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Part 1 Oral cavity, pharynx and esophagus
Figures
Physiology of oral cavity, pharynx and upper esophageal sphincter
Figure 1 : Diagrammatic illustration of motor events of swallowing reflex.
Figure 2 : Origin of cranial nerves involved in swallowing.
Figure 3 : Origin of cranial nerves involved in swallowing.
Figure 4 : Distribution of hypoglossal (XII) nerve.
Figure 5 : Sensory nerve supply of the mucous membrane of the oral cavity and pharynx.
Figure 6 : Distribution of the CN IX (glossopharyngeal).
Figure 7 : Distribution of the vagus nerve (X) to oral and pharyngeal areas.
Upper esophageal sphincter
Figure 1 : Anatomy of the closing and some opening muscles of the upper esophageal sphincter (UES).
Figure 2 : Relationship of upper esophageal high-pressure zone (UEHPZ) to the pharyngoesophageal muscles.
Figure 3 : Strain-energy relationship of the cricopharyngeus (CP) muscle.
Figure 4 : Effect of transection of various motor nerves on the motor responses of the UES closing muscles during swallowing.
Figure 5 : Effect of electrical nerve stimulation on electrical response and tension of UES closing muscles.
Figure 6 : Effect of stress on UES pressure.
Figure 7 : Relationship of CP and TP EMG activities to UES pressure during rest and excitation.
Figure 8 : High variability of CP but not TP EMG.
Figure 9 : Temporal relationship of UES pressure, opening and CP EMG during 4-mL barium swallow relative to hyoid movement.
Figure 10 : Temporal relationship among UES pressure, trans-UES flow, and movement of the hyoid and larynx during 5-mL barium swallow.
Figure 11 : Movement of the hyoid bone during belching (a) and swallowing (b).
Figure 12 : Response of UES muscles during swallowing.
Figure 13 : Responses of superior and inferior hyoid muscles during swallowing.
Figure 14 : Temporal relationship among function of the glottis, UES, hyoid bone, and esophageal and stomach pressures during belching induced by rapid injection of 40 mL of air into the esophagus.
Figure 15 : Electromyography (EMG) responses of the opening and closing muscles of the UES during belching and swallowing activated by injection of 100 mL of air into the stomach of a chronically instrumented dog.
Figure 16 : Effects of belching on the UES closure muscles.
Figure 17 : Role of UES closure and opening muscles during the three phases of vomiting.
Figure 18 : Effect of esophago-UES contractile reflex on the UES closure muscles.
Figure 19 : Role of UES closure muscles in esophago-UES relaxation reflex.
Figure 20 : Respiratory rhythm of the UES closure muscles.
Anatomy and development and physiology of the larynx
Figure 1 : Structure and function of the larynx viewed phylogenetically (according to Negus)
Figure 2 : The nasolaryngeal relationship.
Figure 3 : Human larynx and pharynx viewed from behind.
Figure 4 : Frontal section through the human larynx demonstrating the valvular structure of the false and true cords.
Figure 5 : Laryngoscopic view of the intrinsic muscles responsible for activating vocal cord position.
Figure 6 : Organizational models.
Figure 7 : Stimulation of right internal branch of superior laryngeal nerve.
Figure 8 : Intrathoracic pressure is plotted with respect to time (t) in the spontaneously breathing animal.
Figure 9 : Threshold of the adductor reflex is plotted with respect to respiratory phase.
Figure 10 : Threshold of the adductor reflex is plotted with respect to arterial pCO2.
Figure 11 : The increasing pattern of adductor responses (upper) and integrated responses (lower) by 8-Hz stimulation of the superior laryngeal nerve (SLN) (0.6 V, 0.1 msec) under conditions of (a) pCO2 60 mmHg; (b) pCO2 40 mmHg; and (c) pCO2 25 mmHg.
Figure 12 : Threshold of the adductor reflex is plotted with respect to arterial pO2.
Figure 13 : The pattern of adductor responses (upper) and integrated responses (lower) by 8-Hz stimulation of SLN (0.6 V, 0.1 msec) under conditions of (a) pO2 25 mmHg; (b) pO2 100 mmHg; and (c) pO2 150 mmHg.
Figure 14 : Threshold of the adductor reflex is plotted with respect to intrathoracic pressure.
Figure 15 : Influence of body temperature on threshold and latency in (a) 3-week-old puppies; (b) 6-week-old puppies; (c) 12-week-old puppies; (d) adult dogs.
Figure 16 : Influence of body temperature on threshold in four age groups.
Figure 17 : Evoked adductor responses elicited by single-shock stimulation of SLN in (a) 3-week-old puppies; (b) 6-week-old puppies; (c) 12-week-old puppies; (d) adult dogs. S, stimulus artifact.
Figure 18 : Influence of body temperature on latency in four age groups.
Figure 19 : Laryngeal abductor activity.
Figure 20 : Laryngeal abductor activity.
Figure 21 : Cricothyroid EMG (upper tracing) and phrenic EMG (lower tracing).
Figure 22 : Glottic alteration produced by cricothyroid (CT) and posterior cricoarytenoid action (PCA) alone and in combination.
Figure 23 : Cricothyroid response to mechanical ventilation at rates of (a) 20 per minute, (b) 30 per minute, (c) 40 per minute.
