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==Overview==
==Overview==
The exact pathogenesis of dumping syndrome is not fully understood. Relatively few recent studies have been devoted to elucidating the mechanisms involved in early and late dumping syndromes, and much of our current knowledge is based on older literature<ref name="pmid17859417">{{cite journal |vauthors=Machella TE |title=The Mechanism of the Post-gastrectomy "Dumping" Syndrome |journal=Ann. Surg. |volume=130 |issue=2 |pages=145–59 |year=1949 |pmid=17859417 |pmc=1616289 |doi= |url=}}</ref>. Symptoms of early and late dumping syndrome appear to be caused by distinct pathophysiological mechanisms.
The exact [[pathogenesis]] of dumping syndrome is not completely understood. [[Symptoms]] of early and late dumping syndrome appear to be caused by distinct [[pathological]] mechanisms. The pathogenesis can be divided into accelerated gastric emptying and reduced gastric volume.


==Pathophysiology==
==Pathophysiology==
=== Pathogenesis ===
Dumping syndrome occurs secondary to various conditions such as after [[gastric]] [[surgery]] (especially on taking meals high in [[carbohydrates]] after the procudure), [[diabetes mellitus]], [[Zollinger-Ellison syndrome]], and [[Ehlers-Danlos syndrome]]. The [[pathogenesis]] of dumping syndrome varies according to the [[etiology]] but the most essential component is the rapid gastric emptying. The exact cause is not yet concluded, although several known phenomena may contribute to the development of early dumping [[symptoms]].<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref><ref name="pmid17859417">{{cite journal |vauthors=Machella TE |title=The Mechanism of the Post-gastrectomy "Dumping" Syndrome |journal=Ann. Surg. |volume=130 |issue=2 |pages=145–59 |year=1949 |pmid=17859417 |pmc=1616289 |doi= |url=}}</ref>


===Early dumping===
The main [[pathogenesis]] can be subdivided into the following:
 
* Accelerated [[gastric]] emptying
Although the exact reason isn't yet concluded several known phenomena may contribute to the development of early dumping symptoms<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref>.
* Reduced [[gastric]] volume
* Decreased gastric volume <ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref>
** Due to gastric surgery
* Pyloric Dysfunction<ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref>
** Due to gastric surgery
* Esophageal surgery may also impair gastric retentive capacity because the accompanying vagotomy causes rapid liquid emptying. Hyperosmolar nutrients in the small bowel presumably cause a shift of fluid from the intravascular compartment (i.e. plasma) to the intestinal lumen, resulting in a reduction in plasma volume, tachycardia, and, rarely, syncope. Movement of fluid into the small bowel may also cause distention and contribute to cramp-like contractions, bloating and diarrhoea. Whether this fluid shift contributes to the pathophysiology of dumping syndrome or is mainly a consequence of this process remains unknown. In favour of the latter interpretation, intravenous fluid substitution is not effective in preventing early dumping symptoms<ref name="pmid14452070">{{cite journal |vauthors=JOHNSON LP, SLOOP RD, JESSEPH JE |title=Etiologic significance of the early symptomatic phase in the dumping syndrome |journal=Ann. Surg. |volume=156 |issue= |pages=173–9 |year=1962 |pmid=14452070 |pmc=1466323 |doi= |url=}}</ref>. Another important mechanism involved in the pathophysiology of early dumping syndrome (and also late dumping syndrome as described below) involves the increased release of multiple GI hormones including vasoactive agents (e.g. neurotensin and vasoactive intestinal peptide [VIP]), incretins (e.g. gastric inhibitory polypeptide [GIP] and GLP-1), and glucose modulators (e.g. insulin and glucagon)<ref name="pmid17643905">{{cite journal |vauthors=Tack J |title=Gastric motor disorders |journal=Best Pract Res Clin Gastroenterol |volume=21 |issue=4 |pages=633–44 |year=2007 |pmid=17643905 |doi=10.1016/j.bpg.2007.04.001 |url=}}</ref>. Enhanced release of these GI hormones may induce discoordinated GI motility and inhibit secretion, as well as elicit hemodynamic effects; for example, neurotensin and vasoactive intestinal polypeptide induce splanchnic vasodilation that results in hypotension and systemic hemoconcentration<ref name="pmid3985800">{{cite journal |vauthors=Sirinek KR, O'Dorisio TM, Howe B, McFee AS |title=Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome |journal=Arch Surg |volume=120 |issue=5 |pages=605–9 |year=1985 |pmid=3985800 |doi= |url=}}</ref>.
*
 
