University:
Michigan State University
Course:
MED 615 | Gastroenterology Clerkship
Academic year:

2021
Views:

176

Pages:

72
Author:

Charlee Buchanan

Diseases of the esophagus  A hollow, highly distensible muscular tube  Extends from the epiglottis to the GEJ, located just above the diaphragm Diseases that affect the esophagus  1. Obstruction: mechanical or functional.  2. vascular diseases: varices.  3. Inflammation: esophagitis.  4. Tumours. Mechanical Obstruction  Congenital or acquired.  Examples:  Atresia  Fistulas  Duplications  Agenesis (v rare)  Stenosis. Atresia  Thin, noncanalized cord replaces a segment of esophagus.  Most common location: at or near the tracheal bifurcation  +- fistula (upper or lower esophageal pouches to a bronchus or trachea). Clinical presentation:  Shortly after birth: regurgitation during feeding  Needs prompt surgical correction (rejoin).  Complications if w/ fistula:  Aspiration  Suffocation  Pneumonia  Severe fluid and electrolyte imbalances. Esophageal stenosis  Acquired>>>Congenital.  Fibrous thickening of the submucosa & atrophy of the muscularis propria.  Due to infammation and scarring  Causes:  Chronic GERD.  Irradiation  Ingestion of caustic agents Clinical presentation  Progressive dysphagia  Difficulty eating solids that progresses to problems with liquids. Functional Obstruction  Efficient delivery of food and fluids to the stomach requires coordinated waves of peristaltic contractions.  Esophageal dysmotility: discoordinated peristalsis or spasm of the muscularis.  Achalasia: the most important cause. Achalasia  Triad:  Incomplete LES relaxation  Increased LES tone  Esophageal aperistalsis.  Primary >>>secondary. Primary achalasia  Failure of distal esophageal inhibitory neurons.  Idiopathic  Most common Secondary achalasia  Degenerative changes in neural innervation  Intrinsic  Vagus nerve  Dorsal motor nucleus of vagus  Chagas disease, Trypanosoma cruzi infection>>destruction of the myenteric plexus>> failure of LES relaxation>> esophageal dilatation. Clinical presentation  Difficulty in swallowing  Regurgitation  Sometimes chest pain. Achalasia-like disease  Diabetic autonomic neuropathy  Infiltrative disorders (malignancy, amyloidosis, or sarcoidosis)  Dorsal motor nuclei lesions (produced by polio or surgical ablation). Vascular diseases: Esophageal Varices  Tortuous dilated veins within the submucosa of the distal esophagus and proximal stomach.  Diagnosis by: endoscopy or angiography. Dilated varices beneath intact squamous mucosa Pathogenesis:  Portal circulation: blood from GIT>>portal vein>>liver (detoxification)>>inferior vena cava.  Diseases that impede portal blood flow >> portal hypertension >>esophageal varices.  Distal esophagus : site of Porto-systemic anastomosis.  Portal hypertension>>collateral channels in distal esophagus>>shunt of blood from portal to systemic circulation>>dilated collaterals in distal esophagus>>varices Causes of portal hypertension  Cirrhosis is most common Alcoholic liver disease.  Hepatic schistosomiasis 2nd most common worldwide. Clinical Features  Often asymptomatic.  Rupture leads to massive hematemesis and death.  50% of patients die from the first bleed despite interventions.  Death due to: hemorrhage, hepatic coma, and hypovolemic shock  Rebleeding in 20%. ESOPHAGITIS  Esophageal Lacerations.  Mucosal Injury  Infections  Reflux Esophagitis  Eosinophilic Esophagitis Esophageal Lacerations  Mallory weiss tears are most common  Due to : severe retching or prolonged vomiting  Present with hematemesis.  Failure of gastroesophageal musculature to relax prior to antiperistaltic contraction associated w/ vomiting >> stretching >>>tear.  Linear lacerations  longitudinally oriented  Cross the GEJ.  Superficial  Heal quickly , no surgical intervention Chemical Esophagitis  Damage to esophageal mucosa by irritants  Alcohol,  Corrosive acids or alkalis  Excessively hot fluids  Heavy smoking  Medicinal pills (doxycycline and bisphosphonates)  Iatragenic (chemotx, radiotx , GVHD) Clinical symptoms & morphology  Ulceration and acute inflammation.  Only self-limited pain, odynophagia (pain with swallowing).  Hemorrhage, stricture, or perforation in severe cases Infectious esophagitis  Mostly in debilitated or immunosuppressed.  Viral (HSV, CMV)  Fungal (candida >>> mucormycosis & aspergillosis)  Bacterial: 10%.  Candidiasis :  Adherent.  Gray-white pseudomembranes  Composed of matted fungal hyphae and inflammatory cells  Herpes viruses  Punched-out ulcers  Histopathologic:  Nuclear viral inclusions  Degenerating epithelial cells ulcer edge  Multinucleated epithelial cells.  