Oesophagus 1 & 2 PDF

OESOPHAGUS 1 AND 2 Department of Anatomical Pathology Outline Congenital abnormalities Oesophageal obstruction Achalasia Oesophageal varices Oesophagitis Tumours Anatomy Cranial portion of the foregut 3rd Week...

OESOPHAGUS 1 AND 2 Department of Anatomical Pathology Outline Congenital abnormalities Oesophageal obstruction Achalasia Oesophageal varices Oesophagitis Tumours Anatomy Cranial portion of the foregut 3rd Week Hollow, highly distensible muscular tube Epiglottis- gastroesophageal Junction Congenital Abnormalities A variety of developmental anomalies can affect the GI tract The presence of congenital GI disorders should prompt evaluation of other organs Atresia and fistulae Oesophageal atresia Atresia – absence or closure of a natural passage of the body Absence/agenesis, of the eosophagus: extremely rare, but atresia is more common. Shortly after birth: regurgitation during feeding. Incompatible with life. Surgery Associated with: - Congenital heart defects - Genitourinary malformations - Neurologic diseases Oesophageal atresia Thin, non-canalized cord replaces a segment of oesophagus  mechanical obstruction Proximal & distal blind pouches connect to the pharynx & stomach, respectively Most common: tracheal bifurcation +/- fistula FISTULA Upper/ lower esophageal pouches- to a bronchus/trachea Complications: Aspiration Suffocation Pneumonia Severe fluid & electrolyte imbalances Hiatal Hernia Characterized by separation of the diaphragmatic crura & protrusion of the stomach into the thorax through the resulting gap Congenital hiatal hernias are recognized in infants & children, but many are acquired in later life. Symptoms, including heartburn & regurgitation of gastric juices, are similar to GORD Oesophageal Obstruction Swallowing must be accompanied by a coordinated wave of peristaltic contractions for efficient food/fluid delivery Oesophageal dysmotility interferes with this process & can take several forms. Nutcracker oesophagus: High-amplitude oesophageal contractions where outer longitudinal layer of smooth muscle contracts before the inner circular layer. Can cause periodic short-lived oesophageal obstruction Diffuse oesophageal spasm Motor disorders of the oesophagus can result in functional obstruction Increases oesophageal wall stress  can cause small diverticulae to form Oesophageal stenosis Narrowing of the lumen Caused by fibrous thickening of the submucosa Occasionally congenital, stenosis is most often due to inflammation & scarring that may be caused by:  Chronic gastroesophageal reflux  Irradiation  Caustic injury Associated with atrophy of the muscularis propria and secondary epithelial damage Oesophageal Obstruction The dysphagia associated with stenosis is usually progressive, - Solids to liquids Obstruction develops slowly, - Modification of diet to favour soft foods & liquids - Unaware of their condition until the obstruction is nearly complete Oesophageal mucosal webs Uncommon ledge-like protrusions of mucosa that may cause obstruction Women >40y Pathogenesis; unknown Webs are often associated with: Gastroesophageal reflux Chronic graft-versus-host disease Blistering skin disease Upper oesophageal webs accompanied by iron-deficiency anaemia, glossitis, & cheilosis are part of the Paterson-Brown-Kelly or Plummer-Vinson syndrome Oesophageal mucosal webs Most common in the upper oesophagus Semi-circumferential, eccentric lesions that protrude less than 5 mm & have a thickness of 2 to 4 mm Microscopically Fibrovascular connective tissue & overlying epithelium Main symptom; dysphagia associated with incompletely chewed food Oesophageal rings, or Schatzki rings Similar to webs, but are circumferential & thicker Rings include mucosa, submucosa, & in some cases, hypertrophic muscularis propria. A rings : when present in the distal esophagus, above the gastroesophageal junction & are covered by squamous mucosa In contrast, those located at the squamocolumnar junction of the lower esophagus are designated B rings & may have gastric cardia-type mucosa on their undersurface Achalasia Achalasia Increased tone of the lower oesophageal sphincter (LES), as a result of impaired smooth muscle relaxation Important cause of oesophageal obstruction Release of nitric oxide & vasoactive intestinal polypeptide from inhibitory neurons, along with interruption of normal cholinergic signaling, allows the LES to relax during swallowing. Achalasia Primary achalasia (idiopathic) :failure of distal oesophageal inhibitory neurons Degenerative changes in neural innervation; - intrinsic to the oesophagus - extraoesophageal vagus nerve - dorsal motor nucleus of the vagus Is characterized by the triad of: - Incomplete LES relaxation - Increased LES tone - Aperistalsis of the oesophagus Achalasia Secondary achalasia - Chagas disease (Trypanosoma cruzi) - Destruction of the myenteric plexus, - Failure of peristalsis - Oesophageal dilatation. Achalasia-like disease may be caused by:  Diabetic autonomic neuropathy  Lesions of dorsal motor nuclei, particularly polio or surgical ablation  Infiltrative disorders such as:  Malignancy  Amyloidosis  Sarcoidosis  Treatment: laparoscopic myotomy & pneumatic balloon dilatation Botulinum neurotoxin (Botox) injectionto inhibit LES cholinergic neurons Oesophageal Varices Oesophageal varices Venous blood from the GI tract is delivered to the liver via the portal vein before reaching the inferior vena cava Diseases that impede this flow cause portal hypertension & can lead to the development of oesophageal varices, an important cause of oesophageal bleeding Oesophageal varices Pathogenesis  Portal hypertension results in the