Figure 24 : Duration of positive pressure stimulation determines duration of cricothyroid-evoked activity.
Figure 25 : a: Vagotomy produces spontaneous inspiratory hyperactivity of cricothyroid motoneurons.
Figure 26 : The threshold of cricothyroid elicitation in response to rate of tracheal pressure change measures 30 cmH2O/sec in normocapnia.
Figure 27 : Thyroarytenoid action potentials elicited by single-shock stimuli applied to the ipsilateral superior laryngeal nerve.
Figure 28 : Thyroarytenoid action potentials elicited by repetitive stimulation of ipsilateral superior laryngeal nerve in control dogs.
Figure 29 : Thyroarytenoid action potentials elicited by superior laryngeal stimulation in tracheostomized dogs.
Figure 30 : Thyroarytenoid action potentials produced by 16-Hz superior laryngeal stimulation in chronically tracheostomized dogs.
Figure 31 : Laryngeal abductor activity 1 week posttracheostomy.
Figure 32 : Laryngeal abductor activity 4 weeks posttracheostomy.
Figure 33 : Placement of pressure transducer.
Figure 34 : Organizational model of the glottic closure reflex pathway demonstrating the effect of a unilateral SLN section.
Figure 35 : Organizational model demonstrating the effect of converting a unilateral recurrent laryngeal nerve (RLN) section (a) to a combined unilateral RLN-superior laryngeal nerve (SLN) section (b) when motor neurons involved ipsilaterally are exceeded by those contralaterally.
Figure 36 : Organizational model demonstrating the effect of converting a unilateral RLN section (a) to a combined unilateral RLN-SLN section (b) when motor neurons involved ipsilaterally are exceeded by those contralaterally.
Figure 37 : Organizational model demonstrating the effect of converting a unilateral RLN section (a) to a combined unilateral RLN-SLN section (b) when motor neurons involved ipsilaterally outnumber those contralaterally.
Anatomy, development, and physiology of the lungs
Figure 1 : Intersection of respiratory and gastrointestinal (GI) tracts.
Figure 2 : Comparison of gills and lungs.
Figure 3 : Schematic diagram of lung anatomy with cross-sections of bronchi, bronchioles alveolar ducts, and alveoli.
Figure 4 : Lung volumes.
Figure 5 : Flow-volume loops.
Figure 6 : Effects of intrathoracic and extrathoracic obstruction on the caliber of airways.
Figure 7 : Dead space.
Figure 8 : Measurement of dead space.
Figure 9 : Oxyhemoglobin curve.
Figure 10 : Effect of shunting.
Figure 11 : The effect of mismatched ventilation
and perfusion 
on arterial oxygenation.Figure 12 : Membrane diffusion.
Electrophysiologic characterization of the swallowing pattern generator in the brainstem
Figure 1 : Swallowing motor pattern and sequential activity of vagal motor fibers in species with striated (a, sheep) or striated and smooth muscle (b, baboon) esophagus.
Figure 2 : Brainstem swallowing sites and activity of swallowing neurons.
Figure 3 : Neuronal swallowing patterns.
Figure 4 : Diagram showing the opposite gradients in the firing frequency and the burst duration of the different types of swallowing neurons.
Figure 5 : Diagram of the oropharyngeal and esophageal circuits.
Figure 6 : Effect of sensory inputs on the burst discharge of swallowing neurons.
Figure 7 : Inhibitory effects on the burst firing of swallowing neurons.
Figure 8 : Activity of cortical neurons during swallowing.
Figure 9 : Possible mechanisms of the swallowing pattern generation.
Figure 10 : Cellular properties of NTS neurons recorded in vitro on rat brainstem slices.
Figure 11 : Schematic representations of the swallowing central pattern generator (CPG).
Neural circuits and mediators regulating swallowing in the brainstem
Figure 1 : Cytodendroarchitecture of the rat ambiguus complex.
Figure 2 : Subnuclear divisions of rat nucleus tractus solitarii (boxed insert) and distribution of central terminals of afferents coursing in the superior laryngeal nerve (SLN).
Figure 3 : Proposed network circuit controlling the oral stage of swallowing.
Figure 4 : Proposed network circuit controlling the pharyngeal stage of swallowing.
Figure 5 : Proposed network circuit controlling the esophageal stage of swallowing.
Figure 6 : Map of deglutitive response loci in the rat NTS as determined by pressure pulse microejection of L-glutamate or excitatory amino acid agonists.
Coordination of respiration and swallowing
Figure 1 : Dorsal and lateral views of the brainstem structures involved in the central control of swallowing.
Figure 2 : Dorsal view of brainstem and cervical spinal cord indicating regions involved in control of breathing and progression of labeling with a viral tracer injected into the phrenic nerve.
Reflex interaction of pharynx, esophagus, and airways
Figure 1 : Relationship of deglutitive vocal cord kinetics to other events of the oropharyngeal phase of swallowing during 5-mL barium swallows.
Figure 2 : An example of vocal cord closure pressure during cough.
Figure 3 : Comparison of intercordal and intratracheal pressure during straining, swallowing, coughing, and phonation.
Figure 4 : Example of intercordal and intratracheal pressure during phonation.
