Esophageal and Gastric Pathology Flashcards
Describe the developmental process of the esophagus
Starts out as a single tube with trachea. Then laryngotracheal diverticulum forms…becomes epithelial ridges and eventually forms full trachea
How does epithelium change over course of fetal development?
From psedustratified columnar to columnar epithelium with mutinous secretion to non-keratinizing stratified squamous epithelium
Describe the embyronic development process of the stomach
Fusiform dilitation of the foregut and rotation
There is no epithelial changes
What is esophageal atresia?
Esophagus “not perforated”– basically the tube forms a dead end
Which is the most common developmental anomaly?
Esophageal atresia where esophagus not continuous and part that should be connected is continuous with stomach
What is a tracheoesophageal fistula?
Narrowing of tube with connection between esophagus and trachea
Esophogeal duplication: How does it present?
How is it treated?
It’s discovered after birth due to regurgitation during feeds. It requires prompt surgical repair because it is incompatible with life
Gastric Ectopia (inlet patch)
Presence of ectopic gastric mucosa in upper 1/3 of esophagus
Intantile hypertrophic pyloric stenosis: Epidemiology and presentation
More common in white males
Presents between 3rd/6th week of life with regurgitation, projectile vomiting
What are the types of obstruction? How do they present?
Webs– eccentric thin membranes often in proximal region
Ring: Diaphragm of tissue located in distal esophagus
Schatzki ring: both mucosa/submucosa
Often are asymptomatic
What is a pulsion diverticula?
Diverticulum due to increased intraluminal pressure. Located in proximal/distal esophagus
Secondary to motility disturbances such as achalasia
Describe a traction diverticula
Extrinsic inflammation retracts/pulls bowel outwards
Located in mid esophagus
Less common
Name some of the etiologies of esophagitis
Mechanical (achalasia), reflux, corrosive injuryies, pills/drugs, infections, allergies, radiation, GVHD, systemic disorders
What is mechanism of injury in achalasia?
Injury to myenteric plexus from toxins, trauma, viruses, bacteria, autoimmune
How does achalasia appear on barium swallow?
“Bird’s beak”– dilatation of esophagus with acute tapering at LES and narrowing of GEJ
What is boerhaave syndrome?
Rupture of the esophagus post vomiting due to sudden increase in intraluminal esophageal pressure
What are Mallory-Weirs tears?
Mucosal lacerations in distal esophagus and proximal stomach due to retching, vomiting, straining, coughing (often after heavy alc use)
How does viral esophagitis appear grossly?
On high magnification?
Gross: Shallow punched out ulcers
Histo: Herpes=Multinucleated squamous epithelial cells with intranuclear inclusions. CMV=big cells with nuclear/cytoplasmic inclusions
How does candida esophagitis appear? Both gross and high power.
Gross: Lots of white patches
Histology: pseudo hyphae and budding yeast
How does eosinophilic esophagitis appear on endoscopy?
“Trachealization”– ringed appearance with linear furrows
How does eosinophilic esophagitis present? Eli and symptoms
Epi: Children or adults, males, concurrent with other allergic conditions
Px: feeding difficulty, nausea, vomiting, dysphagia as a result of fibrosis of submucosa
How does scleroderma-caused esophageal sclerosis appear on high power?
Inner circular layer of smooth muscle is not well observed due to deposition of collagenous material– atrophy/fibrosis leads to LES defect, GERD, pulmonary infections
Which esophageal cancer is most common in the Western hemisphere? World wide?
Western hemisphere: adenocarcinoma
Worldwide: Squamous cell carcinoma
Esophageal carcinoma: Epidemiology
Associated with Barrett’s esophagus
RFs: males, age, longstanding reflux, obesity
How is Barrett’s esophagus diagnosed?
Endoscopy: columnar type mucosa on endoscopy
Biopsy: shows intestinal metaplasia (i.e goblet cells)
NEED BOTH
What is the difference between short segment and long segment Barrett’s esophagus? What’s the clinical significance
Short is less than 3cm. Long is greater than 3cm
Long segment BE carries much higher risk of developing adenocarcinoma
Describe the epidemiology of esophageal squamous cell carcinoma
Most common worldwide; males more commonly affected
RFs: tobacco, alcohol, vitamin dificiency, food/water rich in nitrates
HPV IS NOT A RF
Which part of esophagus is most commonly affected?
Middle third
What are the different types of squamous cell carcinoma on histology?
Keratinizing (appear pinker)– they are more differentiated
Non-keratinizing– poorly differentiated
What is chyme? How is it formed?
Rhythmic contractions of gastric musculature breaks down ingested food particles and mixes it with gastric fluid. The result is called chyme
What are the three phases of gastric acid secretion?
Cephalic phase: thought of food leads to stimulation of vagus nerve causing parietal cells to secrete acid
Intestinal phase: As food bolus enters stomach, gastric dilitation occurs that causes gastrin/histamine release by endocrine cells
Intestinal phase: Once food exits stomach, negative regulation by intestinal hormones prevents further acid secretion
Compare/contrast acute vs. chronic gastritis
Acute: Mucosal barrier breakdown, may see neutrophils. Causes: stresses (cushings, curling, toxic, circulatory)
Chronic: Observe inflammatory cells. Causes: H Pylori, autoimmune
How does acute gastritis appear histologically?
Observe surface erosion/fibrin
Lack of chronic inflammatory cells
How does a chronic H Pylori gastritis appear histologically?
Can do special stain to detect– CLOtest detects ureas.
Otherwise, observe superficial inflammation (lymphocytes/plasma cells)
What is atrophic gastritis? What are etiologies?
Loss of parietal/chief cells of gastric glands that can progress to lymphoma/carcinoma
Etiology: Autoimmune or H pylori
How does autoimmune atrophic gastritis appear histologically?
Antralized gastric glands– destruction of parietal cells and intestinal metaplasia of surface epithelium
How does autoimmune gastritis lead to carcinogenesis?
Loss of parietal cells but gastrin signaling still intact: get ECL hyperplasia
Intestinal metaplasia from autoimmune destruction leads to dysplasia and eventually adenocarcinoma
How does autoimmune gastritis appear grossly?
Loss of rugal folds, mucosal atrophy
What is the difference between funds glandular polyp and hyper plastic polyp?
Site of enlargement: glands vs. epithelium
What is cause of hypertrophic gastropathy? How does it appear grossly and microscopically?
ZE Syndrome:
Observe diffuse hypertrophy of rugal folds
On high power, see hyperplasia of parietal cells . Epithelial compartment is not expanded
Marginal Zone B Cell Lymphoma (MALT)
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What are the two types of gastric adenocarcinomas?
Intestinal type: Gland forming
Signet ring type: single cells
What is the difference in progression between intestinal type and Signet ring type adenocarcinomas?
Intestinal: Chronic gastritis–>Metaplasia–>dysplasia–>adenocarcinoma
Signet ring: no chronic gastritis, instead mutation involving E-cadherin
Diffuse type gastric carcinoma: How does it appear grossly and histologically?
Gross: leather bottle stomach (linnets plastica)
HIsto: Signet ring cells
GI Stromal Tumors: Where do most arise? How do most arise? (cell or origin, mutation)
70% arise in stomach
Arise from ICC cells; defined by reactivity to c-KIT (a tyrosine kinase)
How are GI Stromal tumors treated?
Imatinib/gleevec, which targets tyrosine kinase receptor
How do GI Stromal tumors appear grossly? Histologically?
Gross: submucosal with areas of hemorrhage and necrosis
Histo: Subepithelial, spindle cells