===Late dumping===
 
In contrast to the multiple pathophysiologic factors involved in early dumping syndrome, the pathophysiology of late dumping is largely attributable to the development of hyperinsulinemic or reactive hypoglycemia<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref>. Rapid delivery of undigested carbohydrates to the small intestine results in high glucose concentrations that induce a hyperinsulinemic response, resulting in subsequent hypoglycemia and related late dumping symptoms<ref name="pmid1213650">{{cite journal |vauthors=Eloy R, Garaud JC, Moody A, Jaeck D, Grenier JF |title=Jejunal factor stimulating insulin release in the isolated perfused canine pancreas and jejunum |journal=Horm. Metab. Res. |volume=7 |issue=6 |pages=461–7 |year=1975 |pmid=1213650 |doi=10.1055/s-0028-1093704 |url=}}</ref>. Enteral glucose administration is known to induce enhanced insulin release relative to intravenous administration, a process known as the incretin effect. Two GI hormones are believed to play a pivotal role in the incretin effect: glucose-dependent insulinotropic polypeptide or gastric inhibitory polypeptide and GLP-1. An increased GLP-1 response has been reported in patients after gastric surgery, and a positive correlation has been observed between increasing GLP-1 levels and insulin release<ref name="pmid9794105">{{cite journal |vauthors=Toft-Nielsen M, Madsbad S, Holst JJ |title=Exaggerated secretion of glucagon-like peptide-1 (GLP-1) could cause reactive hypoglycaemia |journal=Diabetologia |volume=41 |issue=10 |pages=1180–6 |year=1998 |pmid=9794105 |doi=10.1007/s001250051049 |url=}}</ref>. An additional study suggests that GLP-1 analogues may actually stabilize glucose levels in patients with postprandial hypoglycemia after gastric bypass surgery<ref name="pmid24086087">{{cite journal |vauthors=Abrahamsson N, Engström BE, Sundbom M, Karlsson FA |title=GLP1 analogs as treatment of postprandial hypoglycemia following gastric bypass surgery: a potential new indication? |journal=Eur. J. Endocrinol. |volume=169 |issue=6 |pages=885–9 |year=2013 |pmid=24086087 |doi=10.1530/EJE-13-0504 |url=}}</ref>. Therefore, an exaggerated endogenous GLP-1 response appears to be the key mediator of the hyperinsulinemic and hypoglycemic effect that is characteristic of late dumping syndrome<ref name="pmid24315990">{{cite journal |vauthors=Salehi M, Gastaldelli A, D'Alessio DA |title=Blockade of glucagon-like peptide 1 receptor corrects postprandial hypoglycemia after gastric bypass |journal=Gastroenterology |volume=146 |issue=3 |pages=669–680.e2 |year=2014 |pmid=24315990 |pmc=3943944 |doi=10.1053/j.gastro.2013.11.044 |url=}}</ref>. However, the precise mechanism by which GLP-1 contributes to glucose homeostasis and late dumping syndrome is likely to be complex and remains to be fully elucidated.
 
