GASTRITIS

1. GASTRITIS

2. Definition: Inflammation of the gastric mucosa • group of disorders with inflammatory changes in the gastric mucosa (G.M.) that have different clinical features, histological characteristics and pathogenesis. • A. ACUTE GASTRITIS • B. CHRONIC GASTRITIS

3. A. ACUTE HEMORAGIC GASTRITIS (EROSIVE) Examinationshows: EDEMA MUCOSAL FRIABILITY EROSIONS: limited to the mucosa ! SITES OF BLEEDING: diffusely through the G. M. localized to the body, antrum of the stomach HISTOLOGIC EXAMINATIONof the G.M. reveals infiltration of the lamina propria with: – mononuclear cells – PMN leukocytes – extravasations of blood in the mucosa

4. ETIOLOGY & PATHOGENESIS: Erosive gastritis – 89 - 90 % of critically ill hospitalized patients (medical) surgical intensive care units Stress – induced gastritis Mechanism: a) ischemia of the G.M. b) acid diffusion from the gastric lumen into gastric mucosal tissues c) bile acid / duodenal pancreatic secretions refluxed into the gastric lumen a + b  CRUCIAL in the ethiopathogenesis of the STRESS – INDUCED GASTRITIS AGENTS  injure the G.M. - aspirin – injure the small vessels in the G.M. by: –inhibitory of prostacyclin in the walls of vessels –synthesis of tromboxane by platelets - NSAIDS - bile acids - pancreatic enzymes - ethanol Reduction in tissue PG – principal in damage the G.M.

5. CLINICAL FEATURES PHYSICAL EXAMINATION • Hematemesis / melena Pallor • Anemia Tachycardia • Epigastric pain Hypotension • Nausea • Vomiting • BIOLOGICAL ASPECTS • - leucocytosis / leukopenia

6. DIAGNOSIS • blood in the stool / gastric aspirate • Upper GI endoscopy: • mucosal hemorrhages • friability + congestion • erosions • superficial / deep ulcerations in the fundus / body of the stomach • Radiographic examination – much less reliable in detecting acute hemoragic erosive gastritis • TREATMENT • A. General supportive measures • - maintenance of oxygen, blood volume, fluid and electrolyte requirements • B. H2 – R antagonist (i.v.) QUAMATEL 20 – 40 mg/day • Embolization / vasopressin infusion of the left gastric artery • IPP – Controloc 40 mg i.v. • Surgical treatment should not be performed unless is absolutely necessary.

7. ACUTE GASTRITIS + HELICOBACTER PYLORI - short spiral – shaped, microaerophitic gram - bacillus - in gastric samples by histological examination, culture, increase activity, by endonuclease analysis. - hematoxylin – positive - UBT 13C, 14C - antibodies (Ig G, Ig A) to H.P. 90 – 100 % Hp + antral biopsy specimens of DU patients 70 % - G.U. 80 % - chronic gastritis involving the antral mucosa 50 % - non ulcer dyspepsia

8. CHRONIC GASTRITIS Definition: Chronic inflammatory cells, predominately lymphocytes and plasma cells. HISTOLOGIC CLASSIFICATION I. SUPERFICIAL GASTRITIS - Inflammatory changes in the lamina propia of the superficial mucosa of the upper half of G.M. and the glands are preserved II. ATROPHIC GASTRITIS - the inflammatory infiltrate extends to the deep positions of the mucosa - profound loss of the glandular structures which are separated widely by connective tissue, with a greatly reduced / absent inflammatory infiltrate. - the mucosa is thin, revealing the prominence of its underlying vessels by endoscope examination. Gastritis progresses – changes in the morphology of the gastric glandular elements. Intestinal metaplasia – conversion of gastric glands to the small-intestinal mucosal glands with goblet cells.

