Peptic Ulcer Disease

2. Peptic Ulcer Disease
Presented By,
Dr.Sajid Hasan
MBBS
Army Medical College Chattogram

3. Introduction
Ulcer is the breach of the continuity of skin, epithelium or mucous
membrane caused by sloughing out of inflamed necrotic tissue, e.g.,
apthous ulcer, peptic ulcer, stress ulcer.
Among different types of ulcer, peptic ulcer disease is one of the
common type of ulcer affecting people.

4. Peptic ulcer disease
The word “peptic” means that the cause of the problem is due to acid.
Peptic ulcer is an acid-induced lesion of the digestive tract that is
usually located in the stomach or proximal duodenum, and is
characterized by denuded mucosa with the defect extending into the
submucosa or muscularis propria.
Ref:J. Clin. Med. 2019, 8, 179

6. Types
Peptic ulcer disease (PUD) is of two types-
Gastric ulcers: They are located in the stomach.
Duodenal ulcers: They are found in duodenum, at the beginning of the
small intestine.
A person can have both the ulcer at a time.
Ref: Peptic Ulcer Disease - American College of Gastroenterology

7. Risk Factors
Most common risk factors of PUD are-
H. pylori infection
NSAIDs
Medications- steroids, chemotherapeutic agents.
Others includes-
Zollinger-Ellison syndrome
Stress (Acute illness, burns, head injury)
Viral infection
Ref:J. Clin. Med. 2019, 8, 179

8. Cont…
Vascular insufficiency
Crohn disease
Malignancy (gastric/lung cancer, lymphomas)
Chemotherapy
Radiotherapy
Histamine
Eosinophilic infiltration,
Gastric bypass surgery, and
Metabolic disturbances
Ref:J. Clin. Med. 2019, 8, 179

9. Pathophysiology
Different etiology has different pathophysiology in case of PUD.
NSAIDs & H. pylori being the most common risk factor, their
mechanism are-
H. Pylori mediated
 H. pylori infection can result in either hypochlorhydria or
hyperchlorhydria, thus determining the type of peptic ulcer.
 The main mediators of H. pylori infection are cytokines that inhibit
parietal cell secretion, but H. pylori can directly affect the H+/ATPase-
subunit, activate calcitonin gene-related peptide (CGRP) sensory
neurons linked to somatostatin or inhibit the production of gastrin .
Ref:J. Clin. Med. 2019, 8, 179

10. Cont…
 Although the formation of gastric ulcers is associated with hyposecretion,
10–15% of patients with H. pylori infection have increased gastric
secretion caused by hypergastrinemia and reduced antral somatostatin
content .
 This leads to increased histamine secretion, and subsequently the increased
secretion of acid or pepsin from parietal and gastric cells.
 Additionally, the eradication of H. pylori leads to a decrease in gastrin
mRNA expression and an increase in somatostatin mRNA expression. In
the remaining majority of patients, gastric ulcers are associated with
hypochlorhydria and mucosal atrophy.
Ref:J. Clin. Med. 2019, 8, 179

11. NSAIDs mediated:
The main mechanism of NSAID-associated damage of the gastro
duodenal mucosa is the systemic inhibition of constitutively expressed
cyclooxygenase-1 (COX-1), which is responsible for prostaglandin
synthesis, and is associated with decreased mucosal blood flow, low
mucus and bicarbonate secretion, and the inhibition of cell proliferation
Cont…

12. Clinical feature
Features of Gastric ulcer:
Pain in epigastric region after taking food, lasting up to two hours. Pain
is uncommon during night. It is relieved by vomiting or by inducing
vomiting.
Periodicity: Symptom free interval may be 2–6 months. Often with
seasonal variation.
Vomiting relieves pain and often it is induced by the patient for relief of
pain.
Ref: SRB's Manual of Surgery

13. Cont…
Haematemesis and melena: Haematemesis is more common.
Appetite is good but hesitant to eat, because eating induces pain and
that results in loss of weight. But once complications occur, appetite
decreases. Aversion to spicy, fried foods occurs.
Tenderness: On deep palpation, tenderness is felt in epigastric region.
Ref: SRB's Manual of Surgery

