PEPTIC ULCER

DISEASE
“something is eating at
me”
PREPARED BY:
BOB–JHONSON B. TAGUBA
BSN - III
ANATOMY AND PHYSIOLOGY OF
GI TRACT
PEPTIC ULCER
 A peptic ulcer is an excavation (hollowed-out area)
that forms in the mucosal wall of the stomach, in
the pylorus (opening between stomach and
duodenum), in the duodenum (first part of small
intestine), or in the esophagus.
 A peptic ulcer is frequently referred to as a gastric,
duodenal, or esophageal ulcer, depending on its
location, or as peptic ulcer disease.
 Erosion of a circumscribed area of mucous
membrane is the cause.
PEPTIC ULCER DISEASE
STOMACH DEFENSE SYSTEMS
 Mucous layer
 Coats and lines the stomach
 First line of defense
 Bicarbonate
 Neutralizes acid
 Prostaglandins
 Hormone-like substances that keep blood vessels
dilated for good blood flow
 Thought to stimulate mucus and bicarbonate
production
DUODENAL ULCERS
 Duodenal ulcers have a higher incidence than
gastric ulcers. These ulcers usually occur within 1.5
cm (0.6 inch) of the pylorus and are usually
characterized by high gastric acid secretion.
 Hypersecretion of acid is attributed to a greater
mass of parietal cells.
 Stimuli for acid secretion include protein-rich
meals, alcohol consumption, calcium, and vagal
stimulation.
 Clients with a duodenal ulcer experience low pH
levels in the duodenum for longer periods. The
stomach lining is more sensitive to gastrin and
secretes excess gastrin.
 Finally, clients with duodenal ulcers have more
rapid gastric emptying.
 the combined effect of hypersecretion of acid and
rapid emptying of food from the stomach reduces
the buffering effect of food and results in large
acid load in the duodenum.
 Within the duodenum, inhibitory mechanisms and
pancreatic secretion (an alkaline solution) may be
insufficient to control the acid load.
GASTRIC ULCERS
 Gastric ulcers, which tend to heal within a few weeks,
from within 1 inch (2.5 cm) of the pylorus of the
stomach in an area where gastritis in common.
 Gastric ulcers are probably caused by break in the
mucosal barrier.
 The reflux of bile acids through an incompetent
pylorus into the stomach may break the mucosal
barrier.
 Decreased blood flow to the gastric mucosa may also
alter the defensive barrier and may make the duodenum
more susceptible to gastric acid and pepsin trauma.
 The recurrence rate of gastric ulcer is lower than that of
duodenal ulcer.
 CLASSIFICATION OF PEPTIC ULCER
ASSESSMENT DATA DUODENAL ULCERS GASTRIC ULCERS

Location of ulcer ¼ to 1 inch from pylorus Junction of fundus and

pylorus, some in antrum

Acid secretion Increased Normal to decreased

Serum pepsinogen I Increased Normal

Serum gastrin
Fasting Normal Elevated
Postprandial Elevated
Blood group Most frequently type O No difference

Age at onset 25-50 years Peaks at 45-54 years

Gender predominance Men to women, 4:1 Men to women, 2:1

ASSESSMENT DATA DUODENAL ULCERS GASTRIC ULCERS

Associated gastritis None Common and increased

Pain Occurs on empty stomach, Variable pain pattern; may

2-3 hr after meals or in be made worse by food;
middle of night; relieved antacids ineffective
by food and antacids
Nutritional status Usually well nourished Probably malnourished

