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The document summarizes the normal anatomy and histology of the stomach as well as various pathologies that can affect the stomach. It describes the layers of the normal gastric wall and the different cell types present in each region. It then discusses various inflammatory conditions like acute and chronic gastritis, peptic ulcers, hyperplastic gastropathies including Menetrier's disease, and neoplastic conditions such as Zollinger-Ellison syndrome. For each condition, it provides details on pathogenesis, morphology, clinical features, and complications.
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- 1. Pathology ofPathology of The Stomach - 1The Stomach - 1 Dr.CSBR.Prasad, M.D.,
- 2. 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 1. Submucosa 2. Muscularis propria and 3. Subserosa
- 3. 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)
- 4. GLANDULAR COMPARTMENT OF THE BODY MUCOSA The pale cells: Parietal cells Darker cells: Chief cells
- 5. 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.
- 6. 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
- 7. ARTERIAL AND LYMPHATIC SUPPLY OF THE STOMACH
- 8. Acute Gastritis • Transient mucosal inflammatory process • Erosion, ulceration, hemorrhages, hematemesis, melena • Pathogenesis: Imbalance between defensive and damaging forces
- 10. 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)
- 11. Pathogenesis NSAID-induced ulcers: cyclooxygenase inhibition • synthesis of prostaglandins Role of prostaglandins: – Enhance bicarbonate secretion – Inhibit acid secretion – Promote mucin synthesis and – Increase vascular perfusion
- 12. 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)
- 13. Morphology Gross: • 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
- 14. Clinical Features • S/S of underlying condition • Bleeding • Perforation • Out come depends on the underlying precipitation condition
- 15. Chronic gastritis Clinical features: • Nausea • Upper abdominal discomfort • Vomiting Causes: • Helicobacter pylori – most common • Psychological stress • Caffeine, alcohol, tobacco • Autoimmune gastritis • Bile reflux • Radiation • Crohn’s • GVHD
- 16. 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
- 17. 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
- 18. 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
- 19. Intraepithelial neutrophils and subepithelial plasma cells are characteristic of H. pylori gastritis
- 20. 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
- 22. Diagnosis • Ab to H.pylori • Fecal bacterial detection • Urea breath test • Biopsy specimen: – Rapid urease test – Culture – DNA detection by PCR
- 24. AUTOIMMUNE GASTRITIS • < 10% of cases of chronic gastritis • Spares the antrum • Hypergastrinemia
- 25. Autoimmune gastritis is characterized by: • Antibodies to: – Parietal cells – Intrinsic factor • Reduced serum pepsinogen I • Antral endocrine cell hyperplasia • Vitamin B12 deficiency • Achlorhydria
- 26. 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
- 27. 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
- 28. Gastric atrophy
- 29. 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
- 30. 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
- 33. 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
- 34. 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
- 35. 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
- 36. Menetrier's Disease The 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
- 37. 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
- 38. 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
- 39. 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”
- 42. • 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
- 44. 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
- 46. Peptic Ulcer SyndromePeptic Ulcer Syndrome
- 47. 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]
- 48. 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
- 49. Peptic UlcerPeptic Ulcer • Young adults / Middle age • Remitting & relapsing disease • H.pylori
- 50. Peptic Ulcer -Peptic Ulcer - PathogenesisPathogenesis • Imbalance between mucosal defenses and damaging forces • Acid and pepsin are required for peptic ulceration • H.pylori infection
- 52. 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
- 53. 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
- 55. 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
- 56. 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)
- 57. Gastric ulcer: Elliptical shape Radiating rugal folds (in spoke wheel pattern) Clean floor Punched out edges
- 58. Cross section of ulcer BASE OF THE ULCER FLOOROF THE ULCER
- 59. Peptic Ulcer -Peptic Ulcer - Microscopy Four zones: 1.Zone of exudation (thin layer of fibrinoid necrosis) 2.Zone of inflammatory cell infiltration 3.Zone of granualtion tissue 4.Zone of cicatrization - scarring Blood vessels may show thickening of wall and thrombus in their lumina
- 62. Complications • Bleeding • Perforation • Obstruction • Anemia
- 63. 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
- 64. Malignant ulcer Gastric carcinoma: Heaped up and sloping margins Ironed out mucosa
- 65. Benign tumors • Lipoma • Leiomyoma • Adenomas
- 66. Gastric Lipoma
- 67. Gastric leiomyoma – Massive upper GI bleeding
- 69. E N DE N D
Editor's Notes
- NORMAL CARDIAC MUCOSA: The pit and glandular compartments are approximately equal in height. Scattered glands are dialated. CORPUS, FUNDIC MUCOSA: The pit compartment is about one fourth of the entire mucosal thickness, resulting in a pit to gland ratio of 1 to 3. The glands are tightly clustered. The superficial lamina propria has few cells. ANTRAL (PYLORIC) MUCOSA: The pit and glandular compartments are about the same height. The glands are clustered and less densely packed than are the body glands.
