1. 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
2. A. ACUTE HEMORAGIC GASTRITIS
(EROSIVE)
Examination shows:
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 EXAMINATION of the G.M. reveals infiltration of
the lamina propria with:
– mononuclear cells
– PMN leukocytes
– extravasations of blood in the mucosa
3. 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. 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.
6. 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
7. 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.
8. 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
9. 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
10. 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
11. 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
12. 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
13. 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
14. 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.
