Transcript Peptic Ulcers

(Relates to Chapter 42,
“Nursing Management:
Upper Gastrointestinal Problems,”
in the textbook)
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Peptic Ulcer Disease (PUD)
 500,000 new cases of ulcers diagnosed
each year
 4 million recurrences each year
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Peptic Ulcer Disease
 Erosion of GI mucosa resulting from
digestive action of HCl acid and pepsin
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Peptic Ulcer Disease
 Ulcer development can occur in
 Lower esophagus
 Stomach
 Duodenum
 Margin of gastrojejunal anastomosis after
surgical procedures
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Types of PUD
 Gastric vs. duodenal
 Location
 Acute vs. chronic
 Depends on degree/duration of mucosal
involvement
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Types of PUD
 Acute
 Superficial erosion
 Minimal inflammation
 Short duration, resolves quickly when
cause is identified and removed
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Peptic Ulcers
Fig. 42-10. Peptic ulcers, including an erosion, an acute ulcer, and a chronic
ulcer. Both the acute ulcer and the chronic ulcer may penetrate the entire
wall of the stomach.
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Types of PUD
 Chronic
 Muscular wall erosion with formation of
fibrous tissue
 Long duration—present continuously for
many months or intermittently
 More common than acute erosion
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Peptic Ulcer of the Duodenum
Fig. 42-11. Peptic ulcer of the duodenum.
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Etiology and Pathophysiology
 Develops only in the presence of an
acid environment
 Excess of gastric acid not necessary for
ulcer development
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Etiology and Pathophysiology
 Pepsinogen is activated to pepsin in
presence of HCl acid and at pH of
2 to 3.
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Etiology and Pathophysiology
 Stomach normally protected from
autodigestion by gastric mucosal
barrier
 Surface mucosa of stomach is renewed
about every 3 days.
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Pathophysiology of Ulcer
Development
Fig. 42-12. Disruption of gastric mucosa
and pathophysiologic consequences of
back diffusion of acids.
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Etiology and Pathophysiology
 Mucosa can continually repair itself,
except in extreme instances.
 Water, electrolytes, and water-soluble
substances can pass through barrier.
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Etiology and Pathophysiology
 Mucosal barrier prevents back diffusion
of acid and pepsin from gastric lumen
through mucosal layers to underlying
tissue.
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Etiology and Pathophysiology
 Mucosal barrier can be impaired, and
back diffusion can occur.
 Cellular destruction and inflammation
occur.
 Release of histamine



Vasodilation
Increased capillary permeability
Secretion of acid and pepsin
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Relationship of Mucosal Blood Flow
and Gastric Mucosal Barrier
Fig. 42-13. Relationship between mucosal blood
flow and disruption of the gastric mucosal barrier.
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Etiology and Pathophysiology
 Destroyers of mucosal barrier
 Helicobacter pylori
 Produces enzyme urease

Mediates inflammation, making mucosa more
vulnerable
 Aspirin and NSAIDs
 Inhibit syntheses of prostaglandins

Cause abnormal permeability
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Etiology and Pathophysiology
 Destroyers of mucosal barrier (cont’d)
 Corticosteroids
 ↓ rate of mucosal cell renewal

