Peptic ulcers diseases in human bein.ppt

Talk about peptic ulcer disease

1. Peptic Ulcer Disease
Dr. Husham Aldaoseri
8.NOV.2023

2. Peptic Ulcer Disease (PUD)
Objectives:
1.Define the following terms: peptic ulcer, gastric ulcer,
2.Discuss the different etiologic factors of PUD
3.List the role of H.pylori as the main cause of PUD.
4.Discuss the different diagnostic methods of PUD
5.Discuss the complications of PUD
6.Discuss the treatment of PUD

3. Peptic ulcer
refers to erosion of the mucosa lining any portion of the G.I. tract.
It is defined as : A circumscribed ulceration of the gastrointestinal
mucosa occurring in areas exposed to acid and pepsin and most often
caused by Helicobacter pylori infection.
gastric ulcer : the ulcer that occurs in the stomach lining ,some of
them may be malignant
duodenal ulcer : most often seen in first portion of duodenum
(>95%)
Peptic Ulcer Disease (PUD)

4. Ulcer
1.Peptic ulcer
2.Stress ulcers (acute gastric ulcers)
Ulcer: a breach in the mucosa of
the alimentary tract tha may
extend through muscularis
mucosa into submucosa or
deeper.
About 6% of patients attending a
dentist office will have peptic
ulcer disease
The lifetime prevalence of peptic
ulcers ranges from 11 to 14% for
men and 8 to 11% for women.

5. Normal
Esophagus & Stomach

6. Peptic ulcer disease

7. Pathogenesis of Ulcers
Aggressive Factors
Acid, pepsin
Bile salts
Drugs (NSAIDs)
H. pylori
Defensive Factors
Mucus, bicarbonate layer
Blood flow, cell renewal
Prostaglandins
Phospholipid
Free radical scavengers

8. The causes of peptic ulcer disease include the following:
 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.
 Excess acid production in the stomach . The hormone gastrin
stimulates the production of acid in the stomach; therefore, any factors
that increase gastrin production will in turn increase the production of
stomach acid.
Drugs: Chronic use of aspirins and NSAIDs, or Corticosteroids
Peptic Ulcer Disease

9. ETIOLOGIC FACTORS OF PUD

10. Most common infection in the world (20%)
H. pylori is observed in the gastric mucosa in 90 to 100% of
patients with duodenal ulcers and 70 to 90% of patients with
gastric ulcers.
H. pylori are noted in the gastric antrum in more than 80% of
cases of duodenal ulcers
Helicobacter pylori

11. Helicobacter pylori
Gram negative, Spiral bacilli
Spirochetes
Do not invade cells – only mucous
Breakdown urea - ammonia
Break down mucosal defense
Chronic Superficial inflammation

12. duodenal sites are 4x as common as
gastric sites
most common in middle age with peak
30-50 years
Male to female ratio—4:1
Genetic link: 3x more common in 1st
degree relatives
more common with blood group O
associated with increased serum
pepsinogen
H. pylori infection common,up to 95%
smoking is twice as common
common in late middle age.
incidence increases with age.
Male to female ratio—2:1
More common with bl. group A
Use of NSAIDs: associated with a
three- to four-fold increase in risk
of gastric ulcer
Less related to H. pylori than
duodenal ulcers : about 80%
10 - 20% of patients with a gastric
ulcer have a concomitant duodenal
ulcer
Duodenal Ulcer Vs. Gastric Ulcer

13. Clinical features
•Epigastric pain (the most common symptom)
–Gnawing or burning sensation
–Occurs 2-3 hours after meals
–Relieved by food or antacids
–Patient
 awakens with pain at night.
Some present with complications such as iron deficiency
anemia, obstruction, frank hemorrhage, or perforation.

14. Oral manifestations of peptic ulcer disease
Rare unless there is severe anemia from gastrointestinal
bleeding or persistent regurgitation of gastric acid as a result
of pyloric stenosis that leads to dental erosion, typically of the
palatal aspect of the maxillary teeth.
Vascular malformations of the lip have been reported and
range from a very small macule to a large venous pool.
H. pylori has been islolated from dental plaque implicating the
oral cavity as a potential source of this organism which is
responsible for both peptic ulcer disease and gastric cancer.

15. Endoscopy
Barium meal – contrast x-ray
Biopsy – bacteria & malignancy
H.Pylori:
Endoscopy cytology
Biopsy – Special stains
Culture - difficult
Urease Breath test.
Diagnosis

16. Urease Breath Test.

17. Bleeding – Chronic, Acute, Massive
Fibrosis, Stricture obstruction – pyloric stenosis.
Perforation – Peritonitis- emergency.
Gastric carcinoma. (not duodenal carcinoma)
Complications

18. Non-pharmacological Treatment of
Peptic ulcer
1-Avoid spicy food.
2-Avoid xanthin containing beverges.
3-Avoid Alcohol.
4-Avoid Smoking.
5-Avoid heavy meals.
6-Encourage small frequent low caloric
meals.
7-Avoid ulcerating drugs e.g. NSAIDs,
corticosteroids, xanthines and
parasympathomimetics

19. Treatment
Triple therapy for 14 days is considered the ttt of choice.
Proton Pump Inhibitor + clarithromycin and amoxicillin
Omeprazole
Lansoprazole
Rabeprazole
Esomeprazole (Nexium):
Clarithromycin
 and Amoxicillin
•Can substitute Flagyl 500 mg PO bid for 14 d if allergic to Penicillin.

20. lengthy dental procedures should be avoided or divided over
shorter appointments to minimize stress.

To avoid aspirations, patients should not be left in a supine or
subsupine position for lengthy periods during dental appointments.
Dentists should avoid administering aspirin and other NSAIDs.
Instead, acetaminophen products should be recommended.
the antacids contain calcium, magnesium, and aluminum salts that
bind antibiotics, such as erythromycin and tetracycline, may
decrease the absorption of the antibiotic as much as 75 to 85%.

21. Exogenous steroid administration should be avoided.
 treated the hyposalivation and dry mouth (xerostomia).
Prior to extensive oral surgical or periodontal procedures,
physicians should be consulted