قراءة
عرض

Gastritis

Acute
Causes: infectious, chemical
Histologically: Edema, hyperemia, mucosal erosions and hemorrhage.
Chronic
Helicobacter pylori infection (type B, antral, chronic active with lymphoid follicles)
Autoimmune (type A, body, atrophy, pernicious anemia)
Chemical (induced by drugs, bile reflux, alcohol, regenerative mucosal changes)
The pathogenesis of acute ulceration
NSAID-induced ulcers are caused by direct chemical irritation as well as cyclooxygenase inhibition, which prevents prostaglandin synthesis.
This eliminates the protective effects of prostaglandins, which include enhanced bicarbonate secretion and increased vascular perfusion.
Lesions associated with intracranial injury are thought to be caused by direct stimulation of vagal nuclei, which causes gastric acid hypersecretion.
Acute gastric ulcers
Macroscopic(gross)finding
It range in depth from shallow erosions caused by superficial epithelial damage to deeper lesions that penetrate the mucosa.
Acute ulcers are rounded and typically are less than 1 cm in diameter.
The ulcer base frequently is stained brown to black by acid digested extravasated red cells, in some cases associated with transmural inflammation and local serositis. While these lesions may occur singly, more often multiple ulcers are present within the stomach and duodenum.
Acute stress ulcers are sharply demarcated, with essentially normal adjacent mucosa, although there may be suffusion of blood into the mucosa and submucosa and some inflammatory reaction.
Chronic gastritis
Epithelial damage: increase of nuclei, distorsion of foveolae and glands)
Mucosal infiltrates of lymphocytes and plasma cells
Active process: neutrophil granulocytes (acute damage of epithelial cell)
Atrophy: chief and parietal cell loss and replacement by intestinal type epithelial cells
Intestinal metaplasia: acid mucin containing goblet cells, microvilli, Panneth cells
Regenerative changes: foveolar hyperplasia, increase of myofibroblasts and capillaries
Helicobacter associated chronic gastritis
Gross: red mucosa, coarser texture than normal, may have thickened rugal folds or thin/flat mucosa; with long term disease, mucosa may be thin/flat; usually affects antrum (particularly in children), and cardia .
Micro: bacteria is curved, spirochete-like, in superficial mucus layer and along microvilli of epithelial cells; are not invasive; are usually not seen in areas of intestinal metaplasia; associated with chronic inflammatory infiltrate with germinal centers (follicular gastritis) and plasma cells in lamina propria; active inflammation if neutrophils in glandular or surface epithelial layer.
PEPTIC ULCER DISEASE
Ulcer: focal destruction of mucosa or deeper (necrosis)
Erosion: less than full thickness focal loss of mucosa, can progress to ulcer or heal without scarring.
Peptic : primary autodigestive lesion caused by the action of gastric juice.
Sites: Esophagus, stomach, duodenum and ectopic mucosa
Hyperacidity.
Decreased mucosal protection.
Complications of ulcer
Bleeding
Perforation
Obstruction
Penetration
Pain
Predisposing factors for peptic ulcer of stomach and duodenum
Helicobacter pyIori
direct mucosal injury
increased acid secretion
inflammatory reaction
Trauma: burns, surgery, fractures (Curling ulcer)
Stress.
Cerebral Lesions.
Vagus nerve stimulation (hypothalamus)
Smoking.
Zollinger-Ellison syndrome.
gastrin overproduction, tumor (gastrinoma)
Genetic Factors.
Steroid hormons and Nonsteroidal anti-inflammatory drugs.
blocks prostaglandin synthesis.
Complications of gastric ulcer:
Bleeding
Occurs in 15% to 20 % of patients.
Most frequent complication.
May be life-threatening.
Accounts for 25% of ulcer deaths.
May be the first indication of an ulcer.
Perforation
Occurs in up to 5% of patients.
Accounts for two thirds of ulcer deaths.
It is rarely the first indication of an ulcer.
Obstruction
Mostly in chronic ulcers.
Secondary to edema or scarring.
Occurs in about 2% of patients.
Most often associated with pyloric channel ulcers.
May occur with duodenal ulcers.
Causes incapacitating crampy abdominal pain.
Can rarely cause total obstruction and intractable vomiting.
TUMORS
Benign Epithelial Tumors:
Hyperplastic and inflammatory polyps
True adenomas rare and not the leading cause of carcinoma
Malignant Epithelial Tumors:
Carcinoma, Adenocarcinoma
Malignant Non - Epithelial Tumors:
Lymphoma
Potentially Malignant Tumors:
Endocrine tumors (carcinoid)
GIST
Etiologic factors of stomach carcinoma
Related to socioeconomic level and diet.
High incidence in Japan, actually is decreasing in the Western world, continue to be high in Asia and Russia.
Smoked, salted foods.
Low fresh vegetable diet.
Nitrosamines.
Chronic gastritis with atrophy and metaplasia.
H. pylori infection.
Intestinal reflux.
Blood group A.
Relatives with stomach cancer.
Precancerous lesions
Dysplasia
Enlarged, hyperchromatic, irregularly outlined, crowded nuclei.
Irregular glands, mitoses.
High grade dysplasia = in situ carcinoma = intraepithelial neoplasia.
Adenoma
Carcinoma of the stomach
Sites: classically prepyloric, antral and lesser curvature.
Macroscopic types (Borrmann I-IV):
polypoid, ulcerative, ulcerating and infiltrating, infiltrating.
Microscopic types (Laurens):
Intestinal:
Gland forming, distal, better differentiated, usually old.
Diffuse:
Proximal, intracellular mucus, signet ring cells, less differentiated, usually young patient.



رفعت المحاضرة من قبل: Hatem Saleh
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