definition: inflammation of the gastric mucosa -group of disorders with inflammatory changes in the...
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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
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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
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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.
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CLINICAL FEATURES PHYSICAL EXAMINATION•Hematemesis / melena Pallor•Anemia Tachycardia•Epigastric pain Hypotension•Nausea•Vomiting
BIOLOGICAL ASPECTS- leucocytosis / leukopenia
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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.
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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
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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.
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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
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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
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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
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CORROSIVE GASTRITIS
- corrosive chemicals antrum injury(HCl, H2SO4, NaOH)
Symtoms:burning of the mouth, throat, retrosternal areaepigastric painvomitinghemorrhage / perforation
Treatment: supportive therapy
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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
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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
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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.
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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
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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
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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
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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
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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
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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
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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.
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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.
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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.
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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.