The document discusses peptic ulcer disease. It defines peptic ulcers as breaks in the stomach or duodenal lining that can be caused by an imbalance of factors like acid and pepsin production. About 70-90% of ulcers are associated with Helicobacter pylori bacteria. The document covers topics like anatomy, causes, symptoms, complications, diagnosis and treatment of peptic ulcers.

1. PEPTIC ULCER
Forth group
Prepared by :-
 Thanoon Alromidy
Abdulkader Alhaj
Burhan Alyousfy
Ammar yaser
Basheer Alsomaiey
Asmaa Abdulqaher
Hajer Edrees
Fathia Baalwey

2.  Introduction and definition
 Anatomy and pathophysiology
 Epidemiology
 Etiology ( Causes & Risk factors )
 Signs & Symptoms
 Complication
 Diagnosis
 Treatment
 Prevention
Outlines

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

8.  ANTRUM
comprises the distal 25% to 30% of the
stomach.
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

16. PATHOPHYSIOLOGY

17.  Smoking
 Illicit drugs (cocaine) that reduce mucosal blood flow
Endocrine cell hyperplasia (can stimulate parietal cell growth and gastric
acid secretion)
Alcoholic cirrhosis (primary duodenal PUD)
Psychological stress (can increase gastric acid secretion)
Viral infection ( CMV, herpes simplex virus )
RISK FACTORS

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

27.  Drug therapy
 Antacids
 H₂ receptor blockers
 PPIs
 Antibiotics
 Anticholinergics
 Cytoproctective therapy
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

34.  Surgical procedures
 Gastroduodenostomy
 Gastrojejunostomy
 Vagotomy
 Pyloroplasty
TREATMENT

35.  Surgical procedures
 Gastroduodenostomy
 Gastrojejunostomy
 Vagotomy
 Pyloroplasty
TREATMENT

36. • Stop smoking
• Eat a high fiber diet
• Avoid food that irritates the stomach
• Avoid alcohol
• Avoid caffeine
• Avoid aspirin
PREVENTION

37. • Avoid anti-inflammatory medications
 Ibuprofen
 Naproxen
 Ketoprofen
• Eat small meals more frequently
PREVENTION

38. THE END
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