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Flashcards in 7 Esophageal Physiology Deck (28):
1

Organs involved in swallowing

  • The organs involved in swallowing 
  • primary functions
  • Deglutition/
    • Peristaltic contractions/
      • The failure or lack of coordination of peristaltic contractions/
    • This leads to the symptoms of/
    • The reflux of gastric contents into the esophagus and pharynx is prevented primarily by/
      • Their failure to do so may lead to/

  • The organs involved in swallowing
    • the oral cavity, pharynx and esophagus -
  • primary functions:
    • to form and then transport a bolus from the oropharynx to esophagus (deglutition),
    • to propel this bolus into the stomach,
    • to prevent the reflux of gastric contents into the esophagus, pharynx and respiratory tract.
    • to protect the esophagus from the potential injury due to reflux of acidic material from the stomach.
  • Deglutition is a complex process that involves several striated muscles and cranial nerves, the hard palate and the larynx.
    • Peristaltic contractions of the muscular walls of the esophagus propel swallowed materials into the stomach.
      • The failure or lack of coordination of peristaltic contractions may disrupt the propulsion of swallowed material along the conduit.
    • This leads to the symptoms of dysphagia (difficulty swallowing) or odynophagia (painful swallowing).
    • The reflux of gastric contents into the esophagus and pharynx is prevented primarily by specialized, tonically contracted sphincter muscles that impede the retrograde movement of gastric and esophageal contents, respectively.
      • Their failure to do so may lead to reflux esophagitis and heartburn or pyrosis (a substernal and epigastric burning sensation).

2

Structure and Function of the Swallowing Organs (p.3-4)

  • The esophagus 
    • ?
    • three functionally distinct segments
  • The pharynx and esophagus form/
  • The pharynx 
    • ?
    • The muscular wall of the pharynx is composed of/
    • The most caudal of these muscles/
    • The cricopharyngeus/

  • The esophagus
    • a tubular structure of about 20 - 22 cm in length.
    • three functionally distinct segments:
      • upper esophageal sphincter (UES)
        • high resting tone; relaxes with swallowing
      • tubular esophagus
        • no resting tone; propagating contractions
      • lower esophageal sphincter (LES)
        • high resting tone; relaxes with swallowing
  • The pharynx and esophagus form a tubular conduit made up of distinct neuromuscular elements that are functionally integrated to perform the task of swallowing.
  • The pharynx
    • a tapered hollow cylinder that connects the mouth and nasopharyngeal cavity to the esophagus and trachea.
    • The muscular wall of the pharynx is composed of three overlapping sheets of striated muscle, the pharyngeal constrictors.
    • The most caudal of these muscles, the inferior pharyngeal constrictor, thickens to give rise to a distinct band of striated muscle, the cricopharyngeus.
    • The cricopharyngeus is positioned at the inlet of the esophagus where it functions as the upper esophageal sphincter.

3

Structure and Function of the Swallowing Organs

  • Below the pharyngo-esophageal junction, the esophagus forms/
    • The esophageal musculature consists of/
    • There is a transition zone/
    • what makes up the distal esophagus
    • The circular muscle layer thickens/
  • At rest,
    • the pharyngeal musculature generates/
    • The upper esophageal sphincter (cricopharyngeus) generates/
    • the tonic contraction of the lower esophageal sphincter/
    • The striated and smooth muscle portions of the esophagus between the two sphincters form/

  • Below the pharyngo-esophageal junction, the esophagus forms a continuous tube to the stomach.
    • The esophageal musculature consists of outer longitudinal and inner circular layers that are named according to the axial orientation of their constituent muscle cells.
    • There is a transition zone of several centimeters at about the level of the tracheal bifurcation over which the striated muscle mixes with and is replaced by smooth muscle
    • Smooth muscle makes up the distal esophagus.
    • The circular muscle layer thickens a little at the esophagogastric junction to form a muscular ring called the lower esophageal sphincter.
  • At rest,
    • the pharyngeal musculature generates a weak tonic contraction that stiffens the pharyngeal wall without occluding the lumen.
    • The upper esophageal sphincter (cricopharyngeus) generates a powerful, tonic contraction at rest which occludes the lumen at the junction between the pharynx and esophagus.
    • the tonic contraction of the lower esophageal sphincter completely occludes the lumen at the gastro-esophageal junction.
    • The striated and smooth muscle portions of the esophagus between the two sphincters form a flaccid tube without tone at rest.

