Esophagus/Stomach Key Concepts Flashcards
- absence of ganglion cells (may be grossly normal or contracted)
- rectum always affected, length of additional segment varies
- normally innervated segment of bowel undergoes progressive dilation, becoming massively distended -> may stretch and thin to the point of rupture, most frequently near the cecum
- mucosal inflammation or shallow ulcers may also be present in normally innervated segments
- intraoperative frozen-section analysis is commonly used to confirm the presence of ganglion cells at the anastomotic margin
Hirschsprung disease
what is the most common form of congenital intestinal atresia?
imperforate anus
what is the most common site for fistulization?
esophagus
thickened wall and partial or complete luminal obstruction
stenosis
what are acquired forms of stenosis often due to?
inflammatory scarring
incomplete diaphragm develppment and herniation of abdominal organs into the thorax
diaphragmatic hernia
what does a diaphragmatic hernia often result in?
pulmonary hypoplasia
what are omphalocele and gastroschisis?
ventral herniation of abdominal organs outside the baby’s body, exiting in a hole near (gastroschisis) or out of (omphalocele) the belly button
normally formed tissues in an abnormal site
ectopia
where is the most common location of ectopic gastric mucosa?
upper third of the esophagus
true diverticulum, defined by the presence of all three layers of the bowel wall, that reflects failed involution of the vitelline duct
- common and is a frequent site of gastric ectopia, which may result in occult bleeding
Meckel diverticulum
form of obstruction that presents between the third and sixth weeks of life
- ill-defined genetic component, more common in males
congenital hypertrophic pyloric stenosis
dense infiltrates of neutrophils present in most cases, leading to outright necrosis of the esophageal wall
infectious esophagitis
strictures that impede passage of luminal contents
- ulceration accompanied by superficial necrosis with granulation tissue ad eventual fibrosis
pill-induced esophagitis
Candidiasis is characterized by a gray-white pseudomembrane composed of what?
densely matted fungal hyphae and inflammatory cells covering the esophageal mucosa
what type of infectious agent causes:
- punched-out ulcers
- nuclear viral inclusions within a rim of degenerating epithelial cells at the margin of the ulcer
Herpes
what type of infectious agent causes:
- shallow ulcerations
- nuclear and cytoplasmic inclusions within capillary endothelium and stromal cells
cytomegalovirus (CMV)
esophageal involvement
- basal epithelial cell apoptosis
- mucosal atrophy
- submucosal fibrosis without significant acute inflammatory infiltrates
esophageal graft-versus-host disease
simple hyperemia, evident to the endoscopist as redness (may be only alteration)
- eosinophils are recruited into the squamous mucosa followed by neutrophils
- basal zone hyperplasia exceeding 20% of the total epithelial thickness and elongation of lamina propria papillae, such that they extend into the upper third of the epithelium may also be present
reflux esophagus
tortuous dilated veins lying primarily within the submucosa of the distal esophagus and proximal stomach
- venous channels directly beneath the esophageal epithelium may also become massively dilated
- rupture results in hemorrhage into the lumen r the esophageal wall, in which case the overlying mucosa appears ulcerated and necrotic
esophageal varices
one or several patches of red, velvety mucosa extending upward from the gastroesophageal junction
- metaplastic mucosa alternates with smooth, pale squamous (esophageal) mucosa and interfaces with light-brown columnar (gastric) mucosa
Barrett esophagus
what is considered “long segment” Barrett esophagus?
involves 3cm or more
what is considered “short segment” Barrett esophagus?
less than 3 cm involved
diagnosis of what requires endoscopic evidence of metaplastic columnar mucosa above the gastroesophageal junction?
Barrett esophagus
microscopically, intestinal-type metaplasia is seen as replacement of what in Barrett esophagus?
squamous esophageal epithelium with goblet cells
atypical mitoses, nuclear hyperchromasia, irregularly clumped chromatin, increased nucear-cytoplasmic ratio, failure of epithelial cells to mature as they migrate
dysplasia
usually occurs in the distal third of the esophagus, may invade the adjacent gastric cardia
- initially appears as flat or raised patches on intact mucosa
- large masses may develop (>5cm)
- tumors may infiltrate diffusely or ulcerate and infiltrate deeply
- tumors may be composed of diffusely infiltrative signet-ring cells (similar to those seen in diffuse gastric cancers)
esophageal adenocarcinoma
what is frequently present adjacent to esophageal adenocarcinoma?
Barrett esophagus
half of these cancers occur in the middle third of the esophagus
- begins as in situ lesion (dysplasia)
- early lesions appear as small, gray-white, plaque-like thickenings
- over months-years they grow into tumor masses that may be polypoid, or exophytic, and protrude into/obstruct the lumen
- most are moderately to well differentiated
- symptomatic tumors are generally very large at diagnosis and have already invaded the esophageal wall
squamous cell carcinoma
incomplete LES relaxation, increased LES tone, and esophageal aperistalsis
- can be primary or secondary
achalasia
mucosal tear at the gastroesophageal junction that develops as a result of severe retching or vomiting,
Mallory-Weiss tear
what is the most prevalent cause of esophagitis?
