Peptic Ulcer Disease: by Aniedu, Ugochukwu

Peptic Ulcer Disease
By
Aniedu, Ugochukwu
OUTLINE
• Introduction
• Pathophysiology
• Etiology/ Risk factors
• Types of PUD
• Clinical Presentation
• Investigation/ Diagnostic test
• Complications of PUD
• Management
• Summary
• References.
INTRODUCTION
• Peptic Ulcer is a lesion in the lining
(mucosa) of the digestive tract, typically in
the stomach or duodenum, caused by the
digestive action of pepsin and stomach
acid.
Lesion may subsequently occur into the lamina
propria and submucosa to cause bleeding. –
Most of peptic ulcer occur either in the
duodenum, or in the stomach – Ulcer may also
occur in the lower esophagus due to reflexing of
gastric content – Rarely in certain areas of the

PATHOPHYSIOLOGY
Under normal conditions, a physiologic balance
exists between gastric acid secretion and
gastroduodenal mucosal defense. Mucosal injury
and, thus, peptic ulcer occur when the balance
between the aggressive factors and the
defensive mechanisms is disrupted. Aggressive
factors, such as NSAIDs, H pylori infection,
alcohol, bile salts, acid, and pepsin, can alter the
mucosal defense by allowing back diffusion of
hydrogen ions and subsequent epithelial cell
injury.
ETIOLOGY/ RISK FACTORS
• Lifestyle • Gender
– Smoking – Duodenal: are increasing
– Acidic drinks in older women
– Medications • Genetic factors
– More likely if family
• H. Pylori infection member has Hx
– 90% have this bacterium • Other factors: stress
– Passed from person to can worsen but not the
person (fecal-oral route cause
or oral-oral route)
• Age
– Duodenal 30-40
– Gastric over 50
TYPES
• GASTRIC PEPTIC ULCER
• DUODENAL PEPTIC ULCER
Gastric and Duodenal Ulcers
CLINICAL PRESENTATION
INVESTIGATION/ DIAGNOSTIC TEST
INVESTIGATION
• Stool examination for fecal occult blood.
• Complete blood count (CBC) for decrease

in blood cells.
DIAGNOSTIC TEST
• 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
• Exhaled carbon dioxide is then measured
In all patients with “Alarming symptoms” endoscopy
is required.
Dysphagia.
Weight loss.
Vomiting.
Anorexia.
Hematemesis or Melena
Complications of Peptic Ulcers
• 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 food spill into
peritoneum=peritonitis
• Narrowing and obstruction (pyloric)
– Swelling and scarring can cause obstruction of food leaving
stomach=repeated vomiting
MANAGEMENT
• LIFE STYLE MODIFICATION
• HYPOSECRETORY DRUG THERAPY
• H. pylori ERADICATION THERAPY
• SURGERY
Hyposecretory Drugs
• Proton Pump Inhibitors • Prostaglandin Analogs
– Suppress acid production – Reduce gastric acid and
– Prilosec, Prevacid enhances mucosal
• resistance to injury
H2-Receptor Antagonists
– Cytotec
– Block histamine-stimulated
gastric secretions • Mucosal barrier fortifiers
– Zantac, Pepcid, Axid – Forms a protective coat
• Antacids • Carafate/Sucralfate
– cytoprotective
– Neutralizes acid and
prevents formation of pepsin
(Maalox, Mylanta)
– Give 2 hours after meals
and at bedtime
H. pylori Eradication Therapy:
Indications:
Failure of medical treatment.
Development of complications
High level of gastric secretion and
combined duodenal and gastric ulcer.
Principle:
Reduce acid and pepsin
secretion.
Types of Surgical Procedures
• GASTROENTEROSTOMY
Creates a passage between
the body of stomach to small
intestines.
Allows regurgitation of alkaline
duodenal contents into the
stomach.
Keeps acid away from ulcerated
area
• VAGOTOMY
– Cuts vagus nerve
– Eliminates acid-
secretion stimulus
• PYLOROPLASTY
– Widens the pylorus
to guarantee
stomach emptying
even without vagus
nerve stimulation
• ANTRECTOMY/ SUBTOTAL GASTRECTOMY

