This document provides an overview of peptic ulcer disease (PUD), including its causes, symptoms, diagnostic methods, treatment approaches, and complications. The major causes of PUD are Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use. Diagnosis involves endoscopy or imaging tests. Treatment involves reducing acid secretion with proton pump inhibitors, eradicating H. pylori with antibiotic therapy, and managing complications such as bleeding. PUD is decreasing due to reduced H. pylori infections and increased access to treatments, but still requires proper diagnosis and management to prevent complications.

1. Peptic Ulcer Disease
Understanding, Diagnosis and Treatment

2. A review on diagnosis and treatment of peptic ulcer disease
Project submitted to
Vaish Institute of Pharmaceutical Education and Research
Rohtak (Haryana)
In partial fulfilment for the award of the degree of Bachelor of Pharmacy (2019-2023)
Under Supervision of By
Ms. Aarti Bhoria Sahil
Associate Professor Reg. No. - 19-VIR-42
VIPER, Rohtak Uni. Roll No. : 968727

3. What are Ulcers?
 An ulcer is a discontinuity or break in a bodily membrane that impedes normal function of
the affected organ.
 According to Robbins's pathology, "ulcer is the breach of the continuity of skin, epithelium
or mucous membrane caused by sloughing out of inflamed necrotic tissue.

4. Types of ulcer
 Corneal ulcer
 Foot ulcer
 Mouth ulcer
 peptic ulcer
 Genital ulcer
 Bed sore
Some other classes of ulcers are:
 Pressure ulcers
 Stress ulcers

5. Peptic Ulcer Disease
 A peptic ulcer is a defect in the upper gastrointestinal mucosa that extends through the
muscularis mucosa into deeper layers of the gut wall.
 Peptic ulcer disease is characterized by discontinuation in the inner lining of the
gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the
muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and
proximal duodenum. It may involve lower oesophagus, distal duodenum or jejunum.
Synonyms: stomach ulcer, gastric ulcer, deudonal ulcer

6. Classification of Stomach Ulcer:
A classification of gastric ulcers is suggested:
 Type I, true gastric ulcers;
 Type II, combined gastric and duodenal ulcers;
 Type III, supra-pyloric and pyloric ulcers;
 Type IV, multiple ulcers of the stomach;
 Type V, secondary gastric ulcers.

7. Causes of Peptic Ulcer Disease
Major Causes:
 H. pylori induced peptic ulcer
 Pain relieving NSAIDs induced peptic ulcer
Rare Causes:
 Zollinger - Ellison Syndrome
 Malignancy (lung/gastric cancer, lymphoma)
 Crohn’s disease
 Vascular insufficiency
 Viral infection
 Radiation therapy
 Chemotherapy
 Stress (Acute illness, burns, head injury)
 Smoking
 Alcohol and Diet
 Genetic factors
 Hypercalcemia

8. Helicobacter pylori associated PUD
 H. pylorus is a gram negative bacillus that is found within the gastric epithelial cells. This
bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers.
 H. pylori infection is more prevalent among those with a lower socioeconomic status and is
commonly acquired during childhood. The organism has a wide spectrum of virulence
factors allowing it to adhere to and inflame the gastric mucosa. This results in
hypochlorhydria or achlorhydria leading to gastric ulceration.
Virulence Factors of Helicobacter pylori:
 Urease: Secretion of urease breaks down urea into ammonia and protects the organism by
neutralizing the acidic gastric environment.
 Toxins: CagA/ VacA are associated with stomach mucosal inflammation and host tissue
damage.
 Flagella: Provides motility and allows movement toward the gastric epithelium.

9. NSAIDs associated PUD
 Nonsteroidal anti-inflammatory drugs, or NSAIDs (pronounced en-saids), are the most
prescribed medications for treating conditions such as arthritis. Most people are familiar
with over-the-counter, non-prescription NSAIDs, such as aspirin, ibuprofen, and naproxen.
 Non-steroidal anti-inflammatory drugs and aspirin use is the second most common cause of
PUD after H. pylori infection. The gastric mucosa is normally protected by secretion of
prostaglandin. NSAIDs block prostaglandin synthesis by inhibiting COX1 enzyme
resulting in a decrease in gastric mucus and bicarbonate production and a decrease in
mucosal blood flow.

10. Pathogenesis of Peptic Ulcer Disease
The peptic ulcer disease (PUD) mechanism results from an imbalance between gastric mucosal
protective and destructive factors.
Risk factors predisposing to the development of PUD:
 H. pylori infection
 NSAID use
 First-degree relative with PUD
 Emigrant from a developed nation
 African American/Hispanic ethnicity
H. pylori is known to colonize the gastric mucosa and causes inflammation. The H. pylori also
impairs the secretion of bicarbonate, promoting the development of acidity and gastric metaplasia.
With peptic ulcers, there is usually a defect in the mucosa that extends to the muscularis mucosa.
Once the protective superficial mucosal layer is damaged, the inner layers are susceptible to acidity.
Further, the ability of the mucosal cells to secrete bicarbonate is compromised.

