4. Inflammatory and ulcerative disorders of the stomach

Last updated on April 24, 2019 at 14:51

Many things can go wrong with the GI-tract, and the stomach is not excluded. Let’s look at the pathologies found here.

First, let’s clarify some terms:

  • An erosion never goes deeper than the muscularis mucosae, i.e. only the mucosa is affected
  • An ulceration goes deeper than the muscularis mucosae, i.e. also the submucosa is affected. It can even perforate the wall.
  • Hypochlorhydria is the condition where the level of stomach acid is lower than normal
  • Achlorhydria is the condition where there is no stomach acid
Congenital malformations

Fortunately, congenital pathologies of the stomach are rare.

  • Atresia – complete occlusion of pyloric outlet
  • Microgastria – Babies born with abnormal small stomach and limbs
  • Duplication – Abnormal growth of a solid tumor or cyst in the GI. Can also appear as bleedings or perforations.
  • Gastric diverticulum

All of those above are very rare. Let’s look at some that are still uncommon, but more frequently found than the latter ones.

  • Infantile hypertrophic pyloric stenosis – The mucosa of the pylorus is so hypertrophied that it can obstruct the gastric outlet. The infant will therefore projectile vomit after every meal. The mucosa also appears edematous, will have patchy erosions and be full of ulcers. This is not the same as atresia.
  • Pancreas heterotopy – This means that the pancreatic tissue can be found outside the pancreas, and in approximately in 1-2 % of the population, it’s found in the stomach.
Inflammatory disorders of the stomach

1. Acute erosive gastritis

This type of inflammation is a gastric mucosal erosion, which is typically caused by damage to the mucosal defense. Acute peptic ulcers are the most severe form of this type of gastritis. It will be covered later in this topic.

It can be caused by:

  • Heavy use of NSAIDs, such as aspirin
  • Alcoholism
  • Heavy smoking
  • Chemotherapy
  • Bile reflux
  • Uremia
  • Infections which can be systemic, like Salmonella
  • Severe stress like trauma, burns and surgery
    • Curling-ulcus after burning
    • Cushing-ulcus after CNS injury
  • Ischemia and shock
  • Ingestion of acids and alkaloids (suicide attempts)
  • Nasogastric tube leading to mechanical trauma to the stomach
  • Distal gastrectomy
  • Freezing
    • Wischnevsky spots

This inflammation is the major cause of hematemesis, vomiting of blood, in alcoholics. Also, it’s found in 25 % of patients with rheumatoid arthritis due to the daily use of aspirin against the pain. Most of them develop bleeding, and this can be fatal to 5 % of them.

2. Autoimmune metaplastic atrophic gastritis (AMAG)

This gastritis occurs in only 1 % of the population, and in 90 % of all cases, it is caused by anti-parietal cell antibodies. 60 % have also anti-intrinsic factor antibodies. Recall that this type of cells is found in the fundus and the corpus of the stomach.

Since the parietal cells have the proton pump, H+/K+ ATPase, these patients suffer from hypochlorhydria or achlorhydria because they lose their parietal cells. If the disease is severe enough, the gastrin levels increase in the serum as well. However, there are usually no symptoms, so the patients slowly develop atrophy of the mucosa in the corpus and fundus!

Also, the parietal cells secrete intrinsic factor, which is needed to absorb vitamin B12 in the terminal ileum. Therefore, AMAG leads to pernicious anemia.

It may also eventually lead to carcinoid tumors and G-cell hyperplasia.

3. B(acterial) gastritis – Helicobacter Pylori associated

This infection by Helicobacter Pylori is chronic and is found in 2/3 of the population worldwide. However, the prevalence is decreasing due to sanitation and antibiotics, but still 90 % of the population is infected in developing countries. While the infection usually occurs in childhood in developing countries, it usually occurs in adulthood in industrialized countries. The spiral- or curve shaped bacilli is found in almost all cases of gastric ulcers.

In 80% of infected individuals the infection is asymptomatic and lasts the whole life. In those that have symptoms can the consequences however be fatal.

  • The infection gives a 15-20 % lifetime risk of peptic ulcer disease.
  • It has also been linked to 70 % of gastric cancers, especially intestinal types and gastric lymphoma.
    • The atrophy, intestinal metaplasia and intestinal dysplasia are perfect seedbeds for carcinoma.
    • The acquired mucosal associated lymphoid tissue, MALT, is a seedbed for H. pylori associated gastric lymphoma.
  • Bacterial toxins, like e.g. cagA, VacA, urease and ammonia are toxic to the epithelial cells
  • Mast cells react to the bacterium and release platelet activating factors, which disturbs microcirculation and can cause ischemia and erosions.
  • The different types of H. pylori have different potentials for carcinogenesis.

3. C(hemical) gastritis

This one affects approx. 15 % of the population, and is caused by chemical, toxic or reactive agents which destroys the gastric mucosa. We distinguish between endogenic and exogenic factors.

  • Endogenic factors:
    • Bile or pancreas-fluid reflux
  • Exogenic factors
    • Alcohol
    • Drugs like NSAIDs and steroids

The injuries are almost always found in the antrum and can be seen as foveolar hyperplasia with hyperemia. This type of gastritis is considered mild.

4. D-Gastritis

Here we can find various types of gastritides, which are caused by different factors.

It wasn’t easy to find relevant information for this, so I guess this isn’t that important to know in detail.

  • Opportunistic gastritides by cytomegalovirus (CMV) or yeast infection.
  • Granulomatous gastritis
  • Lymphocytic gastritis
  • Collagenous gastritis
  • Eosinophilic gastritis
  • Gastritis cystica profundal
  • Graft vs. host gastritis (GVH-gastritis)
  • Allergic gastritis
Peptic ulcer disease

Peptic ulcer disease is most often associated with H. Pylori infection or excessive NSAID use and is characterized by “holes” in the mucosa that at least reach the submucosa.

This mucosal defect is caused by disturbance in the equilibrium of the protective and the aggressive factors of the gastric mucosa. You can see the different factors on the figure below.

The red factors on the left are the factors that protect against acidity. The green factors on the right are the aggressive factors.

The ulcers may occur in any part of the GI-tract that is exposed to acidic gastric juices but is most commonly found in the minor curvature of the stomach, gastric antrum and first portion of duodenum. It is 3 times more common in men than in women.

We distinguish between acute and chronic ulcers, where the acute type is the most severe form of acute erosive gastritis. The causes are the same as above. Let’s take a look at their differences:

Acute ulcer Chronic ulcer
Mostly smaller than 1 cm 2-4 cm
Often multiple Often just one
Round or oval Radiating mucosal folds around it
At the level of the mucosa
Ulcer base: covered by fibrin or hematin Ulcer base: clear
Ulcer edge: grayish, yellow and flat Ulcer edge: Hyperemic and straight walls
Complications: bleeding, perforation, peritonitis Complications: Bleeding, perforation, penetration, scarring formation

Zollinger-Ellison syndrome

This syndrome is characterized by multiple peptic ulcerations in the stomach, duodenum and even jejunum. This happens due to neuroendocrine tumors that produce gastrin, called gastrinomas, and they are often located in the pancreas, duodenum or the lymph nodes of the abdomen. Increased gastrin means increased stomach acid.

Classification of gastritides – Sydney system

The Sydney system is used to combine the topography, morphology and the etiological information so it’s easier to come up with a diagnosis.

Grading of atrophy – OLGA

The OLGA grading system uses at least five biopsies from five different parts of the stomach to establish which stage the gastritis is in.


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3. Diseases of the oesophagus

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5. The benign and malignant tumours of the stomach

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