Esophagus Flashcards
A 28-year-old man with eosinophilic esophagitis (EoE) presented with gastrointestinal bleeding to the hospital. He has a history of iron deficiency anemia (but no melena) and was on 40 mg pantoprazole twice a day for 6 months prior to the admission. His laboratory test results prior to admission show hemoglobin 11 mg/dL (normal: 14-17 g/dL), MCV 70 fL (normal: 80-100 fL), ferritin 12 ng/mL (normal: 15-200 ng/mL), and iron saturation of 10% (normal: 20-50%). He had been on adequate iron replacement therapy for 4 months without a change in the ferritin levels. Upon admission, his hemoglobin was 9 mg/dL. His vitals are stable. He reports 8 days of “black” stool (he is on iron). He still has some dysphagia. An Image from his endoscopy is shown in the figure.
He is discharged on esomeprazole 40 mg orally twice a day. During admission, gastric biopsies for H. pylori are interpreted as normal. Gastrin levels are not elevated significantly. He follows up in clinic 8 weeks later without any further complaints – hemoglobin is 8 (from 9 at time of discharge) and you decide to repeat the endoscopy where you see a new ulcer not seen at time of bleeding. You check a pH level in the stomach and it is 5. He confirms that he is not on nonsteroidal medications. Which of the following is the best next step?
A. Check H. pylori again on biopsies and in stool.
B. Recheck gastrin level to confirm that there is no gastrinoma.
C. Take at least 4 biopsies in the gastric body and 4 in the gastric antrum and request eosinophil counts.
D. Perform a colonoscopy to determine whether Crohn’s disease is the cause of the ulceration.
E. Start empiric therapy for H. pylori.
- EoE increases one’s risk for eosinophilic gastritis (EG) with up to 10% of EoE patients reporting a diagnosis of EG. The diagnosis of EG remains elusive as it is not always seen in pathologic interpretation unless eosinophil counts are requested.
- The current diagnostic criteria is that of 30 eosinophils/HPF in the stomach in 5 total HPF. This must be requested by endoscopists.
- Gastrinoma is essentially ruled out with fairly normal gastrin levels and non-acidic pH in stomach. Crohn’s is increased in EoE but is less likely to affect the gastric tissue than eosinophilic disease in EoE without other symptoms than EG
A 50-year-old man with obesity has longstanding heartburn. EGD performed shows the esophagus in the figure. What LA grade of esophagitis does this image show?
A. LA Grade A
B. LA Grade B
C. LA Grade C
D. LA Grade D
- Grade A: Mucosal break(s) ≤5 mm, without continuity across mucosal folds
- Grade B : Mucosal break(s) >5 mm, without continuity across mucosal folds
- Grade C: Mucosal break(s) continuous between ≥2 mucosal folds, involving <75% of the esophageal circumference
- Grade D: Mucosal break(s) involving ≥75% of the esophageal circumference
A 67-year-old woman with a history of oral and vaginal lichen planus presents with progressive dysphagia to solids over 2 years. Upper endoscopy is performed, with this finding immediately distal to the cricopharyngeus [figure]. The adult gastroscope (diameter 9.8 mm) was unable to pass this area. What is the best next step in management?
A. Pass a 38-French non-wire-guided bougie dilator, then pass the gastroscope after dilation.
B. Thread a 15-mm through-the-scope balloon under fluoroscopic visualization and dilate.
C. Refer to thoracic surgery for esophagectomy.
D. Switch to 5-mm pediatric endoscope to pass lesion, dilate with 8-mm wire-guided bougie dilator.
This patient most likely has esophageal lichen planus, given history of oral lichen planus and endoscopic appearance. This stricture is approximately 6-7 mm in diameter. Of the dilation sizes listed, only an 8-mm dilator would be recommended – initially dilating with a larger size would be higher risk for perforation. Additionally, it would not be recommended to blindly pass a non-wire-guided bougie dilator in this type of lesion, but rather either downsizing the scope or using fluoroscopy to pass a guidewire. While esophagectomy is very rarely used for resistant strictures, lichen planus is responsive to endoscopic dilation, which should be tried first.
A 65-year-old man with long segment Barrett’s esophagus presents for surveillance endoscopy. Based on the endoscopic image seen in the figure, what is the best next step in management?
A. Radiofrequency ablation of the lesion
B. Radiofrequency ablation of the lesion and the surrounding Barrett’s
C. Endomicroscopic evaluation of the lesion
D. Endoscopic resection of the lesion
E. Repeat EGD in 3 months after patient has been on PPI twice daily
- This is a subtle area of slightly depressed Barrett’s mucosa and is concerning for dysplasia or early cancer. Any depressed lesion within Barrett’s esophagus should NOT undergo radiofrequency ablation.