== Pathogenesis ==
 
=== Provoking factors ===


=== Role of splanchnic vasodilation ===
====Accelerated gastric emptying====
*Alteration of the [[Pylorus|pyloric]] [[muscle]] that holds the [[gastric]] contents till complete digestion, leads to a rapid transit of [[gastric]] contents into the [[small intestine]]. This rapid descent of partially digested food into the intestines causes an [[osmotic]] shift of fluids from the extracellular compartment leading to [[hypotension]] which leads to the activation of the [[sympathetic nervous system]]
*Reactive [[hypoglycemia]] occurs secondary to [[hyperinsulinemia]] caused by high concentration of [[carbohydrates]] in the proximal [[small intestine]] and rapid absorption of [[glucose]] (late dumping)<ref name="pmid1549803">{{cite journal |vauthors=Eagon JC, Miedema BW, Kelly KA |title=Postgastrectomy syndromes |journal=Surg. Clin. North Am. |volume=72 |issue=2 |pages=445–65 |year=1992 |pmid=1549803 |doi= |url=}}</ref><ref name="pmid27487971">{{cite journal |vauthors=Laurenius A, Engström M |title=Early dumping syndrome is not a complication but a desirable feature of Roux-en-Y gastric bypass surgery |journal=Clin Obes |volume=6 |issue=5 |pages=332–40 |year=2016 |pmid=27487971 |doi=10.1111/cob.12158 |url=}}</ref>


=== Rapid emptying of stomach contents ===
*Removal of a part of the [[stomach]] and [[small intestine]] causes the food to bypass the [[stomach]] and rapidly descent through to the [[ileum]] or [[jejunum]] which may lead to [[osmotic]] shifting<ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref>


=== Role of autonomic nervous system ===
*Dumping syndrome is most common in patients with certain types of [[stomach]] surgery, such as a [[gastrectomy]] or [[gastric bypass surgery]], that allow the [[stomach]] to empty rapidly. Dumping syndrome can also occur as a result of complications after a [[cholecystectomy]] ([[gallbladder]] removal)<ref name="pmid14452070">{{cite journal |vauthors=JOHNSON LP, SLOOP RD, JESSEPH JE |title=Etiologic significance of the early symptomatic phase in the dumping syndrome |journal=Ann. Surg. |volume=156 |issue= |pages=173–9 |year=1962 |pmid=14452070 |pmc=1466323 |doi= |url=}}</ref>


=== Changes in serum glucose levels and plasma volume ===
*Patients with [[esophageal cancer]] who undergo [[esophagectomy]] to remove the [[cancerous]] portion of their [[esophagus]] are also at an increased risk of developing dumping syndrome. The [[stomach]] is pulled into the [[chest]] and attached to what remains of the esophagus, leaving a short [[digestive tract]]<ref name="pmid9200302">{{cite journal |vauthors=Vecht J, Masclee AA, Lamers CB |title=The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment |journal=Scand. J. Gastroenterol. Suppl. |volume=223 |issue= |pages=21–7 |year=1997 |pmid=9200302 |doi= |url=}}</ref>


