Peptic Ulcers By Sarah Hofman

Peptic ulcers They are ulcerations of the mucous membrane or deeper structures of the GI tract. Most commonly occur in the stomach and duodenum. They are the result of acid and pepsin imbalance. Older adults are effect more, perhaps because use of NSAIDs. Symptoms are common between the ages of 25-50 with the peak at age 40. H. pylori is thought to be a dominant factor in promotion of peptic ulcers. (doesn’t develop the disease)

Factors that aid in forming peptic ulcers An excess of gastric acid (duodenal ulcers) Decrease in the natural ability of the GI mucosa to protect itself from acid and pepsin (gastric ulcers) Infection with spiral- shaped bacteria helicobacter pylori Gastric injury from NSAIDs.

Gastric ulcers Reflux of duodenal content (bile acids) also cause severe gastric mucosal damage. Gastric ulcers may occur on the surface of a gastric tumor because of interference with the blood supply Occurs in distal half of stomach. Cause is unclear Once gastric mucosal barrier is damaged, acid secretion is stimulated. Ulcers occur once cell death and erosion have occurred Can occur in some within 1 hour of taking acetylsalicylic acid.

Physiological stress ulcers Acute ulcers that develop following a major physiological insult such as trauma or surgery. Form of erosive gastritis Believed that the gastric mucosa of the body of the stomach undergoes a period of transient ischemia (loss of blood flow) with hypotension, severe injury, extensive burns, and complicated surgery. This is a compensatory mechanism. The decrease of blood flow produces an imbalance between the destructive properties of hydrochloric acid and pepsin and protective factors of the stomach’s mucosal barrier, especially in the fundus portion, resulting in ulceration.

Duodenal Ulcers Term given to a group of disorders that may or may not be caused by hypersecretion. 40% of people with these ulcers have excessive production or excess release of gastrin or increased sensitivity to gastrin. In the other 60%, the amount of acid produced is normal but perhaps the buffering ability is lacking in the duodenum. Risk factors include: H. pylori, infection, NSAIDs, cigarette smoking, and coffee. Ulceration occurs when the acid secretion exceeds the buffering factor.

Assessment time Subjective: With gastric ulcer pt has pain associated with food intake that doesn’t awaken them as with duodenal ulcer. Nausea, eructation, and distention (dyspepsia) Objective: Observe for hemorrhage especially with gastric Duodenal ulcers are apt to perforation. Monitor for GI bleed by watching for vomiting blood (hematemesis) that has a “coffee grounds” appearances Monitor for presence of melena (tarlike, fetid-smelling stool with undigested blood)

Just a few facts!! Bleeding from gastric ulcers is more difficult to control that bleeding from duodenal ulcers. Surgical intervention is indicated if the pt remains unstable after receiving blood over several hours. Perforation occurs when the ulcer crater penetrates the entire thickness of the wall of the stomach or duodenum. It is considered the most lethal complication of peptic ulcers. Gastric outlet obstruction is a complication of peptic ulcer disease that can occur at any time and in ulcers close to the pylorus. It is relieved by constant NG aspiration of stomach content. This allows ability of normal flow of gastric content through the pylorus.

Diagnostics Fiberoptic endoscopy can detect both gastric and duodenal ulcers, called esophagogastroduoden-oscopy. It is more reliable than barium contrast studies. Can view entire esophagus and gastric and duodenal mucosa. Used to determine ulcer healing. During procedure a specimen can be obtained for identification of H.pylori

H.pylori breath test!!! Pt drinks a solution of 13 carbon- enriched urea, natural, nonradioactive substance. That breaks down compound to 13 carbon dioxide. 30 min. later pt exhales into a collection bag. It is sent to manufacture for analysis.

Primary med. management Proton pump inhibitor: antisecretory agent to inhibit secretion of gastrin by parietal cells of the stomach; these include Prevacid and Prevacid. Mucosal healing agents: heal ulcers without antisecretory properties, possibly by adhering to proteins in the ulcer base; sucralfate (Carafate) Antisecretory and cytoprotective:Inhibits gastric acid secretion and protects gastric mucosa; misoprostol (Cytotec) (only drug approved for prevention of ulcers induced by NSAIDs. The primary treatment for peptic ulcers is to reduce sins and symptoms by reducing or neutralizing normal gastric acidity with drug therapy: Antacids: neutralize or reduce the acidity of the stomach content; these are Maalox, Gaviscon, Rolaids etc. Histamine receptor blockers: decrease acid secretions by blocking histamine receptors; these include cimetidine (Tagamet), ranitidine (Zantac) etc.

Time for surgery!!!! Antrectomy: removal of the entire antrum. ( the gastric- producing portion of the lower stomach) to eliminate the main stimuli to acid production. Gastroduodenostomy (Billroth I): fundus of the stomach is directly anastomosed to the duodenum ( to remove ulcers or cancer located in the antrum of the stomach) Gastrojejunostomy (Billroth II): duodenum is closed, and the fundus of the stomach is anastomosed into the jejunum (to remove ulcers or cancer located in the body of the fundus) Total gastrectomy: removal of the entire stomach ( rarely with cancer pt) Vagotomy: removal of the vagal innervation to the fundus, to decrease acid produced by the parietal cells of stomach. Pyloroplasty: surical enlargementof the pylorus to provide drainage of the gastric content.

Top left: antrectomy with Billroth I Top right: Billroth II Bottom: pyloroplasty

Dumping syndrome A rapid gastric emptying causing distention of the duodenum or jejunum produced by bolus of hypertonic food. Can occur after gastric resection procedures. Approximately one third to one half of patients experience dumping syndrome after peptic ulcer surgery. Treatment includes eating six small meals daily that are high in protein and fat and low carbohydrates, eating slowly and avoiding fluids during meals. -Anticholinergic agents to decrease stomach motility -Reclining for approximately 1 hour after meals.

Patients with NG or GI tubes Gi intubation is a new and frightening experience Inability to chew, taste, and swallow food and liquid may contribute to anxieties. A patient with an NG or intestinal tube is usually on NPO status. Occasionally ice chips An NG tube is connected to either continuous or intermittent suctioning, usually 100 mm Hg The nurse must implement frequent position changes to enhance tube functioning and prevent complications of immobility.

Nursing intervention Emphasis on patient care should always be on prevention and early detection of pain in the epigastric region, hematemesis, melena, or tenderness and rigidity of abdomen.

And the prognosis is…… Recurrence of an ulcer is possible and may happen within 2 years in about 1/3 of all patients Among patients whose H.pylori is treated with antibiotics, the peptic ulcer reccurence drops to 2%. Patients who do not receive antibiotics have a relapse of close to 75-90% The likelihood of recurrence is lessened by eliminating foods that aggravate the condition. If symptoms recur, the prognosis is better in patients who resume antacid medication hourly and seek further medical treatment.