projectile vomiting in the 2nd week of life (young infants).  Palpable epigastric mass (the abnormally thicken pylorus). Congenital pyloric stenosis  Gastritis Acute gastritis: Transient mucosal inflammation. Common causes:  Drugs: chronic use of NSAID particularly aspirin.  Irritation by heavy smoking & excessive alcohol. Less common causes:  Severe stress (e.g. burns, surgical operations).  Uremia, ischemia, shock, systemic infections, irradiation some chemotherapeutics, ingestion of acids or alkalis. Gross appearance (by endoscope):  Mucosal edema and hyperemia.  Ulceration of the superficial epithelium and hemorrhage. Microscopic:  Infiltration of the epithelial layer by neutrophils. Clinical manifestations:  Epi-gastric pain.  Hematemesis. Chronic gastritis: Chronic inflammation of the gastric mucosa, leading to atrophy (chronic atrophic gastritis). Types: A) Fundic type: (type A):  Auto-immune atrophic gastritis.  Involves the fundus and the body.  Auto-antibodies to parietal cells and/or intrinsic factor are found in the serum of the patient.  Decreased acid secretion (achlorhydria).  Increased serum gastrin (G-cell hyperplasia).  Pernicious anemia: (megalo-blastic anemia) may be accompanied disorder due to lack of intrinsic factor which results in B12 mal-absorption. Gross appearance:  Loss of rugal folds (the normal mucosal folds) in fundus and body of the stomach. Microscopic:  Partial mucosal atrophy with loss of glands and parietal cells.  Chronic inflammation (lymphocytes & plasma cells).  Intestinal metaplasia.  Dysplasia in some cases. There is a risk for gastric carcinoma. B) Antral type (type B) (H. Pylori gastritis):  Common disease.  Due to infection by Helicobacter pylori organisms. Microscopic: Helicobacter pylori organisms are visible in the mucosa, intracellular and extracellular. Chronic inflammation of the mucosa and lymphoid follicles may be seen.  Hypertrophic gastropathy  Uncommon conditions.  Enlargement of gastric rugal folds. There are two types A) Ménétrier disease: The classic symptom triad of Menetrier disease is gastrointestinal symptoms (epigastric pain, anorexia, vomiting), peripheral edema, and giant gastric folds Hyperplasia of mucous cells, accompanied by fundic gland atrophy. There is excess mucus secretion Decreased acid production. B) Gastric gland hyperplasia (Zollinger-Ellison syndrome): Excessive gastrin secretion by gastrinoma (gastrin- secreting tumor in pancreas) which stimulate gastric glands hyperplasia and excessive acid secretion. Excessive acid secretion due to parietal-cell hyperplasia. Multiple ulcers in the stomach and duodenum. Symptoms include abdominal pain, nausea, vomiting (can be bloody), weight loss, and diarrhea.  Chronic peptic ulcers Peptic ulcers are open sores on the inner lining of the stomach and/or the upper part of the small intestine (the duodenum)  Usually are solitary ulcers that caused by exposure to gastric secretions. Sites:  Duodenal (80%)  Gastric (20%) Pathogenesis: Peptic ulcers are produced due to imbalance between the gastro-duodenal mucosal defense mechanisms and damaging forces. Defense mechanisms include mucus and bicarbonate secretion, mucosal blood flow, and rapid epithelial regeneration. Damaging forces include excess gastric acid and pepsin, H. pylori infection, beside SAIDs e.g. aspirin, cigarette smoking, and excess alcohol ingestion. Gross appearance of peptic ulcers: Round or oval in shape. Sharply demarcated. Clean ulcer bases. Radiating mucosal folds. Gastric ulcers about 2-4 cm in diameter, duodenal are smaller. Microscopic: The base and margins show necrotic debris. Zone of active inflammation all around with granulation tissue. Some areas of fibrous collagenous scary tissue can be noticed. Complications of peptic ulcers: Hemorrhage: hematemesis, melena. Perforation of the ulcer producing peritonitis. Penetration of the ulcer into an adjacent solid organ e.g. liver and pancreas. Healing by fibrous tissue resulting in pyloric stenosis or (hourglass) and stomach deformity. Malignant change: carcinoma develops in about 1% of gastric ulcer, but not recognized in chronic duodenal ulcer. Duodenal peptic ulcer: More common than gastric ulcers (4:1). Usually accompanied by: H. pylori infection (~100%) due to secretion of urease, protease and phospholipase enzymes. Increased gastric acid secretion. Increased rate of gastric emptying. Zollinger-Ellison syndrome is one of main causes. Site: anterior wall of the first portion of duodenum Clinical manifestations: Burning epigastric pain 1-3 hours after meals. Gastric peptic ulcer: Associated with H. Pylori infection in 75% of cases. Site: lesser curvature near the pyloric antrum. Clinical features: Burning epigastric pain, which worsens with eating. Chronic peptic ulcers  Gastric polyp  They are hyperplastic or inflammatory (90%).  Common in chronic gastritis.  Have no malignant potential. Gross appearance:  Usually multiple, have smooth surface, sessile or pedunculated. Microscopic:  Composed of tubules and cysts lined by columnar cells, interspersed with an inflammatory stroma. Gastric polyp  Composed of tubules and cysts lined by columnar cells.  Edematous stroma containing inflammatory cells  Gastric tumors Benign gastric tumors: Adenomas (adenomatous neoplastic polyps).  90% of all gastric benign tumors.  Polypiod mass.  Single or multiple, sessile or pedunculated.  Have a malignant potential Other benign tumors: leiomyoma, lipoma, hemangioma. Gastric adenoma, endoscopic  The mucosa of the stomach shows multiple sessile polypoid masses. Gastric carcinoma: Pathogenesis: (risk factors) Dietary factors: Preservatives in the food (nitrates) Lack of fresh fruits and vegetables. H pylori infection with chronic gastritis. Autoimmune gastritis. Cigarette Smoking. Gastric adenoma. Gross appearance:  Sites: Most common in the lesser curvature of the gastric antrum.  Morphological Types: Exophytic or polypoid type: it forms a projecting intraluminal mass. Excavated or ulcerative type: the ulcer shows heaped- up margins, necrotic floor and indurated base. Flat or infiltrating type: It may invade the whole wall of the stomach resulting in a small contracted stomach (linitis plastica). Ulcerative gastric carcinoma  Opened stomach, showing an ulcer with irregular heaped-up margins.  Extensive excavation of the gastric mucosa and necrotic floor are seen. Microscopic appearance: Adenocarcinoma pattern which may be: Well differentiated (intestinal type). Mucinous forming pools of mucin. Signet-ring cell carcinoma. Gastric carcinoma, microscopic  Malignant cells forming glands and invading the muscular wall of the stomach on the left side. Gastric carcinoma  Signet-ring cells (arrow).  Mucin producing malignant cells. Clinical features: Asymptomatic (90%) until late in the course. Weight loss. Epigastric pain or fullness. Occult bleeding (in the stool). Prognosis: 5 year survival for early resected gastric cancer is 90%. 5 year survival for advanced cases is 10%. Other less common malignant gastric tumors:  Lymphoma “mucosa associated lymphoid tissue lymphoma” MALToma, less than 15% of gastric tumors.  Leiomyosarcoma (1-3% )  Carcinoid tumor.  Gastric malignant schwannoma  Comparison between peptic ulcer and malignant ulcer Peptic ulcer Malignant ulcer Age younger age: 30-40 Older age: 50-70 years years Gastric acidity Usually increased Normal or absent Shape of the ulcer Sloping edge, the base Heaped-up margins, is fibrotic, & the muscle necrotic floor, layer is destroyed indurated base. The muscle layer is infiltrated by the tumor cells