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Pathology of Pathology of The Stomach - 1The Stomach - 1
Dr.CSBR.Prasad, M.D.,
NORMAL ANATOMY
The normal gastric wall has the same layers as does the rest of the gut:
1. Mucosa:• Epithelium and • Lamina propria• Muscularis mucosae at the base
2. Submucosa3. Muscularis propria and 4. Subserosa
Mucosa has two compartments: 1-Superficial pit or foveolar
compartment 2-Deep glandular compartment
NORMAL CARDIAC MUCOSA (1:1)
CORPUS, FUNDIC MUCOSA (1:3)
ANTRAL (PYLORIC) MUCOSA (1:1)
GLANDULAR COMPARTMENT OF THE BODY MUCOSA
The pale cells: Parietal cells
Darker cells: Chief cells
NECK REGION OF THE ANTRAL MUCOSA
The pits are at the top and the glands at the base. In between, the tubules are lined by a mucus-containing epithelium with nuclei that are slightly larger than in either the pits or the glands. This is the neck region,
the proliferative zone for all gastric mucosae. The pale, pear-shaped cells with finely granular, gray cytoplasm at the base of the necks and glands are the gastrin-producing or G cells.
NORMAL ANATOMY• The Lamina Propria. The lamina propria is sparse throughout the normal
stomach. Most of the cells are smooth muscle, a few macrophages, and rare lymphocytes and plasma cells. Arterioles, venules, and capillaries are present at all levels. In contrast, lymphatics are present in the basal lamina propria
• The Muscularis Mucosae. The muscularis mucosae is a thin double layer of smooth muscle that defines the base of the mucosa and separates it from the submucosa.
• The Submucosa. This is a loose connective tissue layer containing blood vessels, lymphatics, nerves, and ganglion cells of the submucosal (Meissner) plexus; a few adipocytes;
• The Muscularis Propria. the stomach has three muscle layers: inner oblique, middle circular, and outer longitudinal. The nerves and ganglion cells of the myenteric (Auerbach) plexus are found between the outer two muscle layers.
• The Subserosa and Serosa. the stomach has a thin covering of subserosal collagen, the subserosa. The subserosa is covered by a single layer of flat mesothelium
ARTERIAL AND LYMPHATIC SUPPLY OF THE STOMACH
Acute Gastritis
• Transient mucosal inflammatory process• Erosion, ulceration, hemorrhages,
hematemesis, melena• Pathogenesis: Imbalance between
defensive and damaging forces
Acute Gastritis
Acute Gastric Ulceration
• Focal, acute, gastric mucosal defects• Specific names depending on location &
clinical association:– Stress ulcer (Shock, sepsis, trauma)– Curling’s ulcer (Burns)– Cushing’s ulcer (Intracranial disease)
Pathogenesis
NSAID-induced ulcers: cyclooxygenase inhibition
• synthesis of prostaglandinsRole of prostaglandins:
– Enhance bicarbonate secretion– Inhibit acid secretion– Promote mucin synthesis and – Increase vascular perfusion
Pathogenesis
Intracranial injury: • Stimulation of vagal nuclei
(Hypersecretion of gastric acid)• Systemic acidosis (lowers intracellular
pH of mucosal cells)• Splanchnic vasoconstriction (hypoxia,
reduced blood flow)
MorphologyGross:• Anywhere in the stomach • Multiple • Ulcers are round and < 1 cm in diameter• Base is frequently stained brown to black• Gastric rugal folds are normal• Margins and base of the ulcers are not indurated Microscopy:• Sharply demarcated, with essentially normal adjacent
mucosa • No scarring • Healing with complete re-epithelialization occurs after
the injurious factors are removed
Clinical Features
• S/S of underlying condition• Bleeding• Perforation • Out come depends on the underlying
precipitation condition
Chronic gastritisClinical features:• Nausea• Upper abdominal discomfort• VomitingCauses:• Helicobacter pylori – most common• Psychological stress• Caffeine, alcohol, tobacco• Autoimmune gastritis• Bile reflux• Radiation• Crohn’s• GVHD
HELICOBACTER PYLORI GASTRITIS
• H. pylori : spiral-shaped or curved bacilli • H. pylori –
– 90% chronic antral gastritis– 100% in duodenal ulcer