4

Swallowing (p.6)

  • Swallowing starts as a phase of/
    • The tongue
  • As the swallow is initiated, the tongue/
  • As the bolus is propelled into the pharynx, the soft palate/
  • At about the same time
    • the larynx/
    • the arytaenoids/

  • Swallowing starts as a phase of preparation including mastication of the food and the formation of the bolus to be swallowed.
    • The tongue assumes a cup shape to hold the bolus in the oral cavity.
  • As the swallow is initiated, the tongue elevates against the palate in a sequential manner from anterior to posterior to squeeze the bolus into the pharynx.
  • As the bolus is propelled into the pharynx, the soft palate elevates to make contact with the posterior pharyngeal wall.
    • This seals the oropharynx from the nasopharynx so that nasopharyngeal reflux does not occur.
  • At about the same time
    • the larynx is elevated, moved anteriorly
    • the arytaenoids are displaced anterior to make contact with the epiglottis, thereby closing the laryngeal opening.

5

Swallowing (p.6)

  • Two types of pharyngeal contraction facilitate/
  • Early in the swallow
    • the pharynx/
    • this also/
  • A peristaltic contraction of the pharyngeal musculature behind the bolus/
  • The tonically contracted upper esophageal sphincter/
  • The peristaltic contraction/
  • The tonically contracted lower esophageal sphincter/
  • Arrival of the peristaltic contraction at the lower esophageal sphincter/

  • Two types of pharyngeal contraction facilitate the movement of the bolus towards the esophagus.
  • Early in the swallow
    • the pharynx shortens in its long axis, decreasing the distance the bolus must travel in transit through the pharynx.
    • Pharyngeal shortening also obliterates the laryngeal vestibule and the pyriform sinuses so that none of the bolus is caught in these recesses.
  • A peristaltic contraction of the pharyngeal musculature behind the bolus occludes the pharyngeal lumen as it sweeps caudal to force the bolus towards the esophagus.
  • The tonically contracted upper esophageal sphincter
    • relaxes as the pharyngeal peristaltic contraction advances towards the esophagus
    • is actively pulled open as the larynx is elevated and moved anteriorly.
    • contracts powerfully as the pharyngeal peristaltic sequence occurs and then rapidly reestablishes its basal tone.
      • This facilitates the transfer of the bolus from the oropharynx to the esophagus.
  • The peristaltic contraction sweeps without interruption from the upper esophageal sphincter, along the esophageal body, to the stomach.
  • The tonically contracted lower esophageal sphincter
    • relaxes long before the peristaltic contraction reaches the gastroesophageal junction.
    • remains relaxed until the peristaltic contraction arrives to strip the bolus into the gastric cavity.
  • Arrival of the peristaltic contraction at the lower esophageal sphincter closes the sphincter with a transient, forceful contraction which soon subsides to the tonic contraction of the resting state.

6

Neuromuscular Control of Swallowing (p.7-16)

  • the swallowing organs composed of striated muscle
  • The contractile behavior of these organs is controlled by/
    • Axons from nerve cell bodies in these nuclei project/
    • The continuous discharge of these nerves is responsible for/
  • Relaxation of these muscles results from/
  • The peristaltic contraction that sweeps along these organs represents/
    • The contraction is peristaltic because/

  • the swallowing organs composed of striated muscle
    • the pharynx, upper esophageal sphincter, and proximal esophageal body
  • The contractile behavior of these organs is controlled by somatic nerves that originate in the nuclei of the glossopharyngeal (IX) and vagus (X) nerves.
    • Axons from nerve cell bodies in these nuclei project via cranial nerves, without synaptic interruption, to end in motor end plates on the striated muscle cells.
    • The continuous discharge of these nerves is responsible for the maintenance of tone in the striated muscle of the oropharynx and upper esophageal sphincter.
  • Relaxation of these muscles results from the inhibition of this tonic somatic neural discharge.
  • The peristaltic contraction that sweeps along these organs represents a vigorous discharge of their somatic innervation.
    • The contraction is peristaltic because the motor units, single motor neurons and striated muscle cells that they supply, are activated in a fixed craniocaudal sequence.

