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INTRODUCTION
Physiologically, a certain amount of acid is secreted by the gastric cells lining
the stomach as a natural mechanism which serves to activate the digestive
enzymes and help in the digestion and assimilation of important proteins so that
they can be easily absorbed by the body.

Acid peptic disease is a collective term used to include many conditions such
as gastro-esophageal reflux disease (GERD), gastritis, gastric ulcer, duodenal
ulcer, esophageal ulcer, Zollinger Ellison Syndrome (ZES) and Meckels
diverticular
ulcer.
The commonest ulcers are the gastric and the duodenal ulcer.
Symptoms of peptic ulcers include abdominal pain, nausea, water brash,
vomiting, loss of appetite and weight loss. Complications include bleeding,
perforation, obstruction in the digestive tract and sometimes cancer.
Peptic ulcer is diagnosed using blood and stool tests, breath tests, and
endoscopy and barium radiography. The patient is treated with drugs that reduce
acidity and sometimes in addition with certain antibiotics to eliminate the H
pylori causing the infection (described below). Surgery may be required in some
cases.
MEANING
Acid peptic disorders include a number of conditions whose pathophysiology is
believed to be the result of damage from acid and pepsin activity in the gastric
secretions. This talk focuses on gastro esophageal reflux disease (GERD) and
peptic ulcer disease, the two most common and well defined disease states

PEPTIC ULCER DISEASE

definition
peptic ulcers(gastric and duodenal) are defects in the in the gastrointestinal
mucosa that extend through the muscularis mucosa.
CAUSES
Acid peptic disease is a result of either a decreased gastric mucosal defense or
an
excessive
acid
production.
Causes

of

acid

peptic

disease

include:

Helicobacter pylori: H.pylori is responsible for around 60%-90% of all

gastric and duodenal ulcers.
Gastrin stimulates the production of gastric acid by parietal
cells. In H. pylori colonization responses to increased gastrin,
the increase in acid can contribute to the erosion of
the mucosa and therefore ulcer formation.
NSAIDs: Prostaglandins protect the mucus lining of the stomach. Non steroidal
anti-inflammatory drugs (NSAIDs) such as aspirin, diclofenac and naproxen
prevent the production of these prostaglandins by blocking cyclo-oxygenase
enzyme
leading
to
ulceration
and
bleeding.
Smoking, alcohol and tobacco: Cigarettes, alcohol and tobacco cause an
instant and intense acid production which acts as though gasoline is poured over
a
raging
fire!
Blood group O: People with blood group O are reported to have higher
risks for the development of stomach ulcers as there is an increased formation
of antibodies against the Helicobacter bacteria, which causes an inflammatory
reaction
and
ulceration.
Heredity: Patients suffering from peptic ulcer diseases usually have a family
history of the disease, particularly the development of duodenal ulcer which
may
occur
below
the
age
of
20.
Steroids/Other medicines: Drugs like corticosteroids, anticoagulants like
warfarin (Coumadin), niacin, some chemotherapy drugs, and spironolactone can
aggravate
or
cause
ulcers.

Diet: Low fiber diet, caffeinated drinks and fatty foods are linked to peptic
ulcer.
Other diseases: Chronic liver, lung and kidney diseases especially tumors of
the acid producing cells all predispose to peptic ulcers. Zollinger-Ellison
Syndrome (ZES) is a rare pre-cancerous condition which causes peptic ulcer
disease. It is a syndrome disorder wherein tumors in the pancreas and
duodenum also known as gastrinomas produce a large amount of gastrin which
is a hormone that stimulates gastric acid secretion. Endocrine disorders such as
hyperparathyroidism are also implicated in the development of pepticulcers.
Stress: Stress and neurological problems can also be associated with the
Cushing ulcer and peptic ulcer.
Risk Factors
Although some studies have found correlations between smoking and ulcer
formation . Some suggested risk factors such as diet, and spice consumption,
Caffeine and coffee, also commonly thought to cause or exacerbate ulcers,
Similarly alcohol consumption increases risk when associated with H.
pylori infection,
Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also
cause multiple and difficult-to-heal ulcers.

