Pathology of GIT Stomach Oct Prof. Dr. Faeza Aftan Col of Med. Aliraqia University

 STOMACH Acute Gastritis Acute Gastric Ulcer Chronic Gastritis - HELICOBACTER PYLORI GASTRITIS - AUTOIMMUNE GASTRITIS PEPTIC ULCER DISEASE Hypertrophic Gastropathies ZOLLINGER-ELLISON SYNDROME Gastric Polyps and Tumors

Normal Esophagus & Stomach Stomach

Microscopic Anatomy of the Stomach

 CONGENITAL ABNORMALITIES  Diaphragmatic Hernia, Omphalocele, and Gastroschisis  Ectopia. (Gastric heterotopia, ectopic gastric mucosa in the small bowel or colon).  Pyloric Stenosis

3-4 times more in males occurs 1/ live births. genetic basis. 2 nd or 3 rd week presents in 2 nd or 3 rd week as regurgitation and projectile vomiting. hyperperistalsis O/E; hyperperistalsis firm, ovoid mass. and a firm, ovoid mass. Acquired pyloric stenosis Acquired pyloric stenosis Rx: Rx: myotomy Congenital hypertrophic pyloric stenosis

ACID PROTECTION MUCUS HCO3- EPITHELIAL BARRIERS BLOOD FLOW PROSTAGLANDIN E, I

 STOMACH Acute Gastritis Acute Gastric Ulcer Chronic Gastritis - HELICOBACTER PYLORI GASTRITIS - AUTOIMMUNE GASTRITIS PEPTIC ULCER DISEASE Hypertrophic Gastropathies ZOLLINGER-ELLISON SYNDROME Gastric Polyps and Tumors

ACUTE GASTRITIS NSAIDs NSAIDs Stress Stress Others Others asymptomatic pain, N & V. ACUTE, HEMORRHAGIC ACUTE, HEMORRHAGIC mucosal erosion, ulcer, Hge, hematemesis, melena, blood loss

Acute Peptic Ulceration NSAIDs. NSAIDs. Stress Stress less than 1 cm less than 1 cm Multiple Multiple Superficial Superficial nausea, vomiting, nausea, vomiting, coffee-ground hematemesis. coffee-ground hematemesis. Bleeding in 1% to 4% perforation,

ACUTE” ULCERS

 NSAID cyclooxygenase inhibition prevents synthesis of PG.  PG ; HCO3- secretion, mucin synthesis, & vascular perfusion. HCL secretion.  intracranial injury  intracranial injury ___ vagal nuclei, __increase HCL

Chronic Gastritis H. Pylori; 90% of cases H. Pylori Autoimmune; 10%

Chronic Gastritis Helicobacter pylori Helicobacter pylori Antrum Antrum Chronic antral H. pylori gastritis Chronic antral H. pylori gastritis increased acid secretion increased acid secretion NO EROSIONS, NO EROSIONS, NO HEMORRHAGENO HEMORRHAGE PU PU Gastric Ca Gastric Ca Gastric Lymphoma. Gastric Lymphoma.

Lymphocytes, +/- PMN lymphoid follicles –METAPLASIA, intestinal –ATROPHY, mucosal “thinning” –DYS-PLASIA Chronic Gastritis

Helicobacter pylori

H. pylori virulence  H. pylori virulence: Flagella, Adhesins, Urease, Urea _Urease_ Amonia (Increase local pH) Toxins, encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer

Helicobacter pylori:  Gram negative, Spiral bacilli  Spirochetes  Do not invade cells – only mucous  Breakdown urea - ammonia  Break down mucosal defense  Chronic Superficial inflammation

Helicobacter pylori Causes chronic gastritis Causes 80 % of gastric peptic ulcers Causes 100% of duodenal peptic ulcers Causes gastric carcinomas Causes MALT lymphomas

 AUTOIMMUNE GASTRITIS less than 10% of cases of chronic gastritis. median age is 60 years, female predominance Antibodies to parietal cells & IF diffuse atrophy, parietal and chief cell damage Achlorhydria. Reduced serum pepsinogen. (chief cell loss) Vitamin B 12 deficiency Atrophy, pernicious anemia, adenocarcinoma

H. pylori–Associated and Autoimmune Gastritis H. pylori–AssociatedAutoimmune LocationAntrumBody Acid productionIncreasedDecreased GastrinNormal to decreasedIncreased SerologyAbs to H. pyloriAbs to parietal cells (H +, K + - ATPase, intrinsic factor) SequelaePeptic ulcer, adenocarcinoma Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor AssociationsLow socioeconomic status, poverty, residence in rural areas Autoimmune disease; thyroiditis, diabetes mellitus, Graves disease

PEPTIC ULCERS

4 times PU are 4 times more in proximal duodenum than in stomach. Duodenal ulcers occur within a few cm of the pyloric valve & involve anterior duodenal wall. Gastric ulcers are located along lesser curvature near the interface of the body & antrum. PU are solitary in more than 80%. Classic PU is a round, sharply punched-out defect

H. pylori NSAID., H. pylori & NSAID., are the primary causes of PUD. Although more than 70% of individuals with PUD are infected by H. pylori, fewer than 10% of H. pylori–infected individuals develop PU.  Clinical picture Young - middle-aged or older adults epigastric pain (burning or aching, 1-3 hrs after meals & worse at night, is relieved by alkali or food). PEPTIC” ULCERS

PEPTIC ULCERS active ulcer The base of active ulcer; Thin layer of fibrinoid debris PMN infiltrate. Granulation tissue Fibrous scar forms the ulcer base. Vessel walls within the scarred area are thickened. Size and site do not differentiate benign and malignant ulcers. However, the gross appearance of chronic PU is virtually diagnostic

Chronic gastric ulcer Malignant gastric ulcer

chronic NSAID smoking, impairs mucosal bl flow & healing corticosteroids, suppress PG synthesis & healing. stress, increase gastric acid production. Ch Dis; alcoholic cirrhosis & ch. obstructive pulmonary dis. Ch. renal failure, and hyperparath, hypercalcemia, stimulates gastrin and increases acid secretion. Cofactors in PUD

PEPTIC ULCERS  Complications. Bleeding – Occurs in 15% to 20% of patients – Accounts for 25% of ulcer deaths Perforation – Occurs in about 5% of patients – Accounts for two thirds of ulcer deaths Obstruction from edema or scarring – Occurs in about 2% of patients – Most often due to pyloric channel ulcers Fe. Def. Anemia Malignant transformation of peptic ulcers is very rare.

Acute gastric perforation in a patient presenting with free air under the diaphragm. A, Mucosal defect with clean edges. B, The necrotic ulcer base (arrow) is composed of granulation tissue

Zollinger-Ellison syndrome Multiple peptic ulcerations in the stomach, duodenum, & even jejunum gastrin-secreting tumor of the pancreas (Gastrinoma), that stimulates acid-secreting cells of the stomach to maximal activity, with consequent GIT mucosal ulceration. ZES may occur sporadically or as part of an AD familial syndrome (MEN 1).

Ménétrier disease Rare, acquired, premalignant disease of the stomach Massive gastric folds, excessive mucous production protein loss, little or no acid production. RUGAL PROMINENCE (cerebriform) HYPERPLASIA of MUCOSA

BEZOARS PHYTO-bezoar (plant material) TRICHO-bezoar (hairball) NON-food material in PSYCH patients – pins – nails – razor blades – coins – Gloves – A large obstructive bezoar usually takes on the shape and contour of the stomach