Peptic ulcers are chronic most often solitary, lesions that occur in any portion of gastrointestinal tract exposed

to the aggressive action of acid-peptic juices Clinical Manifestation: Remitting, relapsing lesion Most often diagnosed in middle aged to older adults but may first become evident in young adult life. Epigastric burning or aching pain. Pain worse at night and 1 to 3 hours after meal. Nausea, vomiting, bloating , belching and weight loss occur. Complication: Anemia, hemorrhage, perforation, obstruction. Malignant formation is rare and related to underlying gastritis. Sites of Peptic ulcer Duodenum: First portion ( few cms from the pyloric ring). Anterior wall is more often affected. Stomach: Usually antrum. Lesser curvature (common) . Anterior and posterior wall and greater curvature (less common). Gross features Base of ulcer: Smooth and clean (peptic digestion of any exudate). Thrombosed or patent blood vessels are evident at the base. Surrounding gastric mucosa: Puckering of surrounding mucosa. The mucosal fold radiates from the crater in a spoke- like fashion. Edematous and reddened due to gastritis. Precipitating Factors: Gastric wall: *Food Poisoning (Ingestion of H. Pylori) Scarring involve the entire thickness . Subserosal *Impaired mucosal defense . The gastric acid and pepsin levels are normal and no H.pylori are present. fibrosis and inflammation present. Chronic use of NSAIDs (aspirin) Cigarette smoking impair Regional lymphnodes are enlarged.
healing and favor recurrences. Alcoholic cirrhosis. Personality, psychological stress, ischemia. Zollinger Ellison Syndrome Critically ill patients

PATHOPHYSIOLOGY Predisposing Factors: *Race: Americans *Gender: Male * Age: Middle- late adulthood

No H. Pylori

Causative Agent H. Pylori H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus) or phospholipases.

Site (gastroduodenal mucosa)

Inability to withstand the digestive action of gastric acid (HCl) and pepsin

Bacterial lipopolysaccharide attracts inflammmatory cells to the mucosa

Increased concentration or activity of acid-pepsin and decreased resistance of the mucosa

A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries

Mucosal damage allows leakage of tissue nutrients in the surface microenvironment , sustaining the bacillus Erosion/damage of the mucosa Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion. Inflammation of the gastric mucosa

Inability to secrete enough mucus to act as a barrier against HCl

Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration Inability to secrete enough mucus to act as a barrier against HCl and gastrinomas (islet cell tumors) in the pancreas

Ulcers occur at sites of chronic inflammation

PEPTIC ULCER DISEASE