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Cirrhosis pathophysiology

2022-10-11T16:51:27Z

44.197.72.169: /* Overview */

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{{Cirrhosis}}
{{CMG}};{{AE}}{{Cherry}}

==Overview==
Cirrhosis occurs due to long term [[liver]] injury which causes an imbalance between [[matrix]] production and degradation. The pathological hallmark of cirrhosis is the development of [[scar tissue]] which leads to replacement of normal [[liver]] [[parenchyma]], leading to blockade of [[Portal vein|portal blood flow]] and disturbance of normal [[liver]] function. When [[fibrosis]] of the [[liver]] reaches an advanced stage where distortion of the [[Liver|hepatic]] [[Circulatory system|vasculature]] also occurs, it is termed as cirrhosis of the [[liver]]. The [[pathogenesis]] of cirrhosis involves [[inflammation]], [[Ito cell|hepatic stellate cell]] activation, [[angiogenesis]], and [[Fibrosis|fibrogenesis]]. [[Kupffer cell|Kupffer cells]] are [[Liver|hepatic]] [[Macrophage|macrophages]] responsible for [[Ito cell|hepatic stellate cell]] activation during injury. [[Ito cell|Hepatic stellate cells (HSC)]] which are located in the [[Space of Disse|subendothelial space of Disse]], become activated in areas of [[liver]] injury and secrete [[TGF-beta|transforming growth factor-beta 1]] ([[TGF beta 1|TGF-β1]]), which leads to a [[Fibrosis|fibrotic]] response and proliferation of [[connective tissue]]. Cirrhosis may also lead to [[Liver|hepatic]] [[Microvascular bed|microvascular]] changes including the formation of intra-[[Liver|hepatic]] [[Shunt (medical)|shunts]] (due to [[angiogenesis]] and loss of [[Parenchyma|parenchymal cells]]) and [[Endothelium|endothelial]] dysfunction. [[Fibrosis]] eventually leads to formation of [[Septum (disambiguation)|septae]] that grossly distort the [[liver]] architecture which includes both the [[liver]] [[parenchyma]] and the [[Circulatory system|vasculature]], accompanied by regenerative [[Nodule (medicine)|nodule]] formation. HAYOP

==Pathophysiology==
The [[pathogenesis]] of cirrhosis is as follows:<ref name="pmid7932316">{{cite journal |vauthors=Arthur MJ, Iredale JP |title=Hepatic lipocytes, TIMP-1 and liver fibrosis |journal=J R Coll Physicians Lond |volume=28 |issue=3 |pages=200–8 |year=1994 |pmid=7932316 |doi= |url=}}</ref><ref name="pmid8502273">{{cite journal |vauthors=Friedman SL |title=Seminars in medicine of the Beth Israel Hospital, Boston. The cellular basis of hepatic fibrosis. Mechanisms and treatment strategies |journal=N. Engl. J. Med. |volume=328 |issue=25 |pages=1828–35 |year=1993 |pmid=8502273 |doi=10.1056/NEJM199306243282508 |url=}}</ref><ref name="pmid8682489">{{cite journal |vauthors=Iredale JP |title=Matrix turnover in fibrogenesis |journal=Hepatogastroenterology |volume=43 |issue=7 |pages=56–71 |year=1996 |pmid=8682489 |doi= |url=}}</ref><ref name="pmid7959178">{{cite journal |vauthors=Gressner AM |title=Perisinusoidal lipocytes and fibrogenesis |journal=Gut |volume=35 |issue=10 |pages=1331–3 |year=1994 |pmid=7959178 |pmc=1374996 |doi= |url=}}</ref><ref name="pmid17332881">{{cite journal |vauthors=Iredale JP |title=Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ |journal=J. Clin. Invest. |volume=117 |issue=3 |pages=539–48 |year=2007 |pmid=17332881 |pmc=1804370 |doi=10.1172/JCI30542 |url=}}</ref><ref name="pmid11984538">{{cite journal |vauthors=Arthur MJ |title=Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C |journal=Gastroenterology |volume=122 |issue=5 |pages=1525–8 |year=2002 |pmid=11984538 |doi= |url=}}</ref>
* When an injured [[Tissue (biology)|tissue]] is replaced by a [[Collagen|collagenous]] [[scar]], it is termed as [[fibrosis]]. The development of [[fibrosis]] requires several months, or even years of ongoing [[injury]].
* The [[pathological]] hallmark of cirrhosis is the development of [[scar tissue]] that leads to replacement of normal [[liver]] [[parenchyma]], leading to blockade of [[Portal vein|portal blood flow]] and disturbance of normal [[liver]] function.
* When [[fibrosis]] of the [[liver]] reaches a point where distortion of the [[Liver|hepatic]] [[Circulatory system|vasculature]] also occurs, it is termed as cirrhosis of the [[liver]]. If the damage progresses, panlobular cirrhosis may result.
* The [[cellular]] mechanisms responsible for cirrhosis are similar regardless of the type of initial insult and site of injury within the [[Hepatic lobule|liver lobule]].
* [[Hepatitis|Viral hepatitis]] involves the periportal region, whereas involvement in [[alcoholic liver disease]] is largely pericentral.
* Cirrhosis involves the following steps:<ref name="pmid7737629">{{cite journal |vauthors=Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G |title=Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension |journal=Hepatology |volume=21 |issue=5 |pages=1238–47 |year=1995 |pmid=7737629 |doi= |url=}}</ref>
** [[Inflammation]]
** [[Ito cell|Hepatic stellate cell]] activation
** [[Angiogenesis]]
** [[Fibrosis|Fibrogenesis]]
'''Hepatic stellate cell activation'''

The role of [[Kupffer cell|hepatic stellate cells]] in the pathogenesis of cirrhosis is described below:
* [[Kupffer cell|Kupffer cells]] are [[Liver|hepatic]] [[Macrophage|macrophages]] responsible for [[Ito cell|hepatic stellate cell]] activation during injury.
* The [[Ito cell|stellate cell]], (also known as the [[Ito cell|perisinusoidal cell]] or [[Ito cell]]) is a type of [[cell]] that normally stores [[vitamin A]] and plays a pivotal role in the development of cirrhosis.
* [[Ito cell|Hepatic stellate cells (HSC)]] are usually located in the [[Space of Disse|subendothelial space of Disse]] and become activated to a [[myofibroblast]]-like [[cell]] in areas of [[liver]] injury. This contractile [[Cell (biology)|cell]] (known as a [[myofibroblast]]) obstructs [[blood flow]] in the [[Circulatory system|circulation]].
* The [[stellate cell]] secretes [[TGF-β|transforming growth factor-beta 1]] ([[TGF beta 1|TGF-β1]]), which leads to a [[Fibrosis|fibrotic]] response and [[proliferation]] of [[connective tissue]].
* [[Connective tissue]] [[proliferation]] leads to the formation of [[extracellular matrix]] around [[hepatocytes]] that is composed of [[collagen]]s (especially type I, III, IV), [[glycoprotein]] and [[proteoglycan]]s.
* [[Collagen]] and non-[[collagenous]] [[matrix]] [[Protein|proteins]] responsible for [[fibrosis]] are produced by the activated [[Stellate cell|hepatic stellate cells]] ([[Ito cell|HSC]]).
* [[Hepatocyte]] damage causes the release of [[lipid]] [[Peroxidase|peroxidases]] from injured [[Cell membrane|cell membranes]] leading to [[necrosis]] of [[Parenchyma|parenchymal cells]].
* Activated [[Ito cell|HSC]] induce the production of numerous [[Cytokine|cytokines]] and their receptors, such as [[platelet-derived growth factor]] ([[Platelet-derived growth factor|PDGF]]) and [[Transforming growth factor|TGF-f31]], which are responsible for [[Fibrosis|fibrogenesis]].
* The matrix formed due to [[Ito cell|HSC]] activation is deposited in the [[space of Disse]] and leads to loss of fenestrations of [[Endothelium|endothelial cells]], through a process called capillarization.
* [[Stellate cell]] activation leads to disturbance of the balance between [[matrix metalloproteinase]]s and the naturally occurring inhibitors ([[TIMP1|TIMP 1]] and [[TIMP2]]). This is followed by [[matrix (biology)|matrix]] breakdown and replacement by [[connective tissue]]-secreted [[matrix]].<ref>Iredale JP. Cirrhosis: new research provides a basis for rational and targeted treatments. [[British Medical Journal|BMJ]] 2003;327:143-7.[http://bmj.bmjjournals.com/cgi/content/full/327/7407/143 Fulltext.] PMID 12869458.</ref>
* [[Matrix metalloproteinase]] (MMP) are [[calcium]] dependent [[enzymes]] that specifically degrade [[collagen]] and non [[Collagen|collagenous]] substrate.
* [[Matrix metalloproteinase|MMP]]-2 and stromyelysin-1 are produced by [[Ito cell|stellate cells]].
* [[Matrix metalloproteinase|MMP]]-2 degrades [[collagen]] and stromelysin-1 degrades [[proteoglycan]] and [[glycoprotein]].
'''Microvascular changes'''

Cirrhosis leads to [[Liver|hepatic]] microvascular changes characterised by:<ref name="pmid19157625">{{cite journal |vauthors=Fernández M, Semela D, Bruix J, Colle I, Pinzani M, Bosch J |title=Angiogenesis in liver disease |journal=J. Hepatol. |volume=50 |issue=3 |pages=604–20 |year=2009 |pmid=19157625 |doi=10.1016/j.jhep.2008.12.011 |url=}}</ref>
* Formation of intra [[Liver|hepatic]] [[Shunt (medical)|shunts]] (due to [[angiogenesis]] and loss of [[Parenchyma|parenchymal cells]])
* [[Liver|Hepatic]] [[Endothelium|endothelial]] dysfunction

* [[Sinusoid (blood vessel)|Sinusoidal]] [[Endothelium|endothelial cells]] are also important contributors of early [[fibrosis]]. [[Endothelial cell]]s from a normal [[liver]] produces [[collagen]], [[laminin]] and [[fibronectin]].<ref>{{cite journal |author=Maher JJ, McGuire RF |title=Extracellular matrix gene expression increases preferentially in rat lipocytes and sinusoidal endothelial cells during hepatic fibrosis in vivo |journal=J. Clin. Invest. |volume=86 |issue=5 |pages=1641–8 |year=1990 |month=November |pmid=2243137 |pmc=296914 |doi=10.1172/JCI114886 |url=}}</ref><ref>{{cite journal |author=Herbst H, Frey A, Heinrichs O, ''et al.'' |title=Heterogeneity of liver cells expressing procollagen types I and IV in vivo |journal=Histochem. Cell Biol. |volume=107 |issue=5 |pages=399–409 |year=1997 |month=May |pmid=9208331 |doi= |url=}}</ref>
* The [[Endothelium|endothelial]] dysfunction is characterised by:<ref name="pmid22504334">{{cite journal |vauthors=García-Pagán JC, Gracia-Sancho J, Bosch J |title=Functional aspects on the pathophysiology of portal hypertension in cirrhosis |journal=J. Hepatol. |volume=57 |issue=2 |pages=458–61 |year=2012 |pmid=22504334 |doi=10.1016/j.jhep.2012.03.007 |url=}}</ref>
** Insufficient release of [[Vasodilator|vasodilators]], such as [[nitric oxide]] due to [[oxidative stress]]
** Increased production of [[Vasoconstrictor|vasoconstrictors]] (mainly [[adrenergic]] stimulation and activation of [[Endothelin|endothelins]] and [[Renin-angiotensin system|RAAS]])
* The [[liver]] responds to injury with new [[blood vessel]] formation. Mediators involved in [[angiogenesis]] include:
**[[Platelet-derived growth factor|Platelet derived growth factor]] ([[Platelet-derived growth factor|PDGF]])
**[[Vascular endothelial growth factor]] ([[Vascular endothelial growth factor|VEGF]])
**[[Nitric oxide]]
**[[Carbon monoxide]]
'''Angiogenesis'''
*[[Angiogenesis]] in cirrhosis results in the production of immature and permeable [[vascular endothelial growth factor]] ([[Vascular endothelial growth factor|VEGF]]) induced neo-[[Blood vessel|vessels]] that further exacerbate [[liver]] injury.<ref>{{cite journal |author=Lee JS, Semela D, Iredale J, Shah VH |title=Sinusoidal remodeling and angiogenesis: a new function for the liver-specific pericyte? |journal=Hepatology |volume=45 |issue=3 |pages=817–25 |year=2007 |month=March |pmid=17326208 |doi=10.1002/hep.21564 |url=}}</ref><ref>{{cite journal |author=Rosmorduc O, Housset C |title=Hypoxia: a link between fibrogenesis, angiogenesis, and carcinogenesis in liver disease |journal=Semin. Liver Dis. |volume=30 |issue=3 |pages=258–70 |year=2010 |month=August |pmid=20665378 |doi=10.1055/s-0030-1255355 |url=}}</ref>
'''Fibrosis'''

The role of [[fibrosis]] in the pathogenesis of cirrhosis is described below:
* [[Fibrosis]] eventually leads to formation of [[Septum (disambiguation)|septae]] that grossly distort the [[liver]] architecture which includes both the [[liver]] [[parenchyma]] and the [[Circulatory system|vasculature]].
* A cirrhotic [[liver]] compromises [[Hepatic sinusoids|hepatic sinusoidal]] exchange by shunting [[Artery|arterial]] and [[Portal vein|portal blood]] directly into the [[Central vein|central veins]] ([[Liver|hepatic]] outflow).
* [[Vascularity|Vascularized]] [[Fiber|fibrous]] [[Septum (disambiguation)|septa]] connect [[Central vein|central veins]] with [[Portal triad|portal tracts]] leading to islands of [[Hepatocyte|hepatocytes]] surrounded by [[Fiber|fibrous]] bands without [[Central vein|central veins]].<ref name="pmid18328931">{{cite journal |vauthors=Schuppan D, Afdhal NH |title=Liver cirrhosis |journal=Lancet |volume=371 |issue=9615 |pages=838–51 |year=2008 |pmid=18328931 |pmc=2271178 |doi=10.1016/S0140-6736(08)60383-9 |url=}}</ref><ref name="pmid15094237">{{cite journal |vauthors=Desmet VJ, Roskams T |title=Cirrhosis reversal: a duel between dogma and myth |journal=J. Hepatol. |volume=40 |issue=5 |pages=860–7 |year=2004 |pmid=15094237 |doi=10.1016/j.jhep.2004.03.007 |url=}}</ref><ref name="pmid11079009">{{cite journal |vauthors=Wanless IR, Nakashima E, Sherman M |title=Regression of human cirrhosis. Morphologic features and the genesis of incomplete septal cirrhosis |journal=Arch. Pathol. Lab. Med. |volume=124 |issue=11 |pages=1599–607 |year=2000 |pmid=11079009 |doi=10.1043/0003-9985(2000)124<1599:ROHC>2.0.CO;2 |url=}}</ref>
* These mechanisms simultaneously occurring in the [[liver]] lead to [[Fibrous tissue|fibrous tissue band]] (septa) and regenerative [[hepatocyte]] [[Nodule (medicine)|nodule]] formation, which eventually replace the entire [[liver]] architecture, leading to decreased [[blood flow]] throughout.
* The formation of [[Fibrosis|fibrotic]] bands is accompanied by regenerative [[Nodule (medicine)|nodule]] formation in the [[Liver|hepatic]] [[parenchyma]].
* Advancement of cirrhosis may lead to [[Parenchyma|parenchymal]] dysfunction and development of [[portal hypertension]].
* The pathological hallmark of cirrhosis is the development of [[scar tissue]] that replaces normal [[parenchyma]], leading to blockade of [[Portal vein|portal blood flow]] and disturbance of normal [[liver]] function.
* Due to [[portal hypertension]], the [[spleen]] becomes congested, which leads to [[hypersplenism]] and increased [[platelet]] sequestration.
'''Pathogenesis of cirrhosis according to cause'''

[[Pathogenesis]] of cirrhosis based upon the underlying cause is as follows:
* '''[[Alcoholic liver disease]]''': [[Alcohol]] seems to injure the [[liver]] by blocking the normal metabolism of [[protein]], [[fat]]s, and [[carbohydrate]]s. Patients may also have concurrent [[alcoholic hepatitis]] with [[fever]], [[hepatomegaly]], [[jaundice]], and [[anorexia]]. [[Liver]] damage due to [[alcoholic hepatitis]] may progress to cirrhosis.
* '''Chronic hepatitis C''': Infection with the [[hepatitis C]] virus causes [[inflammation]] and low grade damage to the [[liver]] that may eventually lead to cirrhosis after decades.
* '''[[Non-alcoholic fatty liver disease|Non-alcoholic steatohepatitis]]''' (NASH): In [[Non-alcoholic fatty liver disease|NASH]], fat builds up in the [[liver]] and eventually causes [[scar tissue]]. This type of [[hepatitis]] appears to be associated with [[diabetes]], [[protein malnutrition]], [[obesity]], [[coronary artery disease]], and treatment with [[corticosteroid]] medications.
* '''[[Primary sclerosing cholangitis]] (PSC):''' [[Primary sclerosing cholangitis|PSC]] is a progressive [[Cholestasis|cholestatic]] disorder presenting with [[pruritus]], [[steatorrhea]], [[Fat soluble vitamins|fat soluble vitamin]] deficiencies, and [[metabolic]] bone disease.
** There is a strong association with [[inflammatory bowel disease]] (IBD), especially [[ulcerative colitis]].
* '''[[Autoimmune hepatitis]]''': [[Immunological|Immunologic]] damage to the [[liver]] leads to [[inflammation]], [[Scar|scarring]] and cirrhosis.

* [[Portal hypertension]] may result from a combination of the following:
** Structural disturbances associated with advanced [[liver]] disease account for 70% of total [[Liver|hepatic]] [[vascular resistance]].
** Functional abnormalities such as [[Endothelium|endothelial]] dysfunction and increased [[Liver|hepatic]] [[vascular]] tone account for 30% of total [[Liver|hepatic]] [[vascular resistance]].

