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Chronic Gastritis. Ulcer of Stomach and Duodenum.

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Chronic Gastritis.
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 Is inflammation of the gastric mucosa  Is clinical and morphological diagnosis  Is a histological diagnosis nowadays, although it can

Gastritis

sometimes be recognised at endoscopy.  Is not a single disease but rather a group of disorders that all induce inflammatory changes in the gastric mucosa but that differ in their clinical features, histologic characteristics, and causative mechanisms.

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TYPE  Acute  Chronic  Uncommon forms

Sydney Classification of Gastritis, 1990

AETIOLOGY  Infectious – H.Pylori (HP)  Non-infectious (alcohol, NSAID, autoimmune,…)  Unknown factors

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Sydney Classification of Gastritis, 1990
TOPOGRAPHY  Antral-predominant  Body-predomonant  Pangastritis MORPHOLOGY  Inflammation (activity)  Atrophy  Intestinal metaplasia
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Endoscopic classification

 Superficial gastritis  Atrophic gastritis

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Chronic Gastritis
 Type A (autoimmune) – 5-20%  Type B (HP) – up to 80%  Type AB  Indeterminant type

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Type A gastritis
 Rare  Antibodies to parietal cells and to intrinsic
factor have been shown to be cytotoxic for gastric mucosal cells  Parietal cells are invariably destroyed atrophy  Parietal cells inability to secrete hydrochloric acid achlorhydria  It results in malabsorption of vitamin B12 anemia progression

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Type A gastritis
 Not young age  No complains – during many years, but:  Nausea  Epigastrium discomfort  Appetite lowering  Air belching  Abdominal fullness or early satiety  Tendency to diarrhea
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Type A gastritis
            
Inspection: - anemia signs (pallor of mucous and skin) - flatting of papillas (bald tongue) - diffusive epigastral abdominal tenderness Common blood test – normal or anemia Gastrinemia Endoscopic investigation: - pallor of mucous - hypotonic and hypokinetic stomach wall Histology: - parietal cells atrophy - intestinal metaplasia - minimal inflammation

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Type A gastritis
     
Treatment: Diet № 2 Replaceable therapy – natural gastric juice - “acidin-pepsin”, “Pepsidil”,.. Increasing of gastric secretion (Euphyllin) Vitamins (e.g. B12)
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Type B gastritis
Synonyms:  Antral-Predominant Gastritis  HP Gastritis  Environmental Gastritis

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Some factors influence the virulence of HP

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Type B gastritis
 Since young age  Often – with duodenitis  Increasing of gastric secretion  Epigastrium discomfort and pain  Reluctance to eat due to anticipate
discomfort  Nausea  Appetite lowering sometime  Air belching sometime

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 Inspection:  - tongue: white fur and enlargement with        

Type B gastritis

dental pits in sides - local epigastral abdominal tenderness in the pyloroduodenal part Endoscopic investigation: - hyperemia and oedema of mucous - folder’s hyperplasia - pylorospasm Histology: - inflammation (lymphocytes, plasmocytes) - HP

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Methods for the diagnosis of HP
 
Non-invasive: Serological (population studies) Urea breath test (high sensitivity and specificity) Invasive: Histology (antral biopsy) Rapid urease tests (“Pyloritek”) Microbiological culture (“Gold standart”) defines anbiotic sensitivity
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  

 Diet № 1  Antibiotics for HP (eradication therapy)    
– in ulcer only Antacids (Maalox, Almagel, Phosphalugel) H2-receptors antagonists (Cimetidine, Famotidine, Ranitidine) Proton pump inhibitors (PPIs) – Omeprazole, Lansoprazole) Prokinetic agents (Metoclopramide, Domperodone)

Treatment

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Ulcer of Stomach and Duodenum
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Ulcers
 
peptic ulcer (язвенная болезнь) symptomatic ulcers

 A peptic ulcer is  a mucosal lesion of the stomach or
duodenum  Anatomical and clinical conception

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Aetiology
         
HP Nervous stress Food taking regimen violating Smoking Gene-factors (1 blood group) Immunological theory Severe inner diseases Old age NSAIDs taking Gastrinoma

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Pathogenesis of peptic ulcer
 Balance disturbance between
aggressive factors and defense mucosal factors.

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Aggressive factors

 Gastric acid  Pepsins

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Protective mucosal factors

 Gastric mucus  Bicarbonate  Prostaglandins

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Duodenal ulcer
 The prevalence of DU is estimated to range
from 6 to 15 % of Western populations  The frequency of DU has been decreasing in the United States and England, especially in males.  Current estimates suggest that approximately 10 % of the population has clinical evidence of DU at some time in their lives.
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Pathogenesis of DU

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Clinical features of DU
 Recurrent abdominal pain - sharp,
burning, or gnawing  Pain occurs 90 min to 3 h after eating and frequently awakens the patient at night (“hungry pain”)  Localisation - epigastrium and right hypochondrium  Irradiation – lower part of interscapular space (X-XII thor.vert.)

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Clinical features of DU
 During spring and autumn (season’s
character of the pain)  Episodic occurrence  Vomiting "coffee grounds" material  Black, tarry stools  Weakness and fatigue (silent bleeding)
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Physical examination
 See gastritis Type B  May be forced position – “posture of
shoemaker”  Epigastric tenderness is the most frequent finding

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DIAGNOSIS
 Barium examination of the upper GI
tract (X-ray)  Endoscopic examination of the upper GI tract  In most patients with typical DUs, specific diagnostic testing for H. pylori may be unnecessary because the organism can be assumed to be present
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Complications
 Penetration (often posteriorly into the
pancreas)  Pylorostenosis = gastric outlet obstruction  Perforation  Bleeding

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Treatment
 Diet 1 (  Eradication of HP (so-called triple therapy)  H2 receptor antagonist  Antacids  Anticholinergic Agents (now rare) (  Coating Agents (sucralfate and Colloidal bismuth
compounds)  Prostaglandins  Proton Pump Inhibitors

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Ulcer of Stomach
 The incidence of GU peaks in the sixth
decade, approximately 10 years later than for DU  Slightly more than half of GUs occur in males  The precise incidence of GU is not known, since many GUs are asymptomatic  Why some persons infected with H. pylori develop DU and others develop GU (in the absence of NSAID use) is not clear.

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 Epigastric pain, but the pattern is less     

Clinical features of GU compare to DU

characteristic The pain may be precipitated or accentuated by food Nausea and vomiting without pylorostenosis Weight loss Complication – see DU + tendency to be malignant (> 3 cm in diameter) Treatment – see DU + surgical in complications
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