Constipation pathophysiology: Difference between revisions

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=== Colonic Function ===
=== Colonic Function ===
* Water absorbtion
* [[Water absorption]]
** About 1.5 liter fluid is entered the colon from small intestine every day. Colon has to excrete out only 200-400 mL stool.
** About 1.5 liter fluid is entered the [[colon]] from [[small intestine]] every day. [[Colon]] has to excrete out only 200-400 mL [[stool]].
** Colon absorbed water and transit the stool into rectum to store and then expel. The amount of water that is absorbed in rectum is depend of the state of hydration.<ref name=":0">{{cite book | last = Sleisenger | first = Marvin | title = Sleisenger and Fordtran's gastrointestinal and liver disease : pathophysiology, diagnosis, management | publisher = Saunders/Elsevier | location = Philadelphia | year = 2010 | isbn = 9781437727678 }}</ref>
** [[Colon]] absorbed water and transit the [[stool]] into [[rectum]] to store and then expel. The amount of [[water]] that is absorbed in [[rectum]] is depend of the state of [[hydration]].<ref name=":0">{{cite book | last = Sleisenger | first = Marvin | title = Sleisenger and Fordtran's gastrointestinal and liver disease : pathophysiology, diagnosis, management | publisher = Saunders/Elsevier | location = Philadelphia | year = 2010 | isbn = 9781437727678 }}</ref>
** Both sodium and chloride are the key elements in reabsorbing water in colon. The more time stool remained in colon, the drier it can become.<ref name="pmid22114753">{{cite journal| author=Andrews CN, Storr M| title=The pathophysiology of chronic constipation. | journal=Can J Gastroenterol | year= 2011 | volume= 25 Suppl B | issue=  | pages= 16B-21B | pmid=22114753 | doi= | pmc=3206564 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22114753  }}</ref>
** Both [[sodium]] and [[chloride]] are the key elements in reabsorbing [[water]] in [[colon]]. The more time [[stool]] remained in [[colon]], the drier it can become.<ref name="pmid22114753">{{cite journal| author=Andrews CN, Storr M| title=The pathophysiology of chronic constipation. | journal=Can J Gastroenterol | year= 2011 | volume= 25 Suppl B | issue=  | pages= 16B-21B | pmid=22114753 | doi= | pmc=3206564 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22114753  }}</ref>
* Motility
* [[Motility]]
** There are two kinds of gross motility in colon, include:<ref name=":0" />
** There are two kinds of gross [[motility]] in colon, include:<ref name=":0" />
*** Repetitive non-propulsive contractions: The main type of contraction in mixing and absorption of contents
*** Repetitive non-propulsive [[contractions]]: The main type of [[contraction]] in mixing and absorption of contents
*** High-amplitude propagated contractions (HAPCs): Large coordinated contraction in charge of pushing the stool forward. Increased forms are seen in the morning and after drinking or eating.
*** High-amplitude propagated [[contractions]] (HAPCs): Large coordinated [[contraction]] in charge of pushing the [[stool]] forward. Increased forms are seen in the morning and after drinking or eating.
** Normal colonic transition is about 20-72 hours.<ref name="pmid19488763">{{cite journal |vauthors=Southwell BR, Clarke MC, Sutcliffe J, Hutson JM |title=Colonic transit studies: normal values for adults and children with comparison of radiological and scintigraphic methods |journal=Pediatr. Surg. Int. |volume=25 |issue=7 |pages=559–72 |year=2009 |pmid=19488763 |doi=10.1007/s00383-009-2387-x |url=}}</ref>
** Normal colonic transition is about 20-72 hours.<ref name="pmid19488763">{{cite journal |vauthors=Southwell BR, Clarke MC, Sutcliffe J, Hutson JM |title=Colonic transit studies: normal values for adults and children with comparison of radiological and scintigraphic methods |journal=Pediatr. Surg. Int. |volume=25 |issue=7 |pages=559–72 |year=2009 |pmid=19488763 |doi=10.1007/s00383-009-2387-x |url=}}</ref>
** HAPCs are decreased mainly in constipation, maybe as the main pathophysiology.<ref name="pmid19824935">{{cite journal |vauthors=Dinning PG, Smith TK, Scott SM |title=Pathophysiology of colonic causes of chronic constipation |journal=Neurogastroenterol. Motil. |volume=21 Suppl 2 |issue= |pages=20–30 |year=2009 |pmid=19824935 |pmc=2982774 |doi=10.1111/j.1365-2982.2009.01401.x |url=}}</ref>
** HAPCs are decreased mainly in [[constipation]], maybe as the main [[pathophysiology]].<ref name="pmid19824935">{{cite journal |vauthors=Dinning PG, Smith TK, Scott SM |title=Pathophysiology of colonic causes of chronic constipation |journal=Neurogastroenterol. Motil. |volume=21 Suppl 2 |issue= |pages=20–30 |year=2009 |pmid=19824935 |pmc=2982774 |doi=10.1111/j.1365-2982.2009.01401.x |url=}}</ref>
** On molecular basis, the main movements of the gut (peristalsis) are regulated through serotonin (5-hydroxytriptamine [5HT]). 5HT is released from enterochromaffin cells in case bowel wall undergo traction (e.g., due to food or bolus). There are seven subtypes of the 5HT receptors, among which 5HT<sub>4</sub> and 5HT<sub>3</sub> are the most important ones. 5HT<sub>4</sub> is to drive 5HT effect on the gut and 5HT<sub>3</sub> is in charge of bowel sensation.<ref name="pmid16678554">{{cite journal |vauthors=Grundy D, Al-Chaer ED, Aziz Q, Collins SM, Ke M, Taché Y, Wood JD |title=Fundamentals of neurogastroenterology: basic science |journal=Gastroenterology |volume=130 |issue=5 |pages=1391–411 |year=2006 |pmid=16678554 |doi=10.1053/j.gastro.2005.11.060 |url=}}</ref>
** On [[molecular]] basis, the main movements of the [[gut]] ([[peristalsis]]) are regulated through [[serotonin]] ([[5 hydroxytryptamine|5-hydroxytriptamine [5HT]]]). [[5HT]] is released from [[enterochromaffin]] [[cells]] in case [[bowel]] wall undergo traction (e.g., due to food or [[bolus]]). There are seven subtypes of the [[5-HT receptor|5HT receptors]], among which [[5HT4 receptor|5HT<sub>4</sub>]] and [[5-HT receptor|5HT<sub>3</sub>]] are the most important ones. [[5HT4|5HT<sub>4</sub>]] is to drive [[5HT]] effect on the gut and [[5HT|5HT<sub>3</sub>]] is in charge of [[bowel]] sensation.<ref name="pmid16678554">{{cite journal |vauthors=Grundy D, Al-Chaer ED, Aziz Q, Collins SM, Ke M, Taché Y, Wood JD |title=Fundamentals of neurogastroenterology: basic science |journal=Gastroenterology |volume=130 |issue=5 |pages=1391–411 |year=2006 |pmid=16678554 |doi=10.1053/j.gastro.2005.11.060 |url=}}</ref>