Figure 5 : An example of temporal relationship of deglutitive (10-mL barium swallow) nasopharyngeal closure (NPC) with other swallowing events.
Figure 6 : Upper esophageal sphincter pressure increases in response to gastroesophageal reflux events.
Figure 7 : a: Example of esophagoglottal closure reflex evoked by 20 mL room air injected into mid-esophagus.
Figure 8 : a: Esophagoglottal closure reflex.
Figure 9 : Electromyographic recording from interarytenoid and lateral cricoarytenoid muscles.
Figure 10 : Relationship between the duration of vocal cords closure and magnitude of the esophageal distention by a balloon.
Figure 11 : Effect of pharyngeal water injection on UES resting pressure.
Figure 12 : Pharyngoglottal closure reflex: effect of pharyngeal water stimulation on myoelectrical activity.
Figure 13 : Upper esophageal sphincter pressure response to laryngeal air stimulation.
Figure 14 : Comparison of response/deflection ratio between young and elderly subjects.
Figure 15 : Coordination between the UES and glottal function during belching.
Figure 16 : Inhibition of progressing primary esophageal peristalsis.
Radiographic evaluation of motility of mouth and pharynx
Figure 1 : Lateral sagittal views of the pharynx comparing line drawings with contrast radiographs at rest and during phonation.
Figure 2 : Comparisons between line drawings and radiographs in the coronal (frontal) plane.
Figure 3 : Line drawing of the normal swallow.
Figure 4 : Selected stop-frame prints from a cinepharyngogram demonstrate several stages of a normal swallow.
Figure 5 : Oral decompensations with abnormal retained bolus.
Figure 6 : Weakness of the soft palate.
Figure 7 : Premature leakage.
Figure 8 : Nasopharyngeal regurgitation.
Figure 9 : Multiple abnormalities.
Figure 10 : Pharyngeal paresis.
Figure 11 : Normal epiglottic tilt.
Figure 12 : Laryngeal penetration.
Figure 13 : Aspiration.
Figure 14 : Multiple abnormalities.
Figure 15 : Cricopharyngeal bar with jet phenomenon.
Endoscopic evaluation of oral and pharyngeal phases of swallowing
Figure 1 : Order of events in swallowing.
Figure 2 : a: Supplies needed for a FEES examination. b: Food needed for a fiberoptic endoscopic evaluation of swallowing (FEES) examination.
Figure 3 : Inpatient FEES examination.
Figure 4 : Outpatient FEES examination.
Figure 5 : Photographs of part I findings.
Figure 6 : Nasal regurgitation of liquid.
Figure 7 : Sensitivity of FEES to penetration vs. residue.
Electromyography in oral and pharyngeal motor disorders
Figure 1 : Single motor unit action potential (MUAP).
Figure 2 : Train (MUAPT) of single MUAPs from the thyroarytenoid muscle displayed in Figure 1.
Figure 3 : Firing pattern from a collection of MUAPs from the medial thyroarytenoid muscle.
Figure 4 : Simultaneous EMG recording from the superior pharyngeal constrictor (SPC), thyroarytenoid (TA), interarytenoid (IA), and submental muscles (SM) during swallow.
Figure 5 : Simultaneous EMG recording of two swallows from the superior pharyngeal constrictor (SPC), thyroarytenoid (TA), cricopharyngeus (CP), and submental muscles (SM) during swallow.
Figure 6 : Rectified EMG recording from the superior pharyngeal constrictor muscles of a patient with unilateral pharyngeal paralysis.
Head and neck disorders affecting swallowing
Figure 1 : Laryngeal clefts classification.
Figure 2 : Mechanism of epiglottic downfolding.
Figure 3 : Pharyngeal lye injection.
Figure 4 : Radial artery forearm free flap reconstruction of cervical esophagus.
Figure 5 : Transoral laser assisted cricopharyngeal myotomy.
Figure 6 : Tongue reconstruction with radial forearm free flap.
Figure 7 : Pharyngeal closure with pectoralis major skin and muscle flap.
Figure 8 : Barium swallow study after cranial nerve injury (IX, X, and XII) with asymmetric hyoid elevation.
Figure 9 : Open laryngoplasty to medialize a paralyzed vocal cord.
Figure 10 : Invasive thyroid cancer.
Figure 11 : Laryngopharyngeal candidiasis with characteristic plaques.
Clinical disorders of the upper esophageal sphincter
Figure 1 : Intrabolus pressure and maximal sagittal upper esophageal sphincter (UES) diameter expressed as a function of swallowed bolus volume.
Figure 2 : Barium radiographs of a typical posterior pharyngeal (Zenker's) diverticulum.
Figure 3 : Hypopharyngeal intrabolus pressure is an indirect measure of UES compliance.
Figure 4 : Example of increased hypopharyngeal intrabolus pressure in a patient with Zenker's diverticulum compared with a normal on the left.
Figure 5 : Normal cricopharyngeus muscle (left) compared to that from a patient with Zenker's (right).
Figure 6 : Tracing derived from an ambulatory dual (esophageal, pharyngeal) pH study.
Figure 7 : Two examples from the same patient, showing different patterns of regurgitation.
Figure 8 : Example of esophagopharyngeal regurgitation captured during prolonged manometric and dual pH recording.
Figure 9 : Example of esophagopharyngeal acid regurgitation occurring during a transient UES relaxation, but aided by strain.
