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.
2. It is a medical condition characterized by Ulcers
in;
Lower esophagus
Stomach
Duodenum
Jejunum
Ileum (adjacent to Meckel's Diverticulum)
INTRODUCTION
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3. Ulcer is breach in
mucosal lining.
WHAT IS ULCER???
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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
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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
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8. H. Pylori
Depletion of antral D Cell Somatostatin
Increased gastric release from G cells
Increased Acid Secretion
Inflammation & Ulcers
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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
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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
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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
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12. Anorexia & nausea.
Gastric ulcer pain increases with food.
Duodenal ulcer pain is relieved with
food.
CLINICAL FEATURES OF PEPTIC ULCERS
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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
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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
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