7

Neuromuscular Control of Swallowing (p.7-16)

  • The neuromuscular control of the smooth muscle esophagus
    • The central innervation of the smooth muscle portion of the esophagus arises from/
    • Axons from these preganglionic parasympathetic neurons travel/
    • The terminal motor innervation of the smooth muscle of the esophagus, the postganglionic neurons, comes from/
  • The neural systems seem to be inactive/
    • The resting contraction of the lower esophageal sphincter reflects/
    • however, some fluctuations in baseline tone may represent/
  • The first swallow-induced event in the smooth muscle esophagus/
    • This results from/

  • The neuromuscular control of the smooth muscle esophagus
    • The central innervation of the smooth muscle portion of the esophagus arises from nerve cell bodies in the dorsal motor nucleus of the vagus.
    • Axons from these preganglionic parasympathetic neurons travel with the vagus nerve to synapse with neurons in the myenteric plexus.
    • The terminal motor innervation of the smooth muscle of the esophagus, the postganglionic neurons, comes from these nerve cell bodies in the myenteric plexus.
  • The neural systems seem to be inactive at rest in the smooth muscle segment of the esophagus.
    • The resting contraction of the lower esophageal sphincter reflects, mainly, the myogenic tone of the sphincter muscle rather than a strong tonic discharge of nerves;
    • however, some fluctuations in baseline tone may represent neural activity.
  • The first swallow-induced event in the smooth muscle esophagus is relaxation of the lower esophageal sphincter.
    • This relaxation results from the vagal activation of inhibitory myenteric nerves that release nitric oxide.

8

Neuromuscular Control of Swallowing (p.7-17)

  • The progressive nature of the peristaltic contraction in the smooth muscle esophageal segment 
    • not programmed in/
    • controlled by/
  • Nitric oxide-releasing myenteric nerves supply/
  • Swallowing activates/
  • The duration of the inhibition is progressively longer at/
  • Excitation that follows the period of inhibition is responsible for/

  • The progressive nature of the peristaltic contraction in the smooth muscle esophageal segment 
    • not programmed in the brainstem.
    • controlled by neuromuscular mechanisms that are intrinsic to the esophagus.
  • Nitric oxide-releasing myenteric nerves supply the circular muscle of the smooth muscle esophagus.
  • Swallowing activates these inhibitory nerves simultaneously throughout the esophageal body, to cause a nearly simultaneous inhibition along the length of the smooth muscle esophagus.
  • The duration of the inhibition is progressively longer at the more distal sites in the smooth muscle esophagus.
  • Excitation that follows the period of inhibition is responsible for the progressive nature of the peristaltic contraction.

9

Heartburn (Pyrosis) and Gastroesophageal Reflux (p.23-25)

  • Heartburn
    • frequency
    • may indicate/
    • If associated with objective signs of mucosal damage (most often erosions)
    • The inflammatory process is usually initiated and maintained by/
  • Gastroesophageal reflux most often occurs either because/
  • This situation is exacerbated if/

  • Heartburn
    • common symptom in the general population
    • may indicate the presence of mucosal inflammation in the distal esophagus.
    • If associated with objective signs of mucosal damage (most often erosions), the diagnosis of gastroesophageal reflux disease (GERD) is established.
    • The inflammatory process is usually initiated and maintained by the reflux of gastric contents (acid and/or bile) into the esophagus.
  • Gastroesophageal reflux most often occurs either because
    • the lower esophageal sphincter does not maintain adequate tone at rest
    • the lower esophageal sphincter relaxes inappropriately, at other times besides swallowing, to allow the retrograde movement of gastric contents into the esophagus
  • This situation is exacerbated if
    • esophageal peristalsis is disordered so that gastric contents are not cleared from the esophagus
    • the motor function of the stomach is impaired so that it does not empty in a timely fashion
    • there is a decrease in saliva production

10

Heartburn (Pyrosis) and Gastroesophageal Reflux (p.26-29)

  • Hiatal hernias
  • link between these herniations and reflux
  • Not every patient with heartburn/
    • 60-70 % of patients with typical reflux symptoms/
    • symptoms are still caused by/
  • Causes of heartburn
  • pyrosis does not always mean/

  • Hiatal hernias
    • often equated with gastroesophageal reflux disease
    • often asymptomatic
  • link between these herniations and reflux
    • recurrent reflux is the main mechanism leading to formation of the hernia.
    • mucosal injury results in contractions of the muscularis mucosae, which has a longitudinal orientation.
    • Over time, such contractions may disrupt the diaphragmatic attachments of the esophagus, allowing shortening and formation of a hiatal hernia.
    • The hernia, in turn, creates a small reservoir of gastric acid above the diaphragm that facilitates reflux.
  • Not every patient with heartburn has reflux disease.
    • 60-70 % of patients with typical reflux symptoms will not have mucosal disease.
    • symptoms are still caused by reflux, but it is not really GERD as there are no mucosal lesions, leading to non-erosive reflux disease (NERD).
  • Causes of heartburn
    • most commonly caused by reflux
    • other illnesses that are clearly less frequently, such as infections like Candida albicans, CMV or Herpes virus.
    • patients who do not take pills with adequate amounts of fluids will have them lodge in the distal esophagus to cause inflammation and heartburn.
  • pyrosis does not always mean injury or inflammation of the mucosa
    • up to one third of healthy volunteers experience esophageal distension as heartburn
    • the availability of effective acid-lowering medications has changed the landscape of reflux disease.

