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neopastic disease of the stomach

الكلية كلية طب حمورابي     القسم الكلية ذات القسم الواحد     المرحلة 4
أستاذ المادة هديل عبد الاله رزوقي كربل       23/10/2016 19:52:46
NEOPLASTIC DISEASE OF THE STOMACH L4

Gastric Polyps
Polyps, nodules or masses that project above the level of the surrounding mucosa, are identified in up to 5% of upper gastrointestinal tract endoscopies.
Inflammatory and Hyperplastic Polyps

Approximately 75% of all gastric polyps are inflammatory or hyperplastic polyps. They most commonly affect persons between 50 and 60 years of age, usually arising in a background of chronic gastritis that initiates the injury and reactive hyperplasia that cause polyp growth.
MORPHOLOGYNEOPLASTIC DISEASE OF THE STOMACH L4

Gastric Polyps
Polyps, nodules or masses that project above the level of the surrounding mucosa, are identified in up to 5% of upper gastrointestinal tract endoscopies.
Inflammatory and Hyperplastic Polyps

Approximately 75% of all gastric polyps are inflammatory or hyperplastic polyps. They most commonly affect persons between 50 and 60 years of age, usually arising in a background of chronic gastritis that initiates the injury and reactive hyperplasia that cause polyp growth.
MORPHOLOGY
The polyps frequently are multiple and characteristically are ovoid in shape, less than 1 cm in diameter, and covered by a smooth surface.
On microscopic examination, polyps have irregular, cystically dilated, and elongated foveolar glands. The lamina propria typically is edematous with variable degrees of acute and chronic inflammation, and surface erosions may be present.

Gastric Adenoma
Gastric adenomas represent as many as 10% of all gastric polyps. Patients usually are between 50 and 60 years of age, and males are affected three times more often than females. adenomas almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia. The risk for development of adenocarcinoma in gastric adenomas is related to the size of the lesion and is particularly elevated with lesions greater than 2 cm in diameter. Overall, carcinoma may be present in up to 30% of gastric adenomas.
MORPHOLOGY
Gastric adenomas are most commonly located in the antrum and typically are composed of intestinal-type columnar epithelium.
All gastrointestinal adenomas exhibit epithelial dysplasia, which can be classified as low- or high grade. Both grades may include enlargement, elongation, and hyperchromasia of epithelial cell nuclei, epithelial crowding, and pseudostratification. High-grade dysplasia is characterized by more severe cytologic atypia and irregular architecture, including glandular budding and gland-within-gland, or cribriform, structures.

Gastric Adenocarcinoma
Adenocarcinoma is the most common malignancy of the stomach, comprising more than 90% of all gastric cancers.
Gastric cancer rates vary markedly with geography. The incidence is up to 20 times higher in Japan, Chile, Costa Rica, and Eastern Europe than in North America, northern Europe, Africa, and Southeast Asia.
Gastric cancer is more common in lower socioeconomic groups and in persons with multifocal mucosal atrophy and intestinal metaplasia.
PATHOGENESIS
Gastric cancers are genetically heterogeneous but certain molecular alterations are common.
Mutations Germ line mutations in CDH1, which encodes E-cadherin, a protein that contributes to epithelial intercellular adhesion, are associated with familial gastric cancers, usually of the diffuse type. Thus, the loss of E-cadherin function seems to be a key step in the development of diffuse gastric cancer.
Sporadic intestinal-type gastric cancer is associated with several genetic abnormalities including acquired mutations of ?-catenin, a protein that binds to both E-cadherin and APC protein.
H. pylori: Chronic gastritis, most commonly due to H. pylori infection, promotes the development and progression of cancers that may be induced by diverse genetic alterations.
EBV: While H. pylori is most commonly associated with gastric cancer, approximately 10% of gastric adenocarcinomas are associated with Epstein-Barr virus (EBV) infection.
MORPHOLOGY
Gastric adenocarcinomas are classified according to their location in the stomach as well as gross and histologic morphology. The Lauren classification that separates gastric cancers into intestinal and diffuse types.
Intestinal-type cancers tend to be bulky and are composed of glandular structures similar to esophageal and colonic adenocarcinoma. Intestinal-type adenocarcinomas typically grow to form either an exophytic mass or an ulcerated tumor.
The neoplastic cells often contain apical mucin vacuoles, and abundant mucin maybe present in gland lumina.
Diffuse gastric cancers display an infiltrative growth pattern and are composed of discohesive cells with large mucin vacuoles that expand the cytoplasm and push the nucleus to the periphery, creating a signet ring cell morphology. These cells permeate the mucosa and stomach wall individually or in small clusters.
A mass may be difficult to appreciate in diffuse gastric cancer, but these infiltrative tumors often evoke a desmoplastic reaction that stiffens the gastric wall and may cause diffuse rugal flattening
and a rigid, thickened wall that imparts a “leather bottle” appearance termed linitis plastica.

