Peptic Ulcer Disease

Carrie Jones
Definition
A circumscribed ulceration of
the gastrointestinal mucosa
occurring in areas exposed to
acid and pepsin and most often
caused by Helicobacter pylori
infection.
(Uphold & Graham, 2003)
Peptic Ulcers:
Gastric & Dudodenal
PUD Demographics
 Higher prevalence in developing countries
 H. Pylori is sometimes associated with
socioeconomic status and poor hygiene
 In the US:
 Lifetime prevalence is ~10%.
 PUD affects ~4.5 million annually.
 Hospitalization rate is ~30 pts per 100,000 cases.
 Mortality rate has decreased dramatically in the
past 20 years
 approximately 1 death per 100,000 cases
Comparing Duodenal
and Gastric Ulcers
Duodenal Ulcers
 duodenal sites are 4x as common as gastric sites
 most common in middle age
 peak 30-50 years
 Male to female ratio—4:1
 Genetic link: 3x more common in 1st degree relatives
 more common in patients with blood group O
 associated with increased serum pepsinogen
 H. pylori infection common
 up to 95%
 smoking is twice as common
Gastric Ulcers
 common in late middle age
 incidence increases with age
 Male to female ratio—2:1
 More common in patients with blood group A
 Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer
 Less related to H. pylori than duodenal ulcers –
about 80%
 10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer
Etiology
 A peptic ulcer is a mucosal break, 3 mm or greater,
that can involve the stomach or duodenum.
 The most important contributing factors are H pylori,
NSAIDs, acid, and pepsin.
 Additional aggressive factors include smoking,
ethanol, bile acids, aspirin, steroids, and stress.
 Important protective factors are mucus, bicarbonate,
mucosal blood flow, prostaglandins, hydrophobic
layer, and epithelial renewal.
 Increased risk when older than 50 d/t decrease protection
 When an imbalance occurs, PUD might develop.
Subjective Data
 Pain—”gnawing”, “aching”, or “burning”
 Duodenal ulcers: occurs 1-3 hours after a meal and may
awaken patient from sleep. Pain is relieved by food,
antacids, or vomiting.
 Gastric ulcers: food may exacerbate the pain while
vomiting relieves it.
 Nausea, vomiting, belching, dyspepsia, bloating,
chest discomfort, anorexia, hematemesis, &/or
melena may also occur.
 nausea, vomiting, & weight loss more common with Gastric
ulcers
Objective Data
 Epigastric tenderness
 Guaic-positive stool resulting from occult blood loss
 Succussion splash resulting from scaring or edema
due to partial or complete gastric outlet obstruction
 A succussion splash describes the sound obtained by
shaking an individual who has free fluid and air or gas in a
hollow organ or body cavity.
 Usually elicited to confirm intestinal or pyloric obstruction.
 Done by gently shaking the abdomen by holding either side
of the pelvis. A positive test occurs when a splashing noise
is heard, either with or without a stethoscope. It is not valid
if the pt has eaten or drunk fluid within the last three hours.
Differential Diagnosis
 Neoplasm of the stomach
 Pancreatitis
 Pancreatic cancer
 Diverticulitis
 Nonulcer dyspepsia (also called functional
dyspepsia)
 Cholecystitis
 Gastritis
 GERD
 MI—not to be missed if having chest pain
Diagnostic Plan
 Stool for fecal occult blood
 Labs: CBC (R/O bleeding), liver function test,
amylase, and lipase.
 H. Pylori can be diagnosed by urea breath test, blood
test, stool antigen assays, & rapid urease test on a
biopsy sample.
 Upper GI Endoscopy: Any pt >50 yo with new onset of
symptoms or those with alarm markings including
anemia, weight loss, or GI bleeding.
 Preferred diagnostic test b/c its highly sensitive for dx of
ulcers and allows for biopsy to rule out malignancy and rapid
urease tests for testing for H. Pylori.
Treatment Plan: H. Pylori
 Medications: Triple therapy for 14 days is considered the
treatment of choice.
 Proton Pump Inhibitor + clarithromycin and amoxicillin
 Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
 Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN
 In the setting of an active ulcer, continue qd proton pump
inhibitor therapy for additional 2 weeks.