CLASSIFICATION
By region/area

Duodenum (called duodenal ulcer)

Esophagus (called esophageal ulcer)

Stomach (called gastric ulcer)

Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender

with palpation)

Gastric Ulcers
Most common in late middle age
Incidence increase with age
Male to female ratio-2:1
Use of NSAID

Duodenal Ulcers
middle age
30-50yrs
4:1
Genetic Link-ist degree relative,
H.Pyloric infection

Esophageal ulcers
When peptic ulcers occur, they can be found in either the lining of the stomach,
the lining of the duodenum, or in both. Peptic ulcers that occur in the stomach
are named gastric ulcers whereas ulcers found in the duodenum are referred to
as duodenal ulcers. Peptic ulcers can be minor (they only go through the first or
the second layers of the stomach), or can be considered a medical emergency
(they go through every layer of the stomach or duodenum lining causing major
internal bleeding). A peptic ulcer is a defect that occurs in the first part of the
small intestine or in the lining of the stomach. Small ulcers may not be
noticeable, whereas large ulcers are considered medical emergencies.
Abdominal pain is a common symptom seen with multiple types of ulcers.
Common causes of ulcers can be: bacterial infections in the stomach or
duodenum, a weakening of the stomach lining caused by a continuous use of an
anti inflammatory, or the common .
PATHOPHYSIOLOGY

Peptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers, with
common etiologies of Helicobacterpylori infection, NSAID use, and stressrelated mucosal damage .
Ulcers may occur with hypersecretion of hydrochloric acid and pepsin, causing
an imbalance between gastric luminal factors and degradation in the defensive
function of the gastric mucosal barrier.
Mucosal defenses include: Mucus
secretion of bicarbonate
mucosal blood flow, and epithelial cell defense.
When acid and pepsin invade a weakened area of the mucosal barrier,
histamine is released. Histamine will stimulate parietal cells to secrete more

acid. With the continuation of this vicious cycle, erosion occurs to form the
ulcer.
Although over 50% of the population has chronic H pyloriinfection, only 5% to
10% develop ulcers. Hpylori is a pH-sensitive bacterium that can infiltrate the
gastric mucosal layer to reside in a neutral-pH environment. Acutely, the
infection or colonization may ironically produce a hypochlorhydric
environment. It is thought that this protective mechanism for the organism
occurs due to the increase of urease, which hydrolyzes urea and converts it to
ammonia and carbon dioxide. H pylori contributes to mucosal injury by
multiple mechanisms
Ulcers induced by nonselective NSAIDs can occur due to a topical irritation of
the gastric epithelial cells and reduced protective prostaglandin synthesis. Due
to their pharmacologic properties, many acidic NSAIDs cause alterations in the
hydrophobic mucosal gel layer. The topical irritation may be the first insult to
injury; however, inhibition of cyclooxygenase (COX) is the greatest concern.
NSAIDs inhibit the rate-limiting enzyme in the conversion of arachidonic acid
to prostaglandins. COX-2 exists throughout the body, producing prostaglandins
associated with inflammation and pain, whereas COX-1 is located in the
stomach, kidney, intestines, and platelets. Isoforms COX-1 and COX-2 are
inhibited by nonselective NSAIDs. As a result of COX-1 inhibition, adverse
effects such as ulcers or GI bleeds may occur.
SIGNS AND SYMPTOMS
Symptoms of a peptic ulcer can be

abdominal pain, classically epigastric strongly correlated to mealtimes. In

case of duodenal ulcers the pain appears about three hours after taking a
meal; Dull, gnawing pain and a burning sensation in the mid
epigastrium or in the back are characteristic.

Pain is relieved by eating or taking alkali; once the

stomach has emptied or the alkali wears off, the pain
returns.

Sharply localized tenderness is elicited by gentle pressure

on the epigastrium or slightly right of the midline.