=== Defecation ===
=== Defecation ===
* The defecation process is consisted of three important stages, include:<ref name="pmid16771766">{{cite journal |vauthors=Bharucha AE |title=Pelvic floor: anatomy and function |journal=Neurogastroenterol. Motil. |volume=18 |issue=7 |pages=507–19 |year=2006 |pmid=16771766 |doi=10.1111/j.1365-2982.2006.00803.x |url=}}</ref>
* The [[defecation]] process is consisted of three important stages, include:<ref name="pmid16771766">{{cite journal |vauthors=Bharucha AE |title=Pelvic floor: anatomy and function |journal=Neurogastroenterol. Motil. |volume=18 |issue=7 |pages=507–19 |year=2006 |pmid=16771766 |doi=10.1111/j.1365-2982.2006.00803.x |url=}}</ref>
*# Filling of the rectum
*# Filling of the [[rectum]]
*# Feeling the rectum filling
*# Feeling the [[rectum]] filled
*# Relaxation of pelvic floor muscles in a coordinated fashion
*# [[Relaxation]] of [[pelvic floor muscles]] in a coordinated fashion
* Anal sphincters and [[puborectalis]] muscle are anatomical contributors to normal fecal consistency.
* [[Anal sphincter|Anal sphincters]] and [[puborectalis]] [[muscle]] are anatomical contributors to normal [[fecal]] consistency.
* Resting anal sphincter tone is caused by both non-voluntary internal (70%) and voluntary external (30%) anal sphincters tone.
* Resting [[anal sphincter]] tone is caused by both non-voluntary [[Internal anal sphincter|internal]] (70%) and voluntary [[External anal sphincter|external]] (30%) anal [[sphincters]] tone.
* Rectoanal inhibitory reflex (RAIR) is consisted of relaxing the internal anal sphincter in response to rectal distention due to gas or stool. RAIR is completely regulated inside the gut and not controlled by peripheral or central nervous system. Hirschprung's disease is completely ruled out by presence of RAIR.<ref name="pmid22114753" />
* Rectoanal inhibitory reflex (RAIR) is consisted of relaxing the [[internal anal sphincter]] in response to [[rectal]] distention due to gas or [[stool]]. RAIR is completely regulated inside the [[gut]] and not controlled by [[Peripheral nervous system|peripheral]] or [[central nervous system]]. [[Hirschsprung's disease]] is completely ruled out by presence of RAIR.<ref name="pmid22114753" />
* When stool entered in rectum the internal sphincter is relaxed by reflex. If the defecation is inconvenient, the puborectalis muscle is contracted and external sphincter is closed.  In case that defecation is desired, the puborectalis muscle is voluntarily relaxed and external sphincter is opened, therefore defecation would be occurred with [[valsalva maneuver]].<ref name="pmid20601142">{{cite journal |vauthors=Rao SS |title=Advances in diagnostic assessment of fecal incontinence and dyssynergic defecation |journal=Clin. Gastroenterol. Hepatol. |volume=8 |issue=11 |pages=910–9 |year=2010 |pmid=20601142 |pmc=2964406 |doi=10.1016/j.cgh.2010.06.004 |url=}}</ref>
* When [[stool]] entered in [[rectum]] the [[Internal anal sphincter|internal sphincter]] is relaxed by [[reflex]]. If the [[defecation]] is inconvenient, the [[puborectalis muscle]] is contracted and [[External anal sphincter|external sphincter]] is closed.  In case that [[defecation]] is desired, the [[puborectalis muscle]] is voluntarily relaxed and [[External anal sphincter|external sphincter]] is opened, therefore [[defecation]] would be occurred with [[valsalva maneuver]].<ref name="pmid20601142">{{cite journal |vauthors=Rao SS |title=Advances in diagnostic assessment of fecal incontinence and dyssynergic defecation |journal=Clin. Gastroenterol. Hepatol. |volume=8 |issue=11 |pages=910–9 |year=2010 |pmid=20601142 |pmc=2964406 |doi=10.1016/j.cgh.2010.06.004 |url=}}</ref>