SMALL AND LARGE INTESTINES
Malabsorptive Diarrhea
Diarrhea is a common symptom of many intestinal diseases, including those due to infection, inflammation, ischemia, malabsorption, and nutritional deficiency. malabsorption, which manifests most commonly as chronic diarrhea and is characterized by defective absorption of fats, fat- and water-soluble vitamins, proteins, carbohydrates, electrolytes and minerals, and water.
Chronic malabsorption causes weight loss, anorexia, abdominal distention, borborygmi, and muscle wasting. A hallmark of malabsorption is steatorrhea, characterized by excessive fecal fat and bulky, frothy, greasy, yellow or clay-colored stools.
Diarrhea can be classified into four major categories:
• Secretory diarrhea is characterized by isotonic stool and persists during fasting.
• Osmotic diarrhea, such as that occurring with lactase deficiency, is due to osmotic forces exerted by unabsorbed luminal solutes. The diarrheal fluid is more than50 mOsm more concentrated than plasma, and the condition abates with fasting.
• Malabsorptive diarrhea caused by inadequate nutrient absorption is associated with steatorrhea and is relieved by fasting.
• Exudative diarrhea is due to inflammatory disease and characterized by purulent, bloody stools that continue during fasting.
Malabsorption results from disturbance in at least one of the four phases of nutrient absorption:
(1) intraluminal digestion, in which proteins, carbohydrates, and fats are broken down into absorbable forms.
(2) terminal digestion, which involves the hydrolysis of carbohydrates and peptides by disaccharidases and peptidases, respectively, in the brush border of the small intestinal mucosa.
(3) transepithelial transport, in which nutrients, fluid, and electrolytes are transported across and processed within the small intestinal epithelium.
(4) lymphatic transport of absorbed lipids.

Celiac Disease
Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is an immune-mediated enteropathy triggered by the ingestion of gluten-containing cereals, such as wheat, rye, or barley, in genetically predisposed persons.
MORPHOLOGY
The histopathologic picture is characterized by increased numbers of intraepithelial CD8+ T lymphocytes, with intraepithelial lymphocytosis, crypt hyperplasia, and villous atrophy.
This loss of mucosal and brush border surface area probably accounts for the malabsorption. In addition, increased rates of epithelial turnover, reflected in increased crypt mitotic activity, may limit the ability of absorptive enterocytes to fully differentiate and contribute to defects in terminal digestion and transepithelial transport.
Other features of fully developed celiac disease include increased numbers of plasma cells, mast cells, and eosinophils, especially within the upper part of the lamina propria.
With increased serologic screening and early detection of disease-associated antibodies, it is now appreciated that an increase in the number of intraepithelial lymphocytes, particularly within the villus, is a marker of mild forms of celiac disease. Intraepithelial lymphocytosis and villous atrophy are not specific for celiac disease, however, and can be a feature of other disorders, including viral enteritis. The combination of histologic and serologic findings is most specific for diagnosis of celiac disease.

Symptomatic adult celiac disease is often associated with anemia (due to iron deficiency and, less commonly, B12 and folate deficiency), diarrhea, bloating, and fatigue.

The polyps frequently are multiple and characteristically are ovoid in shape, less than 1 cm in diameter, and covered by a smooth surface.
On microscopic examination, polyps have irregular, cystically dilated, and elongated foveolar glands. The lamina propria typically is edematous with variable degrees of acute and chronic inflammation, and surface erosions may be present.


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