14. Features of duodenal ulcer:
Pain is more before food, in early morning and decreases after taking food. It is
classically called as hunger pain as it is relieved by taking food. Night pains are
common.
Periodicity is more common than in chronic gastric ulcer with seasonal
variation.
Water-brash- a rush of saliva after an episode of regurgitation to dilute the acid
in esophagus may be present. Heart burn, vomiting may also be present
Haematemesis and melena: Melena is more common, hematemesis also can
occur.
Cont…
Ref: SRB's Manual of Surgery

15. Diagnosis
Diagnosis of PUD requires-
 History taking
 Physical examination
 Investigation: Invasive
Noninvasive.

16. History taking
A careful history should be obtained and noted for the presence of any
complications.
Patient reporting of epigastric abdominal pain, early satiety, and fullness
following a meal raise suspicion of PUD.
The pain of gastric ulcers increases 2 to 3 hours after a meal and may
result in weight loss whereas pain of duodenal ulcers decreases with meal
resulting in weight gain.
Any patient presenting with anemia, melena, hematemesis or weight loss
should be further investigated for complications of PUD predominantly
bleeding, perforation or cancer.
Ref: National Library of Medicine

17. Physical examination
A physical exam may reveal-
 Abdominal tenderness- an epigastic tenderness can be
present.
 Anemia.
Ref: National Library of Medicine

18. Investigation
1. Esophagogastroduodenoscopy (EGD): Gold standard and most
accurate diagnostic test with sensitivity and specificity up to 90% in
diagnosing gastric and duodenal ulcers.
2. Barium swallow: It is indicated when EGD is contraindicated.
In gastric ulcer: Barium meal X-ray to see niche and notch.
In duodenal ulcer: Barium meal X-ray shows deformed or
absence of duodenal cap (because of spasm).
Ref: National Library of Medicine

19. Cont…
3. Helicobacter pylori testing:
Serologic testing:
 Urea breath test: High sensitivity and specificity. It may be used to
confirm eradication after 4 to 6 weeks of stopping treatment.
 Stool antigen test.
 Urine-based ELISA and rapid urine test.
 Endoscopic biopsy: Culture is not generally recommended as it is
expensive, time-consuming and invasive. It is indicated if eradication
treatment fails or there is suspicion about antibiotic resistance
Ref: National Library of Medicine

20. Treatment
Treatment approaches includes-
General measure
Pharmacological treatment
Maintenance treatment
Surgical approaches
Ref: Davidson’s Principles and practice of medicine

21. General measure
These should be advised to be avoided-
 Cigarette smoking
 NSAIDs
 Aspirin
No dietary modification is required.

22. Pharmacological Treatment
It includes-
 H2 receptor antagonist
 Proton pump inhibitor
 Cytoprotective
 H. pylori eradication therapy- Tripple therapy

23. Pharmacological approaches

24. Medicine Mechanism of action Example Adverse effect
Proton Pump Inhibitors
(PPIs)
Inhibition of the gastric H+/K+-
ATPase (proton pump) enzyme
system
Omeprazole
Rabeprazole
Pantoprazole
Headache, Abdominal pain,
Diarrhea, Nausea, Vomiting
Constipation , Flatulence,
Vitamin B12 deficiency
H2 Receptor Blockers Blocking the action of
histamine at the histamine H2
receptors of parietal cells
Famotidine
Ranitidine
Depression, Dizziness
Cardiovascular events
Cytoprotective
Stimulate mucus production and
enhance blood flow throughout
the lining of the gastrointestinal
tract
Sucralfate Diarrhea, Upper respiratory
tract, inflammation,
Eczema, Constipation, Back
pain, Diarrhoea
Ref:J. Clin. Med. 2019, 8, 179

25. Tripple therapy:
First line Standard triple therapy:
PPI + two antibiotics (clarithromycin + metronidazole or amoxicilin)
Duration:7–14 days
Efficiency-70–85%
Ref:J. Clin. Med. 2019, 8, 179
Cont…

26. Site of action of pharmacological agents
Ref:J. Clin. Med. 2019, 8, 179

27. Surgery
Surgery is now rarely required for peptic ulcer disease but it is
needed in some cases .
The operation of choice for a chronic non-healing gastric ulcer
is partial gastrectomy, preferably with a Billroth I anastomosis,
in
which the ulcer itself and the ulcer-bearing area of the stomach
are resected.
Ref: Davidson’s Principles and practice of medicine

28. Complication of PUD
Hemorrhage
Gastric outlet obstruction
Perforation
Penetration
Carcinoma of stomach
Ref: National Library of Medicine