===Pathophysiology of Cirrhosis due to Alcohol===
Mechanisms of [[alcohol]]-induced [[liver]] damage include:<ref name="pmid25548474">{{cite journal |vauthors=Ceni E, Mello T, Galli A |title=Pathogenesis of alcoholic liver disease: role of oxidative metabolism |journal=World J. Gastroenterol. |volume=20 |issue=47 |pages=17756–72 |year=2014 |pmid=25548474 |pmc=4273126 |doi=10.3748/wjg.v20.i47.17756 |url=}}</ref><ref name="pmid15194557">{{cite journal |vauthors=You M, Crabb DW |title=Recent advances in alcoholic liver disease II. Minireview: molecular mechanisms of alcoholic fatty liver |journal=Am. J. Physiol. Gastrointest. Liver Physiol. |volume=287 |issue=1 |pages=G1–6 |year=2004 |pmid=15194557 |doi=10.1152/ajpgi.00056.2004 |url=}}</ref><ref name="pmid16088993">{{cite journal |vauthors=Freeman TL, Tuma DJ, Thiele GM, Klassen LW, Worrall S, Niemelä O, Parkkila S, Emery PW, Preedy VR |title=Recent advances in alcohol-induced adduct formation |journal=Alcohol. Clin. Exp. Res. |volume=29 |issue=7 |pages=1310–6 |year=2005 |pmid=16088993 |doi= |url=}}</ref><ref name="pmid17590995">{{cite journal |vauthors=Niemelä O |title=Acetaldehyde adducts in circulation |journal=Novartis Found. Symp. |volume=285 |issue= |pages=183–92; discussion 193–7 |year=2007 |pmid=17590995 |doi= |url=}}</ref>
* Impairment of:
** [[Protein synthesis]]
** [[Secretion]]
** [[Glycosylation]]

* [[Ethanol]] intake leads to elevated accumulation of intracellular [[Triglyceride|triglycerides]] by:<ref name="pmid12791698">{{cite journal |vauthors=Fischer M, You M, Matsumoto M, Crabb DW |title=Peroxisome proliferator-activated receptor alpha (PPARalpha) agonist treatment reverses PPARalpha dysfunction and abnormalities in hepatic lipid metabolism in ethanol-fed mice |journal=J. Biol. Chem. |volume=278 |issue=30 |pages=27997–8004 |year=2003 |pmid=12791698 |doi=10.1074/jbc.M302140200 |url=}}</ref><ref name="pmid15578517">{{cite journal |vauthors=You M, Matsumoto M, Pacold CM, Cho WK, Crabb DW |title=The role of AMP-activated protein kinase in the action of ethanol in the liver |journal=Gastroenterology |volume=127 |issue=6 |pages=1798–808 |year=2004 |pmid=15578517 |doi= |url=}}</ref><ref name="pmid16879892">{{cite journal |vauthors=Ji C, Chan C, Kaplowitz N |title=Predominant role of sterol response element binding proteins (SREBP) lipogenic pathways in hepatic steatosis in the murine intragastric ethanol feeding model |journal=J. Hepatol. |volume=45 |issue=5 |pages=717–24 |year=2006 |pmid=16879892 |doi=10.1016/j.jhep.2006.05.009 |url=}}</ref>
** [[Lipoprotein]] secretion
** Decreased [[fatty acid]] [[Redox|oxidation]]
** Increased [[fatty acid]] uptake
* [[Alcohol]] is converted by [[alcohol dehydrogenase]] to [[acetaldehyde]].
* Due to the high reactivity of [[acetaldehyde]], it forms [[acetaldehyde]]-[[protein]] adducts which cause damage to [[Cells (biology)|cells]] by:
** Trafficking of [[Liver|hepatic]] [[Protein|proteins]]
** Interrupting [[microtubule]] formation
** Interfering with [[enzyme]] activities
* [[Reactive oxygen species]] begin to form as a result of [[hepatocyte]] damage that activate [[Kupffer cell|Kupffer cells]].<ref name="pmid11984538">{{cite journal |vauthors=Arthur MJ |title=Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C |journal=Gastroenterology |volume=122 |issue=5 |pages=1525–8 |year=2002 |pmid=11984538 |doi= |url=}}</ref>
*[[Kupffer cell]] activation leads to the production of profibrogenic [[Cytokine|cytokines]] which in turn, stimulates [[Stellate cell|stellate cells]].
*[[Stellate cell]] activation leads to [[connective tissue]] formation due to deposition [[extracellular matrix]] and [[collagen]].
* [[Portal triad|Portal triads]] develop connections with central [[veins]] due to [[connective tissue]] formation in pericentral and periportal zones, leading to the formation of regenerative [[Nodule (medicine)|nodules]].
* Shrinkage of the [[liver]] occurs over years due to repeated insults that lead to:
** Loss of [[Hepatocyte|hepatocytes]]
** Increased production and deposition of [[collagen]] and regenerative [[Nodule (medicine)|nodule]] formation on a background of [[fibrosis]]
===Pathophysiology of Portal Hypertension due to Cirrhosis===
==== Increased resistance ====
* Portal hypertension is related to elevation of resistance in the [[Portal venous system|portal vasculature]].
* Increased resistance in [[Portal venous system|portal system]] may be due to both intra-[[hepatic]] and also [[Portocaval anastomoses|portosystemic collateral]] resistance.
** '''Intra-hepatic resistance'''
*** The main factor responsible for intra-[[hepatic]] resistance is [[hepatic]] vascular [[compliance]], which is greatly decreased in liver [[fibrosis]] or [[cirrhosis]].
*** [[Portal hypertension]] occurs when [[compliance]] is decreased and [[blood flow]] is increased in [[liver]].<ref name="pmid5543903">{{cite journal |vauthors=Greenway CV, Stark RD |title=Hepatic vascular bed |journal=Physiol. Rev. |volume=51 |issue=1 |pages=23–65 |year=1971 |pmid=5543903 |doi= |url=}}</ref>
*** Pre-[[hepatic]] and post-[[hepatic]] [[portal hypertension]] arise due to some secondary obstruction before or after [[liver]] [[vasculature]], respectively.<ref>{{cite book | last = Schiff | first = Eugene | title = Schiff's diseases of the liver | publisher = John Wiley & Sons | location = Chichester, West Sussex, UK | year = 2012 | isbn = 9780470654682 }}</ref>
*** [[Alcoholic hepatitis]] causes both [[sinusoidal]] and post-[[sinusoidal]] pathologies.<ref name="pmid13976646">{{cite journal |vauthors=SCHAFFNER F, POPER H |title=Capillarization of hepatic sinusoids in man |journal=Gastroenterology |volume=44 |issue= |pages=239–42 |year=1963 |pmid=13976646 |doi= |url=}}</ref><ref name="pmid5775031">{{cite journal |vauthors=Reynolds TB, Hidemura R, Michel H, Peters R |title=Portal hypertension without cirrhosis in alcoholic liver disease |journal=Ann. Intern. Med. |volume=70 |issue=3 |pages=497–506 |year=1969 |pmid=5775031 |doi= |url=}}</ref>
*** [[Hepatic]] vascular [[endothelium]] synthesizes and secretes both [[Vasodilator|vasodilators]] (e.g., [[nitric oxide]], [[Prostacyclin|prostacyclins]]) and [[Vasoconstrictor|vasoconstrictors]] (e.g., [[endothelin]] and [[Prostanoid|prostanoids]]).<ref name="pmid1874796">{{cite journal |vauthors=Rubanyi GM |title=Endothelium-derived relaxing and contracting factors |journal=J. Cell. Biochem. |volume=46 |issue=1 |pages=27–36 |year=1991 |pmid=1874796 |doi=10.1002/jcb.240460106 |url=}}</ref><ref name="EpsteinVane1990">{{cite journal|last1=Epstein|first1=Franklin H.|last2=Vane|first2=John R.|last3=Änggård|first3=Erik E.|last4=Botting|first4=Regina M.|title=Regulatory Functions of the Vascular Endothelium|journal=New England Journal of Medicine|volume=323|issue=1|year=1990|pages=27–36|issn=0028-4793|doi=10.1056/NEJM199007053230106}}</ref>
*** Increased resistance due to the elevation of [[vascular]] tone may be caused by excess of [[vasoconstrictors]] or lack of [[vasodilators]].
*** It is postulated that in [[Cirrhosis|cirrhotic liver]] the [[nitric oxide]] level is lower and the response to [[endothelin]] in [[myofibrils]] is stronger than in normal [[liver]].<ref name="pmid8707268">{{cite journal |vauthors=Rockey DC, Weisiger RA |title=Endothelin induced contractility of stellate cells from normal and cirrhotic rat liver: implications for regulation of portal pressure and resistance |journal=Hepatology |volume=24 |issue=1 |pages=233–40 |year=1996 |pmid=8707268 |doi=10.1002/hep.510240137 |url=}}</ref>
** '''Portosystemic collateral resistance'''
*** [[Collateral]] blood circulation develops as a consequence of [[portal hypertension]] which is the main contributor to [[Gastrointestinal varices|esophageal and gastric varices]]
*** The main purpose of the [[collaterals]] is to decompress and bypass [[portal]] [[blood]] flow.
*** However, [[Portocaval anastomoses|portosystemic collaterals]] may not lead to a complete decompression.
*** [[Portocaval anastomoses|Portosystemic circulation]] occurs between the [[short gastric]], [[left gastric vein]], and the [[esophageal]], [[azygos]] and the [[intercostal veins]]; the superior, the middle, and the inferior [[Hemorrhoidal plexus|hemorrhoidal veins]]; the [[Paraumbilical veins|paraumbilical venous plexus]], the [[venous]] system of [[abdominal]] [[organs]] juxtaposed with the [[retroperitoneum]] and [[abdominal wall]]; the left [[renal vein]], the [[splanchnic]], the [[adrenal]], and the [[spermatic veins]].<ref name="pmid1415713">{{cite journal |vauthors=Mosca P, Lee FY, Kaumann AJ, Groszmann RJ |title=Pharmacology of portal-systemic collaterals in portal hypertensive rats: role of endothelium |journal=Am. J. Physiol. |volume=263 |issue=4 Pt 1 |pages=G544–50 |year=1992 |pmid=1415713 |doi= |url=}}</ref>

==== Hyperdynamic circulation in portal hypertension ====
* Peripheral [[vasodilatation]] is the basis for decreased systemic [[vascular resistance]] and [[mean arterial pressure]], [[plasma]] volume expansion, elevated [[splanchnic]] [[blood flow]], and elevated [[cardiac index]].<ref name="pmid1735537">{{cite journal |vauthors=Colombato LA, Albillos A, Groszmann RJ |title=Temporal relationship of peripheral vasodilatation, plasma volume expansion and the hyperdynamic circulatory state in portal-hypertensive rats |journal=Hepatology |volume=15 |issue=2 |pages=323–8 |year=1992 |pmid=1735537 |doi= |url=}}</ref>
* '''Systemic vasodilation'''
** Three main mechanisms which contribute to the peripheral [[vasodilation]] are as follows:
*** Increased [[vasodilators]] production in systemic circulation<ref name="pmid2372062">{{cite journal |vauthors=Genecin P, Polio J, Colombato LA, Ferraioli G, Reuben A, Groszmann RJ |title=Bile acids do not mediate the hyperdynamic circulation in portal hypertensive rats |journal=Am. J. Physiol. |volume=259 |issue=1 Pt 1 |pages=G21–5 |year=1990 |pmid=2372062 |doi= |url=}}</ref>
*** Increased [[vasodilators]] production in local [[endothelium]]<ref name="CasadevallPanés1993">{{cite journal|last1=Casadevall|first1=María|last2=Panés|first2=Julián|last3=Piqué|first3=Josep M.|last4=Marroni|first4=Norma|last5=Bosch|first5=Jaume|last6=Whittle|first6=Brendan J. R.|title=Involvement of nitric oxide and prostaglandins in gastric mucosal hyperemia of portal-hypertensive anesthetized rats|journal=Hepatology|volume=18|issue=3|year=1993|pages=628–634|issn=02709139|doi=10.1002/hep.1840180323}}</ref>
*** Decreased [[vascular]] response to local [[vasoconstrictors]]<ref name="pmid1616049">{{cite journal |vauthors=Sieber CC, Groszmann RJ |title=In vitro hyporeactivity to methoxamine in portal hypertensive rats: reversal by nitric oxide blockade |journal=Am. J. Physiol. |volume=262 |issue=6 Pt 1 |pages=G996–1001 |year=1992 |pmid=1616049 |doi= |url=}}</ref>
* '''Plasma volume'''
** There are several events which contribute to the [[hyperdynamic circulation]] such as:
*** Initial [[vasodilatation]], induced by [[systemic]] and local [[endothelial]] factors
*** Subsequent [[Blood plasma|plasma]] volume expansion<ref name="pmid8425700">{{cite journal |vauthors=Albillos A, Colombato LA, Lee FY, Groszmann RJ |title=Octreotide ameliorates vasodilatation and Na+ retention in portal hypertensive rats |journal=Gastroenterology |volume=104 |issue=2 |pages=575–9 |year=1993 |pmid=8425700 |doi= |url=}}</ref>
==Genetics==

* Certain [[TERT]] ([[Telomerase reverse transcriptase|Telomerase reverese transcriptase]]) [[gene]] variants resulting in reduced [[telomerase]] activity have been found to be a [[risk factor]] for sporadic cirrhosis<ref>{{cite journal |author=Calado RT, Brudno J, Mehta P, ''et al.'' |title=Constitutional telomerase mutations are genetic risk factors for cirrhosis |journal=Hepatology |volume=53 |issue=5 |pages=1600–7 |year=2011 |month=May |pmid=21520173 |pmc=3082730 |doi=10.1002/hep.24173 |url=}}</ref>
* An uncharacterized [[Nucleolar protein, member A1|nucleolar protein]], NOL11, has a role in the [[pathogenesis]] of North American Indian childhood cirrhosis<ref>{{cite journal |author=Freed EF, Prieto JL, McCann KL, McStay B, Baserga SJ |title=NOL11, Implicated in the Pathogenesis of North American Indian Childhood Cirrhosis, Is Required for Pre-rRNA Transcription and Processing |journal=PLoS Genet. |volume=8 |issue=8 |pages=e1002892 |year=2012 |month=August |pmid=22916032 |pmc=3420923 |doi=10.1371/journal.pgen.1002892 |url=}}</ref>
* Loss of interaction between the [[C-terminus]] of a protein called Utp4/cirhin and other SSU processome [[proteins]] may cause cirrhosis in children<ref>{{cite journal |author=Freed EF, Baserga SJ |title=The C-terminus of Utp4, mutated in childhood cirrhosis, is essential for ribosome biogenesis |journal=Nucleic Acids Res. |volume=38 |issue=14 |pages=4798–806 |year=2010 |month=August |pmid=20385600 |pmc=2919705 |doi=10.1093/nar/gkq185 |url=}}</ref>

==Gross Pathology==
On [[gross examination]], the [[liver]] may initially be enlarged, but with progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and the color is often yellow (if associates [[steatosis]]). Depending on the size of the [[Nodule (medicine)|nodules]] there are three macroscopic types: micronodular, macronodular and mixed cirrhosis.
* In the micronodular form ([[René Laennec|Laennec]]'s cirrhosis or portal cirrhosis) regenerating [[Nodule (medicine)|nodules]] are under 3 mm.
* In macronodular cirrhosis (post-necrotic cirrhosis), the [[Nodule (medicine)|nodules]] are larger than 3 mm.
* The mixed cirrhosis consists of a variety of [[Nodule (medicine)|nodules]] with different sizes.
On [[gross pathology]], [[Cirrhosis|cirrhotic liver]], [[splenomegaly]], and [[esophageal varices]] are characteristic findings in portal hypertension.
{| class="wikitable"
|-
|
=== Cirrhosis ===
On [[gross pathology]] there are two types of [[cirrhosis]]:
* Micronodular [[cirrhosis]] which is uniform and diffuse, mostly due to [[alcohol]].
* Macronodular [[cirrhosis]] which is irregular, mostly due to [[viral hepatitis]].
|
[[image:Cirrosi micronodular.1427.jpg|thumb|200px|Micronodular cirrhosis - By Amadalvarez (Own work), via Wikimedia Commons<ref><CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)></ref>]]
|
[[image:Fig78x.jpg|thumb|200px|Macronodular cirrhosis<ref name="urlwww.meddean.luc.edu">{{cite web |url=http://www.meddean.luc.edu/lumen/MedEd/orfpath/images/fig78x.jpg |title=www.meddean.luc.edu |format= |work= |accessdate=}}</ref>]]
|-
|
=== Splenomegaly ===
On [[gross pathology]], diffuse enlargement and [[congestion]] of the [[spleen]] are characteristic findings of [[splenomegaly]].
| colspan="2" |
[[image:Esplenomegalia i hiperplasia linfoide folicular reactiva. IMG 2865.jpg|thumb|200px|center|Splenomegaly - By Amadalvarez (Own work), via Wikimedia Commons<ref>Amadalvarez - Own work, <"https://creativecommons.org/licenses/by-sa/4.0" title="Creative Commons Attribution-Share Alike 4.0">CC BY-SA 4.0, <"https://commons.wikimedia.org/w/index.php?curid=49669333">Link</ref>]]
|-
|
=== Esophageal Varices ===
On gross pathology, prominent, congested, and tortoise [[veins]] in the lower parts of [[esophagus]] are characteristic findings of [[esophageal varices]].
| colspan="2" |
[[image:F21. Venous enlargement in hepatic cirrhosis. Alfred Kast Wellcome L0074357.jpg|thumb|200px|center|Esophageal varices<ref><http://wellcomeimages.org/indexplus/obf_images/29/b4/13f38971164f946a97f9d32ddd93.jpg>Gallery: <"http://wellcomeimages.org/indexplus/image/L0074357.html"><"http://creativecommons.org/licenses/by/4.0> CC BY 4.0, <"https://commons.wikimedia.org/w/index.php?curid=36297209"></ref>]]
|}

=== Images of gross pathology of cirrhosis ===
[http://www.peir.net Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology]
<gallery>
Image:Cirrhosis 001.jpg|Cirrhosis: Gross, external view of micronodular cirrhosis
Image:Cirrhosis 002.jpg|Cirrhosis: Gross, cut section of previous one (an excellent example)
Image:Cirrhosis 003.jpg|Cirrhosis: Gross, close-up image
Image:Cirrhosis 004.jpg|Macronodular cirrhosis and hepatoma
</gallery>

