Gastritis. El Salvador Atlas of Gastrointestinal VideoEndoscopy. A Large Database of Images and Video Clips with Cases Reported.
El Salvador Atlas of Gastrointestinal VideoEndoscopy
Acute gastritis is not a single disease but, rather, a group of disorders that induce inflammatory changes in the gastric mucosa. All of the causative mechanisms differ in their clinical presentation and have unique histologic characteristics. The inflammation may involve the entire stomach (pangastritis) or a region of the stomach (eg, antral gastritis). Acute gastritis can be broken down into the following additional categories: erosive (eg, hemorrhagic erosions, superficial erosions, deep erosions) and nonerosive (generally caused by Helicobacter pylori). ,

Video Endoscopic Sequence 1 of 6.

 Acute Gastritis.

 Acute gastritis is not a single disease but, rather, a group
 of disorders that induce inflammatory changes in the
 gastric mucosa. All of the causative mechanisms differ in
 their clinical presentation and have unique histologic
 characteristics. The inflammation may involve the entire
 stomach (pangastritis) or a region of the stomach
 (eg, antral gastritis). Acute gastritis can be broken down
 into the following additional categories: erosive (eg
 , hemorrhagic erosions, superficial erosions, deep erosions)
 and nonerosive (generally caused by Helicobacter pylori).

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 All endoscopic images shown in this Atlas contain
 video clips. We recommend seeing the video clips in full
 screen mode.
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

Video Endoscopic Sequence 2 of 6.

Acute Gastritis.

 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".
Acute Gastritis. 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. Most classification systems distinguish acute, short-term from chronic, long-term disease. The terms acute and chronic are also used to describe the type of inflammatory cell infiltrate. Acute inflammation is usually associated with neutrophilic infiltration, while chronic inflammation is usually characterized by mononuclear cells, chiefly lymphocytes, plasma cells and macrophages. A practical clinicopathologic framework for the classification of gastritis and gastropathy based upon these factors can be proposed.

Video Endoscopic Sequence 3 of 6.

Acute Gastritis.

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.
  • Most classification systems distinguish acute, short-term from
     chronic, long-term disease. The terms acute and chronic are also
     used to describe the type of inflammatory cell infiltrate. Acute
     inflammation is usually associated with neutrophilic infiltration,
     while chronic inflammation is usually characterized by
     mononuclear cells, chiefly lymphocytes, plasma cells and
     macrophages. A practical clinicopathologic framework for the
     classification of gastritis and gastropathy based upon these factors
     can be proposed.

 
Acute gastritis may produce no symptoms but can be associated with short-lived dyspepsia, lack of appetite, nausea or vomiting. It can occasionally be severe enough to cause gastrointestinal bleeding with melena or hematemesis (see above). The most common cause is ingestion of aspirin or other non-steroidal anti-imflammatory drugs (NSAIDs). It can also occur during the early stages of infection with the bacteria, Helicobacter pylori "HP." Most cases resolve by themselves, but endoscopy and biopsy may be required to exclude other conditions such as peptic ulcer disease or cancer. At endoscopy the inner lining of the stomach (mucosa) may appear swollen, reddened and inflamed. There may be small, shallow erosions (breaks in the surface lining) or even tiny areas of bleeding from the mucosa.

Video Endoscopic Sequence 4 of 6.

 Acute gastritis may produce no symptoms but can be
 associated with short-lived dyspepsia, lack of appetite,
 nausea or vomiting. It can occasionally be severe enough
 to cause gastrointestinal bleeding with melena or
 hematemesis (see above). The most common cause is
 ingestion of aspirin or other non-steroidal
 anti-imflammatory drugs (NSAIDs). It can also occur
 during the early stages of infection with the bacteria,
 Helicobacter pylori "HP." Most cases resolve by
 themselves, but endoscopy and biopsy may be required to
 exclude other conditions such as peptic ulcer disease or
 cancer. At endoscopy the inner lining of the stomach
 (mucosa) may appear swollen, reddened and inflamed.
 There may be small, shallow erosions (breaks in the
 surface lining) or even tiny areas of bleeding from the
 mucosa.

 
Acute gastritis has a number of causes, including certain drugs; alcohol; bacterial, viral, and fungal infections; acute stress (shock); radiation; and direct trauma. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen, and naproxen, can be direct irritants and a cause of gastritis. Because of gravity, the irritants lie on the greater curvature of the stomach, and therefore, gastritis and ulcers are seen distally on or near the greater curvature of the stomach. Gastritis can occur even when NSAIDs are taken systemically or when the drugs are ingested persistently or in large quantities. Alcoholic beverages, such as whisky, vodka, and gin, are direct irritants to the stomach and can cause alcoholic gastritis.

