PEPTIC ULCER

DISEASE
By: Ph. Sara alshehri
Peptic Ulcer
◦ Peptic ulcer disease (PUD) refers to ulcerative disorders of the upper gastrointestinal
(GI) tract that require acid and pepsin for their formation. The three common etiologies
include:

◦ (1) Helicobacter pylori infection,

◦ (2) nonsteroidal anti-inflammatory drug (NSAID) use,

◦ (3) stress-related mucosal damage (SRMD).

Pathophysiology
◦ Pathophysiology is determined by the balance between aggressive factors (gastric acid and pepsin) and protective
factors (mucosal defense and repair). Gastric acid, H. pylori infection, and NSAID use are independent factors that
contribute to disruption of mucosal integrity. Increased acid secretion may be involved in duodenal ulcers, but patients
with gastric ulcer usually have normal or reduced acid secretion (hypochlorhydria).

◦ Nonselective NSAIDs (including aspirin) cause gastric mucosal damage by two mechanisms: (1) a direct or topical
irritation of the gastric epithelium, and (2) systemic inhibition of endogenous mucosal PG synthesis. COX-2 selective
inhibitors have a lower risk of ulcers and related GI complications than nonselective NSAIDs. Addition of aspirin to a
selective COX-2 inhibitor reduces its ulcer-sparing benefit and increases ulcer risk.
RISK FACTORS
◦ H. pylori infection
◦ Chronic NSAID use
◦ Tobacco use
◦ Family history of ulcers
◦ Stress (after acute illness, ventilator support, extensive burns, head injury)
◦ Alcohol use
◦ Medications: corticosteroids (high-dose and/or prolonged therapy), bisphosphonates, potassium chloride,
chemotherapeutic agents
CLINICAL PRESENTATION
◦ Abdominal pain
◦ Pain from duodenal ulcers often occurs 1 to 3 hours after meals and is usually relieved by food
◦ Pain from gastric ulcers often occurs after meals and is usually increase by food
◦ Heartburn, belching, and bloating often accompany pain.
◦ Nausea, vomiting, and anorexia are more common in gastric than duodenal ulcers and may be signs of an
ulcer-related complication.
Ulcer complications
◦ upper GI bleeding,
◦ perforation into the peritoneal cavity,
◦ penetration into an adjacent structure (eg, pancreas, biliary tract, or liver), and gastric outlet obstruction.
◦ Bleeding may be occult or present as melena or hematemesis.
◦ Perforation is associated with sudden, sharp, severe pain, beginning first in the epigastrium but quickly
spreading over the entire abdomen.
◦ Symptoms of gastric outlet obstruction typically occur over several months and include early satiety,
bloating, anorexia, nausea, vomiting, and weight loss
Diagnosis
◦ Physical examination
◦ Routine blood tests are not helpful in establishing a diagnosis of PUD.
◦ Hematocrit, hemoglobin, and stool guaiac tests are used to detect bleeding.
◦ Diagnosis of PUD depends on visualizing the ulcer either by upper GI radiography or endoscopy.
◦ Endoscopy is preferred because it provides a more accurate diagnosis and permits direct visualization of
the ulcer.
Diagnosis
◦ Diagnosis of H. pylori infection can be made using:
◦ endoscopic or non-endoscopic (urea breath test [UBT],
◦ serologic antibody detection, and fecal antigen tests.
◦ Testing for HP is only recommended if eradication therapy is planned.
◦ If endoscopy is not planned, serologic antibody testing is reasonable to determine HP status.
◦ The UBT and fecal antigen tests are the preferred non-endoscopic methods to verify HP eradication but
must be delayed at least 4 weeks after completion of treatment to avoid confusing bacterial suppression
with eradication.
NONPHARMACOLOGIC
TREATMENT
◦ Patients with PUD should eliminate or reduce psychological stress,
◦ cigarette smoking, and use of NSAIDs (including aspirin).
◦ If possible, alternative agents such as acetaminophen should be used for pain relief.
◦ Although there is no need for a special diet, patients should avoid foods and beverages that cause
dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine, and alcohol).
◦ Elective surgery is rarely performed because of highly effective medical management. Emergency
surgery may be required for bleeding, perforation, or obstruction.
PHARMACOLOGIC TREATMENT
◦ First-line therapy to eradicate HP infection is usually initiated with:
◦ proton pump inhibitor (PPI)– based, three-drug regimen for 14 days.
◦ If a second treatment course is required, the salvage regimen should contain different antibiotics or a
four-drug regimen with a bismuth salt, metronidazole, tetracycline, and a PPI.
Eradication
therapy
Eradication therapy
◦ Bismuth-based quadruple therapy is recommended as an alternative for patients allergic to penicillin.
◦ All medications except the PPI should be taken with meals and at bedtime.
◦ In sequential therapy, the antibiotics are administered in a sequence rather than all together.
◦ If initial treatment fails to eradicate HP, second-line (salvage) treatment should:
◦ (1) use antibiotics that were not included in the initial regimen,
◦ (2) use antibiotics that are not associated with resistance,
◦ (3) use a drug that has a topical effect (eg, bismuth),
◦ (4) extend the treatment duration to 14 days.
A 14-day course of the PPI-based bismuth-containing quadruple regimen is the most commonly used
second-line therapy after failure of a PPI–amoxicillin–clarithromycin regimen
NSAID-induced ulcers
◦ Patients with NSAID-induced ulcers should be tested to determine H. pylori status.
◦ If H. pylori positive, start treatment with a PPI-based three-drug regimen.
◦ If H. pylori negative, discontinue the NSAID and treat with a standard four-week regimen of a PPI,
histamine2 -receptor antagonist (H2RA), or sucralfate.
◦ PPIs are preferred because they provide more rapid symptom relief and ulcer healing.
◦ If the NSAID must be continued despite ulceration, initiate treatment with a PPI (if H. pylori negative) or
a PPI-based three-drug regimen (if H. pylori positive).
◦ PPI treatment should be continued for 8 to 12 weeks if the NSAID must be continued. Co-therapy with a
PPI or misoprostol or switching to a selective cyclooxygenase-2 (COX-2) inhibitor is recommended for
patients at risk of developing an ulcer-related complication.
NSAID-induced ulcers