<gallery>
Image:Cirrhosis 005.jpg|Cirrhosis: Gross, close-up, natural color (an excellent example)
Image:Cirrhosis 006.jpg|Cirrhosis: Gross, close-up (an excellent example)
Image:Cirrhosis 007.jpg|Cirrhosis: Gross, close-up view
Image:Cirrhosis 008.jpg|Micronodular cirrhosis: Gross, external view (an excellent example)
</gallery>

<gallery>
Image:Cirrhosis 009.jpg|Micronodular cirrhosis: Gross, close-up image
Image:Cirrhosis 010.jpg|Micronodular cirrhosis: Gross (an excellent example)
Image:Cirrhosis 011.jpg|Macronodular cirrhosis: Gross, natural color (perfect color for cirrhosis), close-up, an excellent example
Image:Cirrhosis 012.jpg|Cirrhosis with portocaval shunt: Gross, severe cirrhosis with extensive liver necrosis due to thrombosis of portocaval shunt (well shown)
</gallery>

<gallery>
Image:Cirrhosis 013.jpg|Endstage cirrhosis: Gross, natural color, close-up (an excellent example)
Image:Cirrhosis 014.jpg|Endstage cirrhosis: Gross, natural color, close-up view is an excellent example for nodules of yellow-orange liver tissue and broad irregular bands of fibrosis
Image:Cirrhosis 015.jpg|Endstage cirrhosis: Gross, natural color, close-up cut surface, very well shown nodules of yellow and necrotic opaque liver tissue with broad and irregular bands of fibrosis (an excellent example)
Image:Cirrhosis 016.jpg|Macronodular cirrhosis: Gross, natural color, external view of liver and very enlarged spleen (liver has variable size nodules up to about 2 cm)
</gallery>

<gallery>
Image:Cirrhosis 017.jpg|Macronodular cirrhosis: Gross, natural color, cut surface, large irregular bands of fibrosis with variable size liver cell nodules up to about 8 mm and all necrotic appears to be an end stage liver disease.
Image:Cirrhosis 018.jpg|Macronodular cirrhosis: Gross, natural color view of frontal sections of liver and spleen showing a contracted macronodular liver and an enlarged spleen as large as the liver
Image:Cirrhosis 019.jpg|Macronodular cirrhosis: Gross, natural color slab of liver
Image:Cirrhosis 020.jpg|Fatty change and early cirrhosis: Gross, natural color, rather close-up image showing typical fatty color, and in lighting at lower right of micrography micronodularity is evident (quite good example)
</gallery>

<gallery>
Image:Cirrhosis 021.jpg|Cirrhosis with portal vein thrombosis: Gross, natural color, sectioned liver with portal vein exposed and filled with red thrombus. A good example of end stage cirrhosis.
Image:Cirrhosis 022.jpg|Endstage cirrhosis with lobular necrosis: Gross, natural color, very close-up view (an excellent example of alcoholic cirrhosis)
Image:Cirrhosis 023.jpg|Micronodular cirrhosis: Gross, natural color view of whole liver through capsule with obvious cirrhosis (note to quite large liver)
Image:Cirrhosis 024.jpg|Micronodular cirrhosis: Gross, natural color, view of whole liver showing external surface typical cirrhotic liver (history of alcoholism)
</gallery>

<gallery>
Image:Cirrhosis 025.jpg|Lung: Idiopathic Interstitial Fibrosis: Gross, natural color, an excellent photo of lung cirrhosis (close-up view)
Image:Cirrhosis 026.jpg|Endstage cirrhosis: Gross, natural color, slice of liver. Portal vein is opened to show size and patency.
Image:Cirrhosis 027.jpg|Endstage cirrhosis: Gross, natural color, severe cirrhosis with bile stasis
Image:Cirrhosis 028.jpg|Portal Vein Thrombosis with cirrhosis: Gross, close-up, micronodular cirrhosis with portal vein thrombosis
</gallery>

<gallery>
Image:Cirrhosis 029.jpg|Lung: Hematite: Gross, natural color, external view of "pulmonary cirrhosis" with typical hematite color
Image:Cirrhosis 030.jpg|Gross, natural color of liver and stomach view from external surfaces, micronodular cirrhosis and hemorrhagic gastritis (as the surgeon would see these in natural color)
</gallery>
==Microscopic Pathology==
*Microscopic pathology reveals the four stages of cirrhosis as it progresses:
**Chronic nonsuppurative destructive [[cholangitis]]: inflammation and necrosis of portal tracts with lymphocyte infiltration leads to the destruction of the [[bile ducts]]
**Development of biliary stasis and [[fibrosis]]
**Periportal [[fibrosis]] progresses to bridging [[fibrosis]]
**Increased proliferation of smaller [[bile ductules]] leads to regenerative [[nodule]] formation
*Microscopically, cirrhosis is characterized by regeneration [[nodules]] surrounded by fibrous septa.
*In these nodules, regenerating [[hepatocyte]]s are present.
*Portal tracts, [[central vein]]s and the radial pattern of hepatocytes are absent.
*Fibrous septa are present and inflammatory infiltrate composed of [[lymphocyte]]s and [[macrophage]]s) are also visible.
*If the underlying cause is [[secondary biliary cirrhosis]], biliary ducts are damaged, proliferated or distended leading to bile stasis.
*Dilated ducts contain inspissated bile which appears as bile casts or bile thrombi (brown-green, amorphous).
*Bile retention may be found also in the parenchyma and are referred to as "bile lakes".<ref>[http://www.pathologyatlas.ro/Cirrhosis.html Pathology atlas], "cirrhosis".</ref>

== Microscopic pathology ==
The main microscopic [[histopathological]] findings in portal hypertension are related to [[Cirrhosis (patient information)|cirrhosis]], [[esophageal varices]], [[Hepatic amyloidosis with intrahepatic cholestasis|hepatic amyloidosis]], and congestive [[hepatopathy]] due to [[heart failure]] or [[Budd-Chiari syndrome]].
{| class="wikitable"
|-
|
=== Cirrhosis ===
Robbins definition of [[microscopic]] [[histopathological]] findings in cirrhosis includes (all three is needed for diagnosis):<ref>{{cite book | last = Mitchell | first = Richard | title = Pocket companion to Robbins and Cotran pathologic basis of disease | publisher = Elsevier Saunders | location = Philadelphia, PA | year = 2012 | isbn = 978-1416054542 }}</ref>
* Bridging [[fibrosis]]
* [[Nodule]] formation
* Disruption of the [[hepatic]] architecture
|
[[image:Cirrhosis.jpg|thumb|200px|Cirrhosis with bridging fibrosis (yellow arrow) and nodule (black arrow) - By Nephron, via Librepathology.org<ref name="urlFile:Cirrhosis high mag.jpg - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/File:Cirrhosis_high_mag.jpg#filelinks |title=File:Cirrhosis high mag.jpg - Libre Pathology |format= |work= |accessdate=}}</ref>]]
|-
|
=== Esophageal varices ===
The main microscopic [[histopathological]] findings in [[esophageal varices]] are:
* Large dilated [[submucosal]] [[veins]] ('''key feature''')
* [[Blood]] (fresh)
* [[Hemosiderin]]-laden [[macrophages]].
|
[[image:Eso-varices.jpg|thumb|200px|Esophageal varices with submucosal vein (black arrow), via Librepathology.org<ref name="urlEsophageal varices - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/Esophageal_varices#cite_note-3 |title=Esophageal varices - Libre Pathology |format= |work= |accessdate=}}</ref>]]
|-
|
=== Hepatic amyloidosis ===
The main [[microscopic]] [[histopathological]] findings in [[Hepatic amyloidosis with intrahepatic cholestasis|hepatic amyloidosis]] is amorphous extracellular pink stuff on [[H&E stain|H&E]] staining.
|
[[image:Amyloidosis - high mag.jpg|thumb|200px|Hepatic amyloidosis with amorphous amyloids (black arrow) and normal hepatocytes (blue arrow), via Librepathology.org<ref name="urlFile:Hepatic amyloidosis - high mag.jpg - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/File:Hepatic_amyloidosis_-_high_mag.jpg |title=File:Hepatic amyloidosis - high mag.jpg - Libre Pathology |format= |work= |accessdate=}}</ref>]]
|-
|
=== Congestive hepatopathy ===
The main [[microscopic]] [[histopathological]] findings in congestive [[hepatopathy]] (due to [[heart failure]] or [[Budd-Chiari syndrome]]) are:
* [[Atrophy]] of the centrilobular zone (zone III)
* Distension of portal [[venule]] ([[central vein]])
* Perisinusoidal [[fibrosis]] which may progress to centrilobular [[fibrosis]] and then diffuse [[fibrosis]]
* [[Sinusoidal]] dilation in all zone III areas ('''key feature)'''
|
[[image:Congestive hepatopathy.jpg|thumb|200px|Congestive hepatopathy with central vein (yellow arrowhead), inflammatory cells, Councilman body (green arrowhead), and hepatocyte with mitotic figure (red arrowhead), via Librepathology.org<ref name="urlFile:2 CEN NEC 1 680x512px.tif - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/File:2_CEN_NEC_1_680x512px.tif |title=File:2 CEN NEC 1 680x512px.tif - Libre Pathology |format= |work= |accessdate=}}</ref>]]
|}

=== Videos ===
{{#ev:youtube|CzKGvWZrUpU}}

{{#ev:youtube|CV8OYeIUXko}}

{{#ev:youtube|Jj8ozr_IttM}}

==References==
{{Reflist|2}}

[[Category:Medicine]]
[[Category:Gastroenterology]]
[[Category:Up-To-Date]]
[[Category:Hepatology]]

Tibial plateau fracture pathophysiology

2022-10-10T17:10:55Z

44.197.72.169: /* Pathophysiology */

__NOTOC__
{{Tibial plateau fracture}}

{{CMG}}; {{AE}} {{Rohan}}

==Overview==
The pattern of fracture and degree of [[comminution]] are the resultant of several factors or variables such as the nature of [[injury]], the bone quality, the [[age]] and [[weight]] of the patient, the [[energy]] involved, and the position of the [[knee]] and [[leg]] at the time of impact. Various combinations of these variables lead to a variety of different [[Bone fracture|fracture]] patterns.

==Pathophysiology==
*The fracture pattern and severity of [[comminution]] depends on multiple factors including:<ref>{{cite book | last = Azar | first = Frederick | title = Campbell's operative orthopaedics | publisher = Elsevier | location = Philadelphia, PA | year = 2017 | isbn = 9780323374620 }}</ref>
**Nature of the fall
**[[Bone]] quality
**[[Age]] of the patient
**[[Weight]] of the patient
**[[Energy]] involved
**Position of the [[knee]] and [[leg]] at the time of impact
* Decrease in [[Bone density|bone mass density]] involves following process:<ref name="pmid23645674">{{cite journal| author=Onal M, Piemontese M, Xiong J, Wang Y, Han L, Ye S et al.| title=Suppression of autophagy in osteocytes mimics skeletal aging. | journal=J Biol Chem | year= 2013 | volume= 288 | issue= 24 | pages= 17432-40 | pmid=23645674 | doi=10.1074/jbc.M112.444190 | pmc=3682543 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23645674 }} </ref>
**[[Autophagy]] is the mechanism through which [[Osteocyte|osteocytes]] evade [[oxidative stress]].
**The capability of [[autophagy]] in cells decreases as they age, a major factor of [[Ageing|aging]].
**As [[Osteocyte|osteocytes]] grow, viability of cells decrease thereby decreasing the [[bone mass density]].

===Anatomy===
{| align="right"
|
[[File:Gray257.png|300px|thumb|Anatomy of tibial plateau.[https://upload.wikimedia.org/wikipedia/commons/8/8b/Gray257.png Source: Case courtesy of Henry Vandyke Carter]]]
|}
*Majority of the [[weight]] in the [[lower leg]] is transmitted through [[tibia]].<ref>{{cite book | last = Rockwood | first = Charles | title = Rockwood and Green's fractures in adults | publisher = Wolters Kluwer Health/Lippincott Williams & Wilkins | location = Philadelphia, PA | year = 2010 | isbn = 9781605476773 }}</ref><ref>{{cite book | last = Azar | first = Frederick | title = Campbell's operative orthopaedics | publisher = Elsevier | location = Philadelphia, PA | year = 2017 | isbn = 9780323374620 }}</ref>
*The tibial plateau is the [[proximal]] portion of the [[tibia]] and forms the part of the [[knee joint]].
*The stronger of the two [[Articular surface|articular surfaces]] is the medial [[tibial condyle]] whereas the lateral [[tibial condyle]] is a weaker portion of the joint.
*The medial from the lateral [[tibial condyle]] are separated by the intercondylar eminence which serves as the attachment for the [[anterior cruciate ligament]] (ACL).

'''Medial Condyle'''
*The medial [[condyle]] is larger than the lateral [[condyle]].
*The [[articular surface]] of medial [[condyle]] is oval and it is long axis is [[anteroposterior]].
*The central part of the medial [[Condyle|condylar]] surface is slightly [[concave]].
*The peripheral part is flat and separated from [[femoral]] [[condyle]] by the medial [[meniscus]].

'''Lateral Condyle'''
*The lateral [[condyle]] overhangs the [[shaft]] of [[tibia]].
*The [[articular surface]] is nearly circular.
*The central part is slightly [[concave]] and comes in direct contact with [[femoral]] [[condyle]].
*The peripheral part is flat and separated from [[femur]] by the lateral [[meniscus]].

===Mechanism of Fracture===
*[[Proximal]] [[tibial]] injuries can occur due to direct [[trauma]] or indirect mechanisms such as [[axial]] compression.<ref name="pmid30059369">{{cite journal| author=Ramponi DR, McSwigan T| title=Tibial Plateau Fractures. | journal=Adv Emerg Nurs J | year= 2018 | volume= 40 | issue= 3 | pages= 155-161 | pmid=30059369 | doi=10.1097/TME.0000000000000194 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30059369 }} </ref>
*The causes of most tibial plateau fractures are a [[valgus]] stress associated with an [[axial]] load.
*Most tibial plateau fractures result from motor vehicle-related injuries followed by sports-associated injuries.
*The bumper of a car striking the lateral [[Condyle|plateau]] during this vehicle–pedestrian-related injury causes a [[valgus]] mechanism of injury.
*[[Motor vehicle accident|Motor vehicle injuries]] are high energy and often result in splitting types of fractures as well as direct [[injury]] to the surrounding [[Soft tissue|soft tissues]].
*Low-energy forces can cause a tibial plateau fracture usually in [[Old age|older]] patients with poor bone quality due to rotational forces.
*Such injuries are primarily seen in women >50 years with [[osteoporosis]] resulting in a depressed pattern plateau fracture.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

[[Category:Orthopedics]]
[[Category:Orthopedic surgery]]
[[Category:Fractures]]
[[Category:Bone fractures]]

Contraction alkalosis

2022-10-09T15:33:28Z

44.197.72.169:

__NOTOC__
{{SI}}

{{CMG}}

==Overview==
'''Contraction alkalosis''' refers to the increase in blood [[pH]] that occurs as a result of fluid losses. The change in pH is especially pronounced with acidic fluid losses caused by problems like [[vomiting]].

==Pathophysiology==
Extracellular fluid (ECF) volume contraction is associated with decreased blood volume and decreased renal perfusion pressure. Three compensation mechanisms engage as a result:
# [[Renin]] secretion is increased
# Production of [[angiotensin II]] is increased
# Secretion of [[aldosterone]] is increased

Increases in angiotensin II causes increased Na+-K+ exchange and increased HCO3- (bicarbonate) reabsorption in the [[proximal tubule]]. Increased aldosterone secretion causes increased [[collecting duct - alpha intercalated cell]] H+ secretion, worsening the metabolic alkalosis. Additionally, increased aldosterone secretion causes increased distal tubule K+ secretion, causing the [[hypokalemia]] seen with contraction alkalosis.

==Treatment==
Treatment consists of [[NaCl]] infusion to correct ECF volume contraction and administration of K+ to replace urinary losses.

==References==
{{Reflist|2}}

[[Category:Intensive care medicine]]
[[Category:Nephrology]]
[[Category:Electrolyte disturbance]]
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Arizona bark scorpion

2022-10-07T22:30:50Z

44.197.72.169: /* Habitat */

__NOTOC__
{{Taxobox
| image = Bbasgen-bark-scorpion.jpg
| name = Arizona bark scorpion
| regnum = [[Animal]]ia
| phylum = [[Arthropod]]a
| subphylum = [[Chelicerata]]
| classis = [[Arachnid]]a
| ordo = [[Scorpion]]es
| familia = [[Buthidae]]
| genus = ''[[Centruroides]]''
| species = '''''C. sculpturatus'''''
| binomial = ''Centruroides sculpturatus''
| binomial_authority = ([[Horatio C Wood, Jr.|Wood]], 1863)
}}
{{SI}}
{{CMG}}
==Overview==
The 'Arizona bark scorpion (Centruroides sculpturatus, included in Centruroides exilicauda, the Baja California bark scorpion) is a small light brown scorpion common to the United States. The range of the scorpion is the Sonoran Desert. An adult male can reach 8 centimeters in his body length, while a pregnant female is slightly smaller, with a maximum length of 7 centimeters.

== Diet ==
The Arizona bark scorpion is nocturnal, prefers to ambush its prey, and usually feeds on crickets or cockroaches.

== Predators ==
Arizona bark scorpions are eaten by a wide variety of animals such as birds, reptiles, and other invertebrates. Some examples include spiders, snakes, peccaries, rodents, and other scorpions. In urban areas house cats may also consume Arizona bark scorpions. Development, pesticides and collecting scorpions for research or the pet trade also has an impact on the Arizona bark scorpion population.

== Life cycle ==
[[File:Basgen-scorpion-compared.JPG|thumb|right|Three adult and four juvenile Arizona bark scorpions]]
Arizona bark scorpions have a gestation period of several months, are born live, and are gently guided onto their mother's back. The female usually gives birth to between 25–35 young, and the young will remain with their mother until their first molt, up to 3 weeks after birth. Arizona bark scorpions may live up to 6 years.

While nearly all scorpions are solitary, the Arizona bark scorpion is a rare exception: during winter, packs of 20 to 30 scorpions can congregate.<ref name=UA>{{cite web | url = http://ag.arizona.edu/pubs/insects/az1223/ | title = Scorpions | work = Cooperative Extension, College of Agriculture & Life Sciences | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100721230743/http://ag.arizona.edu/pubs/insects/az1223/ |archivedate=July 21, 2010}}</ref>

== Habitat ==
The Arizona bark scorpion is particularly well adapted to the desert: layers of fat on its exoskeleton make it resistant to water loss. Nevertheless, Arizona bark scorpions hide during the heat of the day, typically under rocks, wood piles, or tree bark. Bark scorpions do not burrow, and are commonly found in homes, requiring only 1/16 of an inch for entry.

