3. A peptic ulcer, also known as peptic ulcer disease (PUD), is the most
common ulcer of an area of the GIT.
About 70 – 90 % of such ulcers are associated with Helicobacter pylori, a
rod-shaped bacterium that lives in the acidic environment of the stomach
Ulcers can also be caused or worsened by drugs such as aspirin,
ibuprofen, and other NSAIDs.
Introduction
4. Peptic ulcers are produced by an imbalance between the gastro-duodenal
mucosal defense mechanisms and damaging forces of gastric acid and pepsin,
combined with superimposed injury from environmental or immunologic agents.
The mucous membrane lining the digestive tract erodes and causes
a gradual breakdown of tissue. This breakdown causes a gnawing or burning
pain in the upper middle part of the belly
Introduction
5. PEPTIC ULCER DISEASE
PU are focal defects in the gastric or duodenal mucosa that extend into the
submucosa or deeper
May be acute or chronic
PUD is one of the most common Gl disorders in the United States with
a prevalence of about 2% and lifetime cumulative prevalence of about
10% , peaking around age 70 years
Introduction
6. The stomach is located in the upper part of the abdomen
just beneath the diaphragm
ANATOMY
7. FUNDUS
The superior-most part of the stomach .
Bounded superiorly by the diaphragm and
laterally by the spleen..
BODY OF THE STOMACH
contains most of the parietal cells.
ANATOMY
9. • Innervation
Vagus nerves
provide extrinsic parasympathetic innervation
to the stomach.
From the vagal nucleus in the floor of the
fourth cerebral ventricle
ANATOMY
10. • The prevalence of peptic ulcer ( 0.1 – 0.2 % ) is decreasing in many
Western communities as a result of widespread use of Helicobacter pylori
eradication therapy but it remains high in developing countries the male-
to female ratio for duodenal ulcer varies from 5 : 1 to 2 : 1 whilst that for
gastric ulcer is 2 : 1 or less
Chronic gastric ulcer is usually single 90 % are situated on the lesser curve
within the antrum or at the junction between body and antral mucosa
EPIDEMOLOGY
11. • Chronic duodenal ulcer usually occurs in the first part of the duodenum
and 50 % are on the anterior wall. Gastric and duodenal ulcers coexist in
10 % of patients and more than one peptic ulcer is found in 10 – 15 % of
patients
Peptic ulceration is strongly associated with H .Pylori infection
The prevalence in developed nations rises with age, and in the UK
approximately 50 % of people over the age of 50 years are infected
EPIDEMOLOGY
12. • In the developing world, infection is more common, affecting up to 90 %
of adult
• Around 90% of duodenal ulcer patients and 70% of gastric ulcer patients are
infected with H. pylori
The remaining 30% of gastric ulcers are caused by NSAIDs and this proportion
is increasing in Western countries as a result of H. Pylori eradication
strategies.
EPIDEMOLOGY
13. • Peptic ulcers occur mainly in the tissue of gastroduodenal mucosa
because it cannot withstand the digestive action of gastric acid HCl and
pepsin
• A damaged mucosa cannot secrete enough mucus to act as a barrier
against HCl
The use of NSAIDs inhibits the secretion of mucus that protects the
mucosa
PATHOPHYSIOLOGY
14. Stress ulcer refers to the acute mucosal ulceration of the duodenal or
gastric area that occurs after physiologically stressful events, such as
burns, shock, severe sepsis, and multiple organ traumas. Stress ulcer is
usually preceded by shock this leads to decreased gastric mucosal blood
flow and to reflux of duodenal contents into the stomach. In addition,
large quantities of pepsin are released. The combination of ischemia,
acid, and pepsin creates an ideal climate for ulceration
PATHOPHYSIOLOGY
15. Here the surface pH is close to neutral and any acidity is buffered by
the organism’s production of the enzyme urease
This produces ammonia from urea and raises the pH around the
bacterium and between its two cell membrane layers. H. pylori
exclusively colonises gastric-type epithelium and is only found in the
duodenum in association with patches of gastric metaplasia
PATHOPHYSIOLOGY
18. H. pylori infection
NSAIDs (potentiated by corticosteroids)
Low of blood supply to mucosa
CAUSES
19. Burning stomach pain
feeling of ullness bloating
Heartburn
Nausea and vomiting
Unexplaind weight loss
Blak stiky stool ( if bleeding )
feeling faint
Trouble breathing
SIGNS AND SYMPTOMS
20. Hemorrhage ( hematemesis or melena )
• Blood vessels damaged as ulcer erodes into the muscles of stomach
or duodenal wall
• Coffee ground vomitus or occult blood in tarry stools
Perforation
An ulcer can erode through the entire wall
Bacteria and partially digested food spill into peritoneum peritonitis
COMPLICATION
21. Narrowing and obstruction ( pyloric )
Swelling and scarring can cause obstruction of food leaving
stomach repeated vomiting
Healing by fibrosis :- causing obstruction
Malignant transformation :- rare ( 0.5 % of gastric peptic ulcer
COMPLICATION
22. healthcare provider may be able to make the diagnosis just by talking with the
patient about the symptoms and to confirm the diagnosis, you’ll need one of these
tests :-
Endoscopy
If the patient has severe symptom the provider may recommend an upper
endoscopy to determine if the patient has an ulcer this procedure, the doctor inserts
an endoscope through throat and into stomach to look for abnormalities
DIAGNOSIS
23. H. Pylori tests
By breath test is the easiest way to discover H . Pylori
The provider also can look for it with a blood or stool test or by taking
a sample during an upper endoscopy
DIAGNOSIS
24. Imaging tests
imaging tests such as X-rays and CT scans are used to detect ulcers
the patient drink a specific liquid that coats the digestive tract and
makes ulcers more visible to the imaging
DIAGNOSIS
25. Medical regimen consists of
Adequate rest
Dietary modification
Drug therapy
Elimination of smoking
Long-term follow-up care
TREATMENT
26. Aim of treatment program
Degree of gastric acidity
Enhance mucosal defense mechanisms
Minimize harmful effects on mucosa
TREATMENT
28. Histamine receptor blocks (H, R blockers)
Used to manage peptic ulcer disease
Block action of histamine on H₂ receptors
HCI acid secretion
conversion of pepsinogen to pepsin
ulcer healing
Proton pump inhibitors
Block ATPase enzyme that is important for secretion of HCI acid
TREATMENT
29. Antibiotic therapy
Eradicate H. pylori infection
No single agents have been effective in eliminating H .Pylori
Antacids
Used as adjunct therapy for peptic disease
↑gastric pH by neutralizing acid
TREATMENT
30. Anticholinergic drugs
Occasionally ordered for treatment
decease cholinergic stimulation of HCl acid
Cytoprotective drug therapy
Serotonin reuptake inhibitors
TREATMENT
31. Nutritional therapy
Dietary modifications may be necessary so that fo foods and
beverages irritating to patient can be avoided or eliminated
Nonirritating or bland diet consisting of 6 small meals aday
during symptomatic phase
TREATMENT
32. Nutritional therapy
Protein considered best neutralizing food
Stimulates gastric secretions
Carbohydrates and fats are least stimulating to HCl acid secretion
Do not neutralize well
TREATMENT
33. Surgical Treatment
> 20 % of patients with ulcers need surgical intervention
Indications for surgical interventions
• Intractability
• Prepyloric or pyloric ulcers
• Multiple ulcer sites
• Possible existence of a malignant ulcer
• Obstruction
TREATMENT
