Peptic Ulcer Disease

PEPTIC ULCER DISEASE PATHOPHYSIOLOGY

By: Marie Francine Jazelle C. Rivera, RN

Peptic Ulcer Disease (PUD) is a term used to describe a group of ulcerative disorders that occurs in
areas of the gastrointestinal tract that are exposed to acid-pepsin secretion. It is also described as a
break, or ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum.
PUD develops when there is an imbalance between mucosal protective factors and the erosive factors.

ANATOMY & PHYSIOLOGY The small intestine has three parts: duodenum,
jejunum, and ileum. The duodenum begins at
There are three parts of the gastrointestinal the pylorus and ends at a suspensory ligament
tract that are may be affected in peptic ulcer called Treitz ligament joining it to the
disease: lower esophagus, stomach, and first jejunum; the duodenum also contains the
part of the duodenum. The esophagus is a opening of the common bile duct and the main
straight tube, about 25cm (10 in.) in length that pancreatic duct. The end of the jejunum and
lies behind the trachea, and connects the beginning of ileum doesn’t have any
pharynx with the stomach. The esophagus anatomical markers, but are not entirely
functions primarily as a conduit for the different from each other.
passage of food from the pharynx to the
stomach. It has two sphincters, the The peritoneum is a serous membrane
pharyngoesophageal sphincter which keeps air surrounding the organs of the abdomen and
from entering the esophagus and stomach lines the abdominopelvic cavity. It has two
during breathing, and the gastroesophageal layers, the visceral and parietal peritoneum.
sphincter which serves to prevent reflux of The visceral peritoneum lies on the surface of
gastric contents into the esophagus. the organs, and the parietal peritoneum lines
the wall of the body cavity. In between the two
The stomach is a pouch-like structure that lies layers is the peritoneal cavity. This cavity
in the left side of the abdomen and serves as a normally contains enough fluid to lubricate
food reservoir during the early stages of and prevent friction during organ movement.
digestion. It is divided into four parts namely Unlike the intestines, the peritoneum is a
cardia, fundus, body, and pylorus. Cardia is
the first part and is located near the esophageal
opening. The fundus is anatomically superior
to the cardia and functions as a temporary
storage area. The body is the main part of the
stomach. Pyloric antrum is a funnel-shaped
portion that narrows to form the pyloric canal
as it approaches the small intestine. At the end
of the pyloric canal is a circular smooth
muscle forming the pyloric sphincter that acts
as a valve that controls gastric emptying into
the small intestine. The inner surface of the
stomach has longitudinal folds called rugae
which facilitate expansion and filling of the
stomach.

