REFLUX ESOPHAGITIS, ESOPHAGEAL CANCER – Flashcards
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ESOPHAGEAL RINGS AND WEBS
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thin, typically delicate structures that partially or completely compromise the esophageal lumen. - present with dysphagia to solids
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ESOPHAGEAL RING
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concentric, smooth, thin (axial length of 0.3-0.5 cm) extension of normal esophageal tissue consisting of 3 anatomic layers of mucosa, submucosa, and muscle - distal esophagus
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A Ring
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uncommon, it is located approximately 1.5 cm proximal to the squamocolumnar junction, and it is rarely symptomatic.
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B - Schatzki ring
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located at the squamocolumnar junction and are the most common type of esophageal ring
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B - Schatzki ring
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almost always associated with hiatal hernias.
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B - Schatzki ring
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covered with squamous mucosa proximally and columnar epithelium distally
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B - Schatzki ring
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dysphagia is felt at the lower chest level
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C ring
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a rare anatomic finding on radiographic studies referring to the indentation caused by the diaphragmatic crura. - rarely symptomatic
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Esophageal web
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thin (axial length of 0.2-0.3 cm) mucosal fold that protrudes into the lumen and is covered with squamous epithelium
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Esophageal web
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most commonly occur in the upper esophagus, causing focal narrowing in the postcricoid area
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Esophageal web
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consist of mucosa and submucosa
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Esophageal web
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associated with iron-deficiency from various causes - Plummer-Vinson syndrome - chronic iron deficiency anemia
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Esophageal web
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dysphagia is felt in the throat
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Most patients with rings and webs of the esophagus have no symptoms if
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the internal ring diameter is large
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once the internal ring diameter is less than 1.3 cm rings and webs characteristically cause
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solid food dysphagia, particularly evident with meat or bread
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PLUMMER-VINSON SYNDROME
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classic triad of postcricoid dysphagia, iron- deficiency anemia and upper esophageal webs
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PLUMMER-VINSON SYNDROME
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dysphagia is usually painless and intermittent or progressive over years, limited to solids
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PLUMMER-VINSON SYNDROME
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Iron deficiency anemia is usually due to chronic bleeding - increased menstrual blood loss or chronic gastrointestinal bleeding of unknown origin.
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PLUMMER-VINSON SYNDROME
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middle-aged Caucasian women, in the fourth to seventh decade of life
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PLUMMER-VINSON SYNDROME
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15% develop squamous cell carcinoma of the pharynx or upper esophagus.
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Iron deficiency has been implicated as the most important etiological factor in the pathogenesis of
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esophageal webs and postcricoid dysphagia.
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ACHALASIA
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- motility disorder - lower two thirds - smooth muscle segment - of esophagus - caused by degeneration of intramural myenteric plexus neurons
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ACHALASIA
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results in impaired lower esophageal sphincter (LES) relaxation and loss of peristaltic sequencing of esophageal contractions - symptoms of dysphagia, chest pain, and regurgitation
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ACHALASIA
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esophagus is massively dilated - megaesophagus with diameter >6 cm - and filled with food residues
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ACHALASIA
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esophageal wall is thickened due to muscular hypertrophy secondary to longstanding functional obstruction at the LES
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ACHALASIA
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Histologic examination = decreased neurons - ganglion cells - in myenteric plexuses as part of inflammatory reaction; - remaining ganglion cells surrounded by lymphocytes.
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ACHALASIA
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- inhibitory motor neurons relax esophageal smooth muscle by releasing NO and VIP. - excitatory motor neurons contract esophageal smooth muscle by releasing acetylcholine and substance P
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ACHALASIA
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Esophageal myenteric plexus shows loss of the inhibitory neuron = basal sphincter pressure to rise = incapable of normal relaxation
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Primary achalasia
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cause of the inflammatory degeneration of neurons is not known
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Primary achalasia
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associated with a higher than expected prevalence of HLA- DQW1 antigen and affected patients often have circulating antibodies to neurons of the myenteric plexus
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Primary achalasia
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may be triggered by HSV-1 infection.
