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Peptic ulcer
1. PEPTIC ULCER
Dr. S. Parasuraman
Faculty of Pharmacy,
AIMST University, Malaysia
2. The gastrointestinal tract
(GIT, alimentary tract, gut)
• It consists of an irregular tube
about 6 m long, extending from
the mouth to the anus.
• The upper GIT Which includes
the mouth, oesophagus and
stomach.
• The lower GIT Which comprises
the duodenum, jejunum, ileum,
colon, rectum and anus.
• The accessory organs liver,
gallbladder and pancreas
3. Abnormalities of the GIT
• Dysphagia:
– Difficulty swallowing, caused by obstruction of the esophagus
– Obstruction may be caused by
• tumors, congenital narrowing
• Neurologic disorders such as brain injury stroke or Parkinson’s
disease may affect voluntary swallowing or peristalsis of the
esophagus
• Dyspepsia
– Epigastric fullness, discomfort, indigestion
• Odynophagia
– Painful swallowing usually associated with dysphagia
• Heartburn
– Burning sensation retrosternally associated with reflux
4. Abnormalities of the GIT
• Anorexia
– Loss of appetite
• Haematemesis
– Vomiting blood (could be red or altered “coffee ground”)
• Melaena
– Passing of black tarry, offensive stool (usually due to upper GI
bleeding)
• Haematochezia
– Passing blood through rectum (PR bleeding)
• Gastritis
– Inflammation of the gastric mucosa
– Acute gastritis
– Chronic gastritis
5. Abnormalities of the GIT
• Peptic ulcers
A peptic ulcer is an abnormal area of mucosa that has been damaged
by the pepsin and hydrochloric acid of gastric juice, with consequent
inflammation of the underlying and surrounding tissue. Erosion 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 oesophagus due to reflexing of
gastric content
– Rarely in certain areas of the small intestine
6. Epidemiology
• Peptic ulcers are common and it has been estimated that up to
10% of the population has an ulcer and annual incidence of
symptomatic peptic ulcer about 0.3%.
• Duodenal ulcers are four times as common as gastric ulcers and
occur mainly in the duodenal cap.
• Gastric ulcers occurs mostly in the lesser curvature of the
stomach. These are benign, some time develop as a tumors
(5%).
• Gastric malignancy is common in Japan, Chile, Finland and
Iceland than other world countries (because of environmental
and diet factor).
7. Aetology
Aetology of peptic ulcer disease is multifactorial.
• Infection with the bacteria Helicobacter pylori occurs in 80 to
95% of patients with peptic ulcer disease.
• H. pylori infection impairs the protective mechanisms of the G.I.
tract against low pH and digestive enzymes and leads to
ulceration of the mucosa.
• Stress — Emotional, trauma, surgical.
• Injury or death of mucus-producing cells.
• Chronic use of NSAIDs
• Smocking
• Alcohol and diet
• Hypercalcemia (↑gastric secretion)
8. Aetology
• Excess acid production in the stomach. The old hypothesis that
ulceration is caused simply by hyperacidity is not tenable. About
70% of gastric ulcers and 50% of duodenal ulcers are not
associated with abnormally high acid production.
• Genetic factor: The lifetime prevalence of developing ulcer
disease in first-degree relatives of ulcer patients is about three
times greater than the general population. 20-50% of duodenal
ulcer reported a positive family history.
• Ulcers are also more common in blood group O subjects and in
those who do not secrete blood group antibodies into gastric
secretions.
9. Classification of peptic ulcer
• Peptic ulcers classified based on region or location of illness
–
–
–
–
Stomach (called gastric ulcer)
Duodenum (called duodenal ulcer)
Esophagus (called Esophageal ulcer)
Meckel's Diverticulum (called Meckel's Diverticulum ulcer)
Modified Johnson Classification of peptic ulcers
Type I: Ulcer along the lesser curve of stomach
Type II: Two ulcers present - one gastric, one duodenal/prepyloric
Type III: Prepyloric ulcer
Type IV: Proximal gastroesophageal ulcer
Type V: Anywhere (associated with chronic NSAID use)
10. Sites of peptic ulcer
• Duodenum: First portion, Anterior wall
•
Stomach: usually antrum, lesser curvature
(common), anterior and posterior wall,
greater curvature (less common)
•
Meckel’s diverticulum
In the margins of a gastroenterostomy
(stomal ulcer)
•
In the duodenum, stomach or jejunum of
patients with Zollinger- Ellison syndrome.
• Within or adjacent to a Meckel’s
diverticulum.
ZES
11. Symptoms of peptic ulcer
Symptoms of peptic ulcer very with location of the
ulcer and the patient age.
• Abdominal discomfort
• Pain or nausea (pain is located in the epogastrium;
not radiate)
Waterbrash
• Waterbrash
• Loss of appetite and weight loss
• Hematemesis (vomiting of blood) Rarely, ulcer lead
to a gastric or duodenal perforation.
Hematemesis
12. Manifestations of peptic ulcer disease
• Episodes of remission and exacerbation
• Pain that for duodenal ulcers is often relieved by eating or
antacids
• G.I. bleeding and possible hemorrhage (20 to 25% of patients)
• Perforation of ulcers with significant mortality
• Obstruction of G.I. tract
13. Complications of peptic ulcer
• Gastrointestinal bleeding. (Sudden large bleeding can be life
threatening)
• Cancer (Helicobacter pylori as the etiological factor making it 3-6 times
likely to develop stomach cancer)
• Perforation (hole in the wall)
• Penetration.
15. Diagnosis of peptic ulcer
• Radiological Diagnosis: Barium x-ray or upper GI series is a
widely used for diagnosis. Barium x-ray is difficult to analysis
and less sensitive and accurate.
• Laboratory test:
– Noninvasive urea breath test.
– Patient with refractory or recurrent peptic ulcer may have underlying H.
pylori infection, histopathology investigation may req.
– Serologic test for detecting H. pylori (levels of IgG and IgA ELISA test)
– Stool antigen test for non-invasive detecting the presence of H. pylori.
• Endoscopic diagnosis
16. Drugs for Treatment of Peptic Ulcer Disease
• Antibiotics for eradication of H. pylori, if present
(amoxicillin, clarithromycin)
• Antacids (magnesium hydroxide, aluminum hydroxide)
• H2 receptor antagonists (ranitidine, cimetidine)
• Proton-pump inhibitors (omeprazole)
• Mucosal protective agents (bismuth, sucralfate)
17. Management of peptic ulcer
The objectives of management are to:
• relieve pain and discomfort
• accelerate healing
• prevent recurrence and complications
19. Helicobacter pylori & Ulcer
• H. pylori -- causes chronic and
indolent
inflammation
by
damaging the mucosal defense
system by reducing the thickness
of the mucus gel layer, diminishing
mucosal
blood
flow,
and
interacting with the gastric
epithelium throughout all stages
of the infection.
• H. pylori infection can also
increase gastric acid secretion by
producing
various
antigens,
virulence factors, and soluble
mediators
21. Zollinger–Ellison syndrome
• Tumors of the gastrinsecreting endocrine cells of
the pancreas or, less
frequently, the duodenal
wall.
• Leads to excessive acid
production by the G.I. tract.
• Development of serious and
aggressive peptic ulcers.
• Complications can include perforation, hemorrhage and
obstruction.
• Treatment may include resection of tumor, administration of
H2 receptor antagonists, anticholinergics and antacids.
