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| __NOTOC__
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| {{CMG}}; {{AE}} {{SH}} | | {{CMG}}; {{AE}} {{SH}} |
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| ==Overview==
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| The Spleen is the most common affected organ in the abdomen as a consequence of trauma to the abdomen.The trauma can be due to number of reasons such as road traffic accidents,falls and domestic violence.There are a number of non traumatic reasons of splenic rupture due to an underlying pathology.
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| ==Classification==
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| ==Historical Perspective==
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| ==Pathophysiology==
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| ==Causes==
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| ===Common casuses===
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| The most common Cause of the splenic rupture remains blunt trauma to the abdomen.The other common causes of splenic rupture includes.<ref name="pmid19787754">{{cite journal |vauthors=Renzulli P, Hostettler A, Schoepfer AM, Gloor B, Candinas D |title=Systematic review of atraumatic splenic rupture |journal=Br J Surg |volume=96 |issue=10 |pages=1114–21 |year=2009 |pmid=19787754 |doi=10.1002/bjs.6737 |url=}}</ref>
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| * Neoplasms
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| * Infections
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| * Non Infectious
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| * Therapy related
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| * Mechanical Causes
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| ===Less common causes===
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| The less common causes of splenic rupture are difficult to diagnose and can be threatening.
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| Some less common causes of splenic rupture are as follows:
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| * Autologus stem cell transplantation in AL Amyloidosis patients<ref name="pmid29093392">{{cite journal| author=Sato S, Tamai Y, Okada S, Kannbe E, Takeda K, Tanaka E| title=Atraumatic Splenic Rupture due to Ectopic Extramedullary Hematopoiesis after Autologous Stem Cell Transplantation in a Patient with AL Amyloidosis. | journal=Intern Med | year= 2017 | volume= | issue= | pages= | pmid=29093392 | doi=10.2169/internalmedicine.9018-17 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29093392 }} </ref>
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| *
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| *
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| ==Differentiating Splenic Rupture from Other Diseases==
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| ==Epidemiology and Demographics==
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| ==Risk Factors==
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| ==Screening==
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| ==Natural History, Complications and Prognosis==
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| ==Diagnosis==
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| ==Diagnostic Study of Choice==
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| == History and Symptoms==
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| ==Physical Examination==
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| == Laboratory Findings==
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| ==Electrocardiogram==
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| ==X-Ray==
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| ==MRI==
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| ==Other Imaging Findings==
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| ==Other Diagnostic Studies==
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| == Algorithms ==
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| {{familytree/start}}
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| {{familytree | | | | | | | | | | | | | | | | | | | | | | | A01 |A01='''Major molecular events in the pathogenesis of HCC'''}}
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| {{familytree | | | | |,|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|+|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|-|.| | | }}
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| {{familytree | | | | B01 | | | | | | | | | | | | | | | | | B02 | | | | | | | | | | | | | | | B03 |B01='''Genomic alterations'''|B02='''Epigenetic modifications'''|B03='''Growthfactor pathway alterations'''}}
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| {{familytree | | |,|-|^|-|.| | | | | | | | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|-|.| | | | | | | | |!| | |}}
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| {{familytree | | C01 | | C02 | | | | | | | | C03 | | | | | C04 | | | | | | C05 | | | | | | | C06 |C01=Gene Mutations|C02=Gene Amplification|C03=DNA methylation micro RNA|C04=Micro RNA|C05=LNC RNA|C06=Major Signaling pathways}}
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| {{familytree | | |!| | | |!| | | | | | | | | |!| | | | | | |!| | | | | | | |!| | | | | | | | |!| |}}
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| {{familytree |boxstyle=text-align: left; | | D01 | | D02 | | | | | | | | D03 | | | | | D04 | | | | | | D05 | | | | | | | D06 |D01=•TERT promoter<br>•TP53<br>•CTNNB1<br>•AXIN1<br>•AXIN2<br>•ATM<br>•RPS6KA3<br>•JAK1<br>•IL6R<br>•IL6ST<br>•ARID1<br>•ARID2
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| |D02=•CCND1<br>•FGF19<br>•CDKNA2A<br>•CDKNA2B<br>•AXIN1<br>•IRF2<br>•MET|D03=GSTP1<br>•E-Cadherin<br>•CDKNA2<br>•RASSF1A<br>•SOCS-3<br>•MIGMT|D04=•MiR-155<br>•Mir-122<br>•Mir-224<br>•Mir-21|D05=•HULC<br>•HEIH<br>•Dreh<br>•MVIH<br>•HOTAIR<br>•MDIG<br>•LINE1|D06=•Wnt/β –catenin<br>•Tyrosine kinase pathways<br>EGF<br>HGF/c-MET<br>FGF<br>VEGF<br>•IGF<br>•HIF<br>•TGF β <br>•Hedgehog}}
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| {{familytree/end}}
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| [[image:512px-Jaundice08.jpg|thumb|350px|center| Elderly Male with jaundice from pancreatic cancer, By James Heilman, MD (Own work) [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons <ref name="urlFile:Jaundice08.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AJaundice08.jpg |title=File:Jaundice08.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
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| The incidence of HCC has almost tripled since the early 1980s in the United States where it is the fastest rising cause of cancer-related deaths1. According to population based Surveillance Epidemiology and End Results registry data, the overall HCC age adjusted incidence rates for liver and intrahepatic ducts cancer is as high as 8 per 100,000 underling population in 2010 (Fig. 1) of which at least 6 per 100,000 related to HCC. Men are at approximately three times higher risk than women. Asian men (i.e., Chinese, Korean, Filipino, and Japanese) have the highest age-adjusted incidence rates. However, the largest proportional increases have occurred among Hispanics followed by blacks and non-Hispanic whites, whereas the lowest proportional increases have occurred among Asians. In contrast to Asians/Pacific Islanders, HCC incidence rates are reported to be higher among Hispanics born in the United States than among foreign-born Hispanics2. HCC incidence rates have increased in each successive birth cohort born between 1900 and 19593 (Fig. 2). In addition, the age distribution of HCC patients has shifted to younger ages, with the greatest proportional increases among individuals 45–60 years old (Fig. 2). There is a south to north gradient in the incidence and mortality of HCC; Southern states including Texas, Louisiana, and Mississippi have some of the highest HCC incidence rates in the nation (Fig. 3). In one study, Texas Latino and especially South Texas Latinos had the highest age-adjusted HCC incidence rates (as high as 10.6/100,000)4.
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| ==References==
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| {{Reflist|2}}
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