peptic ulcer disease is the presence of one or more ulcerative lesions in the stomach or duodenum. for more informations you can read the following file.

1. Peptic ulcer
disease
Ghadeer Ismail Eideh
Supervised by Dr. Aref Rajabi
From: step up to medicine

2. Introduction
01
02
Clinical features
03
Diagnosis
04
Treatment
05
Causes
Outlines

3. Introduction
01

4. A peptic ulcer is a sore on
the lining of the stomach,
small intestine or
esophagus.
Definition

5. Intoduction
• The term ‘peptic ulcer’ refers to an ulcer in the lower
oesophagus, stomach or duodenum, in the jejunum
after surgical anastomosis to the stomach or, rarely, in
the ileum adjacent to a Meckel’s diverticulum.
• Ulcers in the stomach or duodenum may be acute or
chronic; both penetrate the muscularis mucosa but
the acute ulcer shows no evidence of fibrosis.

6. Causes
Infectious cause
H.Pylori
(one of the most common
cause)
Drugs
NSAID
(one of the most common
cause)
Acid hypersecretory
Zollinger-Ellison syndrome
Other risk factor
a. Smoking
b. Alcohol use
c. Emotional stress and dietary factors
(such as coffee and spice intake)

7. Gastric ulcer
vs duodenal
ulcer
02

9. Types of gastric ulcers

10. Clinical
features
03

11. a. Aching or gnawing in
nature.
b. Nocturnal symptoms
and the effect of food on
symptoms are variable.
Epigastric pain Upper GI bleeding
Clinical features
May be complicated
by upper GI
bleeding.

12. nausea/vomiting Early satiety, and
weight loss
Clinical features

13. In some patients, the ulcer is completely ‘silent’, presenting for the
first time with anemia from chronic undetected blood loss, as
abrupt hematemesis or as acute perforation; in others, there is
recurrent acute bleeding without ulcer pain.
Clinical features

14. DIAGNOSIS
04

15. 1. Endoscopy
a. Most accurate test in diagnosing ulcers.
b. Essential in diagnosis of gastric ulcers because biopsy is
necessary to rule out malignancy.
c. Preferred when severe or acute bleeding is present (can perform
electrocautery of bleeding ulcers).
d. Can obtain endoscopic biopsy for diagnosis of H. pylori.
Diagnosis

16. 2. Barium swallow
a. Sometimes used initially but is less reliable than endoscopy.
b. Double-contrast techniques preferred due to improved
accuracy.
Diagnosis

17. 3. Laboratory test—for diagnosis of H. pylori infection
a. Biopsy: Histologic evaluation of endoscopic biopsy is the gold
standard.
b. Stool antigen test—High sensitivity and ease of testing makes this
ideal for screening.
c. Urease detection via urea breath test is highly sensitive and
specific. It documents active infection and helps to assess the results
of antibiotic therapy.
Diagnosis

18. d. Serology (lower specificity)—The presence of antibodies to H.
pylori does not necessarily indicate current infection—antibodies to
H. pylori can remain elevated for months or even years after
eradication of infection.
The following may lead to false-negative test results: PPIs, bismuth,
many antibiotics, and upper GI bleeding.
4. Serum gastrin measurement—if considering Zollinger–Ellison
syndrome as a diagnosis.
Diagnosis

19. • Gastric ulcers require a biopsy to rule out malignancy; duodenal
ulcers do not require biopsy.
• If a peptic ulcer is uncomplicated, a barium study or endoscopy
is not needed initially. Initiate empiric therapy. However, if you
suspect any of the complications of PUD, order confirmatory
studies.
Diagnosis

20. Treatment
05

21. 1. Medical—Majority of patients with PUD can be successfully
treated by curing H. pylori infection, avoidance of NSAIDs, and
appropriate use of antisecretory drugs.
a. Supportive (patient directives)
• Discontinue aspirin/NSAIDs.
• Restrict alcohol use but do not restrict any foods.
• Stop smoking, decrease emotional stress.
• Avoid eating before bedtime (eating stimulates nocturnal
gastric acid levels).
Treatment

22. b. Acid suppression therapy
• PPIs—omeprazole (Prilosec), lansoprazole (Prevacid), block H+/K+
ATPase pump directly in parietal cell membrane. First line of
therapy, most effective antisecretory agents.
• H2 receptor blockers—cimetidine (Tagamet) and ranitidine
(Zantac). Block histamine-based parietal cell acid secretion. Less
effective than PPIs.
• Antacids—somewhat outdated for primary therapy and more
appropriately used for adjunctive therapy/symptomatic relief.
Examples include aluminum hydroxide (Mylanta), calcium
carbonate (Tums), bismuth subsalicylate (PeptoBismol).
Treatment

23. c. Eradicate H. pylori with triple or quadruple therapy (see Table 3-5).
Once infection is cleared, the rate of recurrence is very low.
• For initial therapy, triple therapy (PPI, amoxicillin, and
clarithromycin) for 14 days.
• Quadruple therapy (PPI, bismuth, metronidazole, and tetracycline)
indicated for patients with risk factors for macrolide resistance.
Treatment

24. Treatment

25. d. Cytoprotection
• Sucralfate—facilitates ulcer healing. Must be taken frequently, is
costly, and can cause GI upset.
• Misoprostol—reduces risk for ulcer formation associated with
NSAID therapy. Costly, and can cause GI upset (common side
effect).
Treatment

26. e. Treatment regimens
• If H. pylori test is positive, begin eradication therapy with either
triple or quadruple therapy (see Table 3-6). Also begin acid
suppression with antacids, an H2 blocker, or a PPI.
• If the patient has an active NSAID-induced ulcer, stop NSAID use
(may switch to acetaminophen). Also begin with either a PPI or
misoprostol. Continue for 4 to 8 weeks, depending on severity. Treat
the H. pylori infection as above if present.
• Antisecretory drugs can be discontinued after 4 to 6 weeks in
patients with uncomplicated ulcers who are asymptomatic. Patients
at increased risk of recurrence (especially if underlying cause of
ulcer is not reversed) may benefit from maintenance therapy.
• H. pylori–negative ulcers that are NOT caused by NSAIDs can be
treated with antisecretory drugs (either H2 blockers or PPI).

27. 2. Surgical
a.Rarely needed electively
b. Required for the complications of PUD (bleeding, perforation,
gastric outlet obstruction).
Treatment

30. Thank you