Laryngeal and pharyngeal complications of gastroesophageal reflux disease
Figure 1 : Laryngeal granulomas in a patient with numerous episodes of pharyngeal acid exposure and no history of intubation.
Figure 2 : Infraglottic edema: a finding highly sensitive but not specific for laryngopharyngeal reflux (LPR).
Figure 3 : a: Ventricular obliteration is secondary to edema of the true vocal folds and false vocal cords.
Figure 4 : Intraoperative photo of polypoid degenerations of the true vocal folds (Reinke's edema).
Figure 5 : An extraordinary degree of diffuse laryngeal edema is seen in an individual with more than 80 episodes of LPR on pH testing.
Figure 6 : Chronic laryngitis in a patient following radiation therapy for glottic carcinoma.
Figure 7 : a: Histoplasmosis mimicking a squamous cell carcinoma.
Figure 8 : Crusting granulation tissue seen in the larynx and subglottis of a patient with Wegener's granulomatosis.
Figure 9 : A patient with subglottic stenosis with no history of intubation of trauma.
Figure 10 : A nonsmoker with severe pH probe documented LPR and squamous cell carcinoma on both true vocal folds.
Figure 11 : Intraoperative image of a laparoscopic fundoplication.
Gastroesophageal reflux and asthma
Figure 1 : Prevalence of pulmonary diseases in patients referred for hiatal hernia surgery.
Figure 2 : Prevalence of gastroesophageal reflux disease (GERD) in adult asthmatics.
Figure 3 : Prevalence of GERD in adult asthmatics: GERD defined as abnormal acid reflux.
Figure 4 : Prevalence of GERD in adult asthmatics: GERD defined as the presence of esophageal mucosal disease.
Figure 5 : Prevalence of GERD in adult asthmatics: GERD defined as the presence of hiatal hernia.
Figure 6 : Prevalence of GERD in adult asthmatics: GERD defined as the presence of any abnormal reflux parameter.
Figure 7 : Effect of lansoprazole on asthma exacerbations.
Figure 8 : Effect of antireflux surgery on asthma symptoms in adults: 14 studies.
Figure 9 : Overall clinical response of asthma to antireflux therapy.
Surgical intervention and treatment of oral, pharyngeal motor disorders
Figure 1 : Weisberger and Huebsch endolaryngeal stent (Montgomery's stent) for treatment of chronic aspiration.
Figure 2 : Eliachar endolaryngeal stent for treatment of chronic aspiration while allowing phonation.
Figure 3 : Supraglottic closure with epiglottic flap incorporating relaxing incision of epiglottis.
Figure 4 : Biller's tube supraglottic laryngoplasty for supraglottic closure.
Figure 5 : Intraoperative photograph of tubed supraglottic laryngoplasty.
Figure 6 : Tracheoesophageal diversion for subglottic closure and complete separation of the alimentary and respiratory passages.
Figure 7 : Laryngotracheal separation obviating the need for esophageal anastomosis by closure of the proximal tracheal stump.
Figure 8 : Modified tracheoesophageal diversion allowing esophageal anastomosis despite high tracheostomy.
Figure 9 : Appearance of larynx after posterior cricoid resection.
Figure 10 : Partial cricoid resection modification of posterior cricoid resection.
Figure 11 : Subperichondrial cricoidectomy for definitive separation of the upper alimentary and respiratory passages.
Figure 12 : Glottic closure for treatment of chronic aspiration.
Figure 13 : Narrow-field laryngectomy for definitive separation of the upper alimentary and respiratory passages.
Figure 14 : External approach to cricopharyngeal myotomy.
Figure 15 : Method of endoscopic cricopharyngeal myotomy.
Figure 16 : Method of percutaneous endoscopic gastrostomy.
Figure 17 : Radiograph of a Cope loop gastrostomy tube in position within the stomach.
Physiology of esophageal motility
Figure 1 : Esophagus: anatomic considerations.
Figure 2 : Anatomic radiographic landmarks of the lower esophageal sphincter (LES).
Figure 3 : Esophageal wall.
Figure 4 : Neurons in myenteric plexus of human esophagus.
Figure 5 : Parallel inhibitory and excitatory innervation of the esophageal smooth muscle.
Figure 6 : Simultaneous manometry and fluoroscopy of barium swallow in a normal subject.
Figure 7 : Demonstration of deglutitive inhibition in human esophagus.
Figure 8 : Diagramatic representation of manometric tracing demonstrating deglutitive inhibition.
Figure 9 : Peristalsis in striated muscle portion of the esophagus.
Figure 10 : Central control of peristalsis in the smooth muscle portion of the esophagus.
Figure 11 : Gradient of cholinergic excitatory and noncholinergic inhibitory nerves in the smooth muscle portion of the esophagus.
Figure 12 : Three mechanisms involved in the regulation of basal LES tone.
Figure 13 : Lower esophageal sphincter (LES) relaxation is lost in neuronal nitric oxide synthase (nNOS)-deficient mice.
Figure 14 : Neural circuit for transient lower esophageal sphincter relaxation (TLESR) elicited by stimulation of subdiaphragmatic vagal afferents.
Esophagus - anatomy and development
Figure 1 : Primordial gut.