↓ protective effects
 Lifestyle factors
 Alcohol, coffee, smoking, psychologic stress
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Gastric Ulcers
 Occur in any portion of stomach
 Western countries—less common than
duodenal ulcers
 Prevalent in women, older adults
 Peak incidence >50 years of age
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Gastric Ulcers
 Risk factors
 H. pylori
 Medications
 Smoking
 Bile reflux
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Duodenal Ulcers
 Occur at any age and in anyone
 ↑ between ages of 35 and 45 years
 Account for ~80% of all peptic ulcers
 Familial tendency
 Person with blood group O ↑ risk
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Duodenal Ulcers
 Associated with increased HCl acid
secretion
 H. pylori is found in 90% to 95% of
patients.
 Not all individuals with H. pylori develop
ulcers.
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Duodenal Ulcers
 Increased risk of duodenal ulcers in
those with
 COPD
 Cirrhosis of liver
 Chronic pancreatitis
 Hyperparathyroidism
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Duodenal Ulcers
 Increased risk of duodenal ulcers
(cont’d)
 Chronic renal failure
 Zollinger-Ellison syndrome
 Smoking and alcohol use
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Stress-Related Mucosal Disease
 Also called physiologic stress ulcer
 Acute ulcers that develop after major
physiologic insult
 Trauma or surgery
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Clinical Manifestations
 Pain high in epigastrium
 1 to 2 hours after meals
 “Burning” or “gaseous”
 Food aggravates pain as ulcer has eroded
through gastric mucosa.
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Clinical Manifestations
 Duodenal ulcer pain
 Midepigastric region beneath xiphoid process
 Back pain—if located in posterior aspect
 2 to 5 hours after meals
 “Burning” or “cramplike”
 Tendency to occur, then disappear, then occur
again
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Complications
 Three major complications include
 Hemorrhage
 Perforation
 Gastric outlet obstruction
 All considered emergency situations
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Hemorrhage
 Most common complication of peptic
ulcer disease
 Develops from erosion of
 Granulation tissue found at base of ulcer
during healing
 Ulcer through a major blood vessel
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Perforation
 Most lethal complication of peptic ulcer
 Common in large penetrating duodenal
ulcers that have not healed and are
located on posterior mucosal wall
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Perforation
Fig. 42-14. Duodenal ulcer of the posterior
wall penetrating into the head of the
pancreas, resulting in walled-off perforation.
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Perforation
 Perforated gastric ulcers often located
on lesser curvature of stomach
 Mortality rates higher with perforation
of gastric ulcers
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Perforation
 When ulcer penetrates serosal surface
with spillage of contents into
peritoneal cavity
 Size proportionate to length of time
ulcer existed
 Large perforations: Immediate surgical
closure
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Perforation
 Clinical manifestations
 Sudden, dramatic onset
 Severe upper abdominal pain spreads
throughout abdomen.
 Tachycardia, weak pulse
 Rigid, board-like abdominal muscles
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Perforation
 Clinical manifestations (cont’d)
 Shallow, rapid respirations
 Bowel sounds absent
 Nausea/vomiting
 History reporting symptoms of
indigestion or previous ulcer
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Perforation
 Bacterial peritonitis may occur within 6
to 12 hours.
 Difficult to determine from symptoms
alone if gastric or duodenal ulcer has
perforated
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Gastric Outlet Obstruction
 Predisposition to gastric outlet
obstruction includes
 Ulcers located in
 Antrum and prepyloric and pyloric areas of
stomach
 Duodenum
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Gastric Outlet Obstruction
 Obstruction due to
 Edema
 Inflammation
 Pylorospasm
 Fibrous scar tissue formation
 All contribute to narrowing of pylorus.
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Gastric Outlet Obstruction
 Early phase: Gastric emptying normal
 Over time, ↑ contractile force needed
to empty stomach
 Hypertrophy of stomach wall
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Gastric Outlet Obstruction
 After long-standing obstruction
 Stomach dilates and becomes atonic.
 Clinical manifestations
 Usually long history of ulcer pain
 Pain progresses to generalized upper
abdominal discomfort.
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Gastric Outlet Obstruction
 Clinical manifestations (cont’d)
 Pain worsens toward end of day as
stomach fills and dilates.
 Relief obtained by belching or vomiting
 Vomiting is common.
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Gastric Outlet Obstruction
 Clinical manifestations (cont’d)
 Constipation is a common complaint.
 Dehydration, lack of roughage in diet
 Swelling in stomach and upper abdomen
 Loud peristalsis
 Visible peristaltic waves
 If stomach grossly dilated, may be
palpable
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Diagnostic Studies
 To determine presence and location of
ulcer
 Similar to those used for acute upper GI
bleed
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Diagnostic Studies
 Endoscopy with biopsy
 Most often used
 Allows for direct viewing of mucosa
 Determines degree of ulcer healing after
treatment
 During procedure, tissue specimens can
be obtained to identify H. pylori and rule
out gastric cancer.
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Diagnostic Studies
 Tests for H. pylori
 Noninvasive tests
 Serum or whole blood antibody tests

Immunoglobin G (IgG)
 Will not distinguish between active and recently
treated disease
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Diagnostic Studies
 Noninvasive tests (cont’d)
 Urea breath test


