Irritable bowel syndrome pathophysiology: Difference between revisions

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*'''Intrinsic gastrointestinal factors'''
*'''Intrinsic gastrointestinal factors'''
**'''Motor abnormalities:'''
**'''Motor abnormalities:'''
***IBS is referred to as ‘[[spastic colon]]’ due to changes in [[Colon (anatomy)|colonic]] motor function.
***IBS is referred to as ‘[[spastic colon]]’ due to changes in [[Colon (anatomy)|colonic]] [[Motor coordination|motor]] function.
***Manometry recordings from the [[Transverse colon|transverse]], [[Descending colon|descending]] and [[sigmoid colon]] have shown that IBS leads to changed patterns of [[Colon (anatomy)|colonic]] and [[Small intestine|small intestinal]] motor function, such as increased frequency and irregularity of luminal contractions.
***Manometry recordings from the [[Transverse colon|transverse]], [[Descending colon|descending]] and [[sigmoid colon]] have shown that IBS leads to changed patterns of [[Colon (anatomy)|colonic]] and [[Small intestine|small intestinal]] [[Motor coordination|motor]] function, such as increased frequency and irregularity of [[Lumen|luminal]] contractions.
***Motor changes lead to symptoms of diarrhea and constipation.<ref name="pmid8789897">{{cite journal |vauthors=Schmidt T, Hackelsberger N, Widmer R, Meisel C, Pfeiffer A, Kaess H |title=Ambulatory 24-hour jejunal motility in diarrhea-predominant irritable bowel syndrome |journal=Scand. J. Gastroenterol. |volume=31 |issue=6 |pages=581–9 |year=1996 |pmid=8789897 |doi= |url=}}</ref><ref name="pmid2865504">{{cite journal |vauthors=Kumar D, Wingate DL |title=The irritable bowel syndrome: a paroxysmal motor disorder |journal=Lancet |volume=2 |issue=8462 |pages=973–7 |year=1985 |pmid=2865504 |doi= |url=}}</ref><ref name="pmid11215731">{{cite journal |vauthors=Simrén M, Castedal M, Svedlund J, Abrahamsson H, Björnsson E |title=Abnormal propagation pattern of duodenal pressure waves in the irritable bowel syndrome (IBS) [correction of (IBD)] |journal=Dig. Dis. Sci. |volume=45 |issue=11 |pages=2151–61 |year=2000 |pmid=11215731 |doi= |url=}}</ref>
***[[Muscle|Motor]] changes lead to symptoms of [[diarrhea]] and [[constipation]].<ref name="pmid8789897">{{cite journal |vauthors=Schmidt T, Hackelsberger N, Widmer R, Meisel C, Pfeiffer A, Kaess H |title=Ambulatory 24-hour jejunal motility in diarrhea-predominant irritable bowel syndrome |journal=Scand. J. Gastroenterol. |volume=31 |issue=6 |pages=581–9 |year=1996 |pmid=8789897 |doi= |url=}}</ref><ref name="pmid2865504">{{cite journal |vauthors=Kumar D, Wingate DL |title=The irritable bowel syndrome: a paroxysmal motor disorder |journal=Lancet |volume=2 |issue=8462 |pages=973–7 |year=1985 |pmid=2865504 |doi= |url=}}</ref><ref name="pmid11215731">{{cite journal |vauthors=Simrén M, Castedal M, Svedlund J, Abrahamsson H, Björnsson E |title=Abnormal propagation pattern of duodenal pressure waves in the irritable bowel syndrome (IBS) [correction of (IBD)] |journal=Dig. Dis. Sci. |volume=45 |issue=11 |pages=2151–61 |year=2000 |pmid=11215731 |doi= |url=}}</ref>
***[[Diarrhea]]-prone IBS patients have increased responses to ingestion, [[Corticotropin-releasing hormone|CRH]] (corticotropin releasing hormone), CCK (cholecystokinin), which increase the peak amplitude of high-amplitude propagating contractions (HAPCs)  and lead to abdominal discomfort with accelerated transit through the [[Colon (anatomy)|colon]]. <ref name="pmid11374689">{{cite journal |vauthors=Chey WY, Jin HO, Lee MH, Sun SW, Lee KY |title=Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea |journal=Am. J. Gastroenterol. |volume=96 |issue=5 |pages=1499–506 |year=2001 |pmid=11374689 |doi=10.1111/j.1572-0241.2001.03804.x |url=}}</ref><ref name="pmid7379673">{{cite journal |vauthors=Whitehead WE, Engel BT, Schuster MM |title=Irritable bowel syndrome: physiological and psychological differences between diarrhea-predominant and constipation-predominant patients |journal=Dig. Dis. Sci. |volume=25 |issue=6 |pages=404–13 |year=1980 |pmid=7379673 |doi= |url=}}</ref><ref