GASTROINTESTINAL DISEASES :

Diseases of The :

Normal: The stomach is divided into five anatomic regions , the cardia is the narrow conical portion of the stomach immediately distal to the gastroesophageal junction. The fundus is the dome-shaped portion of the proximal stomach. The body, or corpus, comprises the remainder of the stomach proximal to the incisura angularis. The stomach distal to this angle is the antrum, demarcated from the by the muscular pyloric sphincter.

The gastric wall, consists of mucosa, submucosa, muscularis propria, and serosa. The interior surface of the stomach exhibits coarse rugae .These infoldings of mucosa and submucosa are most prominent in the proximal stomach, flattening out when the stomach is distended .

Congenital anomaly: :

Congenital hypertrophic pyloric stenosis is encountered in infants as a disorder that affects males three to four times more often than females. Regurgitation and persistent,

1 projectile, nonbilious vomiting usually appear in the second or third week of life. Physical examination reveals visible peristalsis and a firm, ovoid palpable mass in the region of the pylorus or distal stomach, the result of hypertrophy, and possibly hyperplasia, of the muscularis propria of the pylorus. Edema and inflammatory changes in the mucosa and submucosa may aggravate the narrowing. Surgical muscle splitting is curative.

Gastritis:

 Chronic : Is the presence of mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia. Pathogenesis: 1. the most important pathogen is H. pylori.It has a high prevalence rate among adults. H. pylori is non invasive, non spore forming S-shaped gram negative rods. 2. Unknown causes: Seen mostly in Japan. 3. Autoimmune: Autoantibodies directed towards gastric parietal cells leading to gland destruction and mucosal atrophy with loss of acid and intrinsic factor production. This form is seen most often in Scandinavia in association with other forms of autoimmune disorders like Hashimoto’s thyroiditis and Addison’s disease. Intestinal metaplasia of gastric epithelium may be regarded as a precursor for intestinal type gastric carcinoma and proliferation of lymphoid tissue in chronic H. pylori infection could lead to lymphoma. Clinical Features: Pain, and vomiting. Hypochlorhydria or and hypergastrinaemia are characteristic of autoimmune gastritis, along with pernicious anemia. Gastric ulcers could develop.

 Acute Gastritis: Is an acute inflammatory process usually of a transient nature, may be acoompanied by hemorrhage and sloughing of superficial mucosa (erosion). Pathogenesis: Causes: 1. Heavy use of NSAIDs. 2. Extensive alcohol consumption. 3. Heavy smoking. 4. Chemotherapeutic agents.

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5. Uremia. 6. Systemic infection (e.g. typhoid fever). 7. Severe stress (trauma, burns, surgery). 8. Ischemia and shock. 9. Ingestion of acids and alkalins. 10. Mechanical trauma (N.G. tube). 11. After partial gastrectomy with reflux of bile.

Pathophysiology: 1. Disruption of the adherent mucosal layer. 2. Stimulation of acid secretion. 3. Decreased production of bicarbonate. 4. Reduced mucosal blood flow. 5. Direct damage of epithelium.

Microscopically it ranges from superficial involvement to involvement of the entire mucosal thickness, localized or diffuse. Mucosal edema, neutrophilic infiltrate and possibly chronic inflammatory infiltrate,and regenerative replication of epithelial cells in the gastric pits is usually prominent.

Peptic Ulceration: Is a breach in the mucosa that extends through the muscularis mucosae into the submucosa or deeper. 98% of peptic ulcers are either in the first potion of the duodenum or in the stomach in a ratio of 4:1. Duodenal ulcers are more frequent in: 1. Alcoholic . 2. COPD. 3. Chronic renal failure. 4. Hyperparathyroidism: Hypercalcemia causes increased gastrin secretion. Pathogenesis: Induced by imbalance between mucosal defense mechanisms and aggressive forces. Defense mechanisms: 1. Secretion of mucus. 2. Secretion of bicarbonate. 3. Mucosal blood flow. 4. Apical surface membrane transport. 5. Epithelial regenerative capacity. 6. Elaboration of prostaglandins. Aggressive foces: 1. Gastric acidity. 2. H. pylori.

