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Esophageal diseases (varices (Tx (sclerotherapy (thrombotic agent…

- - - - subsides spontaneously 50%
      - 25% die during first episode
      - rebleeding 70% chance within first year, with a similar rate of mortality 25%
- - - - primary: loss of intrinsic inhibitory neurons of LES or idiopathic (viral, or autoimmune)
      - secondary: chagas disease (T.cruzi) destroys myenteric plexus in esophagus, duodenum, colon, and ureter.
        poliomyelitis and DM neuropathy affect dorsal motor nuclei.
        malignancy, amyloidosis, and sarcoidosis are infiltrative.
    - - functional obstruction of esophagus
      - dilation of esophagus above LES
  - - - axial (sliding) (more common)
        bell shaped stomach
        
        regurgitation and heartburn, accentuated by bending forward, lying supine, and obesity.
        
        might be complicated by GERD, mucosal ulceration, bleeding, and perforation
      - non axial (paraesophageal)
        
        rarely induce reflux
        
        might be strangulated or obstructed, or less commonly ulceration, bleeding, and perforation.
  - - - pharyngoesophageal, immediately above UES
      - etiology ass/w disordered cricopharyngeus and maybe GERD
      - can accumulate food, cause dysphagia and food regurgitation, mass in the neck, and high risk for aspiration pneumonia
    - - midpoint of esophagus
      - wall weakening due to TB of mediastinal LN, motor dysfunction, or congenital
      - asymptomatic
    - - immediately above LES
      - discoordination of peristalsis and LES relaxation
      - may lead to nocturnal regurgitation
- - - - inflammation due to acid reflux
      - adults with recurrent heartburn (dominant symptom) dysphagia, regurgitation, and rarely, chest pain.
      - etiology
        
        decreased efficacy of antireflux mechanisms
        
        CNS depressants
        
        alcohol
        
        tobacco
        
        prolonged gastric intubation
        
        sliding hiatal hernia
        
        inadequate clearance of refluxed material
        
        delayed gastric emptying
        
        increased gastric volume
        
        mostly idiopathic
      - gross appearance
        
        depends on the causative agent and duration+severity of exposure to be mild or sever
        
        mild esophagitis: simple hyperemia
        
        severe esophagitis: epithelial erosions or ulceration into submucosa
      - microscopic appearance
        
        intraepithelial eosinophils, with neutrophils if severe
        
        basal zone hyperplasia
        
        elongation of lamina propria papillae and capillary congestion
        
        severity of symptoms is not closely related to the degree of histologic picture
      - serious complication: Barrett's esophagus
        
        metaplastic columnar epithelium in esophagus
        
        affects 10% of those with chronic GERD, esp white males
        
        pathogenesis: chronic GERD -> squamous layer inflamation and ulceration -> reepithelialization with columnar layer (origin: from migration of gastric mucosa or growth and differentiation of stem cells)
        
        grossly
        
        salmon pink, velvety
        
        located bw the smooth pink mucosa of esophagus and the brown mucosa of stomach
        
        may exist as
        
        tongues extending up from the GEJ
        
        arregular circumferentail band
        
        isolated patches in distal esophagus
        
        microscopically
        
        columnar metaplasia (contains goblet cells
        
        may be focal requiring repeated endoscopy and biopsy
        
        grading dyspasia is important
        
        complications
        
        barrett's ulcer
        
        stricture (stenosis)
        
        dysplasia and adenocarcinoma #
        
        around 1% of those with barrett per year
        
        higher risk in higher grade of dysplasia
        
        screening is recommended
- - - - etiology
        
        conginital
        
        acquired
        
        GERD and Barrett's #
        
        scleroderma
        
        radiation
        
        caustic injury
      - fibrous thickening of wall, esp submucosa, atrophy of muscularis propria, epithelium is thinned and maybe ulcerated
      - usually adults complaining of dysphagia
    - - protrusions of mucosa + submucosa into the lumen
      - semicircumferential
      - upper esophagus
      - etiology
        
        congenital
        
        acquired
        
        GERD
        
        chronic GVHD
        
        blistering skin diseases
      - Plummer–Vinson syndrome (PVS) AKA Paterson–Brown–Kelly syndrome = upper esophageal webs + IDA + atrophic glossitis
    - - distal esophagus
      - protrusions of mucosa + submucosa + sometimes hypertrophied muscularis propria
- - - - black adult males more affected
      - high incidence in Iran, China, and South Africa
      - pathogenesis: dysplasia -> CIS -> invasive carcinoma
      - patterns
        
        polypoid exophytic (most common)
        
        ulcerated and necrotic
        
        diffuse and infiltrative; causes thickening of wall + narrowing of lumen
      - 20% in upper third of esophagus
        50% in middle third of esophagus
        30% in lower third of esophagus
      - most important risk factors are alcohol consumption and tobacco abuse, others are here
    - - Barrett's esophagus is the precursor
      - risk factors
        
        tobacco, obesity, and radiation (no association with alcohol)
      - whites are more affected
      - pathogenesis: esophagitis (GERD) -> barrett's (metaplasia) -> dysplasia -> carcinoma
      - grossly
        
        distal one third of esophagus (like barrett's)
        
        may invade gastric cardia
        
        initially appears as flat or raised patches that develop into large nodular masses or ulcerative of diffuse infiltrative patterns
      - microscopically
        
        shows mucin producing glandular tumors of intestinal type
      - clinacally
        
        early asymptomatic
        
        progressive dysplasia and odynophagia
        
        weight loss, anorexia, fatigue, and weakness
      - diagnosis by imaging techniques and endoscopic biopsy
      - prognosis is poor, when symptomatic the tumor is large and has already invaded wall, lymphatics, and adjacent structures
        stage is the most important prognostic factor
      - surgical excision is rarely curative