1. Peptic ulcer disease: circumscribed loss of mucosa, submucosa, or muscle layer of the gastrointestinal tract caused by a decreased resistance of gastric mucosa to acid-pepsin injury. Peptic ulcer disease is a chronic disease and may occur in the distal esophagus, stomach, upper duodenum, or jejunum. Gastric ulcers, located on the lesser curvature of the stomach, are larger and deeper than duodenal ulcers and tend to become malignant. Duodenal ulcers are located on the first part of the duodenum and are more common than gastric ulcers. Esophageal ulcers occur in the esophagus. Stress ulcers, an acute problem, occur after a major insult to the body.

    1. Pathology: failure of the body to regenerate mucous epithelium at a sufficient rate to counterbalance the damage to tissue during the breakdown of protein; decrease in the quantity and quality of the mucus; poor local mucosal blood flow, along with individual susceptibility to ulceration. A peptic ulcer is a hole in the lining of the stomach, duodenum, or esophagus. This hole occurs when the lining of these organs is corroded by the acidic digestive juices secreted by the stomach cells. Excess acid is still considered to be significant in ulcer formation. The leading cause of ulcer disease is currently believed to be infection of the stomach by Helicobacter pylori (H. pylori). Another major cause of ulcers is chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs). Cigarette smoking is also an important cause of ulcers.
    2. Risk factors:
      1. Gastric ulcers.
        1. Infection with H. pylori.
        2. Decreased resistance to acid-pepsin injury.
        3. Increased histamine release -inflammatory reaction.
        4. Ulcerogenic drugs (aggravate pre-existing conditions).
        5. Cigarette smoking.
        6. Increased alcohol and caffeine use (aggravates pre-existing conditions).
        7. Gastric ulcer is thought to be a risk for gastric cancer.
        8. Difficulty coping with stressful situations.
      2. Duodenal ulcers.
        1. Infection with pylori.
        2. Elevated gastric acid secretory rate.
        3. Elevated gastric acid levels postprandially (after eating).
        4. Increased rate of gastric emptying-increased amount of acid in duodenum-irritation and breakdown of duodenal mucosa.
        5. Ulcerogenic medication use (aggravates pre-existing conditions).
        6. Cigarette smoking.
        7. Alcohol and caffeine use (aggravates preexisting condition).
        8. Difficulty coping with stressful situations.
      3. Stress ulcers.
        1. Severe trauma or major illness.
        2. Severe burns (Curling’s ulcer); develop in 72 hours with majority of persons with burns over more than 35% of the body surface.
        3. Head injuries or intracranial disease (Cushing’s ulcer).
        4. Medications in large doses: corticosteroids, salicylates, ibuprofen, indomethacin, phenylbutazone (Butazolidin).
        5. Shock.
        6. Sepsis.
    3. Assessment:
      1. Subjective data:
        1. Gastric ulcers.
          1. Pain.
            1. Type: gnawing, aching, burning.
            2. Location: epigastric, left of midline, localized.
            3. Occurrence: periodic pain, often 2 hours after eating.
            4. Relief: antacids; may be aggravated, not relieved, by food.
            5. Some patients report no discomfort at all.
          2. Weakness.
          3. History of risk factors as above.
        2. Duodenal ulcers.
          1. Pain.
            1. Type: gnawing, aching, burning, hunger like, boring.
            2. Location: right epigastric, localized; steady pain near midline of back may indicate perforation.
            3. Occurrence: 1-3 hours after eating, worse at end of day or during the night; initial attack occurs spring or fall; history of remissions and exacerbations.
            4. Relief: food, antacids, or both.
            5. Some patients report no discomfort at all.
          2. Nausea.
          3. History of risk factors.
        3. Stress ulcers.
          1. Pain: often painless until serious complication (hemorrhage, perforation) occurs.
          2. History of risk factors as above.
      2. Objective data.
        1. Gastric ulcer.
          1. Vomiting blood (hematemesis).
          2. Melena (tarry stools).
          3. Weight loss.
          4. X-ray (upper GI series) confirms “crater” (punched-out appearance, clean base).
          5. Endoscopy confirms presence of ulcer; biopsy for cytology.
          6. Monitor for blood loss: CBC, stool for occult blood.
          7. Orthostatic hypotension.
          8. Lab data: positive for pylori.
        2. Duodenal ulcer.
          1. Eructation.
          2. Vomiting blood (hematemesis).
          3. Regurgitation of sour liquid into back of mouth.
          4. Constipation.
          5. X-ray (upper GI series) confirms ulcer craters and niches, as well as outlet deformities: round or oval funnel-like lesion extending into musculature.
