This document summarizes peptic ulcers, which are ulcers that can form in the esophagus, stomach, or duodenum. Peptic ulcers are commonly caused by H. pylori infections or NSAID use. H. pylori infections are usually treated with a combination of antibiotics and proton pump inhibitors. Treatment aims to eliminate H. pylori and reduce stomach acid levels to allow ulcers to heal. Surgery may be needed for complications like bleeding or perforation. Maintaining a healthy lifestyle can help prevent ulcer recurrence.

1. Sarang Suresh
Hotchandani

2. It is a medical condition characterized by Ulcers
in;
Lower esophagus
Stomach
Duodenum
Jejunum
Ileum (adjacent to Meckel's Diverticulum)
INTRODUCTION
SARANG SURESH HOTCHANDANI

3. Ulcer is breach in
mucosal lining.
WHAT IS ULCER???
SARANG SURESH HOTCHANDANI

4. H. Pylori
Infection
Stress Injury of
mucus
secreting cell
ETIOLOGY OF PEPTIC ULCER
SARANG SURESH HOTCHANDANI

5. Chronic
Use of
NSAIDs
Smoking Alcohol &
Diet
ETIOLOGY OF PEPTIC ULCER
SARANG SURESH HOTCHANDANI

6.  Gastric Ulcer
 Chronic gastric ulcer is usually single.
 Approx. 90% are situated in lesser curvature with the antrum or junction between
body and antral mucosa.
 Duodenal Ulcer
 Chronic duodenal ulcers occurs in 1st part of duodenum.
 Approx. 50% are on anterior wall.
 Gastric & duodenal ulcers co – exists in approx. 10% of patients.
 Multiple peptic ulcers are found in approx. 10 – 15 % of patients.
EPIDEMIOLOGY
SARANG SURESH HOTCHANDANI

7. Approx. 90% of cases of duodenal ulcers patients & approx.
70% of gastric ulcer patients are infected with H. Pylori.
Others are by NSAIDs.
Infection is acquired in childhood from person to person
contact.
Majority of people infected with H. Pylori are asymptomatic &
healthy.
Only small number of people develop symptoms.
PATHOPHYSIOLOGY
SARANG SURESH HOTCHANDANI

8. H. Pylori
Depletion of antral D Cell Somatostatin
Increased gastric release from G cells
Increased Acid Secretion
Inflammation & Ulcers
SARANG SURESH HOTCHANDANI

9.  H. Pylori only grow on gastric
type of mucosa.
 Virulence Factors of H. Pylori;
 Vacoulating cytotoxin A )Vac A)
 Cytotoxin associated gene (Cag A)
 Adhesion (BabA)
 OiPA (Outer inflammatory protein A)
 It is gram –ve, motile & spiral
bacteria
 Uses adhesion molecule (BabA)
to bind Lewis B antigen on
epithelial cells.
 Prevent its damage from acid
by producing urease which
convert ammonia into urea with
protects H. Pylori.
PROPERTIES OF H. PYLORI
SARANG SURESH HOTCHANDANI

10. Increase acid release from
stomach cause metaplasia of
duodenal mucosa which provide
environment for growth of H.
Pylori resulting duodenal ulcer.
H. PYLORI ONLY GROWS ON GASTRIC MUCOSA!
THEN HOW IT GROW IN DUODENUM RESULTING
DUODENAL ULCER
SARANG SURESH HOTCHANDANI

11.  It is a chronic condition with spontaneous relapse & remissions.
 The diagnostic value of individual symptoms for peptic ulcer is poor.
 Most Common Presentation
 Recurrent abdominal pain
 Pain is epigastrium
 relationship to food
 Episodic occurrence
 Vomiting in approx. 40% of patients.
CLINICAL FEATURES OF PEPTIC ULCERS
SARANG SURESH HOTCHANDANI

12. Anorexia & nausea.
Gastric ulcer pain increases with food.
Duodenal ulcer pain is relieved with
food.
CLINICAL FEATURES OF PEPTIC ULCERS
SARANG SURESH HOTCHANDANI

13. H. Pylori infection test.
Non – Invasive
 Serology
 Urea Breath Test (High Specificity
& Sensitivity)
 Fecal antigen test
Invasive
 Histopathology exam
 Rapid urease test
 Microbial culture
INVESTIGATIONS
SARANG SURESH HOTCHANDANI

14. Maintainace
Treatment
Surgical
Treatment.
H. Pylori
Eradication
General
Measures
MANAGEMENT OF PEPTIC ULCER
SARANG SURESH HOTCHANDANI

15. Proton
Pump
Inhibitor
2 Antibiotics
• Amoxicillin
• Clarithromycin
• Metronidazole
H. PYLORI ERADICATION
7 DaysSARANG SURESH HOTCHANDANI

16. Proton
Pump
Inhibitor
Bismuth
Substrate
Metronidazole Tetracycline
H. PYLORI ERADICATION “OR”
10 – 14 DaysSARANG SURESH HOTCHANDANI

17. Diarrhea; approx. 30 – 50% of patients.
Flushing & vomiting when taken with alcohol.
Nausea & vomiting.
Cramps, headache, rashes.
SIDE EFFECTS OF H. PYLORI ERADIATION
THERAPY
SARANG SURESH HOTCHANDANI

18. Chronic proton pump
inhibitor user.
Idiopathic Thrombocyte
Purpura
Iron deficiency anemia
Peptic ulcer
Family history of Gastric
ulcer.
Previous resection of
gastric cancer.
H. Pylori Positive
INDICATIONS OF H. PYLORI ERADICATION
THERAPY
SARANG SURESH HOTCHANDANI

19. Gastro Esophageal Reflux
Disease
Asymptomatic Persons
CONTRAINDICATION OF H. PYLORI ERADICATION
THERAPY
SARANG SURESH HOTCHANDANI

20. AVOID
Smoking
Chronic NSAIDs
Alcohol
GENERAL MEASURES
SARANG SURESH HOTCHANDANI

21. Low dose of Proton
Pump Inhibitors
MAINTAINACE THERAPY
SARANG SURESH HOTCHANDANI

22. Operation of choice for
chronic non – healing
gastric ulcers is
Partial Gastrectomy.
SURGICAL TREATMENT
SARANG SURESH HOTCHANDANI

23. Elective
Gastric outflow
obstruction
Persistent
ulceration
Recurrent ulcer
Emergency
Perforation
Hemorrhage
INDICATIONS OF SURGICAL TREATMENT OF
PEPTIC ULCER
SARANG SURESH HOTCHANDANI

24. Iron deficiency anemia
Metabolic bone disease
Gastric cancer.
Dumpling
Bile reflux gastropathy
Diarrhea & mal digestion
Weight loss
COMPLICATION OF GASTRIC RESECTION
SARANG SURESH HOTCHANDANI

25. Zollinger – Ellison
Syndrome
It is triad of Peptic Ulcer +
Hyperchlorhydra + Non B
Cell tumor of Pancreas
Perforation
Peritonitis
Gastric outlet
obstruction
Bleeding
COMPLICATIONS PEPTIC ULCER
SARANG SURESH HOTCHANDANI

26. Sarang
Suresh
Hotchandani
Final Year
Dentistry
Student
Bibi Aseefa
Dental
College,
SMBBMU,
Larkana,
Sindh,
P A K I S T A N
THE END
SARANG SURESH HOTCHANDANI