GIS10 Pathology Of The Esophagus And Cardia Flashcards
Esophagus pathology
- Congenital anomalies
- Esophagitis (inflammation)
- Barrett’s esophagus
- Neuromuscular dysfunction
- Neoplasia
Congenital anomalies of esophagus
- Esophageal atresia (failure to form)
- Tracheo-esophageal fistula (abnormal connection)
- Duplication
Esophagitis
- Reflux esophagitis
- Infective
- candida
- HSV
- CMV - Irritants, radiation, prolonged gastric intubation
Reflux esophagitis
- frequent and prolonged reflux of gastric contents in the esophagus —> acute esophagitis + ulceration
- markedly red esophagus
- heartburn, regurgitation
Causes:
- ***Hiatus hernia (stomach slip through diaphragm)
- Increased ***intra-abdominal pressure (obesity, frequent hard coughing, heavy lifting)
- Loss of ***diaphragmatic muscular tone with ageing
- Abnormal ***upper GI motility
- **Histological features:
1. Hyperplasia of squamous epithelium
2. Lots of lymphocyte and neutrophil (Polymorphs)
Infective esophagitis
Diagnosis: Biopsies
- Fungal esophagitis
- Candida, Aspergillus, Mucor
- markedly red esophagus
- gastric-esophageal junction blurred
- in immunocompromised patient - Viral esophagitis
- HSV —> **darkened esophagus
- CMV —> **enlarged cell
Barrett’s esophagus
- at lower end of esophagus
- result of prolonged reflux esophagitis —> markedly red esophagus
- Squamous mucosa replaced by metaplastic Columnar epithelium of intestinal type —> more resistant to gastric juice
- Hallmark:
—> **Intestinal metaplasia
—> presence of goblet cells (*Glandular / Simple Columnar epithelium)
- complications: malignancy of lower 1/3 of esophagus (***Adenocarcinoma)
Neuromuscular dysfunction / Achalasia
- failure of relaxation of lower esophageal sphincter during swallowing + no peristalsis (aperistalsis)
Reason:
- ↓ no. / complete absence of myenteric ganglion cells in the esophagus proximal to the LES
—> loss of intrinsic inhibitory (parasympathetic) innervation of the LES and smooth muscle coat of esophagus
—> unable to relax
Progression:
- ***Dilation of esophagus (proximal end)
- ***Fibrosis and thickening of esophagus
Presentation:
- Progressive ***dysphagia
- ***Regurgitation
Treatment:
- may need resection of esophagus to treat abrupt narrowing of opening
Patient group:
- middle life
- young adulthood
- infancy / childhood
Neoplasia of esophagus
Benign:
- small, asymptomatic
1. Squamous papilloma (epithelial tumour)
2. Lipoma (fat tissue tumour)
3. Leiomyoma (smooth muscle tumour)
Malignant:
**1. Squamous cell carcinoma (SCC) (commonest, usually occurs in middle esophagus)
—> irregular edges / surface, dark edges due to **necrosis
—> presence of **intercellular bridges and **keratin production
***2. Adenocarcinoma (Barrett’s esophagus, lower 1/3, ∵ turned into Columnar epithelium)
3. Others (small cell carcinoma)
Etiology:
- ***Diet (restricted diet of cornmeal and pickled vegetable, nitrosamine, trace element deficiency, fungal contaminants)
- Chronic alcoholism + smoking
- Barrett’s esophagus
- Achalasia (esophageal disorder)
- Genetic prediposition
***Gross appearance:
1. Ulcerative (commonest)
2. Polypoid / Fungating
—> new vessel formation cannot keep up with lesion growth
—> ischaemic —> necrotic —> ulcerative
3. Sclerosing / Constrictive
ALL giving rise to progressive **dysphagia due to **obstruction / constriction
Spread:
- Direct: Lungs (esophageal wall perforated), Aorta (rupture into aorta with fatal hematemesis)
- Lymphatic: regional lymph nodes, submucosal spread —> multiple tumour nodules
- Haematogenous spread: liver, brain
Cardia pathology
- Cancer
- Adenocarcinoma (most common) (predisposition: Barrett’s esophagus) - Gastritis
- Peptic ulceration
Esophageal varices
due to Portal hypertension from liver cirrhosis