==
==== Reduced gastric volume ====
*Dumping syndrome is most common in patients with certain types of stomach surgery, such as a [https://www.wikidoc.org/index.php/Gastrectomy gastrectomy] or [https://www.wikidoc.org/index.php/Gastric_bypass_surgery gastric bypass surgery], that allow the stomach to empty rapidly. Dumping syndrome can also occur as a result of complications after a [https://www.wikidoc.org/index.php/Cholecystectomy cholecystectomy] (gallbladder removal).[http://www.drdonnica.com/faqs/00007641.htm <nowiki>[1]</nowiki>]
Surgery is one of the major causes leading to a reduced [[gastric]] volume. The following mechanisms lead to the development of dumping syndrome post surgery:<ref name="pmid19724252">{{cite journal |vauthors=Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R |title=Pathophysiology, diagnosis and management of postoperative dumping syndrome |journal=Nat Rev Gastroenterol Hepatol |volume=6 |issue=10 |pages=583–90 |year=2009 |pmid=19724252 |doi=10.1038/nrgastro.2009.148 |url=}}</ref>
* Changes that affect the storage of food in the [[stomach]] or the alteration and manipulation of the [[Pylorus|pyloric muscle]] cuase delivery of [[hyperosmolar]] material into the intestine. Fluid shifts cause rapid [[small bowel]] distention and an increased [[peristalsis]] (early dumping)
* Supraphysiologic release of [[gastrointestinal]] [[peptides]]/[[vasoactive]] mediators lead to paradoxical [[vasodilation]] in a relatively volume-contracted state
* Removal of a part of the [[stomach]] can cause the contents to not digest and flow down undigested. This leads to a large [[hyperosmolar]] load entering into the [[intestines]]. This [[hyperosmolar]] [[chyme]] leads to an [[osmotic]] shift of fluids from the [[vascular]] compartment to the [[intestinal]] [[Lumen (anatomy)|lumen]]. The major sequelae of this is [[hypotension]] and activation of the [[sympathetic nervous system]]
* [[Pancreatic]] [[islet cell]] [[hyperplasia]], rather than late dumping, is thought to be the underlying mechanism for [[hyperinsulinemic hypoglycemia]] with nesidioblastosis after [[gastric bypass]]. These patients do not respond to treatment for dumping syndrome, and it is difficult to confirm this rare diagnosis.
* [[Glucagon-like peptide-1]] ([[Glucagon-like peptide-1|GLP1]]) plays a key role in the [[pathogenesis]] of late [[hypoglycemia]] after [[gastric bypass]]


*Patients with [https://www.wikidoc.org/index.php/Zollinger-Ellison_syndrome Zollinger-Ellison syndrome], a rare disorder involving extreme [https://www.wikidoc.org/index.php/Peptic_ulcer peptic ulcer] disease and [https://www.wikidoc.org/index.php/Gastrin-secreting_tumors gastrin-secreting tumors] in the [https://www.wikidoc.org/index.php/Pancreas pancreas], may also have dumping syndrome.
===Hormones of dumping syndrome===
The following are [[hormonal]] changes occur in dumping syndrome:<ref name="pmid6780101">{{cite journal |vauthors=Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR |title=Release of vasoactive intestinal peptide in the dumping syndrome |journal=Br Med J (Clin Res Ed) |volume=282 |issue=6263 |pages=507–10 |year=1981 |pmid=6780101 |pmc=1504318 |doi= |url=}}</ref><ref name="pmid3726454">{{cite journal |vauthors=Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A |title=Effect of neurotensin in the dumping syndrome |journal=Scand. J. Gastroenterol. |volume=21 |issue=4 |pages=478–82 |year=1986 |pmid=3726454 |doi= |url=}}</ref><ref name="pmid6372067">{{cite journal |vauthors=Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN |title=Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis |journal=Scand. J. Gastroenterol. |volume=18 |issue=1 |pages=73–80 |year=1983 |pmid=6372067 |doi= |url=}}</ref><ref name="pmid11575444">{{cite journal |vauthors=Gebhard B, Holst JJ, Biegelmayer C, Miholic J |title=Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome |journal=Dig. Dis. Sci. |volume=46 |issue=9 |pages=1915–23 |year=2001 |pmid=11575444 |doi= |url=}}</ref><ref name="pmid17643905">{{cite journal |vauthors=Tack J |title=Gastric motor disorders |journal=Best Pract Res Clin Gastroenterol |volume=21 |issue=4 |pages=633–44 |year=2007 |pmid=17643905 |doi=10.1016/j.bpg.2007.04.001 |url=}}</ref><ref name="pmid3985800">{{cite journal |vauthors=Sirinek KR, O'Dorisio TM, Howe B, McFee AS |title=Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome |journal=Arch Surg |volume=120 |issue=5 |pages=605–9 |year=1985 |pmid=3985800 |doi= |url=}}</ref>


