Pathology of Stomach & Small Bowel Flashcards
Describe the protective and damaging processes that are commonly deranged in gastric disease
1) Pre-epithelium is covered in mucus coat that is protective against hydrogen ions and digestive enzymes.
2) Epithelium has tight junctions between cells that resist the passage of acid/digestive enzymes into the lining of the stomach. If there is damage, mucosal cells w/in the epithelium will migrate the the area and secrete a mucus cap
3) Subepithelium is rich in blood supply that provides nutrients, oxygen and anti-inflammatory agents like prostaglandins to the epithelium
Gastritis results when the mucosal barrier is disrupted. Caused by neutrophilic infiltration of the mucosa. Erosions can be severe enough to cause hemorrhage
List the general features and cases of acute and stress-related gastritis
Acute = transient gastric mucosal inflammation. Commonly caused by disruption of the gastric mucosal barrier by NSAIDs, H. pylori, ingestion of harsh chemicals, excessive alcohol consumption, cigarettes, radiation therapy or chemotherapy
Chronic/Stress = less severe and more persistent than acute. Lymphocytes and plasma cells in lamina propria. Most common cause is H. pylori
Understand the pathophysiology, epidemiology and common sequelae of Helicobacter infection
Ok, I feel like we have lots of other cards that answer this in other lectures. If I’m wrong, please feel free to fill this ou
Understand the pathophysiology and common sequelae of autoimmune gastritis
Corpus restricted chronic atrophic gastritis. Will see lymphocytes and plasma cell infiltrate. Can see intestinal metaplasia
Anti-parietal cell and anti-intrinsic factor antibodies
+/- pernicious anemia
Scandinavian and northern
European descent
Discuss the cause of peptic ulcer disease
Chronic gastritis caused by H. pylori infection (70% of pts with PUD are infected)
Other causes: NSAID, cigarette or alcohol use
Discuss the appearance of peptic ulcer disease
Chronic, recurring lesions of GI mucosa found in gastric atrum and first portion of duodenum
Discuss the complications of peptic ulcer disease
Chronic gastritis → intestinal metaplasia (characterized by a change to a intesintal-type columnar epithelium and “punched-out” goblet cells)→ dysplasia and adenoma polyp formation (progresses from low to high grade dysplasia based on degree of nuclear atypia) → adenocarcinoma
Compare and contrast the appearance of the common types of gastric polyps, their associated conditions, and their relationship to gastric cancter
Three types:
1. Hyperplastic: Most common (75%). Result from abnormal proliferation of epithelium and lamina propria in response to chronic gastritis. NO risk for malignant transformation
- Fundic glands: Associated with prolonged PPI use. Commonly found in patients with FAP. Benign
- Adenomas: Proliferation of dysplastic epithelium secondary to chronic gastritis and intestinal metaplasia of the gastric mucosa. May progress to adenocarinomas
What are the risk factors, epidemiology, associations and natural history of gastric adenocarcinoma
Epithelial tumor derived from malignant transformation of gastric epithelium; malignant behavior; associated with chronic gastritis (especially Helicobacter) and diet
Accounts for 90% of all malignant gastric tumors
High mortality unless detected early
Wnt signally pathway activation. Loss of CDH1. Amplification of Her2/neu
Describe the appearance, natural history and molecular features of gastrointestinal stromal tumors
Mesenchymal neoplasm derived from interstitial cells of Cajal (pacemaker cells controlling peristalsis)
Most contain a mutation in the c-kit oncogene
Used as diagnostic aid on tissue
Targeted therapy with tyrosine kinase inhibitor imatinib
Variable clinical course – indolent to malignant
Risk assessment: location, mitotic rate, and size