=== Pathogenesis ===
=== Pathogenesis ===
* Primary constipation is caused by anorectal and colonic problems, while secondary constipation is caused by organic and metabolic diseases or medications.
* Primary constipation is caused by [[anorectal]] and colonic problems, while secondary constipation is caused by organic and [[metabolic diseases]] or [[medications]].


==== Primary constipation ====
==== Primary constipation ====
* Primary constipation is considered when the secondary causes of constipation became ruled out. Without any certain causes or alarm signs, empiric therapy with dietary fibers and laxatives are administered. If the laxative treatment is successful, there will be no need to additional work up.
* Primary constipation is considered when the secondary causes of [[constipation]] became ruled out. Without any certain causes or alarm signs, [[empiric therapy]] with [[Dietary fiber|dietary fibers]] and [[laxatives]] are administered. If the [[laxative]] treatment is successful, there will be no need to additional work up.
* Colonic transit test is needed if further work up is necessary in constipation. The procedure is consisted of ingestion of marker-contained capsule and taking abdominal X-ray after 120 h (5 days).<ref name="pmid21138500">{{cite journal |vauthors=Rao SS, Camilleri M, Hasler WL, Maurer AH, Parkman HP, Saad R, Scott MS, Simren M, Soffer E, Szarka L |title=Evaluation of gastrointestinal transit in clinical practice: position paper of the American and European Neurogastroenterology and Motility Societies |journal=Neurogastroenterol. Motil. |volume=23 |issue=1 |pages=8–23 |year=2011 |pmid=21138500 |doi=10.1111/j.1365-2982.2010.01612.x |url=}}</ref>
* Colonic transit test is needed if further work up is necessary in constipation. The procedure is consisted of [[ingestion]] of marker-contained capsule and taking [[abdominal X-ray]] after 120 h (5 days).<ref name="pmid21138500">{{cite journal |vauthors=Rao SS, Camilleri M, Hasler WL, Maurer AH, Parkman HP, Saad R, Scott MS, Simren M, Soffer E, Szarka L |title=Evaluation of gastrointestinal transit in clinical practice: position paper of the American and European Neurogastroenterology and Motility Societies |journal=Neurogastroenterol. Motil. |volume=23 |issue=1 |pages=8–23 |year=2011 |pmid=21138500 |doi=10.1111/j.1365-2982.2010.01612.x |url=}}</ref>
* After counting and locating the markers, remaining more than 20% of markers within the colon is defined as slow transit test.
* After counting and locating the markers, remaining more than 20% of markers within the [[colon]] is defined as slow transit [[disease]].
** '''Normal-transit constipation'''
** '''Normal-transit constipation'''
*** The most common form of constipation referred to clinicians is normal transit constipation, which is also known as functional constipation.<ref name="pmid16678561">{{cite journal |vauthors=Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC |title=Functional bowel disorders |journal=Gastroenterology |volume=130 |issue=5 |pages=1480–91 |year=2006 |pmid=16678561 |doi=10.1053/j.gastro.2005.11.061 |url=}}</ref>
*** The most common form of constipation referred to [[clinicians]] is normal transit constipation, which is also known as [[functional constipation]].<ref name="pmid16678561">{{cite journal |vauthors=Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC |title=Functional bowel disorders |journal=Gastroenterology |volume=130 |issue=5 |pages=1480–91 |year=2006 |pmid=16678561 |doi=10.1053/j.gastro.2005.11.061 |url=}}</ref>
*** Most of the times patients experience normal transit time and stool frequency. Most of the times patients meet the criteria for inflammatory bowel syndrome with constipation (IBS-C) or psychological disorders.<ref name="pmid8561138">{{cite journal |vauthors=Ashraf W, Park F, Lof J, Quigley EM |title=An examination of the reliability of reported stool frequency in the diagnosis of idiopathic constipation |journal=Am. J. Gastroenterol. |volume=91 |issue=1 |pages=26–32 |year=1996 |pmid=8561138 |doi= |url=}}</ref>
*** Most of the times patients experience normal transit time and [[stool]] frequency. Most of the times patients meet the criteria for [[Irritable bowel syndrome|irritable bowel syndrome with constipation (IBS-C)]] or [[Psychological|psychological disorders]].