- RFA should only be performed on flat Barrett’s esophagus, with or without dysplasia. Endoscopic resection should be performed of this lesion to obtain a surgical pathology specimen to determine the histology of the lesion and depth of invasion.
- If the lesion is an early T1 cancer with clear margins and low-risk features, then endoscopic resection would have resulted in a curative procedure.
A 72-year-old woman reports a 1-year history of intermittent dysphagia to both liquids and solids. She has not lost any weight. The patient has hypertension and a remote history of colon polyps but no other recent issues. Her medications include a baby aspirin and a diuretic. An EGD was performed which showed a large subepithelial lesion in the distal esophagus [figure]. Subsequent endoscopic ultrasound demonstrated a large, 5.5-cm solid, hypoechoic, homogeneous mass lesion arising from the muscularis propria. The lesion had regular margins and no cystic spaces. What is the most likely diagnosis in this patient?
A. Gastrointestinal stromal tumor
B. Hematoma
C. Leiomyoma
D. Lipoma
- The finding of a solid, hypoechoic mass arising from the muscularis propria of the esophagus on endoscopic ultrasound (EUS) is most consistent with either a leiomyoma, a gastrointestinal stromal tumor (GIST), or schwannoma. EUS-guided fine needle aspiration would show spindle cells that were positive for desmin and smooth muscle actin; negative for CD34, CD 117 and S100 and is indicated for determining a diagnosis. The majority of GISTs are positive for CD34 or CD117; Schwannomas are positive for S100 and Leiomyomas are positive for SMA vimentin and desmin. GISTs are pre-malignant and sometimes malignant lesions that need either surveillance or resection based on location, size, and mitotic figures. The large majority of GISTs occur in the stomach (60-70%) or small intestine (20-30%), and <10% of all GISTs are found in the esophagus, rectum, colon, mesentery, omentum, and retroperitoneum. Since GISTs are rare in the esophagus, the most likely diagnosis in this patient would be a leiomyoma rather than a GIST.
- Esophageal intramural hematomas can present with abrupt, sudden onset of chest pain, dysphagia and odynophagia. Patients can often report a history of vomiting, retching, or may have recently undergone endoscopy with or without biopsy or other endoscopic intervention such as sclerotherapy. Development of an esophageal intramural hematoma can be seen in the setting of anticoagulation or coagulopathy.
- Endoscopically, various abnormalities can be seen in the esophagus including purple discoloration of the mucosa, ulceration, mucosal tear, extrinsic compression with narrowing of the esophageal lumen, or evidence of a subepithelial lesion. On EUS, there can be preservation of the normal wall layers with a heterogeneous, isoechoic lesion with hyperechoic foci and anechoic spaces deep to the mucosal layers or within the submucosa with an intact muscularis propria. This patient’s clinical presentation and endoscopic ultrasound findings are not consistent with an esophageal intramural hematoma.
If asymptomatic no further intervention is needed and surveillance is not warranted. Given this patient is symptomatic resection should be considered.
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Endoluminal fundoplication is an emerging technique for treatment of acid reflux but is not indicated with a hiatal hernia >2 cm in size
61F long history of postprandial heartburn and regurgitation. EGD 5yo LA C esophagitis, with biopsies of the lower esophagus negative for Barrett’s esophagus. The patient’s symptoms initially resolved with daily proton pump inhibitor (PPI) therapy and a repeat upper endoscopy 1 year prior showed a normal lower esophagus both endoscopically and histologically. The patient then, in the setting of a 10-lb weight gain, began developing hoarseness, throat clearing, and cough in the postprandial setting. Both an otolaryngology and pulmonary consultation were unrevealing, and she was told that she may have refractory gastroesophageal reflux disease (GERD) to the PPI. In order to evaluate her current symptoms and association with gastroesophageal reflux, what test is recommended?
A. A wireless pH capsule placed during endoscopy while on PPI therapy
B. An upper endoscopy with routine biopsies of both the upper and lower esophagus
C. An assessment of her esophageal peristalsis on high-resolution manometry
D. A catheter-based pH-impedance test while on PPI therapy
E. A measurement of baseline mucosal impedance on upper endoscopy
- The recent Porto and Lyon international consensus statements attempt to define pathologic GERD based on a variety of diagnostic tests and clinical scenarios. Both agree that an EAET (the time a pH is less than 4 in the lower esophagus on a pH test) of >6% is conclusive evidence of pathologic GERD, as are LA C or D esophagitis, Barrett’s esophagus, or a peptic stricture.
