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28 Cards in this Set
- Front
- Back
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GI System- Path of the Esophagus I, II by Leonard
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GI System- Path of the Esophagus I, II by Leonard
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Clinical Presentations
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Dysphagia (difficulty with swallowing)
Odynophagia (pain with swallowing) Regurgitation Obstruction Weight loss (can’t get food downstream) Vomiting *Chest pain (/retrosternal pain) Heartburn Nocturnal wheezing Nocturnal coughing Bleeding |
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Congenital Abnormalities of the Esophagus:
Esophageal atresia what are the sx's, who do you commonly see it in? |
Sx’s: vomiting, regurgitation
Often seen with fistulas -TE fistula is most common congenital esophageal anomaly (both develop from cranial foregut) -Aspiration pneumonia -seen in infancy |
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Congenital Abnormalities of the Esophagus: Web vs. Ring
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Sx’s: dysphagia
both have abnormal protrusion into the lumen of the esoph. of a portion of the esophagus. creates a narrow lumen for food to pass through. Webs (proximal and not completely circumferencial): Shelf-like protrusions of mucosa into lumen Uncommmon; upper esophagus; not circumferential Plummer-Vinson syndrome -Triad: iron deficiency anemia; glossitis; cheilosis F > M: 40 yo or older Long-standing GERD Rings (Schatzki rings..distal, thicker, involving wall of esoph, circumferencial): Circumferential and thicker: may include hypertrophied muscularis Lower esophagus (A) and GE junction (B) |
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Diverticulae: pseudo vs true
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Sx’s: heartburn, dysphagia
Pseudo-diverticulae (lack ALL wall layers): -Increased esophageal wall stress: high amplitude contractions with poor peristaltic movement (spasms) -Lead to mucosal outpouchings – rare True diverticulae: -Zenker (paraesophageal): just above the UES -May be large; “store” residual food bolus → regurgitation; mass effect -Traction: mid-esophagus -Epiphrenic: just above the LES |
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Ectopic tissue: inlet pouch and pancreatic heterotopia
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Inlet pouch: congenital “islands” of ectopic gastric mucosa
-Seen in as many as ~ 10% upper endoscopies -Most often in the cervical esophagus -May show intestinal type epithelium --Do not confuse with Barrett’s esophagus; unlikely to undergo --neoplastic progression and does not require surveillance --May cause “GERD-like” symptoms Pancreatic heterotopia -Pancreatic acinar tissue; distal esophagus (GE junction); usually not clinically significant ~ 16% of pediatric/young adult endoscopies |
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Structural obstruction of Stenosis
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Stenosis (generally involves fibrosis) – narrowing of the lumen
-Radiation can cause this fibrotic stenosis; prolonged epithelial damage (persistent GERD); severe or prolonged caustic (chemical) or thermal injury |
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Functional obstruction of Achalasia..what is the triad? what does that lead to?
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Achalasia: impaired smooth muscle relaxation (LES)
Triad: incomplete LES relaxation; increased LES tone; aperistalsis → imbalance/failure of inhibitory neurons Primary: idiopathic Secondary: Chagas disease (Trypanosoma cruzi) destroys enteric ganglion cells; infiltrative disorders (e.g., amyloidosis, malignancy; sarcoidosis); diabetic autonomic neuropathy; polio Treatment: Dilatation (balloon); myotomy; Botox |
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Esophageal Varices: presentation and pathophysiology
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Presentation:
Upper GI bleeding (e.g., hematemesis) Other signs/Sx’s of portal hypertension, possibly signs/Sx’s of liver disease Pathophysiology: Development of collateral blood vessels between portal and caval circulation secondary to portal hypertension -Liver cirrhosis (alcoholic liver disease); hepatic schistosomiasis (worldwide) Congestion & dilatation of these mucosal submucosal venules/veins Sequelae Rupture with massive hematemesis Common cause of death in cases of advanced cirrhosis Inflammation and mucosal erosion Tx Sclerotherapy (endoscopic injection of thrombotic agents) Endoscopic rubber band ligation; Balloon tamponade for bleeding varices |
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Mallory-Weiss tears and Boerhaave syndrome
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Mallory-Weiss tears: lacerations
Longitudinal tears in esophagus near GE junction Severe retching/vomiting 2° acute alcohol intoxication Boerhaave syndrome Distal esophageal rupture and mediastinitis Severe retching/vomiting followed by severe retrosternal chest pain, shock |
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Hiatal Hernia: sliding and paraesophageal
...which is more common... how do they happen. |
Herniation of stomach through the esophageal diaphragmatic hiatus
Sliding hernia (~ 95% of cases) -Common; portion of gastric cardia ascends and pushes lower esophagus upward → bell-shaped dilatation -Minority (~ 10%) of patients are symptomatic (heartburn; regurgitation), and Sx’s typically managed medically Paraesophageal hernia (~ 5% cases) -Less common but more commonly symptomatic -Herniation of portion of gastric fundus alongside esophagus; progressively enlarges --Requires surgical intervention as enlarges |
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Esophagitis... the most common cause is due to what?
