|
|
|
|
|
|
| Benign Gastric Ulcer |
| Etiology •The three most common causes of benign gastric ulcer (GU) are: H.pylori associated chronic gastritis; ingestion of NSAID; and stress (eg: postoperative or shock) •Less common causes include: Gastrinoma (MEN I); Antral G cell hyperplasia; Herpes simplex or CMV; chemotherapy •Miscellaneous risk factors include alcohol and smoking |
| Pathogenesis •Peptic ulcer disease most commonly results from the effect of pepsin and acid on mucosal cells •While hyperacidity alone can cause peptic ulcer disease, acid is more commonly normal or even decreased in GU so that the pathogenesis of peptic ulcer disease is multifactorial and involves breakdown in mucosal defense mechanisms as well as the effects of acid and pepsin •Defense mechanisms include: mucosal mucus layer, duodenal bicarbonate secretion; apical cell barrier of gastric mucosal cells with tight cell junctions resisting passage of acid; intracellular transport mechanisms for removal of excess H+; ability of blood to neutralize and remove excess acid, |
| Epidemiology •Benign ulcer disease of the upper GI tract should be looked at as a common entity whether it involves the stomach or more commonly the duodenum •The ratio of duodenal/gastric ulcer is 4/1 and although some clear differences exist between GU and DU they both fundamentally represent an imbalance between the effect of acid and pepsin vs compromise of normal mucosal defense mechanisms •There is a wide age distribution with peak incidence in middle age •The male/female is 1.5/1 •Prevalence of peptic ulcer is 10% for men and 5% for women |
| General Gross Description •Peptic ulcers are sharply punched out with straight walls and a flat base which is smooth •The adjoining mucosa is flat and the rugal folds extend to the margin of the ulcer and some reddening of the adjoining mucosa may indicate an associated gastritis. The gastric mucosa is often flattened due to the presence of chronic gastritis with atrophy •Acute ulcers may show edema and chronic ulcers show varying degrees of underlying fibrosis •The depth of the ulcer is variable with some showing only mucosal involvement in which case they are called erosions in contrast to deeply penetrating ulcers which involve submucosa and deeper layers •Occasionally evidence of active bleeding may be seen, and deep ulcers may perforate •Benign gastric ulcers are most commonly found along the leser curvature of the antrum •The majority of benign gastric ulcers are <2cm in diameter |
| General Microscopic Description •Acute benign gastric ulcers show coagulative necrosis of the mucosa with infiltration of polys •As time progresses, granulation tissue forms and there may be some regenerative activity of intact epithelium at the margin •The surrounding mucosa appears normal •Chronic ulcers show additional granulation tissue and the formation of dense scar beneath the ulcer •The term erosion indicates superficial necrosis involving only the mucosa, often found with NSAID use and accompanied by hemorrhage in the base of the ulcer •If necrosis extends into the submucosa or below the term ulcer is used •Chronic ulcers typically show endarteritis obliterans in vessels beneath the ulcer, and erosion of vessels may be seen in cases of active bleeding •The depth of ulceration is quite variable and may show full thickness penetration of the gastric wall with evidence of acute peritonitis •The reparative reaction beneath a benign ulcer may be quite exuberant and include large atyical cells which often represent proliferating endothelial cells. Care should be taken not to confuse these cells with malignant cells |
| Clinical Correlation •The classic symptoms of peptic ulcer include: burning epigastric pain occuring 1-3 hours after a meal or waking the patient at night; relief of pain with food or antacids; and episodic pain occuring in clusters •Numerous other changes in eating may occur and the presentation is often atypical •Some ulcers may be silent(pain free) and present with upper GI bleeding or perforation •Chronicity and recurrence are characteristic of peptic ulcers, and at least 50% of patients with gastric ulcers will have recurrent ulcers, although many of these are silent •The major complications of peptic ulcer disease are: bleeding (20%); perforation (5%); and obstruction •Diagnosis can be made clinically in typical cases with imaging and endoscopy used to document or confirm ulcer disease if necessary •Endoscopy with biopsy can document disease, help separate benign from malignant ulcers and diagnose concurrent H.pylori •Initial treatment is medical consisting of decreasing acid production with H2 blockers, removing ulcerogenic substances such NSAID agents and treating concurrent H.pylori •Surgery is reserved for intractable pain, failure of medical regimes, or major complications particularly severe bleeding or perforation |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 773-778 |
| Benign Gastric Ulcer |
| Synopsis by: (T63000M38000)[442] |
| Search Medline at National Library of Medicine Please be patient during transfer. Medline will open in a new window. To return, close the Medline Window |
|
|
|
|
|
|