Overview of Pathological Findings in the Stomach

Table 3.9 Pathological findings in the stomach

Acute gastritis Chronic gastritis Gastric ulcer Masses – Extramural – Intramural – Epithelial Malignancies – Carcinoma – Lymphoma Portal hypertension – Varices – Hypertensive gastropathy Postoperative changes – Total gastrectomy – Partial gastrectomy – Vagotomy and pyloroplasty – Fundoplication Rare findings

 

Fig. 3.70 Acute gastritis

Fig. 3.71 Chronic gastritis

Fig. 3.72 Gastric ulcer

Fig. 3.730 Gastric polyp

Fig. 3.74 Gastric carcinoma

Fig. 3.75 Fundic varices

Fig. 3.76 Billroth II gastroenterostomy

Fig. 3.77 Angiodysplasias

Gastritis: Clinical Aspects

Acute and chronic gastritis are reactions of the gastric mucosa to various noxious agents. They are entirely different conditions, each presenting its own clinical, endoscopic, and histological features (Table 3.10). Both conditions, especially the chronic form, pose a special challenge to the endoscopist because the endoscopic findings correlate very poorly with the histological findings and clinical presentation.

Acute Gastritis

Acute gastritis can be caused by a variety of exogenous and endogenous agents (Table 3.11). More often than in chronic gastritis, endoscopy reveals signs that point to the correct diagnosis (Table 3.12; Fig. 3.78). The endoscopic features do not suggest a specific causative agent of the gastritis, however. The diagnosis of acute gastritis often relies on the clinical presentation (upper abdominal pain, anorexia, nausea, vomiting) plus the endoscopic findings, with histology showing little or no evidence of cellular infiltrate. The main role of biopsy is to distinguish between the various specific forms of gastritis (due to Crohn disease, infection, etc.).

Fig. 3.78 Endoscopic features of acute gastritis

Acute Gastritis: Diagnosis

Fig. 3.79 Criteria for acute gastritis

Acute Gastritis: Differential Diagnosis and Treatment

Fig. 3.80 Differential diagnosis of acute gastritis

Additional Studies

Histological examination of biopsies taken from normal-appearing antral and body mucosa and from grossly abnormal mucosa

Rapid urease test of biopsy specimens from the antrum and body

Treatment

Acute gastritis is often referable to a time-limited cause that can be identified in the patient’s history (gastroenteritis, alcohol ingestion, medications, stress, etc.). Specific treatment is often unnecessary, but the offending substance must be avoided. Dietary measures are also recommended.

If medical treatment is needed, proton pump inhibitors (PPI) are used. Eradication therapy should be considered for severe cases of Helicobacter pylori-positive gastritis.

Chronic Gastritis: Clinical Aspects and Classification

In the past, numerous efforts were made to categorize the phenomenon of chronic gastritis. A widely used classification was based on etiological criteria, subdividing the disease into types A, B, and C. “Special forms” were added as a separate category (Table 3.13). Today a modified version of the Sidney classification (1990, 1996) is most commonly used. It takes into account etiological and histological parameters and the location of the gastritis (Table 3.14).

Fig. 3.81 Chronic gastritis. Chronic inflammation with subtle histological findings

Fig. 3.82a, b Chronic atrophic gastritis

Fig. 3.83 Candidal gastritis in a patient with hepatic cirrhosis

Chronic Gastritis: Diagnosis, Giant Fold Gastritis, and Ménétrier Disease

Additional Studies

Antral biopsy 2-3 cm from the pylorus

Biopsy from the gastric body

Biopsy from grossly abnormal areas

Rapid test for H. pylori

Antibodies against parietal cells (type A gastritis)

Vitamin B₁₂ level (type A gastritis)

Fig. 3.84 Chronic gastritis. Prominent vascular pattern

Fig. 3.85a, b Mucosal atrophy in chronic gastritis

Fig. 3.86 Chronic gastritis. Histology: intestinal metaplasia

Giant Fold Gastritis

Giant fold gastritis refers to the presence of gastric folds more than 10 mm thick that are not effaced when the stomach is inflated with air. These folds are located in the body and fundus of the stomach. They are occasionally seen without discernible cause but also occur in the setting of H. pylori infection, Zollinger-Ellison syndrome, lymphoma, and Ménétrier disease.

Ménétrier Disease

Ménétrier disease is characterized by a hyperplasia of mucus-producing cells combined with gastric protein loss. Endoscopically, the rugal folds appear thickened and show increased tortuosity. Six-month endoscopic follow-ups are recommended initially, mainly to aid differentiation from lymphoma. Later, yearly follow-ups are scheduled due to the risk of malignant change.

