Associated with atrophy of the muscularis propria & secondary epithelial damage
Congenital – occasional
Inflammation and scarring
Due to GERD, irradiation or caustic injury
Congenital esophageal stenosis in a young man with long-standing dysphagia and occasional superimposed food impactions. Double-contrast esophagogram shows an area of mild narrowing in the mid-esophagus with distinctive ring-like indentations (“ringed esophagus”) (arrows) in the region of the stricture.
Most common in upper esophagus (at level of cricopharyngeus or C5-C6)
Main symptom is dysphagia associated with incompletely chewed food
Barium esophagram demonstrates a thin membrane arising from the anterior wall of the cervical esophagus at the level of C5-C6 without circumferential involvement of the lumen characteristic for an esophageal web An upper esophageal web (arrow) in a patient with Plummer-Vinson syndrome.
Alcohol, corrosive acids or alkalis, excessively hot fluids, heavy smoking
Generally causes only self-limited pain, particularly with swallowing
Complications: hemorrhage, stricture, perforation
Corrosive esophagitis. This is a vinegar-induced esophageal burn. The patient had a fish bone in her throat. She ingested vinegar in an attempt to dissolve the fish bone but to no avail; this led to corrosive esophagitis.
Frequently in debilitated or immuno- compromised individuals commonly HSV, CMV, or fungi (Candidiasis most common)
HSV – punched-out ulcers
CMV – shallower ulcerations + char. nuclear and cytoplasmic inclusions
Candida – adherent, gray-white pseudomembranes
This is Candida esophagitis. Tan-yellow plaques are seen in the lower esophagus, along with mucosal hyperemia. The same lesions are also seen at the upper right in the stomach.
Candidiasis (thrush) of the esophagus. A ‘pseudomembrane’ is present (top) on the surface of the stratified squamous epithelium. It consists of desquamated epithelial cells and thin filament-like fungi. The fungi has penetrated the superficial layer of the squamous epithelium which is separated from relatively unaffected basal layer.
Here are two sharply demarcated "punched out" ulcerations of the mid esophagus in an immunocompromised patient with herpes simplex infection.
A herpetic ulcer is seen microscopically to have a sharp margin. The ulcer base at the left shows loss of overlying squamous epithelium with only necrotic debris remaining. Biopsies of these lesions reveals intranuclear inclusions in squamous epithelial cells indicative of herpes simplex virus esophagitis. This patient was immune compromised from chemotherapy.
Cytomegalovirus Infection. Microscopic sections reveal typical intranuclear inclusions Viral particles confirmed by electron microscopy
Gastroesophageal junction + part of stomach protrude into the chest
Gastroesophageal junction stays where it belongs (attached at level of diaphragm) but part of stomach protrudes into the chest beside the esophagus
With sliding or axial hiatal hernia there is thinning and elongation of the phrenoesophageal membrane leading to herniation of the stomach into the posterior mediastinum. As such, there is no potential for incarceration or strangulation. With paraesophageal herniation, visceral elements herniate through a focal weakness in the phrenoesophageal membrane with the potential to lead to the usual array of complications associated with visceral herniation through a constricted aperture. (Source: Modified from Skinner. 15 with permission from American Gastroenterological Association.)
Characterized by intestinal metaplasia within the squamous mucosa (+) goblet cells necessary for diagnosis
Most common in white males, between 40 – 60 yrs old
Increased risk of esophageal adenoCA pre-malignant condition
Patients with Barrett's esophagus have a 30- to 125-fold increased risk of the development of esophageal cancer in comparison with the general population. The disease is most common in white males.
Begins as in situ lesion called squamous dysplasia early lesions small, gray white, plaque-like tumor masses (polypoid or exophytic) over months to years protrude into and obstruct lumen
Most are moderately to well-differentiated
LN metastases vary with tumor location:
Upper 3 rd cervical LN
Middle 3 rd mediastinal, paratracheal, and tracheobronchial nodes
Lower 3 rd gastric & celiac nodes
Esophageal Tumors: Squamous Cell CA Ulcerating Squamous cell carcinoma of the lower end of the esophagus. Malignant tumor of the esophageal squamous mucosa, most common in the middle and lower third of the esophagus, and strongly associated with tobacco and alcohol use.
Microscopically: sharply demarcated, with essentially normal adjacent mucosa
Acute Gastric Ulceration Acute stress ulcers Multiple acute ulcers of the stomach, occurring in a chronically debilitated patient. Microscopically, there was very little fibrous reaction in the ulcer bed.
Acute Gastric Ulceration Curling's ulcer is an acute peptic ulcer of the duodenum resulting as a complication from severe burns.
H. pylori bacteria (red arrow) imbedded in stomach lining. Courtesy of wikimedia commons.
Active chronic H. pylori gastritis. The gastric mucosa contains large numbers of lymphocytes and plasma cells while polymorphs infiltrate the foveolar epithelium. The surface epithelium shows marked degenerative changes. Hematoxylin and eosin; magnification, ×100.