Arizona bark scorpions prefer riparian areas with mesquite, Populus sections, cottonwood, and sycamor groves, all of which have sufficient moisture and humidity to support insects and other prey species. The popularity of irrigated lawns, and other systems which increase environmental humidity in residential areas, has led to a massive increase in the number of these animals in some areas.

== Venom ==
[[Image:Bbasgen-scorpion-front.jpg|thumb|right|Frontal view of a bark scorpion in a defensive posture]]
The bark scorpion is the most [[venom (poison)|venomous]] scorpion in North America, and its venom can cause severe pain (coupled with numbness and tingling) in adult humans, typically lasting between 24 to 72 hours. Temporary dysfunction in the area stung is common; e.g. a hand or possibly arm can be immobilized or experience convulsions. It also may cause the loss of breath for a short period of time. Due to the extreme pain induced, many victims describe sensations of electrical jolts after [[envenomation]].

Fatalities from scorpion envenomation in the USA are rare and are limited to small animals (including small pets), small children, and adults with compromised immune systems. Extreme reaction to the venom is indicated by numbness, frothing at the mouth, paralysis, and a neuromotor syndrome that may be confused with a seizure and that may make breathing difficult, particularly for small children. Two recorded fatalities have occurred in the state of [[Arizona]] since 1968; the number of victims stung each year in Arizona is estimated to be in the thousands. In Mexico, more than 100,000 people are stung annually, and during a peak period in the 1980s, the bark scorpion claimed up to 800 lives there.<ref name=UA />

=== Antivenom ===
An [[antivenom]] was developed for this species at Arizona State University<ref>{{cite news |url=http://www.popularmechanics.com/science/health/snakebites-about-to-get-more-deadly |title=Why snakebites are about to get a lot more deadly |author=Glenn Derene |publisher=[[Popular Mechanics]] |date=May 10, 2010 |accessdate=September 23, 2011}}</ref> and produced in quantities sufficient to treat individuals within the state of [[Arizona]] up until 1999.<ref>{{cite news |url=http://www.azcentral.com/business/articles/2011/08/04/20110804scorpion-antivenin-gets-fda-ok.html |title=Scorpion antivenin gets FDA's OK |author=Ken Alltucker |date=August 4, 2011 |publisher=[[The Arizona Republic]] |accessdate=September 23, 2011}}</ref> FDA approval was not required as it was provided at no charge, and use was restricted to within the state of Arizona; it was very successful in shortening the duration of symptoms and hospitalization. Production of this antivenom ceased by 2000 and the product was unavailable by 2004. A Mexican-produced antivenom, Anascorp [Antivenin Centruroides (scorpion) F(ab′)2, Laboratorios Silanes, Instituto Bioclon SA de CV], is being tested and used in its place.<ref name=UA-medical>{{cite web | year = 2000 | url = http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm | title = Soothing the Scorpion's Sting | author = David Von Behren, MPH | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20090603092350/http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm |archivedate=June 3, 2009}}</ref> On August 3, 2011, the FDA approved Anascorp for use in the United States.<ref name=FDA>{{cite web |url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm266611.htm |title=FDA approves the first specific treatment for scorpion stings |date=August 3, 2011 |publisher=FDA}}</ref>

=== First aid ===
Basic first aid measures can be used to help remediate scorpion stings:<ref name=UA-medical />
* Clean sting site with soap and water
* Apply a cool compress (cool cloth, no ice)
* Take [[paracetamol|acetaminophen]] (paracetamol) or [[ibuprofen]] for local pain and swelling

=== Medical emergencies ===
[[Image:Arizona bark scorption glowing under ultraviolet light.jpg|thumb|An Arizona bark scorpion glowing under [[ultraviolet light]]]]

Since the amount of venom the scorpion injects on a sting varies, Arizona poison control centers suggest immediate medical attention only in the event of extreme pain or stings involving children.<ref name=UA-poison>{{cite web | year = 2008 | url = http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php | title = Poison and Drug Information Center | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100820192450/http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php |archivedate=August 20, 2010}}</ref>

== UV lighting ==
Bark scorpions, like most other scorpions, will glow when exposed to a [[blacklight]]. This is particularly useful in scorpion detection, since bark scorpions are active during the night, and can be easily spotted using this method. Typical UV [[LED]] flashlights are able to readily detect scorpions at a distance of approximately 6 feet. Newly molted scorpions will not glow under [[ultraviolet light]] for a few days after molting.
{{-}}

== References ==
{{Reflist|32em}}

== External links ==
{{commons category|Centruroides sculpturatus|''Centruroides sculpturatus''}}
{{Portal|Arthropods}}
*[http://www.ntnu.no/ub/scorpion-files/c_exilicauda.php Further information on the scorpion]
*{{cite web |url=http://www.scorpsweep.com/facts.html |title=Scorpion Sweepers |last=Holland |first=Ben |year=2008}}

[[Category:Buthidae]]
[[Category:Fauna of the Southwestern United States|Scorpion, Arizona bark]]
[[Category:Animals described in 1863]]

[[cs:Štír zlatý]]
[[de:Arizona-Rindenskorpion]]
[[fr:Centruroides sculpturatus]]
{{WH}}
{{WS}}

Arizona bark scorpion

2022-10-07T22:29:13Z

44.197.72.169: /* Predators */

__NOTOC__
{{Taxobox
| image = Bbasgen-bark-scorpion.jpg
| name = Arizona bark scorpion
| regnum = [[Animal]]ia
| phylum = [[Arthropod]]a
| subphylum = [[Chelicerata]]
| classis = [[Arachnid]]a
| ordo = [[Scorpion]]es
| familia = [[Buthidae]]
| genus = ''[[Centruroides]]''
| species = '''''C. sculpturatus'''''
| binomial = ''Centruroides sculpturatus''
| binomial_authority = ([[Horatio C Wood, Jr.|Wood]], 1863)
}}
{{SI}}
{{CMG}}
==Overview==
The 'Arizona bark scorpion (Centruroides sculpturatus, included in Centruroides exilicauda, the Baja California bark scorpion) is a small light brown scorpion common to the United States. The range of the scorpion is the Sonoran Desert. An adult male can reach 8 centimeters in his body length, while a pregnant female is slightly smaller, with a maximum length of 7 centimeters.

== Diet ==
The Arizona bark scorpion is nocturnal, prefers to ambush its prey, and usually feeds on crickets or cockroaches.

== Predators ==
Arizona bark scorpions are eaten by a wide variety of animals such as birds, reptiles, and other invertebrates. Some examples include spiders, snakes, peccaries, rodents, and other scorpions. In urban areas house cats may also consume Arizona bark scorpions. Development, pesticides and collecting scorpions for research or the pet trade also has an impact on the Arizona bark scorpion population.

== Life cycle ==
[[File:Basgen-scorpion-compared.JPG|thumb|right|Three adult and four juvenile Arizona bark scorpions]]
Arizona bark scorpions have a gestation period of several months, are born live, and are gently guided onto their mother's back. The female usually gives birth to between 25–35 young, and the young will remain with their mother until their first molt, up to 3 weeks after birth. Arizona bark scorpions may live up to 6 years.

While nearly all scorpions are solitary, the Arizona bark scorpion is a rare exception: during winter, packs of 20 to 30 scorpions can congregate.<ref name=UA>{{cite web | url = http://ag.arizona.edu/pubs/insects/az1223/ | title = Scorpions | work = Cooperative Extension, College of Agriculture & Life Sciences | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100721230743/http://ag.arizona.edu/pubs/insects/az1223/ |archivedate=July 21, 2010}}</ref>

== Habitat ==
The bark scorpion is particularly well adapted to the desert: layers of fat on its exoskeleton make it resistant to water loss. Nevertheless, bark scorpions hide during the heat of the day, typically under rocks, wood piles, or tree bark. Bark scorpions do not burrow, and are commonly found in homes, requiring only 1/16 of an inch for entry.<ref name=scorpion-mangement>{{cite web | year = 2008 | url = http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html | title = Scorpion Management Guidelines | accessdate = June 18, 2008 | archiveurl= http://web.archive.org/web/20080602232642/http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html| archivedate= 2 June 2008 | deadurl= no}}</ref>

Arizona bark scorpions prefer [[riparian]] areas with [[mesquite]], [[Populus sect. Aegiros|cottonwood]], and [[Platanus|sycamore]] groves, all of which have sufficient moisture and humidity to support insects and other prey species. The popularity of irrigated lawns, and other systems which increase environmental humidity in residential areas, has led to a massive increase in the number of these animals in some areas.<ref name=naturalhistory>{{cite book | last = Phillips S.; Comus P. | title = A Natural History of the Sonoran Desert | publisher = Arizona Sonora Desert Museum | year = 2000 | isbn =978-0-520-21980-9 | page = 292 }}</ref>

== Venom ==
[[Image:Bbasgen-scorpion-front.jpg|thumb|right|Frontal view of a bark scorpion in a defensive posture]]
The bark scorpion is the most [[venom (poison)|venomous]] scorpion in North America, and its venom can cause severe pain (coupled with numbness and tingling) in adult humans, typically lasting between 24 to 72 hours. Temporary dysfunction in the area stung is common; e.g. a hand or possibly arm can be immobilized or experience convulsions. It also may cause the loss of breath for a short period of time. Due to the extreme pain induced, many victims describe sensations of electrical jolts after [[envenomation]].

Fatalities from scorpion envenomation in the USA are rare and are limited to small animals (including small pets), small children, and adults with compromised immune systems. Extreme reaction to the venom is indicated by numbness, frothing at the mouth, paralysis, and a neuromotor syndrome that may be confused with a seizure and that may make breathing difficult, particularly for small children. Two recorded fatalities have occurred in the state of [[Arizona]] since 1968; the number of victims stung each year in Arizona is estimated to be in the thousands. In Mexico, more than 100,000 people are stung annually, and during a peak period in the 1980s, the bark scorpion claimed up to 800 lives there.<ref name=UA />

=== Antivenom ===
An [[antivenom]] was developed for this species at Arizona State University<ref>{{cite news |url=http://www.popularmechanics.com/science/health/snakebites-about-to-get-more-deadly |title=Why snakebites are about to get a lot more deadly |author=Glenn Derene |publisher=[[Popular Mechanics]] |date=May 10, 2010 |accessdate=September 23, 2011}}</ref> and produced in quantities sufficient to treat individuals within the state of [[Arizona]] up until 1999.<ref>{{cite news |url=http://www.azcentral.com/business/articles/2011/08/04/20110804scorpion-antivenin-gets-fda-ok.html |title=Scorpion antivenin gets FDA's OK |author=Ken Alltucker |date=August 4, 2011 |publisher=[[The Arizona Republic]] |accessdate=September 23, 2011}}</ref> FDA approval was not required as it was provided at no charge, and use was restricted to within the state of Arizona; it was very successful in shortening the duration of symptoms and hospitalization. Production of this antivenom ceased by 2000 and the product was unavailable by 2004. A Mexican-produced antivenom, Anascorp [Antivenin Centruroides (scorpion) F(ab′)2, Laboratorios Silanes, Instituto Bioclon SA de CV], is being tested and used in its place.<ref name=UA-medical>{{cite web | year = 2000 | url = http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm | title = Soothing the Scorpion's Sting | author = David Von Behren, MPH | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20090603092350/http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm |archivedate=June 3, 2009}}</ref> On August 3, 2011, the FDA approved Anascorp for use in the United States.<ref name=FDA>{{cite web |url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm266611.htm |title=FDA approves the first specific treatment for scorpion stings |date=August 3, 2011 |publisher=FDA}}</ref>

=== First aid ===
Basic first aid measures can be used to help remediate scorpion stings:<ref name=UA-medical />
* Clean sting site with soap and water
* Apply a cool compress (cool cloth, no ice)
* Take [[paracetamol|acetaminophen]] (paracetamol) or [[ibuprofen]] for local pain and swelling

=== Medical emergencies ===
[[Image:Arizona bark scorption glowing under ultraviolet light.jpg|thumb|An Arizona bark scorpion glowing under [[ultraviolet light]]]]

Since the amount of venom the scorpion injects on a sting varies, Arizona poison control centers suggest immediate medical attention only in the event of extreme pain or stings involving children.<ref name=UA-poison>{{cite web | year = 2008 | url = http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php | title = Poison and Drug Information Center | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100820192450/http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php |archivedate=August 20, 2010}}</ref>

== UV lighting ==
Bark scorpions, like most other scorpions, will glow when exposed to a [[blacklight]]. This is particularly useful in scorpion detection, since bark scorpions are active during the night, and can be easily spotted using this method. Typical UV [[LED]] flashlights are able to readily detect scorpions at a distance of approximately 6 feet. Newly molted scorpions will not glow under [[ultraviolet light]] for a few days after molting.
{{-}}

== References ==
{{Reflist|32em}}

== External links ==
{{commons category|Centruroides sculpturatus|''Centruroides sculpturatus''}}
{{Portal|Arthropods}}
*[http://www.ntnu.no/ub/scorpion-files/c_exilicauda.php Further information on the scorpion]
*{{cite web |url=http://www.scorpsweep.com/facts.html |title=Scorpion Sweepers |last=Holland |first=Ben |year=2008}}

[[Category:Buthidae]]
[[Category:Fauna of the Southwestern United States|Scorpion, Arizona bark]]
[[Category:Animals described in 1863]]

[[cs:Štír zlatý]]
[[de:Arizona-Rindenskorpion]]
[[fr:Centruroides sculpturatus]]
{{WH}}
{{WS}}

Arizona bark scorpion

2022-10-07T22:27:51Z

44.197.72.169: /* Diet */

__NOTOC__
{{Taxobox
| image = Bbasgen-bark-scorpion.jpg
| name = Arizona bark scorpion
| regnum = [[Animal]]ia
| phylum = [[Arthropod]]a
| subphylum = [[Chelicerata]]
| classis = [[Arachnid]]a
| ordo = [[Scorpion]]es
| familia = [[Buthidae]]
| genus = ''[[Centruroides]]''
| species = '''''C. sculpturatus'''''
| binomial = ''Centruroides sculpturatus''
| binomial_authority = ([[Horatio C Wood, Jr.|Wood]], 1863)
}}
{{SI}}
{{CMG}}
==Overview==
The 'Arizona bark scorpion (Centruroides sculpturatus, included in Centruroides exilicauda, the Baja California bark scorpion) is a small light brown scorpion common to the United States. The range of the scorpion is the Sonoran Desert. An adult male can reach 8 centimeters in his body length, while a pregnant female is slightly smaller, with a maximum length of 7 centimeters.

== Diet ==
The Arizona bark scorpion is nocturnal, prefers to ambush its prey, and usually feeds on crickets or cockroaches.

== Predators ==
Bark scorpions are eaten by a wide variety of animals such as birds, reptiles, and other invertebrates. Some examples include [[spiders]], [[snakes]], [[peccaries]], [[rodents]], and other scorpions. In urban areas [[house cats]] may also consume bark scorpions. Development, pesticides and collecting scorpions for research or the pet trade also has an impact on the bark scorpion population.

== Life cycle ==
[[File:Basgen-scorpion-compared.JPG|thumb|right|Three adult and four juvenile Arizona bark scorpions]]
Arizona bark scorpions have a gestation period of several months, are born live, and are gently guided onto their mother's back. The female usually gives birth to between 25–35 young, and the young will remain with their mother until their first molt, up to 3 weeks after birth. Arizona bark scorpions may live up to 6 years.

While nearly all scorpions are solitary, the Arizona bark scorpion is a rare exception: during winter, packs of 20 to 30 scorpions can congregate.<ref name=UA>{{cite web | url = http://ag.arizona.edu/pubs/insects/az1223/ | title = Scorpions | work = Cooperative Extension, College of Agriculture & Life Sciences | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100721230743/http://ag.arizona.edu/pubs/insects/az1223/ |archivedate=July 21, 2010}}</ref>

== Habitat ==
The bark scorpion is particularly well adapted to the desert: layers of fat on its exoskeleton make it resistant to water loss. Nevertheless, bark scorpions hide during the heat of the day, typically under rocks, wood piles, or tree bark. Bark scorpions do not burrow, and are commonly found in homes, requiring only 1/16 of an inch for entry.<ref name=scorpion-mangement>{{cite web | year = 2008 | url = http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html | title = Scorpion Management Guidelines | accessdate = June 18, 2008 | archiveurl= http://web.archive.org/web/20080602232642/http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html| archivedate= 2 June 2008 | deadurl= no}}</ref>

Arizona bark scorpions prefer [[riparian]] areas with [[mesquite]], [[Populus sect. Aegiros|cottonwood]], and [[Platanus|sycamore]] groves, all of which have sufficient moisture and humidity to support insects and other prey species. The popularity of irrigated lawns, and other systems which increase environmental humidity in residential areas, has led to a massive increase in the number of these animals in some areas.<ref name=naturalhistory>{{cite book | last = Phillips S.; Comus P. | title = A Natural History of the Sonoran Desert | publisher = Arizona Sonora Desert Museum | year = 2000 | isbn =978-0-520-21980-9 | page = 292 }}</ref>

== Venom ==
[[Image:Bbasgen-scorpion-front.jpg|thumb|right|Frontal view of a bark scorpion in a defensive posture]]
The bark scorpion is the most [[venom (poison)|venomous]] scorpion in North America, and its venom can cause severe pain (coupled with numbness and tingling) in adult humans, typically lasting between 24 to 72 hours. Temporary dysfunction in the area stung is common; e.g. a hand or possibly arm can be immobilized or experience convulsions. It also may cause the loss of breath for a short period of time. Due to the extreme pain induced, many victims describe sensations of electrical jolts after [[envenomation]].