development of collateral channels at sites where the portal & caval systems communicate  Although these collateral veins allow some drainage to occur, they lead to development of a congested subepithelial & submucosal venous plexus within the distal oesophagus  These vessels, termed varices, develop in 90% of cirrhotic patients, most commonly in association with alcoholic liver disease  Hepatic schistosomiasis is the second most common cause of varices Oesophageal varices Clinical Features Asymptomatic Rupture, causing massive hematemesis Haemorrhage due to variceal rupture is a medical emergency Morphology Venogram: tortuous dilated veins Variceal rupture results in hemorrhage into the lumen or oesophageal wall, in which case the overlying mucosa appears ulcerated & necrotic Oesophageal Lacerations Mallory-Weiss tears: Longitudinal, roughly linear tears in oesophagus near the gastroesophageal junction Associated with severe retching or vomiting secondary to acute alcohol intoxication Range in length from millimeters to several centimeters Usually cross the gastroesophageal junction, but may also be located in the proximal gastric mucosa Oesophageal Lacerations Up to 10% of upper GI bleeding Often presents as haematemesis Due to superficial oesophageal lacerations such as those associated with Mallory-Weiss syndrome These do not generally require surgical intervention, & healing tends to be rapid & complete Oesophageal Causes of Haematemesis  Lacerations (Mallory-Weiss syndrome)  Oesophageal perforation (cancer or Boerhaave syndrome)  Varices (cirrhosis)  Esophageal-aortic fistula (usually with cancer)  Chemical and pill-induced oesophagitis  Infectious oesophagitis (Candida, Herpes)  Benign strictures  Vasculitis (autoimmune, cytomegalovirus)  Reflux oesophagitis (erosive)  Eosinophilic oesophagitis  Oesophageal ulcers (many etiologies)  Barrett oesophagus  Adenocarcinoma  Squamous cell carcinoma  Hiatal hernia OESOPHAGITIS Chemical oesophagitis The stratified squamous mucosa of the oesophagus may be damaged by a variety of irritants including: Alcohol Corrosive acids or alkalis Excessively hot fluids Heavy smoking Medicinal pills lodge & dissolve in the oesophagus  mucosal injury  pill-induced oesophagitis Causes self-limited pain, particularly dysphagia +/-Haemorrhage, stricture or perforation Iatrogenic oesophageal injury may be caused by: Cytotoxic chemotherapy Radiation therapy Graft-versus-host disease Infectious oesophagitis May occur in otherwise healthy individuals Frequently seen in those who are debilitated or immunosuppressed as a result of disease or therapy In these patients, common oesophageal infections are caused by: Herpes simplex viruses Cytomegalovirus (CMV) Fungal organisms Candidiasis, Mucormycosis & aspergillosis  Candida esophagitis Tan-yellow plaques are seen in the lower esophagus, along with mucosal hyperaemia. The same lesions are also seen at the upper right in the stomach. Chemical and infectious oesophagitis The morphology of chemical & infectious oesophagitis varies with aetiology Dense infiltrates of neutrophils are present in most cases but may be absent following injury induced by chemicals (lye, acids, or detergent), which may result in outright necrosis of the oesophageal wall Pill-induced oesophagitis frequently occurs at the site of strictures that impede passage of luminal contents Chemical & infectious esophagitis Oesophageal irradiation causes: Intimal proliferation Luminal narrowing of submucosal & mural blood vessels Infection by fungi or bacteria can either cause damage or complicate a preexisting ulcer. When present, ulceration is accompanied by superficial necrosis with granulation tissue & eventual fibrosis Herpetic ulcers Reflux oesophagitis The stratified squamous epithelium of the oesophagus is resistant to abrasion from foods but is sensitive to acid Reflux of gastric contents into the lower esophagus is the most frequent cause of oesophagitis The associated clinical condition is termed gastroesophageal reflux disease (GORD)  Incidence: Clinical Features Common in adults over age 40 but also occurs in infants & children Symptoms: Dysphagia Heartburn Regurgitation of sour-tasting gastric contents Complications Oesophageal ulceration Haematemesis & melaena Stricture development Barrett esophagus Reflux oesophagitis Pathogenesis Conditions that decrease lower oesophageal sphincter tone or increase abdominal pressure contribute to GERD & include: Alcohol & tobacco use Obesity Central nervous system depressants Pregnancy Hiatal hernia Delayed gastric emptying Increased gastric volume In many cases, no definitive cause is identified. Reflux oesophagitis Morphology Gross – Hyperemia / redness Mild GERD : unremarkable mucosal histology With more significant disease, eosinophils are recruited into the squamous mucosa followed by neutrophils, which are usually associated with more severe injury Basal zone hyperplasia Barrett oesophagus Is a complication of chronic GERD that is characterized by intestinal metaplasia within the oesophageal squamous mucosa Barrett oesophagus is most common in white males Typically presents between 40 & 60 years of age The greatest concern in Barrett oesophagus is that it confers an increased risk of oesophageal adenocarcinoma Barrett oesophagus Morphology Barrett oesophagus can be recognized as one or several tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction This metaplastic mucosa alternates with residual smooth, pale squamous (oesophageal) mucosa & interfaces with light-brown columnar (gastric) mucosa distally Barrett oesophagus Is sub-classified into: Long segment, > 3 cm Short segment,