11

Evaluation of the Patient with Heartburn:
Historical Features

  • evaluation of the patient with heartburn 
    • most frequently described as/Some patients describe heartburn as/
    • The symptom is almost never described as/
  • The severity of the heartburn/
    • The typical patient with heartburn has the symptom/
  • exacerbations
  • Heartburn is often relieved by/

  • evaluation of the patient with heartburn
    • most frequently described as a burning or hot sensation that is located in the midepigastrium near the xyphoid process or over the lower half of the sternum.
    • Some patients describe heartburn as a “sour stomach” or “indigestion”.
    • The symptom is almost never described as a sharp, crampy or squeezing pain.
  • The severity of the heartburn does not predict the severity of the underlying pathological process.
    • The typical patient with heartburn has the symptom intermittently.
  • exacerbations
    • Most are related to practices by the patient that intensify esophageal inflammation or promote gastroesophageal reflux.
    • Smoking cigarettes or drinking alcohol promotes reflux by decreasing the force of closure of the lower esophageal sphincter.
    • Eating large, fatty meals increases reflux by multiple mechanisms.
      • First, overeating increases the pressure gradient from the stomach to the esophagus.
        • The result is increased reflux across the lower esophageal sphincter.
      • Second, fats entering the duodenum decrease the force of closure of the lower esophageal sphincter and decrease the rate of gastric emptying.
      • Finally, gastric distension increases the spontaneous relaxations of the lower esopahgeal sphincter.
    • Coffee and spicy foods and citrus juices also increase heartburn.
    • When the patient is recumbent, reflux episodes may increase because gravity no longer counteracts the retrograde flow of intragastric contents across the lower esophageal sphincter.
    • vomiting
  • Heartburn is often relieved by
    • avoiding aggravating factors
    • buffering agents like milk or antacids
    • drinking water which presumably works by diluting and clearing acid from the distal esophagus.

12

Evaluation of the Patient with Heartburn:
Associated Symptoms and Illnesses

  • Dysphagia
    • indicative of a complication arising from gastroesophageal reflux.
    • may have mechanical lesions of the esophagus like esophageal cancer, peptic stricture or Schatzki’s ring.
    • Chronic gastroesophageal reflux may also give rise to esophageal motor abnormalities that are known to produce dysphagia.
  • odynophagia (painful swallowing) most often indicates severe focal inflammation in the form of erosions or ulcers of the esophagus.
  • The coexistence of heartburn and respiratory symptoms, like chronic cough, hoarseness, laryngitis, asthma or recurrent pneumonias, should alert the clinician to the possibility that these symptoms are caused by gastroesophageal reflux.
  • patients may describe cardiac problems as heartburn

13

Evaluation of the Patient with Heartburn:
The Therapeutic Trial as a Diagnostic Test

  • therapeutic trial with one of the proton pump inhibitors
    • ?
    • These agents/
    • Failure of the therapeutic trial suggests/
    • This approach should only be employed/
    • Concurrent symptoms/
  • Diagnosis of GERD

  • therapeutic trial with one of the proton pump inhibitors
    • simplest, safest and most cost effective way to determine if heartburn is caused by gastroesophageal reflux
    • These agents significantly inhibit acid production in the stomach.
    • Failure of the therapeutic trial suggests that the symptoms do not arise from acid reflux
    • This approach should only be employed if the patient presents with simple heartburn only.
    • Concurrent symptoms like dysphagia, odynophagia or chest pain are indicative of more serious problems
  • Diagnosis of GERD
    • Typical symptoms (pattern recognition).
    • Diagnostic trial with proton pump inhibitor in patients with uncomplicated GERD.

14

Evaluation of the Patient with Heartburn:
Endoscopy in the Evaluation of the Patient With Heartburn (p.31)

  • Endoscopy
    • the best way to determine/
    • able to identify/
  • a visually normal appearance to the esophageal mucosa does not rule out/
  • the diagnosis of gastroesophageal reflux should be based on/
  • tests are primarily indicated in individuals with/

  • Endoscopy
    • the best way to determine if heartburn is due to reflux and complicated by mucosal injury (esophagitis).
    • able to identify
      • obvious signs of esophageal inflammation, like esophageal ulcers or erosions,
      • subtle inflammatory changes of the esophageal mucosa that are not seen with other methods like the barium swallow.
  • a visually normal appearance to the esophageal mucosa does not rule out gastroesophageal reflux as the etiology for heartburn, as patients may experience symptoms due to acid reflux but do not have mucosal injury,
    • a scenario that accounts for 60-70 % of patients with typical reflux symptoms (NERD).
  • the diagnosis of gastroesophageal reflux should be based on symptoms rather than testing 
  • tests are primarily indicated in individuals with atypical symptoms or potential complications.