Fatalities from scorpion envenomation in the USA are rare and are limited to small animals (including small pets), small children, and adults with compromised immune systems. Extreme reaction to the venom is indicated by numbness, frothing at the mouth, paralysis, and a neuromotor syndrome that may be confused with a seizure and that may make breathing difficult, particularly for small children. Two recorded fatalities have occurred in the state of [[Arizona]] since 1968; the number of victims stung each year in Arizona is estimated to be in the thousands. In Mexico, more than 100,000 people are stung annually, and during a peak period in the 1980s, the bark scorpion claimed up to 800 lives there.<ref name=UA />

=== Antivenom ===
An [[antivenom]] was developed for this species at Arizona State University<ref>{{cite news |url=http://www.popularmechanics.com/science/health/snakebites-about-to-get-more-deadly |title=Why snakebites are about to get a lot more deadly |author=Glenn Derene |publisher=[[Popular Mechanics]] |date=May 10, 2010 |accessdate=September 23, 2011}}</ref> and produced in quantities sufficient to treat individuals within the state of [[Arizona]] up until 1999.<ref>{{cite news |url=http://www.azcentral.com/business/articles/2011/08/04/20110804scorpion-antivenin-gets-fda-ok.html |title=Scorpion antivenin gets FDA's OK |author=Ken Alltucker |date=August 4, 2011 |publisher=[[The Arizona Republic]] |accessdate=September 23, 2011}}</ref> FDA approval was not required as it was provided at no charge, and use was restricted to within the state of Arizona; it was very successful in shortening the duration of symptoms and hospitalization. Production of this antivenom ceased by 2000 and the product was unavailable by 2004. A Mexican-produced antivenom, Anascorp [Antivenin Centruroides (scorpion) F(ab′)2, Laboratorios Silanes, Instituto Bioclon SA de CV], is being tested and used in its place.<ref name=UA-medical>{{cite web | year = 2000 | url = http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm | title = Soothing the Scorpion's Sting | author = David Von Behren, MPH | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20090603092350/http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm |archivedate=June 3, 2009}}</ref> On August 3, 2011, the FDA approved Anascorp for use in the United States.<ref name=FDA>{{cite web |url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm266611.htm |title=FDA approves the first specific treatment for scorpion stings |date=August 3, 2011 |publisher=FDA}}</ref>

=== First aid ===
Basic first aid measures can be used to help remediate scorpion stings:<ref name=UA-medical />
* Clean sting site with soap and water
* Apply a cool compress (cool cloth, no ice)
* Take [[paracetamol|acetaminophen]] (paracetamol) or [[ibuprofen]] for local pain and swelling

=== Medical emergencies ===
[[Image:Arizona bark scorption glowing under ultraviolet light.jpg|thumb|An Arizona bark scorpion glowing under [[ultraviolet light]]]]

Since the amount of venom the scorpion injects on a sting varies, Arizona poison control centers suggest immediate medical attention only in the event of extreme pain or stings involving children.<ref name=UA-poison>{{cite web | year = 2008 | url = http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php | title = Poison and Drug Information Center | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100820192450/http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php |archivedate=August 20, 2010}}</ref>

== UV lighting ==
Bark scorpions, like most other scorpions, will glow when exposed to a [[blacklight]]. This is particularly useful in scorpion detection, since bark scorpions are active during the night, and can be easily spotted using this method. Typical UV [[LED]] flashlights are able to readily detect scorpions at a distance of approximately 6 feet. Newly molted scorpions will not glow under [[ultraviolet light]] for a few days after molting.
{{-}}

== References ==
{{Reflist|32em}}

== External links ==
{{commons category|Centruroides sculpturatus|''Centruroides sculpturatus''}}
{{Portal|Arthropods}}
*[http://www.ntnu.no/ub/scorpion-files/c_exilicauda.php Further information on the scorpion]
*{{cite web |url=http://www.scorpsweep.com/facts.html |title=Scorpion Sweepers |last=Holland |first=Ben |year=2008}}

[[Category:Buthidae]]
[[Category:Fauna of the Southwestern United States|Scorpion, Arizona bark]]
[[Category:Animals described in 1863]]

[[cs:Štír zlatý]]
[[de:Arizona-Rindenskorpion]]
[[fr:Centruroides sculpturatus]]
{{WH}}
{{WS}}

Arizona bark scorpion

2022-10-07T22:27:12Z

44.197.72.169: /* Overview */

__NOTOC__
{{Taxobox
| image = Bbasgen-bark-scorpion.jpg
| name = Arizona bark scorpion
| regnum = [[Animal]]ia
| phylum = [[Arthropod]]a
| subphylum = [[Chelicerata]]
| classis = [[Arachnid]]a
| ordo = [[Scorpion]]es
| familia = [[Buthidae]]
| genus = ''[[Centruroides]]''
| species = '''''C. sculpturatus'''''
| binomial = ''Centruroides sculpturatus''
| binomial_authority = ([[Horatio C Wood, Jr.|Wood]], 1863)
}}
{{SI}}
{{CMG}}
==Overview==
The 'Arizona bark scorpion (Centruroides sculpturatus, included in Centruroides exilicauda, the Baja California bark scorpion) is a small light brown scorpion common to the United States. The range of the scorpion is the Sonoran Desert. An adult male can reach 8 centimeters in his body length, while a pregnant female is slightly smaller, with a maximum length of 7 centimeters.

== Diet ==
The bark scorpion is nocturnal, prefers to ambush its prey, and usually feeds on [[cricket (insect)|cricket]]s or roaches.

== Predators ==
Bark scorpions are eaten by a wide variety of animals such as birds, reptiles, and other invertebrates. Some examples include [[spiders]], [[snakes]], [[peccaries]], [[rodents]], and other scorpions. In urban areas [[house cats]] may also consume bark scorpions. Development, pesticides and collecting scorpions for research or the pet trade also has an impact on the bark scorpion population.

== Life cycle ==
[[File:Basgen-scorpion-compared.JPG|thumb|right|Three adult and four juvenile Arizona bark scorpions]]
Arizona bark scorpions have a gestation period of several months, are born live, and are gently guided onto their mother's back. The female usually gives birth to between 25–35 young, and the young will remain with their mother until their first molt, up to 3 weeks after birth. Arizona bark scorpions may live up to 6 years.

While nearly all scorpions are solitary, the Arizona bark scorpion is a rare exception: during winter, packs of 20 to 30 scorpions can congregate.<ref name=UA>{{cite web | url = http://ag.arizona.edu/pubs/insects/az1223/ | title = Scorpions | work = Cooperative Extension, College of Agriculture & Life Sciences | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100721230743/http://ag.arizona.edu/pubs/insects/az1223/ |archivedate=July 21, 2010}}</ref>

== Habitat ==
The bark scorpion is particularly well adapted to the desert: layers of fat on its exoskeleton make it resistant to water loss. Nevertheless, bark scorpions hide during the heat of the day, typically under rocks, wood piles, or tree bark. Bark scorpions do not burrow, and are commonly found in homes, requiring only 1/16 of an inch for entry.<ref name=scorpion-mangement>{{cite web | year = 2008 | url = http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html | title = Scorpion Management Guidelines | accessdate = June 18, 2008 | archiveurl= http://web.archive.org/web/20080602232642/http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn74110.html| archivedate= 2 June 2008 | deadurl= no}}</ref>

Arizona bark scorpions prefer [[riparian]] areas with [[mesquite]], [[Populus sect. Aegiros|cottonwood]], and [[Platanus|sycamore]] groves, all of which have sufficient moisture and humidity to support insects and other prey species. The popularity of irrigated lawns, and other systems which increase environmental humidity in residential areas, has led to a massive increase in the number of these animals in some areas.<ref name=naturalhistory>{{cite book | last = Phillips S.; Comus P. | title = A Natural History of the Sonoran Desert | publisher = Arizona Sonora Desert Museum | year = 2000 | isbn =978-0-520-21980-9 | page = 292 }}</ref>

== Venom ==
[[Image:Bbasgen-scorpion-front.jpg|thumb|right|Frontal view of a bark scorpion in a defensive posture]]
The bark scorpion is the most [[venom (poison)|venomous]] scorpion in North America, and its venom can cause severe pain (coupled with numbness and tingling) in adult humans, typically lasting between 24 to 72 hours. Temporary dysfunction in the area stung is common; e.g. a hand or possibly arm can be immobilized or experience convulsions. It also may cause the loss of breath for a short period of time. Due to the extreme pain induced, many victims describe sensations of electrical jolts after [[envenomation]].

Fatalities from scorpion envenomation in the USA are rare and are limited to small animals (including small pets), small children, and adults with compromised immune systems. Extreme reaction to the venom is indicated by numbness, frothing at the mouth, paralysis, and a neuromotor syndrome that may be confused with a seizure and that may make breathing difficult, particularly for small children. Two recorded fatalities have occurred in the state of [[Arizona]] since 1968; the number of victims stung each year in Arizona is estimated to be in the thousands. In Mexico, more than 100,000 people are stung annually, and during a peak period in the 1980s, the bark scorpion claimed up to 800 lives there.<ref name=UA />

=== Antivenom ===
An [[antivenom]] was developed for this species at Arizona State University<ref>{{cite news |url=http://www.popularmechanics.com/science/health/snakebites-about-to-get-more-deadly |title=Why snakebites are about to get a lot more deadly |author=Glenn Derene |publisher=[[Popular Mechanics]] |date=May 10, 2010 |accessdate=September 23, 2011}}</ref> and produced in quantities sufficient to treat individuals within the state of [[Arizona]] up until 1999.<ref>{{cite news |url=http://www.azcentral.com/business/articles/2011/08/04/20110804scorpion-antivenin-gets-fda-ok.html |title=Scorpion antivenin gets FDA's OK |author=Ken Alltucker |date=August 4, 2011 |publisher=[[The Arizona Republic]] |accessdate=September 23, 2011}}</ref> FDA approval was not required as it was provided at no charge, and use was restricted to within the state of Arizona; it was very successful in shortening the duration of symptoms and hospitalization. Production of this antivenom ceased by 2000 and the product was unavailable by 2004. A Mexican-produced antivenom, Anascorp [Antivenin Centruroides (scorpion) F(ab′)2, Laboratorios Silanes, Instituto Bioclon SA de CV], is being tested and used in its place.<ref name=UA-medical>{{cite web | year = 2000 | url = http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm | title = Soothing the Scorpion's Sting | author = David Von Behren, MPH | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20090603092350/http://www.opa.medicine.arizona.edu/horizons/2000/fall/pg21.htm |archivedate=June 3, 2009}}</ref> On August 3, 2011, the FDA approved Anascorp for use in the United States.<ref name=FDA>{{cite web |url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm266611.htm |title=FDA approves the first specific treatment for scorpion stings |date=August 3, 2011 |publisher=FDA}}</ref>

=== First aid ===
Basic first aid measures can be used to help remediate scorpion stings:<ref name=UA-medical />
* Clean sting site with soap and water
* Apply a cool compress (cool cloth, no ice)
* Take [[paracetamol|acetaminophen]] (paracetamol) or [[ibuprofen]] for local pain and swelling

=== Medical emergencies ===
[[Image:Arizona bark scorption glowing under ultraviolet light.jpg|thumb|An Arizona bark scorpion glowing under [[ultraviolet light]]]]

Since the amount of venom the scorpion injects on a sting varies, Arizona poison control centers suggest immediate medical attention only in the event of extreme pain or stings involving children.<ref name=UA-poison>{{cite web | year = 2008 | url = http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php | title = Poison and Drug Information Center | publisher = [[University of Arizona]] | accessdate = June 20, 2008 |archiveurl=http://web.archive.org/web/20100820192450/http://www.pharmacy.arizona.edu/outreach/poison/scorpions.php |archivedate=August 20, 2010}}</ref>

== UV lighting ==
Bark scorpions, like most other scorpions, will glow when exposed to a [[blacklight]]. This is particularly useful in scorpion detection, since bark scorpions are active during the night, and can be easily spotted using this method. Typical UV [[LED]] flashlights are able to readily detect scorpions at a distance of approximately 6 feet. Newly molted scorpions will not glow under [[ultraviolet light]] for a few days after molting.
{{-}}

== References ==
{{Reflist|32em}}

== External links ==
{{commons category|Centruroides sculpturatus|''Centruroides sculpturatus''}}
{{Portal|Arthropods}}
*[http://www.ntnu.no/ub/scorpion-files/c_exilicauda.php Further information on the scorpion]
*{{cite web |url=http://www.scorpsweep.com/facts.html |title=Scorpion Sweepers |last=Holland |first=Ben |year=2008}}

[[Category:Buthidae]]
[[Category:Fauna of the Southwestern United States|Scorpion, Arizona bark]]
[[Category:Animals described in 1863]]

[[cs:Štír zlatý]]
[[de:Arizona-Rindenskorpion]]
[[fr:Centruroides sculpturatus]]
{{WH}}
{{WS}}

Bleeding (patient information)

2022-10-06T23:40:52Z

44.197.72.169: /* Medications to avoid */

{{Template:Bleeding (patient information)}}

'''For the WikiDoc page for this topic, click [[Bleeding|here]]'''

{{CMG}}

==Overview==
Bleeding refers to the loss of blood. Bleeding can happen inside the body (internally) or outside the body (externally). It may occur:

Inside the body when [[blood]] leaks from [[blood vessel]]s or [[organ]]s
Outside the body when blood flows through a natural opening (such as the vagina, mouth, or rectum)
Outside the body when blood moves through a break in the skin

Always seek emergency assistance for severe bleeding, and if internal bleeding is suspected. [[Internal bleeding]] can rapidly become life threatening, and immediate medical care is needed.

Serious injuries don't always bleed heavily, and some relatively minor injuries (for example, scalp wounds) can bleed quite a lot. People who take blood-thinning medication or who have a bleeding disorder such as hemophilia may bleed excessively and quickly because their blood does not clot properly. Bleeding in such people requires immediate medical attention.

Direct pressure will stop most external bleeding, and is the most important first aid step.

Always wash your hands before (if possible) and after giving first aid to someone who is bleeding, in order to avoid [[infection]].

Try to use latex gloves when treating someone who is bleeding. Latex gloves should be in every first aid kit. People allergic to latex can use a non-latex, synthetic glove. You can catch viral hepatitis if you touch infected blood, and HIV can be spread if infected blood gets into an open wound -- even a small one.

Although puncture wounds usually don't bleed very much, they carry a high risk of infection. Seek medical care to prevent tetanus or other infection.

Abdominal and chest wounds can be very serious because of the possibility of severe internal bleeding. They may not look very serious, but can result in shock. Seek immediate medical care for any abdominal or chest wound. If organs are showing through the wound, do not try to push them back into place. Cover the injury with a moistened cloth or bandage, and apply only very gentle pressure to stop the bleeding.

Blood loss can cause bruises (blood collected under the skin), which usually result from a blow or a fall. They are dark, discolored areas on the skin. Apply a cool compress to the area as soon as possible to reduce swelling. Wrap the ice in a towel and place the towel over the injury. Do not place ice directly on the [[skin]].

==What are the symptoms of Bleeding?==
* [[Blood]] coming from an open wound
* [[Bruising]]
* [[Shock]], which may cause any of the following symptoms:
* Confusion or decreasing alertness
* [[Clammy skin]]
* Dizziness or light-headedness after an injury
* [[Low blood pressure]]
* Paleness ([[pallor]])
* Rapid pulse, [[increased heart rate]]
* [[Shortness of breath]]
* [[Weakness]]

Symptoms of internal bleeding may also include:

* [[Abdominal pain]] and swelling
* [[Chest pain]]
* External bleeding through a natural opening
* Blood in the stool (appears black, maroon, or bright red)
* [[hematuria|Blood in the urine]] (appears red, pink, or tea-colored)
* [[Hemetemesis|Blood in the vomit]] (looks bright red, or brown like coffee-grounds)
* [[Vaginal bleeding]] (heavier than usual or after [[menopause]])

Skin color changes that occur several days after an injury (skin may black, blue, purple, yellowish green)

==What causes Bleeding?==
Bleeding can be caused by injuries or can occur spontaneously. Spontaneous [[bleeding]] is most commonly caused by problems with the joints or the [[gastrointestinal]] or [[urogenital tract]]s.

==When to seek urgent medical care?==
Seek medical help if:

* Bleeding can't be controlled, required the use of a tourniquet, or was caused by a serious [[injury]]
* The wound might need stitches
* Gravel or dirt cannot be removed easily with gentle cleaning
* You think there may be internal bleeding or [[shock]]
* Signs of infection develop, including increased [[pain]], redness, [[swelling]], yellow or brown fluid, [[swollen lymph node]]s, fever, or red streaks spreading from the site toward the [[heart]]
* The injury was due to an animal or human bite
* The patient has not had a tetanus shot in the last 5-10 years

==Treatment options==
First aid is appropriate for external bleeding. If bleeding is severe, or if shock or internal bleeding is suspected, get emergency help immediately.

* Calm and reassure the person. The sight of blood can be very frightening.
* If the wound is superficial, wash it with soap and warm water and pat dry. Superficial wounds or scrapes are injuries that affect the top layers of skin and bleeding from such wounds is often described as "oozing," because it is slow.
* Lay the person down. This reduces the chances of fainting by increasing blood flow to the brain. When possible, raise up the part of the body that is bleeding.
* Remove any obvious loose debris or dirt from a [[wound]]. If an object such as a knife, stick, or arrow becomes stuck in the body, DO NOT remove it. Doing so may cause more damage and may increase bleeding. Place pads and bandages around the object and tape the object in place.
* Put pressure directly on an outer wound with a sterile bandage, clean cloth, or even a piece of clothing. If nothing else is available, use your hand. Direct pressure is best for external bleeding, except for an [[eye injury]].
* Maintain pressure until the bleeding stops. When it has stopped, tightly wrap the wound dressing with adhesive tape or a piece of clean clothing. Place a cold pack over the dressing. Do not peek to see if the bleeding has stopped.
* If bleeding continues and seeps through the material being held on the wound, do not remove it. Simply place another cloth over the first one. Be sure to seek medical attention.
* If the bleeding is severe, get medical help and take steps to prevent shock. Keep the injured body part completely still. Lay the person flat, raise the feet about 12 inches, and cover the person with a coat or blanket. DO NOT move the person if there has been a head, neck, back, or leg injury, as doing so may make the injury worse. Get medical help as soon as possible.