<ref name="pmid8561138">{{cite journal |vauthors=Ashraf W, Park F, Lof J, Quigley EM |title=An examination of the reliability of reported stool frequency in the diagnosis of idiopathic constipation |journal=Am. J. Gastroenterol. |volume=91 |issue=1 |pages=26–32 |year=1996 |pmid=8561138 |doi= |url=}}</ref>
*** '''''Rome III criteria''''' for functional constipation is presence of two or more than the followings for ≥ 3 months and onset of ≥ 6 months before diagnosis:<ref name="pmid16305718">{{cite journal |vauthors=Cash BD, Chey WD |title=Review article: The role of serotonergic agents in the treatment of patients with primary chronic constipation |journal=Aliment. Pharmacol. Ther. |volume=22 |issue=11-12 |pages=1047–60 |year=2005 |pmid=16305718 |doi=10.1111/j.1365-2036.2005.02696.x |url=}}</ref>
*** '''''Rome III criteria''''' for [[functional constipation]] is presence of two or more than the followings for ≥ 3 months and onset of ≥ 6 months before [[diagnosis]]:<ref name="pmid16305718">{{cite journal |vauthors=Cash BD, Chey WD |title=Review article: The role of serotonergic agents in the treatment of patients with primary chronic constipation |journal=Aliment. Pharmacol. Ther. |volume=22 |issue=11-12 |pages=1047–60 |year=2005 |pmid=16305718 |doi=10.1111/j.1365-2036.2005.02696.x |url=}}</ref>
**** < 3 defecation per week
**** < 3 [[defecation]] per week
**** Straining during defecation
**** Straining during [[defecation]]
**** Lumpy or hard stool
**** Lumpy or hard stool
**** Sensation if incomplete emptying of rectum
**** Sensation if incomplete emptying of [[rectum]]
**** Sensation of in anorectal obstruction
**** Sensation of in [[anorectal]] obstruction
**** Manual support for defecation
**** Manual evacuation need for defecation
*** Most of the patients are cured with dietary fibers, osmotic laxatives, or enterokinetics.
*** Most of the patients are cured with [[Dietary fiber|dietary fibers]], [[osmotic]] [[laxatives]], or enterokinetics.
** '''Slow-transit constipation'''
** '''Slow-transit constipation'''
*** Slow-transit constipation is consisted of significant decreased number of defecation, less than once a week, mostly involved young women.<ref name="pmid3949236">{{cite journal |vauthors=Preston DM, Lennard-Jones JE |title=Severe chronic constipation of young women: 'idiopathic slow transit constipation' |journal=Gut |volume=27 |issue=1 |pages=41–8 |year=1986 |pmid=3949236 |pmc=1433176 |doi= |url=}}</ref>
*** Slow-transit constipation is consisted of significant decreased number of [[Defecation|defecations]], less than once a week, which mostly involve young women.<ref name="pmid3949236">{{cite journal |vauthors=Preston DM, Lennard-Jones JE |title=Severe chronic constipation of young women: 'idiopathic slow transit constipation' |journal=Gut |volume=27 |issue=1 |pages=41–8 |year=1986 |pmid=3949236 |pmc=1433176 |doi= |url=}}</ref>
*** The more severe form, called "colonic inertia", is the condition in which eating and prokinetics do not lead to increase motor activity and HAPCs.<ref name="pmid15300885">{{cite journal |vauthors=Bassotti G, Roberto GD, Sediari L, Morelli A |title=Toward a definition of colonic inertia |journal=World J. Gastroenterol. |volume=10 |issue=17 |pages=2465–7 |year=2004 |pmid=15300885 |pmc=4572142 |doi= |url=}}</ref>
*** The more severe form, called "colonic inertia", is the condition in which eating and [[Prokinetic|prokinetics]] do not lead to increase motor activity and HAPCs.<ref name="pmid15300885">{{cite journal |vauthors=Bassotti G, Roberto GD, Sediari L, Morelli A |title=Toward a definition of colonic inertia |journal=World J. Gastroenterol. |volume=10 |issue=17 |pages=2465–7 |year=2004 |pmid=15300885 |pmc=4572142 |doi= |url=}}</ref>
*** It is postulated that slow-transit constipation is due to decreased number of interstitial cells of Cajal (ICC) and alteration of myenteric plexus neurons which secret substance P.