Pathophysiology/Pathogenesis of PUD The gastric mucosa is often exposed to noxious substances such as gastric acid, bacteria (Helicobacter pylori ) and drugs. The most common important factors that can cause ulcers are infection with H. pylori and non-steroidal anti-inflammatory drugs (NSAIDs. ) NSAIDs are a group of medications typically used to treat pain and are so common because they are available over the counter without a prescription. People, especially the elderly one who take NSAIDs fora long time, at high do ses or both, have a higher risk of developing ulcers than younger persons. NSAIDs are known to inhibit prostaglandin production by inhibiting two isoforms of cyclo- oxygenase (COX) enzymes, called COX-1 and COX-2. COX-1 is involved in GI mucosal protection and platelet function, whereas COX-2 is involved in the induction of prostaglandin production at the inflammatory site in order to mediate inÀammation and pain. Thus, the anti- inÀammatory effects of nonselective NSAIDs are due to COX-2 inhibition. The suppression ofCOX-1 causes a profound reduction of mucosal prostaglandin production which probably causes the harmful effects in the GI tract and platelets. Thus the inhibition of COX-1 by NSAIDs increases the risk of peptic ulcer d isease development and epithelial injury. Treatment goals: 1.To relieve the pain due to peptic ulcer disease (PUD ). 2.To heal peptic ulcer. 3.To prevent the recurrence and complications of PUD.
