Definition
A.Peptic ulcer disease (PUD) is circumscribed ulceration of the gastrointestinal (GI) mucosa occurring in areas exposed to acid and pepsin. The patient’s prior ulcer history tends to predict future behavior and risk of future complications. Complications include bleeding ulcer, perforation, and obstruction.
B.The stomach is divided on the basis of its physiologic functions into two main portions. The proximal two thirds, the fundic gland area, acts as a receptacle for ingested food and secretes acid and pepsin. The distal third, the pyloric gland area, mixes and propels food into the duodenum and produces the hormone gastrin. Peptic
lesions may occur in the esophagus (esophagitis), stomach (gastritis), or duodenum (duodenitis).
C.There is often no correlation between the presence of an active ulcer, noted by endoscopy, and symptoms. The disappearance of symptoms does not guarantee ulcer healing.
Incidence
A.The annual incidence of peptic ulcer is estimated to range from 0.1% to 1.8%. The ulcer incidence in Helicobacter pylori-infected individuals is about 1% per year. The recurrence rate is 50% to 80% during the 6 to 12 months following the initial ulcer healing, although relapses are not always symptomatic. Some peptic ulcers heal spontaneously, and 2% to 20% of patients have multiple simultaneous ulcers.
B.From 16% to 31% of ulcers are caused by nonsteroidal anti-inflammatory drugs (NSAIDs). Epidemiologic studies show that risks of peptic ulcer and death are three to six times higher among people who take NSAIDs.
C.Cigarette smokers are twice as likely to develop ulcers as nonsmokers.
Pathogenesis
A.Although the precise mechanisms of ulcer formation remain incompletely understood, the process appears to involve the interplay of acid production, pepsin secretion, bacterial infection, and mucosal defense mechanisms. Excess acid production is the hallmark of duodenal ulcer (DU) disease. Pepsin secretion is also elevated in DU disease.
B.The relation of aspirin and other NSAIDs to ulcer disease is due largely to the drugs’ potent inhibition of gastric mucosal prostaglandin synthesis. In addition to prostaglandin inhibition, many NSAID preparations produce acute diffuse mucosal injury by means of a direct erosive effect.
Predisposing Factors
A.H. pylori infection is the most common cause of ulceration.
B.Use of NSAIDs, especially aspirin, ibuprofen, and naproxen, is associated with acute erosive gastritis.
C.Smoking.
D.Genetic factors: Family history of ulcer disease.
E.Age:
1.DU occurs between ages 25 and 75.
2.Gastric ulcer (GU) occurs between ages 55 and 65.
F.Gender:
1.The ratio of male-to-female for gastritis is 1:1.
2.The ratio of male-to-female for peptic ulcers is 2:1.
G.Excessive alcohol consumption, which stimulates acid secretion.
H.Medications:
1.Corticosteroids potentiate ulcer risk in patients who use NSAIDs concurrently.
2.Anticoagulants, such as warfarin.
3.Bisphosphonates.
4.Spironolactone.
5.Selective serotonin reuptake inhibitors (SSRIs).
I.Improper diet, irregular meals, and skipped meals.
J.Severe physiologic stress:
1.Burns.
2.Central nervous system (CNS) trauma.
3.Surgery.
4.Severe medical illness:
a.Cirrhosis.
b.Chronic obstructive pulmonary disease (COPD).
c.Renal failure.
d.Crohn’s disease.
K.Other causes:
1.Radiation-induced ulcer.
2.Chemotherapy-induced ulcer.
3.Vascular insufficiency.
4.Duodenal obstruction.
L.Zollinger–Ellison syndrome.
M.Bile reflux.
N.Illicit drugs: Crack cocaine.
Common Complaints
A.Perforated peptic ulcer presents with a sudden severe onset of sharp abdominal pain.
B.Pain described as aching, boring, gnawing, or burning feeling.
C.Epigastric pain in right upper quadrant (RUQ) and left upper quadrant (LUQ) of the abdomen or occasionally below breast.
D.Pain that awakens the patient at night or in early morning.
Other Signs and Symptoms
A.Asymptomatic.
B.GI distress 1 to 3 hours after a meal, on an empty stomach.
C.Pain relieved by food, antacids, or vomiting.
D.Nausea and vomiting.
E.Hematemesis.
F.Chest discomfort.
G.Blood in stools, grape jelly
or maroon-colored stools.
H.Loss of appetite or weight.
I.Weight gain; those with DU may eat more to ease pain.
J.Anemia.
Other Signs and Symptoms
A.Massive bleeding:
1.Acute, bright red hematemesis or large amount of melena with clots in the stool, or grape jelly
stool.
2.Rapid pulse, drop in blood pressure, hypovolemia, and shock.
B.Subacute bleeding:
1.Intermittent melena or coffee-ground emesis.
2.Hypotension.
3.Weakness and dizziness.
C.Chronic bleeding:
1.Intermittent appearance of blood.
2.Increased weakness, paleness, or shortness of breath.
3.Occult blood.
Subjective Data
A.Ask the patient to describe onset, duration, type, and location of pain. Does it occur at any special time, for example, before meals, after meals, or during the night?.
B.Has the patient had a previous ulcer? What was the treatment; if oral treatment was prescribed, did the patient complete the therapy?.
C.Have the patient describe what alleviates pain, such as taking antacids, and what worsens pain, such as use of aspirin, oral steroids, or NSAIDs.