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Peptic Ulcer Disease
sterile part of the GI tract.
GASTRIC AND DUODENAL
SECRETIONS
Gastric secretions serve two purposes,
production of mucus to lubricate and protect
the mucosal layer of the GI tract wall, and to
secrete fluids and enzymes to aid in the
digestion and absorption of nutrients.
Gastric secretion has three phases: cephalic,
gastric, and intestinal phase. Cephalic phase
starts when the parasympathetic impulse is
stimulated by the smell, taste, sight and
thought of food. This parasympathetic impulse
stimulates the pyloric region of the stomach,
specifically the G cells to secrete Gastrin.
Parasympathetic impulse with gastrin will
stimulate the enterochromaffin-like (ECL)
cells in the gastric glands to release Histamine
which causes additional gastric secretion.
Also, parasympathetic impulse will stimulate
the vagus nerve which triggers acetylcholine
secretion that suppresses somatostatin and
stimulates the gastric glands to secrete gastric
juices which leads to increased hydrochloric
acid and pepsin.
Gastric phase starts when a person ingests
food then the walls of the stomach will distend
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causing secretion of Gastrin which binds with
Cholecystokinin Type B receptor cells to
produce hydrogen secretions, which will then
increase gastric juice. As food enters the
stomach and mixes with gastric juice, the pH
of the contents rises, which enhances gastrin
secretion.
For the stomach to secrete hydrochloric acid,
hydrogen ions are actively transported into the
stomach. Hydrogen ions attracts negatively
charged chloride ions from the blood moving
to the stomach, then an equivalent number are
of alkaline bicarbonate are released into the
blood, and the excess bicarbonate will be
excreted in the urine. This phenomenon is
called the alkaline tide.
The intestinal phase begins when food or
chyme leaves the stomach and enters the small
intestine, particularly the duodenum. Entrance
of chyme will cause the small intestinal wall to
secrete intestinal cell hormone intestinal
gastrin which will cause the increase in gastric
gland secretion. This continuous increase in
gastric gland secretion will then stimulate the
sympathetic reflex causing the inhibition of
gastric juice secretion. Another factor that can
also inhibit the secretion of gastric juices is the
secretion of intestinal somatostatin by the
small intestinal wall when chyme reaches the
duodenum.
Chyme which contains proteins and fats will
cause the secretion of cholecystokinin and
release of secretin. Cholecystokinin is secreted
by the mucosa of the jejunum to stimulate the
gall bladder to pour bile into the small
intestine; it also decreases the gastric motility
which aids in digestion and absorption.
Secretin release causes the relaxation of the
hepatopancreatic sphincter that causes the
release of pancreatic juice which is rich in
bicarbonate and it also triggers the contraction
of the gall bladder to release bile which is also
highly alkaline.
Another gland that is stimulated by chyme is
the Brunner’s glands which secrete large
Peptic Ulcer Disease
amounts of alkali mucus that separates
duodenal inner wall from the digestive
enzymes and gastric acid and contributes to
the alkalinisation of chyme.
PEPTIC ULCER DISEASE
Peptic Ulcer Disease is an ulcerative condition
of the gastrointestinal tract that results from
acid-pepsin imbalance. It is thought to develop
when the aggressive proteolytic activities of
the gastric secretions are greater than their
normal protective abilities. An increase in acid
and pepsin secretion may produce ulcerations
if the protective mechanisms are inadequate.
Peptic activity alone is not responsible for any
ulcerations; individual susceptibility is
necessary.
Peptic ulcers are more likely to occur in the
duodenum affecting 70% of the patients with
PUD than gastric ulcers affecting 10% or less
with today’s available treatments.
The most common cause of PUD is the
causative agent Helicobacter Pylori which can
be found in 95%-100% of duodenal ulcer
cases. H. Pylori affect 50% of the world’s
population, and is more common in
developing countries than in developed
countries because of hygiene and
environmental factors. Its mode of
transmission is believed to be oral-oral and
fecal-oral routes. Infection with H. Pylori
mostly doesn’t have any symptoms in the early
stages, but will cause symptoms in the latter
stages of infection.
Second most common cause is the Non-
steroidal anti-inflammatory drugs (NSAIDs)
which cause ulceration in 15%-25% of patients
taking it regularly. It causes topical irritation
of the gastric mucosa through inhibition of
prostaglandin production as a result of COX-1
protein mechanism inhibition.
Other additional factors are the smoking and
alcohol. It is still studied if the nicotine is the
substance that is responsible for the increase in
acid secretion, decrease in prostaglandin and
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bicarbonate production, and a decrease in
mucosal blood flow which inhibits ulcer repair
or epithelial cell restitution which results to
slower ulcer healing. Alcohol is also believed
to be playing a role in increasing acid secretion
contributing to ulceration and also delaying
ulcer healing. Other factors that are believed to
also cause detrimental effect on the stomach
and duodenum are caffeine, spicy foods, and
sodas which don’t have enough study to
support the hypotheses.
Gastric Ulcers more commonly occur in the
age group of 50-70 years old because old age
can cause degeneration of the cells in the
stomach and duodenum which are needed in
producing mucosal protective barriers in the
stomach and duodenum. It was said earlier that
an imbalance between mucosal protective
barriers and erosive factors causes ulceration.
Therefore, even if the secretion of erosive
factors in the stomach of an elderly is low or in
normal amounts, but the protective barrier is
damaged; it will still result to ulceration.
People with gastric ulcers often experience
more weight loss, anorexia, and vomiting
because whenever they eat, the stomach will
be aggravated by food which will cause pain to
the patient and will encourage him/her to not
eat anymore.
Duodenal ulcer most commonly occurs in the
younger age group of 25-50 years old because
of lifestyle and environment factors. Pain in
this type of ulcer happens 2-3 hours after meal
or in the middle of the night when the stomach
is empty. Pain is relieved by ingestion of food
or antacids, thus creating the pain—food—
relief pattern. Some individuals may have no
symptoms, or may have a symptom of
“hunger-like” pain in the epigastric area.
Complications of duodenal ulcer may include
bleeding, perforation, and obstruction in the
duodenum.
Peptic Ulcer Disease

Upon physical examination. Patient

complains of worsening pain, lying motionless
in bed, widespread guarding and percussion
tenderness. Bowel sounds are decreased.

Radiograph result: Duodenal perforation

Admitting Diagnosis: Duodenal perforation

secondary to duodenal ulcer T/C peritonitis

Few hours after admission, the patient

developed peritonitis.

Diagnostics: Hgb: 17.3 g/dL (12.0-15.5 g/dL)

Hct: 48% (35-45%); WBC: 15, 000/cu mm (4,
800-10, 800/cu mm)

Paracentesis: Peritoneal fluid samples contain

blood, pus/exudate, amylase or bile.

Signs and symptoms: Rigid (board-like)

abdomen, constant severe pain, abdominal
distention, hyperthermia
Case Study

Patient’s Information
References:
Name: Mrs. DMP
Age: 48 years old
Occupation: Advertising sales manager
Chief complaint: Severe epigastric pain
(10/10)
History of Present Illness. 3 hours PTA,
patient felt severe stabbing pain in the
epigastric area. She feels the pain radiating to
her back. She also felt nauseated and vomited
once. She had a bowel movement 8 hours ago,
with no reported changes.
Patient has been taking OTC NSAID
(ibuprofen) 400 mg for 18 months, due to knee
pain, caused by a car accident 3 years ago.
Patient also drinks “maybe 3 litres” of alcohol
a week at social events with clients
• Vital signs: BP: 120/80mmHg; PR:
104bpm, regular; RR: 17cpm; Temp.:
37.1 ºc; O2 sat: 99% in room air
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Peptic Ulcer Disease

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