Other symptoms include pyrosis (heartburn) and a

burning sensation in the esophagus and stomach, which
moves up to the mouth, occasionally with sour eructation
(burping).
bloating and abdominal fullness;
waterbrash (rush of saliva after an episode of regurgitation to dilute the
acid in esophagus - although this is more associated withgastroesophageal
reflux disease);

nausea, and copious vomiting;

loss of appetite and weight loss;

hematemesis (vomiting of blood); this can occur due to bleeding directly

from a gastric ulcer, or from damage to the esophagus from
severe/continuing vomiting.

melena (tarry, foul-smelling feces due to presence of oxidized iron

from hemoglobin);
rarely, an ulcer can lead to a gastric or duodenal perforation, which leads
The timing of the symptoms in relation to the meal may
differentiate between gastric and duodenal ulcers:
A gastric ulcer would giveepigastric pain during the meal,
as gastric acid production is increased as food enters the
stomach. Symptoms of duodenal ulcers would initially be
relieved by a meal, as the pyloric sphincter closes to
concentrate the stomach contents, therefore acid is not
reaching the duodenum.
Duodenal ulcer pain would manifest mostly 23 hours after
the meal, when thestomach begins to release digested
food and acid into the duodenum.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and
the patient's age. Furthermore, typical ulcers tend to heal and recur and as a
result the pain may occur for few days and weeks and then wane or
disappear. Usually, children and the elderly do not develop any symptoms
unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and
3 hours commonly accompanies ulcers. This pain can be misinterpreted
as hunger, indigestion orheartburn. Pain is usually caused by the ulcer but it
may be aggravated by the stomach acid when it comes into contact with the
ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the
navel up to the sternum, it may last from few minutes to several hours and it
may be worse when the stomach is empty. Also, sometimes the pain may flare.
DIAGNOSTIC MESURES
The diagnosis is mainly established based on the characteristic symptoms.
History collection-Stomach pain is usually the first signal of a peptic ulcer. In
some cases, doctors may treat ulcers without diagnosing them with specific tests
and observe whether the symptoms resolve, thus indicating that their primary
diagnosis was accurate.
Confirmation of the diagnosis is made with the help of tests such as endoscopies
or barium contrast x-rays. The tests are typically ordered if the symptoms do not
resolve after a few weeks of treatment, or when they first appear in a person
who is over age 45 or who has other symptoms such as weight loss,
because stomach cancer can cause similar symptoms. Also, when severe ulcers
resist treatment, particularly if a person has several ulcers or the ulcers are in
unusual places, a doctor may suspect an underlying condition that causes the
stomach to overproduce acid.
An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as
a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By
direct visual identification, the location and severity of an ulcer can be
described. Moreover, if no ulcer is present, EGD can often provide an
alternative diagnosis.
One of the reasons that blood tests are not reliable for accurate peptic ulcer
diagnosis on their own is their inability to differentiate between past exposure to
the bacteria and current infection. Additionally, a false negative result is
possible with a blood test if the patient has recently been taking certain drugs,
such as antibiotics or proton pump inhibitors.
The diagnosis of Helicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD);

Direct culture from an EGD biopsy specimen; this is difficult to do, and
can be expensive. Most labs are not set up to perform H. pylori cultures;

Direct detection of urease activity in a biopsy specimen by rapid urease

test;

Measurement of antibody levels in blood (does not require EGD). It is

still somewhat controversial whether a positive antibody without EGD is
enough to warrant eradication therapy;

Stool antigen test;

Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon atom to detect H. pylori. To perform this
exam the patient will be asked to drink a tasteless liquid which contains the
carbon as part of the substance that the bacteria breaks down. After an hour, the
patient will be asked to blow into a bag that is sealed. If the patient is infected
with H. pylori, the breath sample will contain radioactive carbon dioxide. This
test provides the advantage of being able to monitor the response to treatment
used to kill the bacteria.
The possibility of other causes of ulcers, notably malignancy (gastric cancer)
needs to be kept in mind. This is especially true in ulcers of the greater (large)
curvature of thestomach; most are also a consequence of chronic H.
pylori infection.
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal
tract (which always contains some air) to the peritoneal cavity (which normally
never contains air). This leads to "free gas" within the peritoneal cavity. If the
patient stands erect, as when having a chest X-ray, the gas will float to a
position underneath the diaphragm. Therefore, gas in the peritoneal cavity,
shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of
perforated peptic ulcer disease.
TREATMENT