name="pmid9691924">{{cite journal |vauthors=Fukudo S, Nomura T, Hongo M |title=Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome |journal=Gut |volume=42 |issue=6 |pages=845–9 |year=1998 |pmid=9691924 |pmc=1727153 |doi= |url=}}</ref><ref name="pmid18456567">{{cite journal |vauthors=Camilleri M, McKinzie S, Busciglio I, Low PA, Sweetser S, Burton D, Baxter K, Ryks M, Zinsmeister AR |title=Prospective study of motor, sensory, psychologic, and autonomic functions in patients with irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=6 |issue=7 |pages=772–81 |year=2008 |pmid=18456567 |pmc=2495078 |doi=10.1016/j.cgh.2008.02.060 |url=}}</ref><ref name="pmid3569764">{{cite journal |vauthors=Kellow JE, Phillips SF |title=Altered small bowel motility in irritable bowel syndrome is correlated with symptoms |journal=Gastroenterology |volume=92 |issue=6 |pages=1885–93 |year=1987 |pmid=3569764 |doi= |url=}}</ref>
***[[Diarrhea]]-prone IBS patients have increased responses to [[ingestion]], [[Corticotropin-releasing hormone|CRH]] ([[Corticotropin-releasing hormone|corticotropin releasing hormone]]), [[Cholecystokinin|CCK]] ([[cholecystokinin]]), which increase the peak amplitude of high-amplitude propagating [[Contraction|contractions]] (HAPCs)  and lead to [[Abdominal pain|abdominal discomfort]] with accelerated transit through the [[Colon (anatomy)|colon]]. <ref name="pmid11374689">{{cite journal |vauthors=Chey WY, Jin HO, Lee MH, Sun SW, Lee KY |title=Colonic motility abnormality in patients with irritable bowel syndrome exhibiting abdominal pain and diarrhea |journal=Am. J. Gastroenterol. |volume=96 |issue=5 |pages=1499–506 |year=2001 |pmid=11374689 |doi=10.1111/j.1572-0241.2001.03804.x |url=}}</ref><ref name="pmid7379673">{{cite journal |vauthors=Whitehead WE, Engel BT, Schuster MM |title=Irritable bowel syndrome: physiological and psychological differences between diarrhea-predominant and constipation-predominant patients |journal=Dig. Dis. Sci. |volume=25 |issue=6 |pages=404–13 |year=1980 |pmid=7379673 |doi= |url=}}</ref><ref name="pmid9691924">{{cite journal |vauthors=Fukudo S, Nomura T, Hongo M |title=Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome |journal=Gut |volume=42 |issue=6 |pages=845–9 |year=1998 |pmid=9691924 |pmc=1727153 |doi= |url=}}</ref><ref name="pmid18456567">{{cite journal |vauthors=Camilleri M, McKinzie S, Busciglio I, Low PA, Sweetser S, Burton D, Baxter K, Ryks M, Zinsmeister AR |title=Prospective study of motor, sensory, psychologic, and autonomic functions in patients with irritable bowel syndrome |journal=Clin. Gastroenterol. Hepatol. |volume=6 |issue=7 |pages=772–81 |year=2008 |pmid=18456567 |pmc=2495078 |doi=10.1016/j.cgh.2008.02.060 |url=}}</ref><ref name="pmid3569764">{{cite journal |vauthors=Kellow JE, Phillips SF |title=Altered small bowel motility in irritable bowel syndrome is correlated with symptoms |journal=Gastroenterology |volume=92 |issue=6 |pages=1885–93 |year=1987 |pmid=3569764 |doi= |url=}}</ref>
***[[Constipation]]-prone IBS patients show fewer high-amplitude propagating contractions (HAPCs) as compared to [[diarrhea]] prone IBS patients, delayed transit through the [[Colon (anatomy)|colon]] and decreased motility.  
***[[Constipation]]-prone [[Irritable bowel syndrome|IBS]] patients show fewer high-amplitude propagating [[Contraction|contractions]] (HAPCs) as compared to [[diarrhea]] prone [[Irritable bowel syndrome|IBS]] patients, delayed transit through the [[Colon (anatomy)|colon]] and decreased [[motility]].  
***Changes in the motor function of the [[Colon (anatomy)|colon]] are responsible for producing the gastrointestinal symptoms of IBS such as altered bowel habits and abdominal pain.<ref name="pmid18456567" />
***Changes in the [[Muscle|motor]] function of the [[Colon (anatomy)|colon]] are responsible for producing the [[Gastrointestinal tract|gastrointestinal]] symptoms of [[Irritable bowel syndrome|IBS]] such as altered [[Intestine|bowel]] habits and [[abdominal pain]].