- When confronted with a patient who has previously met 1 of these criteria for conclusive pathologic GERD, and has symptoms unresponsive to PPI therapy, a catheter-based pH-impedance test while on PPI therapy is recommended to evaluate these symptoms and the possibility of refractory GERD despite PPI therapy.
- A wireless pH capsule test is recommended in evaluations off PPI therapy to look at the baseline burden of gastroesophageal reflux if prior conclusive evidence of pathologic GERD has not been met.
35 M w/ nodular thyroid goiter and a positive family history of breast and thyroid cancer in several first-degree relatives is referred for panendo. During EGD, extensive esophageal glycogenic acanthosis.. Other findings of underlying syndrome?
A. Germline mutation of the STK11 gene
B. Hamartomas of the gastrointestinal tract
C. Microcephaly
D. Multiple small intestinal angiodysplasia
E. Gastric carcinoid tumor
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Cowden syndrome- PTEN hamartoma tumor syndrome
- esophageal glycogenic acanthosis and hamartomatous gastric polyposis
- familial clusters of breast and thyroid cancer supports
- This is not associated with microcephaly (rather macrocephaly)
- Surveillance in Cowden syndrome
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screening for colon, stomach, small bowel, thyroid, breast, uterine, kidney, and skin (melanoma) cancers.
- colon q5 yrs start at 35
- annual thyroid US
- annual breast exam at 25, mmmo at 30
- endometrial biopsy
65M RFA for C4M6 Barrett’s esophagus with high-grade dysplasia. Follow-up EGD- endoscopic and histological absence of Barrett’s esophagus. Follow up?
A. Cessation of PPI, with dietary measures to avoid GERD
B. Endoscopic ultrasound at yearly intervals to detect subsquamous Barrett’s esophagus
C. Periodic upper endoscopy to assess for recurrent Barrett’s esophagus
D. A daily aspirin as an anti-neoplastic measure - not supported
- Recurrent Barrett’s esophagus develops in 25% s/p RFA for dysplastic Barrett’s. Therefore, periodic upper endoscopy as a surveillance tool is suggested, optimal interval unknown.
- PPI cessation is not recommended, given that ablation does not obviate reflux disease, and recurrent BE in the unprotected mucosa is a strong possibility.
Barret’s guidelines
An otherwise healthy 73-year-old man with a history of non-dysplastic Barrett’s esophagus (BE) presents for surveillance endoscopy. Endoscopy reveals long segment BE, Prague classification C4M6, with some nodularity 1 cm proximal to the GE junction. Endoscopic mucosal resection (EMR) of the lesion shows high-grade dysplasia, with a <1-cm focus of adenocarcinoma, with a maximal depth of invasion to the deep-submucosa (sm3). The lateral margins of the EMR are clear of cancer. What is the next most appropriate step?
A. Radiofrequency ablation of the remaining BE
B. Esophagectomy with possible chemoradiation
C. Repeat EMR to achieve a wider excision
D. Repeat EGD with biopsies in 3 months
This patient’s cancer has invaded beyond the superficial submucosa. Although the resected specimen appears clear of disease at its lateral margins, the status at the deep margin is often difficult to ascertain in deep lesions, and the likelihood of lymphatic involvement in lesions that have penetrated beyond the superficial submucosa is substantial, and argues for surgical resection.
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The reproducibility of a diagnosis of low-grade dysplasia is poor. Most studies demonstrate only fair or worse agreement between pathologists for this diagnosis. Therefore, before contemplating changing the therapeutic approach to the patient, the diagnosis should be confirmed by a second pathologist with expertise in gastrointestinal pathology.
Components of elimination diet
- milk
- wheat/grains
- eggs
- soy
- seafood/fist
- nuts
DOnt forget to exclude secondary EoE>vasculitis, crohns, EosGastro, connective tissue diseae
A 65-year-old White man presents with a history of acid reflux disease for several years. He has mild heartburn a few times a month. He does not have dysphagia. He uses a proton pump inhibitor daily and reports good control of his symptoms. He does not smoke. On exam, His BMI is 31, blood pressure is 130/80, pulse 80/min, and respirations 14/min. His oral exam is unremarkable. His chest is clear to auscultation. His heart exam reveals normal S1, S2 with no gallop. His abdominal exam in benign.
On upper endoscopy, he is found to have salmon-colored mucosa in the tubular esophagus extending 2 cm proximal to the gastroesophageal junction. Representative biopsies are taken. A 2-cm hiatal hernia is present [figure A]. Biopsies from the distal esophagus are reviewed by 2 expert GI pathologists [figure B]. These show closely packed, overlapping basal nuclei with hyperchromasia and irregular contours, basal stratification of nuclei, and diminished goblet and columnar cell mucus. What would you recommend next?
