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Pathology miscellaneous fd4defc8

A 45-year-old male alcoholic with a history of poal hypeension presents with vomiting of blood (hematemesis) and hypotension. He denies any history of vomiting nonblood material or retching prior to vomiting blood. During workup he dies suddenly. Based on his history and physical findings, histologic sections from his esophagus would most likely reveal

A
Columnar epithelium in the distal esophagus
B
Decreased ganglion cells in the myenteric plexus
C
Dilated blood vessels in the submucosa
D
Mucosal outpouchings (diveicula) in the distal esophagus
High-Yield Explanation
Most lesions of the esophagus present with similar symptoms, such as heaburn and dysphagia, but the most serious disease, which carries the risk of exsanguination, is bleeding esophageal varices. Varices occur in about two-thirds of all patients with cirrhosis, and in the majority of patients the etiology is alcoholic cirrhosis. The cirrhosis causes poal hypeension, which shunts blood into connecting channels between the poal and caval systems, such as the subepithelial plexus of veins in the lower esophagus. Varices produce no symptoms until they rupture and cause massive bleeding (hematemesis), which may lead to death. Other diseases, such as gastritis, esophageal laceration (Mallory-Weiss tears), or peptic ulcer disease, may cause hematemesis In contrast, columnar epithelium in the distal esophagus is seen with Barrett's esophagus; decreased ganglion cells in the myenteric plexus are seen with achalasia, a disorder that is characterized by aperistalsis, incomplete relaxation of the lower esophageal sphincter (LES) with swallowing, and increased resting tone of the LES, all of which lead to esophageal dilation and symptoms of progressive dysphagia. Reference: Robbins & Cotran Pathologic Basis of Disease, 9edition

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