9. CHRONIC GASTRITIS – TYPES A & B Type A – involves the body and fundus of the stomach – from that may lead to pernicious anemia Antibodies to parietal cells, intrinsec factor in serum  immuno / autoimmuno pathogenesis Parietal cell Antibodies 20% of patients over age 60  20% of patients with – hypoparathyroidism – Addison’s disease – vitiligo Antibodies to intrinsec factor 40 % of those with pernicious anemia. The risk of stomach cancer in patients with type A gastritis and pernicious anemia is three times than the general population Type B: In younger patients  involves the antrum In elderly patients  involves entire stomach The incidence increases with age - Strong associations of H. pylori with type B gastrities - Chronic reflux of: pancreatic – biliary secretions bile acids lysolecithin

10. DIAGNOSIS • - Biopsy of the G.M. provides the most reliable means of identifying and classifying gastritis. • Several biopsies of suspected areas, when safe and possible, are recommended. • TREATMENT • In type A.G. + pernicious anemia • Vit. B12 – indefinite regular parental administration

11. MÉNÉTRIER’S DISEASE • - large tortuoces gastric mucosal folds in gastric body and fundus. • - hyperplasia of surface and glandular mucous cells, which replace most of the chief and parietal cells. • the lamina propria may contain an increased number of lymphocytes and intestinal metaplasia may be present. • Symptoms • epigastric pain • anorexia • nausea, vomiting • weight loss • gastric bleeding – unusual Gastric ulcer / gastric carcinoma many develop ! • Gastric acid secretion is reduced / absent. • Barium examination: large gastric folds • Endoscopic examination: confirm gastric folds • Diagnostic: deep mucosal biopsy • Treatment:ARH2 decrease protein loss • high – protein diet to replace protein loses • gastrectomy in severe disease

12. CORROSIVE GASTRITIS - corrosive chemicals  antrum injury (HCl, H2SO4, NaOH) Symtoms: burning of the mouth, throat, retrosternal area epigastric pain vomiting hemorrhage / perforation Treatment: supportive therapy

13. INFECTIOUS GASTRITIS Phlegmonous G – necrosis, sepsis - streptococci, staphylococci, Proteus, Escherichia coli TREATMENTi.v. antibiotics fluids + electrolyte replacement gastrectomy – in lack of response It can occur in immuno-compromised patients  cytomegalovirus

14. EOSINOPHILIC GASTRITIS • extensive eosinophilic infiltration (e.i) of the wall of the stomach • -biopsy reveals e.i. • - antrum is more frequently involved than G body fundus. • SYMPTOMS: epigastric pain • nausea, vomiting • TREATMENT:glucocorticoids

15. GRANULOMATOUS GASTRITIS Chron’s disease produce: ulceration granulomatous infiltration stricture formation Other’s: histoplasmosis candidosis syphilis tuberculoses Diagnostic: biopsies + cytology to exclude malignancy surgical exploration if the diagnostic is not established by biopsy at endoscopy.

16. DUODENAL ULCER Chronic and recurrent disease ETIOLOGY - Genetic Factors: increase of blood 0 - increase HLA – B5 antigen in white male subjects - 50 % - elevated serum pepsinogen (PG I) - autosomal dominant trait - Smoking – inhibition of pancreatic bicarbonate secretion by nicotine – accelerated emptying of gastric acid into the duodenum - Chronic renal failure - Alcoholic cirrhosis - Gastric colonization with Helicobacter pylori in 80 -100% - Psychological factors: chronic anxiety, stress

17. CLINICAL FEATURES 1. Epigastric pain: sharp, burning, gnawing 10 % - right epigastrium 2. Occurs from 90’ - 3 hours after eating awakens the patients at night - pain is usually relieved by food or antacids - nausea, vomiting - weight loss - anemia (occult blood loss) – iron deficiency - constipation - Penetration - Perforation 6% / complications - Hemorrhage: 15% with 40 % reccurence

18. DIAGNOSIS 1. Barium examinationUGIT 70 – 80 % + discrete crater in the proximal portion of the duodenal bulb 2. Endoscopic examination

19. MEDICAL TREATMENT 1. Antacids:Aluminum hydroxide Magnesium Calcium carbonate Sodium bicarbonate 2. H2 – R antagonists Cimetidine 300 mg x 4 / days 4 weeks Adverse effects: increase transaminase, creatinine, gynecomastia Ranitidine: 150 mg x 2 / day 300 mg at bedtime Nizatidine:300 mg 1 month 150 mg bedtime for reduction of DU recurrence Famotidina: 20 – 40 mg / day 4 weeks 3. Anticholinergic agents:atropine decrease gastric acid secretion (g.a.s.) Pirenzepine – adjunctive therapy

