PEPTIC ULCER DISEASE

DEFINITION:

A peptic ulcer is a break, or ulceration, in the protective mucosal lining of the lower
esophagus, stomach, or duodenum. Such breaks expose submucosal areas to gastric secretions
and autodigestion. Peptic ulcers can be acute or chronic, superficial or deep. Superficial
ulcerations are erosions because they erode the mucosa but do not penetrate the muscularis
mucosae. True ulcers extend through the muscularis mucosae and damage blood vessels, causing
hemorrhage, or perforate the gastrointestinal wall.

Characteristics of Gastric and Duodenal Ulcers

Characteristics Gastric Ulcer Duodenal Ulcer
INCIDENCE
Age at onset 50-70 yr 20-60 yr
Family history Usually negative Positive
Gender (prevalence) Equal in women and men Greater in men
Stress factors Increased Average
Ulcerogenic drugs Normal used Increased use
Cancer risk Increased Not increased
PATHOPHYSIOLOGY
Abnormal mucus May be present May be present
Parietal cell mass Normal or decreased Increased
Acid production Normal or decreased Increased
Serum gastrin Increased Normal
Serum pepsinogen Normal Increased
Associated gastritis More common Usually not present
Helicobacter pylori May be present (60%-80%) Often present (95%-100%)
Stimulates reduced acid Stimulates acid hypersecretion
secretion , gastric atrophy, and
risk of gastric cancer
CLINICAL
MANIFESTATIONS Located in upper abdomen Located in upper abdomen
Pain Intermittent Intermittent
Pain-antacid-relief pattern Pain-antacid or food-relief
Food-pain pattern (when food pattern
in stomach) Nocturnal pain
Chronic ulcer without pattern Pattern of remissions and
Clinical course of remission and exacerbation exacerbation for years
Heals more slowly Heals more quickly

Classification
 Stomach (called gastric ulcer)
 Duodenum (called duodenal ulcer)
 Oesophagus (called Oesophageal ulcer)
 Meckel’s Diverticulum (called Meckel’s Diverticulum ulcer)
Types of peptic ulcers
 Type I: Ulcer along the lesser curve of stomach
 Type II: Two ulcers present – one gastric, one duodenal
 Type III: Prepyloric ulcer
 Type IV: Proximal gastroesophageal ulcer
 Type V: Anywhere along gastric body, NSAID induced

SYMPTOMS:
Abdominal pain is a common symptom but it doesn't always occur. The pain can differ a lot
from person to person.
 Feeling of fullness -- unable to drink as much fluid
 Hunger and an empty feeling in the stomach, often 1 - 3 hours after a meal
 Mild nausea (vomiting may relieve symptom)
 Pain or discomfort in the upper abdomen
 Upper abdominal pain that wakes you up at night

Other possible symptoms include:

 Bloody or dark tarry stools
 Chest pain
 Fatigue
 Vomiting, possibly bloody
 Weight loss
CAUSES & RISK FACTORS:
Normally, the lining of the stomach and small intestines are protected against the
irritating acids produced in your stomach. If this protective lining stops working correctly, and
the lining breaks down, it results in inflammation (gastritis) or an ulcer.
Most ulcers occur in the first layer of the inner lining. A hole that goes all the way
through the stomach or duodenum is called a perforation. A perforation is a medical emergency.
The most common cause of such damage is infection of the stomach by bacteria called
Helicobacter pylori (H.pylori). Most people with peptic ulcers have these bacteria living in their
gastrointestinal (GI) tract. Yet, many people who have such bacteria in their stomach do not
develop an ulcer.
RISK FACTORS: Peptic Ulcer
 Drinking too much alcohol
 Regular use of aspirin, ibuprofen, naproxen, or other nonsteroidal anti-inflammatory
drugs (NSAIDs). Taking aspirin or NSAIDs once in a while is safe for most people.
 Smoking cigarettes or chewing tobacco
 Being very ill, such as being on a breathing machine
 Radiation treatments
 Advanced age
 Alcohol intake
 Chronic diseases, such as emphysema, rheumatoid arthritis, cirrhosis, and diabetes
**A rare condition called Zollinger-Ellison syndrome causes stomach and duodenal
ulcers. Persons with this disease have a tumor in the pancreas that releases high levels of a
hormone, which causes an increase in stomach acid.
PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE

Contributory factor: Precipitating factors:

 Diet: caffeine intake  Age: 50-70 years old
 Alcohol and smoking  Gender: male
 Presence of Helicobacter
pylori infection

Increase hydrochloric acid (HCL)

production

Irritation of the lining (mucosal) of the

stomach, duodenum, proximal of small
intestines

Damaged mucosal barrier Inflammatory process

Decreased function of mucosal cells S/Sx: Abdominal

Decreased quality of mucus Pain
Loss of tight junctions between cells

Back diffusion of acid into gastric

mucosa

Conversion of pepsinogen Formation of liberation of

to pepsin histamine

Increase acid secretion

Local vasodilation
Further mucosal erosion
Destruction of blood
Stimulation of cholinergic
vessels Increase capillary permeability
intramural plexus,
Loss of plasma proteins
Mucosal injury Ulceration causing muscle spasm
Mucosal edema
Loss of plasma into gastric
lumen
Bleeding/
Hemorrhage