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-Defined as epithelial damage and inflammation
-Endoscopic appearance: irregular regions of redness (hyperemia, erosion (from prolonged inflamm process...wearing down of epithelium), hemorrhage, loss of normal superficial squamous epithelium) -5% incidence in USA (all types) -Most common cause is GERD -Histologic changes may not reflect severity of clinical symptoms |
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Types of esophagitis
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GERD (most common)
Eosinophilic/Allergic Infectious (candida, CMV, HSV) GVHD (incr epithelial apoptosis) |
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Eosinophilic Esophagitis (EE).. where are the eosinophils?
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-Eosinophilic inflammation is common to all forms of esophagitis
-Eosinophilic gastroenteritis or other more systemic eosinophilic processes may involve the esophagus --Peripheral blood eosinophilia -“True” EE is restricted to esophagus --Epithelial infiltration by many eosinophils, especially in the *proximal and mid-esophagus* --+/- peripheral blood eosinophilia Tx: *corticosteroids*, allergen avoidance (if clearly allergic) Ddx: *GERD (eosinophils are restricted to *distal esophagus) Fungal or parasitic infection Systemic allergic or collagen vascular diseases |
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Infectious Esophagitis: HSV
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Typically occurs in immunocompromised pts
-HIV, ChemoTx, transplant Viruses or fungi most common Viral -HSV: herpes esophagitis Sx: chest pain, odynophagia, upper GI bleeding Herpetic ulcers may serve as portal of entry for other pathogens (lead to pneumonitis) Typically HSV 1, but HSV 2 or varicella-zoster possible |
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Viral Esophagitis: CMV...common in who?
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Common in HIV-AIDS
-Most common viral infection of the esophagus in HIV Multiple, well-circumscribed ulcers -CMV viral inclusions seen in nuclei of endothelial cells and fibroblasts, NOT epithelial cells (unlike HSV) Accurate Dx important for appropriate therapy -Acyclovir is ineffective against CMV *seen in the endothelial cells and fibroblastas, NOT epithelial cells (like in HSV) |
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Candida Esophagitis
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HIV-AIDS, transplant, immune-suppressive disorder, or diabetes
-~ 30% pts with HIV-AIDS have esophageal infection, of which esophageal Candidiasis is most common Candida organisms are part of the normal flora of GI tract -Presence of budding yeast forms not adequate for diagnosis; need to I.D. PSEUDOHYPHAE within tissue Sx” dysphagia, odynophagia; may be asymptomatic Endoscopy: small white mucosal plaques -May be confused with “glycogenation” of squamous mucosa or with ectopic sebaceous glands Tx: responds well to antifungals, except in cases with HIV-AIDS |
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AIDS Esophagitis, the CD4 count, and the typical organisms involved
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>200 HSV, VZV
100-200 Candida, HSV <100 Candida, CMV, HSV <50 idiopathic esophageal ulceration |
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THE most common cause of esophagitis is...
