Dysphagia pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
=== Physiology of normal swallowing ===
=== Physiology of normal swallowing ===
Anatomically, swallowing can be divided into three phases:<ref name="CookKahrilas1999">{{cite journal|last1=Cook|first1=Ian J.|last2=Kahrilas|first2=Peter J.|title=AGA technical review on management of oropharyngeal dysphagia|journal=Gastroenterology|volume=116|issue=2|year=1999|pages=455–478|issn=00165085|doi=10.1016/S0016-5085(99)70144-7}}</ref><ref name="pmid24772045">{{cite journal| author=Aslam M, Vaezi MF| title=Dysphagia in the elderly. | journal=Gastroenterol Hepatol (N Y) | year= 2013 | volume= 9 | issue= 12 | pages= 784-95 | pmid=24772045 | doi= | pmc=3999993 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24772045  }} </ref><ref name="pmid21915488">{{cite journal| author=Cassiani RA, Santos CM, Parreira LC, Dantas RO| title=The relationship between the oral and pharyngeal phases of swallowing. | journal=Clinics (Sao Paulo) | year= 2011 | volume= 66 | issue= 8 | pages= 1385-8 | pmid=21915488 | doi= | pmc=3161216 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21915488  }} </ref>
Anatomically, swallowing can be divided into three phases:<ref name="CookKahrilas1999">{{cite journal|last1=Cook|first1=Ian J.|last2=Kahrilas|first2=Peter J.|title=AGA technical review on management of oropharyngeal dysphagia|journal=Gastroenterology|volume=116|issue=2|year=1999|pages=455–478|issn=00165085|doi=10.1016/S0016-5085(99)70144-7}}</ref><ref name="pmid24772045">{{cite journal| author=Aslam M, Vaezi MF| title=Dysphagia in the elderly. | journal=Gastroenterol Hepatol (N Y) | year= 2013 | volume= 9 | issue= 12 | pages= 784-95 | pmid=24772045 | doi= | pmc=3999993 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24772045  }} </ref><ref name="pmid21915488">{{cite journal| author=Cassiani RA, Santos CM, Parreira LC, Dantas RO| title=The relationship between the oral and pharyngeal phases of swallowing. | journal=Clinics (Sao Paulo) | year= 2011 | volume= 66 | issue= 8 | pages= 1385-8 | pmid=21915488 | doi= | pmc=3161216 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21915488 }} </ref><ref name="pmid2333995">{{cite journal| author=Dantas RO, Kern MK, Massey BT, Dodds WJ, Kahrilas PJ, Brasseur JG et al.| title=Effect of swallowed bolus variables on oral and pharyngeal phases of swallowing. | journal=Am J Physiol | year= 1990 | volume= 258 | issue= 5 Pt 1 | pages= G675-81 | pmid=2333995 | doi=10.1152/ajpgi.1990.258.5.G675 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2333995 }} </ref>
* Oral preparatory phase
* Oral preparatory phase
* Oral voluntary phase
* Oral voluntary phase

Revision as of 18:07, 29 January 2018

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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. There are a number of causes of different types of dysphagia of which the most common is stroke among the elderly.

Effect of aging on swallowing mechanism

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

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

The following table elaborates 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 Strictures: The following genes can be involved:
  • CTC1
  • DKC1
  • NHP2
  • NOP10
  • RTEL1
  • TERC
  • WRAP53
•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
•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[12] 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

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. 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.
  10. 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.
  11. 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.
  12. 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.

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