<ref name="pmid18456567" />
**'''Visceral hypersensitivity:'''  
**'''Visceral hypersensitivity:'''  
**IBS is associated with a decreased threshold for perception of visceral stimuli (i.e. visceral hypersensitivity).<ref name="pmid18456567" /><ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref><ref name="pmid2323511">{{cite journal |vauthors=Whitehead WE, Holtkotter B, Enck P, Hoelzl R, Holmes KD, Anthony J, Shabsin HS, Schuster MM |title=Tolerance for rectosigmoid distention in irritable bowel syndrome |journal=Gastroenterology |volume=98 |issue=5 Pt 1 |pages=1187–92 |year=1990 |pmid=2323511 |doi= |url=}}</ref>[[Rectum|Rectal]] distension produces painful and non-painful sensations at lower volumes in IBS patients as compared to healthy controls, suggesting the presence of afferent pathway disturbances in visceral innervation<ref name="pmid7797041">{{cite journal |vauthors=Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA |title=Altered rectal perception is a biological marker of patients with irritable bowel syndrome |journal=Gastroenterology |volume=109 |issue=1 |pages=40–52 |year=1995 |pmid=7797041 |doi= |url=}}</ref><ref name="pmid2338274">{{cite journal |vauthors=Prior A, Maxton DG, Whorwell PJ |title=Anorectal manometry in irritable bowel syndrome: differences between diarrhoea and constipation predominant subjects |journal=Gut |volume=31 |issue=4 |pages=458–62 |year=1990 |pmid=2338274 |pmc=1378424 |doi= |url=}}</ref><ref name="pmid17919487">{{cite journal |vauthors=Posserud I, Syrous A, Lindström L, Tack J, Abrahamsson H, Simrén M |title=Altered rectal perception in irritable bowel syndrome is associated with symptom severity |journal=Gastroenterology |volume=133 |issue=4 |pages=1113–23 |year=2007 |pmid=17919487 |doi=10.1053/j.gastro.2007.07.024 |url=}}</ref><ref name="pmid12055583">{{cite journal |vauthors=Bouin M, Plourde V, Boivin M, Riberdy M, Lupien F, Laganière M, Verrier P, Poitras P |title=Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds |journal=Gastroenterology |volume=122 |issue=7 |pages=1771–7 |year=2002 |pmid=12055583 |doi= |url=}}</ref>.  
**IBS is associated with a decreased threshold for perception of [[Viscus|visceral]] stimuli (i.e. [[Viscus|visceral]] [[hypersensitivity]]).<ref name="pmid18456567" /><ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref><ref name="pmid2323511">{{cite journal |vauthors=Whitehead WE, Holtkotter B, Enck P, Hoelzl R, Holmes KD, Anthony J, Shabsin HS, Schuster MM |title=Tolerance for rectosigmoid distention in irritable bowel syndrome |journal=Gastroenterology |volume=98 |issue=5 Pt 1 |pages=1187–92 |year=1990 |pmid=2323511 |doi= |url=}}</ref>[[Rectum|Rectal]] [[distension]] produces painful and non-painful sensations at lower volumes in [[Irritable bowel syndrome|IBS]] patients as compared to healthy controls, suggesting the presence of [[afferent]] pathway disturbances in [[Viscus|visceral]] [[Nerve|innervation]]<ref name="pmid7797041">{{cite journal |vauthors=Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA |title=Altered rectal perception is a biological marker of patients with irritable bowel syndrome |journal=Gastroenterology |volume=109 |issue=1 |pages=40–52 |year=1995 |pmid=7797041 |doi= |url=}}</ref><ref name="pmid2338274">{{cite journal |vauthors=Prior A, Maxton DG, Whorwell PJ |title=Anorectal manometry in irritable bowel syndrome: differences between diarrhoea and constipation predominant subjects |journal=Gut |volume=31 |issue=4 |pages=458–62 |year=1990 |pmid=2338274 |pmc=1378424 |doi= |url=}}</ref><ref name="pmid17919487">{{cite journal |vauthors=Posserud I, Syrous A, Lindström L, Tack J, Abrahamsson H, Simrén M |title=Altered rectal perception in irritable bowel syndrome is associated with symptom severity |journal=Gastroenterology |volume=133 |issue=4 |pages=1113–23 |year=2007 |pmid=17919487 |doi=10.1053/j.gastro.2007.07.024 |url=}}</ref><ref name="pmid12055583">{{cite journal |vauthors=Bouin M, Plourde V, Boivin M, Riberdy M, Lupien F, Laganière M, Verrier P, Poitras P |title=Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds |journal=Gastroenterology |volume=122 |issue=7 |pages=1771–7 |year=2002 |pmid=12055583 |doi= |url=}}</ref>.  
