The Gastrointestinal Tract Part 2, UTHSC Fall 2022
The Gastrointestinal Tract Part 2, UTHSC Fall 2022
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The Gastrointestinal Tract Part 2, UTHSC Fall 2022 D2 Pathology (Answered) Graded A+
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The Gastrointestinal Tract Part 2, UTHSC Fall 2022
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The Gastrointestinal Tract Part 2, UTHSC Fall 2022
The Gastrointestinal Tract Part 2, UTHSC Fall 2022 D2 Pathology
Chronic Gastritis
- Infection with the bacillus H. Pylori, as the most common cause
- Autoimmune gastritis, as the most common cause of diffuse atrophic gastritis in patients without H. pylori infection
- H. pylori infection → mu...
uthsc fall 2022 d2 pathology chronic gastritis infection with the bacillus h pylori
as the most common cause autoimmune gastritis
as the most common cause of
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The Gastrointestinal Tract Part 2, UTHSC Fall 2022 D2
Pathology
Chronic Gastritis
- Infection with the bacillus H. Pylori, as the most common cause
- Autoimmune gastritis, as the most common cause of diffuse atrophic gastritis in
patients without H. pylori infection
- H. pylori infection → multifocal gastritis
- Other causes: radiation injury, chronic bile reflux, mechanical injury, Crohn's disease,
amyloidosis, or GVHD
- Symptoms, less severe but more persistent than acute gastritis
Helicobacter Pylori Gastritis
- H. pylori organisms present in 90% of individuals with chronic gastritis affecting the
antrum.
- Associated with poverty, limited education, rural areas, ...
- Multifocal atrophic gastritis associated with patchy mucosal atrophy
- With increased risk for gastric adenocarcinoma
- Combination of antibiotics and proton pump inhibitors, as effective treatment
H. pylori-associated Gastritis location
Antrum
Autoimmune Gastritis location
Body
H. pylori-associated Gastritis Inflammatory cell
Neutrophils, subepithelial plasma cells
Autoimmune Gastritis Inflammatory cell
Lymphocytes, macrophages
H. pylori-associated Gastritis Acid production
Increased to slightly decreased
Autoimmune Gastritis Acid production
Decreased
H. pylori-associated Gastritis Gastrin
Normal to decreased
Autoimmune Gastritis Gastrin
Increased
H. pylori-associated Gastritis Other lesions
Hyperplastic/ inflammatory polyps
Autoimmune Gastritis Other lesions
Neuroendocrine hyperplasia
H. pylori-associated Gastritis Serology
Antibodies to H. pylori
Autoimmune Gastritis Serology
Antibodies to parietal cells
H. pylori-associated Gastritis Sequelae
Peptic ulcer, adenocarcinoma, MALToma
Autoimmune Gastritis Sequelae
Atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor
, H. pylori-associated Gastritis Associations
Low socioeconomic status, poverty, residence in rural areas
Autoimmune Gastritis Associations
Autoimmune disease; thyroiditis, diabetes mellitus, Grave disease
Virulence Factors of Helicobacter Pylori Gastritis
• Flagella, for motility in mucus
• Urease, an enzyme results in ↑pH→ ↑ bacterial survival
•Adhesins → ↑ bacterial adherence
•Toxins (CagA)
what factor will decide the outcome of a Helicobacter Pylori Gastritis infection?
• Variation in bacterial factors
• Host factors
Helicobacter Pylori Gastritis Histopathologic Features
- Neutrophils within the epithelium and lamina propria
- Lymphoid aggregates, subepithelial plasma cells, as characteristics of H. pylori
Peptic Ulcer Disease (PUD)
- As a complication of chronic gastritis
- Chronic mucosal ulceration affecting the duodenum or stomach
- Associated with H. pylori infection, NSAIDs, or cigarette smoking
Epidemiology of Peptic Ulcer Disease (PUD)
Decreased the incidence of PUD in developed countries along with reduced the
prevalence of H. pylori infection, however, increased the incidence of duodenal PUD in
old patients due to increased NSAID use
Peptic Ulcer Disease (PUD) Morphology
Sharply punched-out defect or a Perforation
Peptic Ulcer Disease (PUD) Clinical Features
- Epigastric burning or aching pain
- Other manifestations such as nausea, vomiting, bloating, and significant weight loss
- Complications: iron deficiency anemia, bleeding, perforation, and obstruction
Zollinger-Ellison syndrome
multiple peptic ulcerations in the stomach, duodenum, and even jejunum, owing to
excess gastrin secretion by a tumor and, hence, excess gastric acid production
what are current therapies for Peptic Ulcer Disease (PUD)?
H.pylori clearance and neutralization of gastric acid
Hypertrophic Gastropathies
- Giant cerebriform enlargement of the rugal folds due to epithelial hyperplasia
- No inflammation
- Excessive growth factor release
- Example: Zollinger-Ellison syndrome
Polyps are identified in up to ___% of upper GI tract endoscopies
5%
GI polyps are a result of
epithelial or stromal hyperplasia, inflammation, ectopia, or neoplasia
Inflammatory and Hyperplastic Polyps
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