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Secondary achalasia
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- number of other diseases can cause. - One of the most common is cancer in the proximal stomach that may directly infiltrate and destroy esophageal myenteric neurons
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Secondary achalasia
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produce immune-mediated myenteric damage of the myenteric plexus as part of a paraneoplastic syndrome.
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ACHALASIA
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most frequent symptoms are (a) dysphagia for solids and liquids and (b) regurgitation of bland undigested food. Substernal chest pain and heartburn occur in approximately 50% of patients
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ACHALASIA
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Barium esophagram demonstrates dilation of the esophagus, narrow esophagogastric junction with "bird-beak" appearance caused by the persistently contracted LES, aperistalsis in the distal two-thirds of the esophagus, and poor emptying of barium.
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ACHALASIA
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Without treatment, patients with achalasia develop progressive dilation of the esophagus. Megaesophagus (>6 cm diameter) represents end-stage achalasia. Patients with achalasia are at increased risk for developing esophageal cancer, which is typically squamous cell type.
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ESOPHAGITIS
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Inflammation of the esophageal mucosa
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GERD (Gastroesophageal reflux disease)
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most common cause of esophagitis
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GERD (Gastroesophageal reflux disease)
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results when acid-containing gastric secretions or bile and acid-containing secretions from the duodenum and stomach are regurgitated into the esophagus causing inflammatory response in the distal esophagus
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GERD (Gastroesophageal reflux disease)
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reflux - normal physiologic phenomenon experienced intermittently by most people, particularly after a meal
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GERD (Gastroesophageal reflux disease)
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occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated inflammation and erosions
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GERD (Gastroesophageal reflux disease)
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Both hiatal hernia and obesity raise the risk - Male 2:1
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The two dominant pathophysiologic mechanisms causing reflux are:
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LES dysfunction and delayed gastric emptying
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LES DYSFUNCTION
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defined by manometry as a zone of elevated intraluminal pressure at the gastroesophageal junction - 2 types: Transient & Permanent
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Transient LES
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physiological mechanism of belching - active, vagally mediated reflex involving not only LES relaxation, but also crural diaphragmatic inhibition, and esophageal shortening by contraction of its longitudinal muscle
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GERD (Gastroesophageal reflux disease)
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Simple hyperemia, evident to the endoscopist as redness, may be the only alteration - In mild cases the mucosal histology is often unremarkable
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GERD (Gastroesophageal reflux disease)
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With more significant disease, scattered eosinophils are accumulated into the squamous epithelium. With more severe injury intraepithelial neutrophils are seen.
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GERD (Gastroesophageal reflux disease)
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With chronic injury, hyperplasia of the squamous epithelium develops - increase in mucosal lymphocytes, neutrophils and eosinophils is usually present
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GERD (Gastroesophageal reflux disease)
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heartburn, regurgitation and dysphagia. Heartburn - pyrosis - is the most common symptom
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GERD (Gastroesophageal reflux disease)
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extraesophageal symptoms: (a) coughing and wheezing, (b) hoarseness, (c) angina - like retrosternal chest pain - noncardiac chest pain
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GERD (Gastroesophageal reflux disease)
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Complications of reflux esophagitis include esophageal ulceration, stricture development, and Barrett esophagus
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Barret esophagus
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presence on biopsy of intestinal metaplasia, that is, goblet cells containing acid mucin.
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Esophageal stricture
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persistent narrowing of the esophagus caused by persistence of ulcers causing an inflammatory and sclerosing damage of the esophageal wall deep to the lamina propria
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Esophageal ulceration
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secondary to necrosis of esophageal epithelium causing ulcers near the gastroesophageal junction
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Barrett esophagus
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replacement of esophageal squamous epithelium by intestinal columnar epithelium (intestinal metaplasia)
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Barrett esophagus
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occurs in the lower third of the esophagus but may extend higher.