Figure 2 : Arterial blood supply of the esophagus
Figure 3 : Venous drainage of the esophagus
Figure 4 : Parasympathetic and sympathetic innervation of the esophagus
Figure 5 : Lymphatic drainage
Figure 6 : Musculature of the esophagus
Figure 7 : Upper esophageal sphincter and upper esophageal musculature
Figure 8 : Gastroesophageal mucosal junction and muscular arrangement at the lower esophagus
Figure 9 : Diaphragmatic crura and esophageal opening viewed from below (a) and as viewed from above (b).
Figure 10 : Main types of tracheoesophageal fistulae
Esophageal peristalsis
Figure 1 : Primary peristalsis as recorded by an intraluminal manometry catheter.
Figure 2 : Diagrammatic representation of deglutitive inhibition.
Figure 3 : Schematic representation of esophageal contractions.
Figure 4 : Electrical stimulation of intrinsic nerves in circular smooth muscle strips.
Figure 5 : Simultaneous recording of electrical and mechanical activity in opossum smooth muscle esophagus.
Figure 6 : Model showing the marked delay in onset of distal esophageal contractions during peristalsis.
Figure 7 : Evidence of dual innervation of esophageal peristalsis.
Figure 8 : Pathways involved in acetylcholine-induced contraction of esophageal circular smooth muscle.
Sphincter mechanisms at the lower end of the esophagus
Figure 1 : Anatomy of the esophagogastric junction.
Figure 2 : Ultrasonographic images of the esophagus (left) and lower esophageal sphincter (LES, right).
Figure 3 : Esophagogastric junction pressure (EGJP) during diaphragmatic contraction recorded by a reverse perfused sleeve sensor equipped with electrodes to record electromyographic activity of the crural diaphragm.
Figure 4 : Reflex contraction of the esophagogastric junction recorded by a reverse perfused sleeve sensor equipped with electrodes to record crural DEMG activity.
Figure 5 : An example of swallow-induced lower esophageal sphincter (LES) relaxation (left) and transient LES relaxation (right).
Figure 6 : Physiologic record of a spontaneous, transient relaxation of the LES.
Figure 7 : Neural pathways to the LES and crural diaphragm.
Signal transduction in lower esophageal sphincter circular muscle
Figure 1 : Signal transduction for lower esophageal sphincter (LES) contraction in response to agonists.
Figure 2 : Signal transduction for LES tone.
Figure 3 : [3H]Arachidonic acid (AA) content and release of LES and esophageal circular smooth muscle.
Figure 4 : Secreted phospholipase A2 (sPLA2) inhibitors and [3H]AA release and LES tone.
Figure 5 : Cyclooxygenase or lipoxygenase inhibitors and LES basal tone.
Figure 6 : Prostaglandin F2
(PGF2)-induced protein kinase C (PKC) activation in LES tone and sustained contraction.Figure 7 : RhoA in LES tone and PGF2
-induced sustained contraction.Figure 8 : Mitogen-activated protein (MAP) kinases mediate PKC-dependent LES basal tone.
Figure 9 : Protein kinase C (PKC)-mediated contraction of LES circular muscle.
Figure 10 : H2O2 and LES.
Figure 11 : Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in esophagitis.
Figure 12 : An in vitro model of esophagitis.
Figure 13 : H2O2 in LES epithelial and circular muscle cells.
Figure 14 : Release of H2O2 in mucosa supernatant.
Esophageal mucosal defense mechanisms
Figure 1 : Preepithelial defense.
Figure 2 : Epithelial defense.
Figure 3 : Transmission electron micrographs of intercellular spaces.
Figure 4 : Diffusion of refluxed gastric acid (H+) into the intercellular space.
Figure 5 : a: Normal esophageal suction biopsy from a healthy subject without esophagitis.
Esophageal sensory physiology
Figure 1 : Schematic diagram of vagal and spinal nerve supply to the esophagus.
Figure 2 : Confocal photomicrograph of anterogradely labeled intraganglionic laminar ending (IGLE) in the proximal striated part of the esophagus of the rat.
Figure 3 : Confocal photomicrograph of a vagal intramuscular arrays (IMA) nerve terminal in a tangential section of the lower esophageal sphincter of a rat.
Figure 4 : Intensity-dependent response of a vagal afferent fiber to graded esophageal distention (ED, 5–80 mmHg, 30 seconds).
Figure 5 : Comparison of mechanosensitive properties of vagal and spinal afferent fibers innervating the esophagus of opossum (Didelphis virginiana).
Figure 6 : Response of a vagal distention-sensitive afferent fiber to graded esophageal distention (ED) before and after acid infusion.
Figure 7 : Transient receptor potential vanilloid-1 (TRPV1)–like immunoreactivity (TRPV1–IR) in rat nodose ganglia.
Figure 8 : Effect of N-methyl-D-aspartate (NMDA) open channel blocker memantine hydrochloride on mechanotransduction property of an esophageal vagal afferent fiber innervating the esophagus of rat.
Figure 9 : Response characteristics of mucosal mechanosensitive afferent fibers.
Figure 10 : Responses of a distention-responsive upper cervical (C2) spinal neuron having convergent inputs from the cervical and thoracic esophagus.
