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Gastritis & Peptic Ulcer Disease

Gastritis & Peptic Ulcer Disease

Review GI Histology

Gastritis is inflammation of the gastric mucosa; it can be diffuse or multi-focal.

Peptic ulcer disease is characterized by ulcers in the stomach and/or duodenum that penetrate the mucosa to reach the deeper layers of the GI tract.

It's important to properly diagnose and treat these conditions, because gastritis can give way to peptic ulcer disease, and chronic inflammation from either disorder can pave the way for malignancy.

As we'll see, infection by H. pylori and use of NSAIDs are top causes of gastritis and peptic ulcer disease.

Signs and symptoms of these disorders include epigastric pain, GI bleeding, and nausea or vomiting; however, be aware that many patients are asymptomatic, especially in the early phases.

Diagnosis relies on upper endoscopy to visualize potential lesions and biopsies to look for signs of inflammation and damage, infection by H. pylori, and malignancy.

Urea breath test and stool antigen tests can also be used to look for H. pylori infection.

Treatment of gastritis and peptic ulcer disease involves proton pump inhibitors, NSAID discontinuation, and, when present, H. pylori eradication with antibiotics.

In the case of H. pylori infection, we need to perform follow-up tests to confirm eradication and avoid relapse.

Non-ulcer dyspepsia is a diagnosis reserved for patients with gastric pain without an identifiable etiology.

Be sure to rule out cancer in those over 55 years old, and treat with proton pump inhibitors.

Pathogenesis

Gastritis is characterized by inflammation and shallow lesions in the mucosa; Peptic ulcer disease is characterized by ulcers.

Healthy GI tissue from deep to superficial: submucosa, muscularis mucosa, mucosa, and the layer of protective mucus that lines the GI tract.

In healthy tissue, damaging and protective factors of the GI tract are in balance.

Then, as injurious factors begin to predominate, the mucosa and mucous layers become inflamed and erosive lesions can form.

Key insults to the GI tract include H. pylori infection, NSAIDs, cigarette smoking, alcohol, and ischemia.

Ulcers develop when the lesion erodes through the mucosa and deeper layers.

Histology would show necrotic debris with leukocyte infiltration and inflammation, and, if inflammation has been present for a while, we'd find fibrosis in the deeper layers.

Gastritis

Characterized by mucosal inflammation (strictly speaking, gastropathy refers to gastric mucosal disorders without inflammation).

We'll follow tradition and discuss acute vs. chronic gastritis. But, be aware that some modern authors consider acute vs. chronic to be a spurious distinction, and prefer to focus on the etiology of the disorder (environmental, such as pathogen or chemical-driven vs. host-related, such as in immune-mediated or systemic disorders).

ACUTE GASTRITIS:

Acute gastritis occurs when there is a sudden insult to the gastric mucosa.

Most common causes: Aspirin, NSAIDs, and alcohol (especially when alcohol and aspirin are combined).

NSAIDs block prostaglandin synthesis, which is necessary for mucous production, whereas alcohol causes direct damage to the mucosal lining.

Stress Ulcers:

"Stress" ulcers form secondary to an acute, severe illness: Curling ulcers develop when systemic burns cause hypovolemia and mucosal ischemia. Cushing ulcers develop when brain injury produces increased vagal stimulation and increased acid production.

Diagnose acute gastritis with endoscopy to look for inflammation with hyperemia, edema, surface erosion, and bleeding in the gastric mucosa.

Histopathology is characterized by interstitial hemorrhaging in the lamina propria, dilation and congestion of mucosal capillaries, with necrotic debris on the surface (the necrotic debris comprises fibrin and neutrophils).

Be aware that hemorrhagic bleeding can be deadly, so prompt treatment with proton pump inhibitors is necessary.

CHRONIC GASTRITIS:

Whatever the cause, chronic inflammation of the stomach lining can lead to atrophy, which is characterized by loss of gastric glands and folds on a backdrop of pale mucosa with increased vascular visibility; note that we also need to look for malignancies, which are increased in atrophic gastritis.

