Types of Gastritis

Inflammation of the gastric mucosa or submucosa after exposure to local irritants or other cause can result in acute gastritis. The early pathologic manifestation of gastritis is a thickened, reddened mucous membrane with prominent rugae, or folds. Various degrees of mucosal necrosis and inflammatory reaction occur in acute disease. The diagnosis cannot be based solely on clinical symptoms. Complete regeneration and healing usually occur within a few days. If the stomach muscle is not involved, complete recovery usually occurs with no residual evidence of gastric inflammatory reaction. If the muscle is affected, hemorrhage may occur during an episode of acute gastritis.

Chronic gastritis appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach. As the disease progresses, the walls and lining of the stomach thin and atrophy. With progressive gastric atrophy from chronic mucosal injury, the function of the parietal (acid-secreting) cells decreases and the source of intrinsic factor is lost. The intrinsic factor is critical for absorption of vitamin B₁₂. When body stores of vitamin B₁₂ are eventually depleted, pernicious anemia results. The amount and concentration of acid in stomach secretions gradually decrease until the secretions consist of only mucus and water.

Chronic gastritis is associated with an increased risk for gastric cancer. The persistent inflammation extends deep into the mucosa, causing destruction of the gastric glands and cellular changes. Chronic gastritis may be categorized as type A, type B, or atrophic.

Etiology and Genetic Risk

Assessment

Interventions

Patients with gastritis are not often seen in the acute care setting unless they have an exacerbation (“flare up”) of acute or chronic gastritis that results in fluid and electrolyte imbalance or bleeding. Collaborative care is directed toward supportive care for relieving the symptoms and removing or reducing the cause of discomfort.

Acute gastritis is treated symptomatically and supportively because the healing process is spontaneous, usually occurring within a few days. When the cause is removed, pain and discomfort usually subside. If bleeding is severe, a blood transfusion may be necessary. Fluid replacement is prescribed for patients with severe fluid loss. Surgery, such as partial gastrectomy, pyloroplasty, and/or vagotomy, may be needed for patients with major bleeding or ulceration. Treatment of chronic gastritis varies with the cause. The approach to management includes the elimination of causative agents, treatment of any underlying disease (e.g., uremia, Crohn’s disease), avoidance of toxic substances (e.g., alcohol, tobacco), and health teaching.

Eliminating the causative factors, such as H. pylori infection if present, is the primary treatment approach. Drugs and nutritional therapy are also used. In the acute phase, the health care provider prescribes drugs that block and buffer gastric acid secretions to relieve pain.

Types of Ulcers

Most duodenal ulcers occur in the upper portion of the duodenum. They are deep, sharply demarcated lesions that penetrate through the mucosa and submucosa into the muscularis propria (muscle layer). The floor of the ulcer consists of a necrotic area residing on granulation tissue and surrounded by areas of fibrosis.

Complications of Ulcers

Minimal bleeding from ulcers is manifested by occult blood in a tarry stool (melena). Melena may occur in patients with gastric ulcers but is more common in those with duodenal ulcers. Gastric acid digestion of blood typically results in a granular dark vomitus (coffee-ground appearance). The digestion of blood within the duodenum and small intestine may result in a black stool.

Gastric and duodenal ulcers can perforate and bleed. Perforation occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away. The stomach or duodenal contents can then leak into the peritoneal cavity. Sudden, sharp pain begins in the midepigastric region and spreads over the entire abdomen. The amount of pain correlates with the amount and type of GI contents spilled. The classic pain causes the patient to be apprehensive. The abdomen is tender, rigid, and boardlike (peritonitis). The patient assumes the knee-chest (“fetal”) position to decrease the tension on the abdominal muscles. He or she can become severely ill within hours. Bacterial septicemia and hypovolemic shock follow. Peristalsis diminishes, and paralytic ileus develops. Peptic ulcer perforation is a surgical emergency and can be life threatening!

Pyloric (gastric outlet) obstruction (blockage) occurs in a small percentage of patients and is manifested by vomiting caused by stasis and gastric dilation. Obstruction occurs at the pylorus (the gastric outlet) and is caused by scarring, edema, inflammation, or a combination of these factors.

Symptoms of obstruction include abdominal bloating, nausea, and vomiting. When vomiting persists, the patient may have hypochloremic (metabolic) alkalosis from loss of large quantities of acid gastric juice (hydrogen and chloride ions) in the vomitus. Hypokalemia may also result from the vomiting or metabolic alkalosis.

Many patients with ulcers have a single episode with no recurrence. However, intractability may develop from complications of ulcers, excessive stressors in the patient’s life, or an inability to adhere to long-term therapy. He or she no longer responds to conservative management, or recurrences of symptoms interfere with ADLs. In general, the patient continues to have recurrent pain and discomfort despite treatment. Those who fail to respond to traditional treatments or who have a relapse after discontinuation of therapy are referred to a gastroenterologist.

Etiology and Genetic Risk

Peptic ulcer development is associated primarily with bacterial infection with H. pylori and NSAIDs. NSAIDs (e.g., ibuprofen) break down the mucosal barrier and disrupt the mucosal protection mediated systemically by cyclooxygenase (COX) inhibition. COX-2 inhibitors (celecoxib [Celebrex]) are less likely to cause mucosal damage but place patients at high risk for cardiovascular events, such as myocardial infarction. In addition, NSAIDs cause decreased endogenous prostaglandins, resulting in local gastric mucosal injury. GI complications from NSAID use can occur at any time, even after long-term uncomplicated use. NSAID-related ulcers are difficult to treat, even with long-term therapy, because these ulcers have a high rate of recurrence.

Incidence/Prevalence

PUD affects millions of people across the world. However, health care provider visits, hospitalizations, and the mortality rate for PUD have decreased in the past few decades. The use of proton pump inhibitors and H. pylori treatment may explain these declines. Duodenal ulcers are increasing in “baby boomers,” however, which may be the result of increased NSAID use for arthritic pain as they age.

History

Collect data related to the causes and risk factors for peptic ulcer disease (PUD). Question the patient about factors that can influence the development of PUD, including alcohol intake and tobacco use. Note if certain foods such as tomatoes or caffeinated beverages precipitate or worsen symptoms. Information regarding actual or perceived daily stressors should also be obtained.

A history of current or past medical conditions focuses on GI problems, particularly any history of diagnosis or treatment for H. pylori infection. Review all prescription and OTC drugs that the patient is taking. Specifically inquire whether the patient is taking corticosteroids, chemotherapy, or NSAIDs. Also ask whether he or she has ever undergone radiation treatments. Assess whether the patient has had any GI surgeries, especially a partial gastrectomy, which can cause chronic gastritis.

A history of GI upset, pain and its relationship to eating and sleep patterns, and actions taken to relieve pain are also important. Inquire about any changes in the character of the pain, because this may signal the development of complications. For example, if pain that was once intermittent and relieved by food and antacids becomes constant and radiates to the back or upper quadrant, the patient may have ulcer perforation. However, many people with active duodenal or gastric ulcers report having no ulcer symptoms.

Physical Assessment/Clinical Manifestations

Physical assessment findings may reveal epigastric tenderness, usually located at the midline between the umbilicus and the xiphoid process. If perforation into the peritoneal cavity is present, the patient has a rigid, boardlike abdomen accompanied by rebound tenderness and pain. Initially, auscultation of the abdomen may reveal hyperactive bowel sounds, but these may diminish with progression of the disorder.