'''DO NOT'''
* DO NOT apply a tourniquet to control bleeding, except as a last resort. Doing so may cause more harm than good. A tourniquet should be used only in a life-threatening situation and should be applied by an experienced person
* If continuous pressure hasn't stopped the bleeding and bleeding is extremely severe, a tourniquet may be used until medical help arrives or bleeding is controllable.
* It should be applied to the limb between the bleeding site and the heart and tightened so bleeding can be controlled by applying direct pressure over the wound.
* To make a tourniquet, use bandages 2 to 4 inches wide and wrap them around the limb several times. Tie a half or square knot, leaving loose ends long enough to tie another knot. A stick or a stiff rod should be placed between the two knots. Twist the stick until the bandage is tight enough to stop the bleeding and then secure it in place.
* Check the tourniquet every 10 to 15 minutes. If the bleeding becomes controllable, (manageable by applying direct pressure), release the tourniquet.
* DO NOT peek at a wound to see if the bleeding is stopping. The less a [[wound]] is disturbed, the more likely it is that you'll be able to control the bleeding
* DO NOT probe a wound or pull out any embedded object from a wound. This will usually cause more bleeding and harm
* DO NOT remove a dressing if it becomes soaked with [[blood]]. Instead, add a new one on top
* DO NOT try to clean a large wound. This can cause heavier bleeding
* DO NOT try to clean a wound after you get the bleeding under control. Get medical help

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==Where to find medical care for Bleeding?==
[http://maps.google.com/maps?q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|map+top+hospital+Bleeding}}}}&oe=utf-8&rls=org.mozilla:en-US:official&client=firefox-a&um=1&ie=UTF-8&sa=N&hl=en&tab=wl Directions to Hospitals Treating Bleeding]

==Prevention of Bleeding==
Use good judgment and keep knives and sharp objects away from small children.

Stay up-to-date on [[vaccination]]s, especially the [[tetanus]] [[immunization]].

==Sources==
http://www.nlm.nih.gov/medlineplus/ency/article/000045.htm
{{WH}}
{{WS}}

[[Category:Patient information]]
[[Category:Medical emergencies]]
[[Category:Blood]]
[[Category:Hematology]]

Genomic imprinting

2022-10-06T20:33:49Z

44.197.72.169: /* Problems associated with imprinting */

{{CMG}}

'''Genomic imprinting''' is a [[genetics|genetic]] phenomenon by which certain [[gene]]s are [[gene expression|expressed]] in a [[parent]]-of-origin-specific manner. Imprinted genes are either expressed only from the allele inherited from the mother (eg. ''[[H19 (gene)|H19]]'' or ''[[CDKN1C]]''), or in other instances from the allele inherited from the father (eg. ''IGF2''). Forms of genomic imprinting have been demonstrated in [[insect]]s, [[mammal]]s and flowering [[plant]]s.

In [[Ploidy#Diploid|diploid]] organisms [[somatic cell]]s possess two copies of the [[genome]]. Each [[autosomal]] gene is therefore represented by two copies, or alleles, with one copy inherited from each parent at [[fertilisation]]. For the vast majority of autosomal genes, expression occurs from both [[allele]]s simultaneously. In mammals however, a small proportion (<1%) of genes are imprinted, meaning that gene expression occurs from only one allele. The expressed allele is dependent upon its parental origin. For example, the gene encoding [[Insulin-like growth factor 2]] (IGF2/Igf2) is only expressed from the allele inherited from the father (DeChiara ''et al.'', 1991).

The phrase "imprinting" was first used to described events in the insect ''Pseudococcus nipae'' (Schrader 1921). In Pseudococcids or [[mealybugs]] (Homoptera, Coccoidea) both the male and female develop from a fertilised egg. In females, all chromosomes remain [[Euchromatin|euchromatic]] and functional. In embryos destined to become males, one [[haploid]] set of chromosomes becomes [[Heterochromatin|heterochromatinised]] after the sixth cleavage division and remains so in most tissues; males are thus functionally haploid (Brown and Nur 1964; Hughes-Schrader 1948; Nur 1990). In insects, imprinting describes the silencing of the paternal genome in males, and thus is involved in sex determination. In mammals, genomic imprinting describes the processes involved in introducing functional inequality between two parental alleles of a gene (Feil and Berger, 2007).

==Imprinted genes in mammals==
Experimental manipulation of mouse embryos in the early 1980s showed that normal development requires the contribution of both the maternal and paternal genomes. Gynogenetic embryos (containing two female genomes) show relatively normal embryonic development, but poor placental development. In contrast, androgenetic embryos (containing two male genomes) show very poor embryonic development but normal placental development. Further investigation identified that these phenotypes were the result of unbalanced imprinted gene expression (Barton ''et al.'', 1984; McGrath and Solter, 1984).

The gynogenetic embryos have twice the normal level of maternally expressed genes, and completely lack expression of paternally expressed genes, whereas the reverse is true for androgenetic embryos. It is now known that there are approximately 80 imprinted genes in humans and mice, many of which are involved in embryonic and placental growth and development (Isles and Holland, 2005; Morison ''et al.'', 2005; Reik and Lewis, 2005; Wood and Oakey, 2006).

No naturally occurring cases of [[parthenogenesis]] exist in mammals because of imprinted genes. Experimental manipulation of a paternal methylation imprint controlling the Igf2 gene has, however, recently allowed the creation of rare individual mice with two maternal sets of chromosomes - but this is not a true parthenogenote. [[Hybrid (biology)|Hybrid]] offspring of two species may exhibit unusual growth due to the novel combination of imprinted genes.<ref>[http://www.hhmi.org/news/tilghman.html HHMI News: Gene Tug-of-War Leads to Distinct Species]</ref>

===Genetic mapping of imprinted genes===
At the same time as the generation of the gynogenetic and androgenetic embryos discussed above, mouse embryos were also being generated that contained only small regions that were derived from either a paternal or maternal source (Cattanach and Kirk, 1985; McLaughlin ''et al.'', 1996). The generation of a series of such uniparental disomies, which together span the entire genome, allowed the creation of an imprinting map.<ref>[http://www.mgu.har.mrc.ac.uk/research/imprinting/largemap.html Untitled Document]</ref> Those regions which when inherited from a single parent result in a discernable phenotype contain imprinted gene(s). Further research showed that within these regions there were often numerous imprinted genes (Bartolomei and Tilghman 1997. Around 80% of imprinted genes are found in clusters such as these, called imprinted domains, suggesting a level of co-ordinated control (Reik and Walter 2001).

===Imprinting mechanisms===
Imprinting is a dynamic process. It must be possible to erase and re-establish the imprint through each generation. The nature of the imprint must therefore be [[epigenetic]] (modifications to the structure of the DNA rather than the sequence). In [[germline]] cells the imprint is erased, and then re-established according to the [[sex]] of the individual; i.e. in the developing sperm, a paternal imprint is established, whereas in developing oocytes, a maternal imprint is established. This process of erasure and [[reprogramming]] is necessary such that the current imprinting status is relevant to the sex of the individual. In both plants and mammals there are two major mechanisms that are involved in establishing the imprint; these are [[DNA methylation]] and [[histone]] modifications.

===Regulation===
The grouping of imprinted genes within clusters allows them to share common regulatory elements, such as non-coding [[RNA]]s and differentially methylated regions (DMRs). When these regulatory elements control the imprinting of several genes in a given region, they are known as imprinting control regions (ICR). The expression of non-coding RNAs, such as ''Air'' on mouse chromosome 17 and ''KCNQ1OT1'' on human chromosome 11p15.5, have been shown to be essential for the imprinting of genes in their corresponding regions.

Differentially methylated regions are generally segments of DNA rich in [[cytosine]] and [[guanine]] nucleotides, with the cytosine nucleotides methylated on one copy but not on the other. Contrary to expectation, methylation does not necessarily mean silencing; instead, the effect of methylation depends upon the default state of the region.

===Functions of imprinted genes===
The control of expression of specific genes by genomic imprinting is unique to placental mammals ([[eutherians]] and [[marsupials]]) and flowering plants. Imprinting of whole chromosomes has been reported in mealybugs (Brown and Nur. 1964; Hughes-Schrader. 1948; Schrader 1921; Nur. 1990) and a [[fungus gnat]] (''Sciara'') (Metz. 1938). It has also been established that [[X-chromosome]] inactivation occurs in an imprinted manner in the extra-embryonic tissues of mice, where it is always the paternal X-chromosome which is silenced (Alleman and Doctor, 2000; Reik and Walter, 2001).

The majority of imprinted genes in mammals have been found to have roles in the control of embryonic growth and development, including development of the placenta (Isles and Holland 2005; Tycko and Morison 2002). Other imprinted genes are involved in post-natal development, with roles affecting suckling and metabolism (Constancia ''et al.'', 2004; Tycko and Morison, 2002).

===Theories on the origins of imprinting===
Imprinting appears to be able to increase the [[Fitness (biology)|evolutionary fitness of genes]] in two ways, so either or both could be responsible for its origins.

Perhaps the most widely accepted explanation for the occurrence of genomic imprinting is the "parental conflict hypothesis" (Moore and Haig 1991). This hypothesis states that the inequality between parental genomes due to imprinting is a result of the [[sexual conflict|differing interests of each parent]] in terms of the [[Fitness (biology)|evolutionary fitness of their genes]]. The [[father]] is more interested in the growth of his offspring, at the expense of the [[mother]]. The mother's interest is to conserve resources for her own survival while providing sufficient nourishment to current and subsequent litters. Accordingly, paternally expressed genes tend to be growth promoting whereas maternally expressed genes tend to be growth limiting (Moore and Haig 1991).

Another hypothesis behind the origins of genomic imprinting is that this phenomenon evolved to silence foreign DNA elements, such as genes of viral origin. There appears to be an over-representation of [[Transposon|retrotransposed]] genes, that is to say genes that are inserted into the genome by [[virus]]es, among imprinted genes. It has also been postulated that if the retrotransposed gene is inserted close to another imprinted gene, it may just acquire this imprint (Chai et. al 2001).

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==Examples==
===Prader-Willi and Angelman Syndrome===
Several [[genetic disorder|genetic diseases]] that map to 15q11 (band 11 of the long arm of chromosome 15) in humans are due to abnormal imprinting. This region is differently imprinted in maternal and paternal chromosomes, and both imprintings are needed for normal development. In a normal individual, the maternal allele is methylated, while the paternal allele is unmethylated. It is possible for an individual to fail to inherit a properly imprinted 15q11 from one parent, as a result either of deletion of the 15q11 region from that parent's chromosome 15 or, less frequently, of [[uniparental disomy]] (in which both copies have been taken from the other parent's genes).

* If neither copy of 15q11 has ''paternal imprinting'', the result is [[Prader-Willi syndrome]] (characterised by [[hypotonia]], [[obesity]], and [[hypogonadism]]).
* If neither copy has ''maternal imprinting'', the result is [[Angelman syndrome]] (characterised by [[epilepsy]], [[tremors]], and a perpetually smiling [[facial expression]]).

===NOEY2===
[[NOEY2]] is a paternally expressed imprinted gene located on chromosome 1 in humans. Loss of NOEY2 expression is linked to an increased risk of ovarian and breast cancers; in 41% of breast and ovarian cancers the protein transcribed by NOEY2 is not expressed, suggesting that it functions as a [[tumor suppressor gene|tumour suppressor]]<ref name ="NOEY2">

{{
cite news
|url=http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=9874798
|publisher=The National Academy of Sciences
|title=NOEY2 (ARHI), an imprinted putative tumor suppressor gene in ovarian and breast carcinomas
|date=January 5, 1999

}}</ref> Therefore, if a person inherits both chromosomes from the mother, the gene will not be expressed and the individual is put at a greater risk for breast and ovarian cancer.

==Imprinted genes in plants==
Decades after imprinting was demonstrated in the mouse, a similar phenomena was observed in [[flowering plant]]s (angiosperms). During fertilisation of the embryo in flowers, a second separate fertilisation event gives rise to the [[endosperm]], an extraembryonic structure that nourishes the [[seed]] similar to the mammalian [[placenta]]. Unlike the embryo, the endosperm often contains two copies of the maternal genome and fusion with a male gamete results in a triploid genome. This uneven ratio of maternal to paternal genomes appears to be critical for seed development. Some genes are found to be expressed from both maternal genomes while others are expressed exclusively from the lone paternal copy (Nowack ''et al.'', 2007).

==See also==
* [[Metabolic imprinting]]
* [[Bookmarking]]
* [[Epigenetics]]

==Notes==
<references/>

==References==
===Scientific journals===
{{refbegin|2}}
* {{cite journal | author = Bartolomei, M. S. and Tilghman, S. M. | date = 1997 | title = Genomic imprinting in mammals | journal = Annu Rev Genet | volume = 31 | pages = 493-525 | doi = 10.1146/annurev.genet.31.1.493 | url = http://arjournals.annualreviews.org/doi/full/10.1146/annurev.genet.31.1.493 | format = subscription required }}
* {{cite journal | author = Barton, S. C. | coauthors= ''et al'' | date = 1984 | title = Role of paternal and maternal genomes in mouse development | journal = [[Nature (journal)|Nature]] | volume = 311 | issue = 5984 | pages = 374-376 | doi = 10.1038/311374a0 | pmid = 6482961 | url = http://www.nature.com/nature/journal/v311/n5984/abs/311374a0.html }}
* {{cite journal | author = Brown S.W. and Nur U. | date = 1964 | title = Heterochromatic chromosomes in the coccids| journal = [[Science (journal)|Science]] | volume = 145 | pages = 130-136 | pmid = 14171547 | doi= 10.1126/science.145.3628.130 | url = http://www.sciencemag.org/cgi/content/citation/145/3628/130 }}
*Cattanach, B. M. and Kirk, M. 1985. Differential activity of maternally and paternally derived chromosome regions in mice. Nature 315(6019), pp. 496-498
*Chai, J.H. et al. 2001. Retrotransposed genes such as Frat3 in the mouse Chromosome 7C Prader-Willi syndrome region acquire the imprinted status of their insertion site. Mamm. Genome 12, 813–821
*Constancia, M. et al. 2004. Resourceful imprinting. Nature 432(7013), pp. 53-57
*DeChiara, T. M. et al. 1991. Parental imprinting of the mouse insulin-like growth factor II gene. Cell 64(4), pp. 849-859
*Feil, R and Berger, F 2007. Convergent evolution of genomic imprinting in plants and mammals. Trends in Genetics 23(4) pp. 192-199
*Hughes-Schrader, S. 1948. Cytology of Coccids (Coccoidea-Homoptera). Adv. Genet. 2, pp127-203.
*Isles, A. R. and Holland, A. J. 2005. Imprinted genes and mother-offspring interactions. Early Hum Dev 81(1), pp. 73-77.
*McGrath, J. and Solter, D. 1984. Completion of mouse embryogenesis requires both the maternal and paternal genomes. Cell 37(1), pp. 179-183.
*McLaughlin, K. J. et al. 1996. Mouse embryos with paternal duplication of an imprinted chromosome 7 region die at midgestation and lack placental spongiotrophoblast. Development 122(1), pp. 265-270.
*Metz, C.W. 1938. Chromosome behavior, inheritance and sex determination in Sciara. Am. Nat. 72, pp. 485-520.
*Moore, T. and Haig, D. 1991. Genomic imprinting in mammalian development: a parental tug-of-war. Trends Genet 7(2), pp. 45-49
*Morison, I. M. et al. 2005. A census of mammalian imprinting. Trends Genet 21(8), pp. 457-465.
*Nowack et al. 2007. Bypassing genomic imprinting allows seed development. Nature 447, pp. 312-316.
*Nur, U. (1990). Heterochromatization and euchromatization of whole genome in scale insects (Coccoidea:Homoptera). Development Suppl. 29-34.
*Reik, W. and Lewis, A. 2005. Co-evolution of X-chromosome inactivation and imprinting in mammals. Nat Rev Genet 6(5), pp. 403-410.
*Reik, W. and Walter, J. 2001. Genomic imprinting: parental influence on the genome. Nat Rev Genet 2(1), pp. 21-32.
*Schrader, F. 1921. The chromosomes of Pseudococcus nipae. Biol Bull. 40, pp 259-270.
*Tycko, B. and Morison, I. M. 2002. Physiological functions of imprinted genes. J Cell Physiol 192(3), pp. 245-258
*Wood, A.J. and Oakey, R.J. 2006. Genomic Imprinting in Mammals: Emerging Themes and Established Theories. PLoS Genetics 2(11), e147.
{{refend}}

==External links==
*[http://igc.otago.ac.nz/ Imprinted Gene and Parent-of-origin Effect Database]
*[http://www.mgu.har.mrc.ac.uk/research/imprinting/ MRC Harwell Imprinting Resource]
*[http://geneimprint.com/ geneimprint.com]
*[http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/I/Imprinting.html J. Kimball's Imprinted Genes Site]
* {{MeshName|Genomic+imprinting}}

 

[[Category:Molecular genetics]]
[[Category:Gene expression]]
[[Category:Epigenetics]]

[[de:Imprinting]]
[[es:Impronta genética]]
[[he:החתמה גנומית]]
[[ja:ゲノムインプリンティング]]
[[pl:Imprinting (genetyka)]]
[[pt:Imprinting genômico]]
[[sk:Imprinting]]
[[sr:Утискивање]]
[[fi:Leimautuminen]]
[[zh:基因銘印]]

{{WH}}
{{WikiDoc Sources}}

Mitral stenosis echocardiography

2022-10-06T18:01:19Z

44.197.72.169: /* Echocardiographic Assessment of Mitral Stenosis Severity */

__NOTOC__
{{Mitral stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}

==Overview==
[[Transthoracic echocardiography]] (TTE) may be helpful in the [[diagnosis]] of mitral stenosis. Findings on a [[transthoracic echocardiography]] ([[Echocardiography|TTE]]) should be performed among [[patients]] with suspected mitral stenosis to confirm the [[diagnosis]] and to establish the baseline severity of [[disease]]. It should then be performed to monitor the course of [[disease]] over time. [[Echocardiography]] findings of mitral stenosis include decreased opening of the [[mitral valve]] leaflets and increased [[blood]] flow velocity during [[diastole]]. The trans-[[Mitral valve|mitral]] gradient as measured by [[Doppler echocardiography]] is the [[gold standard (test)|gold standard]] in the evaluation of the severity of mitral stenosis. [[TEE]] should also be performed prior to [[percutaneous mitral balloon commissurotomy]] for the evaluation of the presence of [[left atrial]] [[thrombus]].