Figure 11 : Typical firing patterns of three types of neurons in the nucleus tractus solitarius centralis (NTSc) region receiving synaptic input from the vagal afferent fibers.
Esophageal motility disorders
Figure 1 : Pathophysiologic classification of motor disorders of smooth muscle portion of esophagus.
Figure 2 : Motility patterns in esophageal smooth muscle disorders.
Figure 3 : Radiologic appearance of some motor disorders of smooth muscle portion of the esophagus.
Figure 4 : Gross appearance of esophagus in classical achalasia.
Figure 5 : Chest film of a patient with longstanding achalasia.
Figure 6 : Cricopharyngeal contraction in achalasia.
Figure 7 : Illustration of hypotensive (incompetent) peristaltic contractions.
Figure 8 : Three different mechanisms of LES incompetence in gastroesophageal reflux.
Figure 9 : Scleroderma esophagus peptic stenosis as seen in a double-contrast examination of the esophagus.
Heartburn and esophageal pain
Figure 1 : Distribution of acid reflux times in patients with nonerosive esophageal reflux disease (NERD), erosive esophagitis (EE), and Barrett's esophagus (BE).
Figure 2 : Proposed algorithm for defining gastroesophageal reflux disease based on endoscopic findings and the results of pH studies.
Figure 3 : Schematic of visceral pain. Visceral pain is mediated by visceral afferents that are processed in the dorsal root ganglion.
Figure 4 : Latency of cortical responses to painful esophageal stimuli based on neuroanatomy and gender.
Figure 5 : Esophageal wall thickness in patients with chest pain and controls.
Figure 6 : Esophageal pH (a), manometric pressure (b), and esophageal wall thickness (c) as measured by high-frequency intraluminal ultrasound.
Figure 7 : Simultaneous readings of esophageal pH, muscle layer thickness, and manometric pressure in patients with heartburn.
Figure 8 : Schematic of vanilloid receptor 1 (VR1).
Figure 9 : VR1 activation in nerve endings triggers the release of substance P (SP), calcitonin gene-related-peptide (CGRP), and neurokinin A.
Figure 10 : Acid-sensing ion channels (ASIC) function as proton-gated channels.
Figure 11 : Anion-sensing ion channel 1 (ASIC1) is inhibited by amiloride and its derivatives.
Figure 12 : The effect of ketamine on acid-induced pain thresholds in the proximal esophagus and the foot.
Endoscopic evaluation of esophageal motility disorders
Figure 1 : a: Barium esophagram showing a dilated, tortuous esophagus and a "bird's beak" appearance of the lower esophageal sphincter (LES).
Figure 2 : Dilated, fluid-filled esophagus in a patient with achalasia.
Figure 3 : Candida esophagitis in a patient with achalasia.
Figure 4 : Two examples of a puckered lower esophageal sphincter in patients with achalasia.
Figure 5 : Retroflexed view showing a patulous gastroesophageal junction in a patient with scleroderma.
Figure 6 : A fairly normal-appearing esophagus in a patient with symptomatic nutcracker esophagus.
Figure 7 : Several epiphrenic diverticula in a patient with reflux esophagitis and a peptic stricture.
Figure 8 : Zenker's diverticulum.
Figure 9 : Barium x-ray swallowing study showing a large mid-esophageal pulsion diverticulum.
Figure 10 : Multiple esophageal rings.
Figure 11 : Fine circumferential folds, which disappear with continued air insufflation.
Esophageal manometry
Figure 1 : Schematic representation of various options for manometric recording configurations for pharyngoesophageal manometry.
Figure 2 : Normal upper esophageal sphincter (UES) relaxation recorded by a sleeve–side-hole assembly.
Figure 3 : Normal esophageal motility.
Figure 4 : An example of a normal esophageal response to a water swallow displayed as a conventional line plot (left panel) and as a colored topographical plot (right panel).
Figure 5 : Schematic representation of several configurations for esophageal manometric assemblies.
Figure 6 : Schematic depiction of the various elements of pharyngoesophageal motility analysis.
Figure 7 : Recording of pharyngoesophageal motility in a patient with dysphagia due to a cricopharyngeal bar.
Figure 8 : Schematic representation of an approach to the analysis of esophageal manometric recordings.
Figure 9 : Schematic representation of an approach to the analysis of esophageal body motility.
Figure 10 : Representative recording of esophageal motility from a patient with achalasia.
Figure 11 : Representative recording of esophageal motility from a patient with diffuse esophageal spasm. Note the simultaneous pressure in the midesophagus.
Figure 12 : Representative recording of esophageal motility from a patient with a nonspecific esophageal motor disorder.
Figure 13 : Representative recording of esophageal motility from a patient with an isolated abnormality of lower esophageal sphincter (LES) relaxation.
Figure 14 : Representative recording of esophageal motility from a patient with scleroderma.
Gastroesophageal reflux monitoring: pH and impedance
Figure 1 : Ambulatory pH catheter placement.
Figure 2 : Catheter free pH monitoring system (Bravo system).
Figure 3 : Reflux episode identified by pH monitoring as a rapid drop in pH from above to below 4.0 distally longer than proximal.
Figure 4 : Ambulatory pH monitoring tracings.
Figure 5 : Artifacts during pH monitoring.
Figure 6 : Impedance changes produced by liquid, mixed, or gas boluses.
