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 GASTRITISB. CHRONIC GASTRITIS

A. ACUTE HEMORAGIC GASTRITIS (EROSIVE)

Examination shows:EDEMAMUCOSAL FRIABILITYEROSIONS: limited to the mucosa !SITES OF BLEEDING: diffusely through the G. M.localized to the body, antrum of the stomach

HISTOLOGIC EXAMINATION of the G.M. reveals infiltration of the lamina propria with: – mononuclear cells

– PMN leukocytes– extravasations of blood in the mucosa

ETIOLOGY & PATHOGENESIS:Erosive gastritis – 89 - 90 % of critically ill hospitalized patients (medical) surgical intensive care unitsStress – induced gastritis

Mechanism:a) ischemia of the G.M.b) acid diffusion from the gastric lumen into gastric mucosal tissuesc) bile acid / duodenal pancreatic secretions refluxed into the gastric lumena + 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- ethanolReduction in tissue PG – principal in damage the G.M.

CLINICAL FEATURES PHYSICAL EXAMINATION•Hematemesis / melena Pallor•Anemia Tachycardia•Epigastric pain Hypotension•Nausea•Vomiting

BIOLOGICAL ASPECTS- leucocytosis / leukopenia

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

TREATMENTA. General supportive measures- maintenance of oxygen, blood volume, fluid and electrolyte requirements

B. H2 – R antagonist (i.v.) QUAMATEL 20 – 40 mg/dayEmbolization / vasopressin infusion of the left gastric artery IPP – Controloc 40 mg i.v.Surgical treatment should not be performed unless is absolutely necessary.

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

CHRONIC GASTRITISDefinition: 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.

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 antrumIn elderly patients involves entire stomachThe incidence increases with age- Strong associations of H. pylori with type B gastrities- Chronic reflux of: pancreatic – biliary secretions

bile acidslysolecithin

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 anemiaVit. B12 – indefinite regular parental administration

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.

Symptomsepigastric painanorexianausea, vomitingweight lossgastric bleeding – unusualGastric ulcer / gastric carcinoma many develop !

Gastric acid secretion is reduced / absent.Barium examination: large gastric foldsEndoscopic examination: confirm gastric folds

Diagnostic: deep mucosal biopsy

Treatment: ARH2 decrease protein losshigh – protein diet to replace protein losesgastrectomy in severe disease

CORROSIVE GASTRITIS

- corrosive chemicals antrum injury(HCl, H2SO4, NaOH)

Symtoms:burning of the mouth, throat, retrosternal areaepigastric painvomitinghemorrhage / perforation

Treatment: supportive therapy

INFECTIOUS GASTRITIS

Phlegmonous G – necrosis, sepsis

- streptococci, staphylococci, Proteus, Escherichia coli

TREATMENT i.v. antibiotics

fluids + electrolyte replacement

gastrectomy – in lack of response

It can occur in immuno-compromised patients cytomegalovirus

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 painnausea, vomiting

TREATMENT: glucocorticoids

GRANULOMATOUS GASTRITIS

Chron’s disease produce: ulcerationgranulomatous infiltrationstricture formation

Other’s: histoplasmosiscandidosissyphilistuberculoses

Diagnostic: biopsies + cytology to exclude malignancysurgical exploration if the diagnostic is not

established by biopsy at endoscopy.

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

CLINICAL FEATURES

1. Epigastric pain: sharp, burning, gnawing10 % - 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

DIAGNOSIS

1. Barium examination UGIT 70 – 80 % + discrete crater in the proximal portion of the duodenal bulb

2. Endoscopic examination

- size- shape- location

- in detecting D.U. in the absence of Rx image- in identifying ulcers too small / superficial to be recognized by X-ray- excluding an ulcer as the source of active GI Hemorrhage

MEDICAL TREATMENT

1. Antacids: Aluminum hydroxideMagnesiumCalcium carbonateSodium bicarbonate

2. H2 – R antagonistsCimetidine 300 mg x 4 / days 4 weeksAdverse effects: increase transaminase, creatinine, gynecomastiaRanitidine: 150 mg x 2 / day

300 mg at bedtimeNizatidine: 300 mg 1 month

150 mg bedtime for reduction of DU recurrenceFamotidina: 20 – 40 mg / day 4 weeks

3. Anticholinergic agents: atropine decrease gastric acid secretion (g.a.s.)Pirenzepine – adjunctive therapy

4. Coating agentsSucralfate increase mucosal defense!Colloidal bismuth

5. Prostaglandins reduce 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 stresseat 5 times / day in small meals

GASTRIC ULCER (G.U.)- the pick incidence for G.U. is in the sixth decade

ETIOLOGYAcid- 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

DIAGNOSIS1. Barium examination2. Endoscopy: size, location, histological characteristicsUlcer > 3 cm diameter are > often malignant 4% of GU appears benign on X-Ray plane to be malignant by endoscopic biopsy / surgery!

MEDICAL TREATMENTH2RASulcralfate 4/ 8 weeksAntacidsBenign 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.

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 adenocarcinomas10% non// Hodgkin's lymphomas and leiomyosarcomas.

ETIOLOGYLong/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.

DIAGNOSISDouble-contrast radiographic examination.Deep Gastroscopic biopsy and brush cytology.

TREATMENTSurgical 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.