CAUSES & RISK FACTORS: Normally, the lining of the stomach and small intestines are protected against

the irritating acids produced in your stomach. If this protective lining stops working correctly, and the lining breaks down, it results in inflammation (gastritis) or an ulcer. Most ulcers occur in the first layer of the inner lining. A hole that goes all the way through the stomach or duodenum is called a perforation. A perforation is a medical emergency. The most common cause of such damage is infection of the stomach by bacteria called Helicobacter pylori (H.pylori). Most people with peptic ulcers have these bacteria living in their gastrointestinal (GI) tract. Yet, many people who have such bacteria in their stomach do not develop an ulcer. RISK FACTORS: Peptic Ulcer Drinking too much alcohol Regular use of aspirin, ibuprofen, naproxen, or other nonsteroidal anti-inflammatory drugs (NSAIDs). Taking aspirin or NSAIDs once in awhile is safe for most people. Smoking cigarettes or chewing tobacco Being very ill, such as being on a breathing machine Radiation treatments Advanced age Alcohol intake Chronic diseases, such as emphysema, rheumatoid arthritis, cirrhosis, and diabetes **A rare condition called Zollinger-Ellison syndrome causes stomach and duodenal ulcers. Persons with this disease have a tumor in the pancreas that releases high levels of a hormone, which causes an increase in stomach acid.

PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE

Contributory factor: Diet: caffeine intake Alcohol and smoking Presence of Helicobacter pylori infection Precipitating factors: Age: 50-70 years old Gender: male

Increase hydrochloric acid (HCL) production

Irritation of the lining (mucosal) of the stomach, duodenum, proximal of small intestines

Damaged mucosal barrier

Inflammatory process

Decreased function of mucosal cells Decreased quality of mucus Loss of tight junctions between cells

S/Sx: Abdominal Pain

Back diffusion of acid into gastric mucosa

Conversion of pepsinogen to pepsin Increase acid secretion Further mucosal erosion Destruction of blood vessels Mucosal injury Ulceration Bleeding/ Hemorrhage Decreased oxygen carrying capacity as manifested by decreased hemoglobin and hematocrit level S/Sx: black tarry stools, vomiting with the presence of blood

Formation of liberation of histamine Local vasodilation Stimulation of cholinergic intramural plexus, causing muscle spasm Increase capillary permeability Loss of plasma proteins Mucosal edema Loss of plasma into gastric lumen

S/Sx: Pallor, Lightheadedness, and weakness