Gastritis: It is inflammation of the lining of the stomach. Gastritis may be acute or chronic.
Acute gastritis may be caused by drugs like aspirin, NSAIDS, steroids, iron tablets, alcohol, H.pylori, viruses like Hepatitis viruses, infectious mononucleosis, stress etc. It presents with upper abdominal discomfort or pain, bloating, nausea and vomiting.
Chronic gastritis is seen in H.pylori infections, post gastric surgery , autoimmune disorders like atrophic gastritis, Crohn’s disease, HIV/AIDs etc. It is frequently asymptomatic, symptoms may result from anemia due to Vit. B12 deficiency.
Microscopic examination shows infiltration of the mucosa with lymphocytes, plasma cells, neutrophils and sometimes eosinophils; mucosal atrophy and intestinal metaplasia. In chronic erosive gastritis caused by NSAIDS, superficial mucosal erosions are seen. Granulomas are present in Crohn’s disease, TB, sarcoidosis and other granulomatous disease. Predominantly eosinophilic infiltrate is seen in eosinophilic gastritis associated with food allergies.
Dyspepsia: It is a common symptom described as an uncomfortable feeling in the epigastrium, upper abdominal pain, bloating, heartburn, nausea, vomiting and/or indigestion. It can be due to peptic ulcer disease, gastritis, GERD, alcohol and drugs like NSAIDS, aspirin, stress, spicy or fatty foods, caffeine or gastric cancers.
Peptic ulcer: It is ulceration of the epithelial lining of the stomach and/or duodenum as a result of action of pepsin, HCl and loss of protective mucous layer. It may be caused by H.pylori infections, NSAIDS, stress, burns, TB, Crohn’s disease, cirrhosis, renal failure, sarcoidosis, CMV, surgery, critical illness or smoking. Multiple ulcers are seen in Zollinger-Ellison syndrome. Duodenal ulcers are more common than gastric ulcers. Clinical features of peptic ulcers include episodic gnawing pain or burning epigastric pain that is aggravated by food intake in gastric ulcers and relieved by food intake in duodenal ulcers. Other symptoms include indigestion, nausea, vomiting, weight loss and loss of appetite. Gastric ulcers are typically located on the lesser curvature while duodenal ulcers are located at the duodenal bulb. On gross examination, the ulcer is round or oval, “punched-out” lesion, superficial (involves only mucosa) or deep (penetrates the muscularis layer). Microscopic examination shows a necrotic base, zone of fibrocollagenous tissue and overlying granulation tissue. Obstruction and malignant change are more common in gastric ulcers than duodenal, while perforation is more common in duodenal ulcers. Treatment includes eradication of H.pylori, H2 blockers, PPIs (first choice), sucralfate and rarely surgery (vagotomy, partial gastrectomy).
GIST or gastrointestinal stromal tumors: GIST tumors arise from the interstitial cells of Cajal. They are typically seen in adults between 40-70 years of age. They can be benign or malignant. Many cases are asymptomatic. Presentation is with abdominal pain, nausea, fatigue, GI bleeding and weight loss. Skin changes like urticaria pigmentosa or cutaneous mastocytosis which presents with itchy brown macules and papules may be seen. Mutations in the KIT and PDGFRA genes are associated with GIST. These mutations lead to persistent activation of signalling pathways that lead to abnormally increased cell proliferation and survival. Some cases have SDH mutations and are deficient in the enzyme succinate dehydrogenase that results in excess accumulation of succinate in the mitochondria. GIST may develop in cases of neurofibromatosis type 1. Tumors may be single or multiple. Biopsy findings include spindle-shaped, epithelioid or mixed cells arranged in fascicles or syncytia, resembling muscle cells. GIST tumors are CD117 and DOG1 marker +. Treatment is by surgical excision or imatinib.
Adenocarcinoma of stomach: It is the most common type of gastric cancer. It has a high incidence in Japan, South America and Eastern Asia. Diets rich in salt, smoked or poorly preserved foods, nitrates, nitrites and secondary amines are associated with an increased risk of gastric cancer. Most cases are sporadic. Familial cases are associated with mutations in p53, BRCA2 and gene coding E-cadherin (high risk). Gastric cancer is seen as part of HNPCC, familial adenomatous polyposis and Peutz-Jeghers syndrome. H.pylori infection especially in blood group A individuals is associated with high risk. Chronic atrophic gastritis with pernicious anemia, obesity and Menetrier’s disease are other risk factors. Patients may remain asymptomatic till late in the disease. Symptoms include dyspepsia, anorexia, vague abdominal pain, early satiety, weight loss and GI bleeding. Distant metastases present as enlarged supraclavicular lymph node (Virchow’s node), periumbilical lymph node (Sister Mary Joseph’s node) and left axillary lymph node (Irish’s node). Peritoneal seeding may cause Krukenberg tumors (bilateral ovarian tumors with signet-ring cells). Gross examination shows a polypoid, fungating mass, ulcerative or diffusely infiltrative lesion. Locally advanced cancers invade the muscularis propria. Linitis plastica is a type of diffusely infiltrative, scirrhous-type, gastric adenocarcinoma that presents as thickened gastric folds and extensive submucous fibrosis with poor distensibility seen on endoscopic ultrasound. Treatment of gastric cancer is surgical with subtotal or total gastrectomy. Chemotherapy with cisplatin, 5FU, etoposide and/or leucovorin, radiotherapy or immunotherapy may be used in advanced cases.
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