==Echocardiography==
*[[Echocardiography]] is the standard and by using various techniques the transmitral flows can be converted to [[valve]] areas.<ref name="MR">Mitral regurgitation https://radiopaedia.org/articles/mitral-stenosis Accessed on December 7, 2016</ref><ref name="pmid24281331">{{cite journal| author=Nunes MC, Tan TC, Elmariah S, do Lago R, Margey R, Cruz-Gonzalez I et al.| title=The echo score revisited: Impact of incorporating commissural morphology and leaflet displacement to the prediction of outcome for patients undergoing percutaneous mitral valvuloplasty. | journal=Circulation | year= 2014 | volume= 129 | issue= 8 | pages= 886-95 | pmid=24281331 | doi=10.1161/CIRCULATIONAHA.113.001252 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24281331 }} </ref>
*The [[mitral valve]] area can be directly planimetered in some cases.<ref name="Carabello2005">{{cite journal|last1=Carabello|first1=Blase A.|title=Modern Management of Mitral Stenosis|journal=Circulation|volume=112|issue=3|year=2005|pages=432–437|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.104.532498}}</ref>
*[[Echocardiographic]] findings also predict the success/failure of [[balloon valvuloplasty]].<ref name="Sravan K ReddyRanjan Shetty2019">{{cite journal|last1=Sravan K Reddy|first1=N.|last2=Ranjan Shetty|first2=K.|last3=Sudhakar Rao|first3=M.|last4=Sree Madhurya Reddy|first4=M.|title=Strain imaging to assess early effects of successful percutaneous balloon mitral valvotomy on left atrium mechanics|journal=The Egyptian Heart Journal|volume=71|issue=1|year=2019|issn=2090-911X|doi=10.1186/s43044-019-0021-3}}</ref>
*Coexisting [[valve]] dysfunction can be identified as well as [[pulmonary hypertension]] and right [[ventricular dysfunction]].<ref name="BaumgartnerHung2009">{{cite journal|last1=Baumgartner|first1=Helmut|last2=Hung|first2=Judy|last3=Bermejo|first3=Javier|last4=Chambers|first4=John B.|last5=Evangelista|first5=Arturo|last6=Griffin|first6=Brian P.|last7=Iung|first7=Bernard|last8=Otto|first8=Catherine M.|last9=Pellikka|first9=Patricia A.|last10=Quiñones|first10=Miguel|title=Echocardiographic Assessment of Valve Stenosis: EAE/ASE Recommendations for Clinical Practice|journal=Journal of the American Society of Echocardiography|volume=22|issue=1|year=2009|pages=1–23|issn=08947317|doi=10.1016/j.echo.2008.11.029}}</ref>
*[[Cardiac catheterization]] is a secondary modality used when surgical/[[percutaneous]] repair is contemplated or if [[Symptom|symptoms]] are out of proportion to noninvasive testing results.<ref name="VahanianAlfieri2012">{{cite journal|last1=Vahanian|first1=Alec|last2=Alfieri|first2=Ottavio|last3=Andreotti|first3=Felicita|last4=Antunes|first4=Manuel J.|last5=Barón-Esquivias|first5=Gonzalo|last6=Baumgartner|first6=Helmut|last7=Borger|first7=Michael Andrew|last8=Carrel|first8=Thierry P.|last9=De Bonis|first9=Michele|last10=Evangelista|first10=Arturo|last11=Falk|first11=Volkmar|last12=Iung|first12=Bernard|last13=Lancellotti|first13=Patrizio|last14=Pierard|first14=Luc|last15=Price|first15=Susanna|last16=Schäfers|first16=Hans-Joachim|last17=Schuler|first17=Gerhard|last18=Stepinska|first18=Janina|last19=Swedberg|first19=Karl|last20=Takkenberg|first20=Johanna|last21=Von Oppell|first21=Ulrich Otto|last22=Windecker|first22=Stephan|last23=Zamorano|first23=Jose Luis|last24=Zembala|first24=Marian|last25=Bax|first25=Jeroen J.|last26=Baumgartner|first26=Helmut|last27=Ceconi|first27=Claudio|last28=Dean|first28=Veronica|last29=Deaton|first29=Christi|last30=Fagard|first30=Robert|last31=Funck-Brentano|first31=Christian|last32=Hasdai|first32=David|last33=Hoes|first33=Arno|last34=Kirchhof|first34=Paulus|last35=Knuuti|first35=Juhani|last36=Kolh|first36=Philippe|last37=McDonagh|first37=Theresa|last38=Moulin|first38=Cyril|last39=Popescu|first39=Bogdan A.|last40=Reiner|first40=Željko|last41=Sechtem|first41=Udo|last42=Sirnes|first42=Per Anton|last43=Tendera|first43=Michal|last44=Torbicki|first44=Adam|last45=Vahanian|first45=Alec|last46=Windecker|first46=Stephan|last47=Popescu|first47=Bogdan A.|last48=Von Segesser|first48=Ludwig|last49=Badano|first49=Luigi P.|last50=Bunc|first50=Matjaž|last51=Claeys|first51=Marc J.|last52=Drinkovic|first52=Niksa|last53=Filippatos|first53=Gerasimos|last54=Habib|first54=Gilbert|last55=Kappetein|first55=A. Pieter|last56=Kassab|first56=Roland|last57=Lip|first57=Gregory Y.H.|last58=Moat|first58=Neil|last59=Nickenig|first59=Georg|last60=Otto|first60=Catherine M.|last61=Pepper|first61=John|last62=Piazza|first62=Nicolo|last63=Pieper|first63=Petronella G.|last64=Rosenhek|first64=Raphael|last65=Shuka|first65=Naltin|last66=Schwammenthal|first66=Ehud|last67=Schwitter|first67=Juerg|last68=Mas|first68=Pilar Tornos|last69=Trindade|first69=Pedro T.|last70=Walther|first70=Thomas|title=Guidelines on the management of valvular heart disease (version 2012)|journal=European Journal of Cardio-Thoracic Surgery|volume=42|issue=4|year=2012|pages=S1–S44|issn=1873-734X|doi=10.1093/ejcts/ezs455}}</ref>

[[Mitral valve]] assessment with [[echocardiography]] maybe include:<ref name="OmranArifi2011">{{cite journal|last1=Omran|first1=A.S.|last2=Arifi|first2=Ahmed A.|last3=Mohamed|first3=A.A.|title=Echocardiography in mitral stenosis|journal=Journal of the Saudi Heart Association|volume=23|issue=1|year=2011|pages=51–58|issn=10167315|doi=10.1016/j.jsha.2010.07.007}}</ref>

*[[Diagnosis]] from the pattern of valve involvement and [[calcification]]
* Severity of mitral stenosis
* Associated [[mitral regurgitation]]
* Other co-existent [[valve]] [[Lesion|lesions]]
* Chamber [[Dilation|dilatation]] and function

Complete [[Echocardiography|echocardiographic]] examination of [[mitral valve]] include M-mode tracing, multiple two dimensional views, and [[Doppler]] flow evaluation.

=== Echocardiographic Assessment of Mitral Stenosis Severity ===

{| style="cellpadding=0; cellspacing= 0; width: 600px;"
|-
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Severity'''|| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Mild'''||style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Moderate''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Severe'''
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |[[Mitral valve]] area || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |2.2 - 1.5 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |1- 1.5 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |<1
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |Pressure Half time (msec) || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |100 - 150 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |150 - 220 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |>220
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |Mean Pressure Gradient ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | <5 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |5-10 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |>10
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |TR velocity || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |<2.7 || style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | 2.7-3 ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | >3
|-
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |[[Pulmonary]] [[artery]] [[pressure]]|| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |<30 ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | 30-50 ||style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | >50
|}

=== M-mode Echocardiography ===

M-mode [[echocardiographic]] assessment of the valve reveals slow early [[Diastole|diastolic]] closure of the [[mitral valve]]. The mid-diastolic closure velocity or E-F slope is remarkably reduced or sometimes even flat. Though least reliable, this can be used to assess the severity of the [[mitral stenosis]] and to determine re-stenosis from serial measurements after [[surgical]] or percutaneous treatment. E-F slope of less than 10 mm/sec (normal is >60 mm/sec) recoded during suspended respiration suggests severe mitral stenosis. E-F slope can also be flat in subjects with normal [[mitral valve]] if the left [[Ventricle (heart)|ventricular]] compliance is reduced.<ref name="NaguehSmiseth2016">{{cite journal|last1=Nagueh|first1=Sherif F.|last2=Smiseth|first2=Otto A.|last3=Appleton|first3=Christopher P.|last4=Byrd|first4=Benjamin F.|last5=Dokainish|first5=Hisham|last6=Edvardsen|first6=Thor|last7=Flachskampf|first7=Frank A.|last8=Gillebert|first8=Thierry C.|last9=Klein|first9=Allan L.|last10=Lancellotti|first10=Patrizio|last11=Marino|first11=Paolo|last12=Oh|first12=Jae K.|last13=Popescu|first13=Bogdan Alexandru|last14=Waggoner|first14=Alan D.|title=Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging|journal=Journal of the American Society of Echocardiography|volume=29|issue=4|year=2016|pages=277–314|issn=08947317|doi=10.1016/j.echo.2016.01.011}}</ref>

Another M-mode feature of mitral stenosis is the anterior movement of posterior [[mitral valve]] leaflet in early [[diastole]]. Opening snap usually coincides with E point.

The images below show decreased E-F slope:
[[Image:Mitral Stenosis.jpg|thumb|450px|left|Mitral Stenosis M Mode]][[Image: M Mode MS.jpg|thumb|450px|center|Mitral Stenosis M Mode. Leaflet tips bright (calcified) and thickened and E/F slope decreased]]

 

=== 2D-Echocardiography ===

* This is a reliable method of assessing the severity of [[stenosis]].<ref name="pmid629495">{{cite journal| author=Wann LS, Weyman AE, Feigenbaum H, Dillon JC, Johnston KW, Eggleton RC| title=Determination of mitral valve area by cross-sectional echocardiography. | journal=Ann Intern Med | year= 1978 | volume= 88 | issue= 3 | pages= 337-41 | pmid=629495 | doi= | pmc= | url= }} </ref><ref name="pmid830199">{{cite journal| author=Nichol PM, Gilbert BW, Kisslo JA| title=Two-dimensional echocardiographic assessment of mitral stenosis. | journal=Circulation | year= 1977 | volume= 55 | issue= 1 | pages= 120-8 | pmid=830199 | doi= | pmc= | url= }} </ref>
* As with any stenotic valve, the main [[Diagnosis|diagnostic]] feature in the parasternal long axis view is the doming of the entire valve into ventricle during diastole. This is due to the reduced mobility of the valve tips compared to the base of the leaflets leading to development of persistent left atrio-ventricular(AV) gradient. With this orientation, maximum opening area of mitral valve during diastole can be measured by direct planimetry of the two dimensional image. Valve orifice area of <1 cm2 is considered severe.<ref name="OmranArifi20112">{{cite journal|last1=Omran|first1=A.S.|last2=Arifi|first2=Ahmed A.|last3=Mohamed|first3=A.A.|title=Echocardiography in mitral stenosis|journal=Journal of the Saudi Heart Association|volume=23|issue=1|year=2011|pages=51–58|issn=10167315|doi=10.1016/j.jsha.2010.07.007}}</ref>
* During atrial contraction when the AV gradient increases, the valves open abruptly producing opening snap and a knee bend appearance on the precordial long axis view. Thickening of the valve leaflets with or without [[calcification]] can be visualized with echocardiography. This can also involve the annulus and the chordae which can be shortened.<ref>{{cite journal|doi=10.3978/j.issn.2225-319X.2015.03.05}}</ref><ref name="Płońska-GościniakLichodziejewska2019">{{cite journal|last1=Płońska-Gościniak|first1=Edyta|last2=Lichodziejewska|first2=Barbara|last3=Szyszka|first3=Andrzej|last4=Kukulski|first4=Tomasz|last5=Kasprzak|first5=Jarosław D.|last6=Dzikowska-Diduch|first6=Olga|last7=Gackowski|first7=Andrzej|last8=Gościniak|first8=Piotr|last9=Pysz|first9=Piotr|last10=Gąsior|first10=Zbigniew|title=Echocardiography in adults|journal=Journal of Ultrasonography|volume=19|issue=76|year=2019|pages=54–61|issn=20848404|doi=10.15557/JoU.2019.0008}}</ref>
* Other associated features may include markedly enlarged [[left atrium]], [[pulmonary hypertension]], right heart enlargement and [[tricuspid regurgitation]]. There may be involvement of other valves as well.<ref name="MaederWeber2018">{{cite journal|last1=Maeder|first1=Micha T.|last2=Weber|first2=Lukas|last3=Buser|first3=Marc|last4=Gerhard|first4=Marc|last5=Haager|first5=Philipp K.|last6=Maisano|first6=Francesco|last7=Rickli|first7=Hans|title=Pulmonary Hypertension in Aortic and Mitral Valve Disease|journal=Frontiers in Cardiovascular Medicine|volume=5|year=2018|issn=2297-055X|doi=10.3389/fcvm.2018.00040}}</ref>

====Orifice Area by Planimetry====
* A well validated technique for assessing severity
* In parasternal short [[axis]] view
* The [[mitral valve]] is funnel shaped, so the area needs to be measured at the tip of the [[valves]] (the narrowest portion).
* Be sure to turn the gain down to have low overall 2D gain.
* Trace the inner edge of the [[valve]] orifice during the maximum opening in diastole.
* Not useful if heavily [[Calcification|calcified]] [[Heart valve|valves]] or after valvotomy
* Sometimes chordae can mimic the [[valve]] orifice.

[[Echocardiogram]] below shows knee bend with opening snap (Time 0:00-0:07), decreased E-F slope (Time 0:08-0:12), measurement of orifice area (Time 0:25-0:37)
{{#ev:youtube|Jks98rwwsh8}}

=== Doppler Echocardiography ===

====Mean Transmitral Valve Gradient====
Can be measured by tracing the area-under-the-curve of the mitral E and A waves obtained by continuous Doppler. The severity of stenosis can be assessed as mild (<5), moderate (5-10) and severe (>10).
Peak transmitral gradient can be calculated from velocity of mitral inflow using modified [[Bernoulli equation]]:

{|class="wikitable" border="1" style="background:FloralWhite"
|- align="center"
|Peak transmitral gradient= 4 x (peak velocity)2
|}

====Pressure Half Time====

The rate of pressure decline across the stenotic orifice is determined by the cross sectional area of the orifice. Smaller the orifice leads to slower rate of [[pressure]] decline. [[Pressure]] half time is defined as the time interval between maximum early [[Diastole|diastolic]] [[pressure gradient]] and the point at which the [[pressure]] gradient is half the [[maximum]] [[Value (mathematics)|value]].

By [[echocardiography]], this is measured in apical-4-chamber view with continuous wave [[Doppler ultrasound|doppler]] aligned with the inflow jet of [[mitral valve]]. The spectral trace is recorded and the slope of the flow is measured from the beginning of E-wave ignoring the A-wave.

Based on the [[Bernoulli equation]], the velocity of pressure half time can be derived as V1/2 = 0.7 Vmax

{|class="wikitable" border="1" style="background:FloralWhite"
|- align="center"
|The mitral valve area can be calculated as MV area (cm2) = 220 ÷ Pressure half time (msec)
|}

====Limitations of Pressure Half Time====

* Assumes normal left atrial and [[Left ventricle|left ventricula]]<nowiki/>r [[compliance]]. This is not true immediately post [[valvuloplasty]] (72 hrs) and in [[left ventricular hypertrophy]]

* [[Aortic regurgitation]] leads to increased [[Left ventricle|left ventricular]] [[diastolic pressure]] and thus shorter [[pressure]] half time. Hence [[mitral valve]] area is over estimated.

* Angle needs constant intercept angle parallel to the flow

* [[Atrial fibrillation]] - several beats need to be averaged.

* [[Atrial septal defect]] - left to right shunt, shortened [[pressure]] half time and hence [[mitral valve]] area over estimated.

* [[Mitral regurgitation]] does not affect [[pressure]] half time.

