4. Peptic Ulcer Disease: Causes and Mechanisms

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Questions and Answers

Which of the following best describes the primary mechanism contributing to the formation of peptic ulcers in the duodenum?

Increased gastric acid secretion and decreased duodenal bicarbonate secretion. (correct)

Ectopic gastric mucosa in the fundus.

Atrophy of the gastric fundus leading to decreased acid production.

Decreased gastric acid secretion and increased duodenal bicarbonate secretion.

A patient with peptic ulcer disease is a chronic smoker, uses NSAIDs regularly and has tested positive for H. pylori. Which of these factors is LEAST likely to be directly involved in the pathogenesis of their ulcers?

Smoking

Parietal cell hyperplasia (correct)

NSAID use

H. pylori infection

Hyperplastic polyps of the stomach are most commonly associated with which of the following?

Adenomatous changes with tendency towards malignancy.

Chronic _H. pylori_ infection (correct)

Familial adenomatous polyposis.

Long term usage of proton pump inhibitors

Which of the following characteristics is most consistent with intestinal-type gastric adenocarcinoma?

Large, exophytic, ulcerated mass Signup and view all the answers

A patient with a history of smoking and COPD is diagnosed with a duodenal ulcer. Which of the following risk factor is most directly related to the ulcer formation?

Smoking Signup and view all the answers

What is a key differentiating factor between gastritis and gastropathy?

The presence of inflammatory cells. Signup and view all the answers

Which of the following is a common cause of gastropathy?

NSAIDs, alcohol, and bile. Signup and view all the answers

What is the role of foveolar cells in protecting the stomach lining?

They secrete alkaline fluid to neutralize stomach acid Signup and view all the answers

What distinguishes erosive gastritis from other forms of gastritis?

Loss of mucosa Signup and view all the answers

How does H. pylori contribute to the development of gastritis?

By producing urease, which increases ammonium levels. Signup and view all the answers

What is the significance of observing neutrophils above the basement membrane in the gastric mucosa?

It is a sign of active inflammation (gastritis). Signup and view all the answers

Which of the following is a direct consequence of NSAID use in the stomach?

Inhibition of cyclooxygenase (COX) Signup and view all the answers

What are the common signs and symptoms associated with acute gastritis?

Asymptomatic, epigastric pain, nausea/vomiting, mucosal erosion, and hemorrhage. Signup and view all the answers

Which bacterial factor allows H. pylori to move through the viscous mucus in the stomach?

Flagella Signup and view all the answers

What is the primary function of urease produced by H. pylori in the stomach environment?

To neutralize stomach acid via ammonia production Signup and view all the answers

What is the role of adhesins in the pathogenesis of H. pylori infection?

They enhance the bacteria's adherence to surface foveolar cells. Signup and view all the answers

Which of the following is a typical morphological finding in a gastric biopsy of a patient with H. pylori gastritis?

Increased presence of plasma cells and lymphocytes in the lamina propria Signup and view all the answers

What does the presence of neutrophils within the lamina propria, specifically in pit abscesses, suggest?

An acute inflammatory response, often seen in H. pylori infection. Signup and view all the answers

Where are H. pylori bacteria characteristically found in the gastric mucosa?

Adhering to the surface of the epithelial cells or mucus layer. Signup and view all the answers

What is the cytotoxin-associated gene A (CagA) associated with regarding H. pylori?

Potential for cancer or ulcer development. Signup and view all the answers

In a gastric biopsy from a patient with H. pylori infection, what is a key characteristic of the inflammatory infiltrate observed in the lamina propria?

Increased numbers of lymphocytes and plasma cells. Signup and view all the answers

Which layer of the gastrointestinal (GI) tract is primarily responsible for nutrient absorption?

Mucosa Signup and view all the answers

What is the primary physiological function of segmentation in the GI tract?

Mixing of chyme in the small intestine to aid digestion and nutrient absorption Signup and view all the answers

What is the key cellular component seen in histological analysis of inflamed GI tissue?

Infiltration of inflammatory cells such as neutrophils and lymphocytes Signup and view all the answers

Which diagnostic method provides direct visualization of ulcerations in the gastrointestinal tract?

Endoscopy Signup and view all the answers

Which of the following is NOT a characteristic feature of inflammation in the GI tract?

