peptic ulcer

2. By the end of the session learners will be able to:
 Review the anatomy and physiology of
gastrointestinal system (GIT)
 Define Peptic Ulcer disease.
 Discuss the causes, pathophysiology and
manifestation of Peptic Ulcer disease.
 Discuss the diagnostic and medical and surgical
management of Peptic Ulcer disease.
 Apply nursing management for patient with Peptic
Ulcer disease.
 5. Develop a teaching plan for a client experiencing
Peptic Ulcer disease.

7.  A peptic ulcer is an excavation that forms in
the mucosal wall of the stomach, in the
pylorus, in the duodenum, or in the
esophagus.
 The erosion of a circumscribed area may
extend as deep as the muscle layers or
through the muscle to the peritoneum.
 A peptic ulcer may be referred to as a
gastric, duodenal, or esophageal ulcer,
depending on its location.

8.  Gastric ulcer. Gastric ulcer tend to occur in
the lesser curvature of the stomach, near the
pylorus.
 Duodenal ulcer. Peptic ulcers are more
likely to occur in the duodenum than in the
stomach.
 Esophageal ulcer. Esophageal ulcer occur
as a result of the backward flow of HCl from
the stomach into the esophagus

10.  Erosion. The erosion is caused by the increased
concentration or activity of acid-pepsin or by
decreased resistance of the mucosa.
 Damage. A damaged mucosa cannot secrete
enough mucus to act as a barrier against HCl.
 Acid secretion. Patients with duodenal ulcers
secrete more acid than normal, while patients with
gastric ulcers tend to secrete normal or decreased
levels of acid.
 Decreased resistance. Damage to the
gastroduodenal mucosa results in decreased
resistance to bacteria and thus infection from the H.
pylori bacteria may occur.

11.  Helicobacter pylori. Research has documented
that peptic ulcers result from infection with the
gram-negative bacteria H. pylori, which may be
acquired through ingestion of food and water. H.
pylori damage the mucous coating that protects the
stomach and duodenum.
 Salicylates and NSAIDs. Encourages ulcer
formation by inhibiting the secretion of
prostaglandins.
 Various illnesses. Pancreatitis, hepatic disease,
Crohn’s disease, gastritis, and Zollinger-Ellison
syndrome are also known causes.

12.  Excess HCl. Excessive secretion of HCl in the
stomach may contribute to the formation of
peptic ulcers.
 Irritants. Ingestion of milk and caffeinated
beverages and alcohol also increase HCl
secretion. These contribute by accelerating
gastric emptying time and promoting mucosal
breakdown.
 Blood type. Gastric ulcers tend to strike people
with type A blood while duodenal ulcers tend to
afflict people with type O blood.

13. Symptoms of ulcer may last for a few days, weeks,
months, and may disappear only to reappear, often
without an identifiable cause.
 Pain. As a rule, the patient with an ulcer
complains of dull, gnawing pain or a burning
sensation in the midepigastrium or the back that
is relieved by eating.
 Pyrosis. Pyrosis (heartburn) is a burning
sensation in the stomach and esophagus that
moves up to the mouth.

14.  Vomiting. Vomiting results
from obstruction of the pyloric orifice, caused
by either muscular spasm of the pylorus or
mechanical obstruction from scarring.
 Constipation and diarrhea. Constipation or
diarrhea may occur, probably as a result of diet
and medications.
 Bleeding. 15% of patients may present with GI
bleeding as evidenced by the passage
of melena (tarry stools).

15.  Hemorrhage. Hemorrhage, the most common
complication, occurs in 10% to 20% of patients with
peptic ulcers in the form of hematemesis or melena.
 Perforation and penetration. Perforation is the erosion
of the ulcer through the gastric serosa into the peritoneal
cavity without warning, while penetration is the erosion of
the ulcer through the gastric serosa into adjacent
structures.
 Pyloric obstruction. Pyloric obstruction occurs when the
area distal to the pyloric sphincter becomes scarred and
stenosed from spasm or edema or from scar tissue that
forms when an ulcer alternately heals and breaks down.

16.  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.

17.  Pharmacologic therapy. Currently, the most
commonly used therapy for peptic ulcers is a
combination of antibiotics, proton pump
inhibitors, and bismuth salts that suppress or
eradicate the infection.
 Stress reduction and 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.

18.  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.
 Dietary modification. Avoiding extremes of the
temperature of food and beverages and
overstimulation from consumption of meat
extracts, alcohol, coffee, and other caffeinated
beverages, and diets rich in cream and milk
should be implemented.

19.  Pyloroplasty. Pyloroplasty involves
transecting nerves that stimulate the acid
secretion and opening the pylorus.
 Antrectomy. Antrectomy is the removal of
the pyloric portion of the stomach with
anastomosis to either the duodenum or
jejunum.

21.  Assessment for a description of pain.
 Assessment of relief measures to relieve the
pain.
 Assessment of the characteristics of the
vomitus.
 Assessment of the patient’s usual food
intake and food habits.

22.  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
the diet.
 Deficient knowledge about prevention of
symptoms and management of the condition.

23.  Relief of pain.
 Reduced anxiety.
 Maintenance of nutritional requirements.
 Knowledge about the management and
prevention of ulcer recurrence.
 Absence of complications.

24.  Administer prescribed medications.
 Avoid aspirin, which is an anticoagulant, and foods
and beverages that contain acid-enhancing
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 modifications.
 Encourage relaxation techniques

25.  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.

26.  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 fluid 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.

27.  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).

28.  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 acid-producing 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.

29.  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).

30.  Relief of pain.
 Reduced anxiety.
 Maintained nutritional requirements.
 Knowledge about the management and
prevention of ulcer recurrence.
 Absence of complications.

31.  https://nurseslabs.com/peptic-ulcer-disease/