Peptic ulcer disease

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* The term “peptic ulcer” refers to an ulcer in:Lower esophagus Stomach Duodenum Jejunum after surgical anastomosis to stomachRarely, ileum adjacent to Meckel’s diverticulum. It may be acute or chronic Both penetrate muscularis mucosae Acute ulcer shows no evidence of fibrosis Erosions do not penetrate muscularis mucosae

* Peptic Ulcer Disease

H. Pylori infection
NSAIDs
Smoking
Other factors affecting Acid-pepsin versus Mucosal resistance


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* Chronic gastric ulcer: It is usually single 90% are situated on the lesser curve within the antrum or at the junction between the body and antral mucosa Chronic duodenal ulcer: It usually occurs in the 1st part of the duodenum just distal to the junction of the pyloric and duodenal mucosa. 50% are on the anterior wall Gastric & duodenal ulcers coexist in 10% of patients More than one peptic ulcer is found in 10-15% of patients Chronic ulcer shows 4 layers: Surface debris An infiltrate of neutrophils Granulation tissue Collagen

* Natural history of spontaneous relapse & remission lasting for decades, if not for life. Recurrent abdominal pain: Localization to the epigastrium Relationship to food Episodic occurrence Vomiting: Occurs in 40% of cases Persistent daily vomiting suggests gastric outlet obstruction. In 1/3rd of patients the history is less characteristic particularly in elderly especially those under treatment with NSAIDs Occasionally, the only symptom is: Anorexia & nausea Sense of undue repletion after meals

* In some patients the ulcer is completely silent and the patients present for the 1st time with; Anemia from chronic undetected blood loss Abrupt hematemesis Acute perforation In other patients, there is recurrent acute bleeding without ulcer pain between the attcks It should be noted that: The diagnostic value of individual symptoms for peptic ulcer disease is poor The history is often a poor predictor of the presence of an ulcer.


* The diagnosis can be made by either: Double contrast barium meal. Endoscopy: It is the preferred method because: It is more accurate Suspicious lesions and H. pylori status can be evaluated by biopsy. For those with duodenal ulcer seen at barium meal, urea breath testing will accurately define H. pylori status. Endoscopy & biopsy is mandatory when gastric ulcer is detected at barium meal because of the risk of being malignant. In addition, repeated endoscopy examination is indicated in cases of gastric ulcer after suitable treatment. It is not necessary to repeat the endoscopy in cases of treated duodenal ulcer as follow up tool

* Fundus

Radiating folds
Ulcer Creator

* Ulcer

Towards pylorus

* Ulcer

Radiating Mucosal folds
Macroscopic features of gastric ulcer

* Deep duodenal ulcer

Duodenal loop
Duodenal cup
Antrum of stomach

* Duodenal ulcer

* Multiple duodenal ulcers in case suspected to have Zollinger Ellison syndrome

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* The aims of management are to: Relieve symptoms Induce ulcer healing in the short term Cure the ulcer in the long term H. pylori eradication is the cornerstone of therapy of peptic ulcer, as this will: Prevent ulcer relapse and complications Eliminate the need for long-term therapy in the majority of the patients. Improve quality of life

* Treatment of Peptic ulcer

H. pylori eradication
General measures
Surgical Treatment
Maintenance treatment
Short-term management


* Indications: Definite: Peptic Ulcer MALToma Not indicated: Asymptomatic GERD Uncertain: Family history of gastric cancer Non-ulcer dyspepsia Long-term NSAIDs users



* Antibiotic regimens: First-line therapy including: Proton pump inhibitor at standard dose (12 hourly) + Amoxicillin 1 g 12-hourly + Clarithromycin 500 mg 12 hourly or Metronidazole 400 mg 12-hourly All three drugs for 7 days

* Second-line therapy (recommended in case of failure of 1st line therapy): Proton pump inhibitor in standard dose, 12-hourly Bismuth 120 mg 6-hourly Metronidazole 400 mg 12-hourly Tetracycline 500 mg 6-hourly All of the above FOUR drugs for 7 days

* Only 50% of peptic ulcer patients are treated Only 50% receive adequate antibiotics

* Common side effects of H. pylori eradication therapy: Diarrhea: 30-50% of patients, usually mild but Clostrdium deficille-associated colitis can occur Metronidazole; Metallic taste (common) Peripheral neuropathy (rare) Flushing & vomiting when taken with alcohol Nausea, vomiting Abdominal cramp Headache Rash

* The patients should avoid: Cigarette smoking Aspirin & NSAIDs Alcohol in moderation is not harmful No special dietary advice is required.

* Many different drugs are available for the short-term management of acid-peptic symptoms including: Antacids: Relieve minor dyspeptic symptoms Calcium compounds cause constipation Aluminium compounds cause: Diarrhea Block absorption of digoxin, tetracycline, & dietary phosphate Most have high sodium content (can exacerbate CHF)


* Histamine H2-receptor antagonist drugs H+/K+ ATPase (proton pump) inhibitors Colloidal bismuth compounds Sucralfate Synthetic prostaglandin analogues (misoprostol)


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* Continuous maintenance treatment should not be necessary after successful H. pylori eradication. For the minority who require maintenance treatment, the lowest effective dose should be used.

* Indications for surgery in peptic ulcer: Emergency: Perforation Hemorrhage Elective: Complications e.g. gastric outflow obstruction Recurrent ulcer following gastric surgery


* Follow-up evaluation PU patients
DU
GU
Symptoms relieved
Symptoms persisting
Re-endoscopy
1- Another diagnosis 2- Irritable Gut
Healed
Non-Healed (Biopsy)
Persisting H. Pylori infection
Non-H. pylori ulcer


* Persisting H. pylori infection: Poor compliance Resistant H. pylori Inadequate treatment
Non-H. pylori ulcer:False negative H. pylori Inadequate biopsy Proton pump inhibitor or Bismuth intake Continues use of NSAIDsDelayed healing Dense fibrosis Smoking Big ulcer Hypersecretory state Non-peptic ulcer:Tuberculosis Cancer Crohn’s disease

GASTRINOMAS (zollinger-Ellison syndrome) is caused by ectopic secretion of gastrin by a PET (i.e., gastrinoma), which causes excessive gastric acid secretion, characteristically causing peptic disease (often severe) and/or gastroesophageal reflux disease (GERD). It is characterized by Prominent gastric folds on UGI endoscopy or X-ray (90%), Multiple peptic ulcers or ulcers in unusual locations (1%-5%), Complicated PUD (gastric outlet obstruction, 10%; perforation, 7%; recurrent bleeding, 5%-10%) and Esophageal stricture caused by PUD (3%-4%). The diagnosis of ZES requires the demonstration of acid hypersecretion in the presence of hypergastrinemia (assessments of fasting serum gastrin levels that will be increased), if the fasting serum gastrin level is normal, especially in repeated determinations, the diagnosis of ZES is very unlikely.