15

Evaluation of the Patient with Heartburn

  • Ambulatory Intraesophageal pH Monitoring (p.33)
    • ?
    • performed by/
    • identifies patients with/
    • does not prove that/
    • The diagnosis of esophagitis requires/
    • symptom severity/
    • ambulatory pH monitoring should not be considered/
  • Barium Swallow (p.32)
    • provides information about/
    • usefullness / sensitivity
    • documents/

  • Ambulatory Intraesophageal pH Monitoring
    • a simple method that quantifies esophageal acid exposure.
    • performed by placing the probe into the distal esophageal lumen.
      • The pH electrode is attached via a nasal tube to a recording device or transmits information via radio waves to records intraesophageal pH values for 24 – 48 hours.
      • Standard analytical methods display the intraesophageal pH over the recording time and allow to correlate acid exposure to symptoms or precipitating factors.
    • identifies patients with abnormal gastroesophageal reflux,
    • does not prove that these patient have esophagitis.
    • The diagnosis of esophagitis requires demonstrating the presence of inflammation of the esophageal mucosa.
    • symptom severity does not necessarily correlate with the amount of esophageal acid exposure.
    • ambulatory pH monitoring should not be considered a first line test for the evaluation of heartburn.
  • Barium Swallow
    • provides information about significant structural changes within the esophagus.
    • useful, but lower sensitivity than endoscopy in the recognition of mucosal lesions.
    • documents the presence and extent of a hiatal hernia.

16

Evaluation of the Patient with Heartburn:
Treatment of Reflux Disease (p.35-37+45)

  • Gastroesophageal reflux 
    • prevalence
    • lifestyle/
    • Many patients learn to/
    • lifestyle modification/
    • additional steps
  • For many patients requiring medical therapy, reflux / 
    • If esophageal erosions were seen endoscopically/
  • The alternative could be surgery/

  • Gastroesophageal reflux
    • highly prevalent in Western countries, suggesting
    • lifestyle contributes to its pathogenesis and to symptoms.
    • Many patients learn to avoid other foods that trigger symptoms, largely due to acidity or direct interactions with nerves (OJ, spicy foods).
    • lifestyle modification plays an important role but often does not suffice.
    • additional steps are needed.
      • The most commonly used interventions focus on the acidity (aggressiveness) of the refluxing material.
      • By decreasing gastric acid production, we can significantly improve symptoms and accelerate healing of mucosal injury.
      • Proton pump inhibitors are significantly more effective than histamine-2 receptor antagonists, as PPIs are the more effective blockers of acid production.
  • For many patients requiring medical therapy, reflux is a chronic problem.
    • If esophageal erosions were seen endoscopically, only 10-20 % of patients will continue doing well 180 days after discontinuation of therapy.
    • Thus, maintenance is needed.
  • The alternative could be surgery, which constructs a valve-like structure around the distal esophagus (fundoplication).
    • While as effective as medication (85 % success rate), surgery has more acute complications and may not be able to deliver long-term cure. 

17

Evaluation of the Patient with Heartburn:
Complications of Reflux Disease (p.46)

  • repair and scar formation, which may ultimately narrow the lumen (stricture formation).
  • injury triggers changes in epithelial behavior with cells differentiating into cylindrical rather than the typical squamous epithelium (Barrett’s metaplasia).
  • reflux may affect more proximal areas.
    • these extraesophageal manifestations of reflux may involve the airways and could contribute to chronic hoarseness, recurrent airway infections or atypical asthma.

18

Evaluation of the Patient with Heartburn:
Barrett's Esophagus (p.47-48+52)

  • Hallmark
  • Barrett’s esophagus has been linked to/
  • The main reason for our concern/
  • the actual cancer incidence/
  • Esophageal adenocarcinomas primarily affect/
  • surgical management of reflux/

  • Hallmark
    • Metaplasia of the esophageal epithelium with cylindrical epithelium and goblet cells (‘specialized intestinal metaplasia’)
  • Barrett’s esophagus has been linked to reflux disease.
  • The main reason for our concern is the potential progression toward cancer.
    • Adenocarcinoma of the esophagus typically arises in metaplastic (=Barrett’s) epithelium.
    • There's a significant association between adenocarcinoma and reflux, while no such correlation existed for squamous cell cancers.
    • There's a gradual evolution of cancer via increasing degrees of dysplasia as the morphologic manifestation of progressive genetic alterations.
  • the actual cancer incidence remains low, albeit rising.
    • In patients with Barrett’s esophagus, the annual cancer incidence is around 0.3% or lower.
  • Esophageal adenocarcinomas primarily affect older Caucasian males.
  • surgical management of reflux did not demonstrate any protective effect compared to medical management