A. Increase use of PPI to twice a day.
B. Begin aspirin 81 mg daily.
C. Repeat esophageal biopsies in 6 months with Seattle protocol (4 quadrant biopsies every 1-2 cm).
D. Endoscopic treatment with radiofrequency ablation
E. Endoscopic mucosal resection
- This patient has Barrett’s with low-grade dysplasia (LGD). He has controlled reflux symptoms with once a day PPI, and endoscopy does not show esophagitis; therefore, an increase in PPI is not recommended.
- Routine use of twice daily PPI in Barrett’s is not recommended.
- Chemoprevention with NSAIDs or ASA for Barrett’s is not recommended.
- ACG guidelines recommend radiofrequency ablation treatment of Barrett’s esophagus with LGD. An alternate option of repeating biopsies in 12 months is also acceptable. The patient does not have nodular disease; therefore, EMR is not indicated as first-line therapy.
A 67-year-old woman presents with 6 months of progressive dysphagia to solids. She has no other significant medical history and denies taking both prescription and over-the-counter medications. Upper endoscopy is performed [figure A] with biopsy. Pathology [figure B] reveals a lymphocyte-rich inflammatory infiltrate involving the interface/crossing the basement membrane between mucosa and submucosa along with multiple visualized apoptotic bodies. What is the best medication to treat this patient’s condition?
A. Oral viscous budesonide 3 mg twice daily
D. High-dose PPI twice daily
- This patient has esophageal lichen planus based on the endoscopic appearance — white, lacy stricture, and pathologic description of apoptotic bodies (“Civatte bodies”) and lymphocyte-rich inflammatory infiltrate involving the interface/crossing the basement membrane between mucosa and submucosa.
- tx topical corticosteroid like budesonide
- role of PPI in esophageal lichen planus is unclear
Lymphocytic esophagitis is different from lichen planus
- Lymphocytes in the esophagus can be present due to a variety of conditions including reflux, stasis in the setting of esophageal motility disorders, Crohn’s disease, or an inflammatory condition with similarities to eosinophilic esophagitis.
- Endoscopic findings range from normal, to webs, rings, and strictures. Lymphocytic esophagitis is often characterized by intraepithelial lymphocytes, peripapillary distribution, and have had varying counts reported in the literature.
- Treatment often is based on PPI therapy, topical steroids, and endoscopic dilations.
A 48-year-old man presents with dysphagia to solids after undergoing Nissen fundoplication 6 months prior. Barium esophagram revealed an intact fundoplication. On EGD, no stricture was visualized, but there was resistance to endoscope passage through the esophago-gastric junction. Fundoplication appears intact on retroflex view, and there is no other mass or evidence of hiatal hernia. Esophageal biopsies are normal. Endoscopic dilation is performed with a 20-mm through-the-scope balloon. The patient continues to complain of dysphagia.
After the above dilation, the patient undergoes esophageal manometry. Median IRP is 23, a representative swallow is shown in the figure. What is the best next step to treat this patient’s dysphagia?
A. Injection of botulinum toxin 100 units into the lower esophageal sphincter
B. Surgical referral for conversion to Toupet fundoplication
C. Dilation of esophagus with 36 French bougie dilator
D. Peroral endoscopic myotomy (POEM)
- A recent retrospective study demonstrated efficacy of surgical conversion of the Nissen fundoplication (360 degrees) to a Toupet fundoplication (270 degrees) for the management of post-Nissen dysphagia
A 68-year-old woman is referred to your practice for a history of esophageal squamous high-grade intraepithelial neoplasia (HGIN). Staining of the mucosa with 1.5% Lugol’s iodine yields the appearance shown in the figure. Which of the following statements is correct?
A. Biopsy of the dark-staining mucosa has a high yield for neoplasia.
B. Treatment of this lesion with radiofrequency ablation results in complete eradication of neoplasia in a minority of patients.
C. Endoscopic mucosal resection of this lesion carries a high risk of stricturing.
D. Eradication of this tissue will require higher doses of energy than if it were columnar.
The lesion above shows a 4-cm circumferential nonstaining area. Endoscopic mucosal resection of such a long, circumferential area of squamous neoplasia has a high risk of stricturing. After staining with Lugol’s iodine, it is the nonstaining - not the staining areas - which are likely to be neoplastic. RFA of this lesion results in complete eradication of neoplasia in >80% of patients in most studies. Ablation for squamous epithelium can be successfully performed at energy densities lower than that used for columnar epithelium, to reduce risk of stricturing.