          6. Endoscopy for direct visualization.
          7. Monitor for blood loss: CBC, stool for occult blood.
          8. Orthostatic hypotension.
          9. Lab data: positive for pylori.
        3. Stress ulcer.
          1. GI bleeding.
          2. Multiple, superficial erosions affecting large area of gastric mucosa.
    4. Analysis/nursing diagnosis (all types):
      1. Pain related to erosion of gastric lining.
      2. Ineffective individual coping related to inability to change lifestyle.
      3. Altered nutrition, less than body requirements, related to inadequate intake.
      4. Knowledge deficit regarding preventive measures.
      5. Risk for injury related to possible hemorrhage or perforation.
    5. Nursing care plan/implementation (all types):
      1. Goal: promote comfort.
        1. Medications as ordered to decrease pain.
        2. Prepare for diagnostic tests.
        3. X-rays; upper GI series (barium swallow); lower GI (barium enema).
        4. Endoscopy.
        5. Gastric analysis, to determine amount of hydrochloric acid in GI tract.
      2. Goal: prevent/recognize signs of complications.
        1. Monitor vitals for shock.
        2. Check stool for occult blood/hemorrhage.
        3. Palpate abdomen for perforation (rigid, board like); arterial bleeding.
      3. Goal: provide emotional support.
        1. Stress-management techniques.
        2. Restful environment.
        3. Prepare for surgery, if necessary.
      4. Goal: health teaching.
        1. Medications:
          1. Antibiotics. Sometimes antibiotics work best if given in combination with Prilosec, H2 blockers, or Pepto Bismol. Caution: use of antibiotic treatment can cause allergic reactions, diarrhea, and severe antibiotic induced colitis.
            1. Tetracycline.
            2. Amoxicillin.
            3. Metronidazole (Flagyl).
            4. Clarithromycin (Biaxin).
          2. Histamine antagonists: given with meals/bedtime to block the action of histamine-stimulated gastric secretions (basal and stimulated); inhibit pepsin secretion and reduce the volume of gastric secretions.
            1. Cimetidine (Tagamet) inhibits gastrin release; can be given PO, IV, or IM; cannot be given within 1 hour of antacid therapy.
            2. Ranitidine (Zantac) has greater reduction of acid secretion, longer duration, less frequent administration (bid vs. qid), and fewer side effects than cimetidine.
            3. Nizatidine (Axid).
            4. Famotidine (Pepcid).
          3. Proton pump inhibitors (gastric acid inhibitors): superior in treating esophageal ulcers; equal to other H2 receptors for gastric and duodenal ulcers.
            1. Omeprazole (Prilosec).
            2. Lansoprazole (Prevacid).
            3. Pantoprazole.
          4. Antiulcers: give 1-3 hours after meals and at bedtime to decrease pain by lowering acidity; monitor for:
            1. Diarrhea (seen most often with magnesium carbonate and magnesium oxide [Maalox, Mylanta]).
            2. Constipation (seen most often with calcium carbonate [Turns] or aluminum hydroxide [Amphojel)).
            3. Electrolyte imbalance (seen with systemic antacid, soda bicarbonate).
            4. Best 1-3 hours after meals.
            5. Liquids more effective than tablets; if taking tablets, chew slowly.
          5. Sucralfate and misoprostol (Cytotec): given 1 hour before meals and at bedtime.
            1. Locally active topical agent that forms a protective coat on mucosa, prevents further digestive action of both acid and pepsin.
            2. Must not be given within 30 minutes of antacids.
          6. Anticholinergic-when used, given before meals to decrease gastric acid secretion and delay gastric emptying.
          7. Cisapride, a serotonin-4 receptor agonist used to treat ulcers, gastric reflux, dyspepsia, gastroparesis, and chronic constipation.
          8. Important: avoid aspirin (could increase bleeding possibility).
        2. Diet:
          1. Change diet only to relieve symptoms; diet may not influence ulcer formation.
          2. Avoid foods that increase acidity- caffeine and alcohol in moderation.
          3. Plan:
            1. Small, frequent meals (to prevent exacerbations of symptoms related to an empty stomach).
            2. Weight control.
        3. Complications-signs and symptoms:
          1. Gastric ulcers may be premalignant.
          2. Perforation.
          3. Hemorrhage.
          4. Obstruction.
        4. Lifestyle changes:
          1. Decrease:
            1. Smoking.
            2. Noise.
            3. Rush.
            4. Confusion.
          2. Increase:
            1. Communication.
            2. Mental/physical rest.
            3. Compliance with medical regimen.
    6. Evaluation/outcome criteria:
      1. Avoids foods/liquids that cause irritation.
      2. Takes prescribed medications.
      3. Pain decreases.
      4. No complications.
      5. States signs and symptoms of complications.
      6. Participates in stress-reduction activities.
      7. Stops smoking.