The term GASTRITIS encompasses a series of conditions
that present with inflammation of the gastric mucosa or inner lining of
the stomach. Several forms of this disease are described:
ACUTE GASTRITIS: This cause of upper abdominal pain
is a frequent affliction in our population. Clinically pain is felt in
the epigastric region, frequently associated with nausea, and vomiting
or a feeling of burning in your stomach, It has nothing to do with gas.
Frequently symptoms associated with gastro-esophageal reflux , such as
"heartburn" are observed. These epigastric symptoms are relieved
by ingestion of
foods, specially milk.
Emotional stress may play some role.
Question:Is my gastritis curable?
Answer: Yes, your Doctor with a professional diagnosis having to rule
out other diseases with the the most accurate test called gastroscopy
or video-endoscopy and using a modern therapy gastritis is complete curable.
A definite and precise diagnosis of this condition can be made through
endoscopy of the upper G.I. Tract.The doctor eases a gastroscope, a thin
tube containing a tiny camera, through your mouth and down into your stomach
to look at the stomach lining. The doctor will check for inflammation
and may remove a tiny sample of tissue for tests. This procedure to remove
a tissue sample is called a biopsy which is needed to rule out in some
cases a malignancy.
Endoscopically one can observe diverse patterns of reddening of the gastric
mucosa, which can adopt different shapes ( flame-shaped discoloration
or a pattern specific to subepithelial hemorrhage) and can affect only
a small area or the whole stomach. Histopathologically, one observes infiltration
of polymorphonuclear cells in the tissue under the microscope. Diverse
causes of gastritis are known amongst which one must mention idiopathic
causes, alcohol abuse, use of some oral analgesics such as aspirin, piroxicam
or indomethacine as well as cigarette smoking and a certain bacteria named
Injury to the gastric mucosa is associated with epithelial cell damage
and regeneration. The term gastritis is used to denote
inflammation associated with mucosal injury. However, epithelial cell
injury and regeneration are not always accompanied by mucosal inflammation.
This distinction has caused considerable confusion since gastritis is
often used to describe endoscopic or radiologic characteristics of the
gastric mucosa rather than specific histologic findings. Epithelial cell
damage and regeneration without associated inflammation is properly referred
to as "gastropathy."
The causes, natural history, and therapeutic implications of gastropathy
differ from gastritis:
Gastropathy is usually caused by irritants such as
drugs (eg, nonsteroidal antiinflammatory agents and alcohol), bile reflux,
hypovolemia, and chronic congestion.
Gastritis is usually due to infectious agents (such
as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
DIAGNOSIS A mucosal biopsy is required to distinguish
between acute or chronic gastritis and gastropathy since the endoscopic
features may be similar
Helicobacter pylori testing Noninvasive testing for Helicobacter
pylori has high sensitivity and specificity for infection and gastritis
Biopsy Accurate histologic assessment of gastritis and
gastropathy depends upon optimizing the site and number of biopsy specimens.
Gross abnormalities should be biopsied and sent for histologic examination
(in separate containers) along with biopsies of normal-appearing mucosa
adjacent to the lesion. Biopsy of the incisura is also useful since it
approximates the transition zone between the antrum and body, where intestinal
metaplasia and atrophy are most frequently found in environmental metaplastic
Pathophysiology: The mechanisms of mucosal injury in
gastritis and PUD are thought to be an imbalance of aggressive factors,
such as acid production or pepsin, and defensive factors, such as mucus
production, bicarbonate, and blood flow.
Erosive gastritis usually is associated with serious illness or with
various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory
drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable
to normal gastric secretions.
Infection with Helicobacter pylori, a short, spiral-shaped, microaerophilic
gram-negative bacillus, is the leading cause of PUD and is associated
with virtually all ulcers not induced by NSAIDs. H pylori colonize the
deep layers of the mucosal gel that coats the gastric mucosa and presumably
disrupts its protective properties. H pylori is thought to infect virtually
all patients with chronic active gastritis.
NSAIDs and aspirin also interfere with the protective mucus layer by
inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal
prostaglandins. Many people with known H pylori colonization or who are
taking NSAIDs do not suffer from gastritis or PUD, which indicates other
important causative factors must be involved.
|Fig. 1: This Videoendoscopic image shows a severely inflamed
gastric mucosa typical of acute gastritis.
|Fig 2: After treatment normal gastric folds are observed.
Acute Gastritis (Pangastritis).
The mechanisms of mucosal injury in gastritis and The
mechanisms of mucosal injury in gastritis and Peptic ulcer
disease are thought to be an imbalance of aggressive
factors, such as acid production or pepsin, and defensive
factors, such as mucus production, bicarbonate, and blood
Download the video clip by clicking on the endoscopic image.
Acute Gastritis (Pangastritis).
The most common causes of acute gastritis are infectious.
Acute infection with H. pylori induces gastritis. However,
H. pylori acute gastritis has not been extensively studied.
Reported as presenting with sudden onset of epigastric
pain, nausea, and vomiting, limited mucosal histologic
studies demonstrate a marked infiltrate of neutrophils with
edema and hyperemia. If not treated, this picture will
evolve into one of chronic gastritis. Hypochlorhydria
lasting for up to 1 year may follow acute H. pylori infection.
The less common of the two forms involves primarily the
fundus and body.