Can determine active infection
Stool antigen test

Not as accurate as breath test
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Diagnostic Studies
 Tests for H. pylori (cont’d)
 Invasive tests
 Endoscopic procedure
 Biopsy of stomach

Rapid urease test
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Diagnostic Studies
 Barium contrast studies
 Reserved for patient who cannot undergo
endoscopy
 Not accurate for shallow, superficial ulcers
 Used in diagnosis of gastric outlet
obstruction
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Diagnostic Studies
 X-ray studies
 Ineffective in distinguishing a peptic ulcer
from a malignant tumor
 Do not show degree of healing
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Diagnostic Studies
 Gastric analysis
 Analyze gastric contents for acidity and
volume
 NG tube is inserted, and gastric contents
are aspirated.
 Contents analyzed for HCl acid
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Diagnostic Studies
 Laboratory analysis
 CBC
 Anemia
 Urinalysis
 Liver enzyme studies
 Serum amylase determination
 Pancreatic function
 Stool examination
 Presence of blood
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Collaborative Care
 Medical regimen consists of
 Adequate rest
 Dietary modification
 Drug therapy
 Elimination of smoking and alcohol
 Long-term follow-up care
 Stress management
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Collaborative Care
 Aim of treatment program
 Reduce degree of gastric acidity
 Enhance mucosal defense mechanisms
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Collaborative Care
 Generally treated in ambulatory care
clinics
 Ulcer healing requires many weeks of
therapy.
 Pain disappears after 3 to 6 days.
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Collaborative Care
 Complete healing may take 3 to 9
weeks.
 Should be assessed by means of x-rays or
endoscopic examination
 Aspirin and nonselective NSAIDs may
be stopped.
 Smoking cessation
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Drug Therapy
 Use of
 H2R blockers
 PPIs
 Antibiotics
 Antacids
 Anticholinergics
 Cytoprotective therapy
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Drug Therapy
 Histamine-2 receptor blockers (H2R
blockers)
 Frequently used
 Block action of histamine on H2 receptors
 ↓ HCl acid secretion
 ↓ conversion of pepsinogen to pepsin
 ↑ ulcer healing
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Drug Therapy
 H2R blockers (cont’d)
 Therapeutic effects last up to 12 hours.
 Oral or IV
 Examples
 Cimetidine
 Ranitidine
 Famotidine
 Nizatidine
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Drug Therapy
 Proton pump inhibitors (PPI)
 Block ATPase enzyme—important for
secretion of HCl acid
 ↑ effective than H2R blockers—reducing
acid and promoting healing
 Examples


Esomeprazole
Omeprazole
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Drug Therapy
 Antibiotic therapy
 Eradicates H. pylori infection
 Most important in treatment if
H. pylori present
 No single agent has been effective in
eliminating H. pylori.
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Drug Therapy
 Antibiotic therapy (cont’d)
 Usual treatment 7 to 14 days
 Example of therapy
 Dual therapy—ranitidine bismuth citrate
(Tritec) with clarithromycin (Biaxin)
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Drug Therapy
 Antacids
 Adjunct therapy for PUD
 Increase gastric pH by neutralizing HCl
acid
 Effects on empty stomach 20 to 30
minutes
 If taken after meals, may last 3 to 4 hours
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Drug Therapy
 Antacids (cont’d)
 Systemic vs. nonsystemic
 Systemic




Rarely used for PUD
Extremely soluble and absorbed into circulation
Long-term use can cause alkalosis.
Sodium bicarbonate (Alka-Seltzer)
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Drug Therapy
 Antacids (cont’d)

Nonsystemic



Insoluble and poorly absorbed
Magnesium hydroxide (Mag-Ox)
 Watch for diarrhea.
Aluminum hydroxide (Amphojel)
 Watch for constipation.
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Drug Therapy
 Antacids (cont’d)
 ↑ sodium preparations: Not to be used in
elderly or patients with ↑BP, heart failure,
liver cirrhosis, or renal disease
 Magnesium preparations: Not to be used
in patients with renal failure
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Drug Therapy
 Antacids (cont’d)
 Interact unfavorably with some drugs
 Health care provider must know all drugs
being taken before therapy is begun.
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Drug Therapy
 Cytoprotective drug therapy
 Used for short-term treatment
 Protection for esophagus, stomach, and
duodenum
 Accelerates ulcer healing
 Example


