PEPTIC ULCER

a case analysis

BRIX ALVIN L. VALDRIZ

BSN 4C – GROUP 1

2021

PEPTIC ULCER
Definition of Peptic Ulcer
A peptic ulcer may be referred to as a gastric, duodenal, or esophageal ulcer,
depending on its location. A peptic ulcer is an excavation (hollowed-out area) that forms in
the mucosal wall of the stomach, in the pylorus (the opening between the stomach and
duodenum), in the duodenum (the first part of the small intestine), or in the esophagus.
Erosion of a circumscribed area of mucous membrane is the cause. This erosion may extend
as deeply as the muscle layers or through the muscle to the peritoneum.
Peptic ulcers are more likely to occur in the duodenum than in the stomach. As a
rule, they occur alone, but they may occur in multiples. Chronic gastric ulcers tend to occur
in the lesser curvature of the stomach, near the pylorus. Esophageal ulcers occur as a result
of the backward flow of HCl from the stomach into the esophagus (gastroesophageal reflux
disease [GERD]).

Types of Peptic Ulcer

Gastric Ulcer
Forms in the lining of the stomach.
Duodenal Ulcer
Form in the upper small intestine.

Risk Factors
People used to think that stress or certain foods could cause ulcers. But researchers
haven’t found any evidence to support those theories. Instead, studies have revealed two
main causes of ulcers:
o H. pylori bacteria. The H. pylori bacteria stick to the layer of mucus in the
digestive tract and cause inflammation (irritation), which can cause this
protective lining to break down. This breakdown is a problem because your
stomach contains strong acid intended to digest food. Without the mucus
layer to protect it, the acid can eat into stomach tissue.
o NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are a group of medications
typically used to treat pain. There are many drugs in this group. A few of
these include: aspirin (Bayer®), ibuprofen (Motrin®, Advil®), naproxen
(Aleve®, Naprosyn®), ketorolac (Toradol®) and oxaprozin (Daypro®). NSAIDs
are also included in some combination medications, such as Alka-Seltzer®,
Goody’s Powder® and BC Powder®. Acetaminophen (Tylenol®) is NOT an
NSAID and is therefore the preferred non-prescription treatment for pain in
patients at risk for peptic ulcer disease. NSAID use is very common because
many are available over the counter without a prescriptionand therefore
they are a very common cause of peptic ulcers. NSAIDs cause ulcers by
interrupting the natural ability of the stomach and the duodenum to protect
themselves from stomach acid. NSAIDs also can interfere with blood clotting,
which has obvious importance when ulcers bleed.
o Hypersecretory states. Excessive secretion of HCl in the stomach may
contribute to the formation of peptic ulcers, and stress may be associated

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 with its increased secretion. The ingestion of milk and caffeinated beverages,
smoking, and alcohol also may increase HCl secretion. Stress and eating spicy
foods may make peptic ulcers worse. Peptic ulcers are found in rare cases in
patients with tumors that cause secretion of excessive amounts of the
hormone gastrin. The Zollinger-Ellison syndrome (ZES) consists of severe
peptic ulcers, extreme gastric hyperacidity, and gastrin-secreting benign or
malignant tumors of the pancreas.
Pathophysiology
 Peptic ulcers occur mainly in the gastroduodenal mucosa because this tissue cannot
withstand the digestive action of gastric acid (HCl) and pepsin.
 The erosion is caused by the increased concentration or activity of acid–pepsin or by
decreased resistance of the mucosa. A damaged mucosa cannot secrete enough
mucus to act as a barrier against HCl.
 The use of NSAIDs inhibits the secretion of mucus that protects the mucosa.
Patients with duodenal ulcers secrete more acid than normal, whereas
patients with gastric ulcers tend to secrete normal or decreased levels of
acid.
 Damage to the gastroduodenal mucosa results in decreased resistance to
bacteria, and thus infection from H. pylori bacteria may occur.
 Once acid or pepsin penetrates the mucosal barrier, the tissues are exposed to
continued damage because acid diffuses into the gastric wall. Ulcers may erode more
deeply into the muscularis and eventually may perforate the wall. An area of
inflammation surrounds the crater.
 When the erosion invades a blood vessel wall, bleeding takes place. Bleeding may
involve persistent loss of small amounts of blood or massive hemorrhage, depending
on the size of the blood vessel involved. Chronic blood loss may be detected by the
presence of iron deficiency anemia or occult blood in the stool; one of these may be
the first indicator of peptic ulcer.
 The development of peptic ulcers begins with a breakdown of the mucosal barrier,
which results from an imbalance between the mucosal defense system and forces
that are potentially damaging to it.
 Healing of peptic ulcers is difficult because the lesion cannot be isolated from the
irritants in the environment. During the healing process, granulation tissue forms
deep in the cavity, and new epithelial tissue regenerates from the edges. This
granulation tissue often breaks down because it is subject to damage by the chyme.
 Because a longer time is often required for healing, more fibrous scar tissue develops
at the site. The ulcers tend to recur because predisposing factors remain or the scar
tissue itself interferes with the blood supply to the area.

