Dysphagia pathophysiology: Difference between revisions

Jump to navigation Jump to search
Line 309: Line 309:


===Esophagitis===
===Esophagitis===
[[Image:Eosinophilic esophagiits path.jpg|thumb|centre|150px|[[H&E]] stain of [[esophagus]] [[biopsy]] showing eosinophilic esophagitis, manifested by an infiltration of [[eosinophils]] in the [[lamina propria]]]]
[[Image:Eosinophilic esophagiits path.jpg|thumb|150px|[[H&E]] stain of [[esophagus]] [[biopsy]] showing eosinophilic esophagitis, manifested by an infiltration of [[eosinophils]] in the [[lamina propria]]]]
 
===Esophageal stricture===
===Esophageal stricture===
[[File:Esophagus path.jpg|300px|thumb|centre|Esophageal stricture <"https://commons.wikimedia.org/wiki/File%3ATinci%C3%B3n_hematoxilina-eosina.jpg"> via Wikimedia Commons<nowiki></ref></nowiki>]]
[[File:Esophagus path.jpg|300px|thumb|centre|Esophageal stricture <"https://commons.wikimedia.org/wiki/File%3ATinci%C3%B3n_hematoxilina-eosina.jpg"> via Wikimedia Commons<nowiki></ref></nowiki>]]

Revision as of 18:08, 5 February 2018

Dysphagia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Dysphagia from other Conditions

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Barium Swallow

Endoscopy

CT

MRI

Echocardiography and Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Dysphagia pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Dysphagia pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Dysphagia pathophysiology

CDC on Dysphagia pathophysiology

Dysphagia pathophysiology in the news

Blogs on Dysphagia pathophysiology

Directions to Hospitals Treating Dysphagia

Risk calculators and risk factors for Dysphagia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Overview

Dysphagia can result from propulsive failure, motility disorders, structural disorders, intrinsic or extrinsic compression of the oropharynx or esophagus. Propulsive failure can result from dysfunction of the central nervous system control mechanisms, intrinsic musculature, or peripheral nerves. Structural abnormalities may result from surgery, neoplasm, caustic injury, or congenital anomalies.

Pathophysiology

Physiology of normal swallowing

Anatomically, swallowing can be divided into three phases:[1][2][3][4]

  • Oral preparatory phase
  • Oral voluntary phase
  • Pharyngeal phase
  • Esophageal phase

(a)Oral preparatory phase:

  • This phase involves mastication and formation of a bolus in the oral cavity.

(b)Oral voluntary phase:

  • It is characterized by propelling the bolus into the pharyngeal phase.
  • It is controlled by the corticobulbar tracts and cranial nerves V(trigemenal),VII(facial)and XII(hypoglossal).

(c)Pharyngeal phase:

  • This phase is a reflex
  • It is controlled by the cranial nerves V(trigemenal),X(vagus)XI(accessory) and, XII(hypoglossal).

(d)Esophageal phase:

Pathogenesis of Dysphagia

The pathogenesis of dysphagia can be explained on the basis of etiology. It can be

  • Physiological
  • Pathological

{{#ev:youtube|X4ryV6wGK1Y}}

Effect of aging on swallowing mechanism

Physiological dysphagia

Normal aging results in following changes in the swallowing mechanism:[6][7][8][9][10]

  • Reduced lingual movement
  • Delayed onset of the pharyngeal swallow
  • Delayed upper esophageal sphincter manometric relaxation during swallowing
  • Diminished pharyngolaryngeal sensory discrimination
  • Cerebral atrophy
  • Decreased nerve function
  • Decline in muscle mass

Pathological dysphagia

Following mechanisms can lead to pathological dysphagia.

