Pathophysiology:

The mechanisms of mucosal injury in gastritis and PUD are thought to be mainly caused by H pylori infections, coupled an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood flow.

Erosive gastritis usually is associated with serious illness or with various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric secretions.

Helicobacter Pylori:

Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of PUD.H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective properties.

NSAIDs:

NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins.such as dyspepsia or gastroesophageal reflux disease (GERD).

Severe physiologic stress:

• Burns
• CNS trauma(Head injuries)
• Surgery
• Severe medical illness
• Chronic medical comditions like cirrhosis, chronic obstructive pulmonary disease, renal failure.

Hypersecretoryconditions:

• Gastrinoma (Zollinger-Ellison syndrome)

Common ulcer symptoms include:

• A burning sensation or pain  in the epigastric regoin.

                      - Occurs 2-3 hours after meals.

                       -Relieved by food or antacids

                      -The pain sometimes extends to the back.

• Nausea

                      - Dyspepsia, including belching, bloating, distention, and fatty food intolerance

                      - Heartburn

                      - Loss of appetite and weight loss.

                      - Bloating or nausea after eating. 

Less common but more serious symptoms of ulcers include:

• Vomiting after meals,which might be related to partial or complete gastric outlet obstruction.
• Vomiting blood and/or material that looks like coffee grounds.
• Black stools that look like tar, or stools that contain dark red blood. 

Symptoms of ulcers in the upper small intestine (duodenal ulcers) and in the stomach (gastric ulcers) are similar, except for when pain occurs:

• Pain from a duodenal ulcer may occur several hours after eating (when the stomach is empty) and may improve after eating. Pain also may wake you frequently in the middle of the night.

• Pain from a gastric ulcer may occur shortly after eating (when food is still in the stomach).

Silent ulcers: 

Silent ulcers  are more common in older adults, people who have diabetes,

or people who use nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen (Advil), or naproxen (Aleve).

Complications of an ulcer :

• Bleeding

• Perforation, penetration, or obstruction of the digestive tract.

• Complications can happen in both silent ulcers and ulcers that cause symptoms.

In children, symptoms vary with age:

• Toddlers and young children may complain of general stomach pain.
• Teenagers may have symptoms more like those experienced by adults.

Diagnostic tests:

Upper GI endoscopy:

• Preferred diagnostic test in the evaluation of patients with suspected PUD
• Highly sensitive for the diagnosis of gastric and duodenal ulcers
• Allows for biopsies and cytologic brushings in the setting of a gastric ulcer to differentiate a benign ulcer from a malignant lesion
• Allows for detection of H pylori infection with antral biopsies for a rapid urease test and/or histopathology in patients with PUD

Nonendoscopic or noninvasive tests :

• Serum H pylori antibody detection, fecal antigen tests, and urea breath tests.

Special tests:

• A fasting serum gastrin level to screen for Zollinger ellison syndrome
• A secretin stimulation test for the diagnosis of Zollinger-Ellison syndrome  

Treatment:

Medical treatment:

H2-receptor blockers(Cimetidine,Ranitidine,Famotidine):

These agents selectively block H2-receptors on parietal cells, resulting in diminished acid secretion and ulcer healing.

Long-term use can have tachyphalaxis. 

Proton pump inhibitors (PPIs):

Proton pump inhibitors bind to and inhibit the H+/K+ -adenosine triphosphatase (ATPase) pump of the parietal cell,

resulting in a marked decrease in acid secretion.These drugs are an important part of triple therapy, the treatment of choice

for H pylori infection.Can be used as primary therapy to heal ulcers not associated with H pylori infection. 

Helicobacter pylori eradication:

Most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of NSAIDs,

along with the appropriate use of antisecretory therapy.

Triple therapy for H.Pylori:

PPI-based triple therapies for H pylori are considered the first-line therapies for the treatment of H pylori.

These regimens consist of a PPI, amoxicillin, and clarithromycin for 7-14 days. 

Cytoprotectants(Misoprostol):

These agents have the ability to induce prostaglandin synthesis and, thus, cytoprotective effects in the GI tract.

Surgical treatment:

 Indications for surgical treatment  are: 

• Intractable pain
• Haemorrhage(bleeding)
• Perforation
• Gastric outlet obstruction 

Open surgical procedures: 

• Truncal vagotomy and pyloroplasty
• Truncal vagotomy and gastrojejunostomy
• Truncal vagotomy and antrectomy

• Highly selective vagotomy

• Anterior seromyotomy and posterior truncal vagotomy

Laparoscopic peptic ulcer operations: 

• Thoracoscopic truncal vagotomy and pyloric stretch
• Truncal vagotomy and pyloric stretch
• Highly selective vagotomy
• Posterior truncal vagotomy and selective anterior vagotomy
• Posterior truncal vagotomy and anterior seromyotomy.