Figure 7 : Direction of intraluminal bolus movement as detected by multichannel intraluminal impedance.
Figure 8 : Combined multichannel intraluminal impedance and pH catheter.
Figure 9 : Gastroesophageal reflux detected by combined multichannel intraluminal impedance and pH (MII-pH) monitoring.
Figure 10 : Suggested diagnostic gastroesophageal reflux disease (GERD) algorithm.
Pathophysiology of gastroesophageal reflux disease
Figure 1 : A simple overview of the pathogenesis of gastroesophageal reflux disease.
Figure 2 : Gastroesophageal reflux disease initiates a vicious cycle of increasing esophageal acid exposure.
Figure 3 : The odds ratio (95% confidence intervals) for prevalence of H. pylori in patients with esophagitis in North America24, 25, 26, 27, 28, 29, 30 and the Far East.19, 20, 21, 22, 23
Figure 4 : The structure of the lower esophageal sphincter (LES).
Figure 5 : Body position and gastroesophageal reflux causing mucosal injury.
Figure 6 : The phrenoesophageal ligament at the gastroesophageal junction in normal and hiatal hernia.
Figure 7 : Attachment of phrenoesophageal ligand to lower esophageal sphincter.
Figure 8 : Duration (% time) of esophageal pH <4 in control subjects and patients with increasing severity of gastroesophageal reflux disease (GERD).
Nonerosive reflux disease
Figure 1 : Phenotypic presentations of gastroesophageal reflux disease (GERD) and the subclassification of nonerosive reflux disease (NERD).
Figure 2 : Natural history of NERD.
Figure 3 : The global distribution of NERD and erosive esophagitis (EE).
Figure 4 : The effectiveness of proton pump inhibitor therapy in NERD as compared to erosive esophagitis (EE).
Figure 5 : The proportion of patients who failed symptomatically proton pump inhibitor (PPI) once daily in each of the GERD groups.
Barrett's adenocarcinoma
Figure 1 : Endoscopic image of Barrett's adenocarcinoma using high-resolution endoscopy.
Figure 2 : Closer view of the nodular mucosa of Barrett's adenocarcinoma (green arrow) using high-resolution endoscopy
Figure 3 : Algorithm for staging and treatment of early cancers.
Figure 4 : Algorithm for staging and treatment of advanced cancers.
Figure 5 : Endoscopic mucosal resection of early Barrett's adenocarcinoma using the banding technique.
Figure 6 : Barrett's adenocarcinoma specimen in situ post–endoscopic mucosal resection.
Figure 7 : Endoscopic picture of the distal esophagus post–endoscopic mucosal resection.
Figure 8 : Specimen retrieval post–endoscopic mucosal resection using a net basket.
Hiatus hernia
Figure 1 : Anatomy of the diaphragmatic hiatus.
Figure 2 : Demonstration of "physiologic herniation" during swallow using endoscopically placed mucosal clips.
Figure 3 : Anatomic features of a sliding hiatus hernia viewed radiographically during swallowing.
Figure 4 : Radiograph of a patient with a small axial hiatal hernia (case 1).
Figure 5 : Radiograph of a patient with a small axial hiatal hernia (case 2).
Figure 6 : Alteration of the hiatal anatomy associated with sliding hiatal hernia.
Figure 7 : Sliding versus paraesophageal hiatal hernia.
Figure 8 : Type I hiatal hernia. In this example, the herniated gastric cardia is evident at rest, after completion of esophageal emptying.
Figure 9 : Three-dimensional representation of the progressive anatomic disruption of the EGJ as occurs with development of a type I hiatus hernia.
Figure 10 : Type II paraesophageal hiatal hernia.
Figure 11 : Organoaxial volvulus.
Figure 12 : Mesenteroaxial volvulus.
Figure 13 : Type III paraesophageal hiatal hernia.
Figure 14 : Computed tomography image through the chest showing a type IV paraesophageal hiatal hernia.
Figure 15 : The "pinchcock" action of the pelvic and crural diaphragms on the alimentary canal as it enters and exits the abdominal cavity.
Figure 16 : Success or failure of individual provocative maneuvers (coughing, leg lifting, abdominal compression, Valsalva) at eliciting gastroesophageal reflux as a function of lower esophageal sphincter (LES) pressure among groups of normal controls, patients without hiatus hernia and patients with radiographically defined hiatus hernia.
Figure 17 : Model of the relationship among lower esophageal sphincter pressure (x axis), size of hernia (y axis), and the susceptibility to gastroesophageal reflux induced by provocative maneuvers that increase abdominal pressure as reflected by the reflux score (z axis).
Figure 18 : Esophagogastric junction high pressure zone relative to the diaphragmatic hiatus.
Figure 19 : Esophagogastric junction (EGJ) opening diameter during deglutitive relaxation.
Figure 20 : Concurrent manometric and videofluorographic recording of a 10-mL barium swallow in a subject with a reducing hiatal hernia characterized by late retrograde flow.
Figure 21 : Concurrent manometric and video recording of a 10-mL barium swallow characterized by early retrograde flow in a subject with a nonreducing hiatal hernia.
Figure 22 : Esophageal emptying results among subject groups based on 10 test swallows.
Figure 23 : Graphic depiction of a radionuclide acid clearance study in a subject with a hiatus hernia.