1.Luminal Stenosis

Esophageal lumen can be narrowed by the following factors:[11][12][13][14]

  • Stricture
  • Inflammation
  • Web
  • Malignancy

2.Non-obstructing gastro-esophageal disease

Many patients that describe dysphagia will have normal investigations including UGE and high-resolution manometry (HRM), suggesting that a dysfunction of the somatosensory as opposed to neuromuscular apparatus might be present[15]

3.Primary motility disorder

The pathophysiological process in primary motility disorder is:

  • An imbalance between inhibitory and excitatory neurons of the myenteric plexus at the distal oesophageal sphincter.
  • There is a decrement in inhibitory innervation (nitrous oxide, or vasoactive intestinal peptide) leading to aperistalsis
  • Failure of relaxation of the lower oesophageal sphincter during swallowing.

4.Rheumatological conditions

The underlying pathophysiological mechanism of dysphagia in rheumatological conditions is as follows:

  • The smooth muscle of the mid and lower oesophagus is replaced by fibrous tissue secondary to the underlying autoimmune pathology leading to incompetence of the lower oesophageal sphincter (LOS) and subsequently to GORD and dysphagia.

Examples:

  • CREST syndrome
  • Sjogren’s syndrome
  • Systemic lupus erythematosus (SLE)
  • Mixed connective tissue disease (MCTD)
  • Rheumatoid arthritis

5.Medication induced

6.Neurological disorders

The following table summarizes the mechanism, genetic association, gross pathology features and microscopic findings of each cause.

Cause of dysphagia Type of food Type of progression Pathophysiological changes Genetic association Gross pathology features Microscopic findings
Oropharyngeal dysphagia Soilds Liquids Intermittent/Progressive
•Zenker's diverticulum

•Webs

Yes No Progressive •Zenker's diverticulum(ZD): Diverticulum or a sac is seen in the esophagus
•Webs
•Neoplasm Yes Yes Progressive •Neoplasm
Myogenic causes

•Myasthenia gravis

•Connective tissue disorder

•Myotonic dystrophy

Neurogenic causes

•ALS

•Parkinsonism

•Stroke

Yes Yes Progressive
Esophageal dysphagia
•Pill esophagitis

•Caustic injury

•Chemotherapy

Yes No
•Strictures

•Esophageal Cancer

Yes No Progressive Esophageal stricture is the result of:[16][17] The following genes can be involved:
  • CTC1
  • DKC1
  • NHP2
  • NOP10
  • RTEL1
  • TERC
  • WRAP53
On gross pathology, circumferential thickening of the lower esophageal wall are characteristic finding of esophageal stricture due to gastroesophageal reflux disease.[18] On microscopic histopathological analysis, characteristic findings of esophageal stricture due to gastroesophageal reflux disease are:[22]
•Esophageal Cancer:

Mutations in the following genes can cause esophageal cancer:

  • Chromosomal losses (4q, 5q, 9p, and 18q)
  • Chromosomal gains (8q, 17q, and 20q)
  • Gene amplifications (7, 8, and 17q)
  • PT53 genes and P16 genes 
  • Variants in ADH and/or ALDH2 genes
Squamous cell carcinoma or adenocarcinoma of the esophagus may appear as:[24]
  • Polypoid lesion 

Nuclear atypia of malignancy:

•Rings

•Webs

Yes No Intermittent Rings:

Webs: Multiple theories have been found:

•Achalasia

•Diffuse esophageal spasm(DES)

Yes Yes Intermittent •Achalasia:
•Diffuse esophageal spasm(DES):
  • Impairment of inhibitory myenteric plexus neurons
  • Dysregulation of endogenous NO synthesis or/and degradation
There is a genetic association between DES and achalasia[29] Gross thickening of muscularis propria layer and lower esophageal sphincter (LES) due to hyperplasia are characteristic findings of DES There is degeneration of vagal fibres, inflammatory infiltration of myenteric plexus, and hyperplasia of smooth muscles are characteristic findings of DES
•Scleroderma Yes Yes Progressive

Gallery

Zenkers diverticulum

Zenkers diverticulumSource: Libre Pathology

Esophageal cancer

Esophageal squamous cell carcinoma by Nephron - Own work BY-SA 3.0
Esophageal adenocarcinoma by Nephron - Own work, CC BY-SA 3.0

