GASTRITIS

GASTRITIS MANAGEMENT
DR. P. SATYA SRINIVAS M.S

PROFESSOR
DEPARTMENT OF GENERAL SURGERY
GGH,GUNTUR
surgical anatomy of stomach
1. The superior-most part of the stomach is the distensible fundus, bounded
superiorly by the diaphragm and laterally by the spleen.
2. The body of the stomach contains most of the parietal (oxyntic) cells,
some of which are also present in the cardia and fundus
BLOOD SUPPLY OF STOMACH
1.celiac artery provides majority of blood supply to the stomach
2. four main arteries a.)left gastric rtery
b.) right gastric artery
c.) left gastroepiploic rtery
d.) right gastroepiploic artery.
lymphatic drainage - parallels the vasculature drains into 4
zones of lymph nodes
innervation- the extrinsic innervation of stomach is both
parasympathetic(vagus) and sympathetic(celiac plexuses)
Physiology of stomach
• Gastric function is under neural (sympathetic and parasympathetic) and hormonal control
(peptides or amines that interact with target cells in the stomach).
Gastric barrier function
• Blood flow plays a critical role in gastric mucosal defense

• Decreased gastric mucosal blood flow has minimal effects on ulcer formation until it approaches
50% of normal.
• After damage occurs, injured surface epithelial cells are replaced rapidly by the migration of surface
mucous cells located along the basement membranes.
• This process is referred to as restitution or reconstitution.
GASTRITIS
• Definition- Inflammation associated with gastric mucosal injury
• ACUTE – Short term inflammation with neutrophilic infiltrate
• CHRONIC – Long standing with mononuclear cell infiltrate especially

lymphocyte/macrophages
CLASSIFICATION OF GASTRITIS
• ACUTE GASTRITIS –
A)Acute H .pylori infection
B) other acute infectious agents
1] Bacterial(other than H . pylori) – H.heilmani , streptococci ,staphylococci , E.coli ,TB,
proteus, clostridia.
2] Phlegmonous - severe tansmural infection of gastric wall. { hemophilic streptococci ,
staphylococcus, pneumococcus , enterococcus. }
3] mycobacterial
4] syphilitic
5] viral- EBV , CMV , coxasackie virus
6] parasitic- Anisakiasis
7] fungal – candida albicans, histoplasmosis
• CHRONIC ATROPHIC GASTRITIS –
1)TYPE A : Auto immune, BODY predominant
2) TYPE B : H.PYLORI related, ANTRAL predominant
UNCOMMON FORM OF GASTRITIS –

1)Reflux
2) erosive
3) stress- fundus of stomach
4) lymphocytic
5) eosinophilic
6)granulomatous
7)crohn’s
8) sarcoidosis
HELICOBACTER PYLORI
• Most common human infection involving 50%of the world population.

• It is involved in a wide range of gastroduodenal diseases which leads to CHRONIC GASTRITIS and
PEPTIC ULCER disease.
• WHO TYPE-1 CARCINOGEN
• It is spiral shaped, microaerophilic, gram negative bacterium
• UREASE appears to be vital for its survival and colonization
• The infection is usually acquired during early age (less than 10 years)
• Gastric mucosal barrier is alkaline (1mm thick)
• CHARACTERISTICS: Hydrolyses urea. Production of ammonia. Effect of ammonia on
antral G cells release of gastrin (via negative feedback mechanism). Hyper gastrenemia
gastric acid hypersecretion.
• The potential four mechanisms by which H. Pylori causes ULCER formation:
•1.Production of toxic products that cause local tissue injury.
•2. Induction of local mucosal immune response.
•3.Increased gastrin levels and changes in acid secretion.
•4. Gastric metaplasia occurring in the duodenum.
• STAINS USED FOR H.PYLORI:
• Geimsa stain
• Silver stain
• Genta stain
• SENSITIVITY : 95% ; SPECIFICITY :99%

➢ Cytotoxins associated with H. Pylori:
o CAG-A: Cytotoxin associated gene –A Associated with chronic gastritis, peptic ulcer ,
gastric carcinoma
o VAC-A : Vacuolating cytotoxin –A
➢ H. pylori is associated with MALT LYMPHOMA ,dyspepsia ,hyperplastic gastric polyps , ITP,
➢ Spread of H .Pylori : fecal/feco-oral routes, oro-oral routes