*Dumping is also common for [https://www.wikidoc.org/index.php/Esophageal_cancer esophageal cancer] patients who have had an [https://www.wikidoc.org/index.php/Esophagectomy esophagectomy]; surgery to remove the cancerous portion of their esophagus.  The [https://www.wikidoc.org/index.php/Stomach stomach] is pulled into the chest and attached to what remains of the esophagus, leaving a short digestive tract.  Both early and late dumping syndrome can occur.
{| class="wikitable"
! style="background:#4479BA; color: #FFFFFF;" ! |Hormone
! style="background:#4479BA; color: #FFFFFF;" ! |Role
|-
| style="background:#DCDCDC;" align="center" |ANP
|[[Vasoconstriction]]
|-
| style="background:#DCDCDC;" align="center" |[[Gastric inhibitory polypeptide]] ([[Gastric inhibitory polypeptide|GIP]])
|Delays emptying, [[insulin]] secretion
|-
| style="background:#DCDCDC;" align="center" |[[Vasoactive intestinal peptide]] ([[Vasoactive intestinal peptide|VIP]])
|Relaxation of [[gastrointestinal tract]], [[vascular]] relaxation
|-
| style="background:#DCDCDC;" align="center" |[[Glucagon-like peptide-1]] ([[Glucagon-like peptide-1|GLP-1]])
|[[Insulin]] secretion, slows [[Gastrointestinal tract|gastrointestinal]] transit time
|-
| style="background:#DCDCDC;" align="center" |[[Peptide YY]]
|Inhibits [[gastric acid]] secretion, delays emptying
|-
| style="background:#DCDCDC;" align="center" |[[Neurotensin]]
|Relaxation, [[splanchnic]] [[vasodilation]]
|-
| style="background:#DCDCDC;" align="center" |[[Serotonin]]
| -
|}
The following are effects caused by specific [[hormones]]:
{| class="wikitable"
! style="background:#4479BA; color: #FFFFFF;" ! |Effect
! style="background:#4479BA; color: #FFFFFF;" ! |Hormone
|-
| style="background:#DCDCDC;" align="center" |[[Insulin]] secretion
|[[Gastric inhibitory polypeptide|GIP]], [[Glucagon-like peptide-1|GLP-1]]
|-
| style="background:#DCDCDC;" align="center" |[[Vasodilation]]
|[[Neurotensin]], [[Vasoactive intestinal peptide|VIP]]
|-
| style="background:#DCDCDC;" align="center" |Slows [[Gastrointestinal tract|GIT]]
|[[Peptide YY]], [[Vasoactive intestinal peptide|VIP]], [[neurotensin]]
|-
| style="background:#DCDCDC;" align="center" |Inhibits absorption
|[[Vasoactive intestinal peptide|VIP]]
|-
| style="background:#DCDCDC;" align="center" | -
|Serotonin
|}


*Finally, patients with [https://www.wikidoc.org/index.php/Connective_tissue connective tissue] conditions such as [https://www.wikidoc.org/index.php/Ehlers-Danlos_syndrome Ehlers-Danlos syndrome] can experience "late" dumping as a result of decreased motility.
===Approach to pathophysiology of dumping syndrome===