<ref name="pmid10611149">{{cite journal |vauthors=He CL, Burgart L, Wang L, Pemberton J, Young-Fadok T, Szurszewski J, Farrugia G |title=Decreased interstitial cell of cajal volume in patients with slow-transit constipation |journal=Gastroenterology |volume=118 |issue=1 |pages=14–21 |year=2000 |pmid=10611149 |doi= |url=}}</ref> cv<ref name="pmid8980942">{{cite journal |vauthors=Tzavella K, Riepl RL, Klauser AG, Voderholzer WA, Schindlbeck NE, Müller-Lissner SA |title=Decreased substance P levels in rectal biopsies from patients with slow transit constipation |journal=Eur J Gastroenterol Hepatol |volume=8 |issue=12 |pages=1207–11 |year=1996 |pmid=8980942 |doi= |url=}}</ref>
*** It is postulated that slow-transit constipation is due to decreased number of [[Interstitial cells of Cajal|interstitial cells of Cajal (ICC)]] and alteration of [[Myenteric plexus|myenteric plexus neurons]] which secret [[substance P]].<ref name="pmid10611149">{{cite journal |vauthors=He CL, Burgart L, Wang L, Pemberton J, Young-Fadok T, Szurszewski J, Farrugia G |title=Decreased interstitial cell of cajal volume in patients with slow-transit constipation |journal=Gastroenterology |volume=118 |issue=1 |pages=14–21 |year=2000 |pmid=10611149 |doi= |url=}}</ref><ref name="pmid8980942">{{cite journal |vauthors=Tzavella K, Riepl RL, Klauser AG, Voderholzer WA, Schindlbeck NE, Müller-Lissner SA |title=Decreased substance P levels in rectal biopsies from patients with slow transit constipation |journal=Eur J Gastroenterol Hepatol |volume=8 |issue=12 |pages=1207–11 |year=1996 |pmid=8980942 |doi= |url=}}</ref>
*** Hypoganglionosis, inflammatory neuropathy, and leiomyopathy are other causes of slow-transit constipation.
*** Hypoganglionosis, [[inflammatory]] [[neuropathy]], and leiomyopathy are other causes of slow-transit constipation.
** '''Defecation disorder'''
** '''Defecation disorder'''
*** Straining and spending long times in toilet are the main findings of patients with defecation disorder.
*** Straining and spending long times in toilet are the main findings of patients with [[defecation]] disorder.
*** Patients with defecation disorder often have problems even with liquid and firm stools. Therefore, laxatives are not effective mostly.
*** Patients with [[defecation]] disorder often have problems even with liquid and firm stools. Therefore, [[laxatives]] are not effective mostly.
*** Anorectal manometery and balloon expulsion test are the gold-standard tests for diagnosing functional defecation disorder.<ref name="pmid15984989">{{cite journal |vauthors=Rao SS, Ozturk R, Laine L |title=Clinical utility of diagnostic tests for constipation in adults: a systematic review |journal=Am. J. Gastroenterol. |volume=100 |issue=7 |pages=1605–15 |year=2005 |pmid=15984989 |doi=10.1111/j.1572-0241.2005.41845.x |url=}}</ref>
*** [[Anorectal]] [[Manometry|manometery]] and balloon expulsion test are the [[Gold standard (test)|gold-standard]] tests for diagnosing functional defecation disorder.<ref name="pmid15984989">{{cite journal |vauthors=Rao SS, Ozturk R, Laine L |title=Clinical utility of diagnostic tests for constipation in adults: a systematic review |journal=Am. J. Gastroenterol. |volume=100 |issue=7 |pages=1605–15 |year=2005 |pmid=15984989 |doi=10.1111/j.1572-0241.2005.41845.x |url=}}</ref>
*** Most of the functional defecation disorders are due to dyssynergia. Dyssynergia is an acquired condition due to disorganized toilet habits, pain during defecation, obstetrics and back injuries.<ref name="pmid187939972">{{cite journal |vauthors=Rao SS |title=Dyssynergic defecation and biofeedback therapy |journal=Gastroenterol. Clin. North Am. |volume=37 |issue=3 |pages=569–86, viii |year=2008 |pmid=18793997 |pmc=2575098 |doi=10.1016/j.gtc.2008.06.011 |url=}}</ref>
*** Most of the functional defecation disorders are due to dyssynergia. Dyssynergia is an acquired condition due to disorganized toilet habits, pain during [[defecation]], [[obstetrics]] and back injuries.<ref name="pmid187939972">{{cite journal |vauthors=Rao SS |title=Dyssynergic defecation and biofeedback therapy |journal=Gastroenterol. Clin. North Am. |volume=37 |issue=3 |pages=569–86, viii |year=2008 |pmid=18793997 |pmc=2575098 |doi=10.1016/j.gtc.2008.06.011 |url=}}</ref>
*** The main pathogenesis in dyssynergia is lack of coordination among abdominal, rectoanal, and pelvic floor muscles contractions during defecation process.<ref name="pmid187939972" />
*** The main [[pathogenesis]] in dyssynergia is lack of coordination among [[Abdominal muscles|abdominal]], [[Anorectal|rectoanal]], and [[pelvic floor muscles]] contractions during [[defecation]] process.<ref name="pmid187939972" />
***  
***  


