patoloji-ders-notlari

Title

Serdar Balcı

Pathology of the Stomach

Serdar BALCI, MD

Stomach

ACUTE GASTRITIS

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Acute Gastritis

Transient mucosal inflammatory process

May be asymptomatic

Cause variable degrees of epigastric pain, nausea, and vomiting

In severe cases mucosal erosion, ulceration, hemorrhage, hematemesis, melena, massive blood loss

Robbins Basic Pathology

Protective mechanisms of gastric epithelium

Disruption of protective mechanisms result in gastritis

Morphology of gastritis

ACUTE PEPTIC ULCERATION

Acute Peptic Ulceration

Pathogenesis

Morphology of ulcer

Erosions superficial epithelial damage

Ulcers deeper lesions penetrate the mucosa

Robbins Basic Pathology

CHRONIC GASTRITIS

Chronic Gastritis

H. pylori

Helicobacter pylori Gastritis

H. pylori virulence

H. pylori

H. pylori shows tropism for gastric foveolar epitheleum

Generally not found in areas of intestinal metaplasia, acid-producing mucosa of the gastric body, or duodenal epithelium

Antral biopsy is preferred for evaluation of H. pylori gastritis

Robbins Basic Pathology

concentrated within the superficial mucus overlying epithelial cells in the surface and neck regions

Robbins Basic Pathology

neutrophils within the lamina propria

Some cross the basement membrane

intraepithelial location

accumulate in the lumen of gastric pits to create pit abscesses

Robbins Basic Pathology

superficial lamina propria includes large numbers of plasma cells, often in clusters or sheets

increased numbers of lymphocytes and macrophages

inflammatory infiltrates may create thickened rugal folds, mimicking infiltrative lesions

Lymphoid aggregates, some with germinal centers

Induced form of mucosa-associated lymphoid tissue (MALT) -potential to transform into lymphoma

Robbins Basic Pathology

Intestinal metaplasia

Goblet cells and columnar absorptive cells

Associated with increased risk of gastric adenocarcinoma

Robbins Basic Pathology

Diagnostic methods for H.pylori

H.pylori vs Autoimmune Gastritis

Robbins Basic Pathology

Autoimmune gastritis

Antibodies against parietal cells

Loss of glands

Decreased acid, decreased intrinsic factor

Increased gastrin production by Neuroendocrine cells

Hypergastrinemia and hyperplasia of antral gastrin-producing G cells

No intrinsic factor, no ileal vitamin B 12 absorption, B12 deficiency, megaloblastic anemia (pernicious anemia)

Reduced serum concentration of pepsinogen reflects chief cell loss

Netter’s Illustrated Human Pathology, Second Edition

Netter’s Illustrated Human Pathology, Second Edition

PEPTIC ULCER DISEASE

Peptic ulcers develop anywhere in the gastrointestinal tract in contact with acid-pepsin secretion. Majority are found in the duodenum or stomach.

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Netter’s Illustrated Human Pathology, Second Edition

Netter’s Illustrated Human Pathology, Second Edition

Peptic Ulcer Disease

Cofactors in peptic ulcerogenesis

Gastric hyperacidity

H. pylori infection

Parietal cell hyperplasia

Excessive secretory responses

Impaired inhibition of stimulatory mechanisms

Zollinger-Ellison syndrome

Uncontrolled release of gastrin by a neuroendocrine tumor

Massive acid production

Multiple peptic ulcerations in the stomach, duodenum, jejunum

Peptic ulcers

Round to oval

Sharply punched-out defect

Robbins Basic Pathology

Base of ulcers

Smooth and clean

Result of peptic digestion of exudate

Granulation tissue

Robbins Basic Pathology

OTHER DISEASES

Gastric candidiasis

Autopsy Pathology: A Manual and Atlas

**Iatrogenic ulceration **

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Ménétrier disease

Rare disorder

Excessive secretion of transforming growth factor α (TGF-α)

Diffuse hyperplasia of the foveolar epithelium of the body and fundus

Hypoproteinemia due to protein-losing enteropathy