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GERD (3-5% of general population); most common outpatient GI dx in US of A;Reflux of gastric contents into distal esophagus
Etiology: decreased competence of LES, delayed gastric emptying Causes: alcohol, tobacco, CNS depressants, hypothyroidism, pregnancy, hiatal hernia, systemic sclerosis Pathophysiology: chronic exposure to gastric juices impairs natural reparative capacity of mucosa Sx: heartburn, regurgitation, chest pain; may involve bronchospasm/asthma Severity of Sx’s NOT correlated with histologic findings |
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diagnosis and treatment of GERD
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Dx:
Intraesophageal pH monitoring Endoscopy & histology -Hyperemic mucosa, erosions, ulceration -Intraepithelial inflammatory cells (PMNs, eos, lymphs) Empiric treatment No gold standard Dx Treatment: Pharmacologic: promote motility, H2 receptor antagonists, PPI Surgical: reduce hiatal hernia, interrupt gastric vagal innervation |
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Chronic GERD Sequelae
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Barrett Esophagus: *intestinal goblet cell metaplasia within distal esophageal mucosa*
-Metaplastic change in response to chronic irritation; may be irreversible -Requires *correlation between endoscopic findings and histologic finding of intestinal goblet cell metaplasia -Incidence: ~ 10-12% with symptomatic GERD --Mean age Dx: ~ 60 yo (M>F) -Important risk factor for esophageal andenocarcinoma --RR: 30-125 (i.e., esophageal adenocarcinoma is 30-125 times more likely in individuals with Barrett esophagus than those without Barrett esophagus) --Prevalence of adenocarcinoma at time of Dx of Barrett esophagus = ~ 10% |
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Barrett Esophagus: Long segment vs. short segment
and treatment |
Long segment vs. short segment
Long segment: extends 3 cm or more above GE junction Short segment: extends < 3cm above GE junction Tx Anti-reflux therapy Endoscopy every 1-2 years with four quadrant bx’s at 2 cm intervals through length of Barrett mucosa -Screen for glandular epithelial dysplasia or adenocarcinoma |
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Barrett’s Related Dysplasia
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Neoplastic change in glandular epithelial cells in metaplastic area
-Patchy, irregular distribution Endoscopic appearance -Polypoid (small mass) or thickened velvety mucosa) Grade the dysplasia: low- vs. high- grade -Cytologic and architectural features |
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Differentiate low grade and high grade dysplasia
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Management of Barrett dysplasia is controversial and evolving:
Low grade dysplasia -Variable management: routine follow-up for Barrett esophagus or repeat endoscopy and bx. 6-12 mos. High grade dysplasia -Up to 50% increased risk of adenocarcinoma -Tends to be multifocal and coexistent with intramucosal (non-invasive) carcinoma -Aggressive surveillance --Repeat bx’s “immediately” – 4 quadrant, every 1 cm length to better characterize nature of the lesion Tx: Photodynamic therapy, laser ablation, endoscopic mucosal resection, esophagectomy |
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Esophageal Neoplasms
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Present with dysphagia, odynophagia, weight loss, obstruction
Vast majority are carcinomas: squamous or adenocarcinoma Adenocarcinoma -Usually (> 95%) arise in a background of long-standing GERD and Barrett mucosa --Distal 1/3 of esophagus -Additional risks: tobacco, EtOH, obesity, irradiation -M >> F (7:1) -Dramatic increase in incidence over past 40 years --Now represent ~ 50% of all esophageal cancer (only ~5% in 1970) |
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Esophageal Adenocarcinoma, and TNM staging
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Stepwise progression: accumulation of genetic and epigenetic effects
TNM staging (AJCC) -Most present with invasion into or through the muscularis propria (T2-T4) --10-20% 5-year survival -Tumors limited to the mucosa or submucosa have much better prognosis --80-100% 5-year survival Tx: surgery & neoadjuvant chemo/XRT |
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Squamous Cell Carcinoma
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M > F (4:1); > ~ 45 yo; A-A>Caucasians
Risk factors -Tobacco, EtOH, thermal and caustic chemical injury, Plummer-Vinson syndrome, achalasia, poverty (rural and underdeveloped areas); irradiation; HPV (types 16, 18) Majority occur in the middle 1/3 of the esophagus (50-60%) -~ 30% in distal 1/3; 10-20% in the proximal 1/3 Tx: surgery & neoadjuvant chemo/XRT |
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Squamous Cell Carcinoma and TNM staging.
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T
Superficial (mucosal or submucosal invasion) ~ 20% of cases 70% 5-year survival More often are multifocal than more aggressive tumors Deep (into and through muscularis propria) 10-50% 5-year survival Some studies show that for both SCC and adenocarcinoma, overall 5-year survival is poor: ~ 10-15% N ~ 60% of cases present with lymph node metastases M Common distant metastases are to liver or lung |