Esophagitis

H&E stain of esophagus biopsy showing eosinophilic esophagitis, manifested by an infiltration of eosinophils in the lamina propria

Esophageal stricture

Esophageal stricture <"https://commons.wikimedia.org/wiki/File%3ATinci%C3%B3n_hematoxilina-eosina.jpg"> via Wikimedia Commons</ref>
Esophageal stricture due to GERD, via wikipedia.org[30]

References

  1. Cook, Ian J.; Kahrilas, Peter J. (1999). "AGA technical review on management of oropharyngeal dysphagia". Gastroenterology. 116 (2): 455–478. doi:10.1016/S0016-5085(99)70144-7. ISSN 0016-5085.
  2. Aslam M, Vaezi MF (2013). "Dysphagia in the elderly". Gastroenterol Hepatol (N Y). 9 (12): 784–95. PMC 3999993. PMID 24772045.
  3. Cassiani RA, Santos CM, Parreira LC, Dantas RO (2011). "The relationship between the oral and pharyngeal phases of swallowing". Clinics (Sao Paulo). 66 (8): 1385–8. PMC 3161216. PMID 21915488.
  4. Dantas RO, Kern MK, Massey BT, Dodds WJ, Kahrilas PJ, Brasseur JG; et al. (1990). "Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing". Am J Physiol. 258 (5 Pt 1): G675–81. doi:10.1152/ajpgi.1990.258.5.G675. PMID 2333995.
  5. Stein HJ, DeMeester TR (1992). "Outpatient physiologic testing and surgical management of foregut motility disorders". Curr Probl Surg. 29 (7): 413–555. PMID 1606845.
  6. Masoro EJ (1987). "Biology of aging. Current state of knowledge". Arch Intern Med. 147 (1): 166–9. PMID 3541821.
  7. Carucci LR, Turner MA (2015). "Dysphagia revisited: common and unusual causes". Radiographics. 35 (1): 105–22. doi:10.1148/rg.351130150. PMID 25590391.
  8. Cook IJ, Weltman MD, Wallace K, Shaw DW, McKay E, Smart RC; et al. (1994). "Influence of aging on oral-pharyngeal bolus transit and clearance during swallowing: scintigraphic study". Am J Physiol. 266 (6 Pt 1): G972–7. doi:10.1152/ajpgi.1994.266.6.G972. PMID 8023945.
  9. Shaw DW, Cook IJ, Gabb M, Holloway RH, Simula ME, Panagopoulos V; et al. (1995). "Influence of normal aging on oral-pharyngeal and upper esophageal sphincter function during swallowing". Am J Physiol. 268 (3 Pt 1): G389–96. doi:10.1152/ajpgi.1995.268.3.G389. PMID 7900799.
  10. Easterling, Caryn S.; Robbins, Elizabeth (2008). "Dementia and Dysphagia". Geriatric Nursing. 29 (4): 275–285. doi:10.1016/j.gerinurse.2007.10.015. ISSN 0197-4572.
  11. Starmer HM, Riley LH, Hillel AT, Akst LM, Best SR, Gourin CG (2014). "Dysphagia, short-term outcomes, and cost of care after anterior cervical disc surgery". Dysphagia. 29 (1): 68–77. doi:10.1007/s00455-013-9482-9. PMID 23943072.
  12. Inayat F, Hussain Q, Shafique K (2017). "Dysphagia Caused by Extrinsic Esophageal Compression From Mediastinal Lymphadenopathy in Patients With Sarcoidosis". Clin Gastroenterol Hepatol. 15 (7): e119–e120. doi:10.1016/j.cgh.2016.11.010. PMID 27840183.
  13. Oda K, Iwakiri R, Hara M, Watanabe K, Danjo A, Shimoda R; et al. (2005). "Dysphagia associated with gastroesophageal reflux disease is improved by proton pump inhibitor". Dig Dis Sci. 50 (10): 1921–6. doi:10.1007/s10620-005-2962-5. PMID 16187198.