Signs and Symptoms

Symptoms of an ulcer may last for a few days, weeks, or months and may disappear
only to reappear, often without an identifiable cause. Many people with ulcers have no
symptoms, and perforation or hemorrhage may occur in 20% to 30% of patients who had
no preceding manifestations.
As a rule, the patient with an ulcer complains of dull, gnawing pain or a burning
sensation in the midepigastrium or the back. It is believed that the pain occurs when the
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increased acid content of the stomach and duodenum erodes the lesion and stimulates the
exposed nerve endings. Another theory suggests that contact of the lesion with acid
stimulates a local reflex mechanism that initiates contraction of the adjacent smooth
muscle. Pain is usually relieved by eating, because food neutralizes the acid, or by taking
alkali; however, once the stomach has emptied or the alkali’s effect has decreased, the pain
returns. Sharply localized tenderness can be elicited by applying gentle pressure to the
epigastrium at or slightly to the right of the midline.
Other symptoms include pyrosis (heartburn), vomiting, constipation or diarrhea, and
bleeding. Pyrosis is a burning sensation in the stomach and esophagus that moves up to the
mouth. Heartburn is often accompanied by sour eructation, or burping, which is common
when the patient’s stomach is empty. Although vomiting is rare in uncomplicated duodenal
ulcer, it may be a symptom of a complication of an ulcer. It results from obstruction of the
pyloric orifice, caused by either muscular spasm of the pylorus or mechanical obstruction
from scarring or acute swelling of the inflamed mucous membrane adjacent to the ulcer.
Vomiting may or may not be preceded by nausea; usually it follows a bout of severe pain
and bloating, which is relieved by vomiting. Emesis often contains undigested food eaten
many hours earlier.
Constipation or diarrhea may occur, probably as a result of diet and medications.
Fifteen percent of patients with peptic ulcer experience bleeding. Patients may present with
GI bleeding as evidenced by the passage of melena (tarry stools). A small portion of patients
who bleed from an acute ulcer have only very mild symptoms or none at all (Barba,
Fitzgerald & Wood, 2007).