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ESOPHAGITIS
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Prolonged exposure of the esophagus to the acid refluxate causes esophagitis, i.e., promotes inflammatory cell infiltrate, and ultimately causes epithelial necrosis and erosion of the esophageal mucosa
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Barrett esophagus
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chronic damage is believed to promote the replacement of healthy esophageal epithelium with the metaplastic columnar cells, the cellular origin of which remains unknown. - = increased risk for cancer
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Barrett esophagus
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one or several tongues of salmon-pink, velvety mucosa extending upward from the gastroesophageal junction
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Barrett esophagus
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metaplastic mucosa alternates with residual smooth, pale squamous mucosa of the normal esophagus and interfaces with light-brown columnar (gastric) mucosa distally
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Barrett esophagus
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Three types of columnar metaplasia have been discerned: fundic, cardia, and specialized intestinal metaplasia - presence of goblet cells.
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Barrett esophagus
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defined only as the presence of intestinal metaplasia
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Barrett esophagus
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increased epithelial proliferation, often with atypical mitoses, nuclear hyperchromasia and
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Barrett esophagus
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Dysplasia - stratification, increased nuclear-to-cytoplasmic ratio. Gland architecture is frequently abnormal and is characterized by budding, irregular shapes, and cellular crowding
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Barrett esophagus
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a pre-malignant condition. - risk of transformation into adenocarcinoma correlates with the length of esophagus involved and the degree of dysplasia
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Barrett esophagus
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Males 3:1 Smokers 2:1
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Eosinophilic esophagitis
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chronic esophageal inflammatory disorder, allergic in nature and of unknown origin that is characterized by dense infiltration by eosinophilic granulocytes that is restricted to the esophagus
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Eosinophilic esophagitis
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great majority of patients have a history of atopy (asthma, rhinitis, conjunctivitis, drug and food allergies), blood eosinophilia, increased serum IgE levels, and positive results in multiple allergy skin tests
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Eosinophilic esophagitis
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endoscopic is often characteristic with transverse ridges (which can resemble the trachea) and small white plaques
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Eosinophilic esophagitis
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most characteristic microscopic finding is a high number of eosinophils infiltrating the esophageal epithelium
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Eosinophilic esophagitis
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Treatment strategies include the exclusion of sensitizing foods, systemic and topical corticosteroids
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Candida esophagitis
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In mild cases, a few small, elevated white plaques are surrounded by a hyperemic zone in the middle or lower third of the esophagus
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Candida esophagitis
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In severe cases, confluent pseudomembranes lie on a hyperemic and edematous mucosa
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Candida esophagitis
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pseudomembrane contains fungal mycelia, necrotic debris and fibrin
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Herpes esophagitis
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viral infection of the esophagus caused by Herpes simplex virus
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Herpes esophagitis
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development of small vesicles that subsequently rupture to form discrete superficial ulcers on the mucosa
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Herpes esophagitis
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Squamous epithelial cells in herpetic vesicles exhibit typical nuclear herpetic inclusions and occasional multinucleation
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Cytomegalovirus esophagitis
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Characteristic cytomegalovirus inclusion bodies are seen in endothelial cells and granulation tissue fibroblasts
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Chemical esophagitis
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results from ingestion of corrosive agents
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Chemical esophagitis
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reflects accidental poisoning in children, attempted suicide in adults or contact with medication ("pill esophagitis")
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Chemical esophagitis
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Ingestion of strong alkaline agents (e.g., lye) or strong acids (e.g., sulfuric or hydrochloric acid), both of which are used in various cleaning solutions, can produce
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Iatrogenic esophagitis
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External irradiation for treatment of thoracic cancers
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Iatrogenic esophagitis
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Nasogastric tubes may cause pressure ulcers when they are in place for prolonged periods, although acid reflux also plays a role in these cases.