Sucralfate (Carafate)
Misoprostol (Cytotec)
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Drug Therapy
 Anticholinergic drugs
 Occasionally used
 ↓ cholinergic stimulation of HCl acid
 ↓ gastric motility: Not used for gastric
outlet obstruction
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Drug Therapy
 Tricyclic antidepressants
 Pain relief
 Anticholinergic properties
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Nutritional Therapy
 Dietary modifications: Food and
beverages irritating to patient are
avoided or eliminated.
 Bland diet may be recommended.
 Six small meals a day during
symptomatic phase
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Therapy Related to Complications
 Acute exacerbation
 Treated with same regimen used for
conservative therapy
 Situation is more serious because of
possible complications of perforation,
hemorrhage, and gastric outlet
obstruction.
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Therapy Related to Complications
 Acute exacerbation (cont’d)
 Accompanied by bleeding, increased pain
and discomfort, nausea, and vomiting
 Endoscopic evaluation

Reveals degree of inflammation or bleeding
and ulcer location
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Therapy Related to Complications
 Perforation
 Immediate focus:
 Stop spillage of gastric or duodenal contents
into peritoneal cavity.
 Restore blood volume.
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Therapy Related to Complications
 Perforation (cont’d)
 NG tube is placed into stomach.
 Continuous aspiration
 Placement of tube near to perforation site
facilitates decompression.
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Therapy Related to Complications
 Perforation (cont’d)
 Circulating blood volume: Replaced with
lactated Ringer’s and albumin solutions
 Blood replacement in form of packed
RBCs may be necessary.
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Therapy Related to Complications
 Perforation (cont’d)
 Central venous pressure line inserted and
monitored hourly
 Indwelling urinary catheter inserted and
monitored hourly
 ECG—if history of cardiac disease
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Therapy Related to Complications
 Perforation (cont’d)
 Broad-spectrum antibiotics
 Pain medication
 Open or laparoscopic repair
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Therapy Related to Complications
 Gastric outlet obstruction
 Decompress stomach.
 Correct any existing fluid and electrolyte
imbalances.
 Improve patient’s general state of health.
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Therapy Related to Complications
 Gastric outlet obstruction (cont’d)
 NG tube inserted in stomach, attached to
continuous suction
 Continuous decompression allows



Stomach to regain its normal muscle tone
Ulcer to begin to heal
Inflammation and edema to subside
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Therapy Related to Complications
 Gastric outlet obstruction (cont’d)
 After several days, NG clamped and
residual volumes checked
 Common to clamp tube overnight for
8 to 12 hours and measure residual in
morning
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Therapy Related to Complications
 Gastric outlet obstruction (cont’d)
 When aspirate below 200 mL
 Within normal range
 Oral intake of clear liquids can begin
 Watch patient carefully for signs of
distress or vomiting.
 As residual ↓, solid foods added and tube
removed
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Therapy Related to Complications
 Gastric outlet obstruction (cont’d)
 IV fluids and electrolytes
 Administered according to degree of
dehydration, vomiting, electrolyte imbalance
 Pyloric obstruction: Endoscopically
treated with balloon dilations
 Surgery may be necessary to remove scar
tissue.
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Nursing Assessment
 Past health history
 Medication usage
 Heartburn
 Weight loss
 Black, tarry stools
 Epigastric tenderness
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Nursing Assessment
 Nausea and vomiting
 Abnormal laboratory values
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Nursing Diagnoses
 Acute pain
 Ineffective self-health management
 Nausea
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Nursing Management
 Overall goals
 Comply with prescribed therapeutic
regimen.
 Experience a reduction in or absence of
discomfort.
 Exhibit no signs of GI complications.
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Nursing Management
 Overall goals (cont’d)
 Have complete healing.
 Lifestyle changes can prevent recurrence.
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Nursing Implementation
 Health promotion
 Identify patients at risk.
 Provide early detection and treatment.
 Encourage patients to take ulcerogenic
drugs with food or milk.
 Teach patient to report to health care
provider symptoms related to gastric
irritation.
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Nursing Implementation
 Acute intervention
 General complaints include increased
pain, nausea, vomiting, and some
bleeding.
 Convey treatment measures to
patient/family.
 Provide regular mouth care.
 Cleanse and lubricate nares if NG tube is
in place.
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Nursing Implementation
 Acute intervention (cont’d)
 Vital signs hourly
 Monitor I/O
 Physical and emotional rest
 Sedatives can mask symptoms of shock.
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Nursing Implementation
 Hemorrhage
 Changes in vital signs, ↑ in amount and
redness of aspirate