Diagnostic Procedures
Blood studies such as amylase which is performed to detect and monitor the clinical
course of pancreatitis. It is frequently ordered when a patient presents with acute
abdominal pain. In cases of ulcer, there will be increased levels since peptic ulcer penetrates
the posterior wall of the duodenum into the pancreas. his causes a localized pancreatitis
with elevated amylase levels (normal: 60–120 Somogyi units/dL or 30–220 units/L (SI units)).
Gastrin is a test used in the evaluation of patients with peptic ulcers to diagnose Zollinger-
Ellison (ZE) syndrome or G-cell hyperplasia. In ZE syndrome, there would be increased levels
which is associated with a pancreatic islet cell gastrin-producing tumor (normal: 0–180
pg/mL or 0–180 ng/L (SI units)). Lipase is a test that is used in the evaluation of pancreatic
disease. In peptic ulcers, there would be increased levels in which the pathophysiology of
this observation is not well understood. Certainly, in perforated peptic disease the lipase in
the gastrointestinal (GI) contents leaks out into the peritoneum, where it is picked up by the
bloodstream. Lipase levels rise (normal: 0–160 units/L or 0–160 units/L (SI units)).
Pepsinogen is a test used to identify pernicious anemia (PA), gastric atrophy, or peptic
disease. It is also used to identify precancerous changes in those at great risk for gastric
carcinoma. In peptic ulcer, there would be decreased levels, it might be related to the
reactive inflammatory changes associated with active ulcer disease (normal: Pepsinogen I:
28–100 ng/mL ; Pepsinogen II: <22 ng/mL).
For endoscopic studies, esophagogastroduodenoscopy is performed to visualize the
lumen of the esophagus, stomach, and duodenum. In peptic ulcers, this benign, acid-
induced ulcer usually occurs in the duodenum but may occur in the distal stomach. It is a
small to moderate-sized ulcer seen in the mucosa of the organ.
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 For x-ray studies, upper gastrointestinal tract x-ray provides visualization of the
mucosa of the esophageal, gastric, and duodenum lumens. It is indicated in patients with
upper abdominal pain, dyspepsia, dysphagia, early satiety, or suspected gastroduodenal
obstruction. For ulcers, they are most commonly seen in the first portion of the duodenum,
called the bulb.

Medical Managements
Once the diagnosis is established, the patient is informed that the condition can be
controlled. Recurrence may develop; however, peptic ulcers treated with antibiotics to
eradicate H. pylori have a lower recurrence rate than those not treated with antibiotics. The
goals are to eradicate H. pylori and to manage gastric acidity. Methods used include
medications, lifestyle changes, and surgical intervention.

Pharmacologic Managements
Antacids
The most commonly used agents are mixtures of aluminum hydroxide and
magnesium hydroxide. Aluminum hydroxide can produce constipation and phosphate
depletion; magnesium hydroxide may cause loose stools. Many of the commonly used
antacids (e.g., Maalox, Mylanta) have a combination of both aluminum and magnesium
hydroxide in order to avoid these side effects. The magnesium-containing preparation
should not be used in chronic renal failure patients because of possible hypermagnesemia,
and aluminum may cause chronic neurotoxicity in these patients.
Proton Pump Inhibitors
Omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole are
substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H+,K+-
ATPase. Esomeprazole is the S-enantiomer of omeprazole, which is a racemic mixture of
both S- and R-optical isomers. The R-isomer of lansoprazole, dexlansoprazole, is the most
recent PPI approved for clinical use. Its reported advantage is a dual delayed-release system,
aimed at improving treatment of gastroesophageal reflux disease (GERD). These are the
most potent acid inhibitory agents available. Omeprazole and lansoprazole are the PPIs that
have been used for the longest time. Both are acid-labile and are administered as enteric-
coated granules in a sustained-release capsule that dissolves within the small intestine at a
pH of 6. Lansoprazole is available in an orally disintegrating tablet that can be taken with or
without water, an advantage for individuals who have significant dysphagia. Absorption
kinetics are similar to the capsule. In addition, a lansoprazole-naproxen combination
preparation that has been made available is targeted at decreasing NSAID-related GI injury
(see below). Omeprazole is available as nonenteric-coated granules mixed with sodium
bicarbonate in a powder form that can be administered orally or via gastric tube.