19

Dysphagia - Difficulty Swallowing (p.54)

  • Dysphagia 
  • Normally, people are aware only of/
  • The symptom of dysphagia/

  • Dysphagia
    • the perception of having difficulty swallowing.
    • Impaired bolus transit along the pharyngo-esophageal conduit
  • Normally, people are aware only of the oral and most of the pharyngeal phases of swallowing;
    • chewing motions, the formation of a bolus in the mouth, and the initiation of a peristaltic sequence in the oropharynx.
  • The symptom of dysphagia
    • may be only a nondescript feeling that something is amiss after the pharyngeal portion of the swallow,
    • may be a sensed as an evanescent slowing of the food bolus in its transit to the stomach,
    • may be the sensation of food getting stuck.

20

Dysphagia - Difficulty Swallowing (p.54-55)

  • Dysphagia may be associated with other symptoms, such as/
    • These symptoms arise when/
  • Dysphagia can be differentiated based on/
    • neuromuscular mechanisms controlling these regions/
    • the pathological processes that underlie disordered swallowing in them/
    • Oropharyngeal dysphagia most commonly arises from/
  • Oropharyngeal dysphagia
    • Localization
    • Manifestation
  • Esophageal dysphagia
    • Localization
    • Manifestation

  • Dysphagia may be associated with other symptoms, such as aspiration and regurgitation.
    • These symptoms arise when transport of a swallowed bolus along the pharyngo-esophageal conduit is impaired by either a mechanical obstruction of the lumen or neuromuscular failure causing disordered peristalsis.
  • Dysphagia can be differentiated based on symptoms into oropharyngeal or esophageal.
    • neuromuscular mechanisms controlling these regions are dissimilar
    • the pathological processes that underlie disordered swallowing in them are different
    • Oropharyngeal dysphagia most commonly arises from either neuromuscular disorders or structural abnormalities such as oropharyngeal tumors.
  • Oropharyngeal dysphagia
    • Localization: Anterior throat above suprasternal notch.
    • Manifestation: Difficulty initiating swallows, cough, choking, nasal regurgitation, nasal speech
  • Esophageal dysphagia
    • Localization: Suprasternal notch or substernal, rarely epigastric. Location does not predict level of lesion
    • Manifestation: Fullness, foreign body sensation or pain, regurgitation, aspiration.

21

Evaluation of the Patient with Dysphagia (p.57-59)

  • Historical Features - Characteristics of Dysphagia
    • where s/he senses the dysphagia
      • oropharyngeal
      • Esophageal
    • location of the sensation vs. level of the lesion
  • Physical Findings

  • Historical Features - Characteristics of Dysphagia
    • where s/he senses the dysphagia.
      • The perception of things sticking anterior in the throat above the suprasternal notch predicts fairly reliably that the dysphagia is oropharyngeal in origin.
      • Esophageal dysphagia is sensed at the suprasternal notch, substernally or on the anterior chest wall;
    • location of the sensation does not predict the level of the lesion.
      • In most cases, the sensation is cephalic to the lesion.
      • Dysphagia is seldom perceived in the middle of the back or epigastrium.
  • Physical Findings
    • facial asymmetries, for example the consequences of a stroke,
    • a dry oral mucosa or pharyngeal lesions,
    • an impaired mobility of the tongue or larynx
    • an absent gag reflex.
    • Skin changes, such as telangiectasias or sclerodactyly suggest the presence of a systemic disease with likely esophageal involvement.

22

Evaluation of the Patient with Dysphagia:
Exacerbating and Relieving Factors

  • oropharyngeal dysphagia 
    • exacerbating
    • relieving
  • esophageal dysphagia arising from mechanical lesions obstructing the lumen of the esophagus 
    • exacerbating
    • relieving
  • Dysphagia with both solids and liquids suggests/
  • Dysphagia brought on or worsened by drinking very cold liquids or eating ice cream is characteristic of/

  • oropharyngeal dysphagia
    • more difficulty swallowing liquids than solids.
    • cautious eating and swallowing or getting the head into certain positions brings some relief.
  • esophageal dysphagia arising from mechanical lesions obstructing the lumen of the esophagus
    • worse with solids than with liquids.
      • Those foods that are most troublesome are things that are not chewed well; meats, breads and peanut butter.
    • may gain relief by “washing it down” with liquids.
  • Dysphagia with both solids and liquids suggests
    • a near complete obstruction of the esophagus, a disordered esophageal motor function,
    • a severe inflammation of the esophageal mucosa.
  • Dysphagia brought on or worsened by drinking very cold liquids or eating ice cream is characteristic of esophageal motility problems.

