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Flashcards in GI Deck (117)
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Esophageal Atresia

  • portion of conduit replaced by thin, noncanalized cord with blind pouches above and below atretic segment.
  • associated with congenital heart defects, GU malformations, and neurologic disorders.
  • presentation: regurgitation during feeding.


Imperforate Anus

  • most common congenital intestinal atresia.
  • failure of cloacal membrane to involute.


Esophageal Fistula

  • connection btw esophagus and trachea or mainstem bronchus.
  • swallowed material or gastric fluid can enter the respiratory tract.
  • associated with: congenital heart defects, GU malformations, and neurologic disorders.
  • presentation: regurgitation during feeding.


Esophageal Stenosis

  • incomplete form of atresia.
  • lumen reduced by fibrous, thickened wall.
  • can be congenital or from inflammatory scarring (chronic reflux, irradiation, scleroderma)


Congenital Duplication Cysts

  • cystic masses with redundant smooth muscle layers throughout GI tract.


Diaphragmatic Hernia

  • incomplete formation of diaphragm allows cephalad displacement of abd viscera.
  • leads to pulmonary hypoplasia incompatable with life.



  • abdominal musculature is incomplete and viscera herniate into ventral membranous sac
  • associated with other birth defects in 40%.



  • all layers of abd wall fail to develop (peritoneum to skin).
  • viscera herniate into ventral membranous sac.


GI Ectopia

  • most common gastric mucosa ectopia is proximal esophagus.
    • dysphagia and esophagitis.
  • in small bowel/colon ⇒ occult blood loss or peptic ulceration.


Pancreatic Heterotopia

  • ectopic in esophagus and stomach.
  • in pylorus ⇒ inflammation, scarring, and obstruction.


Meckel Diverticulum

  • 2% of population, 2:1 male:female
  • persistence of vitelline duct ⇒ outpouching within 85cm of ileocecal valve.
  • can have pancreatic tissue or heterotopic gastric mucosa (with peptic ulceration).



  • blind pouch leading off alimentary tract, lined by mucosa and including all three layers of bowel wall (mucosa, submucosa, and muscularis propria)


Pyloric Stenosis

  • congenital hypertrophic pyloric stenosis: 1 in 500 births.  4:1 male:female.  
    • associated with Turner syndrome and trisomy 18.
    • presentation: regurgitation and projectile vomiting within 3 wks of birth, externally visible peristalsis, palpable firm ovoid mass.
    • tx: myotomy (full thickness muscle spitting incision).
  • acquired pyloric stenosis: from chronic antral gastritis, peptic ulcers close to pylorus, and malignancy.


Hirschsprung Disease

  • aka congenital aganglionic megacolon.
  • from arrested migration of neural crest cells into the gut ⇒ aganglionic segment lacking peristaltic contractions ⇒ functional obstruction and progressive dilation and hypertrophy of unaffected proximal colon.
  • pathogenesis: loss of function mutation in RET tyrosine kinase receptor in 15% sporadic and most familial.
    • 4:1 male:female.  
  • presentation: neonatal failure to pass meconium or abd distention with megacolon.
    • risk of peroration, sepsis, or enterocolitis with fluid derangement.
    • acquired megacolon with Chagas disease (lose ganglia), bowel obstruction, IBD, and psychosomatic disorders.


Esophageal Spasm

  • short or long-lived, focal or diffuse.
  • diffuse ⇒ functional obstruction.
  • ↑ wall stress can cause diverticula.


Zenker Diverticulum

  • aka pharyngeoesophageal diverticulum.
  • occurs immediately above upper esophageal sphincter.
  • contains one or more wall layers, can accumulate food if large and present as a mass with food regurgitation.


Traction Diverticulum

  • occurs at esophageal mid-point.
  • contains one or more wall layers, when large can accumulate food and present as mass with food regurgitation.


Epiphrenic Diverticulum

  • occurs immediately above lower esophageal sphincter.
  • contains one or more wall layers, when large can accumulate food and present as mass with food regurgitation.


Mucosal Webs

  • ledgelike protrusions of fibrovascular tissue and overlying epithelium.
  • mostly in upper esophagus in women >40yrs.


Plummer-Vinson Syndrome

  • aka Paterson-Brown-Kelly Syndrome.
  • constellation of webs, iron deficiency anemia, glossitis, and cheilosis.


Esophageal Rings

  • aka Schatzki rings.
  • similar to webs but circumferential and thicker.
  • include mucosa, submucosa, and occasionally hypertrophic muscularis propria.
  • A rings = above esophageal junction.
    • squamous epithelium.
  • B rings = at squamocolumnar junction.  
    • contain gastric cardia-type mucosa.



  • triad: incomplete relaxation of LES, ↑ LES tone (cholinergic signaling), and esophageal aperistalsis.
  • primary: idiopathic, from failure of distal esophageal neurons to induce LES relaxation during swallowing, or degenerative changes in neural innervation.
  • secondary: with Chagas disease, disorders of vagal dorsal motor nuclei (polio, surgical ablation), diabetic autonomic neuropathy, infiltrative disorders (amyloid, sarcoid, cancer).
  • tx: myotomy, balloon dilation, botulinum toxin injection to inhibit LES cholinergic neurons.


