Digestive system disease

1Diseases of Digestive

System

Chen Jian

Department of Pathology and Physiopathology

School of Medicine, ZhejiangUniversity

cj@zju.edu.cn

88208199Summary

•Gastritis

•Peptic ulceration

•Appendicitis

•Inflammatory bowel disease

•Barrett esophagus

•Gastric carcinoma, colorectal cancer

•Viral hepatitis

•Alcoholic liver disease

•Liver cirrhosis

•Primary carcinoma of the liver

This is the normal appearance of the gastric antrumextending to the

pylorusat the right of center. The first portion of the duodenum(duodenal

bulb) is at the far right. In the endoscopicviews below, the normal

appearance of the pylorus is seen at the left, with the first portion of the

duodenum at the right. Anatomy and histology of the stomach. A,Gross anatomy. B,

Microscopic view of antralmucosa. C,Microscopic view of

fundicmucosa.

2This is the normal appearance of the gastric fundalmucosa, with

short pits lined by pale columnar mucus cells leading into long

glands which contain bright pink parietal cells that secrete

hydrochloric acid. Acute Gastritis

•Acute gastritis is an acute mucosal

inflammatory process, usually of a

transient nature.

•Hemorrhage into the mucosa

•Sloughing of the superficial mucosal

epithelium (erosion)

•Important cause of acute gastrointestinal

bleeding

Pathogenesis

–Heavy use of nonsteroidalanti-inflammatory drugs

(NSAIDs)

–Excessive alcohol consumption

–Heavy smoking

–Treatment with cancer chemotherapeutic drugs

–Uremia

–Systemic infections

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

–Ischemia and shock

–Suicide attempts with acids and alkali

–Mechanical trauma (e.g., nasogastricintubation)

–Reflux of bilious material after distal gastrectomyMorphology

•Diffuse, and from superficial inflammation to

involvement of the entire mucosal thickness with

hemorrhage and focal erosions.

•Concurrent erosion and hemorrhage are readily

visible by endoscopyand termed acute erosive

gastritis.

•Mucosal edema and an inflammatory infiltrate of

neutrophilsand possibly by chronic inflammatory

cells.

•Regenerative replication of epithelial cells in the

gastric pits is usually prominent.

This is a more typical acute gastritis with a diffusely hyperemic gastric

mucosa. There are many causes for acute gastritis: alcoholism, drugs,

infections, etc. Here are some larger areas of gastric hemorrhage that could bestbe termed

"erosions" because the superficial mucosa is eroded away. Such erosions are

typical for the pathologic process termed gastropathy, which describes gastric

mucosal injury without significant inflammation. The findings here fit with acute

erosive gastropathy, but there are other patterns. Etiologies for the various

gastropathiescan include: alcohol, drugs such as NSAIDS, stress, uremia, bile

reflux, portal hypertension, radiation, and chemotherapy.

3At high power, gastric mucosa demonstrates infiltration by neutrophils. This

is acute gastritis. Clinical Features

•May be entirely asymptomatic.

•Variable epigastricpain with nausea and

vomiting.

•Overt hematemesis, melena, and

potentially fatal blood loss.

•NSAID-induced gastritis

Chronic Gastritis

•The presence of chronic inflammatory

changes in the mucosa

•Helicobacter pylori, HP

•Mucosal atrophy

•Epithelial metaplasia

•In the Western world, the prevalence of

histologicchanges indicative of chronic

gastritis is higher than 50% in the later

decades of life. Pathogenesis

•The bacillus H. pylori.

•Immunologic (autoimmune),in association with

pernicious anemia

•Toxic, as with alcohol and cigarette smoking

•Postsurgical, especially following antrectomy

with gastroenterostomywith reflux of bilious

duodenal secretions

•Radiation

•Miscellaneous-amyloidosis, graft-versus-host

disease, uremia

Helicobacter pylori, HP

•Identification in 1982

•The 2005 Nobel Prize in Medicine

•H. pyloridoes not invade the tissues, it

induces an intense inflammatory and

immune response.

•strains producing VacAand CagAcause

more intense tissue inflammation, more

severe epithelial damage, and higher

cytokine production. Helicobacter pylorigastritis. A Steiner silver stain demonstrates the numerous

darkly stained Helicobacterorganisms along the luminal surface of the gastric

epithelial cells. There is no tissue invasion by bacteria. (Courtesy of Dr. Melissa

Upton, Department of Pathology, University of Washington, Seattle,

Washington.)