  14. Roman S, Kahrilas PJ (2014). "The diagnosis and management of hiatus hernia". BMJ. 349: g6154. doi:10.1136/bmj.g6154. PMID 25341679.
  15. Philpott H, Nandurkar S, Royce SG, Thien F, Gibson PR (2014). "Risk factors for eosinophilic esophagitis". Clin Exp Allergy. 44 (8): 1012–9. doi:10.1111/cea.12363. PMID 24990069.
  16. Holzheimer, R (2001). Surgical treatment : evidence-based and problem-oriented. München New York: Zuckschwerdt. ISBN 3-88603-714-2.
  17. Belevich VL, Ovchinnikov DV (2013). "[Treatment of benign esophageal stricture]". Vestn. Khir. Im. I. I. Grek. (in Russian). 172 (5): 111–4. PMID 24640761.
  18. Yamasaki, Yasushi; Ozawa, Soji; Oguma, Junya; Kazuno, Akihito; Ninomiya, Yamato (2016). "Long peptic strictures of the esophagus due to reflux esophagitis: a case report". Surgical Case Reports. 2 (1). doi:10.1186/s40792-016-0190-1. ISSN 2198-7793.
  19. Maejima, Ryuhei; Uno, Kaname; Iijima, Katsunori; Fujishima, Fumiyoshi; Noguchi, Tetsuya; Ara, Nobuyuki; Asano, Naoki; Koike, Tomoyuki; Imatani, Akira; Shimosegawa, Tooru (2016). "A Japanese case of lymphocytic esophagitis". Digestive Endoscopy. 28 (4): 476–480. doi:10.1111/den.12578. ISSN 0915-5635.
  20. Contini, Sandro (2013). "Caustic injury of the upper gastrointestinal tract: A comprehensive review". World Journal of Gastroenterology. 19 (25): 3918. doi:10.3748/wjg.v19.i25.3918. ISSN 1007-9327.
  21. Wilcox CM (2013). "Overview of infectious esophagitis". Gastroenterol Hepatol (N Y). 9 (8): 517–9. PMC 3980995. PMID 24719600.
  22. "Esophageal stricture - Libre Pathology".
  23. Sugarbaker, David (2015). Adult chest surgery. New York: McGraw-Hill Education. ISBN 0071781897.
  24. "Squamous cell carcinoma of the esophagus".
  25. Paladini F, Cocco E, Cascino I, Belfiore F, Badiali D, Piretta L; et al. (2009). "Age-dependent association of idiopathic achalasia with vasoactive intestinal peptide receptor 1 gene". Neurogastroenterol Motil. 21 (6): 597–602. doi:10.1111/j.1365-2982.2009.01284.x. PMID 19309439.
  26. Alahdab YO, Eren F, Giral A, Gunduz F, Kedrah AE, Atug O; et al. (2012). "Preliminary evidence of an association between the functional c-kit rs6554199 polymorphism and achalasia in a Turkish population". Neurogastroenterol Motil. 24 (1): 27–30. doi:10.1111/j.1365-2982.2011.01793.x. PMID 21951831.
  27. de León AR, de la Serna JP, Santiago JL, Sevilla C, Fernández-Arquero M, de la Concha EG; et al. (2010). "Association between idiopathic achalasia and IL23R gene". Neurogastroenterol Motil. 22 (7): 734–8, e218. doi:10.1111/j.1365-2982.2010.01497.x. PMID 20367798.
  28. Frieling T, Berges W, Borchard F, Lübke HJ, Enck P, Wienbeck M (1988). "Family occurrence of achalasia and diffuse spasm of the oesophagus". Gut. 29 (11): 1595–602. PMC 1433819. PMID 3061886.
  29. From en.wikipedia.org, Public Domain, <"https://commons.wikimedia.org/w/index.php?curid=1931423">

Template:WH Template:WS