==== Secondary constipation ====
==== Secondary constipation ====
* Most of medications can lead to constipation as a side effect. Therefore, a detailed drug history is needed in every patients with constipation.<ref name="pmid21332973">{{cite journal |vauthors=Fosnes GS, Lydersen S, Farup PG |title=Constipation and diarrhoea - common adverse drug reactions? A cross sectional study in the general population |journal=BMC Clin Pharmacol |volume=11 |issue= |pages=2 |year=2011 |pmid=21332973 |pmc=3049147 |doi=10.1186/1472-6904-11-2 |url=}}</ref><ref name="pmid21194659">{{cite journal |vauthors=Simonson W, Han LF, Davidson HE |title=Hypertension treatment and outcomes in US nursing homes: results from the US National Nursing Home Survey |journal=J Am Med Dir Assoc |volume=12 |issue=1 |pages=44–9 |year=2011 |pmid=21194659 |doi=10.1016/j.jamda.2010.02.009 |url=}}</ref><ref name="pmid20658791">{{cite journal |vauthors=Dolder C, Nelson M, Stump A |title=Pharmacological and clinical profile of newer antidepressants: implications for the treatment of elderly patients |journal=Drugs Aging |volume=27 |issue=8 |pages=625–40 |year=2010 |pmid=20658791 |doi=10.2165/11537140-000000000-00000 |url=}}</ref><ref name="pmid12809835">{{cite journal |vauthors=Talley NJ, Jones M, Nuyts G, Dubois D |title=Risk factors for chronic constipation based on a general practice sample |journal=Am. J. Gastroenterol. |volume=98 |issue=5 |pages=1107–11 |year=2003 |pmid=12809835 |doi=10.1111/j.1572-0241.2003.07465.x |url=}}</ref><ref name="pmid21375137">{{cite journal |vauthors=Rosti G, Gatti A, Costantini A, Sabato AF, Zucco F |title=Opioid-related bowel dysfunction: prevalence and identification of predictive factors in a large sample of Italian patients on chronic treatment |journal=Eur Rev Med Pharmacol Sci |volume=14 |issue=12 |pages=1045–50 |year=2010 |pmid=21375137 |doi= |url=}}</ref>
* Most of [[medications]] can lead to constipation as a [[side effect]]. Therefore, a detailed drug history is needed in every patients with constipation.<ref name="pmid21332973">{{cite journal |vauthors=Fosnes GS, Lydersen S, Farup PG |title=Constipation and diarrhoea - common adverse drug reactions? A cross sectional study in the general population |journal=BMC Clin Pharmacol |volume=11 |issue= |pages=2 |year=2011 |pmid=21332973 |pmc=3049147 |doi=10.1186/1472-6904-11-2 |url=}}</ref><ref name="pmid21194659">{{cite journal |vauthors=Simonson W, Han LF, Davidson HE |title=Hypertension treatment and outcomes in US nursing homes: results from the US National Nursing Home Survey |journal=J Am Med Dir Assoc |volume=12 |issue=1 |pages=44–9 |year=2011 |pmid=21194659 |doi=10.1016/j.jamda.2010.02.009 |url=}}</ref><ref name="pmid20658791">{{cite journal |vauthors=Dolder C, Nelson M, Stump A |title=Pharmacological and clinical profile of newer antidepressants: implications for the treatment of elderly patients |journal=Drugs Aging |volume=27 |issue=8 |pages=625–40 |year=2010 |pmid=20658791 |doi=10.2165/11537140-000000000-00000 |url=}}</ref><ref name="pmid12809835">{{cite journal |vauthors=Talley NJ, Jones M, Nuyts G, Dubois D |title=Risk factors for chronic constipation based on a general practice sample |journal=Am. J. Gastroenterol. |volume=98 |issue=5 |pages=1107–11 |year=2003 |pmid=12809835 |doi=10.1111/j.1572-0241.2003.07465.x |url=}}</ref><ref name="pmid21375137">{{cite journal |vauthors=Rosti G, Gatti A, Costantini A, Sabato AF, Zucco F |title=Opioid-related bowel dysfunction: prevalence and identification of predictive factors in a large sample of Italian patients on chronic treatment |journal=Eur Rev Med Pharmacol Sci |volume=14 |issue=12 |pages=1045–50 |year=2010 |pmid=21375137 |doi= |url=}}</ref>
{| class="wikitable"
{| class="wikitable"
!Group
!Group
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!Alternatives
!Alternatives
|-
|-
| rowspan="3" |'''Antihypertensives'''
| rowspan="3" |'''[[Antihypertensives]]'''
|Clonidine
|[[Clonidine]]
| rowspan="3" |
| rowspan="3" |
* Beta-blockers
* [[Beta-blockers]]
* Angiotensin-converting enzyme inhibitors