CMV :  Shallower ulcerations.  Biopsy: nuclear and cytoplasmic inclusions in capillary endothelium and stromal cells Reflux Esophagitis  Reflux of gastric contents into the lower esophagus  Most frequent cause of esophagitis  Most common complaint by patients  Gastroesophageal reflux disease, GERD  Squamous epithelium is sensitive to acids  Protective forces: mucin and bicarbonate, high LES tone Pathogenesis  Decreased lower esophageal sphincter tone (alcohol, tobacco, CNS depressants)  Increase abdominal pressure ( obesity,, pregnancy, hiatal hernia, delayed gastric emptying, and increased gastric volume)  Idiopathic!! MORPHOLOGY  Macroscopy (endoscopy)  Depends on severity (Unremarkable, Simple hyperemia (red)  Microscopic:  Eosinophils infiltration  Followed by neutrophils (more severe).  Basal zone hyperplasia  Elongation of lamina propria papillae Clinical Features  Most common over 40 years.  May occur in infants and children  Heartburn , dysphagia,  Regurgitation of sour-tasting gastric contents  Rarely: Severe chest pain, mistaken for heart disease  Tx: proton pump inhibitors Complications  Esophageal ulceration  Hematemesis  Melena  Strictures  Barrett esophagus (precursor of Ca.) Eosinophilic Esophagitis          Chronic immune mediated disorder Symptoms: Food impaction and dysphagia in adults Feeding intolerance or GERD-like symptoms in children Endoscopy: Rings in the upper and mid esophagus. Microscopic: Numerous eosinophils w/n epithelium Far from the GEJ.  Most patients are: atopic (atopic dermatitis, allergic rhinitis, asthma) or modest peripheral eosinophilia.  Tx:  Dietary restrictions( cow milk and soy products)  Topical or systemic corticosteroids.  Refractory to PPIs. Barrett Esophagus  Complication of chronic GERD  Intestinal metaplasia within the esophageal squamous mucosa.  10% of individuals with symptomatic GERD  Males>>females, 40-60 yrs  Direct precursor of esophageal adenocarcinoma  Metaplasia >> 0.2-1% /year >>dysplasia>> adenocarcinoma. MORPHOLOGY Endoscopy:  Red tongues extending upward from the GEJ.       Histology: Gastric or intestinal metaplasia Presence of goblet cells +-Dysplasia : low-grade or high-grade Intramucosal carcinoma: invasion into the lamina propria. Management of Barrett  Periodic surveillance endoscopy with biopsy to screen for dysplasia.  High grade dysplasia & intramucosal carcinoma needs interventions. ESOPHAGEAL TUMORS  Squamous cell carcinoma (most common worldwide)  Adenocarcinoma (on the rise, half of cases) Adenocarcinoma  Background of Barrett esophagus and long-standing GERD.  Risk factors: dysplasia associated Barrett, smoking, obesity, radioTx.  Male : female (7:1)  Geographic & racial variation (devloped countries) Pathogenesis  From Barrett>>dysplasia>>adenocarcinoma  Acquisition of genetic and epigenetic changes.  Chromosomal abnormalities and TP53 mutation. MORPHOLOGY  Distal third.  Early: flat or raised patches  Later: exophytic infiltrative masses  Microscopy:  Forms glands and mucin. Clinical Features  Pain or difficulty swallowing  Progressive weight loss  Chest pain  Vomiting.  Advanced stage at diagnosis: 5-year survival <25%.  Early stage: 5-year survival 80% Squamous Cell Carcinoma  Male : female (4:1)  Underdeveloped countries.  Risk factors:  Alcohol  Tobacco use  Poverty  Caustic injury  Achalasia .  Plummer-Vinson syndrome  Frequent consumption of very hot beverages  Previous radiation Tx . Pathogenesis  In western : alcohol and tobacco use.  Other areas: polycyclic hydrocarbons, nitrosamines, fungus-contaminated foods  HPV infection implemented in high risk regions. MORPHOLOGY  Middle third (50% of cases)  Polypoid, ulcerated, or infiltrative.  Wall thickening, lumen narrowing  Invade surrounding structures (bronchi, mediastinum, pericardium, aorta). Microscopy:  Pre-invasive: Squamous dysplasia & CIS.  Well to moderately differentiated invasive SCC.  Intramural tumor nodules  Lymph node metastases :  Upper 1/3: cervical LNs  Middle 1/3: mediastinalparatracheal, and tracheobronchial LNs.  Lower 1/3: gastric and celiac LNs. Clinical Features  Dysphagia  Odynophagia  Obstruction  Weight loss and debilitation  Impaired nutrition & tumor associated cachexia  Hemorrhage and sepsis if ulcerated.  Aspiration via a tracheoesophageal fistula  Dismal Px: 5 year survival <9%

Diseases of the Esophagus

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