Video Endoscopic Sequence 5 of 6.

Acute Gastritis.

 Acute gastritis has a number of causes, including certain
 drugs; alcohol; bacterial, viral, and fungal infections;
 acute stress (shock); radiation; and direct trauma.

 Nonsteroidal anti-inflammatory drugs (NSAIDs), such as
 aspirin, ibuprofen, and naproxen, can be direct irritants and
 a cause of gastritis. Because of gravity, the irritants lie on
 the greater curvature of the stomach, and therefore,
 gastritis and ulcers are seen distally on or near the greater
 curvature of the stomach. Gastritis can occur even when
 NSAIDs are taken systemically or when the drugs are
 ingested persistently or in large quantities. Alcoholic
 beverages, such as whisky, vodka, and gin, are direct
 irritants to the stomach and can cause alcoholic gastritis.

 
Bacterial infections also can cause gastritis. The most common type of infection is caused by H pylori. H pylori gastritis typically starts in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa. It is also responsible for as many as 80% of gastric ulcers and is associated with a transient increase in gastric acid secretion. The acid secretion drops as the corpus of the stomach is involved. Urease produced by H pylori catalyzes the hydrolysis of urea to ammonia and carbon dioxide. Hydroxide ions generated by the equilibration of water with ammonia are hypothesized to contribute to gastric mucosal epithelial damage. H pylori is thought to be spread from person to person via oral-oral and/or fecal-oral routes.

Video Endoscopic Sequence 6 of 6.

 Bacterial infections also can cause gastritis. The most
 common type of infection is caused by H pylori. H pylori
 gastritis typically starts in the antrum, causing intense
 inflammation, and over time, it may extend to involve the
 entire gastric mucosa. It is also responsible for as many as
 80% of gastric ulcers and is associated with a transient
 increase in gastric acid secretion. The acid secretion drops
 as the corpus of the stomach is involved. Urease produced
 by H pylori catalyzes the hydrolysis of urea to ammonia
 and carbon dioxide. Hydroxide ions generated by the
 equilibration of water with ammonia are hypothesized to
 contribute to gastric mucosal epithelial damage. H pylori is
 thought to be spread from person to person via oral-oral
 and/or fecal-oral routes.

 
Chronic Gastritis. This 60 year-old male, pathologist, is under screening for abdominal pain and jaundice. an upper endoscopy was performed. Chronic gastritis with a depressed lesion was found that had to rule out malignancy. The Cat Scan displayed a Carcinoma of the head of the pancreas.

Video Endoscopic Sequence 1 of 8.

Chronic Gastritis.

 This 60 year-old male, pathologist, is under screening for
 abdominal pain and jaundice. An upper endoscopy was
 performed displaying this image and video clip.
 Chronic gastritis with a depressed lesion was found that
 had to rule out malignancy.
 The Cat Scan displayed a Carcinoma of the head of the
 pancreas.
Chronic Gastritis. A depressed lesion is seen, multiple biopsies were taken to rule out a gastric adenocarcinoma.

Video Endoscopic Sequence 2 of 8

Chronic Gastritis.

 A depressed lesion is seen, multiple biopsies were taken
 to rule out a gastric adenocarcinoma.
Chromoendoscopy using methylene blue.

Video Endoscopic Sequence 3 of 8.

 Chromoendoscopy using methylene blue.
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.

Video Endoscopic Sequence 4 of 8.

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.

Video Endoscopic Sequence 5 of 8.

 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.

H pylori-associated chronic gastritis progresses with the following 2 main topographic patterns that have different clinical consequences: · Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis. · Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.Most of the people who are infected with H pylori do not develop significant clinical complications, and they remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk factors may develop peptic ulcer, gastric mucosa-associated lymphoid tissue (MALT) lymphomas, or gastric adenocarcinomas.

Video Endoscopic Sequence 6 of 8.

 H pylori–associated chronic gastritis progresses with the
 following 2 main topographic patterns that have different clinical
 consequences:

  • Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.
  • Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.
  • Most of the people who are infected with H pylori do not
     develop significant clinical complications, and they remain carriers
     with asymptomatic chronic gastritis. Some individuals who carry
     additional risk factors may develop peptic ulcer, gastric
     mucosa–associated lymphoid tissue (MALT) lymphomas, or
     gastric adenocarcinomas.
Some biopsies were taken to rule out adenocarcinoma.

Video Endoscopic Sequence 7 of 8.

Some biopsies were taken to rule out adenocarcinoma.
An enlarged bulging papilla was found, an ERCP was performed. The Cat Scan displayed a Carcinoma of the head of the pancreas.