Chronic Gastritis: This is an entity which presents with no or
unspecific clinical symptoms, reason why it is primarily diagnosed endoscopically
and histo-pathologically. Endoscopic findings include a pale discoloration
of the mucosa or segments of it. Histo-pathologically one finds a reduced
number of gastric glands in the stomach, which present an abnormal morphology
Synonyms and related keywords: type B nonatrophic gastritis, superficial
nonatrophic gastritis, diffuse antral nonatrophic gastritis, chronic antral
nonatrophic gastritis, interstitial-follicular nonatrophic gastritis,
hypersecretory nonatrophic gastritis, type A atrophic gastritis, diffuse
corporal atrophic gastritis, pernicious anemia–associated gastritis,
metaplastic atrophic gastritis, atrophic pangastritis, progressive intestinalizing
pangastritis, environmental atrophic gastritis, type C reactive gastritis,
reflux, bile, chronic nonsteroidal anti-inflammatory drug gastropathy,
Helicobacter pylori infection, H pylori–associated multifocal atrophic
gastritis, varioliform gastritis, chemical gastritis, reactive gastritis,
Helicobacter gastritis, H pylori–associated chronic gastritis, infectious
granulomatous gastritis, gastritis in patients who are immunosuppressed,
autoimmune gastritis, chronic reactive chemical gastropathy,chronic noninfectious
granulomatous gastritis, lymphocytic gastritis, eosinophilic gastritis,
radiation gastritis, ischemic gastritis
|This Videoendoscopic image of the stomach shows a pale Decoloration
of the mucosa typical of chronic gastritis.
This is an ailment which presents with no or unspecific clinical symptoms,
resason why it is primarily diagnosed endoscopically and histo-pathologically.
Endoscopic findings include a pale discoloration of the mucosa or segments
of it. Histopathologically one finds a reduced number of gastric glands
in the stomach, which present an abnormal morphology and distribution.
H pylori–associated chronic gastritis
H pylori are gram-negative rods that have the ability
to colonize and infect the stomach. The bacteria survive within the mucous
layer that covers the gastric surface epithelium and the upper portions
of the gastric foveolae. The infection usually is acquired during childhood.
Once the organism has been acquired, has passed through the mucous layer,
and has become established at the luminal surface of the stomach, an intense
inflammatory response of the underlying tissue develops.
The presence of H pylori always is associated with tissue damage and
the histological finding of both an active and chronic gastritis. The
host response to H pylori and bacterial products is composed of T- and
B-cell lymphocytes, denoting chronic gastritis, followed by infiltration
of the lamina propria and gastric epithelium by polymorphonuclear leukocytes
that eventually phagocytize the bacteria. The presence of polymorphonuclear
leukocytes in the gastric mucosa is diagnostic of active gastritis.
ATROPHIC GASTRITIS Similar to chronic gastritis, clinical
symptoms are often non-existent or non-specific in this condition, which
is considered by many to be the end-stage of chronic gastritis. Diagnosis
is commonly made by endoscopy and biopsy. Endoscopically this disease
manifests itself with the disappearance of gastric folds, the visualization
of submucosal blood vessels and the total or partial loss of the mucosal
lining. Under the microscope no or only a few gastric glands are observed.
Signs of intestinal metaplasia can be found. There is some discussion
to whether atrophic gastritis should be considered a pre-cancerous lesion.
In my experience I have found a considerable number of gastric cancers
to be embedded in an area of atrophic gastritis which underscores this
theory. It is believed that for a gastric carcinoma to develop as many
as 20 years must transcurr before it becomes evident. Therefore
Atrophic Gastritis. Is seen the submucosal
CHRONIC GASTRITIS ( Erosive)Variliform.
|Erosive gastritis Multiple linear erosions are
observed at the antrum
Erosive gastritis should really be included in the chapters dealing
with Ulcers since the lesions caused by this entity are of similar
nature, differing only in that they are less profound and more superficial
in erosive gastritis, not reaching the muscularis layer and erosions
are multiple and the ulcers
generaly are one
|56 year old female who underwent cholecystectomy several years earlier.
Signs of intestinal metaplasia are seen endoscopically.
Intestinal Metaplasia of the Pre-Piloric
Metaplasia of the antrum as well as biliar reflux.
Metaplasia is a potentially reversible change from a fully
differentiated cell type to another cell type implying
adaptation to environmental stimuli. In the stomach
intestinal type metaplasia is most common. This occurs as
a result of Helicobacter pylori infection or bile reflux.
Intestinal Metaplasia The term metaplasia implies the substitution of
a normal tissue for a another tissue.In the case of intestinal metaplasia,
gastric tissue of the stomach is commonly substituted by intestinal epithelium.
(goblet cell) cells may be found and on occasions gastric glands are substituted
by intestinal crypts and villi. These changes are often a consequence
of inflammation or of prolonged exposure to biliary reflux, as seen in
post-cholecystectomy patients.. Although this diagnosis is confirmed only
by histo-pathologic methods, one can often positively predict this entity
with high resolution video endoscopy.
Hiperplasia of the Mucosa (Foveolar hiperplasia): An entity in which microscopic
findings include enlargement of the base of the (foveolas) as well as
deepening of the foveolas. The (bridges ) are enlogated and adopt a papillary
appearance. In Menetrieres Disease, an ailment which presents with giant
mucosal folds, a diffuse (foveolar hiperplasia) is observed.
Multiple acute erosions and some ulcers
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
aspirin, ibuprofen, and piroxican, can be direct irritants
and can cause of gastritis.