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
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
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.
CLINICAL FEATURES
•Hematemesis / melena
•Anemia
•Epigastric pain
•Nausea
•Vomiting
BIOLOGICAL ASPECTS
- leucocytosis / leukopenia
PHYSICAL EXAMINATION
Pallor
Tachycardia
Hypotension
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.
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 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.
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
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
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
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
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 pain
nausea, vomiting
TREATMENT: glucocorticoids
GRANULOMATOUS GASTRITIS
Chron’s disease produce: ulceration
granulomatous infiltration
stricture formation
Other’s:
Diagnostic:
histoplasmosis
candidosis
syphilis
tuberculoses
biopsies + cytology to exclude malignancy
surgical 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, 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
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 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
4. Coating agents
Sucralfate 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 stress
eat 5 times / day in small meals
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
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.
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.
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.
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.