Younger patients with ulcer-like symptoms are often treated with antacids or H2
antagonists before EGD is undertaken.
Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be
prescribed a prostaglandin analogue (Misoprostol) in order to help prevent
peptic ulcers, which are a side-effect of the NSAIDs.
When H. pylori infection is present, the most effective treatments are
combinations of 2 antibiotics
(e.g. Clarithromycin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton
pump inhibitor (PPI), sometimes together with a bismuth compound. In
complicated, treatment-resistant cases, 3 antibiotics
(e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a
PPI and sometimes with bismuth compound. An effective first-line therapy for
uncomplicated cases would be Amoxicillin + Metronidazole +Pantoprazole (a
PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.
Treatment of H. pylori usually leads to clearing of infection, relief of symptoms
and eventual healing of ulcers.
Ranitidine and famotidine, which are both H2 antagonists, provide relief of
peptic ulcers, heartburn, indigestion and excess stomach acid and prevention of
these symptoms associated with excessive consumption of food and drink.
Ranitidine and famotidine are available over the counter at pharmacies, both as
brand-name drugs and as generics, and work by decreasing the amount of acid
the stomach produces allowing healing of ulcers.
Sucralfate (Carafate) has also been a successful treatment of peptic ulcers.
Perforated peptic ulcer is a surgical emergency and requires surgical repair of
the perforation. Most bleeding ulcers require endoscopy urgently to stop
bleeding with cautery, injection, or clipping.
SURGICAL MANAGEMENT
With the advent of H2receptor antagonists, surgical intervention is less
common.
If recommended, surgery is usually for intractable ulcers (particularly with
ZollingerEllison syndrome), lifethreatening hemorrhage, perforation, or

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obstruction. Surgical procedures include vagotomy, vagotomy with

pyloroplasty, or Billroth I or II.
Billroth I, more formallyBillroth's operation I, is anoperation in which
the pylorus is removed and the proximalstomach is anastomosed directly to
the duodenum.
Billroth II, more formallyBillroth's operation II, is anoperation in which
the greater curvature of the stomach is connected to the first part of the
jejunum in a side-to-side manner. This often follows resection of the lower part
of the stomach (antrum). The antrectomy (resection of thestomach antrum) is
not part of the originally described procedure. The surgical procedure is
called gastrojejunostomy.
The Billroth II is often indicated in refractory peptic ulcer disease and gastric
adenocarcinoma. It was first described by Theodor Billroth.
Complications

Gastrointestinal bleeding is the most common complication. Sudden large

bleeding can be life-threatening, though this is more common in the elderly
population. It occurs when the ulcer erodes one of the blood vessels, such as
the gastroduodenal artery.

Perforation (a hole in the wall of the gastrointestinal tract) often leads to

catastrophic consequences if left untreated. Erosion of the gastro-intestinal
wall by the ulcer leads to spillage of stomach or intestinal content into the
abdominal cavity. Perforation at the anterior surface of the stomach leads to
acute peritonitis, initially chemical and later bacterial peritonitis. The first
sign is often sudden intense abdominal pain; an example is Valentino's
syndrome, named after the silent-film actor who experienced this pain before
his death. Posterior wall perforation leads to bleeding due to involvement of
gastroduodenal artery that lies posterior to the 1st part of duodenum.

Perforation and penetration are when the ulcer continues into adjacent
organs such as the liver and pancreas.

Gastric outlet obstruction is the narrowing of pyloric canal by scarring

and swelling of gastric antrum and duodenum due to peptic ulcers. Patient
often presents with severe vomiting without bile.

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Cancer is included in the differential diagnosis (elucidated

by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6
times more likely to develop stomach cancer from the ulcer.