11. Signs and Symptoms
Signs and symptoms of peptic ulcer disease may vary depending upon the location of the
disease and age. Gastric and duodenal ulcers can be differentiated from the timing of their
symptoms in relation to meals. Nocturnal pain is common with duodenal ulcers. Those with
gastric outlet obstruction commonly report a history of abdomen bloating and/or fullness.
Common signs and symptoms include:
 Epigastric abdominal pain
 Bloating
 Abdominal fullness
 Nausea and vomiting
 Weight loss/weight gain
 Hematemesis
 Melena

12. Diagnostic methods
 Esophagogastroduodenoscopy (EDG)
 Baruim swallow (indicated when EDG is contraindicated)
 Complete blood work
 Serum gastric (ordered if Zollinger Ellison is suspected)
 Computerized tomography
 H. pylori testing
i. Serologic testing
ii. Urea breath test
iii. Stool antigen test
iv. Urine based ELISA and rapid urine test
v. Endoscopic biopsy

13. Approaches for the treatment of Peptic Ulcer
Disease
Reduction of gastric acid secretion
 H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Roxatidine
 Proton pump inhibitors: Omeprazole, Lansoprazole, Pantoprazole, Rabeprazole, Esomeprazole
 Anticholinergics: Pirenzepine, Propantheline, Oxyphenonium
 Prostaglandin analogue: Misoprostol
Neutralization of gastric acid (Antacids)
 Systemic: Sodium bicarbonate, Sodium citrate
 Non-systemic: Magnesium hydroxide, Magnesium trisilicate, Aluminium hydroxide gel,
Magaldrate, Calcium carbonate
Ulcer protectives: Sucralfate, Colloidal bismuth subcitrate (CBS)
Anti-H. pylori drugs: Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline

14. RECOMMENDED H. pylori ANTIBIOTIC
REGIMENS
Antimicrobial Regimens Duration
Bismuth subsalicylate (Pepto Bismol) 525 mg (2 tabs)
q.i.d. + metronidazole 250 mg 9.i.d + tetracycline 500
mg q.i.d. + H2 receptor antagonist'
Antibiotics for 2 weeks
H, antagonist for 4 weeks
Lansoprazole 30 mg or Omeprazole 20 mg b.i.d.
+Clarithromycin 500 mg b.i.d. + Metronidazole 500 mg
b.i.d.
2 weeks
Lansoprazole 30 mg or Omeprazole 200 mg b.i.d.
+Clarithromycin 500 mg b.i.d. + Amoxicillin 1 gm b.i.d.
2 weeks
Bismuth subsalicylate (Pepto Bismol) 525 mg (2 tabs)
q.i.d., Metronidazole 500 mg q.i.d., Tetracycline 500 mg
q.i.d. + Omeprazole 20 mg or Lansoprazole 30 mg q. AM
2 weeks

15. Strategies for management of peptic ulcer bleeding
Before endoscopy
 Risk stratification
Glasgow-Blatchford scores are superior to Rockall scores in prediction of endoscopic treatment and
surgery. A Glasgow-Blatchford score of zero reliably predicts early discharge without intervention.
 Restrictive blood transfusion strategy
 Blood transfusion when haemoglobin values are below 70 g/L leads to less re-bleeding and
better survival than does liberal transfusion.
 Correction of anticoagulation with a target INR of about 1·5
The optimum INR remains undefined, and recommendations are based on expert opinion only.
 Use of pro-kinetic drugs
Pro kinetic drugs lead to improved endoscopic view, and reduce the need for second look endoscopy.
 Pre-emptive PPIs
Pre-emptive PPIs reduce the presence of high-risk stigmata at endoscopy, and reduce the need for
endoscopic therapy.

16. .
Endoscopic treatment
Addition of a second modality to epinephrine injection reduces recurrent bleeding and need for surgery.
 Endoscopy within 24 hours
There is no clear evidence that immediate endoscopy offers advantages over endoscopy done within 24h.
 Combination therapy
 PPIs reduce re-bleeding and the need for surgery.
 After endoscopy
 Maintain or initiate (if not started before endoscopy) PPI therapy.
 Adjuvant PPI therapy
Treatment with high-dose parenteral PPI indicated if high-risk peptic ulcer stigmata present. Oral PPI given if patients had
no high-risk peptic ulcer stigmata.
 High-dose PPI infusion for 72 h
Intermittent high-dose PPI therapy seems similar to continuous high-dose PPI infusion.

17. Complications
Peptic ulcer disease (PUD) if not diagnosed and treated promptly can lead to serious
complications.
Following complications can occur in PUD:
 Upper gastrointestinal bleeding
 Gastric outlet obstruction
 Perforation
 Penetration
 Gastric cancer

18. Conclusion
PUD is a disease with decreasing clinical burden due to the decline in H. pylori infections, as
well as increased accessibility to anti-secretory therapy and more judicious use of NSAIDs.
However, due to its continued high lifetime prevalence and varied clinical presentation,
recognition and appropriate management of PUD are key to avoid and minimize significant
complications. Testing and treating H. pylori as well as limiting mucosal injury caused by
NSAIDs (via concurrent PPI prophylaxis or choosing COX-2 selective NSAIDs if available)
are the strategies to consider when evaluating PUD. Resuscitation, anti-secretory therapy,
endoscopy and management of antithrombotic agents are the key steps in treatment of PUD
bleeding, which is the most common complication.