Malignancy potential Rare, no increase in Occurs in approximately

incidence 10% of clients

Bleeding pattern Melena more common than Hematemesis more

hematemesis common than melena

Recurrence May occurs marginal Recurrence unlikely after

ulcers after surgery surgery
STRESS-INDUCED AND DRUG-INDUCED ULCERS
 Besides peptic ulcers, acute gastric erosion, frequently
called stress ulcers or stress erosive gastritis, can occur
after an acute medical crisis. Major assaults that give
rise to gastroduodenal ulcerations include the following:
-Severe trauma or major illness
-Severe burns (may cause what is known as Curling’s
ulcers)
-Head injury or intracranial disease (frequently called
Cushing’s ulcers)
-Ingestion of a drug (e.g., aspirin, NSAIDs, steroids, and
alcohol) that acts on the gastric mucosa
-Shock
-Sepsis
 ETIOLOGY AND RISK
FACTORS
 Lifestyle
 Smoking (nicotine)
 Chewing tobacco
 Acidic drinks
 Alcohol
 Medications or drugs (e.g.,
steroids,aspirin,NSAIDS,caffein,)
 Stress
 H. Pylori infection
 90% have this bacterium
 Passed from person to person (fecal-oral route or oral-oral
route)
 Age
 Duodenal: 25-50
 Gastric: 45-54 years old
 Gender
 Duodenal: Men to women, 4:1
 Gastric: Men to women, 2:1
 Medical condition
 Crohn’s disease
 Zollinger-Ellison Syndrome
 Hepatic and Biliary disease
Helicobacter pylori infection
PATHOPHYSIOLOGY
CLINICAL MANIFESTATION
 Acute pain
 Sharp, burning, pyrosis (heartburn),
aching,cramplike, gnawing pain
 Epigastric tenderness
 Gastric:
epigastrium; left of midline
 Duodenal: mid to right of epigastrium
 Nausea and vomiting
 Dyspepsia (indigestion)
 Bleeding
GASTRIC ULCERS
 Pain occurs 1-2 hours after meals
 Pain usually does not wake patient
 Accentuated by ingestion of food
 Risk for malignancy
 Deep and penetrating and usually occur on the
lesser curvature of the stomach
DUODENAL ULCERS
 Pain occurs 2-4 hours after meals
 Pain wakes up patient
 Pain relieved by food
 Very little risk for malignancy
 ASSESSMENT AND DIAGNOSTIC FINDINGS
 Physical assessment may reveal pain, epigastric tenderness, or abdominal
distention.
 A barium study of the upper GI tract may show an ulcer; however,
endoscopy is the preferred diagnostic procedure because it allows direct
visualization of inflammatory changes, ulcers, and lesions.
 Through endoscopy, a biopsy of the gastric mucosa and of any suspicious
lesions can be obtained.
 Stools may be tested periodically until they are negative for occult blood.
 Gastric secretory studies are of value in diagnosing achlorhydria and
ZES.
 H. pylori, infection may be determined by biopsy and histology with
culture.
 There is also a breath test that detects H. pylori, as well as a serologic test
for antibodies to the H. pylori antigen.
 Pain that is relieved by ingesting food or antacids and absence of pain on
arising are also highly suggestive of an ulcer.
DIAGNOSTIC TESTS
 Esophagogastrodeuodenoscopy (EGD)
Endoscopic procedure
 Visualizes ulcer crater
 Ability to take tissue biopsy to R/O cancer and
diagnose H. pylori
Upper gastrointestinal series (UGI)
 Barium swallow
 X-ray that visualizes structures of the upper GI
tract
Urea Breath Testing
 Used to detect H.pylori
 Client drinks a carbon-enriched urea solution
 Excreted carbon dioxide is then measured
COMPLICATIONS OF PEPTIC ULCER
 Hemorrhage
 Blood vessels damaged as ulcer erodes into the
muscles of stomach or duodenal wall
 Coffee ground vomitus or occult blood in tarry stools
 Perforation
 An ulcer can erode through the entire wall
 Bacteria and partially digested fool spill into
peritoneum=peritonitis
 Narrowing and obstruction (pyloric)
 Swelling and scarring can cause obstruction of food
leaving stomach=repeated vomiting
MEDICAL MANAGEMENT
 The primary objective of intervention for peptic
ulcer is to provide stomach rest.
 Approaches include neutralizing or buffering
hydrochloric acid, inhibiting acid secretion,
decreasing the activity of pepsin and hydrochloric
acid, and eradicating H. pylori from the G.I. tract.
SPECIFIC MEASURES INCLUDE:
 Pharmacologic therapy
 Physical and emotional rest
 Dietary management
 Stress reduction and rest
 Smoking cessation
PHARMACOLOGIC THERAPY/PRIMARY GOALS
 Provide pain relief
 Antacids and mucosa protectors
 Eradicate H. pylori infection
 Two antibiotics and one acid suppressor
 Heal ulcer
 Eradicate infection
 Protect until ulcer heals
 Prevent recurrence
 Decrease high acid stimulating foods in susceptible people
 Avoid use of potential ulcer causing drugs
 Stop smoking
HYPOSECRETORY DRUGS
 Prostaglandin Analogs
Proton Pump Inhibitors
 Reduce

