• Upper Esophageal Sphincter (UES): mainly controlled by the crycopharyngeus muscles, inferior pharyngeal constrictor and proximal esophageal muscles; basal tone controlled by tonic excitatory motor stimulation of the crycopharyngeus; located C5-C6
• Lower Esophageal Sphincter (LES): functional zone of esophagus (not true anatomic structure); 3-4 cm at diaphragmatic hiatus; basal tone mostly myogenic, but also has neural and hormonal input
• esophageal body basal tone is flacid
• mouth to stomach play-by-play:
• swallowing is voluntary transient inhibition of tonically active somatic neurons (relax UES)
• vagal action initiates primary peristalsis in the lower 2/3 (smooth muscle portion) of the esophagus
• ‘off response’: inhibitory stimulus is directed at the smooth muscle; after the stimulus is withdrawn, there is a latent period (longer latency closer to stomach); following latency, the muscle contracts once; result is a progressing ring of contraction
• vagal stimulus (non adrenergic or cholinergic) relaxes the LES as the food bolus approaches; adrenergic stimulation modulates LES tone but does not affect sphincter relaxation or peristalsis
• central nervous action transiently inhibits the crural diaphragm

• three classic symptoms of esophageal disorders: dysphagia (impaired transport of bolus); odynophagia (painful swallowing); heartburn (pain originating at the GE junction and traveling anteriorly)
• dysphagia is of two types:
• (1) oropharyngeal dysphagia: difficulty initiating swallowing
• result of: weak pharyngeal peristalsis; uncoordinated peristalsis; UES dysfunction; obstructions
• can result from: tumors; osteophytes (bony strictures); CNS disorders (stroke is most common cause of oropharyngeal dysphagia); skeletal muscle disorders (myestenia gravis, MS, etc)
• aspiration is common and leads to recurring pneumonia
• (2) esophageal dysphagia: problems in transport post-swallow
• impaired peristalsis: interupt normal peristaltic progression or amplitude of contraction or both
• impaired LES function leaves residual pressure at the LES upon swallowing Þ obstruction

Achalasia – disrupts normal progression of peristalsis without affecting amplitude

• neuromuscular disorder: primary disorder may be degeneration in CNS (vagus nerve), vagal trunks (dorsal vagal nucleus), myenteric ganglia (Auerbach’s plexus), purinergic terminals
• results in loss of progressive waves and LES relaxation; spontaneous (tertiary) contractions are still present
• esophageal distension is common
• loss of normal peristalis results in impaired transport; tertiary contractions painful (due to vagal innervation of esophagus)
• loss of LES relaxation leads to esophageal obstruction; LES pressure may be elevated (due to vagal innervation of esophagus)
• aspiration of residual food is common; also fermentation can lead to carcinoma
• symptoms: dysphagia, chest pain, regurgitation; show an air-fluid level in esophagus
• treatment: dilation of sphincter via endoscopy or surgery - both are 80% effective Þ decreased sphincter pressure
• drugs (i.e. botulinum toxin can be used, but are rarely effective) – Ý sensitivity to gastrin and cholinergic drugs
• secondary achalasia: results from tumor in esophagus

Scleroderma – diminishes amplitude of force of contraction without altering the normal orderly progression

• systemic disease that also involves entire GI tract
• early loss of nexal connections in smooth muscle Þ atrophy Þ fibrosis
• leads to loss of LES function, and loss of peristalsis in lower 2/3 of esophagus (smooth muscle portion)
• reflux, esophagitis, stricture formation, delayed gastric emptying
• Raynaud’s phenomenon: cyanotic fingertips; often present in scleroderma
• also called systemic sclerosis or CREST (calcinosis; Raynaud’s; esophageal dysmotility; sclerodactyly; telangiectasia)

• high LES tone, or post relaxation spike in LES pressure

• amplitude of peristaltic waves is very high; but rate of motility is decreased
• however, this occurs in 50% of normal people and is often the result of nervousness Þ difficult diagnosis

• symptoms are dysphagia and severe chest pain similar to angina
• peristalsis is somewhat preserved, but is punctuated with repetitive high amplitude waves
• may progress to acalasia
• LES function is normal, but may be impaired with Ý pressure and partial relaxation