Mallory-Weiss Tears

  • longitudinal lacerations at gastroesophageal junction associated with excessive vomiting with alcohol intoxication.
    • caused by failure of relaxation of LES preceding vomiting.  causes stretching and tearing.
  • presentation: hematemesis.


Chemical and Infectious Esophagitis

  • squamous epithelium damaged by alcohol, corrosive acids or alkalis, excessively hot fluids, heavy smoking, irradiation, chemotherapy, graft-versus-host disease.
  • infections common in immunocompromised: HSV, CMV, candida.
  • morphology: dense neutrophilic infiltrates.
    • granulation tissue if ulceration
    • candidiasis: adherent grey-white pseudomembrane of fungal hyphae and inflammatory cells.
    • HSV: punched-out ulcers.
    • CMV: shallow ulcerations with viral inclusions.
  • presentation: pain and dysphagia.
    • severe/chronic cases: hemorrhage, stricture, perforation.


Reflux Esophagitis

  • foremost cause of esophagitis = GERD.
  • Pathogenesis: reflux of gastric juices from ↓ LES tone and/or ↑ abd pressure.
    • exacerbated by alcohol, tobacco, obesity, CNS depressants, pregnancy, delayed gastric emptying, ↑ gastric volume.
    • can be from hiatal hernia when stomach protrudes into thorax.
  • Morphology: hyperemia, edema, basal zone hyperplasia and thinning of superficial epithelial layers, neutrophile and/or eosinophil infiltration.
  • Presentation: adults >40yrs with dysphagia, heartburn, regurgitation of gastric contents into mouth.
    • complications: ulceration, hematemesis, melena, stricture, Barrett esophagus.
  • tx: proton pump inhibitors and/or H2 histamine receptor antagonists.


Eosinophilic Esophagitis

  • pts have atopic disorders (dermatitis, asthma, etc.)
  • morphology: large numbers of intraepithelial eosinophils.
  • presentation: food impaction and dysphagia.  
    • children: feeding intolerance and GERD-like symptoms.
  • tx: dietary restriction and/or steroids.


Barrett Esophagus

  • complication of 10% chronic GERD.
  • intestinal metaplasia within esophageal squamous mucosa.
  • ↑ risk of esophageal adenocarcinoma.  0.2-2% pts have pre-invasive dysplasia each yr.
  • morphology: patches of red, velvety mucosa up from gastroesophageal junction.
    • intsetinal-type columnar epithelium with mucin-secreting goblet cells.
    • dysplasia is low or high grade.
    • intramucosal carcinoma has neoplastic cell invasion in lamina propria.
  • presentation: white male btw 40-60yrs.  diagnosed both grossly and with biopsy.
  • tx: high grade dysplasia or carcinoma needs esophagectomy.


Esophageal Varices

  • pathogenesis: severe portal HTN ⇒ collateral bypass channels btw portal and caval circulations.
    • congested subepithelial and submucosal veins in distal esophagus = varices.
    • most common cause in west = alcoholic cirrhosis
    • most common worldwide = hepatic schistosomiasis
  • morphology: tortuous dilated veins in distal esophageal and proximal gastric submucosa.
    • irregular luminal protrusion of overlying mucosa with superficial ulceration, inflammation, or adherent blood clots.
  • presentation: silent until rupture with catastrophic hematemesis.
    • rupture from inflammatory erosion, ↑ venous pressure, ↑ hydrostatic pressure from vomiting.
    • 50% die of first bleed from exsanguination or hepatic coma.
    • 50% chance recurrence.
  • tx: scleroherapy, balloon tamponade, band ligation.


Esophageal Adenocarcinoma

  • come from dysplasia in Barret mucosa.
  • 7:1 male:female
  • pathogenesis: early chromosomal and p53 mutations, amplification of c-ERB-B2, cyclin D, E genes, mutated RB, p16/INK4a cyclin dependent kinase inhibitor.
  • morphology: gross = exophytic nodules to excavated and deeply infiltrative masses in distal 1/3 esophagus.
    • micro: form glands, produce mucin, intestinal morphology.  signet ring tumors not common.
  • presentation: white male with dysphagia, weight loss, hematemesis, chest pian, or vomiting.
    • 5 yr survival <25%.


Squamous Cell Carcinoma (Esophageal)

  • adults >45yrs. 4:1 male:female, blacks>whites
  • risk factors: alcohol, tobacco, caustic esophageal injury, achalasia, Plummer-Vinson syndrome, scalding hot beverages.
  • high incidence in Iran, central China, Hong Kong, Brazil, South Africa.
  • morphology: 50% in middle 1/3 of esophagus.
    • begin in situ as gray-white plaque-like mucosal thickenings.
    • expand as exophytic, ulcerate, become diffusely infiltrative with wall thickenings and luminal stenosis.
    • submucosal lymphatic network promotes circumferential and longitudinal spread.
    • mod to well defined.  less comon verrucous, spindle, and basaloid carcinomas.
  • presentation: insidious, late symptoms, dysphagia, obstruction, weight loss, hemorrhage, sepsis from ulceration, respiratory fistulae with aspiration.
    • 5 yr survival is 75% if superficial, otherwise 9%.