D.Review associated symptoms, such as nausea, vomiting, and heartburn.
E.Ask the patient if any first-degree relatives have ulcers.
F.Inquire whether the patient is a smoker. If so, how much and for how long?.
G.Ask the patient about alcohol consumption: How much and for how long?.
H.Inquire whether any blood has ever been vomited or passed in stool. If so, have the patient describe it.
I.Take the patient’s dietary history, including time of meals, frequency of skipped meals, weight loss, and so forth.
J.Review all medications, including a review of over-the-counter (OTC) and herbal products such as ginkgo biloba; special attention should be taken to inquire about aspirin and NSAIDs.
K.Obtain past medical history of associated diseases, such as cirrhosis, pancreatitis, arthritis, COPD, and hyperparathyroidism.
L.If the patient suspects blood in stool, ask if there has been a change in bowel pattern, presence of abdominal pain or tenderness, and what kind of food, such as red beets, the patient recently ingested.
Physical Examination
A.Check temperature (if indicated), pulse, respirations, blood pressure, and weight.
B.Palpate the abdomen for tenderness, rigidity, masses, and liver or spleen enlargement.
C.Percuss the abdomen for hepatosplenomegaly.
D.Auscultate the abdomen for bowel sounds in all quadrants.
E.Rectal exam:
1.Check for tenderness and masses.
2.Take stool specimen.
Diagnostic Tests
A.Complete blood count (CBC).
B.Stool for occult blood.
C.Coagulation studies.
D.Testing for H. pylori:
1.Endoscopy with biopsy is the most accurate test.
2.Rapid urease test is the diagnostic test of choice.
3.Urea breath test (UBT).
4.Serum test for H. pylori antibodies.
5.Stool H. pylori antigen testing—More accurate than antibody testing and less expensive.
E.Radiography with barium meal.
F.Mucosal biopsy, after GI consultation, to rule out cancer.
G.Fasting gastrin level (screening for Zollinger–Ellison syndrome).
H.Proton pump inhibitors (PPIs) are associated with osteopenia/osteoporosis; depending on the length of therapy consider a dual-energy x-ray absorptiometry (DEXA) scan.
Differential Diagnoses
A.PUD.
B.Gastroesophageal reflux disease (GERD).
C.Zollinger–Ellison syndrome: Fasting serum gastrin level 500 pg/mL in the presence of acid hypersecretion is diagnostic.
D.Cancer:
1.Gastric lymphoma.
2.Gastric cancer.
3.Pancreatic cancer.
E.Pancreatitis (acute or chronic).
F.Myocardial ischemia.
G.Abdominal aneurysm.
H.Diverticulitis.
I.Drug-induced dyspepsia:
1.Theophylline.
2.Digitalis.
J.Crohn’s disease (CD) involving the stomach or duodenum.
K.Gastric infections.
L.Cholelithiasis.
Plan
A.General interventions: Goals are to alleviate pain, promote healing, limit complications, and prevent recurrences while minimizing the costs and side effects of treatment:
1.Encourage the patient to stop taking NSAIDs, unless medically indicated:
a.If NSAID use is unavoidable, the lowest possible dose and duration and cotherapy with a PPI based on triple therapy is recommended.
2.Smoking cessation should be highly encouraged at each visit.
B. 
See Section III: Patient Teaching Guide Management of Ulcers.
C.Dietary management: Advise the patient to avoid alcohol; coffee, including decaffeinated; and other caffeine-containing beverages because they stimulate acid secretion (see Appendix B, Bland Diet
).
D.Medical and surgical management:
1.Diagnostic evaluation of the ulcer is by means of endoscopy.
2.Test for H. pylori (carbon isotope-UBT, blood test for antibodies to H. pylori, stool test, or gastric biopsy at the time of esophagogastroduodenoscopy [EGD]):
a.A single negative H. pylori test should be interpreted cautiously, especially in the face of active bleeding. Blood in the stomach can alter the pH indicator in the rapid urease test. False negatives are likely, and additional testing for H. pylori is essential.
b.Concurrent use of a PPI, antibiotics, or bismuth will cause a false negative test.
3.Surgery remains an option for treatment of refractory disease and complications. The most serious indications for surgery include brisk bleeding of 6 to 8 units of blood in 24 hours, recurrent bleeding episodes, perforation, gastric outlet obstruction refractory to medical therapy, and failure of a benign GU to heal after 15 weeks. Emergency intervention may be required, such as withholding food and oral fluids, starting an intravenous (IV), placing a nasogastric (NG) tube, providing oxygen therapy, or performing a blood transfusion. If life-threatening bleeding occurs, treat shock.
E.Pharmaceutical therapy:
A.The treatment of a peptic ulcer begins with the eradication of H. pylori in infected individuals. Empiric therapy for the infection is reasonable for uncomplicated cases in the absence of NSAID use. Documenting infection, even in patients with known ulcers, is an essential step prior to initiating antimicrobial therapy:
1.Triple therapy anti-H. pylori regimen PPI + amoxicillin + clarithromycin:
a.PPI-based regimen (choose one):
i.Rabeprazole (Aciphex) 20 mg twice a day—–tTotal treatment duration 7 days.
ii.Esomeprazole (Nexium) 40 mg once a day—Total treatment duration 10 days.