Signal massive upper GI bleeding
 ↑ amount of blood in gastric contents
 ↓ pain because blood neutralizes acidic
gastric contents
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Nursing Implementation
 Hemorrhage (cont’d)
 Maintain patency of NG tube.
 Prevent blood clot blockage.
 If blocked, distention results.
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Nursing Implementation
 Perforation
 Sudden, severe abdominal pain unrelated
in intensity and location to pain that
brought patient to hospital

Possibility of perforation
 Indicated by a rigid, board-like abdomen
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Nursing Implementation
 Perforation (cont’d)
 Severe generalized abdominal and
shoulder pain
 Shallow, grunting respirations
 Bowel sounds diminished or absent
 Vital signs every 15 to 30 minutes
 Stop all oral, NG feeds/drugs until health
care provider notified.
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Nursing Implementation
 Perforation (cont’d)
 IV fluids may be increased to replace
volume lost.
 Ensure any known allergies are reported
on chart.

Antibiotic therapy is usually started.
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Nursing Implementation
 Perforation (cont’d)
 Surgical or laparoscopic closure may be
necessary if perforation does not heal
spontaneously.
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Nursing Implementation
 Gastric outlet obstruction
 Can occur at any time
 Likely in patients whose ulcer is located close
to pylorus
 Gradual onset
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Nursing Implementation
 Gastric outlet obstruction (cont’d)
 Constant NG aspiration of stomach
contents may relieve symptoms.
 If occurs during treatment of acute
exacerbation


Regular irrigation of NG tube
Repositioning from side to side
 IV fluids for hydration
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Nursing Implementation
 Gastric outlet obstruction (cont’d)
 Accurate I/O
 Surgery may be performed if conservative
treatment not successful
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Ambulatory and Home Care
 Patient teaching
 Disease
 Teach basic etiology/pathophysiology.
 Drugs
 Actions, side effects, danger of taking any
medication without health care provider
approval
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Ambulatory and Home Care
 Patient teaching (cont’d)
 Lifestyle changes
 Appropriate changes in diet
 Regular follow-up care
 Discuss medications.
 Encourage compliance with plan of care.
 Importance of immediate reporting of N/V,
epigastric pain, bloody emesis, or tarry stools
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Surgical Therapy
 Uncommon because of antisecretory
agents
 Indications for surgical interventions
 Unresponsive to medical management
 Concern about gastric cancer
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Surgical Therapy
 Surgical procedures
 Billroth I: Gastroduodenostomy
 Partial gastrectomy with removal of distal 2/3
stomach and anastomosis of gastric stump to
duodenum
 Billroth II: Gastrojejunostomy
 Partial gastrectomy with removal of distal 2/3
stomach and anastomosis of gastric stump to
jejunum
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Surgical Therapy
Fig. 42-15. A, Billroth I procedure (subtotal gastric resection with
gastroduodenostomy anastomosis). B, Billroth II procedure (subtotal
gastric
resection
anastomosis).
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© 2007, with
2004, gastrojejunostomy
2000, Mosby, Inc., an affiliate
of Elsevier Inc. All Rights Reserved.
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Surgical Therapy
 Surgical therapies (cont’d)
 Vagotomy
 Severing of vagus nerve
 Can be total or selective
 Pyloroplasty
 Surgical enlargement of pyloric sphincter
 Commonly done after vagotomy
 ↓ gastric motility and gastric emptying
 If accompanying vagotomy, ↑ gastric emptying
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Postoperative Complications
 Most common
 Dumping syndrome
 Postprandial hypoglycemia
 Bile reflux gastritis
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Postoperative Complications
 Dumping syndrome
 20% of patients experience after surgery.
 Direct result of surgical removal of a large
portion of stomach and pyloric sphincter
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Postoperative Complications
 Dumping syndrome
 ↓ ability of stomach to control amount of
gastric chyme entering small intestine


