Module 2: GI: Barretts and Esophageal Cancers and Non-Neoplastic Stomach Lesions Flashcards
The last non neoplastic condition of the esophagus is Barrett’s Esophagus, what is the etiology for this?
Long standing acid reflux esophagitis — GERD
- -what causes GERD?
1. obesity
2. limited scleroderma (CREST syndrome–calcinosis, Raynaud’s phenomenon, esophageal dysmotility (GERD) , sclerodactyly, telangectasia)
3. Anti-centromere positive
4. Hiatal Hernia (sliding)
What is the presentation for Barrett’s Esophagus?
1.Heart Burn
2. Waterbrush (bad metallic taste of acid in the mouth)
3. Dyspepsia
4. Epigastric pain
5. Substernal discomfort relieved with antacids
(more common in whites)
The definitive diagnosis for Barrett’s Esophagus is an upper GI endoscopy with biopsy, what would the findings be?
Normal Epithelium: stratified squamous non-keratinized
Intestinal Metaplasia: Tall columnar with goblet cells as a protective mechanism
Endoscopy: normal pearly white esophageal squamous mucosa — velvety pink columnar mucosa (serpiginuos salmon colored patch)
What is the pathogenesis for Barrett’s Esophagus?
Decreased tone in the LES — genetic reprogramming of stem cells in the lower 1/3rd of the esophagus
What are the complications for Barrett’s Esophagus?
1 risk factor for intestinal dysplasia —- adenocarcinoma of the esophagus (always due to Barrett’s)
—most common in the US – almost always distal 1/3rd of esophagus and preceded by chronic acid reflux
–globally SCC of esophagus is more common
Progressive dysphagia and odynophagia – difficulty and painful swallowing
Melena — iron deficiency anemia
There are two neoplasms of the esophagus, Squamous Cell Carcinoma (SCC) and Adenocarcinoma. First we will discuss SCC. What is the etiology for SCC?
Chronic Alcoholism
Smoking
Plummer-Vinson Syndrome (Patterson Brown Kelly Syndrome)
Achalasia
p16,p53 and Rb mutations (tumor suppressor genes)
What is the pathogenesis for SCC?
Usually in upper 2/3rd of esophagus (middle 1/3rd to be specific)
–growth pattern: exophytic, excavated and infiltrative
What is the presentation for SCC?
Progressive dysphagia (initially solids than liquids due to gradual luminal narrowing)
Odynophagia
Cachexia
Fatigue (due to melena and iron deficiency anemia)
What demographic of the population presents with SCC?
Black and Asian Males greater than 50
–highest incidence in central Asia and Northern China
What are the two investigations done for SCC?
Barium Swallow: shows obstruction or narrowing of lumen (however need a Upper GI scope to confirm)
GI endoscopy w/Biopsy: malignant squamous cells invading into the submucosa and muscularis propria
In regards to SCC, explain the two histological slides 5c
Pic on left: Malignant squamous cells invading into the submucosa and muscularis propria. without keratin pearls so a worse dx
Pic on right: squamous cell whirls of keratin (Better prognosis because its well differentiated in function)
What is a complication of SCC?
- Obstruct — regurgitation —- aspiration pneumonia
- Bleeding — melena —- iron deficiency anemia
- Form a TE fistula (food can get into the lungs –aspiration pneumonia —- lung abscess)
- Can spread to cervical, mediastinal, paratracheal, tracheobronchial, gastric and celiac nodes depending on site of tumor
Now moving onto the next malignancy of the esophagus is Adenocarcinoma. What is the etiology for this?
Barrett Esophagus (due to chronic GERD) is the precursor lesion
- -risk varies from 30 fold to 100 fold
- -more common than SCC
What is the pathogenesis for Adenocarcinoma?
Usually in the lower 1/3rd of the esophagus
–growth pattern: multistep process through dysplasia
What is the presentation for Adenocarcinoma?
Progressive Dysphagia Odynophagia Cachexia Fatigue (due to melena --- iron deficiency anemia) --commonly seen in white males
What investigations are done for Adenocarcinoma?
Barium Swallow: shows obstruction of lumen (need to confirm with scope)
GI endoscopy with biopsy: malignant glandular epithelium invading into the submucosa and muscularis propria