Peptic ulcers are chronic, recurring lesions that occur most often in middle-aged to older adults without obvious precipitating conditions, other than chronic gastritis. A majority of peptic ulcers come to clinical attention after patient complaints of epigastric burning or aching pain, although a significant fraction manifest with complications such as iron deficiency anemia, frank hemorrhage, or perforation. The pain tends to occur 1 to 3 hours after meals during the day, is worse at night, and is relieved by alkali or food. Nausea, vomiting, bloating, and belching may be present. Healing may occur with or without therapy, but the tendency to develop subsequent ulcers remains.
Fig. 15.15 Pepticulcerdisease.(A)EndoscopicviewoftypicalantralulcerassociatedwithNSAIDuse.(B)Grossviewofasimilarulcerthatwasresectedduetogastricperforation,presentingasfreeairunderthediaphragm.Notethecleanedges.(C)Thenecroticulcerbaseiscomposedofgranulationtissueoverlaidbydegradedblood.(Endoscopic image courtesy of Dr. Ira Hanan,The University of Chicago, Chicago, Illinois.) http://ebooksmedicine.net
PUD causes much more morbidity than mortality. A variety of surgical approaches were formerly used to treat PUD, but current therapies are aimed at H. pylori eradication with antibiotics and neutralization of gastric acid, usually through use of proton pump inhibitors. These efforts have markedly reduced the need for surgical management, which is reserved primarily for treatment of ulcers with uncontrollable bleeding or perforation.
Long-standing chronic gastritis may be associated with intestinal metaplasia, recognized by the presence of goblet cells. This is strongly associated with increased risk for development of gastric adenocarcinoma. In addition, the achlorhydria of gastric mucosal atrophy, which is commonly associated with intestinal metaplasia, permits overgrowth of bacteria that produce carcinogenic nitrosamines. Intestinal metaplasia caused by chronic H. pylori gastritis may regress after eradication of the organism.
Chronic gastritis exposes the epithelium to inflammation-related free radical damage and proliferative stimuli. Over time, this can lead to the accumulation of genetic alterations that result in carcinoma. Preinvasive in situ lesions can be recognized histologically as dysplasia, which is marked by variations in epithelial size, shape, and orientation along with coarse chromatin texture, hyperchromasia, and nuclear enlargement. These overlap with and are sometimes difficult to distinguish from injury-associated regenerative changes.
Gastritisisamucosalinflammatoryprocess.Wheninflammatorycellsareabsentorrare,thetermgastropathy canbeapplied.
Thespectrumofacutegastritisrangesfromasymptomaticdiseasetomildepigastricpain,nausea,andvomiting.Causativefactorsincludeanyagentordiseasethatinterfereswithgastricmucosalprotection.Acutegastritiscanprogresstogastriculceration.
ThemostcommoncauseofchronicgastritisisH. pylori infection;mostremainingcasesarecausedbyNSAIDs,alcohol,or autoimmune gastritis.
H. pylori gastritistypicallyaffectstheantrumandisassociatedwithincreasedgastricacidproduction.
H. pylori gastritisinducesmucosa-associatedlymphoidtissue(MALT)thatcangiverisetoB-celllymphomas(MALTomas).
Autoimmune gastritis causesatrophyofthegastricbodyoxynticglands,whichresultsindecreasedgastricacidproduction,antralG-cellhyperplasia,achlorhydria,andvitaminB12deficiency.Anti–parietalcellandanti–intrinsicfactorantibodiesaretypicallypresent.