**Visceral hypersensitivity contributes to IBS by involving the following:  
**[[Viscus|Visceral]] [[hypersensitivity]] contributes to [[Irritable bowel syndrome|IBS]] by involving the following:  
**'''[[Spinal cord|Spinal]] hyperexcitability'''
**'''[[Spinal cord|Spinal]] hyperexcitability'''
***Secondary to activation of  neurotransmitters such as:  
***Secondary to activation of  [[Neurotransmitter|neurotransmitters]] such as:  
***[[NMDA receptor|N-methyl D aspartate (NMDA) receptor]]  
***[[NMDA receptor|N-methyl D aspartate (NMDA) receptor]]  
***[[nitric oxide]]   
***[[nitric oxide]]   
**'''Activation of specific gastrointestinal mediators''' that lead to afferent nerve fiber sensitization:
**'''Activation of specific [[Gastrointestinal tract|gastrointestinal]] mediators''' that lead to [[Afferent nerve|afferent]] [[nerve]] fiber sensitization:
***[[kinins]]   
***[[kinins]]   
***[[serotonin]]   
***[[serotonin]]   
**'''Central ([[Brain stem|brainstem]] and [[Cerebral cortex|cortical]]) modulation''' with increased activation of anterior cingulate cortex, [[thalamus]] and [[Insular cortex|insula]].
**'''Central ([[Brain stem|brainstem]] and [[Cerebral cortex|cortical]]) modulation''' with increased activation of anterior [[cingulate cortex]], [[thalamus]] and [[Insular cortex|insula]].
***These structures are involved in processing of pain.   
***These structures are involved in processing of pain.   
***Cortical and brain stem modulation translate into long term hypersensitivity due to neuroplasticity.  
***[[Cortical area|Cortical]] and [[brain stem]] modulation translate into long term hypersensitivity due to [[neuroplasticity]].  
***Semi permanent changes(seen on functional magnetic resonance imaging and positron emission tomography)  in the neural response to visceral stimulation contribute to visceral hypersensitivity.''<ref name="pmid21537962" /><ref name="pmid10784583">{{cite journal |vauthors=Mertz H, Morgan V, Tanner G, Pickens D, Price R, Shyr Y, Kessler R |title=Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention |journal=Gastroenterology |volume=118 |issue=5 |pages=842–8 |year=2000 |pmid=10784583 |doi= |url=}}</ref>  ''  
***Semi permanent changes(seen on functional [[magnetic resonance imaging]] and [[positron emission tomography]])  in the [[Nervous system|neural]] response to [[Viscus|visceral]] stimulation contribute to [[Viscus|visceral]] [[hypersensitivity]].''<ref name="pmid21537962" /><ref name="pmid10784583">{{cite journal |vauthors=Mertz H, Morgan V, Tanner G, Pickens D, Price R, Shyr Y, Kessler R |title=Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention |journal=Gastroenterology |volume=118 |issue=5 |pages=842–8 |year=2000 |pmid=10784583 |doi= |url=}}</ref>  ''  
**'''Recruitment of peripheral silent nociceptors''' cause increased end organ sensitivity due to  
**'''Recruitment of peripheral silent [[Nociceptor|nociceptors]]''' cause increased end [[Organ (anatomy)|organ]] sensitivity due to  
***hormonal activation ( increased serotonin affects gastrointestinal motility and visceral pain perception)  
***[[Hormone|hormonal]] activation ( increased [[serotonin]] affects [[Gastrointestinal tract|gastrointestinal]] [[motility]] and [[Viscus|visceral]] [[pain]] perception)  
***immune activation(recruitment of inflammatory mediators)<ref name="pmid21537962" />  
***[[Immunity (medical)|immune]] activation(recruitment of [[Inflammation|inflammatory]] mediators)<ref name="pmid21537962" />  
{{familytree/start |summary=PE diagnosis Algorithm.}}
{{familytree/start |summary=PE diagnosis Algorithm.}}
{{familytree | | | | | | | | | |,|-| A01 |-| A02 | | | |A01=[[Spinal cord|Spinal]] hyperexcitability |A02= Activation of <br>• [[NMDA receptor|N-methyl D aspartate (NMDA) receptor]] <br>• [[nitric oxide]] }}
{{familytree | | | | | | | | | |,|-| A01 |-| A02 | | | |A01=[[Spinal cord|Spinal]] hyperexcitability |A02= Activation of <br>• [[NMDA receptor|N-methyl D aspartate (NMDA) receptor]] <br>• [[nitric oxide]] }}