• Routes of infection:– Oral– Fecal-oral– Environmental spread
Pathogenesis
• Infection results in increased acid production
• Four features are linked to H. pylori virulence: – Flagella, Urease, Adhesins, Toxins
• Chronic antral H. pylori gastritis pangastritis multifocal atrophic gastritis
Morphology• The organism is concentrated within the superficial
mucus overlying epithelial cells• Frequently found in the antrum • Mucosa is erythematous • Inflammatory cells:
– Neutrophils Intraepithelial, pit abscesses – Subepithelial plasma cells
• Mucosa: – Thickened - initial stages – Atrophic - later stages
• Lymphoid aggregates, with germinal centers – May progress to Lymphoma
Intraepithelial neutrophils and subepithelial plasma cells are
characteristic of H. pylori gastritis
Helicobacter pylori gastritis: A, Spiral-shaped H. pylori are highlighted in this Warthin-Starry silver stain. Organisms are abundant within surface mucus. B, Intraepithelial and lamina propria neutrophils are prominent. C, Lymphoid aggregates with germinal centers and abundant subepithelial plasma cells within the superficial lamina propria are characteristic of H. pylori gastritis
Diagnosis
• Ab to H.pylori• Fecal bacterial detection• Urea breath test• Biopsy specimen:
– Rapid urease test– Culture– DNA detection by PCR
Urease breath test
AUTOIMMUNE GASTRITIS
• < 10% of cases of chronic gastritis • Spares the antrum• Hypergastrinemia
Autoimmune gastritis is characterized by:
• Antibodies to:– Parietal cells– Intrinsic factor
• Reduced serum pepsinogen I• Antral endocrine cell hyperplasia• Vitamin B12 deficiency• Achlorhydria
Pathogenesis• CD4+ T cells directed against parietal cell
components, including the H+,K+-ATPase, are the principal agents of injury
• Loss of parietal cells:– absence of acid production – hypergastrinemia and – hyperplasia of G cells
• Lack of intrinsic factor – Pernicious anemia
• no evidence of an autoimmune reaction to chief cells
Morphology
• Diffuse atrophy of gastric mucosa– body and fundus appears markedly thinned, and rugal
folds are lost • Infiltrated by lymphocytes, plasma cells• Inflammation extends deep into mucosa• Loss of parietal and chief cells• Intestinal metaplasia • Antral endocrine cell hyperplasia
– multicentric, low-grade carcinoid tumors
Gastric atrophy
Autoimmune gastritis:A, Low-magnification image of gastric body demonstrating deep inflammatory infiltrates, primarily
composed of lymphocytes, and glandular atrophy. B, Intestinal metaplasia, recognizable as the presence of goblet cells admixed with gastric foveolar
epithelium
Clinical Features • Slow onset • Median age at diagnosis is 60 yrs • May be associated with other autoimmune
diseases• Atrophic glossitis (beefy red tongue)• Peripheral neuropathy - paresthesias and
numbness • Spinal cord lesions: loss of vibration and position
sense • Cerebral manifestations: personality changes
and memory loss to psychosis
Clinical Features
HYPERPLASTIC HYPERPLASTIC GASTROPATHIESGASTROPATHIES
HYPERPLASTIC GASTROPATHIES
• The normal gastric folds or rugae are composed of cores of submucosa covered by mucosa
• The status of the folds depends, to a great extent, upon the degree of gastric distention
HYPERPLASTIC GASTROPATHIES• Unusually large folds, therefore, are defined as those
that persist even in the distended stomach • DEF:
– Radiographic large folds are those greater than 8 mm in width– Endoscopic large folds are greater than 1 cm in height
CLASSIFICATION OF GIANT FOLDS 1. Normal variant, including common gastritis 2. Menetrier's disease and variants 3. Zollinger-Ellison syndrome 4. Lymphocytic gastritis 5. Extensive or diffuse neoplastic infiltrates 6. Other causes
Menetrier's DiseaseThe full blown syndrome includes:• Giant folds • Gastric protein loss and
• Decreased gastric acid production Histologically:• Foveolar hyperplasia and distortion • Glandular atrophy and
• Edema but little inflammation, in the lamina propria