Large bolus of hypertonic fluid enters
intestine
↑ fluid drawn into bowel lumen
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Postoperative Complications
 Dumping syndrome (cont’d)
 Occurs at end of meal or 15 to 30 minutes
after eating
 Symptoms include


Weakness, sweating, palpitations, dizziness,
abdominal cramps, borborygmi, urge to
defecate
Last no longer than an hour
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Postoperative Complications
 Postprandial hypoglycemia
 Variant of dumping syndrome
 Result of uncontrolled gastric emptying of
a bolus of fluid high in carbohydrate into
small intestine


↑ blood sugar
Release of excessive amounts of insulin into
circulation
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Postoperative Complications
 Postprandial hypoglycemia (cont’d)
 Secondary hypoglycemia occurs with
symptoms ~2 hours after meals.
 Symptoms include sweating, weakness,
mental confusion, palpitations,
tachycardia, and anxiety.
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Postoperative Complications
 Bile reflux gastritis
 Surgery can result in reflux alkaline
gastritis.



Prolonged contact of bile causes damage to
gastric mucosa.
May result in back diffusion of H+ ions through
gastric mucosa
PUD may reoccur.
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Postoperative Complications
 Bile reflux gastritis (cont’d)
 Continuous epigastric distress that ↑ after
meals
 Administration of cholestyramine
(Questran) relieves irritation.
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Nutritional Therapy Postoperatively
 Start as soon as immediate
postoperative period has successfully
passed.
 Patient should be advised to reduce
drinking fluid (4 oz) with meals.
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Nutritional Therapy Postoperatively
 Diet should consist of
 Small, dry feedings daily
 Low carbohydrates
 Restricted sugar with meals
 Moderate amounts of protein and fat
 30 minutes of rest after each meal
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Surgical Therapy for PUD
 Preoperative care
 Laparoscopic or open surgery techniques
 Surgeon should educate family/patient on
surgical procedure.
 Nurse can clarify questions.
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Surgical Therapy for PUD
 Postoperative care
 Similar to postop care after abdominal
laparotomy
 NG tube used to decompress and
decrease pressure on suture line
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Surgical Therapy for PUD
 Postoperative care (cont’d)
 Aspirate observed for
 Color




Bright red at first with darkening within first 24
hours
Color changes to yellow-green within 36 to 48
hours.
Amount
Odor
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Surgical Therapy for PUD
 Postoperative care (cont’d)
 NG suction must be in working order, and
patency maintained.
 Observe for signs of ↓ peristalsis and
lower abdominal discomfort.

Intestinal obstruction
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Surgical Therapy for PUD
 Postop care (cont’d)
 Accurate I/O essential
 Vital signs every 4 hours
 Frequent position changes
 IV therapy
 Observe for signs of infection.
 Long-term complication—pernicious
anemia
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Gerontologic Considerations
 ↑ patients >60 years of age
 ↑ use of NSAIDs
 First manifestation may be frank
gastric bleeding or ↓ hematocrit.
 Treatment similar to younger adults
 Emphasis placed on prevention of both
gastritis and peptic ulcers
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Audience Response Question
Diagnostic testing is planned for a patient with a suspected
peptic ulcer. The nurse explains to the patient that the most
reliable test for determining the presence and location of an
ulcer is a(n):
1. Endoscopy.
2. Gastric analysis.
3. Barium swallow.
4. Serologic test for Helicobacter pylori.
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Case Study
 55-year-old man complains of pain and
burning pressure around stomach 2 to 3
hours after eating.
 He has a history of former alcohol
abuse and smoking.
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Case Study
 He has had 10-lb weight loss in 2
months accompanied by nausea,
vomiting, and decreased appetite.
 EGD reveals ulcers; biopsy sample
positive for H. pylori
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Discussion Questions
1. He asks you how this happened. What
are his risk factors?
2. What are his treatment options?
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Discussion Questions
3. What are complications of peptic
ulcer disease?
4. What lifestyle modifications are
necessary to ensure healing?
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