*In addition, people with this syndrome often suffer from low blood sugar, or [https://www.wikidoc.org/index.php/Hypoglycemia hypoglycemia], because the rapid "dumping" of food triggers the [https://www.wikidoc.org/index.php/Pancreas pancreas] to release excessive amounts of [https://www.wikidoc.org/index.php/Insulin insulin] into the bloodstream. This type of hypoglycemia is referred to as "alimentary hypoglycemia".
The following illustraion outlines the major events involved in the [[pathogenesis]] of dumping syndrome (early and late):<ref name="van BeekEmous2017">{{cite journal|last1=van Beek|first1=A. P.|last2=Emous|first2=M.|last3=Laville|first3=M.|last4=Tack|first4=J.|title=Dumping syndrome after esophageal, gastric or bariatric surgery: pathophysiology, diagnosis, and management|journal=Obesity Reviews|volume=18|issue=1|year=2017|pages=68–85|issn=14677881|doi=10.1111/obr.12467}}</ref><ref name="urlwww.practicalgastro.com">{{cite web |url=https://www.practicalgastro.com/pdf/February06/UklejaArticle.pdf |title=www.practicalgastro.com |format= |work= |accessdate=}}</ref>{{Familytree/start}}
<br><br><br>
{{familytree/start}}
{{familytree | | | | | | | | | | | | | | | | A01 | | | | | |A01=Meal (Hyperosmolar)}}
{{familytree | | | | | | | | | | | | | | | | |!| | | | | | | | }}
{{familytree | | | | | | | | | | | | | | | | |)|-|-|-|-|-|-|.| }}
{{familytree | | | | | | | | | | | | | | | | B02 | | | | | B03 |B02=Rapid gastric emptying |B03=Reduced gastric volume}}
{{familytree | | | | | | | | | | | | |,|-|-|-|+|-|-|-|.| | |}}
{{familytree | | | | | | | | | | | | C01 | | C02 | | C03 |C01=Hyperosmolar chyme jejunum |C02=Release of GI hormones |C03=Rapid glucose absorption into blood}}
{{familytree | | | | | | | | | | | | |!| | | |!| | | |!| | }}
{{familytree |boxstyle=text-align: left; | | | | |,|-|-|-|v|-|-|-|(| | | D04 | | |!| | |D04=•VIP<br> ··Vasodilation<br> ··Relaxation of GIT<br> ··Inhibits Absorption<br> •PYY<br> ··Slows GIT<br> •Neurotensin<br> ··Vasodilation (relaxation)<br> •GIP<br> ··Insulin secretion<br> •GLP-1<br> ··Slows GIT<br> ··Insulin secretion<br>}}
{{familytree | | | | D01 | | D02 | | D03 | | |!| | | D05 | |D01=Distention of intestine |D02=Increased contractility |D03=Fluid shift from Blood to GI|D05=Postprandial hyperglycemia}}
{{familytree | | | | |!| | | |!| | |,|^|.| | |!| | | |!| | }}
{{familytree | | | | E01 | | E02 | |!| |!| | E05 | | E06 |E01=•Nausea<br> •Abdominal pain (cramps)<br>|E02=•Diarrhea<br> •Bloating<br> |E05=Systemic and GI symptoms |E06=Increased release of GLP-1}}
{{familytree | | | | | | | | | | | |!| |!| | | | | | |!| | }}
{{familytree | | | | | | | | | | E03 | | E04 | | | | E07 | | | |E03=Peripheral vasodilation |E04= Hypovolemia |E07=Exaggerated insulin release}}
{{familytree | | | | | | | | | | | |!| | |!| | | | | | |!| | }}
{{familytree | | | | | | | | | | F01 | | F02 | | | | F03 | | |F01=Hemoconcentration (Dehydrated blood) |F02=Hypotension |F03=Late reactive hypoglycemia}}
{{familytree | | | | | | | | | | | | |,|-|^|-|.| | | |!| | }}
{{familytree |boxstyle=text-align: left; | | | | | | | | | | | | G01 | | G02 | | G03 | |G01=Increased heart rate |G02=•Decreased ANP<br> •Increased Aldosterone<br> |G03=•Hunger<br> •Tremor<br> •Perspiration<br> }}
{{familytree | | | | | | | | | | | | |!| | | | | | | | | | }}
{{familytree |boxstyle=text-align: left; | | | | | | | | | | | | G04 | | | | | | | | |G04=•Flushing<br> •Dizziness<br> •Palpitations<br> }}
{{Family tree/end}}


== Genetics ==
<br><br>
==== Exceptional diseases ====
There are a few diseases that have a different mechanism compared to conventional [[risk factors]] such as surgery leading to dumping syndrome. The following are the diseases:
*[[Zollinger-Ellison syndrome]]:
**A rare disorder involving extreme [[peptic ulcer]] disease and [[Gastrinoma|gastrin-secreting tumor]]<nowiki/>s in the [[pancreas]], may also have dumping syndrome


== Gross Pathology ==
*[[Connective tissue disease|Connective tissue disorders]] such as [[Ehlers-Danlos syndrome]]
**Can experience "late" dumping as a result of decreased motility.