23

Evaluation of the Patient with Dysphagia:
Chronology of Symptoms

  • esophageal dysphagia symptoms started as/
  • Dysphagia that remains intermittent and is not progressive, or only slowly progressive, over a long period of time suggests/
  • Long asymptomatic periods punctuated by brief episodes of relatively severe dysphagia suggest/
  • The sporadic nature of the dysphagia results from/
  • Dysphagia that worsens relentlessly over time and progresses from occurring only with solid boluses to occurring with both solids and liquids is suggestive of /
  • The sudden onset of dysphagia is/

  • esophageal dysphagia symptoms started as only mild, intermittent dysphagia and progressed over time. 
  • Dysphagia that remains intermittent and is not progressive, or only slowly progressive, over a long period of time suggests a benign cause like a stable stricture or a motility abnormality.
  • Long asymptomatic periods punctuated by brief episodes of relatively severe dysphagia suggest the presence of an esophageal mucosal ring (Schatzki’s ring).
  • The sporadic nature of the dysphagia results from the repeated formation of a thin mucosal ring that is ruptured by the bolus that is transiently lodged in the ring.
  • Dysphagia that worsens relentlessly over time and progresses from occurring only with solid boluses to occurring with both solids and liquids is suggestive of esophageal neoplasms.
  • The sudden onset of dysphagia is uncommon and should make the physician think of such things as foreign body impaction or an infectious cause.

24

Evaluation of the Patient with Dysphagia:
Associated Symptoms or Illnesses

  • People with oropharyngeal dysphagia will complain of/
  • Heartburn associated with dysphagia suggests/
  • Chronic esophagitis may lead to the formation of /
  • odynophagia (painful swallowing) associated with dysphagia suggests/
  • Immunocompromised patients may have/
    • The most common infectious agents are/
    • Dysphagia may also be a manifestation of/

  • People with oropharyngeal dysphagia will complain of difficulties initiating the swallowing process, nasopharyngeal reflux of swallowed liquids and choking or coughing with swallowing, and other symptoms of the neuromuscular disease that underlies there swallowing problem 
  • Heartburn associated with dysphagia suggests that an inflammatory process, usually chronic gastroesophageal reflux disease (GERD), is in some way responsible for the dysphagia.
  • Chronic esophagitis may lead to the formation of
    • an esophageal stricture
    • an abnormality of esophageal motor function that interferes with esophageal transit.
  • odynophagia (painful swallowing) associated with dysphagia suggests a more severe inflammatory process like
    • esophageal ulcers resulting from GERD,
    • improperly taken pills lodging in the esophagus
    • infections (Cytomegalovirus, Herpes or Candida).
  • Immunocompromised patients; i.e. those being treated with cancer chemotherapeutic agents, transplant patients and those suffering from AIDS, may have dysphagia arising from infectious processes.
    • The most common infectious agents are Cytomegalovirus, Herpes, Candida, or Kaposi's sarcoma
    • Dysphagia may also be a manifestation of systemic diseases like collagen vascular diseases (especially scleroderma), diabetes mellitus and hypothyroidism.

25

Causes of Dysphagia (p.56+60)

  • Neuromuscular Diseases
    • Diseases of the Central Nervous System
    • Diseases of the Peripheral Nervous System
    • Myopathic Diseases
    • Structural Abnormalities
  • Esophageal Dysphagia
    • Mechanical Obstruction
    • Esophagitis
    • Myopathic Diseases
    • Peripheral Neuropathies
    • Primary Motor Abnormalities