Vasoconstriction Signup and view all the answers

Microscopic examination of a biopsy from a GI ulcer is most likely to reveal which of the following?

Erosion of the mucosal layer and inflammatory infiltrate Signup and view all the answers

Which of the following is a primary effect of anti-inflammatory agents such as corticosteroids on the GI tract?

Reduce inflammatory responses by dampening immune cell activity Signup and view all the answers

In the context of GI infections, what is the consequence of pathogen invasion into the tissues?

Compromise of tissue integrity through inflammation. Signup and view all the answers

Study Notes

Diseases of the Stomach

This presentation covers diseases of the stomach.
The learning objectives include applying knowledge of GI anatomy, histology, and physiology; describing the pathophysiology of acute and chronic gastritis; identifying features of H. Pylori infection; defining peptic ulcer disease (PUD); and recognizing differences between duodenal and gastric ulcers.

Acute Gastritis

Inflammation of the gastric mucosa
Characterized by the presence of neutrophils (white blood cells)

Gastropathy

Stomach dysfunction
Absence of inflammatory cells
Often results from NSAIDs, alcohol, or bile

Gastritis

Gastric pH = 1
Foveolar cells produce mucus and phospholipids to protect the epithelial cells.
Neutral pH fluid protects epithelial cells.
NSAID, COX-1 and COX-2 can decrease stomach pH
Uremia or H. Pylori (urease) increase ammonia and decrease H3CO2.
Lamina propria edema, and vascular congestion cause damage.
Erosion (loss of mucosa) with neutrophils, pus, and fibrin = hemorrhagic erosive gastritis

Mechanisms of Injury

NSAIDs inhibit the synthesis of prostaglandins.
NSAIDs affect all protective barriers.
NSAIDs reduce acid secretion in the stomach.
COX-2 inhibitors can cause stomach inflammation.
Ammonia from uremia or H. pylori inhibit gastric bicarbonate transporters.
Reduced mucin and bicarbonate secretion occurs in older adults with gastritis.
Decreased oxygen delivery may exacerbate gastritis, particularly at high altitudes.

Morphology (Gastritis)

Neutrophils are above the basement membrane and within contact with epithelial cells.
Inflammation signifies active inflammation.

Morphology (Gastropathy)

There is hyperplasia (increase in size) of foveolar mucus cells, typically present.
The surface epithelium (a type of cell) is usually intact.
Neutrophils, lymphocytes, and plasma cells are less prominent.

Helicobacter Pylori Gastritis

Four features are linked to H. pylori virulence:
- Flagella: allows bacteria to move in mucus
- Urease: creates ammonia that elevates pH in the stomach
- Adhesion molecules: help bacteria adhere to cells
- Toxins: may contribute to ulcer development, e.g., CagA (cytotoxin-associated gene A)
Morphology: Features found in a stomach biopsy with Helicobacter Pylori infection include a higher concentration of mucus overlying epithelial cells, neutrophils within the lamina propria, and the bacteria adhering to the surface of gastric cells.

Chronic Gastritis

H. Pylori likely causes autoimmune atrophy in a small subset of cases (10%). Other cases involve bile reflux, mechanical causes and ulcerative lesions.
Nausea and epigastric pain are common symptoms.
Antral area infection may cause duodenal ulcers.
Body or fundus infection may lead to multifocal atrophy, reduced parietal cells, reduction in stomach acid and an increase in the risk of gastric cancer.

Occurs in patients with severe trauma, extensive burns, intracranial disease, or major surgery.
More than 75% of critically ill patients develop visible gastric lesions within 3 days.
Commonly caused by stress, shock, sepsis, or severe trauma.
Curling ulcers appear in the proximal duodenum in patients with severe burns or trauma.
Cushing ulcers appear in the stomach, duodenum, or esophagus in the presence of intracranial disease.
Characterized by high incidence of perforation.
Pathogenesis is usually due to local ischemia caused by hypotension or reduced blood flow, as well as the release of endothelin-1.
Cushing ulcers are thought to be caused by direct stimulation of vagal nuclei, which results in hypersecretion.
Systemic acidosis contributes in mucosal injury due to lowering the intracellular pH.

