Peptic Ulcer: Classification, Etiology, Risk Factors, Clinical Manifestation, Diagnosis & Management

By March 7, 2017 No Comments
Peptic Ulcer: Classification, Etiology, Risk Factors, Clinical Manifestation, Diagnosis & Management

Peptic Ulcer is an erosion of the Gastric mucosa resulting from the digestive action of hydrochloric acid and pepsin. Any portion of the GI tract that comes into contact with gastric secretions is susceptible to ulcer development, including the lower esophagus, stomach, duodenum, and margin of gastrojejunal anastomosis after the surgical procedure.

Classification of peptic ulcer disease

A peptic ulcer can be classified as acute or chronic depending on the degree of mucosal involvement and gastric or duodenal according to the location.

The acute ulcer is associated with superficial erosion and minimal inflammation. It is of short duration and resolves quickly when the cause is identified and removed.

A chronic ulcer is one of long duration eroding through the muscular wall with the formation of fibrous tissue. Ti is present continuously for many months or intermittently throughout the person’s lifetime.

Peptic ulcer disease occurs in approximately 10% of the population. Gastric ulcer is more likely to occur during the 5th and 6th decade of life; duodenal ulcers more commonly occurs during 4th and 5th decades for men. For women, the occurrences are about 10 years later in life. Men are more likely to have both gastric and duodenal ulcer.

Gastric ulcer

A gastric ulcer which tends to heal within a few weeks, form within 1 inch (2.5cm) of the pylorus of the stomach in an area where gastritis is common. Gastric ulcer is probably caused by a break in the mucosal barrier. The barrier which differs from the layer of glycoprotein mucus that overlies the gastric epithelium, normally allows hydrochloric acid to be secreted into the stomach without injury to the epithelial cells. An incompetent pylorus may decrease the production of mucus, the usual gastric defense. The reflux of bile acids through an incompetent pylorus into the stomach may break the mucosal barrier. Decreased blood flow to the gastric mucosa may also alter the defensive barrier and may make the duodenum more susceptible to gastric acid and pepsin trauma. The reoccurrence rate is lower than that of duodenal ulcer.

Duodenal ulcer

The duodenal ulcer has a higher incidence than a gastric ulcer. These ulcers usually occur within 1.5 cm (0.6inch) of the pylorus and are usually characterized by high gastric acid secretion. Some are associated with a normal gastric secretion that is associated with rapid emptying of the stomach. Hypersecretion of acid is attributed to a greater mass of parietal cells. Stimuli for acid secretion include protein-rich meals, alcohol consumption, calcium and vagal stimulation.

Clients with a duodenal ulcer experiences low PH levels in the duodenum for longer periods. The stomach lining is more sensitive to gastric and secretes excess gastrin.

Finally, clients with duodenal ulcers have more rapid gastric emptying. The combined effect of hypersecretion of acid and rapid emptying of food from stomach reduces the buffering effects of food and results in large acid load in the duodenum. Within the duodenum, inhibitory mechanism and pancreatic secretion (an alkaline solution) may be insufficient to control the acid load.

Stress-induced and drug-induced ulcers

Besides peptic ulcers, acute gastric erosion, frequently called stress ulcers or stress erosive gastritis, can occur after an acute medical crisis. Major assaults that give rise to gastroduodenal ulceration include following:

Etiology and risk factors of Peptic Ulcer

  • The causal factor in more than 90% of all peptic ulcers has been attributed to H.pylori
  • The side effects of NSAIDs administration

These factors target the mucosal defenses of the stomach and duodenum and can eventually lead to ulceration. The other factors which are related: decreasing or increasing of gastric secretions lead to a peptic ulcer.

Clinical manifestations of peptic ulcer

  • Acute pain
  • Nausea/vomiting: patients with duodenal ulcers usually have a normal appetite unless a pyloric obstruction is present. Carcinoma, gastric ulcers, or gastritis may be associated with anorexia, weight loss, and dysphagia. Vomiting occurs more often in a gastric ulcer that the uncomplicated duodenal ulcer. It also occurs more frequently when the ulcer is in the pylorus or antrum of the stomach.

Bleeding: patients with ulcers often bleed when the ulcer erodes through a blood vessel. Bleeding may occur as massive hemorrhage or may be occult, with slow oozing.

Duodenal ulcer Gastric ulcer
  1. Pain
  • Episodic in nature lasting 30 min to 2 hours
  • Epigastric location near midline may radial around coastal border to back
  • Described as gnawing, burning, aching
  • Occurs 1-3 hours after meals and at night (12-3AM)
  • Dull epigastric location near midline
  • Easily satiety
  • Often relived  by food or antacid
  • Not usually relieved by food or antacid

In both, there is common manifestation including dyspepsia, anorexia, and weight loss.

Diagnostic studies

The diagnostic measures used to determine the presence and location of peptic ulcers are as following:

  • Complete blood count
  • Urinalysis
  • Liver enzymes
  • Gastric cytology
  • H-pyloric testing of breath, urine, and bloody stools

Management of peptic ulcer 

When the patient’s clinical manifestation and health history suggest the diagnosis of a peptic ulcer and diagnostic studies its presence, a medical regimen is instituted.

Medical management

The primary objective of intervention for peptic ulcer is to provide stomach rest.

  • Adequate rest benefits the patient to an elimination of stressors, help decrease the stimulus for overproduction of HCL acid.
  • Dietary modification may be necessary so that foods and beverages irritating to the patient can be avoided or eliminated. A bland diet consisting of six small meals may be suggested
  • Medications have a major role in the treatment of peptic ulcers.
  • Antacids are weak bases that neutralize free HCL acid to prevent irritation and permit mucosal healing
  • Histamine receptor antagonists inhibit HCL secretion by binding to the H2 receptor on stomach cells and blocking, the release of histamine which is secretagogue for HCL.
  • Basom pump inhibitors more effective than H2 receptor antagonists
  • Mucosal protective agents
  • Antibiotic therapy is instituted for patients verified with H.pylori
  • Should stop smoking

Surgical management

When the medical therapy has been tried and proved unsuccessful the surgery is indicated.

  • Vagotomy: it is performed to eliminate the acid-secreting stimulus to gastric cells.
  • Vagotomy with pyloroplasty: it involves cutting the right and left vagus nerves acid widening the existing exit of the stomach at the pylorus.
  • Gastroenterostomy: it permits regurgitation of alkaline duodenal contents, thereby neutralizing gastric acid. A drain is made in the bottom of the stomach and sewn to an opening made in the jejunum.

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