  • Neuromuscular Diseases
    • Diseases of the Central Nervous System
      • Cerebral Vascular Accident
      • Multiple Sclerosis
      • Amyotrophic Lateral Sclerosis
      • Parkinson’s Disease
      • Tumors of the Brainstem
    • Diseases of the Peripheral Nervous System
      • Poliomyelitis
      • Myasthenia Gravis
      • Peripheral Neuropathies (Diabetes Mellitus)
    • Myopathic Diseases
      • Muscular Dystrophies
      • Polymyositis, Dermatomyositis
      • Metabolic Myopathic Processes (myxedema ,thyrotoxicosis, steroid-induced myopathy)
    • Structural Abnormalities
      • Neoplasms (squamous cell carcinoma, lymphoid tumors)
      • Infectious processes
      • Compression form External Lesions (enlarged thyroid, lymph nodes,cervical vertebral osteophytes)
      • Esophageal Rings or Webs (Plummer-Vinson syndrome, congenital webs)
  • Esophageal Dysphagia
    • Mechanical Obstruction
      • Esophageal Neoplasms (mucosal or intramural tumors)
      • Peptic Stricture
      • Foreign Bodies
      • Paraesophageal Hernia
      • Mediastinal tumors
    • Esophagitis
      • peptic
      • chemical
      • eosinophilic
      • infecitous
    • Myopathic Diseases
      • as above
    • Peripheral Neuropathies
      • diabetes
    • Primary Motor Abnormalities
      • Achalasia
      • Diffuse Esophageal Spasm

26

A Practical Approach (p.62+70-71+73)

  • Dysphagia for solids only is typically due to/
    • the most common cause
    • other causes
  • Endoscopy
  • Dysphagia for solids and liquids is more often due to/
    • what will also cause such symptoms.

  • Dysphagia for solids only is typically due to a structural abnormality. 
    • the most common cause is the reflux-associated esophageal stricture.
    • other causes are cancer and eosinophilic esophagitis 
  • Endoscopy
    • the most appropriate diagnostic strategy
    • allows obtaining biopsies or even correcting the problem by simple and safe interventions, such as dilations.
  • Dysphagia for solids and liquids is more often due to functional disturbances, such as achalasia
    • advanced lesions that nearly occlude the esophageal lumen will also cause such symptoms.

27

Special Cases: Eosinophilic Esophagitis (p.63-66+68)

  • like the/
  • increased prevalence with/
  • manifests/
  • The typical symptom
  • The diagnosis requires/
    • There appear to be/
  • interaction between acid reflux and the allergic response. 
    • the impaired esophageal function/
    • acid-induced injury/
  • In some patients, we thus see improvement or even resolution with/
    • Should this not be the case, we should try to/
  • Treatment 

  • like the asthma equivalent of the esophagus.
  • increased prevalence with distinct regional differences.
  • manifests in childhood, but is increasingly seen in young adults, with a slight male predominance.
  • The typical symptom is intermittent dysphagia for solids.
  • The diagnosis requires biopsies, which prove extensive eosinophilic infiltration of the epithelium.
    • There appear to be altered signaling processes involving IL5, which increases eosinophil proliferation plus excess production of eotaxins. .
  • interaction between acid reflux and the allergic response.
    • the impaired esophageal function alters defense mechanisms against reflux, secondarily often worsening distal esophageal inflammation.
    • acid-induced injury weakens the epithelial barrier function and may worsen the response to the allergen.
  • In some patients, we thus see improvement or even resolution with PPI therapy.
    • Should this not be the case, we should try to identify an underlying allergy (can be food and air-born allergies) to avoid exposure and improve inflammation.
  • Treatment
    • acid suppression and topical steroids, which should be swallowed rather than being inhaled.

28

Special Cases: Dysmotility (p.74-77)

  • Disruption of esophageal motility 
    • can cause/
    • the best defined motility disorders are/
  • achalasia
    • patients have /
    • Swallows trigger/
    • the abnormalities result in/
    • Morphologic studies have demonstrated/
    • treatment
  • Diffuse esophageal spasm 
    • swallows trigger/
    • Difference b/n this and achalasia
    • Symptoms

  • Disruption of esophageal motility
    • can cause significant symptoms, including dysphagia.
    • the best defined motility disorders are achalasia and esophageal spasm
  • achalasia
    • patients have
      • a loss of normal peristaltic contractions within the tubular esophagus
      • an incomplete or completely absent relaxation of the lower esophageal sphincter.
    • Swallows trigger only simultaneous contractions along the axis of the esophagus, which poorly propel the bolus.
    • Combined with the ongoing closure of the lower esophageal sphincter the abnormalities result in dysphagia, chest pressure or pain and regurgitation of indigested material.
    • Morphologic studies have demonstrated inflammation within the myenteric ganglia with a progressive loss of ganglion cells.
    • Considering the loss of neurons, treatment cannot restore normal function.
      • it focuses on removing the primary obstacle to bolus transfer, the non-relaxing lower esophageal sphincter.
      • By lowering the sphincter forces (using medications, stretching forces or surgery), symptoms improve quite a bit.
  • Diffuse esophageal spasm
    • swallows also only trigger simultaneous, non-propagating contractions along the axis of the esophagus.
    • However, the lower esophageal sphincter relaxes.
    • Thus, symptoms are not as severe in the majority of patients.