Suppressgastric acid and enhances mucosal resistance to injury
acid production
 Cytotec

Prilosec, Prevacid

 Mucosal barrier
H2-Receptor fortifiers
Antagonists
 Forms a protective coat
 Block histamine-stimulated gastric secretions
 Carafate/Sucralfate
 Zantac, Pepcid, Axid
 cytoprotective
 Antacids
 Neutralizes acid and prevents formation of pepsin (Maalox,
Mylanta)
 Give 2 hours after meals and at bedtime
DIETARY MANAGEMENT
 The intent of dietary modification for patients
with peptic ulcers is to avoid oversecretion of acid
and hypermotility in the G.I. tract.
 These can be minimized by avoiding extremes of
temperature 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).
STRESS REDUCTION AND REST
 Reducing environmental stress requires physical and
physiological modifications on the patient’s part as well
as the aid and cooperation of family members and s.o.
 The patient may need help in identifying situations that
are stressful and exhausting.
 A rushed lifestyle and an irregular schedule may
aggravate symptoms and interfere with the regular meals
taken in relaxed setting and 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, or behavior modification may be
helpful.
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.
 Smoking cessation support groups and other
smoking cessation approaches are helpful for
many patients.
SURGICAL MANAGEMENT
TYPES OF OPERATIONS
 VAGOTOMY- is performed to eliminate

the acid-secreting stimulus to gastric cells.

Three types of vagotomy:
 TRUNCAL VAGOTOMY- each vagus nerve is
completely cut.
 SELECTIVE VAGOTOMY- the surgeon partially severs
the nerves to preserve the hepatic and celiac branches.
 PROXIMAL VAGOTOMY- partial cutting is
performed, but only the parietal cell mass is
denervated; innervation of both the antrum and the
pyloric sphincter is preserved.
 VAGOTOMY WITH PYLOROPLASTY
-involves cutting the right and left vagus nerves
and widening the existing exit of the stomach at the
pylorus. This procedure prevents stasis and enhances
emptying, thereby preventing belching, weight loss,
and feelings of fullness.

 GASTROENTEROSTOMY

-a simple gastroenterostomy permits

regurgitation of alkaline duodenal contents, thereby
neutralizing gastric acid.
 ANTRECTOMY

-is performed to reduce the acid-secreting portions of the

stomach. The procedure removes the entire antrum of he
stomach; thus the cells that secrete gastrin secreted.

 SUBTOTAL GASTRECTOMY

-a generic term referring to any surgery that involves

partial removal of the stomach, may be accomplished by
either a Billroth I or Billroth II procedure.
 BILLROTH I- the surgeon removes part of the distal
portion of the stomach, including the antrum. The
remainder of the stomach is anastomosed to the
duodenum. This combined procedure is more properly
called gastroduodenostomy. It decreases the incidence of
dumping syndrome that often occurs after a Billroth II
procedure.
 BILLROTH II- resection involves reanastomosis
of the proximal remnant of the stomach to the
proximal jejunum. Pancreatic secretions and bile
continue to be secreted into the duodenum, even
after gastrectomy.
 TOTAL GASTRECTOMY

-total resection of the stomach is the principal

intervention for extensive gastric cancer. This
surgery involves removal of the stomach, with
anastomosis of the esophagus to the jejunum, an
esophagojejunostomy.
SUBTOTAL GASTRECTOMY
COMPLICATIONS OF
GASTRIC SURGERIES
 Marginal Ulcers
 Hemorrhage
 Alkaline Reflux Gastritis
 Acute Gastric Dilation
 Nutritional Problems
 Dumping Syndrome
 Gastrojejunocolic Fistula
 Pyloric Obstruction
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