== Microscopic Pathology ==
*Low [[blood sugar]], or [[hypoglycemia]]:
*  
**Because the rapid "dumping" of food triggers the [[pancreas]] to release excessive amounts of [[insulin]] into the [[bloodstream]]. This type of [[hypoglycemia]] is referred to as "[[Alimentary tract|alimentary]] [[hypoglycemia]]".
*[[Diabetes mellitus|Diabetes]]:
**[[Neuropathy]] can cause damage to the [[nerves]] supplying the [[Gastrointestinal tract|GIT]]


==References==
==References==

Latest revision as of 18:44, 21 December 2017

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

Overview

The exact pathogenesis of dumping syndrome is not completely understood. Symptoms of early and late dumping syndrome appear to be caused by distinct pathological mechanisms. The pathogenesis can be divided into accelerated gastric emptying and reduced gastric volume.

Pathophysiology

Pathogenesis

Dumping syndrome occurs secondary to various conditions such as after gastric surgery (especially on taking meals high in carbohydrates after the procudure), diabetes mellitus, Zollinger-Ellison syndrome, and Ehlers-Danlos syndrome. The pathogenesis of dumping syndrome varies according to the etiology but the most essential component is the rapid gastric emptying. The exact cause is not yet concluded, although several known phenomena may contribute to the development of early dumping symptoms.[1][2]

The main pathogenesis can be subdivided into the following:

Accelerated gastric emptying

Reduced gastric volume

Surgery is one of the major causes leading to a reduced gastric volume. The following mechanisms lead to the development of dumping syndrome post surgery:[5]

Hormones of dumping syndrome

The following are hormonal changes occur in dumping syndrome:[7][8][9][10][11][12]

Hormone Role
ANP Vasoconstriction
Gastric inhibitory polypeptide (GIP) Delays emptying, insulin secretion
Vasoactive intestinal peptide (VIP) Relaxation of gastrointestinal tract, vascular relaxation
Glucagon-like peptide-1 (GLP-1) Insulin secretion, slows gastrointestinal transit time
Peptide YY Inhibits gastric acid secretion, delays emptying
Neurotensin Relaxation, splanchnic vasodilation
Serotonin -

The following are effects caused by specific hormones:

Effect Hormone
Insulin secretion GIP, GLP-1
Vasodilation Neurotensin, VIP
Slows GIT Peptide YY, VIP, neurotensin
Inhibits absorption VIP
- Serotonin

Approach to pathophysiology of dumping syndrome

The following illustraion outlines the major events involved in the pathogenesis of dumping syndrome (early and late):[13][14]




 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Meal (Hyperosmolar)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Rapid gastric emptying
 
 
 
 
Reduced gastric volume
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hyperosmolar chyme jejunum
 
Release of GI hormones
 
Rapid glucose absorption into blood
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
•VIP
··Vasodilation
··Relaxation of GIT
··Inhibits Absorption
•PYY
··Slows GIT
•Neurotensin
··Vasodilation (relaxation)
•GIP
··Insulin secretion
•GLP-1
··Slows GIT
··Insulin secretion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Distention of intestine
 
Increased contractility
 
Fluid shift from Blood to GI
 
 
 
 
 
 
Postprandial hyperglycemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
•Nausea
•Abdominal pain (cramps)
 
•Diarrhea
•Bloating
 
 
 
 
 
 
 
Systemic and GI symptoms
 
Increased release of GLP-1
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Peripheral vasodilation
 
Hypovolemia
 
 
 
Exaggerated insulin release
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hemoconcentration (Dehydrated blood)
 
