Gastric dumping syndrome pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact pathogenesis of dumping syndrome is not completely understood. 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 ===
=== 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, Zolinger-Ellison syndrome, and Ehler-Danlos syndrome. The pathogenesis of dumping syndrome varies according to the etiology but the most essential component is the increased 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>
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>


The main pathogenesis can be subdivided into the following:
The main [[pathogenesis]] can be subdivided into the following:
* Accelerated gastric emptying
* Accelerated [[gastric]] emptying
* Reduced gastric volume
* Reduced [[gastric]] volume


'''Accelerated gastric emptying'''
====Accelerated gastric emptying====
*Alteration of the pyloric muscle that holds the gastric contents till complete digestion, will cause a free fall of gastric contents into the small intestine. This rapid descent will cause an osmotic shift leading to hypotension which will activate the sympathetic nervous system and its associated side effects.
*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>
*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>


*Removal of a part of the stomach and small intestine will cause bypassing of the gastric contents straight through to the ileum or jejunum which can cause rapid descent and 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>
*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>


*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>] <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>
*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>


*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.<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>  
*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 ====
==== Reduced gastric volume ====
Surgery is one of the major causes leading to a reduced 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>
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 in the stomach or the pyloric muscle cuase delivery of hyperosmolar material into the intestine. Fluid shifts cause rapid small bowel distention and an increased peristalsis (early dumping).
* 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 GI peptides/vasoactive mediators lead to paradoxical vasodilation in a relatively volume-contracted state.
* 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 in a hyperosmolar manner. This hyperosmolar chyme will cause an osmotic shift from the blood circulation to the intestinal lumen . This my may cause hypotension which will in turn activate the sympathetic nervous system and its associated side effects.
* 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.
* [[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.
* Glucagonlike peptide-1 (GLP1) plays a key role in the pathogenesis of late hypoglycemia after gastric bypass
* [[Glucagon-like peptide-1]] ([[Glucagon-like peptide-1|GLP1]]) plays a key role in the [[pathogenesis]] of late [[hypoglycemia]] after [[gastric bypass]]


===Hormones of Dumping Syndrome===
===Hormones of dumping syndrome===
The following are hormones and their association with 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>
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>


{| class="wikitable"
{| class="wikitable"
Line 40: Line 40:
|-
|-
| style="background:#DCDCDC;" align="center" |ANP
| style="background:#DCDCDC;" align="center" |ANP
|Vasocontriction
|[[Vasoconstriction]]
|-
|-
| style="background:#DCDCDC;" align="center" |GIP
| style="background:#DCDCDC;" align="center" |[[Gastric inhibitory polypeptide]] ([[Gastric inhibitory polypeptide|GIP]])
|Delays emptying, Insulin secretion
|Delays emptying, [[insulin]] secretion
|-
|-
| style="background:#DCDCDC;" align="center" |VIP
| style="background:#DCDCDC;" align="center" |[[Vasoactive intestinal peptide]] ([[Vasoactive intestinal peptide|VIP]])
|Relaxation of GIT, vascular relaxation
|Relaxation of [[gastrointestinal tract]], [[vascular]] relaxation
|-
|-
| style="background:#DCDCDC;" align="center" |GLP-1
| style="background:#DCDCDC;" align="center" |[[Glucagon-like peptide-1]] ([[Glucagon-like peptide-1|GLP-1]])
|Insulin secretion, Slows GIT
|[[Insulin]] secretion, slows [[Gastrointestinal tract|gastrointestinal]] transit time
|-
|-
| style="background:#DCDCDC;" align="center" |Peptide YY
| style="background:#DCDCDC;" align="center" |[[Peptide YY]]
|Inhibits gastric acid secretion, Delays emptying
|Inhibits [[gastric acid]] secretion, delays emptying
|-
|-
| style="background:#DCDCDC;" align="center" |Neurotensin
| style="background:#DCDCDC;" align="center" |[[Neurotensin]]
|Relaxation, Sphlancnic vasodilation
|Relaxation, [[splanchnic]] [[vasodilation]]
|-
| style="background:#DCDCDC;" align="center" |[[Serotonin]]
| -
|}
|}
The following are effects caused by specific hormones:
The following are effects caused by specific [[hormones]]:
{| class="wikitable"
{| class="wikitable"
! style="background:#4479BA; color: #FFFFFF;" ! |Effect
! style="background:#4479BA; color: #FFFFFF;" ! |Effect
! style="background:#4479BA; color: #FFFFFF;" ! |Hormone
! style="background:#4479BA; color: #FFFFFF;" ! |Hormone
|-
|-
| style="background:#DCDCDC;" align="center" |Insulin secretion
| style="background:#DCDCDC;" align="center" |[[Insulin]] secretion
|GIP, GLP-1
|[[Gastric inhibitory polypeptide|GIP]], [[Glucagon-like peptide-1|GLP-1]]
|-
|-
| style="background:#DCDCDC;" align="center" |Vasodilation
| style="background:#DCDCDC;" align="center" |[[Vasodilation]]
|Neurotensin, VIP
|[[Neurotensin]], [[Vasoactive intestinal peptide|VIP]]
|-
|-
| style="background:#DCDCDC;" align="center" |Slows GIT
| style="background:#DCDCDC;" align="center" |Slows [[Gastrointestinal tract|GIT]]
|PYY, VIP, Neurotensin
|[[Peptide YY]], [[Vasoactive intestinal peptide|VIP]], [[neurotensin]]
|-
|-
| style="background:#DCDCDC;" align="center" |Inhibits absorption
| style="background:#DCDCDC;" align="center" |Inhibits absorption
|VIP
|[[Vasoactive intestinal peptide|VIP]]
|-
| style="background:#DCDCDC;" align="center" | -
|Serotonin
|}
|}


===Approach to Pathophysiology of Dumping Syndrome===
===Approach to pathophysiology of dumping syndrome===


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}}
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><br>
{{familytree/start}}
{{familytree/start}}
{{familytree | | | | | | | | | | | | | | | | A01 | | | | | |A01=Meal (Hyperosmolar)}}
{{familytree | | | | | | | | | | | | | | | | A01 | | | | | |A01=Meal (Hyperosmolar)}}
Line 101: Line 107:
{{Family tree/end}}
{{Family tree/end}}


<br><br>
==== Exceptional diseases ====
==== 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:
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:
*[https://www.wikidoc.org/index.php/Zollinger-Ellison_syndrome 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.
**A rare disorder involving extreme [[peptic ulcer]] disease and [[Gastrinoma|gastrin-secreting tumor]]<nowiki/>s in the [[pancreas]], may also have dumping syndrome


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


*Low blood sugar, or [https://www.wikidoc.org/index.php/Hypoglycemia hypoglycemia],
*Low [[blood sugar]], or [[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".
**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
*[[Diabetes mellitus|Diabetes]]:
**Neuropathy can cause damage to the nerves supplying the GIT
**[[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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