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 Cytoprotective Agents
Sucralfate. Sucralfate is a complex sucrose salt in which the hydroxyl groups have
been substituted by aluminum hydroxide and sulfate. This compound is insoluble in water
and becomes a viscous paste within the stomach and duodenum, binding primarily to sites
of active ulceration. Sucralfate may act by several mechanisms: serving as a physicochemical
barrier, promoting a trophic action by binding growth factors such as EGF, enhancing
prostaglandin synthesis, stimulating mucus and bicarbonate secretion, and enhancing
mucosal defense and repair. Toxicity from this drug is rare, with constipation being most
common (2–3%). It should be avoided in patients with chronic renal insufficiency to prevent
aluminum-induced neurotoxicity. Hypophosphatemia and gastric bezoar formation have
also been reported rarely. Standard dosing of sucralfate is 1 g qid.
Prostaglandin Analogues. In view of their central role in maintaining mucosal
integrity and repair, stable prostaglandin analogues were developed for the treatment of
PUD. The mechanism by which this rapidly absorbed drug provides its therapeutic effect is
through enhancement of mucosal defense and repair. The most common toxicity noted with
this drug is diarrhea (10–30% incidence). Other major toxicities include uterine bleeding and
contractions; misoprostol is contraindicated in women who may be pregnant, and women
of childbearing age must be made clearly aware of this potential drug toxicity. The standard
therapeutic dose is 200 μg qid.
Other Medical Therapies
Diet Modification
The intent of dietary modification for patients with peptic ulcers is to avoid
oversecretion of acid and hypermotility in the GI tract. These can be minimized by avoiding
extremes of temperature of food and beverage and overstimulation from consumption of
meat extracts, alcohol, coffee (including decaffeinated coffee, which also stimulates acid
secretion) and other caffeinated beverages, and diets rich in milk and cream (which
stimulate acid secretion). In addition, an effort is made to neutralize acid by eating three

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regular meals a day. Small, frequent feedings are not necessary as long as an antacid or a
histamine blocker is taken. Diet compatibility becomes an individual matter: The patient
eats foods that are tolerated and avoids those that produce pain.
Smoking Cessation
Studies have shown that smoking decreases the secretion of bicarbonate from the
pancreas into the duodenum, resulting in increased acidity of the duodenum. Research
indicates that continued smoking may significantly inhibit ulcer repair (Suzuki, et al., 2006).
Therefore, the patient is strongly encouraged to stop smoking.
Stress Reduction & Rest
Reducing environmental stress requires physical and psychological modifications on
the patient’s part as well as the aid and cooperation of family members and significant
others. The nurse assists the patient to identify situations that are stressful or exhausting. A
hectic lifestyle and an irregular schedule may aggravate symptoms and interfere with
regular meals taken in relaxed settings along with the regular administration of medications.
The patient may benefit from regular rest periods during the day, at least during the acute
phase of the disease. Biofeedback, hypnosis, behavior modification, massage, or
acupuncture may be helpful.
Surgery
The introduction of antibiotics to eradicate H. pylori and of H2 receptor antagonists
as treatment for ulcers has greatly reduced the need for surgical intervention. However,
surgery is usually recommended for patients with intractable ulcers (those that fail to heal
after 12 to 16 weeks of medical treatment), life-threatening hemorrhage, perforation, or
obstruction and for those with ZES that is unresponsive to medications (Ramakrishnan &
Salinas, 2007). Surgical procedures include vagotomy, with or without pyloroplasty
(transecting nerves that stimulate acid secretion and opening the pylorus) (Severing of the
vagus nerve. Decreases gastric acid by diminishing cholinergic stimulation to the parietal
cells, making them less responsive to gastrin. May be performed via open surgical approach,
laparoscopy, or thoracoscopy), and antrectomy, which is removal of the pyloric (antrum)
portion of the stomach with anastomosis (surgical connection) to either the duodenum
(gastroduodenostomy or Billroth I) (Removal of the lower portion of the antrum of the
stomach (as well as a small portion of the duodenum and pylorus. The remaining segment is
anastomosed to the duodenum) or jejunum (gastrojejunostomy or Billroth II) (Removal of
lower portion (antrum) of stomach with anastomosis to jejunum. Dotted lines show portion
removed. A duodenal stump remains and is oversewn.). Patients who require surgery may
have had a long illness. They may be discouraged and have had interruptions in their work
and pressures in their family life that affect their outlook on surgery and resolution of their
disease.