Gastric Ulcer: Clinical Aspects and Diagnosis

Fig. 3.87 Gastric ulcer

Gastric Ulcer: Management

– Tests for detecting H. pylori (see p. 104)

– Histological examination

– Rapid urease test

– Breath test

– Serological testing

– Culture method

Radiography: Precede endoscopy with abdominal plain film if perforation is suspected.

Treatment and Follow-Up

Pharmacological Therapy

PPI are administered. If H. pylori is detected, the following regimen is used for eradication:

1. PPI, for example, pantoprazol, 40 mg 1-0-1
   
2. Clarithromycin, 500 mg 1-0-1
   
3. Amoxicillin, 1000 mg 1-0-1

Irritants, nicotine, and NSAIDs should be withdrawn.

Complications

Oozing hemorrhage

Massive hemorrhage (treatment, see p. 151 ff.)

Perforation

Gastric outlet stenosis

Follow-Ups

Endoscopy is repeated at four to six weeks, and new specimens are obtained. Additional follow-ups are scheduled according to the progression of healing.

Problems

Refractory ulcer

Dieulafoy ulcer (see p. 155)

Fig. 3.88 Gastric ulcer

Gastric Ulcer: Helicobacter pylori

Tests for Detection of Helicobacter pylori

Rapid Urease Test

Principle	Based on the ability of the organism to convert urea into carbon dioxide and ammonia. A specimen of mucosa is placed into a test medium that contains urea and an indicator dye. If H. pylori is present, the pH rises, producing a characteristic color change, depending on the indicator used.
Sensitivity	90-95%
Specificity	95%
Advantages	Economical
	Fast (15 minutes to three hours)
Disadvantages	Does not indicate degree of inflammation
Evaluation	Fast, simple, low-cost test to detect or exclude H. pylori colonization

Histological Detection

Principle	Staining and direct histological identification of the organism in a tissue specimen (Fig. 3.89)
Sensitivity	85-95%
Specificity	95-100%
Advantages	Standard method
	Provides information on inflammatory activity
Disadvantages	Invasive
Evaluation	Standard method

C₁₃ Breath Test

Principle	The breath test, like the rapid urease test, is based on the ability of H. pylori to break down urea. The patient consumes a test meal containing C13-labeled urea. The H. pylori urease splits the urea, and C13-labeled carbon dioxide is exhaled. The exhaled air is collected and analyzed by mass or infrared spectroscopy.
Sensitivity	90%
Specificity	95%
Advantages	Noninvasive
Disadvantages	High cost
	Does not indicate degree of inflammation
Evaluation	Ideal for confirming eradication

Serological Testing

Principle	Serological tests are based on the detection of IgG and IgA antibodies against H. pylori in the serum. High titers of these antibodies are found during or immediately after a florid infection.
Sensitivity	85%
Specificity	75-80%
Advantages	Noninvasive
Disadvantages	Not useful for confirming eradication
	Relatively low sensitivity and specificity
	Does not indicate degree of inflammation
Evaluation	Very useful for epidemiological studies
	Not useful for planning treatment or evaluating response

Culture Method

Principle	It is possible to culture and identify H. pylori in special laboratories.
Sensitivity	70-90%
Specificity	100%
Advantages	Can be used to test antibiotic sensitivity
Disadvantages	Invasive
	very costly
	Relative Not a routine method, should be reserved for special investigations
Evaluation	Not a routine method, should be reserved for special investigations

 

Fig. 3.89 Histological detection of H. pylori a Low-grade, inactive gastritis b With Warthin–Starry staining, even a relatively low-power view shows H. pylori organisms (black) densely colonizing the ridgesummits and pit epithelium (from: Hahn and Riemann, Klinische Gastroenterologie. Vol. I, 3rd ed. Stuttgart: Thieme 1996)

Mass, Tumor, Malignancy: Overview

When distended by air insufflation, the stomach wall assumes a uniform appearance in which normal gastric folds are easily distinguished from the conspicuous mass effect produced by an extrinsic indentation, an intramural process, or a lesion in the mucosa (Table 3.15; Fig. 3.90).

Masses that bulge into the gastric lumen from the smooth or regularly folded surface often present the examiner with serious difficulties.

The endoscopic diagnosis is frequently uncertain.

The nomenclature of these changes, especially polyps, is confusing.

Role of Endoscopy

Endoscopy has a pivotal role in the definitive investigation of these findings.

First the mass is visualized endoscopically and its morphology is described.

Endoscopy makes it possible to obtain tissue samples, although some limitations apply (see Leiomyoma).

Based on the endoscopic findings, the need for further testing is assessed. Endosonography is particularly rewarding in equivocal cases.

Fig. 3.90 Location of masses in the stomach

Synopsis

Mass, Tumor, Malignancy: Diagnosis

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