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STOMACH Cell types: Mucosal surface & foveolae:  Surface foveolar cells - secrete mucous Mucous neck cells - progenitor cells  Glands: Mucous cells.

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Presentation on theme: "STOMACH Cell types: Mucosal surface & foveolae:  Surface foveolar cells - secrete mucous Mucous neck cells - progenitor cells  Glands: Mucous cells."— Presentation transcript:

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3 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

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5 Congenital Anomalies

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

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

8 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

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

13 - Reduced mucosal blood flow - Direct damage to mucosal epithelium

14 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

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

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23 / dysplasia

24 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

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

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

27 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%

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

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46 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

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53 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

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59 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

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62 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

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68 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

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70 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

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72 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)

73 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)

74 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)

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

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79 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

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