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==Historical Perspective==
====Classification Gastritis==
 
{| class="wikitable"
===Discovery===
!colspan="2" | Gastritis
*In 1869, Paul Langerhans first described pancreatic [[Islet cell|islet cells]], when he was still a medical student.
!Etiology
*In 1902, Nicholls discovered the first adenoma of [[pancreatic islets]].<ref name="pmid20187464">{{cite journal| author=Stamatakos M, Safioleas C, Tsaknaki S, Safioleas P, Iannescu R, Safioleas M| title=Insulinoma: a rare neuroendocrine pancreatic tumor. | journal=Chirurgia (Bucur) | year= 2009 | volume= 104 | issue= 6 | pages= 669-73 | pmid=20187464 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20187464  }} </ref>
!Gasstritis synonyms
*In 1922, Frederick Banting and Charles Best were the first to discover insulin from a dog’s [[pancreas]].
|-
*In 1926, Wilder-et-al associated [[hyperinsulinism]] and functional islet tumor after a surgery on a person who had [[hypoglycemia]] and found an [[Islet cell carcinoma|islet cell cancer]] with [[liver]] metastasis.<ref name="WilderAllan1927">{{cite journal|last1=Wilder|first1=Russell M.|last2=Allan|first2=Frank N.|last3=Power|first3=M. H.|last4=Robertson|first4=H. E.|title=CARCINOMA OF THE ISLANDS OF THE PANCREAS|journal=Journal of the American Medical Association|volume=89|issue=5|year=1927|pages=348|issn=0002-9955|doi=10.1001/jama.1927.02690050014007}}</ref>
|colspan="2" | Non-atrophic
 
|
*In 1927, William J Mayo was the first to discover the association between [[hyperinsulinism]] and a functional [[Pancreatic islet cell tumors|pancreatic islet cell tumor]]. In 1927, the insulinoma was first described in Mayo clinic, which was dissected in 1929 in Toronto.<ref name="pmid20187464">{{cite journal| author=Stamatakos M, Safioleas C, Tsaknaki S, Safioleas P, Iannescu R, Safioleas M| title=Insulinoma: a rare neuroendocrine pancreatic tumor. | journal=Chirurgia (Bucur) | year= 2009 | volume= 104 | issue= 6 | pages= 669-73 | pmid=20187464 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20187464  }} </ref>
*Helicobacter pylori
 
*Other factors
*In 1929, the first surgical cure was performed by Roscoe Graham.<ref name="pmid17856569">{{cite journal |vauthors=Whipple AO, Frantz VK |title=ADENOMA OF ISLET CELLS WITH HYPERINSULINISM: A REVIEW |journal=Ann. Surg. |volume=101 |issue=6 |pages=1299–335 |year=1935 |pmid=17856569 |pmc=1390871 |doi= |url=}}</ref>
|
 
Superficial
* In 1935, Whipple suggested a [[diagnostic criteria|diagnostic criterion]] for the diagnosis of [[insulinoma]] called as [[Whipple's triad]]. <ref name="pmid17856569">{{cite journal |vauthors=Whipple AO, Frantz VK |title=ADENOMA OF ISLET CELLS WITH HYPERINSULINISM: A REVIEW |journal=Ann. Surg. |volume=101 |issue=6 |pages=1299–335 |year=1935 |pmid=17856569 |pmc=1390871 |doi= |url=}}</ref>
Diffuse antral gastritis (DAG)
 
Chronic antral gastritis (CAG)
 
Interstitial - follicular
Hypersecretory
Type B*
|-
|rowspan="4" |Atrophic
|Autoimmune
|
*Autoimmunity
|
Type A*
Diffuse corporal
Pernicious anemia-associated
|-
|rowspan="3"|Multifocal atrophic
|Helicobacter pylori
|Type B*, type AB*
|-
|Dietary
|Environmental
|-
|Environmental factors
|Metaplastic
|-
|rowspan="7"| Special form
|rowspan="4"| Chemical
|Chemical irritation
|Reactive
|-
|
*Bile
|
*Reflux
|-
|
*NSAIDs
|
*NSAID
|-
|
*Other agents
|
*Type C*
|-
|Radiation
|Radiation injury
|
|}


==Risk assessment table==
==Risk assessment table==

Revision as of 16:03, 6 November 2017

==Classification Gastritis

Gastritis Etiology Gasstritis synonyms
Non-atrophic
  • Helicobacter pylori
  • Other factors

Superficial Diffuse antral gastritis (DAG) Chronic antral gastritis (CAG) Interstitial - follicular Hypersecretory Type B*

Atrophic Autoimmune
  • Autoimmunity

Type A* Diffuse corporal Pernicious anemia-associated

Multifocal atrophic Helicobacter pylori Type B*, type AB*
Dietary Environmental
Environmental factors Metaplastic
Special form Chemical Chemical irritation Reactive
  • Bile
  • Reflux
  • NSAIDs
  • NSAID
  • Other agents
  • Type C*
Radiation Radiation injury

Risk assessment table

Scoring criteria for risk assessment*
Scoring system Score Risk
IMPROVEDD Score[1] Predicted % VTE risk through 42 days
0 0.4%
1 0.6%
2 0.8%
3 1.2%
4 1.6%
5-10 2.2%
Predicted % VTE risk through 77 days
0 0.5%
1 0.7%
2 1.0%
3 1.4%
4 1.9%
5-10 2.75
IMPROVE score[2] Predicted % VTE risk through 3 months
0 0.5%
1 1.0%
2 1.7%
3 3.1%
4 4%
5-8 11%
Padua Score[3] < 4 Low risk for VTE
≥ 4 High risk for VTE
Caprini score[4] 0-1 Low risk of VTE
2 Moderate of VTE
3-4 High risk of VTE
≥ 5 Highest risk for VTE

References

  1. ↑ . doi:10.1055/s-0037-160392910.1055/s-0037-1603929. Missing or empty |title= (help)
  2. ↑ Spyropoulos AC, Anderson FA, Fitzgerald G, Decousus H, Pini M, Chong BH; et al. (2011). "Predictive and associative models to identify hospitalized medical patients at risk for VTE". Chest. 140 (3): 706–14. doi:10.1378/chest.10-1944. PMID 21436241.
  3. ↑ Barbar S, Noventa F, Rossetto V, Ferrari A, Brandolin B, Perlati M; et al. (2010). "A risk assessment model for the identification of hospitalized medical patients at risk for venous thromboembolism: the Padua Prediction Score". J Thromb Haemost. 8 (11): 2450–7. doi:10.1111/j.1538-7836.2010.04044.x. PMID 20738765.
  4. ↑ Caprini JA, Arcelus JI, Hasty JH, Tamhane AC, Fabrega F (1991). "Clinical assessment of venous thromboembolic risk in surgical patients". Semin Thromb Hemost. 17 Suppl 3: 304–12. PMID 1754886.
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