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Presented by Robb Wilentz, M.D. and prepared by Bahram R. Oliai, M.D.
Case 2: An 81 year old female with a long history of gastroesophageal reflux.
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1. Question
Week 56: Case 2
An 81 year old female with a long history of gastroesophageal reflux./images/2115a.jpg
/images/2115b.jpg
/images/2115c.jpgCorrect
Answer: High-grade dysplasia arising with Barrett esophagus of the distinctive type
Histology: This case shows a markedly atypical villiform epithelium on top of ducts and glands and adjacent to squamous epithelium. There are scattered goblet cells, which are consistent with Barrett mucosa of the distinctive type. The atypical epithelium is diagnostic of high-grade dysplasia because it shows
(1) prominent architectural distortion,
(2) loss of cellular polarity, even at the very surface of the epithelium,
(3) marked cytologic atypia, including nuclear hyperchromasia and irregularity, and
(4) a lack of significant inflammation. No invasive carcinoma is seen within this specimen.Discussion: Barrett esophagus is a well-recognized entity in which the squamous mucosa is replaced by metaplastic columnar epithelium. The metaplastic columnar epithelium may or may not show intestinal metaplasia, characterized by the presence of goblet cells containing neutral mucin and staining blue on a periodic-acid Schiff/Alcian blue stain (pH=2.5). When intestinal metaplasia is seen, the epithelium is termed “Barrett mucosa of the distinctive type.” The recognition of distinctive-type Barrett mucosa is important because its presence is more closely linked with the development of adenocarcinoma than is that of non-distinctive-type epithelium. It is important to note, however, that the finding of goblet cells is not absolutely diagnostic of Barrett mucosa of the distinctive type. Scattered goblet cells may be seen in the setting of chronic gastritis within the gastric cardia. Therefore, it is important that there is good communication between the pathologist and endoscopist as to the location of a biopsy when one is taken in the area of the gastroesophageal junction.
Just like in the colon (and in the pancreas—see case #1 in this week’s conference), Barrett mucosa may undergo a progression through stages of dysplasia to invasive adenocarcinoma. Thus, when the diagnosis of Barrett mucosa is entertained, the pathologist should indicate in his or her report the presence (or absence) of dysplasia and the degree of that dysplasia. A detailed discussion of the types of dysplasia can be found at http://pathology2.jhu.edu/beweb/study.htm. Briefly, the diagnosis of dysplasia is made by evaluating the surface of the epithelium, the architecture of the epithelium, the cytology within the epithelium, and the presence (or absence) of inflammation within the epithelium. A recent study has shown that while there can be significant disagreement among pathologists regarding the exact grade of dysplasia, there is actually excellent intra- and interobserver agreement when dysplasia is divided into two important groups based on treatment modalities (no dysplasia, indefinite for dysplasia, low-grade dysplasia versus high-grade dysplasia and carcinoma). Patients with high-grade dysplasia and carcinoma undergo immediate treatment with surgery or ablation therapies, while patients with less advanced forms of dysplasia require follow-up.
Incorrect
Answer: High-grade dysplasia arising with Barrett esophagus of the distinctive type
Histology: This case shows a markedly atypical villiform epithelium on top of ducts and glands and adjacent to squamous epithelium. There are scattered goblet cells, which are consistent with Barrett mucosa of the distinctive type. The atypical epithelium is diagnostic of high-grade dysplasia because it shows
(1) prominent architectural distortion,
(2) loss of cellular polarity, even at the very surface of the epithelium,
(3) marked cytologic atypia, including nuclear hyperchromasia and irregularity, and
(4) a lack of significant inflammation. No invasive carcinoma is seen within this specimen.Discussion: Barrett esophagus is a well-recognized entity in which the squamous mucosa is replaced by metaplastic columnar epithelium. The metaplastic columnar epithelium may or may not show intestinal metaplasia, characterized by the presence of goblet cells containing neutral mucin and staining blue on a periodic-acid Schiff/Alcian blue stain (pH=2.5). When intestinal metaplasia is seen, the epithelium is termed “Barrett mucosa of the distinctive type.” The recognition of distinctive-type Barrett mucosa is important because its presence is more closely linked with the development of adenocarcinoma than is that of non-distinctive-type epithelium. It is important to note, however, that the finding of goblet cells is not absolutely diagnostic of Barrett mucosa of the distinctive type. Scattered goblet cells may be seen in the setting of chronic gastritis within the gastric cardia. Therefore, it is important that there is good communication between the pathologist and endoscopist as to the location of a biopsy when one is taken in the area of the gastroesophageal junction.
Just like in the colon (and in the pancreas—see case #1 in this week’s conference), Barrett mucosa may undergo a progression through stages of dysplasia to invasive adenocarcinoma. Thus, when the diagnosis of Barrett mucosa is entertained, the pathologist should indicate in his or her report the presence (or absence) of dysplasia and the degree of that dysplasia. A detailed discussion of the types of dysplasia can be found at http://pathology2.jhu.edu/beweb/study.htm. Briefly, the diagnosis of dysplasia is made by evaluating the surface of the epithelium, the architecture of the epithelium, the cytology within the epithelium, and the presence (or absence) of inflammation within the epithelium. A recent study has shown that while there can be significant disagreement among pathologists regarding the exact grade of dysplasia, there is actually excellent intra- and interobserver agreement when dysplasia is divided into two important groups based on treatment modalities (no dysplasia, indefinite for dysplasia, low-grade dysplasia versus high-grade dysplasia and carcinoma). Patients with high-grade dysplasia and carcinoma undergo immediate treatment with surgery or ablation therapies, while patients with less advanced forms of dysplasia require follow-up.