Nursing Managements
Assessment
The nurse asks the patient to describe the pain and strategies used to relieve it (eg,
food, antacids). The patient usually describes peptic ulcer pain as burning or gnawing; it
occurs about 2 hours after a meal and frequently awakens the patient between midnight
and 3 AM. Taking antacids, eating, or vomiting often relieves the pain. If the patient reports

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a recent history of vomiting, the nurse determines how often emesis has occurred and notes
important characteristics of the vomitus: Is it bright red, does it resemble coffee grounds, or
is there undigested food from previous meals? Has the patient noted any bloody or tarry
stools?
The nurse also asks the patient to list his or her usual food intake for a 72-hour
period and to describe food habits (eg, speed of eating, regularity of meals, preference for
spicy foods, use of seasonings, use of caffeinated beverages and decaffeinated coffee).
Lifestyle and other habits are a concern as well. Does the patient use irritating substances?
For example, does he or she smoke cigarettes? If yes, how many? Does the patient ingest
alcohol? If yes, how much and how often? Are NSAIDs used? The nurse inquires about the
patient’s level of anxiety and his or her perception of current stressors. How does the
patient express anger or cope with stressful situations? Is the patient experiencing
occupational stress or problems within the family? Is there a family history of ulcer disease?
1052 Unit 7 Digestive and Gastrointestinal Function The nurse assesses the patient’s vital
signs and reports tachycardia and hypotension, which may indicate anemia from GI
bleeding. The stool is tested for occult blood, and a physical examination, including
palpation of the abdomen for localized tenderness, is performed.

Nursing Diagnosis
 Acute pain related to the effect of gastric acid secretion on damaged
tissue
 Anxiety related to an acute illness
 Imbalanced nutrition related to changes in diet
 Deficient knowledge about prevention of symptoms and management of
the condition

Nursing Interventions
1. Relieving Pain
 Pain relief can be achieved with prescribed medications. The patient
should avoid aspirin, foods and beverages that contain caffeine, and
decaffeinated coffee.
 In addition, meals should be eaten at regularly paced intervals in a
relaxed setting. Some patients benefit from learning relaxation
techniques to help manage stress and pain.
2. Maintaining Optimal Nutrition
 The nurse assesses the patient for malnutrition and weight loss. After
recovery from an acute phase of peptic ulcer disease, the patient is
advised about the importance of complying with the medication regimen
and dietary restrictions.
3. Monitoring and Managing Potential Complications
 HEMORRHAGE
 The nurse assesses the patient for faintness or dizziness and
nausea, which may precede or accompany bleeding.
 It is important to monitor vital signs frequently and to evaluate
the patient for tachycardia, hypotension, and tachypnea.

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  Other nursing interventions include monitoring the hemoglobin
and hematocrit, testing the stool for gross or occult blood, and
recording hourly urinary output to detect anuria or oliguria
(absence of or decreased urine production
 Inserting a peripheral IV line for the infusion of saline or lactated
Ringer’s solution and blood products. The nurse may need to
assist with the placement of a central venous catheter for rapid
infusion of large amounts of blood and fluids as well as
hemodynamic monitoring. Blood component therapy is initiated if
there are signs of shock (eg, tachycardia, sweating, coldness of the
extremities).
 Inserting an NG tube to distinguish fresh blood from “coffee
grounds” material, to aid in the removal of clots and acid, to
prevent nausea and vomiting, and to provide a means of
monitoring further bleeding
 Inserting an indwelling urinary catheter and monitoring urinary
output
 Monitoring oxygen saturation and administering oxygen therapy
 Placing the patient in the recumbent position with the legs
elevated to prevent hypotension, or placing the patient on the left
side to prevent aspiration from vomiting
 PERFORATION AND PENETRATION
 The perforation must be closed as quickly as possible and the
abdominal cavity lavaged of stomach or intestinal contents.
 During surgery and postoperatively, the stomach contents are
drained by means of an NG tube. The nurse monitors fluid and
electrolyte balance and assesses the patient for localized infection
or peritonitis (increased temperature, abdominal pain, paralytic
ileus, increased or absent bowel sounds, abdominal distention).
 Antibiotic therapy is administered parenterally as prescribed.
 PYLORIC OBSTRUCTION
 In treating the patient with pyloric obstruction, the first
consideration is to insert an NG tube to decompress the stomach.
Confirmation that obstruction is the cause of the discomfort is
accomplished by assessing the amount of fluid aspirated from the
NG tube. A residual of more than 400 mL strongly suggests
obstruction.
 Decompression of the stomach and management of extracellular
fluid volume and electrolyte balances may improve the patient’s
condition and avert the need for surgical inter

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