Menetrier's Disease
• There is no known cause • Excessive growth factors Clinical features:• Adults, mean age of 55 to 60 yrs• Epigastric pain• Peripheral edema due to hypoproteinemia
Menetrier's Disease - Morphology
• Enlarged folds in the gastric body and fundus
• Rougae have knobby, lobulated, or even cerebriform surfaces
• There is abundant mucus on the surface • Microscopy: florid pit hyperplasia
accompanied by atrophy of glands, superficial edema
Menetrier's Disease - Morphology
• The pits are unusually elongated• frequently extend from the surface to the
base of the mucosa• Occasionally, they penetrate the
muscularis mucosae – “gastritis cystica profunda”
• Replacement of the glandular compartment by the expanding pit compartment results in hypochlorhydria or achlorhydria
Tx – Resection: • The most common indication for
resection is the hypoproteinemia that leads to uncontrollable peripheral edema and even anasarca
Zollinger-Ellison SyndromeZollinger-Ellison Syndrome
Zollinger-Ellison Syndrome
Characterized by:• Intractable peptic ulcers involving
duodenum and jejunum, often multiple • Hypergastrinemia, usually from a gastrin-
producing tumor Typical features of ZE syndrome:• Hypergastrinemia • Parietal cell hyperplasia
Zollinger-Ellison Syndrome
Peptic Ulcer SyndromePeptic Ulcer Syndrome
Peptic Ulcer SyndromePeptic Ulcer Syndrome
Peptic ulcers are solitary lesion that can occur in any part of the GIT which is
exposed to acid-peptic juices
Acid peptic digestion[Acid & Pepsin are required for peptic ulceration]
Peptic UlcerPeptic Ulcer
Sites:• Duodenum• Stomach• GE junction• Gastrojejunostomy site• Jejunum in ZE-syndrome• Meckel’s diverticulum with gastric mucosa• At the “inlet patch” in esophagus
Peptic UlcerPeptic Ulcer
• Young adults / Middle age• Remitting & relapsing disease• H.pylori
Peptic Ulcer - Peptic Ulcer - PathogenesisPathogenesis
• Imbalance between mucosal defenses and damaging forces
• Acid and pepsin are required for peptic ulceration
• H.pylori infection
Peptic UlcerPeptic Ulcer
Peptic Ulcer - Peptic Ulcer - PathogenesisPathogenesis
• Increase in parietal cell mass• Increased sensitivity of parietal cells to
secretory stimuli• Increased basal acid secretory drive• Impaired inhibition of stimulatory
mechanisms eg: gastrin release
Peptic Ulcer - Peptic Ulcer - PathogenesisPathogenesis• NSAIDs• Smoking• Alcoholism• Corticosteroids• Rapid gastric emptying• Hyperparathyroidism• COPD• Cirrhosis• Psychosomatic disorder
Hypercalcemia due to any
cause stimulates
Gastrin production
Ischemia
Peptic Ulcer - Peptic Ulcer - MorphologyMorphology
• Duodenum – first part, anterior wall• Stomach – lesser curvature, junction of
corpus and antrum• 0.3cm (erosions) to 0.6cm (ulcers)• 50% measure >2cms
Peptic Ulcer - Peptic Ulcer - MorphologyMorphology
• Shape: Round to oval• Margins: Punched out • Edge: Overhanging • Floor: clean• Base: Firm• Depth may vary• Scarring -> puckering -> radiating mucosal
folds (like spokes)
Gastric ulcer:Elliptical shape
Radiating rugal folds (in spoke wheel pattern)
Clean floor
Punched out edges
Cross section of ulcer
BASE OF THE
ULCER
FLOOROF THE
ULCER
Peptic Ulcer - Peptic Ulcer - Microscopy
Four zones:1.Zone of exudation (thin layer of fibrinoid
necrosis)2.Zone of inflammatory cell infiltration3.Zone of granualtion tissue4.Zone of cicatrization - scarring
Blood vessels may show thickening of wall and thrombus in their lumina
Peptic UlcerPeptic Ulcer
Complications
• Bleeding• Perforation• Obstruction• Anemia
DD Benign & malignant ulcers
Feature Benign ulcer Malignant ulcer
Margins Punched out Heaped up / sloping
Floor Clean Necrotic debris
Surrounding mucosa
Spoke wheel pattern Ironed out
Malignant ulcer
Gastric carcinoma:Heaped up and sloping margins
Ironed out mucosa
Benign tumors
• Lipoma• Leiomyoma• Adenomas
Gastric Lipoma
Gastric leiomyoma – Massive upper GI bleeding
Gastric leiomyoma
E N DE N D
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