Zollinger-Ellison syndrome pathophysiology: Difference between revisions

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*Zollinger-Ellison syndrome is a disorder where increased levels of [[gastrin]] are produced, causing the [[stomach]] to produce excess [[hydrochloric acid]]. Often, the cause is a [[tumor]] ([[gastrinoma]]) of the [[duodenum]] or [[pancreas]] producing the hormone [[gastrin]]. Gastrin then causes an excessive production of acid which can lead to [[peptic ulcers]] (in almost 95% of patients).<ref name="wikipedia">wikipedia.2015.https://en.wikipedia.org/wiki/Zollinger%E2%80%93Ellison_syndrome</ref>
*Zollinger-Ellison syndrome is a disorder where increased levels of [[gastrin]] are produced, causing the [[stomach]] to produce excess [[hydrochloric acid]]. Often, the cause is a [[tumor]] ([[gastrinoma]]) of the [[duodenum]] or [[pancreas]] producing the hormone [[gastrin]]. Gastrin then causes an excessive production of acid which can lead to [[peptic ulcers]] (in almost 95% of patients).<ref name="wikipedia">wikipedia.2015.https://en.wikipedia.org/wiki/Zollinger%E2%80%93Ellison_syndrome</ref>
*The gastrinoma tumor cells secrete excessive amounts of gastrin which leads to [[hyperplasia]] of the fundic [[parietal cells]] and increased basal [[gastric acid]] output. The excessive [[gastric acid]] output breaches the mucosal defenses of the gastric as well as the duodenal wall, causes [[ulceration]], and inactivates [[pancreatic]] digestive enzymes with resultant fat [[malabsorption]] and [[diarrhea]]. Inhibition of absorption of sodium and water by the [[small intestine]] results in a secretory component of the [[diarrhea]]. <ref name="pmid28722872">{{cite journal |vauthors=Cingam S, Karanchi H |title= |journal= |volume= |issue= |pages= |year= |pmid=28722872 |doi= |url=}}</ref>
*The gastrinoma tumor cells secrete excessive amounts of gastrin which leads to [[hyperplasia]] of the fundic [[parietal cells]] and increased basal [[gastric acid]] output. The excessive [[gastric acid]] output breaches the mucosal defenses of the gastric as well as the duodenal wall, causes [[ulceration]], and inactivates [[pancreatic]] digestive enzymes with resultant fat [[malabsorption]] and [[diarrhea]]. Inhibition of absorption of sodium and water by the [[small intestine]] results in a secretory component of the [[diarrhea]]. <ref name="pmid28722872">{{cite journal |vauthors=Cingam S, Karanchi H |title= |journal= |volume= |issue= |pages= |year= |pmid=28722872 |doi= |url=}}</ref>
*Gastrin works on stomach [[parietal cell]]s causing them to [[Hydrogen potassium ATPase|secrete]] more [[hydrogen ion]]s into the stomach lumen. In addition, [[gastrin]] acts as a trophic factor for [[parietal cells]], causing [[parietal cell]] [[hyperplasia]]. Thus, there is an increase in the number of acid secreting cells and each of these cells produces acid at a higher rate. The increase in acidity contributes to the development of [[peptic ulcer]]s in the stomach and [[duodenum]]. High acid levels lead to multiple [[ulcer]]s in the [[stomach]] and [[small bowel]].
*The pathophysiology of ZES is related to the trophic action of gastrin on parietal cells of the gastric antrum and the resulting hypersecretory acid milleu. <ref name="pmid24319020">{{cite journal |vauthors=Epelboym I, Mazeh H |title=Zollinger-Ellison syndrome: classical considerations and current controversies |journal=Oncologist |volume=19 |issue=1 |pages=44–50 |year=2014 |pmid=24319020 |pmc=3903066 |doi=10.1634/theoncologist.2013-0369 |url=}}</ref>
*The pathophysiology of ZES is related to the trophic action of gastrin on parietal cells of the gastric antrum and the resulting hypersecretory acid milleu. <ref name="pmid24319020">{{cite journal |vauthors=Epelboym I, Mazeh H |title=Zollinger-Ellison syndrome: classical considerations and current controversies |journal=Oncologist |volume=19 |issue=1 |pages=44–50 |year=2014 |pmid=24319020 |pmc=3903066 |doi=10.1634/theoncologist.2013-0369 |url=}}</ref>
*An overwhelming majority of patients with this disease consequently develop [[peptic ulcers]], often large and multiple, frequently in distal [[duodenum]] and even proximal [[jejunum]] (an uncommon location for [[ulcers]] resulting from [[Helicobacter pylori]] or the use of [[nonsteroidal anti-inflammatory drugs]]). <ref name="pmid24319020">{{cite journal |vauthors=Epelboym I, Mazeh H |title=Zollinger-Ellison syndrome: classical considerations and current controversies |journal=Oncologist |volume=19 |issue=1 |pages=44–50 |year=2014 |pmid=24319020 |pmc=3903066 |doi=10.1634/theoncologist.2013-0369 |url=}}</ref>
*An overwhelming majority of patients with this disease consequently develop [[peptic ulcers]], often large and multiple, frequently in distal [[duodenum]] and even proximal [[jejunum]] (an uncommon location for [[ulcers]] resulting from [[Helicobacter pylori]] or the use of [[nonsteroidal anti-inflammatory drugs]]). <ref name="pmid24319020">{{cite journal |vauthors=Epelboym I, Mazeh H |title=Zollinger-Ellison syndrome: classical considerations and current controversies |journal=Oncologist |volume=19 |issue=1 |pages=44–50 |year=2014 |pmid=24319020 |pmc=3903066 |doi=10.1634/theoncologist.2013-0369 |url=}}</ref>

Revision as of 18:47, 17 August 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2] Mohamad Alkateb, MBBCh [3]

Overview

Development of Zollinger-Ellison syndrome is the result of increased levels of gastrin due to an existing gastrinoma in the duodenum or pancreas.

Pathogenesis

Genetics

  • Approximately 80% of the time, the primary causative lesion is thought to arise sporadically; in the remainder of recorded cases, this entity exists as part of MEN-1, an autosomal dominant disorder characterized by tumors of the pituitary, the parathyroid, and the pancreas. [4]

Associated Conditions

Gross Pathology

  • Gross pathology presents as enlarged fundic mucosal folds with cerebriform pattern.

Microscopic Pathology

References

  1. wikipedia.2015.https://en.wikipedia.org/wiki/Zollinger%E2%80%93Ellison_syndrome
  2. 2.0 2.1 2.2 2.3 Cingam S, Karanchi H. PMID 28722872. Missing or empty |title= (help)
  3. 3.0 3.1 Epelboym I, Mazeh H (2014). "Zollinger-Ellison syndrome: classical considerations and current controversies". Oncologist. 19 (1): 44–50. doi:10.1634/theoncologist.2013-0369. PMC 3903066. PMID 24319020.
  4. Thakker RV, Newey PJ, Walls GV, Bilezikian J, Dralle H, Ebeling PR; et al. (2012). "Clinical practice guidelines for multiple endocrine neoplasia type 1 (MEN1)". J Clin Endocrinol Metab. 97 (9): 2990–3011. doi:10.1210/jc.2012-1230. PMID 22723327.

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