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Julio Alejandro Murra-Saca MD.
Gastroenterologist, Coloproctologist
Tel : (503) 226-3131, (503) 225-3087, Celular (503) 887-2507
Email
  
Edificio Centro Scan, Colonia Médica, San Salvador, El Salvador.

 

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Notes on Cyber Gastroenterology

 

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 Helicobacter Pylori.
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 atrophic gastritis.
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.
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 flow.                                                   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,

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
flow.

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 and distribution.
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.

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 vassels


Variliform Gastritis.

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 Antrum.

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 are observed.
Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
aspirin, ibuprofen, and piroxican, can be direct irritants
and can cause of gastritis.

 

 

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