Chronic H. pylori gastritis. This low-power view shows marked glandular atrophy, lymphoid follicles, and centrally a focus of intestinal metaplasia. H&E ×25.
The inner lining of the stomach consists of a very thick mucosal layer consisting of tall rows of glandular cells running parallel to each other. The thick mucosa has a deep narrow gap extending to the bottom of the mucosa. This gap is the ulcer. Normal stomach mucosa (40X2.8) Stomach mucosa with ulcer (40X2.0)
Chronic Gastritis Complications: PUD Feature Gastric Ulcers Duodenal Ulcers % of ulcer cases 25% 75% Epidemiology Male:female ratio 1:1 Smoking does not cause PUD but delays healing Male:female ratio 2:1 Risk increased with MEN I, cirrhosis, COPD, renal failure, hyperparathyroidism H. pylori ~ 80% of cases 90 – 95% of cases Pathogenesis Defective mucosal barrier due to H. pylori Mucosal ischemia (reduced PGE), bile reflux, delayed gastric emptying BAO & MAO normal to decreased Defective mucosal barrier due to H. pylori Increased acid prod’n (inc. parietal cell mass) BAO & MAO both increased
Chronic Gastritis Complications: PUD Feature Gastric Ulcers Duodenal Ulcers Location Single ulcer in lesser curvature of antrum (same location for cancer) Single ulcer on anterior portion of 1 st part of duodenum ffed by single ulcer on posterior portion (danger for perforation into pancreas) Complications Bleeding (most commonly in left gastric artery) Perforation Bleeding (most commonly in gastro - duodenal artery) Perforation (air under the diaphragm, pain radiates to left shoulder) Gastric outlet obstruc- tion, pancreatitis Clinical findings Burning epigastric pain soon after eating Burning epigastric pain 1 – 3 hours after eating
Chronic Gastritis Complications: Mucosal Atrophy and Intestinal Metaplasia
Long-standing chronic gastritis loss of parietal cell mass intestinal metaplasia
Presence of goblet cells
Increased risk of gastric adenocarcinoma greatest in autoimmune gastritis
Due to overgrowth of bacteria produce carcinogenic nitrosamines
Diffuse hyperplasia of foveolar epithelium of the body and fundus
Protein-losing enteropathy hypo-proteinemia
Increased risk of gastric adenoCA in adults
Characteristic feature: hyperplasia of foveolar mucous cells
Hypertrophic Gastropathies: Menetrier’s Disease Microscopic appearance of Menétrier's disease. There is marked hyperplasia of the crypts accompanied by mild atrophy of the underlying secretory mucosa.
~75% of all gastric polyps are inflammatory or hyperplasic polyps
Most common in 50 – 60 yrs old individuals
Develop in association with chronic gastritis
Risk of dysplasia correlates with size
Gastric Polyps: Inflammatory & Hyperplastic Polyps Gross appearance of gastric polyps of hyperplastic type. Many of the lesions show central umbilication. Low-power microscopic view of gastric polyps of hyperplastic type. The cystic dilatation of the glands is more evident on the left side.
Gastric Polyps: Fundic Gland Polyps Endoscopic image of fundic gland polyposis taken on retroflexion of gastroscope. This patient was chronically taking proton pump inhibitors. H&E stain of fundic gland polyp showing shortening of the gastric pits with cystic dilatation.
All GI adenomas have epithelial dysplasia that can be classified as low grade or high grade.
Gastric Tumors: Gastric Adenoma Gross appearance of gastric adenomatous polyps. The larger lesion is a tangle of fingerlike projections. Adenomatous polyp. (From Oota K, Sobin LH: Histological typing of gastric and oesophageal tumours, Geneva, World Health Organization, 1977)
May infiltrate stomach wall desmoplastic reaction that stiffens the gastric wall called linitis plastica (leather bottle appearance)
Produce Krukernberg tumors of the ovaries
Gastric Tumors: Gastric Adenocarcinoma Gross appearance of gastric adenocarcinoma of polypoid type. Gross appearance of gastric adenocarcinoma of ulcerative type showing marked resemblance to chronic peptic ulcer.
Gastric Tumors: Gastric Adenocarcinoma Typical gross appearance of diffuse carcinoma of linitis plastica type. Practically the entire wall of the stomach is involved by tumor. Note the prominence of rugal folds.
Gastric Tumors: Gastric Adenocarcinoma Gastric adenocarcinoma of intestinal type. Diffuse type of gastric adenocarcinoma. An Indian file pattern of infiltration of the muscularis externa can be appreciated.
Most common presenting symptoms are dyspepsia and epigastric pain
Gastric Tumors: Lymphoma EXTRANODAL MARGINAL ZONE B-CELL (MALT) LYMPHOMA — This tumor, previously called MALT-type lymphoma or MALT lymphoma is now called extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue in the WHO classification system.
Gastric Tumors: Lymphoma MALT-type malignant lymphoma of stomach involving mucosa and submucosa.