Autoimmune Gastritis

Less than 10% of chronic gastritis cases.
Characterized by sparing of the antrum and causing hypergastrinemia.
Antibodies to parietal cells and intrinsic factor are present.
Reduced serum pepsinogen I levels (loss of chief cells), antral endocrine cell hyperplasia, and vitamin B12 deficiency lead to pernicious anemia.
Impaired gastric acid secretion leads to achlorhydria (absence of hydrochloric acid).

H. Pylori Gastritis vs. Autoimmune Gastritis

Key differences in presentation, location, inflammatory infiltrate, acid production, and presence of other lesions, between H. Pylori and autoimmune gastritis are summarized.
Autoimmune gastritis is characterized by diffuse damage of oxyntic mucosa, in body and fundic areas.

Polyps

Over 75% of gastric polyps are considered hyperplasic or inflammatory, which are often linked to H. Pylori infections.
Polyps lasting 5-6 years or with a size over 1.5cm are typically resectable.
Multiple polyps, smooth or eroded, often occur due to familial adenomatosis syndrome or use of pump inhibitors.
10% of polyps are adenomatous, more common in men.
30% of polyps are malignant.
Solitary polyps are less than 2 cm and usually in the antral region.

Gastric Cancer (Adenocarcinoma)

Most frequent malignant tumor in the stomach.
Intestinal type presents as large masses that can penetrate and appear exofitic or ulcerated.
Diffuse type is infiltrative and thickened, with signet ring cells.
Most cases originate in the antrum and lesser curvature.
Common symptoms include dyspepsia, dysphagia, weight loss, anorexia, early satiety, anemia, and hemorrhage.

Gastric Cancer (Metastasis and Other Risk Factors)

Sites of metastasis are common: periumbilical, left axillary, ovaric, and Douglas Pouch.
Gastric cancer arises in areas with low socioeconomic status and H. pylori infections are prevalent factors driving their origin.
There are no significant differences in incidence in people with ulcers and those without.

Gastric Carcinoma

Loss of CDH1 cadherin (up to 50% of cases) or loss of APC function.
Increased Wnt signaling or gain-of-function in B-catenin expression, TGF-B signaling, BAX regulation of apoptosis or CDKN2 cell cycle control may play a role.
Proinflammatory IL-1β and IL-1 can increase risk.
Apical mucin vacuoles, desmoplastic reaction, subtotal gastrectomy can be involved in the development of disease.
Advanced gastric cancer present in less than 20% of cases.

Gastric Lymphoma

Histology or microscopic description of a section of gastric tissue, taken from biopsy analysis, is observed.

Peptic Ulcer Disease

Gastric ulceration in the duodenum or stomach, primarily due to H. pylori infection, NSAIDs, or smoking.
Gastric antrum and duodenum show increased acid secretion and decreased bicarbonate secretion.
Gastric fundus or body exhibit modest acid secretion and associated atrophy that protects the duodenum and antrum, from developing ulcers.
Ectopic gastric mucosa in parts of the intestines may also lead to ulcers.

Peptic Ulcer Disease: Risk Factors

Risk factors for peptic ulcer disease include:
- H. pylori: Infection with this bacteria is a main factor.
- Smoking
- Chronic obstructive pulmonary disease (COPD): a lung disease.
- Hard drugs or cocaine: often lead to peptic ulcers.
- Nonsteroidal anti-inflammatory drugs (NSAIDs): Often cause stomach upset.
- Alcohol cirrhosis, particularly in the duodenal region.

Hypertrophic Gastropathies

Uncommon diseases characterized by giant cerebriform enlargement of rugal folds (epithelial hyperplasia).
Does not involve inflammation.
Two main types include Menetrier disease (in adults) and Zollinger-Ellison syndrome.

Zollinger-Ellison Syndrome

Gastrin-secreting neuroendocrine tumors (gastrinomas) primarily appear in the small intestine or pancreas, although typically presenting as solitary lesions in 75% cases.
Can be related to MEN Type 1 syndrome.
Duodenal ulcers or chronic diarrhea can be present.
Parietal cell hyperplasia is characteristic, often leading to excessive oxyntic mucosa in the stomach.

Bibliography

This section contains information from the listed publications.

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Description

Test your knowledge on peptic ulcer disease, specifically focusing on duodenal ulcers and their associated risk factors. This quiz covers the pathogenesis of ulcers, the role of H. pylori, and differentiating aspects of gastritis. Challenge yourself with questions that explore the complex interactions contributing to ulcers.