Zollinger-Ellison syndrome pathophysiology: Difference between revisions

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==Pathogenesis==
==Pathogenesis==
*Zollinger-Ellison syndrome is a disorder where the production of increased levels of [[gastrin]] causes the [[stomach]] to release excess amounts of [[hydrochloric acid]]. [[Gastrin]] then results in an excessive production of acid which often may 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 the production of increased levels of [[gastrin]] causes the [[stomach]] to release excess amounts of [[hydrochloric acid]]. [[Gastrin]] then results in an excessive production of acid which often may 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>
*Increased basal [[gastric acid]] output and [[hyperplasia|hyyperplasia]] of the fundic [[parietal cells]] occur as a result of excessive amounts of [[gastrin]] that secreted by the gastrinoma tumor cells. The excessive [[gastric acid]] output overrides the mucosal defense of the [[gastric]] and [[duodenal]] wall thereby causing [[ulceration]], and inactivation of [[pancreatic]] digestive enzymes which therefore results in fat [[malabsorption]] and [[diarrhea]]. Secretory nature of [[diarrhea]]  is a result of the inhibition of absorption of [[sodium]] and water by the [[small intestine]]. <ref name="urlGastrinoma - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK441842/ |title=Gastrinoma - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref>
*Increased basal [[gastric acid]] output and hyperplasia of the fundic [[parietal cells]] occur as a result of excessive amounts of [[gastrin]] that secreted by the gastrinoma tumor cells. The excessive [[gastric acid]] output overrides the mucosal defense of the [[gastric]] and [[duodenal]] wall thereby causing [[ulceration]], and inactivation of [[pancreatic]] digestive enzymes which therefore results in fat [[malabsorption]] and [[diarrhea]]. Secretory nature of [[diarrhea]]  is a result of the inhibition of absorption of [[sodium]] and water by the [[small intestine]]. <ref name="urlGastrinoma - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK441842/ |title=Gastrinoma - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref>
*The pathophysiology of ZES is the stimulatory action of [[gastrin]] on the [[parietal cells]] of the gastric [[antrum]] resulting in hyper-secretory acid milieu. <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 the stimulatory action of [[gastrin]] on the [[parietal cells]] of the gastric [[antrum]] resulting in hyper-secretory acid milieu. <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>
*Majority of patients with ZES also develop [[peptic ulcers]] which are large and multiple in number, usually in the distal [[duodenum]] and  proximal [[jejunum]] (which usually would be an uncommon location for [[ulcers]] arising due to [[Helicobacter pylori]] or by 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>
*Majority of patients with ZES also develop [[peptic ulcers]] which are large and multiple in number, usually in the distal [[duodenum]] and  proximal [[jejunum]] (which usually would be an uncommon location for [[ulcers]] arising due to [[Helicobacter pylori]] or by 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 20:10, 6 September 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

Zollinger-Ellison syndrome results from increased levels of gastrin due to an existing gastrinoma in the duodenum or pancreas.

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Microscopic Pathology

  • A well-differentiated neuroendocrine tumor (NET) histologically typically shows an organ like arrangement of cells with nesting, trabecular, or gyriform patterns. [6]
  • The tumor cells are usually round with regular bland nuclei which produce large number of secretory granules with diffuse immunoexpression of neuroendocrine markers.Where as, the poorly differentiated neuroendocrine tumor (NET) shows a atypical, sheet-like, diffuse and irregular nuclei, less cytoplasmic secretory granules, and limited biomarker immunoexpression. [6]
  • Immunostaining for chromogranin A and synaptophysin is an important step in the diagnosis of neuroendocrine tumors. In order to differentiate from other neuroendocrine tumors gastrin immunostaining may be used. somatostatin scintigraphy is considered an effective localizing tool as gastrinomas tend to express a high density of somatostatin receptors. [6]

References

  1. wikipedia.2015.https://en.wikipedia.org/wiki/Zollinger%E2%80%93Ellison_syndrome
  2. "Gastrinoma - StatPearls - NCBI Bookshelf".
  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.
  5. Ito T, Igarashi H, Uehara H, Jensen RT (2013). "Pharmacotherapy of Zollinger-Ellison syndrome". Expert Opin Pharmacother. 14 (3): 307–21. doi:10.1517/14656566.2013.767332. PMC 3580316. PMID 23363383.
  6. 6.0 6.1 6.2 Cingam S, Karanchi H. PMID 28722872. Missing or empty |title= (help)

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