Decreased oxygen carrying S/Sx: black tarry stools,

capacity as manifested by vomiting with the
decreased hemoglobin and presence of blood
hematocrit level

S/Sx: Pallor,
Lightheadedness, and
weakness
Assessment and Diagnostic Findings
To establish the diagnosis of peptic ulcer, the following assessment and laboratory studies should
be performed:
 Esophagogastroduodenoscopy. Confirms the presence of an ulcer and allows cytologic
studies and biopsy to rule out H. pylori or cancer.
 Physical examination. A physical examination may reveal pain, epigastric tenderness, or
abdominal distention.
 Barium study. A barium study of the upper GI tract may show an ulcer.
 Endoscopy. Endoscopy is the preferred diagnostic procedure because it allows direct
visualization of inflammatory changes, ulcers, and lesions.
 Occult blood. Stools may be tested periodically until they are negative for occult blood.
 Carbon 13 (13C) urea breath test. Reflects activity of H. pylori.

TREATMENT

Treatment Plan: H. Pylori

 Eradication Therapy: Triple therapy for 14 days is considered the treatment of choice.
o Proton Pump Inhibitor + clarithromycin and metronidazole
 Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
 In the setting of an active ulcer, continue qd proton pump inhibitor therapy for
additional 2 weeks.
 Goal: complete elimination of H. Pylori.
Treatment Plan: Not H. Pylori
 Medications—treat with Proton Pump Inhibitors alone or H2 receptor antagonists to
assist ulcer healing + Antacid
o H2 Antagonist: Ranitidine 150mg peroral BD, Cimetidine 400mg peroral BD for up
to 8 weeks
o PPI: Lansoprazole or Omeprazole 20mg peroral OD for 4-8 weeks.
o Topical antacids (eg: Gaviscon, sucralfate, colloidal bismuth) especially for acute
ulceration postoperative or in ITU patients.
Indications for Surgical Intervention
 Gastric outlet obstruction not responsive or suitable for endoscopic dilatation
(pyloroplasty)
 Failure to respond to maximal medical treatment with severe symptoms or due to habitual
recidivism.
 Emergency indication:
o Perforation
o bleeding
Surgery
 People who do not respond to medication, or who develop complications:
 o Vagotomy - cutting the vagus nerve to interrupt messages sent from the brain to
the stomach to reducing acid secretion.
o Antrectomy - remove the lower part of the stomach (antrum), which produces a
hormone that stimulates the stomach to secrete digestive juices. A vagotomy is
usually done in conjunction with an antrectomy.
o Pyloroplasty - the opening into the duodenum and small intestine (pylorus) are
enlarged, enabling contents to pass more freely from the stomach. May be
performed along with a vagotomy.
Lifestyle Changes
 Discontinue NSAIDs and use Acetaminophen for pain control if possible.
 Acid suppression--Antacids
 Smoking cessation
 No dietary restrictions unless certain foods are associated with problems.
 Stress reduction
Complications
 Perforation
 Peritonitis
 Bowel obstruction, Gastric outflow obstruction, & Pyloric stenosis
 Bleeding--occurs in 25% to 33% of cases and accounts for 25% of ulcer deaths.
Evaluation/Follow-up/Referrals
 H. Pylori Positive: retesting for tx efficacy
o Urea breath test—no sooner than 4 weeks after therapy to avoid false negative
results
o Stool antigen test—an 8 week interval must be allowed after therapy.
 H. Pylori Negative: evaluate symptoms after one month. Patients who are controlled
should cont. 2-4 more weeks.
 If symptoms persist then refer to specialist for additional diagnostic testing.
Nursing Interventions
 Monitor the patient for signs of bleeding through fecal occult blood, vomiting, persistent
diarrhea, and change in vital signs.
 Monitor intake and output.
 Monitor the patient’s hemoglobin, hematocrit, and electrolyte levels.
 Administered prescribed I.V. fluids and blood replacements if acute bleeding is present.
 Maintain nasogastric tube for acute bleeding, perforation, and postoperatively, monitor
tube drainage for amount and color.
 Perform saline lavage if ordered for acute bleeding.
 Encourage bed rest to reduce stimulation that may enhance gastric secretion.
 Provide small, frequent meals to prevent gastric distention if not actively bleeding.
 Watch for diarrhea caused by antacids and other medications.
 Restrict foods and fluids that promote diarrhea and encourage good perineal care.
 Advise patient to avoid extremely hot or cold food and fluids, to chew thoroughly, and to
eat in a leisurely fashion to reduce pain.
 Administer medications properly and teach patient dose and duration of each medication.
 Advise patient to modify lifestyle to include health practices that will prevent recurrences
of ulcer pain and bleeding.