❑ TESTS FOR H.PYLORI:
1. Non invasive tests;
o Urea breath test(c13,c14):carbon labelled urea
solution which is detected in breath.It is sensitive and
reliable.
o Stool antigen test
o Serology
DIAGNOSIS:
2. Invasive tests:
o Urease assay
o Histology
o Culture
PPV- positive predictive value
NPV- negative predictive value
•ENDOSCOPY(OESOPHAGO-
GASTRODUODENOSCOPY):
• safe and accurate op procedure
•Endoscopic features of gastritis:

•Erythema, mucosal erosions ,absence of rugal folds ,
presence of visible vessels
•GASTRIC MUCOSAL BIOPSY:

•The gastric mucosal biopsy should be obtained from
the following sites:
PRIMARY
TREATMENT:
Treament is indicated
Only for H.pylori related
Gastric or duodenal
ulceration and not
for asymptomatic
colonisation .
RESCUE
TREATMENT
•KEY POINTS:
• PPI’S require an acidic environment in the

gastric lumen to be active /effective . Hence co
prescription of antacids is discouraged as
there is production of alkaline environment.
• Eradication treatment is indicated only for

H.Pylori related gastritis or duodenitis and not
for mere asymptomatic colonization.
• The treatment efficacy can be evaluated after

4-6 weeks of eradication therapy by stool
antigen (cost effective )/ invasive biopsy /non
invasive urea breath test (risk of radiation) and
if the disease perisits alternate regimens can
be chosen.
Chronic attophic gastritis
• It is of two types type A and type B

• Type A auto immune gastritis
• Type B H PYLORI RELATED GASTRITIS
• Endoscopic view of atrophic gastritis shows
attophied gastric mucosa with inflammation
Autoimmune gastritis
• This is an autoimmune condition in which there are circulating antibodies to the parietal cell.
• malabsorption of vitamin B12, which, if untreated, may result in pernicious anaemia.
• The antrum is not affected and the hypochlorhydria leads to the production of high levels of
gastrin from the antral G cells. This results in chronic hypergastrinaemia.
• Patients with autoimmune gastritis are predisposed to the development of gastric cancer, and
screening such patients endoscopically may be appropriate.
Erosive gastritis
• Patients with autoimmune gastritis are predisposed to the development of gastric cancer, and
screening such patients endoscopically may be appropriate.
• The NSAID-induced gastric lesion is associated with inhibition of the cyclo-oxygenase type 1
(COX-1) receptor enzyme, hence reducing the production of cytoprotective prostaglandins in the
stomach.
Stress gastritis
• Stress gastritis is characterized by multiple superf icial (nonulcerating) erosions that typically
begin in the proximal portion of the stomach and progress distally.
• Stress gastritis can occur after physical trauma, shock, sepsis, , or respiratory failure and may
lead to life-threatening gastric bleeding.
• multifactorial cause related to an imbalance between acid production and mucosal protection.
• The only clinical sign may be painless upper GI bleeding. The bleeding is usually slow and
intermittent
Hypertrophic gastritis (Ménétrier Disease)
• a rare disease characterized by massive gastric folds in the fundus and body of the
stomach, giving the mucosa a cobblestone or cerebriform appearance.
• Antrum is spare
• Histolic features - foveolar hyperplasia , decreased or absent parietal cells
• Medical management with acid supressing agents if not relieved total gastrectomy is
indicated (massive protein loss)
• Follow up with 1-2yr endocopy
THANK YOU

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GASTRITIS MANAGEMENT

DR. P. SATYA SRINIVAS M.S

• Blood flow plays a critical role in gastric mucosal defense

• Definition- Inflammation associated with gastric mucosal injury

• ACUTE – Short term inflammation with neutrophilic infiltrate

• CHRONIC – Long standing with mononuclear cell infiltrate especially

UNCOMMON FORM OF GASTRITIS –

• Most common human infection involving 50%of the world population.

•1.Production of toxic products that cause local tissue injury.

•2. Induction of local mucosal immune response.

•3.Increased gastrin levels and changes in acid secretion.

•4. Gastric metaplasia occurring in the duodenum.

• STAINS USED FOR H.PYLORI:

• SENSITIVITY : 95% ; SPECIFICITY :99%

➢ Spread of H .Pylori : fecal/feco-oral routes, oro-oral routes

•Endoscopic features of gastritis:

•GASTRIC MUCOSAL BIOPSY:

• PPI’S require an acidic environment in the

• Eradication treatment is indicated only for

• The treatment efficacy can be evaluated after

• It is of two types type A and type B

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