STOMACH Cell types: Mucosal surface & foveolae:  Surface foveolar cells - secrete mucous Mucous neck cells - progenitor cells  Glands: Mucous cells - secrete mucous & pepsinogen II Parietal cells - secrete HCl & IF Chief cells - secrete pepsinogen I & II Endocrine cells - secrete peptide & amine hormones

Congenital Anomalies

CONGENITAL ANOMALIES Diaphragmatic Hernia: Defect in diaphragm, away from esophageal hiatus Portions of stomach & SI herniate  pulmonary hypoplasia & respiratory impairment

CONGENITAL ANOMALIES Heterotopic rests: Location: Anywhere in the GIT MC: Pancreatic & gastric S/S: Usually asymptomatic but may cause ulceration

CONGENITAL ANOMALIES Congenital Hypertrophic Pyloric Stenosis:CHiPs M > F (3:1), 1 in 200 infant males, multifactorial inheritance Cause:  Hypertrophy & hyperplasia of circular muscle of pylorus  regurgitation, projectile non- bilious vomiting commences at wks of age  May be due to defective autonomic regulation Dx: Visible peristalsis & palpable mass in RUQ Tx: Pyloromyotomy is curative

ACUTE GASTRITIS Other Causes: Ingestion of strong acids or alkali Ca chemotx Radiation Ischemia & shock NGTs

- Reduced mucosal blood flow - Direct damage to mucosal epithelium

ACUTE GASTRITIS Clinically: Asymptomatic to epigastric pain of varying severity, up to acute abdomen w/ hematemesis & shock major cause of massive hematemesis (esp. alcoholics) Common in those who take daily aspirin for RA

ACUTE GASTRITIS Morphology: Mucosal edema & congestion, PMN infiltration (milder cases) Erosions (not deeper than muscularis mucosa) & hges (acute erosive gastritis)

/ dysplasia

CHRONIC GASTRITIS Pathogenesis: Autoimmune: Abs to parietal cells  parietal cell destruction (  HCl & IF) Environmental:  Chronic infection by H. pylori  Alcohol, tobacco, radiation, bile reflux, Crohn’s disease, uremia, gastric atony

CHRONIC GASTRITIS Gross: Red mucosa (thickened or flattened) Autoimmune  fundus & body H pylori  antrum & body Bile reflux  antrum

CHRONIC GASTRITIS Histology: Lympho & plasma cell infiltrates in LP (superficial or involving entire mucosal thickness) Others: Regenerative atypia Intestinal metaplasia Atrophy Dysplasia

CHRONIC GASTRITIS Clinical: Mild abdominal discomfort, nausea, vomiting, hypochlorhydria Autoimmune gastritis: Hypo- / a- chlorhydria, hypergastrinemia, ~ 10%  overt PA, long-term risk of Ca is 2- 4%

Helicobacter pylori ~ 50% of asymptomatic American adults > 50 yrs are infected Dx: CLO test Diseases Association: Chronic gastritis PUD Gastric ca/ lymphoma

PEPTIC ULCERS Usually solitary ~ cm MC: duodenum & antrum Ratio of duodenal: gastric PU is ~ 4 : 1 ~ 4 M Americans have PU Life-time incidence in USA is 10% for men & 4% for women

PEPTIC ULCERS Clinical: Epigastric pain 1-3 hrs PC & worse at night; nausea; vomiting; belching, weight loss Complications: Hemorrhage - 25% of ulcer deaths Perforation - ~ 2/3 of ulcer deaths Obstruction - causes severe crampy abdominal pain Malignant transformation extremely rare

HYPERTROPHIC GASTROPATHTY Zollinger-Ellison Syndrome: Hypertrophic rugal folds Parietal cell hyperplasia Peptic ulcers Markedly elevated serum gastrin levels Caused by a gastrin secreting tumor (gastrinoma) Pancreas is the usual primary site

HYPERTROPHIC GASTROPATHY Menetrier’s disease: Affects men in 4th to 6th decades Epigastric pain, anorexia, vomitting, wt. loss & peripheral edema Diffuse rugal hypertrophy Marked foveolar hyperplasia, smooth muscle proliferation in LP, glandular atrophy Hypochlorhydria Protein-losing enteropathy

GASTRIC POLYPS Mucosal masses projecting above level of surrounding mucosa > 90% non-neoplastic polyps - no malignant potential Hyperplastic polyps: MC type of gastric polyp Small sessile polyps May be multiple No dysplasia  no malignant potential

GASTRIC POLYPS (CONT.) Adenomatous polyps (Adenomas): May be sessile or pedunculated Usually solitary May reach 3-4 cm in dia Contain proliferating dysplastic epithelium Are true neoplasms Up to 40% contain a focus of ca at time of biopsy Patients with autoimmune gastritis or colonic polyposis Syndromes have an increased incidence Gastric polyps need to be biopsied

GASTRIC CARCINOMA Worldwide distribution variable US 2.5% of all Ca deaths 5-6 fold decline in incidence over last 70 yrs (for unknown reasons)

GASTRIC CARCINOMA Classification: According to Depth of invasion: Early Gastric Ca: Confined to mucosa & submucosa Very good prognosis - ~ 90% 5-year survival, even w/ limited LN spread Advanced Gastric Ca: Extended beyond submucosa Spread by local invasion, lymphatics, blood (to liver, lungs & bone) Virchow node Bilateral ovarian metastases - Krukenberg Poor prognosis (<15% 5-year survival)

GASTRIC CARCINOMA Classification: According to Gross Pattern: Exophytic Flat/depressed Excavated (ulcerative) According to Histologic Pattern: Intestinal type, glandular, expansile Diffuse type, “signet ring cell”, infiltrating (linitis plastica)

GASTRIC CARCINOMA Classification: Pathologic stage is the most important prognostic indicator Less Common Gastric Tumors: Lymphomas (~ 5%) Stromal tumors (~ 2%) Carcinoid tumors (rare)

GASTRIC CARCINOMA Risk Factors: Diet: Nitrites (food preservatives), smoked & salted foods, deficiency of fresh fruits & vegetables Host Factors: chronic gastritis (autoimmune & H. pylori), adenomatous polyps, partial gastrectomy Genetic Factors: only ~ 4% of patient’s w/ gastric CA have a family Hx