* [[Angiotensin-converting enzyme inhibitors]]
* Angiotensin II receptor antagonists
* [[Angiotensin II receptor antagonists]]
|-
|-
|Calcium channel blockers
|[[Calcium channel blockers]]
|-
|-
|Ganglionic blockers
|[[Ganglionic blocker|Ganglionic blockers]]
|-
|-
|'''Antidepressants'''
|'''[[Antidepressants]]'''
|Tricyclic antidepressants
|[[Tricyclic antidepressants]]
|
|
* Selective 5HT reuptake inhibitors  
* [[Selective serotonin reuptake inhibitor|Selective 5HT reuptake inhibitors]]
* 5HT norepinephrine reuptake inhibitors
* [[Serotonin-norepinephrine-dopamine reuptake inhibitor|5HT norepinephrine reuptake inhibitors]]
|-
|-
|'''Cation-containing drugs'''
|'''[[Cations|Cation]]-containing drugs'''
|Oral iron supplementation
|Oral [[iron]] supplementation
|
|
* Intravenous supplementation of iron
* [[Intravenous]] supplementation of [[iron]]
* Addition of a laxative
* Addition of a [[laxative]]
|-
|-
| rowspan="2" |'''Aluminum-containing drugs'''
| rowspan="2" |'''[[Aluminium|Aluminum]]-containing drugs'''
|Sucralfate   
|[[Sucralfate]]  
| rowspan="2" |
| rowspan="2" |
* Proton pump inhibitors
* [[Proton pump inhibitors]]
|-
|-
|Antacids
|[[Antacids]]
|-
|-
| rowspan="2" |'''Analgesics'''
| rowspan="2" |'''[[Analgesics]]'''
|Opiates
|[[Opiates]]
| rowspan="2" |
| rowspan="2" |
* Different class of analgesic drugs  
* Different class of [[analgesic drugs]]
* Using an opiate in combination with a peripherally active opiate receptor antagonist, such as naloxone or methylnaltrexone
* Using an [[opiate]] in combination with a peripherally active [[Opioid antagonist|opiate receptor antagonist]], such as [[naloxone]] or [[methylnaltrexone]]
|-
|-
|Cannabinoids
|[[Cannabinoids]]
|-
|-
| colspan="2" |Anti-Parkinson
| colspan="2" |'''Anti-Parkinson'''
| rowspan="3" |
| rowspan="3" |
* Regular use of laxatives
* Regular use of [[laxatives]]
|-
|-
| colspan="2" |Antiepileptic
| colspan="2" |[[Antiepileptics|'''Antiepileptic''']]
|-
|-
| colspan="2" |Antipsychotic
| colspan="2" |[[Antipsychotic|'''Antipsychotic''']]
|-
|-
| colspan="2" |Antihistamines
| colspan="2" |[[Antihistamines|'''Antihistamines''']]
| rowspan="3" |
| rowspan="3" |
* Replaced with other groups
* Replaced with other groups
|-
|-
| colspan="2" |Antispasmodics
| colspan="2" |[[Antispasmodics|'''Antispasmodics''']]
|-
|-
| colspan="2" |Vinca alkaloids
| colspan="2" |[[Vinca alkaloids|'''Vinca alkaloids''']]
|}
|}
*  
* [[Diseases]] that disturbed the [[nervous system]] may lead to constipation, such as [[diabetes mellitus]], [[autonomic neuropathy]], [[Chagas' disease]], and [[Hirschsprung's disease]].
*
* Both [[hyperglycemia]] and [[hypoglycemia]] can lead to [[bowel movement]] disturbance and constipation.<ref name="pmid12594591">{{cite journal |vauthors=Takahashi T, Matsuda K, Kono T, Pappas TN |title=Inhibitory effects of hyperglycemia on neural activity of the vagus in rats |journal=Intensive Care Med |volume=29 |issue=2 |pages=309–11 |year=2003 |pmid=12594591 |doi=10.1007/s00134-002-1580-3 |url=}}</ref>
*
*
* '''Hardening of the feces''': Improper [[mastication]], low [[dietary fiber]], [[dehydration]] and medications ([[aluminium]], [[calcium]], [[diuretic]], [[iron]]).
* '''Paralysis or slowed transit''': [[Hypothyroidism]], [[hypokalemia]], injured [[Anus|anal sphincter]], medications ([[loperamide]], [[codeine]], [[morphine]], [[tricyclic antidepressants]]) and severe systemic illness due to other causes.
* '''Constriction, where part of the intestine or rectum is narrowed or blocked''': [[Diverticulosis]], [[pelvic masses]] and [[stenosis]].
* '''Psychosomatic constipation''': [[Functional constipation]] and [[irritable bowel syndrome]].<ref>{{cite journal |author=Caldarella MP, Milano A, Laterza F, ''et al'' |title=Visceral sensitivity and symptoms in patients with constipation- or diarrhea-predominant irritable bowel syndrome (IBS): effect of a low-fat intraduodenal infusion |journal=Am. J. Gastroenterol. |volume=100 |issue=2 |pages=383–9 |year=2005 |pmid=15667496 |doi=10.1111/j.1572-0241.2005.40100.x}}</ref>
*
 