NURSING ASSESSMENT

Assess pain and methods used to relieve it; take a thorough history,
including a 72hour food intake history.
If patient has vomited, determine whether emesis is bright red or coffee
ground in appearance. This helps identify source of the blood.
Ask patient about usual food habits, alcohol, smoking, medication use
(NSAIDs), and level of tension or nervousness.
Ask how patient expresses anger (especially at work and with family),
and determine whether patient is experiencing occupational stress or family
problems.
Obtain a family history of ulcer disease.
Assess vital signs for indicators of anemia (tachycardia, hypotension).
Assess for blood in the stools with an occult blood test.
Palpate abdomen for localized tenderness.

NURSING DIAGNOSIS

Acute Pain related to the effect of gastric acid secretion on damaged

tissue

Anxiety related to coping with an acute disease

Imbalanced Nutrition related to changes in diet

Decient Knowledge about preventing symptoms and managing the

condition
Potential Complications

Hemorrhage: upper GI

Perforation

Penetration

Pyloric obstruction (gastric outlet obstruction)

Planning and Goals

The major goals of the patient may include relief of pain, reduced anxiety,
maintenance of nutritional requirements, knowledge about the management
and prevention of ulcer recurrence, and absence of complications.
NURSING INTERVENTIONS
Relieving Pain and Improving Nutrition

Administer prescribed medications.

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Avoid aspirin, which is an anticoagulant, and foods and beverages that

contain acidenhancing caffeine (colas, tea, coffee, chocolate), along with
decaffeinated coffee.

Encourage patient to eat regularly spaced meals in a relaxed atmosphere;

obtain regular weights and encourage dietary modications.

Encourage relaxation techniques.

Reducing Anxiety

Assess what patient wants to know about the disease, and evaluate level
of anxiety; encourage patient to express fears openly and without criticism.

Explain diagnostic tests and administering medications on schedule.

Interact in a relaxing manner, help in identifying stressors, and explain

effective coping techniques and relaxation methods.

Encourage family to participate in care, and give emotional support.

MONITORING AND MANAGING COMPLICATIONS

If hemorrhage is a concern

Assess for faintness or dizziness and nausea, before or with bleeding; test
stool for occult or gross blood; monitor vital signs frequently (tachycardia,
hypotension, and tachypnea).

Insert an indwelling urinary catheter and monitor intake and output; insert
and maintain an IV line for infusing uid and blood.

Monitor laboratory values (hemoglobin and hematocrit).

Insert and maintain a nasogastric tube and monitor drainage; provide

lavage as ordered.

Monitor oxygen saturation and administering oxygen therapy.

Place the patient in the recumbent position with the legs elevated to
prevent hypotension, or place the patient on the left side to prevent
aspiration from vomiting.

Treat hypovolemic shock as indicated.

If perforation and penetration are concerns

Note and report symptoms of penetration (back and epigastric pain not
relieved by medications that were effective in the past).

Note and report symptoms of perforation (sudden abdominal pain,

referred pain to shoulders, vomiting and collapse, extremely tender and
rigid abdomen, hypotension and tachycardia, or other signs of shock).
Home and Community Based Care
TEACHING PATIENTS SELF CARE

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Assist the patient in understanding the condition and factors that help or
aggravate it.
Teach patient about prescribed medications, including name, dosage,
frequency, and possible side effects. Also identify medications such as
aspirin that patient should avoid.
Instruct patient about particular foods that will upset the gastric mucosa,
such as coffee, tea, colas, and alcohol, which have acidproducing potential.
Encourage patient to eat regular meals in a relaxed setting and to avoid
overeating.
Explain that smoking may interfere with ulcer healing; refer patient to
programs to assist with smoking cessation.
Alert patient to signs and symptoms of complications to be reported.
These complications include hemorrhage (cool skin, confusion, increased
heart rate, labored breathing, and blood in the stool), penetration and
perforation (severe abdominal pain, rigid and tender abdomen, vomiting,
elevated temperature, and increased heart rate), and pyloric obstruction
(nausea, vomiting, distended abdomen, and abdominal pain). To identify
obstruction, insert and monitor nasogastric tube; more than 400 mL residual
suggests obstruction.

EVALUATION

Expected Patient Outcomes

Remains free of pain between meals

Experiences less anxiety
Complies with therapeutic regimen
Maintains weight

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