Hollow GI organ lined by non-keratinizing stratified squamous epithelium over lamina propria and a thin muscularis mucosae; submucosa contains mixed mucous glands and a submucosal plexus; muscularis propria has inner circular and outer longitudinal layers with a myenteric plexus; outermost layer is adventitia.
Z-line (squamocolumnar junction) is the mucosal transition; the GEJ anatomically corresponds to the start of gastric rugal folds.
Protection → lubrication → propulsion: stratified squamous mucosa resists mechanical abrasion from food bolus; submucosal glands deliver mucin via squamous-lined ducts to lubricate; coordinated muscularis propria layers with enteric plexus generate peristalsis.
Epithelium: multilayered, non-keratinizing squamous cells; no basal cell hyperplasia, no intercellular edema (spongiosis), and no papillary elongation (changes that would suggest reflux injury).
Lamina propria / muscularis mucosae: thin, without active inflammation or erosion.
Submucosa: loose connective tissue with mucous glands, lymphatics, vessels, nerves, ganglion cells; gland ducts are squamous-lined.
Muscularis propria: inner circular / outer longitudinal smooth muscle with myenteric plexus.
Adventitia: loose connective tissue (no serosa).
Gastric inlet patch (heterotopic gastric mucosa): true gastric-type mucosa in the upper third; unlike normal squamous lining.
Pancreatic metaplasia/heterotopia: benign acini/ducts in esophageal mucosa/submucosa; not present in normal.
Glycogenic acanthosis: squamous epithelial hyperplasia with abundant glycogen in superficial cells; appears as solitary/scattered white plaques endoscopically; when extensive, think Cowden syndrome.
Early GERD changes: spongiosis, basal cell hyperplasia, papillary elongation, scattered intraepithelial inflammatory cells—absent in normal.
Esophagus, (site), biopsy:
- Squamous mucosa without diagnostic abnormality.
- No active esophagitis, dysplasia, or intestinal metaplasia identified.