*


==Genetics==
==Genetics==

Revision as of 19:33, 17 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]

Overview

The underlying pathophysiology of constipation involves several processes such as hardening of the stool, paralysis or slow transit, constriction in the lower gastrointestinal system or psychomotor factors.

Pathophysiology

Colonic Function

Defecation

Pathogenesis

Primary constipation

Secondary constipation

Group Drug Alternatives
Antihypertensives Clonidine
Calcium channel blockers
Ganglionic blockers
Antidepressants Tricyclic antidepressants
Cation-containing drugs Oral iron supplementation
Aluminum-containing drugs Sucralfate
Antacids
Analgesics Opiates
Cannabinoids
Anti-Parkinson
Antiepileptic
Antipsychotic
Antihistamines
  • Replaced with other groups
Antispasmodics
Vinca alkaloids

Genetics

  • [Disease name] is transmitted in [mode of genetic transmission] pattern.
  • Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
  • The development of [disease name] is the result of multiple genetic mutations.

Associated Conditions

Gross Pathology

  • On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

  • On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

  1. ↑ 1.0 1.1 Sleisenger, Marvin (2010). Sleisenger and Fordtran's gastrointestinal and liver disease : pathophysiology, diagnosis, management. Philadelphia: Saunders/Elsevier. ISBN 9781437727678.
  2. ↑ 2.0 2.1 Andrews CN, Storr M (2011). "The pathophysiology of chronic constipation". Can J Gastroenterol. 25 Suppl B: 16B–21B. PMC 3206564. PMID 22114753.
  3. ↑ Southwell BR, Clarke MC, Sutcliffe J, Hutson JM (2009). "Colonic transit studies: normal values for adults and children with comparison of radiological and scintigraphic methods". Pediatr. Surg. Int. 25 (7): 559–72. doi:10.1007/s00383-009-2387-x. PMID 19488763.
  4. ↑ Dinning PG, Smith TK, Scott SM (2009). "Pathophysiology of colonic causes of chronic constipation". Neurogastroenterol. Motil. 21 Suppl 2: 20–30. doi:10.1111/j.1365-2982.2009.01401.x. PMC 2982774. PMID 19824935.
  5. ↑ Grundy D, Al-Chaer ED, Aziz Q, Collins SM, Ke M, Taché Y, Wood JD (2006). "Fundamentals of neurogastroenterology: basic science". Gastroenterology. 130 (5): 1391–411. doi:10.1053/j.gastro.2005.11.060. PMID 16678554.
  6. ↑ Bharucha AE (2006). "Pelvic floor: anatomy and function". Neurogastroenterol. Motil. 18 (7): 507–19. doi:10.1111/j.1365-2982.2006.00803.x. PMID 16771766.
  7. ↑ Rao SS (2010). "Advances in diagnostic assessment of fecal incontinence and dyssynergic defecation". Clin. Gastroenterol. Hepatol. 8 (11): 910–9. doi:10.1016/j.cgh.2010.06.004. PMC 2964406. PMID 20601142.
  8. ↑ Rao SS, Camilleri M, Hasler WL, Maurer AH, Parkman HP, Saad R, Scott MS, Simren M, Soffer E, Szarka L (2011). "Evaluation of gastrointestinal transit in clinical practice: position paper of the American and European Neurogastroenterology and Motility Societies". Neurogastroenterol. Motil. 23 (1): 8–23. doi:10.1111/j.1365-2982.2010.01612.x. PMID 21138500.
  9. ↑ Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC (2006). "Functional bowel disorders". Gastroenterology. 130 (5): 1480–91. doi:10.1053/j.gastro.2005.11.061. PMID 16678561.
  10. ↑ Ashraf W, Park F, Lof J, Quigley EM (1996). "An examination of the reliability of reported stool frequency in the diagnosis of idiopathic constipation". Am. J. Gastroenterol. 91 (1): 26–32. PMID 8561138.
  11. ↑ Cash BD, Chey WD (2005). "Review article: The role of serotonergic agents in the treatment of patients with primary chronic constipation". Aliment. Pharmacol. Ther. 22 (11–12): 1047–60. doi:10.1111/j.1365-2036.2005.02696.x. PMID 16305718.
  12. ↑ Preston DM, Lennard-Jones JE (1986). "Severe chronic constipation of young women: 'idiopathic slow transit constipation'". Gut. 27 (1): 41–8. PMC 1433176. PMID 3949236.
  13. ↑ Bassotti G, Roberto GD, Sediari L, Morelli A (2004). "Toward a definition of colonic inertia". World J. Gastroenterol. 10 (17): 2465–7. PMC 4572142. PMID 15300885.
  14. ↑ He CL, Burgart L, Wang L, Pemberton J, Young-Fadok T, Szurszewski J, Farrugia G (2000). "Decreased interstitial cell of cajal volume in patients with slow-transit constipation". Gastroenterology. 118 (1): 14–21. PMID 10611149.
  15. ↑ Tzavella K, Riepl RL, Klauser AG, Voderholzer WA, Schindlbeck NE, Müller-Lissner SA (1996). "Decreased substance P levels in rectal biopsies from patients with slow transit constipation". Eur J Gastroenterol Hepatol. 8 (12): 1207–11. PMID 8980942.
  16. ↑ Rao SS, Ozturk R, Laine L (2005). "Clinical utility of diagnostic tests for constipation in adults: a systematic review". Am. J. Gastroenterol. 100 (7): 1605–15. doi:10.1111/j.1572-0241.2005.41845.x. PMID 15984989.
  17. ↑ 17.0 17.1 Rao SS (2008). "Dyssynergic defecation and biofeedback therapy". Gastroenterol. Clin. North Am. 37 (3): 569–86, viii. doi:10.1016/j.gtc.2008.06.011. PMC 2575098. PMID 18793997.
  18. ↑ Fosnes GS, Lydersen S, Farup PG (2011). "Constipation and diarrhoea - common adverse drug reactions? A cross sectional study in the general population". BMC Clin Pharmacol. 11: 2. doi:10.1186/1472-6904-11-2. PMC 3049147. PMID 21332973.
  19. ↑ Simonson W, Han LF, Davidson HE (2011). "Hypertension treatment and outcomes in US nursing homes: results from the US National Nursing Home Survey". J Am Med Dir Assoc. 12 (1): 44–9. doi:10.1016/j.jamda.2010.02.009. PMID 21194659.
  20. ↑ Dolder C, Nelson M, Stump A (2010). "Pharmacological and clinical profile of newer antidepressants: implications for the treatment of elderly patients". Drugs Aging. 27 (8): 625–40. doi:10.2165/11537140-000000000-00000. PMID 20658791.
  21. ↑ Talley NJ, Jones M, Nuyts G, Dubois D (2003). "Risk factors for chronic constipation based on a general practice sample". Am. J. Gastroenterol. 98 (5): 1107–11. doi:10.1111/j.1572-0241.2003.07465.x. PMID 12809835.
  22. ↑ Rosti G, Gatti A, Costantini A, Sabato AF, Zucco F (2010). "Opioid-related bowel dysfunction: prevalence and identification of predictive factors in a large sample of Italian patients on chronic treatment". Eur Rev Med Pharmacol Sci. 14 (12): 1045–50. PMID 21375137.
  23. ↑ Takahashi T, Matsuda K, Kono T, Pappas TN (2003). "Inhibitory effects of hyperglycemia on neural activity of the vagus in rats". Intensive Care Med. 29 (2): 309–11. doi:10.1007/s00134-002-1580-3. PMID 12594591.

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