• mucosal layer superficially lined by columnar mucin-producing cells that empty into pits which contain the gastric glands
• parts of stomach
  • proximal stomach (cardia) consists of glands lined by mucin producing cells
  • fundus- mucosa and submucosa re disposed in longitudinal rugae
    • mucosal layer lined by mucin producing neck cells extending into glands lined by parietal cells (eosinophilic) and chief cells (basophilic)
  • antrum- consists entirely of mucin producing cells, G cells, and delimited by pyloric sphincter

• clinical consequence
  • accumulation of stomach contents leading to reflux or projectile vomiting
• two forms
  • congenital- muscular hypertrophy occuring in infants
    • epidemiology- male predominance
  • acquired- secondary to gastric inflammation or fibrous stricture (or neoplasm)

• epidemiology- middle aged males
• presentation
  • nonspecific GI complaings
  • edema (due to protein loss)
• pathogenesis: idopathic overproduction of TGF alpha
• histopathology
  • enlargement of mucosal folds with hyperplasia of surface mucosal cells
  • this results in marked mucus/protein loss
• associated with metastatic change, leading to increased risk for carcinoma

• clinical presentation
  • abdominal pain
  • symptoms associated with gastric ulcers occuring 1-3 hrs after meals and relieved by antacids
• pathogenesis
  • sudden onset (acute) or persistence (chronic) of factors that result in breakdown of mucosal barrier and/or decrease in normal protective mechanisms

related to factors that:

• directly damage mucosal epithelium
• inhibit production of mucin OR
• compromise the normally rich vascular supply required to oxygenate and to carry away and/or neutralize acid in microenvironment

• acute mucosal inflammation with neutrophilic infiltrate and edema
• variable epithelial cell and mucosal necrosis in the form of either
  • erosion
    • superficial necrosis
    • loss of mucosal epithelium only (does not extend to submucosa)
    • often small
  • ulcer
    • mucosal necrosis and loss that extends deeply into or beyond muscularis mucosa (ex: burns, trauma)
    • Curling ulcers or Cushing ulcers

• exogenous- drugs/toxins
  • NSAID's
  • smoking
  • alcohol
  • steroids
  • aspirin
• endogenous
  • stress (endogenous steroids)
  • microvascular ischemia (conditions affecting vascular supply like hypotension/shock)

• presistance of inflammation in gastric mucosa

Usually features of acute gastritis are present (and etiologic facgtors more important for acute an chronic gastritis are likely to be interactive in both phases of gastritis)

• microbiology of H pylori
  • wing shaped
  • gram negative rods
  • sits in mucus overlying epithelial cells
• pathogenesis (usually in antrum)
  • produce toxic ammonia from urease, inciting cytotoxins, and causing inflammatory reaction

• pathogenesis (usually at fundus)- can also be tied to other autoimmune conditions like Hashimoto's thyroiditis
  1. Ab directed against parietal cells
  2. cause loss of gastric acid and pernicious anemia (loss of IF)
  3. leads to hyperplasia of gastrin producing cells in the antrum

• chronic mucosal inflammation with lymphocytes and macrophages
  • associated loss of functional tissue with evidence of ongoing inflammation and repair (fibrosis)
• glandular atrophy (thining of mucosal layer and loss of cells with specialized function)
• inflammatory polyps (regenerative overgrowth of mucosal epithelium above mucosal surface) (NO malignant potential)
• intestinal metaplasia (appearance of villi and goblet cells)
• chronic ulcers

• superficial layer of necroinflammatory debris
• acute inflammation of mucosal layer
• extension beyond muscularis mucosa with reactive granulation tissue (attempt ot heal/wall off)
• fibrosis

• gastric adenocarcinoma
• if H pylori- gastric lymphoid MALToma

• associated with:
  • H pylori
  • blood group O
  • 50% of gastric ulcers have duodenal ulcers as well
• location
  • MOST COMMON: duodenum
  • 2- antrum
  • 3- fundus

• gross pathology
  • punched out appearance
  • radiating mucosal folds
• histopathology- necrotic debris overlying eventual granulation tissue and fibrosis

Malignant ulcers tend to be larger, fungating, with heaped up ulcer margins without orientation of gastric folds.

• multiple ulcers with high level of acid production in response to pancreatic gastrinoma
• results in chronic gastritis

• leiomyomas (most common)
• schwanommas- benign nerve sheath tumors, relatively uncommon in upper GI tract
• adenomatous mucosal polys (uncommon)- have same appearance and malignat potential as polyps elsewhere in the GI tract

• clinically present most frequently as abdominal pain or bleeding
• most common- adenocarcinoma, epithelial carcinomas (epithelials have poor prognosis)
• contributory factors
  • diet (nitrosamines)
  • chronic gastritis causing atrophy/metaplasia
  • H pylori
  • blood group A
• epidemiology- incidence varies around world (Japan is high)

• intestinal type gastric carcinoma
  • histopathology
    • localized with expansile growth
    • gland formation
    • mucus cells exude mucus into their lumens
• diffuse type gastric carcinoma
  • histopathology
    • irregular clusters of single mucus containing singlet ring cells
    • aggressive tumor with depth of invasion the most important criterion for prognosis
  • gross pathology
    • infiltrative in growth with possible mucosal ulceration
    • produce rigid stomach wall (linitis plastica)

• most common site- stomach
• increased incidence in immunosuppressed patients
• relationship to chronically stimulated lymphoid tissue
  • as occurs in setting of chronic infection with H. pylori
• most frequently in people of Mediterranean descent and those with chronic malabsorptive syndromes (ex: sprue)

• gross pathology
  • arise in lymphoid tissue within the wall of GI tract in the MALT
  • tend to inflitrate within wall
    • give stiff "leather-bottle" like appearance to somach on gross exam
  • most B cell type (except sprue associated lypmhomas which are T cell type usually)
  • more frequently involved is stomach
• prognosis- poor for T cell associated with sprue and those occuring in Meditteraneans

• origin- spindle cell tumors arising in the submucosa and muscular layers
  • can be well circumscribed or infiltrative and aggressive dependent on specific tumor type and grade
  • arise from cells of interstitial cells of Cajal (the cells controlling peristalsis)
• genetics- c-kit mutations cause abnormal growth

• microscopic pathology-spindle shaped morphology
• location- most commonly in stomach
• prognosis
  • uncertain malignat potential, but increased size and mitotic rate show rough correlation with tendency for invasion
• tx
  • surgery (but recurrence is posssible)
  • inhibit tyrosine kinase (imatinib)