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ESOPHAGEAL VARICES
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dilated veins immediately beneath the mucosa that are prone to rupture and hemorrhage
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ESOPHAGEAL VARICES
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arise in the lower third of the esophagus - virtually always in patients with cirrhosis and portal hypertension
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ESOPHAGEAL VARICES
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response to portal hypertension is the development of a collateral circulation diverting the obstructed portal blood flow to the caval veins - portocaval collaterals
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ESOPHAGEAL VARICES
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most important portosystemic anastomoses are the gastroesophageal collaterals
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ESOPHAGEAL VARICES
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native veins laying within the wall of the esophagus and draining into the azygos vein.
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ESOPHAGEAL VARICES
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appear as tortuous dilated veins lying primarily within the submucosa of the distal esophagus and proximal stomach
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ESOPHAGEAL VARICES
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If exceed 0.5 cm in diameter, they tend to rupture, leading to life-threatening massive upper gastrointestinal hemorrhage.
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MALLORY-WEISS SYNDROME
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bleeding from tears in mucosa at gastroesophageal junction - usually caused by severe retching, coughing, or vomiting
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MALLORY-WEISS SYNDROME
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most patients present with a single tear involving mucosa and submucosa but not the muscular layer
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MALLORY-WEISS SYNDROME
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On average, the tear is 2-3 cm in length and a few millimeters in width
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Most common benign tumor
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leiomyomas
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Squamous papillomas
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sessile lesions with a central core of connective tissue and a hyperplastic papilliform squamous mucosa.
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SCC
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- thoracic esophagus - AA males - Smoking/Alcohol - in US - over 45, males 4:1
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Adenocarcinoma
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- Caucasian males - linked to GERD/Barrett esophagus
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SCC
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middle and upper thirds of the esophagus
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SCC
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tumors may be polypoid exophytic masses that protrude into the lumen leading to obstruction or cancerous ulcerations that infiltrate deeply within the esophageal wall and gradually narrow the lumen by circumferential compression
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SCC
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neoplastic squamous cells range from well- differentiated forms, characterized by presence of epithelial "pearls," to poorly differentiated forms in which the evidence of squamous differentiation is minimal or absent
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SCC
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rich lymphatic drainage of the esophagus provides a route for most metastases
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SCC
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tumors of the upper third metastasize to cervical, internal jugular and supraclavicular nodes
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SCC
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Metastases to liver and lung are common
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SCC
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Cancer of the middle third spreads to paratracheal and hilar lymph nodes and to nodes in the aortic, cardiac and paraesophageal regions
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SCC
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Because the lower third of the esophagus is fed by the left gastric artery, lower esophageal tumors spread via accompanying lymphatics to retroperitoneal, celiac and left gastric nodes
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SCC
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most common presenting complaint is dysphagia, but by the time a patient complains of dysphagia, most tumors are unresectable
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SCC
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cachectic owing to difficulty in swallowing
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SCC
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Odynophagia occurs in half of patients, and persistent pain suggests mediastinal extension of the tumor or involvement of spinal nerves
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SCC
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Compression of the recurrent laryngeal nerve causes hoarseness, and tracheoesophageal fistula is manifested clinically by a chronic cough
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ADENOCARCINOMA
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arises in a background of Barrett esophagus and long-standing GERD
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ADENOCARCINOMA
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Caucasian men 7:1
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ADENOCARCINOMA
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distal third of the esophagus and may invade the adjacent gastric cardia
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ADENOCARCINOMA
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Initially appearing as flat or raised patches in otherwise intact mucosa
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ADENOCARCINOMA
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Chromosomal abnormalities and mutation or overexpression of p53 are present at early stages
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ADENOCARCINOMA
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amplification of c-ERB-B2, cyclin D1, and cyclin E genes; mutation of the retinoblastoma tumor suppressor gene; and allelic loss of the cyclin-dependent kinase inhibitor p16/INK4a. In other instances p16/INK4a is epigenetically silenced by hypermethylation