H. pylori

Chronic gastritis is often due to infection by H. pylori (the acute phase of H. pylori infection is often asymptomatic, so goes undetected).

H. pylori is a gram-negative spirochete bacterium that raises stomach pH via urease, among other insults; because it causes chronic inflammation and tissue damage, H. pylori is classified as a class I carcinogen.

H. pylori is present in nearly half the world's population, but not everyone infected with H. pylori infection develops gastritis or cancer, and the specific reasons for variability in outcomes is uncertain.

H. pylori gastritis is asymptomatic in most people, but it increases the risk of peptic ulcer disease, gastric cancer, and primary gastric MALT lymphomas.

Lesions are typically found in the antrum but may be multi-focal.

Autoimmune gastritis

Characterized by T-cell mediated destruction of parietal cells (aka, oxyntic cells, which secrete hydrogen ions and intrinsic factor). Loss of parietal cells can lead to pernicious anemia.

Be aware that patients are likely to have other autoimmune disorders, and that auto-immune gastritis can be concomitant with H. pylori infection (so even if auto-immune gastritis is indicated, we still need to check for and treat H. pylori infections).

Peptic Ulcer Disease

Peptic ulcers are the most common cause of upper GI bleeding (though most ulcers do not bleed).

As in gastritis, top causes include H. pylori infection and NSAID use; cigarette smoking is an important risk factor.

Contrary to popular belief, psychological stress and spicy foods do not cause peptic ulcers.

Thanks to improvements in sanitation, peptic ulcers caused by H. pylori are on the decline; however, cases due to NSAID use are increasing (possibly due to an aging population relying on NSAIDs for age-related pain relief).

We typically define peptic ulcers as gastric or duodenal; be aware that patients can have both.

Gastric ulcers are typically the result of reduced mucosal protection against gastric acids.

H. pylori infection*is present in approximately 70% of cases.

Early detection and treatment of gastric ulcers is crucial because of their higher risk of malignancy rate (5-10%).

Be aware that Zollinger-Ellison syndrome is a rare cause of gastric ulcers.

Duodenal ulcers are typically caused by increased acid production, with possible reduced mucosal protection.

H. pylori is present in approximately 90% of cases.

Duodenal ulcers are typically benign.

Gastric ulcer pain increases upon eating, leading patients to avoid food and lose weight, whereas duodenal ulcer pain relieves pain and may therefore be associated with weight gain.

However, be aware that these patterns are not always consistent.

Peptic ulcer complications:

Hemorrhage is the most common complication; it can be treated with endoscopic hemostasis therapies and proton pump inhibitors.

Perforation occurs when an ulcer creates a hole in the GI tract; this is an emergency, and can cause peritonitis.

Perforation has a high mortality rate (up to 30%).

Patients tend to present with sudden abdominal pain, tachycardia, and abdominal rigidity.

With imaging we'll see free abdominal air under the diaphragm; this is called pneumoperitoneum.

Be aware that "penetration" occurs when a peptic ulcer erodes into another organ instead of opening into the peritoneum.

Gastric outlet obstruction is mechanical blockage.

In acute cases, obstruction is due to inflammation and edema in acute cases; in chronic cases, obstruction is due to fibrosis and scarring.

Patients experience early satiety with nausea, vomiting, bloating, and pain.

Imaging will show gastric distention, and endoscopy can reveal the cause.

Try treatment of the peptic ulcer disease before attempting surgical solutions.

Diagnostic Work-up Pearls

For patients who are younger than 60 years-old without alarming symptoms: weight loss, anemia, bloody stools, or dysphagia (trouble with swallowing), the focus should be on diagnosis of active H. pylori infection with non-invasive testing and response to a proton pump inhibitor (PPI, (eg, omeprazole)).

The urea breath test or stool antigen test are non-invasive tests for H. pylori.

Note that H. pylori antibody serologies do not distinguish between active and inactive disease.

For patients who are older than 60 years-old or with any alarming symptoms**: weight loss, anemia, bloody stools, or dysphagia (trouble with swallowing), upper endoscopy should be performed.

Gastritis & Peptic Ulcer Disease

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