Video Endoscopic Sequence 8 of 8.

 An enlarged bulging papilla was found, an ERCP was
 performed.
 The Cat Scan displayed a Carcinoma of the head of the
 pancreas.

 
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.

Video Endoscopic Sequence 1 of 10.

 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.  
Pangastritis. H. pylori infection was associated with a decrease in gastric juice ascorbic acid concentration, and this effect was more pronounced in patients with the CagA-positive strain. Pangastritis was more common in patients whose H. pylori. infection was accompanied by anemia.

Video Endoscopic Sequence 2 of 10.

Pangastritis.

 H. pylori infection has been associated with a decrease in
 gastric juice ascorbic  acid concentration, and this effect
 was more pronounced in patients with the  CagA-positive
 strain. Pangastritis was more common in patients whose H.
 pylori. infection was accompanied by anemia.

.
Acute Gastritis.

Video Endoscopic Sequence 3 of 10.

 Acute Gastritis.

 
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,

Video Endoscopic Sequence 4 of 10.

 Acute Gastritis.

 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 may produce no symptoms but can be associated with short-lived dyspepsia, lack of appetite, nausea or vomiting. It can occasionally be severe enough to cause gastrointestinal bleeding with melena or hematemesis.

Video Endoscopic Sequence 5 of 10.

 Acute gastritis may produce no symptoms but can be
 associated with short-lived dyspepsia, lack of appetite,
 nausea or vomiting. It can occasionally be severe enough
 to cause gastrointestinal bleeding with melena or
 hematemesis.

 
Acute Gastritis. In pangastritis (coexisting antral gland gastritis and fundic gland gastritis), the fundic gland gastritis is characterized by less severe inflammation than the antral gland gastritis. Pangastritis can result in extensive mucous gland (pseudopyloric) metaplasia and varying amounts of intestinal metaplasia. Nests of parietal cells commonly occur, even in the presence of achlorhydria.

Video Endoscopic Sequence 6 of 10.

Acute Gastritis.

 In pangastritis (coexisting antral gland gastritis and fundic
 gland gastritis), the fundic gland gastritis is characterized
 by less severe inflammation than the antral gland gastritis.
 Pangastritis can result in extensive mucous gland
 (pseudopyloric) metaplasia and varying amounts of
 intestinal metaplasia. Nests of parietal cells commonly
 occur, even in the presence of achlorhydria.
Acute Gastritis.

Video Endoscopic Sequence 7 of 10.

Acute Gastritis.

 
Acute Gastritis.

Video Endoscopic Sequence 8 of 10.

Acute Gastritis.

 
Acute Gastritis.

Video Endoscopic Sequence 9 of 10.

Acute Gastritis.

 
Acute Gastritis.

Video Endoscopic Sequence 10 of 10.

Acute Gastritis.
Redness of the mucosa. Acute inflammation and chronic inflammation usually are distinguishable by general histophatology. In the gastric mucosa, hyperemia and exudation (the endoscopic sign of acute inflammation) The classification of gastritis is based on the intensity of the inflammatory process and its effects on the glandular structures.

Severe Acute Gastritis.

Redness of the Mucosa.

 Acute inflammation and chronic inflammation usually are
 distinguishable by general histophatology. In the gastric
 mucosa, hyperemia and exudation (the endoscopic sign of
 acute inflammation) The classification of gastritis is based
 on the intensity of the inflammatory process and its effects
 on the glandular structures.

 
Acute Gastritis of the gastric fundus. Reddened gastric folds. Fundic (oxyntic) gland gastritis (type A) can be associated with diffuse severe mucosal atrophy and pernicious anemia. Diffuse severe atrophic fundic gland gastritis primarily affects elderly patients, who develop achlorhydria, but with a residual ability to absorb vitamin B12. Patients with pernicious anemia generally have antibodies against parietal cells (90%) and intrinsic factor (60%). Antiparietal cell antibodies also occur in 50% of patients with gastric atrophy without pernicious anemia (but without anti-intrinsic factor antibodies) and in 10 to 15% of normal persons.

Acute Gastritis of the Gastric Fundus.

Reddened Gastric folds.