– Lower half of stomach (antrum) makes most of the
acid
– Removing this portion (antrectomy) decreases acid
production
• SUBTOTAL GASTRECTOMY
– Removes ½ to 2/3 of stomach
• Remainder must be reattached to the rest of the
bowel
– Billroth I
– Billroth II
Billroth I
• Distal portion of the

stomach is removed
• The remainder is
anastomosed to the
duodenum
Billroth II
• The lower portion

of the stomach is
removed and the
remainder is
anastomosed to
the jejunum
Postoperative Care
– NG tube – care and management

– Monitor for post-operative complications
Post-op Complications
• Dumping Syndrome.
– Prevalent with sub total gastrostomies
– Early-30 minutes after meals
• Bleeding – Vertigo, tachycardia, syncope, sweating,
– Occurs at the anastomosed site pallor, palpitations
– Late – 90 min-3 hours after meals
– First 24 hours and post-op days
• Rx: Decrease CHO intake, Eat slowly, Avoid
4-7
fluids during meals, Increase fat, Eat small,
• Duodenal stump leak frequent meals
– Billroth II
– Severe abdominal pain • Anemia
– Bile stained drainage on – Rapid gastric empyting decreases
absorption of iron
dressing
• Malabsorption of fat
• Gastric retention – Decreased acid secretions, decreased
– WILL NEED TO PUT NG TUBE pancreatic secretions, increased upper
BACK IN GI mobility
Summary
• H. pylori is the most common cause of PUD and
is a risk factor for gastric cancer
• H Pylori eradication reduces risk of disease
recurrence
• Test-and-Treat strategy is recommended for
patients with undifferentiated dyspepsia
• Intial evaluation with endoscopy is recommended
for those with alarm symptoms or those failing
treatment
• Optimum treatment regimens are 14d multidrug
with antibiotics and acid suppressants(Triple
therapy)
REFERENCES
• http://emedicine.medscape.com/article/181753-overview#showall. Retrieved 28th Jan,
2016
• Fendrick M, Forsch R etal. Peptic Ulcer Disease Guidleines for Clinical Care.
University of Michigan Health System May 2005
• American Gastroenterological Association medical position statement: evaluation of
dyspepsia. Gastroenterology 1998;114:579-81.
• Krogfelt K, Lehours P, Mégraud F. Diagnosis of Helicobacter pylori Infection.
Helicobacter 2005 10:s1 5
• Meurer L, Bower D. Management of Helicobacter pylori Infection. American Family
Physician Vol 65, No. 7, 2002 pp 1327-1336
• Standards of Practice Committee of the American Society for Gastrointestinal
Endoscopy; The role of endoscopy in dyspepsia. Gastrointestinal Endoscopy Vol 54,
No. 6, 2001 pp 815-817
• Vaira D, Gatta L, Ricci C, et al. Peptic ulcer and Helicobacter pylori: update on testing
and treatment. Postgrad Med 2005;117(6):17-22, 46

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Peptic Ulcer Disease: by Aniedu, Ugochukwu

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Peptic Ulcer Disease

• Peptic Ulcer is a lesion in the lining

(mucosa) of the digestive tract, typically in

the stomach or duodenum, caused by the

digestive action of pepsin and stomach

propria and submucosa to cause bleeding. –

Most of peptic ulcer occur either in the

duodenum, or in the stomach – Ulcer may also

occur in the lower esophagus due to reflexing of

gastric content – Rarely in certain areas of the

• Complete blood count (CBC) for decrease

• LIFE STYLE MODIFICATION

• HYPOSECRETORY DRUG THERAPY

• H. pylori ERADICATION THERAPY

• ANTRECTOMY/ SUBTOTAL GASTRECTOMY

• Distal portion of the

• The lower portion

– NG tube – care and management

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