GERD
strongly associated with food allergy, allergic rhinitis, asthma, or modest peripheral eosinophilia
- common cause of GERD-like symptoms in children in developed countries
eosinophillic esophagitis
consequence of portal hypertension, are present in nearly half of cirrhosis patients
gastroesophageal varices
what esophageal cancer is associated with alcohol/tobacco use, poverty, caustic esophageal injury, achalasia, tylosis (hyperkeratosis of palms/soles), and Plummer-Vinson syndrome?
esophageal squamous cell carcinoma
lamina propria shows only mild edema/slight vascular congestion, and surface epithelium is intact
- but foveolar cell hyperplasia, with characteristic corkscrew profiles and epithelial proliferation are present
acute gastritis
the presence of what, above the basement membrane in direct contact with epithelial cells, is abnormal in all parts of the GI tract and signifies active inflammation
neutrophils
erosion denotes loss of what?
- resulting in a superficial mucosal defect
epithelium
concurrent erosion and hemorrhage is called what?
acute erosive hemorrhagic gastritis
sharply demarcated under microscope, with essentially normal adjacent mucosa
- may be a slow spread of blood into the mucosa and submucosa, and an inflammatory reaction
- are found anywhere in the stomach, there may be multiple
- ulcer base is frequently stained brown/black by acid digestion, may be associated with transmural inflammation and local serositis (serous membrane inflammation)
acute stress ulcer
gastric biopsy specimen demonstrates concentrations within the superficial mucus overlying epithelial cells in the surface and neck regions (most often in antrum of the stomach)
- distribution can be irregular, with areas of heavy colonization adjacent to those with few organisms
- display tropism for gastric epithelia and are generally not found in association with intestinal metaplasia or duodenal epithelium
H. pylori
what is the preferred evaluation of H. pylori gastritis?
antral biopsy
endoscopically, antral mucosa is erythematous and has a coarse or even nodular appearance
- inflammatory infiltrate generally includes variable numbers of neutrophils within the lamina propria, including some that cross the basement membrane to assume an intraepithelial location
- accumulate in the lumen of gastric pits to create pit abscesses
- inflammatory infiltrates may create thickened rugal folds, mimicking the appearance of early cancers
- lymphoid aggregates frequently present -> MALToma**
H. pylori gastritis
in contrast to autoimmune gastritis, H. pylori gastritis is usually what?
- biopsies of the gastric body can show intact oxyntic glands adjacent to antral-type glands
a patchy process
diffuse mucosal damage of the oxyntic (acid-producing) mucosa within the body and fundus of the stomach
- mucosa appears markedly thinned, rugal folds are lost
- megaloblastic anemia (vit B12 def)
- inflammatory infiltrate typically composed of lymphocytes, macrophages, and plasma cells, often in association with lymphoid aggregates and follicles
- inflammatory reaction is deeper than H. pyloriand centered on the gastric glands
autoimmune gastritis
what hyperplasia can be difficult to apreciate on H&E stain, but is clearly demonstrated with immuno-stains for proteins like chromogrannin A
- parallels the degree of mucosal atrophy, and is a physiologic response to decreased acid production
autoimmune gastritis
overtime, hypergastrinemia can stimulate what? what can this rarely progress to?
endocrine cell hyperplasia in the fundus and body
- small, multicentric, low-grade neuroendocrine (cancinoid) tumors
most commonly occur in the proximal duodenum, where they occur within a few centimeters of the pyloric valve and involve the anterior duodenal wall
- solitary in more than 80% of patients
- round to oval, sharply punched-out defect
- the base is smooth and clean as a result of peptic digestion of exudate
peptic ulcers
predominantly located along the lesser curvature near the interface of the body and antrum
gastric ulcers
what rarely (if ever) occurs to peptic ulcers, and are more likely cases in which a lesion thought to be a chronic peptic ulcer was actually an ulcerated carcinoma from the start?
malignant transformation
what is the most common cause of acute gastritis?
H. pylori infection
typically affecting the antrum, associated with increased gastric acid production.
- in later disease, the body can be involved and the resulting glandular atrophy can lead to mildly reduced acid production
- induces MALT that can give rise to B cell lymphoma
H. pylori gastritis
what is the most frequent etiology of noninfectious chronic gastritis?