H. pylori is present in all patients with duodenal ulcers and 70% of gastric ulcers. Mehanisms of H. pylori pathogenesis: 1. Secretion of urease, proteases and phospholipases. 2. Neutrophils produce myeloperoxidase and monochloramine. 3. H. pylori cause thrombotic occlusion of surface capillaries. 4. Elaboration of lipopolysaccharides.

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Most peptic ulcers are rounded with sharply punched out crater, 2-4 cm in diameter, smaller in the duodenum in the anterior and posterior walls and lesser curvature of the stomach. The margins of the crater are punched out with no significant elevations of the edges. Histologically, 4 zones are identified: 1. The base and margins of thin necrotic fibrinoid debris. 2. Active non-specific inflammatory cell infiltration mostly neutrophils. 3. Granulation tissue. 4. Fibrous collagenous scar. Chronic gastritis occurs in 85-100% of duodenal ulcers and 65% of gastric ulcers.

Acute Ulceration: Appear after severe stress, are multiple located mainly in the stomach and occasionally in the duodenum. Causes: 1. Severe trauma. 2. Extensive burns (Curling’s ulcers). 3. CNS injury (Cushing’s ulcer). 4. Chronic exposure to NSAIDs and corticosteroids.

Tumors

BENIGN TUMORS  The mucosal polyps are classified as non-neoplastic or neoplastic. Gastric polyps are uncommon. Although they are usually found incidentally, dyspepsia or anemia

MORPHOLOGY: majority of gastric polyps (up to 90%) are non-neoplastic and appear to be of a hyperplastic nature composed of a mixture of hyperplastic surface epithelium (foveolar epithelium) and cystically dilated glandular tissue, with a lamina propria containing increased inflammatory cells and smooth muscle . Most hyperplastic polyps are small and sessile and are commonly located in the antrum .

The adenoma of the stomach constitutes 5% to 10% of the polypoid lesions in the stomach. adenoma contains proliferative dysplastic epithelium and so has malignant potential. Gastric adenomas may be sessile (without a stalk) or pedunculated (stalked). The most common location is the antrum.

 Lipomas. Lipomas are a benign neoplasm of adipose tissue, usually present in the submucosa

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Malignant tumor: Carcinomas: 90-95% Lymphomas: 4% Carcinoids: 3% GISTs: 2%

There are two types of gastric carcinomas: 1. Intestinal: arise on intestinal metaplasia, M:F ratio is 2:1. 2. Diffuse: Seen in patients younger than 50 yrs. M:F ratio is 1:1.

Pathogenesis:  Intestinal type: A- Diet: Nitrites, smoked food and pickles, excess salt intake and decreased intake of fresh vegetables. B- Infection with H. pylori. C- Pernicious anemia. D- Altered anatomy: Subtotal gastrectomy. E- Cigarette smoking F-Gastric adenomas

 Diffuse type: Unknown. Familial gastric carcinoma syndrome(E-cadherin mutation)

Locations: Pylorus and antrum: 50-60% Cardia: 25% Body And Fundus: 15-25% Lesser curvature: 40% Greater curvature: 12% morphology: Four patterns of growth: 1. Exophytic. 2. Flat or depressed. 3. Excavated: with an erosive crater. 4. Linitis plastica: Diffuse thickening and permeation of the gastric wall.

The intestinal variant is composed of neoplastic intestinal glands resembling those of colonic adenocarcinoma , which permeate the gastric wall . The diffuse variant is composed of gastric-type mucous cells, which generally do not form glands, but permeate the mucosa and wall as scattered individual cells or small clusters in an "infiltrative" growth pattern.

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