- The glands are tightly packed. The pale cells with finely granular cytoplasm are parietal cells; the cells with denser, darker cytoplasm are chief cells.
- 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.
- The Lamina Propria. The lamina propria is sparse throughout the normal stomach. In the body mucosa, there is little stroma between the glands, only scant stroma between the pits and necks, and almost no inflammatory cells of any type Fig-8.5. In the antral and cardiac mucosae, the gland clusters are separated by a few loose collagen fibers and smooth muscle cells and the pits are more widely spaced than in the body mucosa; but even in this more spacious lamina propria, there are few inflammatory cells Fig-8.4, 8.6. 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, but not higher; however, in severe chronic atrophic gastritis, lymphatics may be found much higher in the mucosa. 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. Muscle fibers extend from here into the base of the mucosa, especially in the most distal part of the antrum. 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; and a variety of scattered spindle cells that are a mix of fibroblasts, smooth muscle cells, and mast cells. The Muscularis Propria. In contrast to other parts of the gut, which have a bilayer of inner circular and outer longitudinal smooth muscle in 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. Except where it is attached to omentum, mesocolon, and ligaments, the stomach has a thin covering of subserosal collagen, the subserosa. The subserosa is covered by a single layer of flat mesothelium, the serosa proper, a part of the visceral peritoneum.
- A schematic diagram of the arteries of the stomach illustrates: A: aorta; LG: left gastric artery; H: hepatic artery; RG: right gastric artery; GD: gastroduodenal artery; S: splenic artery; LGE: left gastroepiploic artery; and SPD: superior pancreaticoduodenal artery. The lymph nodes are situated along the arteries and consist of six groups: 1) paracardiac nodes; 2) superior gastric nodes; 3) subpyloric nodes; 4) inferior gastric nodes; 5) splenic nodes; and 6) pancreatic nodes. (Fig. 69 from Fasicle 7, Second Series.)
- FIGURE 17-11 Mechanisms of gastric injury and protection. This diagram illustrates the progression from more mild forms of injury to ulceration that may occur with acute or chronic gastritis. Ulcers include layers of necrosis (N), inflammation (I), and granulation tissue (G), but a fibrotic scar (S), which takes time to develop, is only present in chronic lesions.
- Focal, acutely developing gastric mucosal defects are a well-known complication of therapy with NSAIDs. They may also appear after severe physiologic stress. Some of these are given specific names, based on location and clinical associations. For example: • Stress ulcers are most common in individuals with shock, sepsis, or severe trauma.• Ulcers occurring in the proximal duodenum and associated with severe burns or trauma are called Curling ulcers.• Gastric, duodenal, and esophageal ulcers arising in persons with intracranial disease are termed Cushing ulcers and carry a high incidence of perforation.
- Pathogenesis. The pathogenesis of acute ulceration is complex and incompletely understood. NSAID-induced ulcers are related to cyclooxygenase inhibition. This prevents synthesis of prostaglandins, which enhance bicarbonate secretion, inhibit acid secretion, promote mucin synthesis, and increase vascular perfusion. Lesions associated with intracranial injury are thought to be caused by direct stimulation of vagal nuclei, which causes hypersecretion of gastric acid. Systemic acidosis, a frequent finding in these settings, may also contribute to mucosal injury by lowering the intracellular pH of mucosal cells. Hypoxia and reduced blood flow caused by stress-induced splanchnic vasoconstriction also contribute to the pathogenesis of acute ulcers.
- Pathogenesis. The pathogenesis of acute ulceration is complex and incompletely understood. NSAID-induced ulcers are related to cyclooxygenase inhibition. This prevents synthesis of prostaglandins, which enhance bicarbonate secretion, inhibit acid secretion, promote mucin synthesis, and increase vascular perfusion. Lesions associated with intracranial injury are thought to be caused by direct stimulation of vagal nuclei, which causes hypersecretion of gastric acid. Systemic acidosis, a frequent finding in these settings, may also contribute to mucosal injury by lowering the intracellular pH of mucosal cells. Hypoxia and reduced blood flow caused by stress-induced splanchnic vasoconstriction also contribute to the pathogenesis of acute ulcers.