 Goal: complete elimination of H. Pylori. Once achieved
reinfection rates are low. Compliance!
Treatment Plan: Not H. Pylori
 Medications—treat with Proton Pump
Inhibitors or H2 receptor antagonists to assist
ulcer healing
 H2: Tagament, Pepcid, Axid, or Zantac for up to 8
weeks
 PPI: Prilosec, Prevacid, Nexium, Protonix, or
Aciphex for 4-8 weeks.
Lifestyle Changes
 Discontinue NSAIDs and use Acetaminophen for
pain control if possible.
 Acid suppression--Antacids
 Smoking cessation
 No dietary restrictions unless certain foods are
associated with problems.
 Alcohol in moderation
 Men under 65: 2 drinks/day
 Men over 65 and all women: 1 drink/day
 Stress reduction
Prevention
 Consider prophylactic therapy for the following patients:
 Pts with NSAID-induced ulcers who require daily NSAID therapy
 Pts older than 60 years
 Pts with a history of PUD or a complication such as GI bleeding
 Pts taking steroids or anticoagulants or patients with significant
comorbid medical illnesses
 Prophylactic regimens that have been shown to dramatically
reduce the risk of NSAID-induced gastric and duodenal ulcers
include the use of a prostaglandin analogue or a proton pump
inhibitor.
 Misoprostol (Cytotec) 100-200 mcg PO 4 times per day
 Omeprazole (Prilosec) 20-40 mg PO every day
 Lansoprazole (Prevacid) 15-30 mg PO every day
Complications
 Perforation & Penetration—into pancreas,
liver and retroperitoneal space
 Peritonitis
 Bowel obstruction, Gastric outflow
obstruction, & Pyloric stenosis
 Bleeding--occurs in 25% to 33% of cases and
accounts for 25% of ulcer deaths.
 Gastric CA
Surgery
 People who do not respond to medication, or who
develop complications:
 Vagotomy - cutting the vagus nerve to interrupt messages
sent from the brain to the stomach to reducing acid
secretion.
 Antrectomy - remove the lower part of the stomach
(antrum), which produces a hormone that stimulates the
stomach to secrete digestive juices. A vagotomy is usually
done in conjunction with an antrectomy.
 Pyloroplasty - the opening into the duodenum and small
intestine (pylorus) are enlarged, enabling contents to pass
more freely from the stomach. May be performed along
with a vagotomy.
Evaluation/Follow-up/Referrals
 H. Pylori Positive: retesting for tx efficacy
 Urea breath test—no sooner than 4 weeks after
therapy to avoid false negative results
 Stool antigen test—an 8 week interval must be
allowed after therapy.
 H. Pylori Negative: evaluate symptoms after
one month. Patients who are controlled
should cont. 2-4 more weeks.
 If symptoms persist then refer to specialist for
additional diagnostic testing.
 Reference List
 Fantry, G. T. (2005, May 6). Peptic Ulcer Disease. Retrieved September
4th, 2006, from www.emedicine.com/med/topic1776.htm
 General Practice Notebook (2006). Peptic Ulcer. Retrieved September
10th, 2006, from www.gpnotebook.co.uk/simplepage.cfm?ID=630849536
 Microbe Wiki (2006, August 16). Heliobacter. Retrieved September 10th,
2006, from www.microbewiki.kenyon.edu/index.php/Helicobacter
 Moore, R. A. (1995). Helicobacter pylori and peptic ulcer: A systematic
review of effectiveness and an overview of the economic benefits of
implementing what is known to be effective. Oxford: Cortecs Limited and
Health Technology Evaluation Association.
 Pounder, R. (1994). Peptic ulceration. Medicine International, 22:6, 225-30.
 Rodney, W.M. (2005, Summer). H. Pylori eradication options for peptic
ulcer. Nurse Practitioners Prescribing Reference,12(2), 150.
 Uphold, C. R. & Graham, M. V. (2003). Clinical Guidelines in Family
Practice (4th ed.). Gainesville, FL: Barmarrae Books, Inc.