 Fundic (oxyntic) gland gastritis (type A) can be associated
 with diffuse severe mucosal atrophy and pernicious anemia.
 Diffuse severe atrophic fundic gland gastritis primarily
 affects elderly patients, who develop achlorhydria, but with
 a residual ability to absorb vitamin B12. Patients with
 pernicious anemia generally have antibodies against
 parietal cells (90%) and intrinsic factor (60%). Antiparietal
 cell antibodies also occur in 50% of patients with gastric
 atrophy without pernicious anemia
 (but without anti-intrinsic factor antibodies) and in 10 to 15
 % of normal persons.
The video clip displays acute gastritis taken from endoscopy. Acute Gastritis: The inflammation may involve the entire stomach (pangastritis) or a region of the stomach (eg, fondus gastritis). Acute gastritis can be broken down into the following additional categories: erosive (eg, hemorrhagic erosions, superficial erosions, deep erosions) and nonerosive (generally caused by Helicobacter pylori).

Acute Gastritis of the gastric fundus.

 The image and the video displays a video endoscopy with
 typical acute gastritis.
 
 Acute Gastritis: The inflammation may involve the entire
 stomach (pangastritis) or a region of the stomach
 (eg, fondus gastritis). Acute gastritis can be broken down
 into the following additional categories: erosive
 (eg, hemorrhagic erosions, superficial erosions, deep
 erosions) and nonerosive (generally caused by Helicobacter
 pylori).
Gastric Erosion seen with magnification and high-resolution and chromoendoscopy. H.Pylori infection was found in the biopsies.

Video Endoscopic Sequence 1 of 2.

Gastric Erosion.

 Seen with magnification and high-resolution
 chromoendoscopy.
 H.Pylori infection was found in the biopsies.
Furrow of erosioned mucosal changes. Gastric carcinoma of the intestinal type originates in dysplastic epithelium, which in turn develops in the milieu of atrophic gastritis and intestinal metaplasia. Cancers also may develop less often from gastric adenomatous polyps, which represent dysplastic epithelium arising in a raised lesion. The main causes of chronic atrophic gastritis and gastric atrophy are autoimmune due to pernicious anemia or chronic Helicobacter pylori infection. In the former condition, there is severe atrophy of the corpus (oxyntic mucosa), with the antrum being speared. In contrast, chronic atrophic gastritis consequent to H. pylori infection is a multifocal pangastritis, involving independent foci in the corpus and antrum of the stomach.

Video Endoscopic Sequence 2 of 2.

Cronic Gastritis

Furrow of erosioned mucosal changes.

 Gastric carcinoma of the intestinal type originates in
 dysplastic epithelium, which in turn develops in the milieu
 of atrophic gastritis and intestinal metaplasia. Cancers also
 may develop less often from gastric adenomatous polyps,
 which represent dysplastic epithelium arising in a raised
 lesion. The main causes of chronic atrophic gastritis and
 gastric atrophy are autoimmune due to pernicious anemia
 or chronic Helicobacter pylori infection. In the former
 condition, there is severe atrophy of the corpus (oxyntic
 mucosa), with the antrum being speared. In contrast,
 chronic atrophic gastritis consequent to H. pylori infection
 is a multifocal pangastritis, involving independent foci in
 the corpus and antrum of the stomach.

                 
Follicular Lymphoid Hyperplasia. The lesions are raised, flat or nodular folds, and are often associated with gastric ulceration. The etiology of this condition remains unclear, but Helicobacter pylori infection has been implicated. Microerosions are frequently seen with magnifying endoscopes.

Video Endoscopic Sequence 1 of 4.

Follicular Lymphoid Hyperplasia.

 (Goose pimple stomach).

 The lesions are raised, flat or nodular folds, and are often
 associated with gastric ulceration. The etiology of this
 condition remains unclear, but Helicobacter pylori infection
 has been implicated. Microerosions are frequently seen
 with magnifying endoscopes.
Follicular Lymphoid Hyperplasia. In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori-infection induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis.

Video Endoscopic Sequence 2 of 4.

Follicular Lymphoid Hyperplasia.

 In follicular gastritis, gastric acidity is significantly reduced,
 but can be normalized by eradication of H. pylori. It can
 thus be speculated that inflammatory cytokines or H. pylori
-infection induced prostaglandins might strongly inhibit
 gastric acid secretion in follicular gastritis.
Follicular Lymphoid Hyperplasia. Seen with magnification and high-resolution chromoendoscopy using indigo carmin.

Video Endoscopic Sequence 3 of 4.

Follicular Lymphoid Hyperplasia.

 Seen with magnification and high-resolution
 chromoendoscopy using indigo carmin.
Follicular Lymphoid Hyperplasia.

Video Endoscopic Sequence 4 of 4.

Follicular Lymphoid Hyperplasia.
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.

 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.
 
Lineal erosion at the antrum. In this endoscopic sequence is compared between endoscopic examination using an endoscope with zoom and the next sequence using a magnifying endoscope.

Video Endoscopic Sequence 1 of 2.