20. 4. Coating agents Sucralfate increase mucosal defense! Colloidal bismuth 5. Prostaglandinsreduce basal and stimulated g.a.s. enhances mucosal resistance to tissue injury. 6. Proton Pomp Inhibition - OMEPRAZOLE 20 mg X 2 / DAY 4 – 6 weeks - LANSOPRAZOLE 30 mg / day - PANTOPRAZOLE 40 mg / day - ESOMEPRAZOLE 20 – 40 mg / day DIET - free of spices, fruit juices - avoid coffee, alcohol intake - elimination of smoking - elimination stress eat 5 times / day in small meals

21. GASTRIC ULCER (G.U.) • the pick incidence for G.U. is in the sixth decade • ETIOLOGY • Acid- pepsin appears important in the pathogenesis • - Gastric emptying is delayed • Regurgitation of duodenal contents (bile) induce gastric mucosal injury- gastric ulceration • CLINICAL FEATURES • - Epigastric pain - no relief with eating! • - Nausea, vomiting • - Weight loss • - Upper GI bleeding • - Anemia

22. DIAGNOSIS • 1. Barium examination • 2. Endoscopy: size, location, histological characteristics • Ulcer > 3 cm diameter are > often malignant • 4% of GU appears benign on X-Ray plane to be malignant by endoscopic biopsy / surgery! • MEDICAL TREATMENT • H2RA • Sulcralfate 4/ 8 weeks • Antacids • Benign G.U. should heal completely within 3 months of vigorous therapy. • Avoid - NSAID/ glucocorticoides • - coffee • - smoking • - spices foods • Gastroscopy after 4 weeks of treatment reveal healing of benign ulcers.

23. Surgery in D.U. • - Vagotomy + antrectomy • - vagotomy + pyloroplasty • - truncal or selective vagotomy • - Bilroth IA: stomach + proximal duodenum • Bilroth IIA: stomach + loop of the jejunum • Surgery GU: Antrectomy + G.D. Anastomosis in those who do not respond to medical theraphy/complications. • GASTRIC ADENOCARCINOMA • 90% are adenocarcinomas • 10% non// Hodgkin's lymphomas and leiomyosarcomas.

24. ETIOLOGY • Long/term ingestion of high concentrations of nitrates indried, smoked, salted foods- higher risk. Serial endoscopic examination of the stomach in patients with atrophic gastritis- replacement of the gastric mucosa by intestinal type cells/ cellular atypia/ neoplasia • - Adenomatous polyposis • - Gastric ulcers • - Menetrier's disease • Group AII patients • CLINICAL FEATURES • - Upper abdominal discomfort- steady pain • - Anorexia • - Weight loss • - Nausea + vomiting - tumor of the pylorus • - Disphagya - tumor of cardia • - Palpable abdomen mass-physic examination • - Iron - deficiency anemia • - Migratory thrombophlebitis • - microangiopathie hemolytic anemia • - Achantosis nigricans.

25. DIAGNOSIS • Double-contrast radiographic examination. • Deep Gastroscopic biopsy and brush cytology. • TREATMENT • Surgical removal of the complete T, with resection of adjacent lymph nodes offers the only chance for cure. • Subtotal gastrectomy - distal carcinomas. • Total gastrectomy - proximal tumors. • PROGNOSIS • - degree of tumor penetration into the stomach wall. • - regional lymph node involement/ vascular invasion. • Chemotherapy and/or radiotherapy - metastatic disease (5 FU+ Doxorubicin, Mytomicin + G cisplatin) • PRIMARY GASTRIC LYMPHOMA • 7% of gastric malignancies/ 2% of all lymphomas. • GASTRIC SARCOMA • - 1-3% of all gastric neoplasms • - anterior + posterior walls of the gastric fundus • - spread to the liver and lungs.