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GENERAL PATHOLOGY

Stomach:

Anatomy:

The stomach is a saccular organ. It extends from left of the midline superiorly, where it is joined to the esophagus, to right of the midline inferiorly, where it connects to the duodenum. The concavity of the right, inner curve is called the lesser curvature, and the convexity of the left, outer curve is the greater curvature.

It divided into the following 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 that extends supero-laterally to the gastroesophageal junction. 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 duodenum by the muscular pyloric sphincter.

Histology:

The gastric wall consists of the following layers:

mucosa, submucosa, muscularis propria, and serosa.

The interior surface of the stomach exhibits rugae, which are enfolding of mucosa and submucosa, their function are to increase surface area of the stomach, and to give the distensible ability to the stomach.

Gastric glands contain the following cells:

1- Surface mucous cells.

2- Parietal cells. (gastric acid formation)

3- Chief cells. (pepsin secreting cells).

4-neuroendocrine cells.

5- stem cells.

MUCOSAL PROTECTION

1-Mucus secretion: The thin layer of surface mucus in the stomach and duodenum

2- Bicarbonate secretion: Surface epithelial cells in both the stomach and the duodenum secrete bicarbonate into the boundary zone of adherent mucus, creating an essentially pH-neutral microenvironment immediately adjacent to the cell surface.

3- Epithelial barrier: Intercellular tight junctions provide a barrier to the back-diffusion of hydrogen ions. Epithelial disruption is followed rapidly by restitution, in which existing cells migrate along the exposed basement membrane to fill in the defects and restore epithelial barrier integrity.

4- Mucosal blood flow: The rich mucosal blood supply provides oxygen, bicarbonate, and nutrients to epithelial cells and removes back-diffused acid.

Pathology of the stomach:

Congenital Anomalies

1-Gastric heterotopia, small patches of ectopic gastric mucosa in the duodenum or in more distal sites may present as perplexing sources of bleeding, owing to peptic ulceration of adjacent mucosa.

2-Pyloric stenosis: Congenital hypertrophic pyloric stenosis is encountered in infants as a disorder that affects boys three to four times more often than girls Regurgitation and persistent, projectile, nonbilious vomiting usually appear in the second or third week of life.

ACUTE GASTRITIS

Acute gastritis is an acute mucosal inflammatory process, usually of a transient nature. The inflammation may be accompanied by hemorrhage into the mucosa and, in more severe circumstances, by sloughing of the superficial mucosa.

Pathogenesis:

• increased acid secretion with back-diffusion.

• decreased production of bicarbonate buffer

• reduced blood flow

• direct damage to the epithelium

Causes :

• Heavy use of non-steroidal anti-inflammatory drugs (aspirin).

• Excessive alcohol consumption

• Heavy smoking

• Treatment with cancer chemotherapeutic drugs

• Uremia

• Systemic infections (e.g., salmonellosis)

• Severe stress (e.g., trauma, burns, surgery)

• Ischemia and shock

• Gastric irradiation..

• Mechanical trauma (e.g., nasogastric intubation)

Morphology:

In mild cases , there is lamina propria edema and slight vascular congestion. The surface epithelium is intact, and scattered neutrophils are present among the surface epithelial cells or within the epithelial layer and lumen of mucosal glands.

With more severe mucosal damage, erosion and hemorrhage develop. Erosion is a loss of the superficial epithelium, generating a defect in the mucosa that does not cross the muscularis mucosa. It is accompanied by acute inflammatory infiltrate.

Clinical Features.

Depending on the severity of the anatomic changes, acute gastritis may be entirely asymptomatic . It may cause variable epigastric pain, nausea, and vomiting; or may present with overt hemorrhage, massive hematemesis, melena, and potentially fatal blood loss.

Chronic gastritis:

It is defined as the presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia, usually in the absence of erosions. The epithelial changes may become dysplastic and constitute a background for the development of carcinoma.

Pathogenesis.

• Chronic infection by H. pylori .

• Immunologic ( autoimmune), in association with pernicious anemia

• Toxic, as with alcohol ingestion and cigarette smoking

• Postsurgical (gastroenterostomy), with reflux of bilious duodenal secretions.

• Radiation

• Miscellaneous—amyloidosis.

H. pylori:

It is a gram negative rods.

Chronic infection by Helicobacter pylori, elaborate of urease enzyme, which produces ammonia from endogenous urea, thereby buffering gastric acid in the immediate vicinity of the organism. Patients with chronic gastritis and H. pylori usually improve when treated with antimicrobial agents, and relapses are associated with reappearance of this organism.

Autoimmune gastritis:

This form of gastritis accounts for less than 10% of cases of chronic gastritis.

It results from the presence of auto-antibodies to the gastric gland parietal cells and intrinsic. This uncommon form of gastritis is seen in association with other autoimmune disorders, such as Hashimoto thyroiditis and Addison disease.

Clinical Features.

Chronic gastritis usually causes few symptoms. Nausea, vomiting, and upper abdominal discomfort may occur.

Individuals with advanced gastritis from H. pylori or other environmental causes are often hypochlorhydric, owing to parietal cell damage and atrophy of body-fundic mucosa. When severe parietal cell loss occurs in the setting of autoimmune gastritis, hypochlorhydria or achlorhydria and hypergastrinemia are present.

Peptic ulcer:

An ulcer is defined as a break in the mucosa of the alimentary tract, which extends through the muscularis mucosae into the submucosa or deeper.

It can occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid-peptic juices, Peptic ulcers are usually solitary lesions less than 4 cm in diameter.

Located in the following sites:

1- Duodenum, first portion

2-Stomach, usually antrum

3-At the gastroesophageal junction.

4-Within the margins of a gastrojejunostomy

5-In the duodenum, stomach, or jejunum of patients with Zollinger-Ellison syndrome

6-within Meckel diverticulum that contains ectopic gastric mucosa

Role of H. pylori in peptic ulcer:

• H. pylori secretes a urease, which generates free ammonia.

• Secretes protease, which breaks down glycoproteins in the gastric mucus.

• The organisms also elaborate phospholipases, which damage surface epithelial cells and may release bioactive leukotrienes.

• Neutrophils attracted by H. pylori release myeloperoxidase, which in the presence of ammonia can destroy mammalian cells.

Clinical Features.

The great majority of peptic ulcers cause epigastric pain. The pain tends to be worse at night and occurs usually 1 to 3 hours after meals during the day. Classically the pain is relieved by alkalis or food, but there are many exceptions. other important symptoms are (Nausea, vomiting, bloating, and significant weight loss).

A significant minority first come to light with complications such as anemia, frank hemorrhage, or perforation.

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LECTURE – 10 –

Dr . Ali Zeki

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