GI Flashcards
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.
Omphalocele
- abdominal musculature is incomplete and viscera herniate into ventral membranous sac.
- associated with other birth defects in 40%.
Gastroschisis
- 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).
Diverticulum
- 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.
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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.
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A rings = above esophageal junction.
- squamous epithelium.
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B rings = at squamocolumnar junction.
- contain gastric cardia-type mucosa.
Achalasia
- 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.
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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.
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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.
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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
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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.
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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.
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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.
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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%.
Benign Esophageal Tumors
- mesenchymal origin, in esophageal wall.
-
leiomyomas most common.
- also fibromas, lipomas, hemangiomas, neurofibromas, lymphangiomas.
- take form of mucosal polyps
Acute Gastritis
- transient mucosal inflammatory process.
-
pathogenesis: ↑ acid production with back diffusion, ↓ bicarb or mucin production, or direct mucosal damage.
- chronic use NSAIDs ⇒ ↓ bicarb production and intereres with prostaglandins (which inhibit acid production, promote mucin synthesis and increase vascular perfusion)
- excessive alcohol and smoking are toxic. ischemia and shock injure mucosa too.
-
morphology: moderate edema and hyperemia, some hemorrhage.
- neutrophils invade epithelium, superficial epithelial sloughing (erosion), fibrinous luminal exudate.
- presentation: asymptomatic or with pain, nausea, and vomiting. may have ulceration with hemorrhage = hematemesis or melena.
Acute Gastric Ulceration
- focal, acute mucosal defects.
- complication of NSAID use or phsyiologic stress.
- stress ulcer = from shock, sepsis, severe trauma.
- curling ulcer = proximal duodenum, from burns or trauma.
- cushing ulcer = gastric, duodenal, and esophageal ulcer arising in pt with intracranial disease. ↑ risk perforation.
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pathogenesis: **NSAIDs **⇒ ↓ bicarb production
- brain injury ⇒ direct vagal stimulation ⇒ gastric acid hypersecretion.
- systemic acidosis, hypoxia, ↓ splanchnic blood flow.
- morphology: <1cm, multiple, shallow. anywhere in stomach. base is brown.
- presentation: 10-15% bleed, 5% perforate. outcome determined by ability to correct underlying conditions.
Chronic Gastritis
- ongoing mucosal inflammation with mucosal atrophy.
- can ⇒ dysplasia and carcinoma.
- causes: H. pylori, alcohol, tobacco, psychological stress, caffeine. 10% are autoimmune
- symptoms less severe but persist.
Helicobacter Pylori Gastritis
- most common cause of chronic gastritis.
- spread: fecal-oral, oral-oral, environmental.
- ↑ colonization in lower socioeconomic statuses and crowded areas.
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pathogenesis: in antrum. ↑ acid production and disruption of normal mucosal protection.
- virulence factors: flagella, urease production, bacterial adhesins, toxins.
- ⇒ multifocal atrophic gastritis and intestinal metaplasia.
- associated with polymorphisms in IL-1B and TNF genes.
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morphology: erythematous and coarse/nodular mucosa.
- H pylor in superficial mucus over surface and neck epithelium. pit abscesses with neutrophils, lamina propria has plasma cells/macrophages/lymphocytes.
- long-standing = diffuse mucosal atrophy, prominent lymphoid aggregates with germinal centers.
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presentation: diagnose by Ab serologic test, urea breath test, culture, etc.
- H pylori is risk for: peptic ulcer disease, gastric adenocarcinoma, gastric lymphoma.
Autoimmune Gastritis
- spares antrum, associated with hypergastrinemia.
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pathogenesis: CD4 mediated destruction of parietal cells, also Ab to parietal cells and intrinsic factor.
- get achlorhydria (no gastric acid secretion) ⇒ hypergastrinemia and antral G-cell hyperplasia.
- ↓ production intrinsic factor ⇒ pernicious anemia.
- bystander damage to chief cells ⇒ ↓ pepsinogen I production.
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morphology: rugal folds lost, diffuse mucosal damage of parietal cells in body and fundus.
- inflammatory infiltrate of lymphocytes, macrophages, and plasma cells. may have lymphoid aggregates.
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presentation: AutoAb found early. takes 20-30yrs for gastric atrophy. present with anemia, B12 deficiency with atrophic glossitis, malabsorption, peripheral neuropathy, spinal cord lesions, cerebral dysfunction.
- associted with other autoimmune diseases.
Reactive Gastropathy
- chemical injury from NSAIDs or bile reflux.
- marked by edema, glandular hyperplasia, regenerative changes.
Eosinophilic Gastritis
- has heavy eosinophilic infiltration of mucosa and submucosa.
- from infection, allergies to ingested materials, from systemic collagen-vascular disease (scleroerma).
Lymphocytic Gastritis
- idiopathic disorder in women.
- associated with celiac disease.
- marked accumulation of intraepithelial CD8 cells.
Granulomatous Gastritis
- presence of granulomas.
- sarcoid, Crohn disease, infections.
Peptic Ulcer Disease
- in first part of duodenum or in antrum (4:1).
- from H pylori-induced hyperchlorhydric chronic gastritis and NSAID use.
- 10% risk in men, 4% in women.
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pathogenesis: hyperacidity from infection, parietal cell hyperplasia, excessive secretory response, ↑ gastrin production (from hypercalcemia or tumor).
- NSAIDs and steroids reduce PG effects.
- smoking impairs mucosal blood flow and healing.
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morphology: solitary ulcers, sharply punched out with overhanging mucosal borders and smooth clean ulcer bases.
- thin layers fibrinoid debris, underlying inflammation with granulation tissue and deep scarring. surrounded by chronic gastritis.
-
presentation: epigastric gnawing, burning, or aching pain, worse at night and 1-3 hrs post eating, nausea, vomiting, bloating, belching, weight loss.
- complications: anemia, hemorrhage, perforation, obstruction.
- tx: get rid of H pylori, neutralize/reduce gastric acid production.
Gastric Dysplasia
- combo of free radical damage and proliferative stimuli to exposed epithelium causes genetic alterations and causes carcinoma.
- are pre-invasic in situe lesions.
Ménétrier Disease
- diffuse foveolar cell hyperplasia with protein-losing enteropathy ⇒ systemic hypoproteinemia.
- from overexpression of TGF-alpha
- ↑ risk gastric adenocarcinoma.
Zollinger-Ellison Syndrome
- gastrinomas in small bowel or pancreas.
- 5x ↑ gastrin levels in parietal cells, ↑ in mucous neck cells and gastric endocrine cells.
- 75% sporadic, 25% related to MEN type I.
- 60-90% malignant.
- presentation: multiple duodenal ulcers and/or chronic diarrhea.
Inflammatory and Hyperplastic Polyps
- 75% of gastric polyps.
- btw 50-60yrs and associated with chronic gastritis.
-
morphology: <1cm and usually multiple.
- smooth surface, sometimes superficial erosions.
- irregular, cystically dilated and elongated glands with variable amounts of acute/chronic inflammation.
- ↑ risk dysplasia with size.
- tx: excision if larger than 1.5cm.
Fundic Gland Polyps
- occur sporadically in women >50yrs or with familial adenomatous polyposis.
- ↑ incidence from proton pump inhibitors from ↑ gastrin secretion.
- morphology: single or multiple, smooth, well-circumscribed lesions made of irregular cystically dilated glands, minimal inflammation.