 Lineal erosion at the antrum. In this endoscopic sequence
 is compared between endoscopic examination using
 an endoscope with zoom and the next sequence using a
 magnifying endoscope.

Lineal erosion using a magnifying endoscope.

Video Endoscopic Sequence 2 of 2.

 Lineal erosion using a magnifying endoscope.
Lineal erosive gastritis of the antrum.

Lineal erosive gastritis of the antrum.


 

Hemorrhagic Gastritis. Sub epithelial hemorrhages of the stomach are nonspecific entities that may arise in response to a variety of topical insults such as alcohol, corrosives, and drugs (specially non steroidal anti-inflammatory agents) and in response to a severe physiologic stress.

 Hemorrhagic Gastritis.

 Sub epithelial hemorrhages of the stomach are nonspecific
 entities that may arise in response to a variety of topical
 insults such as alcohol, corrosives, and drugs (specially
 non steroidal anti-inflammatory agents) and in response
 to a severe physiologic stress. 
 

Hemorrhagic Gastritis. A 77 year-old, physician with hemorrhagic gastritis of the fundus. He had been under aspirin treatment.

Hemorrhagic Gastritis.


 A 77 year-old, physician with hemorrhagic gastritis of the
 fundus.
 He had been under aspirin treatment.

Image of chronic gastritis as observed the discoloration of the mucosa.Chronic gastritis, by definition, is a histopathological entity characterized by chronic inflammation of the stomach mucosa. Gastritis can be classified based on the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathological pattern, which may suggest the etiologic agent and clinical course (eg, H pylori–associated multifocal atrophic gastritis). Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although minimal inflammation is observed in some gastropathies, such as those associated with NSAID intake, these entities are discussed in this article because they are frequently included in the differential diagnosis of chronic gastritis.

Chronic Gastritis.

 Image of chronic gastritis as observed the discoloration of
 the mucosa.
 

Chronic gastritis, by definition, is a histopathological
 entity characterized by chronic inflammation of the
 stomach mucosa. Gastritis can be classified based on
 the underlying etiologic agent (eg, Helicobacter pylori,
 bile reflux, nonsteroidal anti-inflammatory drugs
 [NSAIDs], autoimmunity, allergic response) and the
 histopathological pattern, which may suggest the etiologic
 agent and clinical course (eg, H pylori–associated
 multifocal atrophic gastritis). Other classifications are
 based on the endoscopic appearance of the gastric
 mucosa (eg, varioliform gastritis). Although minimal
 inflammation is observed in some gastropathies, such as
 those associated with NSAID intake, these entities are
 discussed in this article because they are frequently
 included in the differential diagnosis of chronic gastritis.

 

 
Follicular Lymphoid Hyperplasia. Diffuse hyperplasia of lymphoid follicles at the antrum. (Goose pimple stomach). Proliferation of submucosal lymphoid follicles in the gastrointestinal tract. Lymph follicles are a normal component of gut associated lymphatic tissue.

Follicular Lymphoid Hyperplasia.

 Diffuse hyperplasia of lymphoid follicles at the antrum.
 (Goose pimple stomach).

 Proliferation of submucosal lymphoid follicles in the
 gastrointestinal tract. Lymph follicles are a normal
 component of gut associated lymphatic tissue.

 
A diffuse Intestinal Metaplasia. An 85 year-old female two years ago, she underwent open cholecystectomy. The patient complained of epigastric discomfort, an upper video gastroscopy was performed. A deformed antrum was appreciated, biliar reflux is observed, biopsies where taken to rule out carcinoma. Intestinal metaplasia is the most dramatic epithelial transformation, the acquisition of the epithelium that is normally observed only in the intestine. Intestinal metaplasia has not only morphologic and biochemical properties of the small intestinal epithelium but also functional ones. The metaplastic stomach changes from a secretory organ to an “intestinal” organ capable of the absorption of certain substances such as lipid, from the gastric lumen.

A diffuse Intestinal Metaplasia.

 An 85 year-old female two years ago, she underwent open
 cholecystectomy. The patient complained of epigastric
 discomfort, an upper video gastroscopy was performed.
 A deformed antrum was appreciated, biliar reflux is
 observed, biopsies where taken to rule out carcinoma.
 Intestinal metaplasia is the most dramatic epithelial
 transformation, the acquisition of the epithelium that is
 normally observed only in the intestine.
 Intestinal metaplasia has not only morphologic and
 biochemical properties of the small intestinal epithelium
 but also functional ones. The metaplastic stomach changes
 from a secretory organ to an “intestinal” organ capable of
 the absorption of certain substances such as lipid, from the
 gastric lumen. 
The video clip displays more intensive areas of Intestinal 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.