Revision as of 23:05, 30 October 2017

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

Overview

IBS is caused by the complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation and psychosocial factors, genetic and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation and mucosal inflammation, altered gut microbiota and abnormal serotonin pathways. Visceral hypersensitivity is a decreased threshold for the perception of visceral stimuli that affects spinal excitability brain stem and cortical modulation, activation of specific gastrointestinal mediators and recruitment of peripheral silent nociceptors. Immune activation and mucosal inflammation involves an interaction of lymphocytes, mast cells and proinflammatory cytokines. Environmental factors encompass dietary changes and infections. Psychosocial factors such as stress, anxiety and depression directly shape adult connectivity in the executive control network consisting of structures such as the insula, anterior cingulate cortex and the thalamus. Semipermanent/permanent changes in complex neural circuits lead to central pain amplification and contribute to abdominal pain in IBS patients. The dorsolateral prefrontal cortex activity (responsible for vigilance and alertness of the human brain) and the mid-cingulate cortex (engaged in attention pathways and responses) is reduced in IBS patients, which may lead to alterations in the subjective sensations of pain. Genetic factors also play a role in IBS. It has high twin concordance and familial aggregation. It is associated with Single nucleotide polymorphisms (SNPs) in genes involved in immune activation, neuropeptide hormone function, oxidative stress, nociception, permeability of the GI tract, host-microbiota interaction, inflammation, and TNF activity.

Pathophysiology

Pathogenesis

IBS is an interplay between four main factors:


 
 
 
 
 
CNS dysregulation and psychosocial factors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intrinsic gastrointestinal factors:
• Motor abnormalities
• Visceral hypersensitivity
• Immune activation and mucosal inflammation
• Altered gut microbiota
• Abnormal serotonin pathways
 
 
IRRITABLE BOWEL SYNDROME
 
 
 
Genetic factors:
• Twin concordance
• Familial aggregation
• Single Nucleotide Polymorphisms(SNPs)
• TNF polymorphism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Environmental factors
 
 
 


 
 
 
 
 
 
 
 
 
 
 
 
Spinal hyperexcitability
 
Activation of
• N-methyl D aspartate (NMDA) receptor
• nitric oxide
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Central (brainstem and cortical) modulation
 
Increased activation of:
• Anterior cingulate cortex
• Thalamus
• insula.
 
 
 
 
 
 
 
 
 
 
 
Visceral hypersensitivity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation of specific gastrointestinal mediators
 
Kinins and serotonin activation lead to afferent nerve fiber sensitization
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Recruitment of peripheral silent nociceptors
 
Increased end organ sensitivity due to hormonal or immune activation
 
 
 
 
 
 




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