Figure 24 : Obstruction and entrapment as a complication of type II paraesophageal hernia with an upside-down stomach.
Eosinophilic esophagitis
Figure 1 : Histologic features of eosinophilic esophagitis.
Figure 2 : Comparison of the radiographic, endoscopic, and histologic findings of a child with eosinophilic esophagitis (1a, 1b, 1c) and a child with peptic esophagitis (2a, 2b, 2c).
Figure 3 : Radiographic and endoscopic studies from an 18-year-old woman with a longstanding history of dysphagia that began in early childhood.
Figure 4 : Endoscopic features of eosinophilic esophagitis.
Figure 5 : Esophageal furrow in a 15-year-old boy with dysphagia.
Surgical therapy for gastroesophageal reflux disease
Figure 1 : Opposing sling and clasp muscle fibers. The longitudinal muscle layer of the stomach has been cut away to show the opposing sling and clasp muscle fibers.
Figure 2 : a. An endoscopic view of a 360-degree fundoplication.
Figure 3 : A typical operating room setup for performing laparoscopic antireflux surgery (LARS).
Figure 4 : Nissen fundoplication.
Figure 5 : Intraoperative view of an esophageal perforation.
Figure 6 : The Hill repair.
Figure 7 : Collis gastroplasty.
Figure 8 : Toupet repair.
Figure 9 : Mechanisms of fundoplication failure.
Pathophysiology of achalasia and diffuse esophageal spasm
Figure 1 : Timed barium swallow.
Figure 2 : Esophageal manometric findings in achalasia.
Figure 3 : Contour plot topographic analysis of esophageal motility in achalasia.
Figure 4 : Esophageal manometric findings in vigorous achalasia.
Figure 5 : Esophageal manometric findings in achalasia variant with preserved LES relaxation.
Figure 6 : Histopathology of achalasia.
Figure 7 : In vitro study demonstrating the effects of electrical field stimulation (EFS) on circular muscle strips from the LES of control subjects (a) and patients with achalasia (b).
Figure 8 : a: Effect of nitro-L-arginine methyl ester (L-NAME) on LES relaxation in the opossum in vivo.
Figure 9 : Effect of recombinant hemoglobin that inactivates nitric oxide on esophageal peristalsis in a human subject.
Figure 10 : Pathophysiology of idiopathic achalasia.
Figure 11 : Esophageal manometry in diffuse esophageal spasm.
Figure 12 : Radiographic examination of diffuse esophageal spasm.
Figure 13 : Contour plot topographic analysis of esophageal motility and esophagram in diffuse esophageal spasm.
Figure 14 : Failed deglutitive inhibition in diffuse esophageal spasm.
Oral, pharyngeal and esophageal motility disorders in systemic diseases
Figure 1 : Sclerodactyly in a patient with systemic sclerosis.
Figure 2 : Aperistalsis and diminished lower esophageal sphincter (LES) pressure in a patient with systemic sclerosis.
Figure 3 : Nonspecific esophageal motility disorder in a long-standing diabetic.
Figure 4 : Vigorous achalasia in a patient with seizures and an elevated antineuronal nuclear antibody 1 (ANNA-1).
Pharyngeal and esophageal diverticula, rings, and webs
Figure 1 : Illustration and radiological appearance of Zenker's mid esophageal and epiphrenic esophageal diverticula.
Figure 2 : Barium swallow of a patient with Zenker's diverticulum.
Figure 3 : Barium swallow of a patient with midthoracic or traction diverticulum.
Figure 4 : Barium swallow of a patient with intramural pseudodiverticulosis.
Figure 5 : Endoscopic appearance of Zenker's diverticulum.
Figure 6 : Postendoscopic resection appearance of the Zenker's diverticulum.
Figure 7 : Illustration of A ring (muscular ring) and B ring (Schatzki mucosal ring) in the lower esophagus.
Figure 8 : Barium swallow of a patient with A and B rings of the distal esophagus.
Figure 9 : Barium swallow appearance of esophageal web.
A patient with chronic severe oropharyngeal dysphagia
Figure 1 : Bolus anterior hold position at anterior floor-of-mouth due to lack of tongue control.
Figure 2 : Evidence for lack of glossopalatal seal predisposing premature spill.
Figure 3 : Soft palate not closed with bolus present in pharynx.
Figure 4 : Evidence for trace aspiration anteriorly just below inferior margin of cricoid cartilage.
Figure 5 : Evidence for barium stasis in valleculae and pyriforms (yellow thin arrows).
How to perform esophageal manometry
Figure 1 : Example of lower esophageal sphincter (LES) rapid pull-through technique (1 cm/s).
Figure 2 : Example of station pull-through technique.
Figure 3 : Example of sleeve device properly positioned within the LES.
Figure 4 : Example of the influence of respiration on esophageal, LES, and gastric pressures.
Figure 5 : Examples of esophageal peristalsis and LES relaxation during three swallows each of 5 mL of water.
Figure 6 : Example of a UES pull-through.
Figure 7 : Example of proximal esophageal manometry.
Figure 8 : Example of pull-through technique for positioning the sleeve sensor within the UES.
Figure 9 : Examples of evaluation of swallow-induced UES relaxation using sleeve device.
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