Hypotension
 
 
 
Late reactive hypoglycemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Increased heart rate
 
•Decreased ANP
•Increased Aldosterone
 
•Hunger
•Tremor
•Perspiration
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
•Flushing
•Dizziness
•Palpitations
 
 
 
 
 
 
 
 



Exceptional diseases

There are a few diseases that have a different mechanism compared to conventional risk factors such as surgery leading to dumping syndrome. The following are the diseases:

References

  1. ↑ 1.0 1.1 Vecht J, Masclee AA, Lamers CB (1997). "The dumping syndrome. Current insights into pathophysiology, diagnosis and treatment". Scand. J. Gastroenterol. Suppl. 223: 21–7. PMID 9200302.
  2. ↑ Machella TE (1949). "The Mechanism of the Post-gastrectomy "Dumping" Syndrome". Ann. Surg. 130 (2): 145–59. PMC 1616289. PMID 17859417.
  3. ↑ Eagon JC, Miedema BW, Kelly KA (1992). "Postgastrectomy syndromes". Surg. Clin. North Am. 72 (2): 445–65. PMID 1549803.
  4. ↑ Laurenius A, Engström M (2016). "Early dumping syndrome is not a complication but a desirable feature of Roux-en-Y gastric bypass surgery". Clin Obes. 6 (5): 332–40. doi:10.1111/cob.12158. PMID 27487971.
  5. ↑ 5.0 5.1 Tack J, Arts J, Caenepeel P, De Wulf D, Bisschops R (2009). "Pathophysiology, diagnosis and management of postoperative dumping syndrome". Nat Rev Gastroenterol Hepatol. 6 (10): 583–90. doi:10.1038/nrgastro.2009.148. PMID 19724252.
  6. ↑ JOHNSON LP, SLOOP RD, JESSEPH JE (1962). "Etiologic significance of the early symptomatic phase in the dumping syndrome". Ann. Surg. 156: 173–9. PMC 1466323. PMID 14452070.
  7. ↑ Sagor GR, Bryant MG, Ghatei MA, Kirk RM, Bloom SR (1981). "Release of vasoactive intestinal peptide in the dumping syndrome". Br Med J (Clin Res Ed). 282 (6263): 507–10. PMC 1504318. PMID 6780101.
  8. ↑ Pedersen JH, Beck H, Shokouh-Amiri M, Fischer A (1986). "Effect of neurotensin in the dumping syndrome". Scand. J. Gastroenterol. 21 (4): 478–82. PMID 3726454.
  9. ↑ Lawaetz O, Blackburn AM, Bloom SR, Aritas Y, Ralphs DN (1983). "Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis". Scand. J. Gastroenterol. 18 (1): 73–80. PMID 6372067.
  10. ↑ Gebhard B, Holst JJ, Biegelmayer C, Miholic J (2001). "Postprandial GLP-1, norepinephrine, and reactive hypoglycemia in dumping syndrome". Dig. Dis. Sci. 46 (9): 1915–23. PMID 11575444.
  11. ↑ Tack J (2007). "Gastric motor disorders". Best Pract Res Clin Gastroenterol. 21 (4): 633–44. doi:10.1016/j.bpg.2007.04.001. PMID 17643905.
  12. ↑ Sirinek KR, O'Dorisio TM, Howe B, McFee AS (1985). "Neurotensin, vasoactive intestinal peptide, and Roux-en-Y gastrojejunostomy. Their role in the dumping syndrome". Arch Surg. 120 (5): 605–9. PMID 3985800.
  13. ↑ van Beek, A. P.; Emous, M.; Laville, M.; Tack, J. (2017). "Dumping syndrome after esophageal, gastric or bariatric surgery: pathophysiology, diagnosis, and management". Obesity Reviews. 18 (1): 68–85. doi:10.1111/obr.12467. ISSN 1467-7881.
  14. ↑ "www.practicalgastro.com" (PDF).

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