- results in atrophy of the gastric body oxyntic glands, leading to decreased gastric acid production, antral G cell hyperplasia, achlorhydria, and vit B12 deficiency
autoimmune gastritis
what develops in both forms of chronic gastritis and is a risk factor for gastric adenocarcinoma
intestinal metaplasia
usually secondary to H. pylori
- ulcers can develop in the stomach or duodenum, and usually heal after suppression of gastric acid production and eradication of H. pylori
peptic ulcer disease
irregular enlargement of the gastric rugae in the body and fundus
- excessive secretion of TGF-a
- diffuse hyperplasia of foveolar mucous cells
- glands are elongated with corkscrew-like appearance and cystic dilation is common
- diffuse or patchy glandular atrophy, evident as hypoplasia of parietal and chief cells
Menetrier disease
irregular, cysticaly dilated, and elongated foveolar glands
- smaller than 1 cm, usually multiple (particularly in those with atrophic gastritis)
- ovoid in shape and have a smooth surface
gastric polyps
- 75% of all gastric polyps are inflammatory or hyperplastic
occur in the gastric body and fundus
- well-circumscribed lesions with a smooth surfae
- may be single or multiple
- cystically dilated, irregular glands lines by flattened parietal and chief cells
- minimal/absent inflammation
fundic gland polyps
solitary lesions, less than 2cm
- located in the antrum (usually the lesser curvature more than the greater curvature)
- intestinal-type columnar epithelium that exhibits varying degrees of dysplasia
- can be classified as low or high grade, both grades may include enlargement, elongation, pseudostratification, and hyperchromasia of epithelial cell nuclei, and epithelial crowding
gastric adenocarcinoma
characterized by more severe cytologic atypia and irregular architecture, including glandular budding and gland-within-gland, or cribiform structures
high grade gastric adenocarcinoma
the risk of what is much higher in gastric adenocarcinomas than intestinal adenocarcinomas?
transformation to invasive cancer
diffuse gastric cancer is generally composed of discohesive cells, likely as a result of what?
E-cadherin loss
cells do not form glands, but instead have large mucin vacuoles that expand the cytoplasm and push the nucleus to the periphery, creating signet-ring cell morphology
- they permeate the mucosa and stomach wall individually or in small clusters, and may be mistaken for inflammatory cells, such as macrophages
- they release extracellular mucin, forming large mucin lakes
diffuse gastric cancer
a mass may be difficult to appreciate in diffuse gastric cancer, but these infiltrative tumors often evoke what?
a desmoplastic reaction that stiffens the gastric wall and may provide valuable diagnostic clue
- large areas of infiltration, diffuse rugal flattening and a rigid, thickened wall may impart a leather bottle appearence called linitis plastica
these take the form of a dense, lymphocytic infiltrate in the lamina propria
- neoplastic lymphocytes infiltrate the gastric glands focally to create diagnostic lymphoepithelial lesions
- reactive B-cell follicles may be present
- plasmacytic differentiation in 40% of tumors
- express B cell markers CD19 and CD20
- positive for CD43 in 25% of cases
- restricted expression of kappa or landa immunoglobulin light chains
- molecular detection of clonal IgH rearrangements
gastric MALToma
intramural or submucosal masses that create small polypoid lesions
- typically arise within ocyntic mucosa in the stomach
- overlying mucosa may be intact or ulcerated (tumors may invade deeply and involve the messentery in the intestines)
- yellow or tan in color, and are very firm as a consequence of desmoplastic reaction (which may cause kinking/obstruction of the bowel)
- minimal pleomorphism, but anaplasia, mitotic activity and necrosis may be present in rare casese
- immunohist stains positive for endocrine granule markers, such as synaptophysin and chromogranin A
carcinoid tumors
large (30cm), solitary, well-circumstribed fleshy mass covered by ulcerated or intact mucosa
- the cut surface shows a whorled appearance
- metastases may take the form of multiple serosal nodules throughout the peritoneal cavity, or as one or more nodules in the liver
- most useful diagnostic marker is KIT, which is detectable in Cajal cells and 95% of these tumors
gastric GI stromal tumor (GIST)
GIST composed of thin elongated cells
spindle cell type
GIST composed of epithelial appearing cells
epitheliod type
caused by gastrin-secreting tumors that cause parietal cell hyperplasia and acid hypersecretion
- 60-90% of gastrinomas are malignant
ZES
occur sporadically, most often as a consequence of PPI therapy, and in familial adenomatous polyposis (FAP) patients
fundic gland polyps
develop in a background of chronic gastritis and are particularly associated with intestinal metaplasia and mucosal (glandular) atrophy
gastric adenoma
gastric tumors with an intestinal histology that form bulky tumors and may be ulcerated, while those composed of signet-ring cells typically display a diffuse infiltrative growth pattern that may thicken the gastric wall without forming a discrete mass
- are linked to H. pylori induced chronic gastritis
gastric adenocarcinoma
derived from MALT, whose development is induced by H. pylori induced chronic gastritis
primary gastric lymphomas
arise from diffuse component of the endocrine system and are most common in the GI tract, particularly the small intestine
- prognosis is based on location, tumors of the small intestine tend to be most aggressive, while those in appendix are typically benign
carcinoid tumors aka neuroendocrine tumors
most common mesenchymal tumor of the abdomen, occurs most often in the stomach, and is related to benign pacemaker cells, or intestinal cells of Cajal
- tumors generally have activating mutations in either KIT or PDGFRA tyrosine kinases and respond to specific kinase inhibitors
GIST