• driving force = positive intra-abdominal pressure and negative intra-thoracic pressure
• some reflux is normal (6-10x per hour after meals; 1-2x per hour at night)
• 75% of esophageal disorders are the result of increased reflux Þ GERD
• often presents as heartburn, belching, bloating, dysphagia, GI bleeding, chest pain; often after meals
• however, symptoms are mild and often relieved with antacids so most people never present at all
• in pediatric cases: recurrent emesis, recurrent pneumonia, asthma, apnea, irritability, hematamesis, dysphagia, sleep disturbance
• reflux can lead to: chest pain, weight loss, anemia, laryngitis, dental enamel decay, dyspepsia, chronic cough
• Barrett’s esophagus, hemorrhage, esophagitis, stricture, aspiration
• normal protection against reflux
• tonic contraction of LES
• anatomic features extrinsic to LES: crural diaphragm (inspiration causes esophageal constriction)
• ‘flap valve’ resulting from acute GE junction angle
• intra-abdominal pressure
• phrenoesophageal ligaments
• mechanisms of reflux
• transient LES relaxation (not associated with swallows) in 95% of cases, only 5% have low LES tone; hypotonic sphincter
• decreased sphincter response to intra-abdominal pressure, hormones, etc (i.e., gastrin)
• stomach distension Þ increased stomach pressure Þ overwhelms LES (explains reflux after meals)
• hiatus hernia: stomach pushes up through diaphragm Þ lose diaphragm/LES interaction
• diaphragm no longer causes constriction at inspiration Þ inspiration decreases pressure in the esophagus and sucks stomach contents up
• under debate whether or not hiatus hernia actually causes reflux (so far no correlation)
• also contributing: esophageal clearance; delayed gastric emptying (distension); gastric acidity; decreased mucous and saliva; mucosal resistance
• diagnostic tests:
• barium swallow: best test for someone presenting with dysphagia; rules out stricture, hernia, ulcer, etc
• upper endoscopy: recommended for chronic heartburn; diagnose state of mucosa; look for Barrett’s
• esophageal manometry: measure pressure; evaluates motility
• intra-esophageal pH monitoring: place pH sensor and wait for reflux; gold standard for reflux disease
• treatment:
• lifestyle modifications: weightloss; red. fat diet (fat relaxes LES); stop smoking (contraindicated drugs)
• antacids only work 1-2 hours; good for intermittent symptoms
• block acid secretion
• augment LES strength with drugs (urecholine, metoclopromide) or surgery (anti-reflux operations)

• causes of esophagitis: chemicals (lye, tetracycline, anti-cancer drugs); infection (candida, herpes); trauma (intubation/reflux); radiation; gastric secretions (acid and pepsin) and duodenal juice (include bile and pancreas secretions)

• basal cells proliferate and are pushed towards lumen where older, injured cells are shed
• often dilation of blood vessels (hyperemia) in lamina propria, edema, inflammatory cells (from lamina propria into stratified squamous epithelium)
• if injury outpaces regeneration Þ ulcers and epithelial destruction

Infectious Esophagitis: usually only in immunosuppressed

• constant repair Þ hyperplastic basal layer and often few flattened squamous cells due to constant shedding
• lengthened vascular papillae
• inflammation (lymphocytes, neutrophils, eosinophils; intraepithelial eosinophils are characteristic of reflux esophagitis)
• can lead to ulceration (loss of continuity of epithelial surface); Barrett’s esophagus; scars and strictures; esophagitis (inflammation, epithelial changes)

• columnar metaplasia of lower esophageal mucosa due to chronic reflux
• may be mucosal transformation or direct metaplasia through ulceration and re-epithelialization with columnar cells with goblet cells
• Barrett’s is a protective response (gastric mucosa is more suited to resist acid than squamous epithelium)
• major risk is progression to adenocarcinoma Þ occurs in 10% of Barrett’s cases

• 60% are adenocarcinomas - most arise from Barrett’s; usually distal
• 40% are squamous carcinomas
• mass of tumor may cause obstruction and dysphagia; ulceration common (diffusely infiltrate esophageal wall Þ localized narrowing and rigidity); metastasis is very common
• in US 10x less frequent than colo-rectal cancer and gastic cancer, but still very common; often diagnosed too late
• alcohol and tobacco use are associated with a higher incidence
• blacks higher incidence than whites

• barium swallow
• primary wave: moves the bolus; accompanied by LES opening and closure
• secondary wave: gets rid of leftovers
• tertiary wave: uncoordinated, no peristalsis, common in elderly
• Barrett’s: high strictures are often seen in radiologic tests
• reflux: difficult to diagnose radiologically, may see ulcers