- Morphology. Lesions described as acute gastric ulcers range in depth from shallow erosions caused by superficial epithelial damage to deeper lesions that penetrate the depth of the mucosa. Acute ulcers are rounded and less than 1 cm in diameter. The ulcer base is frequently stained brown to black by acid digestion of extravasated blood and may be associated with transmural inflammation and local serositis. Unlike peptic ulcers, which arise in the setting of chronic injury, acute stress ulcers are found anywhere in the stomach. The gastric rugal folds are essentially normal, and the margins and base of the ulcers are not indurated. While they may occur singly, more often there are multiple ulcers throughout the stomach and duodenum. Microscopically, acute stress ulcers are sharply demarcated, with essentially normal adjacent mucosa. Depending on the duration of the ulceration, there may be a suffusion of blood into the mucosa and submucosa and some inflammatory reaction. Conspicuously absent are the scarring and thickening of blood vessels that characterize chronic peptic ulcers. Healing with complete re-epithelialization occurs after the injurious factors are removed. The time required for healing varies from days to several weeks.
- Four features are linked to H. pylori virulence: • Flagella, which allow the bacteria to be motile in viscous mucus• Urease, which generates ammonia from endogenous urea and thereby elevates local gastric pH• Adhesins that enhance their bacterial adherence to surface foveolar cells• Toxins, such as cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer development by poorly defined mechanisms
- FIGURE 17-12 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.
- FIGURE 17-13 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. Antibodies to parietal cells and to intrinsic factor are present early in the disease course. Progression to gastric atrophy probably occurs over 2 to 3 decades, and anemia is seen in only a few patients. Because of the slow onset and variable progression, patients are generally diagnosed only after being affected for many years; the median age at diagnosis is 60 years. Slightly more women than men are affected. Pernicious anemia and autoimmune gastritis are often associated with other autoimmune diseases including Hashimoto thyroiditis, insulin-dependent (type I) diabetes mellitus, Addison disease, primary ovarian failure, primary hypoparathyroidism, Graves disease, vitiligo, myasthenia gravis, and Lambert-Eaton syndrome. These associations, along with concordance in some monozygotic twins and clustering of disease in families, support a genetic predisposition. In general, about 20% of relatives of individuals with pernicious anemia also have autoimmune gastritis, although they may be asymptomatic. Despite this strong genetic influence, autoimmune gastritis stands apart from other autoimmune diseases in that there is little evidence of linkage to specific HLA alleles. Clinical presentation may be linked to symptoms of anemia.[15] In addition, vitamin B12 deficiency may cause atrophic glossitis, in which the tongue becomes smooth and beefy red, epithelial megaloblastosis, and malabsorptive diarrhea. Vitamin B12 deficiency may also cause peripheral neuropathy, spinal cord lesions, and cerebral dysfunction. Neuropathic changes include demyelination, axonal degeneration, and neuronal death. The most frequent manifestations of peripheral neuropathy are paresthesias and numbness. The spinal lesions may be associated with a mixture of loss of vibration and position sense, sensory ataxia with positive Romberg sign, limb weakness, spasticity, and extensor plantar responses. Cerebral manifestations range from mild personality changes and memory loss to psychosis. In contrast to anemia, neurologic changes are not reversed by vitamin B12 replacement therapy.
- Hyperplasia may involve: Foveolar compartment or Glandular compartment Hyperplasia of foveolar compartment is associated with loss of protein rich mucin and may present as edema due to hypoproteinemia. Hyperplasia of glandular compartment is associated with excessive acid and pepsin production hence the patient present with the symptoms of peptic ulcer.
- PROMINENT RUGAL FOLDS Top: En face view of the stomach opened along the greater curvature. The antrum is the flattened area to the left. The remainder of the mucosa is covered by long ridges or folds. Bottom: Cross section shows submucosa in the core of each fold. These cores are covered by thick mucosa, in this case characterized by glandular hyperplasia, part of the Zollinger- Ellison syndrome.
- MENETRIER&apos;S DISEASE This is also body mucosa, but compared to figure 9-41, the pits are more prominent, many have a serrated configuration, and many extend to the base of the mucosa, where some of them end as cysts.
- When gastrin is present in excessive quantities, there is hyperplasia and hypertrophy of the parietal cells in the body mucosa
- ZOLLINGER-ELLISON SYNDROME Left: This is a cross section of a rolled gastric wall. The C-shaped structure in the center is the muscularis propria. The long submucosal folds are covered by thick body mucosa. Right: In this typical ZES case, the mucosa has a normally thick pit compartment and an expanded glandular compartment with much of the expansion due to an excess of parietal cells.
- FIGURE 17-11 Mechanisms of gastric injury and protection. This diagram illustrates the progression from more mild forms of injury to ulceration that may occur with acute or chronic gastritis. Ulcers include layers of necrosis (N), inflammation (I), and granulation tissue (G), but a fibrotic scar (S), which takes time to develop, is only present in chronic lesions.
- FIGURE 17-11 Mechanisms of gastric injury and protection. This diagram illustrates the progression from more mild forms of injury to ulceration that may occur with acute or chronic gastritis. Ulcers include layers of necrosis (N), inflammation (I), and granulation tissue (G), but a fibrotic scar (S), which takes time to develop, is only present in chronic lesions.