=== Exercise Doppler Echocardiography ===

* 2008 ACC/AHA guidelines recommend that when there is a discrepancy between resting doppler echocardiographic findings, clinical findings, symptoms, and signs in a patient with MS, exercise doppler echocardiography should be performed.<ref name="pmid18820172">{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172 | doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18820172 }} </ref>
* In those who cannot exercise, [[dobutamine]] can be used to increase the heart rate.<ref name="pmid15013120">{{cite journal| author=Reis G, Motta MS, Barbosa MM, Esteves WA, Souza SF, Bocchi EA| title=Dobutamine stress echocardiography for noninvasive assessment and risk stratification of patients with rheumatic mitral stenosis. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 3 | pages= 393-401 | pmid=15013120 | doi=10.1016/j.jacc.2003.09.037 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15013120 }} </ref>

==== Continuity Equation Mitral Valve Area<ref>Oh J., Seward J.B., Tajik A.J.: The echo manual. 2nd ed. Lippincott-RavenPhiladelphia1999</ref>====
Mitral Valve Area = (LVOT diameter)2 x 0.785 x TVILVOT
----------------------------------
TVIMV

LVOT: Left Ventricular Outflow Tract

TVILVOT: Time Velocity Integral of Left Ventricular Outflow Tract

TVIMV: Time Velocity Integral of Mitral Valve

==Echocardiography Examples of Mitral Stenosis==

*Continuous Wave Doppler Echo
[[Image:Ring Dehis.jpg|thumb|450px|left|Sewing Ring Ring dehiscence leading to Mitral Stenosis Continuous Wave Doppler]]
{{clr}}
*3-D Echo of Rheumatic Mitral Stenosis 1
{{#ev:youtube|-wLGHHFZIrM}}
{{clr}}

* Calcific Mitral Stenosis Continuous Wave Doppler
[[Image:Severe Calcific MS TEE CW.jpg|420px]]
{{clr}}
* Calcific Mitral Stenosis Severe 1
{{#ev:youtube|9yPfTxBAq3s}}
{{clr}}

==2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary<ref name="pmid24589852">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2014 | volume= | issue= | pages= | pmid=24589852 | doi=10.1161/CIR.0000000000000029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24589852 }} </ref>==
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' [[Transthoracic echocardiography]] (TTE) is indicated in patients with signs or symptoms of [[mitral stenosis]] (MS) to establish the diagnosis, quantify hemodynamic severity (mean pressure gradient, mitral valve area, and pulmonary artery pressure), assess concomitant valvular lesions, and demonstrate valve morphology (to determine suitability for mitral commissurotomy). ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: B'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' [[Transesophageal echocardiography]] (TEE) should be performed in patients considered for cutaneous mitral balloon commissurotomy to assess the presence or absence of left atrial thrombus and to further evaluate the severity of [[mitral regurgitation]] (MR). ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: B'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''3.''' Exercise testing with [[doppler]] or invasive hemodynamic assessment is recommended to evaluate the response of the mean mitral gradient and pulmonary artery pressure in patients with [[MS]] when there is a discrepancy between resting doppler echocardiographic findings and clinical symptoms or signs. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|}

==2008 and Incorporated 2006 ACC/AHA Guidelines for the Management of Patients with Valvular Heart Disease (DO NOT EDIT) <ref name="pmid18820172">{{cite journal |author=Bonow RO, Carabello BA, Chatterjee K, ''et al.'' |title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons |journal=Circulation |volume=118 |issue=15 |pages=e523–661 |year=2008 |month=October |pmid=18820172 |doi=10.1161/CIRCULATIONAHA.108.190748 |url=}}</ref>==

===Echocardiography Indications (DO NOT EDIT) <ref name="pmid18820172">{{cite journal |author=Bonow RO, Carabello BA, Chatterjee K, ''et al.'' |title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons |journal=Circulation |volume=118 |issue=15 |pages=e523–661 |year=2008 |month=October |pmid=18820172 |doi=10.1161/CIRCULATIONAHA.108.190748 |url=}}</ref>===

{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' [[Echocardiography]] should be performed in patients for the diagnosis of [[mitral stenosis]], assessment of hemodynamic severity (mean gradient, [[mitral valve]] area, and pulmonary artery pressure), assessment of concomitant valvular lesions, and assessment of valve morphology to determine suitability for [[percutaneous mitral balloon valvotomy (PMBV)]]. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: B'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''2.''' [[Echocardiography]] should be performed for reevaluation in patients with known [[mitral stenosis]] and changing symptoms or signs. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: B'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''3.''' [[Echocardiography]] should be performed for assessment of the hemodynamic response of the mean gradient and pulmonary artery pressure by exercise [[Doppler echocardiography]] in patients with [[mitral stenosis]] when there is a discrepancy between resting Doppler echocardiographic findings, clinical findings, symptoms, and signs. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''4.''' [[Transesophageal echocardiography]] in [[mitral stenosis]] should be performed to assess the presence or absence of left atrial [[thrombus]] and to further evaluate the severity of [[MR]] in patients considered for [[percutaneous mitral balloon valvotomy (PMBV)]]. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''5.''' [[Transesophageal echocardiography]] in [[mitral stenosis]] should be performed to evaluate [[mitral valve|MV]] morphology and hemodynamics in patients when [[transthoracic echocardiography]] provides suboptimal data. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|}

{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightCoral"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]]

|-
| bgcolor="LightCoral"|<nowiki>"</nowiki>'''1.''' [[Transesophageal echocardiography]] in the patient with [[mitral stenosis]] is not indicated for routine evaluation of [[mitral valve|MV]] morphology and hemodynamics when complete transthoracic echocardiographic data are satisfactory. ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|}

{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LemonChiffon"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]

|-
| bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' [[Echocardiography]] is reasonable in the re-evaluation of asymptomatic patients with [[mitral stenosis]] and stable clinical findings to assess pulmonary artery pressure (for those with severe [[mitral stenosis]], every year; moderate [[mitral stenosis]], every 1 to 2 years; and mild MS, every 3 to 5 years). ([[ACC AHA guidelines classification scheme#Level of Evidence|''Level of Evidence: C'']])<nowiki>"</nowiki>
|}

==References==
{{reflist|2}}

[[Category:Valvular heart disease]]
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[[Category:Surgery]]
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Impetigo epidemiology and demographics

2022-10-05T21:44:05Z

44.197.72.169: /* Epidemiology and Demographics */

__NOTOC__
{{‪Impetigo‬}}
{{CMG}}; {{AE}} {{USAMA}}
==Overview==
In 2010, 140 million people suffered from impetigo. Impetigo is more common among children. Impetigo is more prevalent in tropical and pacific countries.<ref name="urlHigh Burden of Impetigo and Scabies in a Tropical Country">{{cite web |url=https://doi.org/10.1371/journal.pntd.0000467 |title=High Burden of Impetigo and Scabies in a Tropical Country |format= |work= |accessdate=}}</ref><ref name="pmid26088526">{{cite journal| author=Romani L, Steer AC, Whitfeld MJ, Kaldor JM| title=Prevalence of scabies and impetigo worldwide: a systematic review. | journal=Lancet Infect Dis | year= 2015 | volume= 15 | issue= 8 | pages= 960-7 | pmid=26088526 | doi=10.1016/S1473-3099(15)00132-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26088526 }} </ref><ref name="pmid23245607">{{cite journal| author=Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M et al.| title=Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. | journal=Lancet | year= 2012 | volume= 380 | issue= 9859 | pages= 2163-96 | pmid=23245607 | doi=10.1016/S0140-6736(12)61729-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23245607 }} </ref>

==Epidemiology and Demographics==
===Incidence===
*In 2010, 140 million people suffered from impetigo.<ref name="pmid23245607">{{cite journal| author=Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M et al.| title=Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. | journal=Lancet | year= 2012 | volume= 380 | issue= 9859 | pages= 2163-96 | pmid=23245607 | doi=10.1016/S0140-6736(12)61729-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23245607 }} </ref>

===Prevalence===
*The [[prevalence]] of impetigo in Australian Aboriginal communities is 49%.<ref name="pmid26088526">{{cite journal| author=Romani L, Steer AC, Whitfeld MJ, Kaldor JM| title=Prevalence of scabies and impetigo worldwide: a systematic review. | journal=Lancet Infect Dis | year= 2015 | volume= 15 | issue= 8 | pages= 960-7 | pmid=26088526 | doi=10.1016/S1473-3099(15)00132-2 | pmc= | url=https://wvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvvv ia amaww.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26088526 }} </ref>
*The [[prevalence]] of impetigo in Solomon Islands is 43%.<ref name="pmid2940770">{{cite journal| author=Eason RJ, Tasman-Jones T| title=Resurgent yaws and other skin diseases in the Western Province of the Solomon Islands. | journal=P N G Med J | year= 1985 | volume= 28 | issue= 4 | pages= 247-50 | pmid=2940770 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2940770 }} </ref>
*Impetigo is more [[Prevalence|prevalent]] in tropical and pacific countries.<ref name="urlHigh Burden of Impetigo and Scabies in a Tropical Country">{{cite web |url=https://doi.org/10.1371/journal.pntd.0000467 |title=High Burden of Impetigo and Scabies in a Tropical Country |format= |work= |accessdate=}}</ref><ref name="pmid26088526">{{cite journal| author=Romani L, Steer AC, Whitfeld MJ, Kaldor JM| title=Prevalence of scabies and impetigo worldwide: a systematic review. | journal=Lancet Infect Dis | year= 2015 | volume= 15 | issue= 8 | pages= 960-7 | pmid=26088526 | doi=10.1016/S1473-3099(15)00132-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26088526 }} </ref>
*In 2006-2007, 25.6% school going children and 12.2% infants had active impetigo in Fiji.<ref name="urlHigh Burden of Impetigo and Scabies in a Tropical Country">{{cite web |url=https://doi.org/10.1371/journal.pntd.0000467 |title=High Burden of Impetigo and Scabies in a Tropical Country |format= |work= |accessdate=}}</ref>

===Age===
*Impetigo is more common among young children between age 2 to 5. Particularly those who attend school or daycare centers.<ref name="pmid25250996">{{cite journal| author=Hartman-Adams H, Banvard C, Juckett G| title=Impetigo: diagnosis and treatment. | journal=Am Fam Physician | year= 2014 | volume= 90 | issue= 4 | pages= 229-35 | pmid=25250996 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25250996 }} </ref><ref name="pmid27617460">{{cite journal| author=Cohen PR| title=Bullous impetigo and pregnancy: Case report and review of blistering conditions in pregnancy. | journal=Dermatol Online J | year= 2016 | volume= 22 | issue= 4 | pages= | pmid=27617460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27617460 }} </ref><ref name="urlHigh Burden of Impetigo and Scabies in a Tropical Country">{{cite web |url=https://doi.org/10.1371/journal.pntd.0000467 |title=High Burden of Impetigo and Scabies in a Tropical Country |format= |work= |accessdate=}}</ref>
*A study showed that almost 69% of children below the age of 16 were affected by impetigo.<ref name="pmid26088526">{{cite journal| author=Romani L, Steer AC, Whitfeld MJ, Kaldor JM| title=Prevalence of scabies and impetigo worldwide: a systematic review. | journal=Lancet Infect Dis | year= 2015 | volume= 15 | issue= 8 | pages= 960-7 | pmid=26088526 | doi=10.1016/S1473-3099(15)00132-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26088526 }} </ref>
*Non-bullous impetigo is rare in children under 2 years.<ref name="pmid24770507">{{cite journal| author=Pereira LB| title=Impetigo - review. | journal=An Bras Dermatol | year= 2014 | volume= 89 | issue= 2 | pages= 293-9 | pmid=24770507 | doi= | pmc=4008061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24770507 }} </ref>

===Gender===
* The distribution of impetigo is not effected by gender of the patient.

===Race===
*Impetigo is very common in Australian Aboriginal communities and Solomon Islands.<ref name="pmid26088526">{{cite journal| author=Romani L, Steer AC, Whitfeld MJ, Kaldor JM| title=Prevalence of scabies and impetigo worldwide: a systematic review. | journal=Lancet Infect Dis | year= 2015 | volume= 15 | issue= 8 | pages= 960-7 | pmid=26088526 | doi=10.1016/S1473-3099(15)00132-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26088526 }} </ref>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

[[Category:Needs content]]
[[Category:Disease]]
[[Category:Bacterial diseases]]
[[Category:Infectious skin diseases]]
[[Category:Dermatology]]
[[Category:Emergency mdicine]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]
[[Category:Gynecology]]
[[Category:Urology]]

Coronary artery bypass surgery maintaining glucose level

2022-10-05T17:41:33Z

44.197.72.169: /* 2022 ACA Revascularization Guideline */

__NOTOC__
{{Coronary artery bypass surgery}}
{{CMG}}; {{AOEIC}} {{Anahita}} {{VK}}
==Overview==

==Maintaining Glucose Level in CABG==
===2022 ACA Revascularization Guideline===
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|Class 1 Recommendation, Level of Evidence: B-R <ref name="pmid34895950">{{cite journal| author=Writing Committee Members. Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM | display-authors=etal| title=2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. | journal=J Am Coll Cardiol | year= 2022 | volume= 79 | issue= 2 | pages= e21-e129 | pmid=34895950 | doi=10.1016/j.jacc.2021.09.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34895950 }} </ref><ref name="pmid10197653">{{cite journal| author=Furnary AP, Zerr KJ, Grunkemeier GL, Starr A| title=Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. | journal=Ann Thorac Surg | year= 1999 | volume= 67 | issue= 2 | pages= 352-60; discussion 360-2 | pmid=10197653 | doi=10.1016/s0003-4975(99)00014-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10197653 }} </ref><ref name="pmid16153268">{{cite journal| author=Hruska LA, Smith JM, Hendy MP, Fritz VL, McAdams S| title=Continuous insulin infusion reduces infectious complications in diabetics following coronary surgery. | journal=J Card Surg | year= 2005 | volume= 20 | issue= 5 | pages= 403-7 | pmid=16153268 | doi=10.1111/j.1540-8191.2005.200472.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16153268 }} </ref><ref name="pmid15006999">{{cite journal| author=Lazar HL, Chipkin SR, Fitzgerald CA, Bao Y, Cabral H, Apstein CS| title=Tight glycemic control in diabetic coronary artery bypass graft patients improves perioperative outcomes and decreases recurrent ischemic events. | journal=Circulation | year= 2004 | volume= 109 | issue= 12 | pages= 1497-502 | pmid=15006999 | doi=10.1161/01.CIR.0000121747.71054.79 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15006999 }} </ref><ref name="pmid26180108">{{cite journal| author=Umpierrez G, Cardona S, Pasquel F, Jacobs S, Peng L, Unigwe M | display-authors=etal| title=Randomized Controlled Trial of Intensive Versus Conservative Glucose Control in Patients Undergoing Coronary Artery Bypass Graft Surgery: GLUCO-CABG Trial. | journal=Diabetes Care | year= 2015 | volume= 38 | issue= 9 | pages= 1665-72 | pmid=26180108 | doi=10.2337/dc15-0303 | pmc=4542267 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26180108 }} </ref><ref name="pmid12771873">{{cite journal| author=Furnary AP, Gao G, Grunkemeier GL, Wu Y, Zerr KJ, Bookin SO | display-authors=etal| title=Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting. | journal=J Thorac Cardiovasc Surg | year= 2003 | volume= 125 | issue= 5 | pages= 1007-21 | pmid=12771873 | doi=10.1067/mtc.2003.181 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12771873 }} </ref><ref name="pmid17395026">{{cite journal| author=Furnary AP, Wu Y| title=Eliminating the diabetic disadvantage: the Portland Diabetic Project. | journal=Semin Thorac Cardiovasc Surg | year= 2006 | volume= 18 | issue= 4 | pages= 302-8 | pmid=17395026 | doi=10.1053/j.semtcvs.2006.04.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17395026 }} </ref>
|-
| bgcolor="LightGreen"| 1. In order to reduce [[Sternum|sternal]] [[wound]] [[infection]] in [[patients]] undergoing [[CABG]] an [[surgery|intraoperative]] [[Intravenous therapy|continuous infusion]] of [[insulin]] should be initiated with the goal to keep [[blood sugar]] lower than 180 mg/dL.
2. In order to reduce [[Sternum|sternal]] [[wound]] [[infection]] in [[patients]] undergoing [[CABG]] an [[surgery|postoperative]] [[Intravenous therapy|continuous infusion]] of [[insulin]] is recommended with the goal to keep an early [[surgery|postoperative]] [[blood sugar]] lower than 180 mg/dL.
|}
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:Yellow"|Class 1 Recommendation, Level of Evidence: B-NR <ref name="pmid34895950">{{cite journal| author=Writing Committee Members. Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM | display-authors=etal| title=2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. | journal=J Am Coll Cardiol | year= 2022 | volume= 79 | issue= 2 | pages= e21-e129 | pmid=34895950 | doi=10.1016/j.jacc.2021.09.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34895950 }} </ref><ref name="pmid999352">{{cite journal| author=Edwards LD| title=The epidemiology of 2056 remote site infections and 1966 surgical wound infections occurring in 1865 patients: a four year study of 40,923 operations at Rush-Presbyterian-St. Luke's Hospital, Chicago. | journal=Ann Surg | year= 1976 | volume= 184 | issue= 6 | pages= 758-66 | pmid=999352 | doi=10.1097/00000658-197612000-00017 | pmc=1345421 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=999352 }} </ref><ref name="pmid17383396">{{cite journal| author=Engelman R, Shahian D, Shemin R, Guy TS, Bratzler D, Edwards F | display-authors=etal| title=The Society of Thoracic Surgeons practice guideline series: Antibiotic prophylaxis in cardiac surgery, part II: Antibiotic choice. | journal=Ann Thorac Surg | year= 2007 | volume= 83 | issue= 4 | pages= 1569-76 | pmid=17383396 | doi=10.1016/j.athoracsur.2006.09.046 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17383396 }} </ref><ref name="pmid27555340">{{cite journal| author=Lazar HL, Salm TV, Engelman R, Orgill D, Gordon S| title=Prevention and management of sternal wound infections. | journal=J Thorac Cardiovasc Surg | year= 2016 | volume= 152 | issue= 4 | pages= 962-72 | pmid=27555340 | doi=10.1016/j.jtcvs.2016.01.060 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27555340 }} </ref><ref name="pmid2796369">{{cite journal| author=Vander Salm TJ, Okike ON, Pasque MK, Pezzella AT, Lew R, Traina V | display-authors=etal| title=Reduction of sternal infection by application of topical vancomycin. | journal=J Thorac Cardiovasc Surg | year= 1989 | volume= 98 | issue= 4 | pages= 618-22 | pmid=2796369 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2796369 }} </ref><ref name="pmid19932261">{{cite journal| author=Steingrímsson S, Gustafsson R, Gudbjartsson T, Mokhtari A, Ingemansson R, Sjögren J| title=Sternocutaneous fistulas after cardiac surgery: incidence and late outcome during a ten-year follow-up. | journal=Ann Thorac Surg | year= 2009 | volume= 88 | issue= 6 | pages= 1910-5 | pmid=19932261 | doi=10.1016/j.athoracsur.2009.07.012 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19932261 }} </ref><ref name="pmid24613159">{{cite journal| author=Kieser TM, Rose MS, Aluthman U, Montgomery M, Louie T, Belenkie I| title=Toward zero: deep sternal wound infection after 1001 consecutive coronary artery bypass procedures using arterial grafts: implications for diabetic patients. | journal=J Thorac Cardiovasc Surg | year= 2014 | volume= 148 | issue= 5 | pages= 1887-95 | pmid=24613159 | doi=10.1016/j.jtcvs.2014.02.022 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24613159 }} </ref>
|-
| bgcolor="Yellow"| A comprehensive approach to decrease the risk of [[Sternum|sternal]] [[wound]] [[infection]] is recommended in [[patients]] undergoing [[CABG]].
|}
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:Lightblue"|Class 2b Recommendation, Level of Evidence: B-R<ref name="pmid34895950">{{cite journal| author=Writing Committee Members. Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM | display-authors=etal| title=2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. | journal=J Am Coll Cardiol | year= 2022 | volume= 79 | issue= 2 | pages= e21-e129 | pmid=34895950 | doi=10.1016/j.jacc.2021.09.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=34895950 }} </ref><ref name="pmid26180108">{{cite journal| author=Umpierrez G, Cardona S, Pasquel F, Jacobs S, Peng L, Unigwe M | display-authors=etal| title=Randomized Controlled Trial of Intensive Versus Conservative Glucose Control in Patients Undergoing Coronary Artery Bypass Graft Surgery: GLUCO-CABG Trial. | journal=Diabetes Care | year= 2015 | volume= 38 | issue= 9 | pages= 1665-72 | pmid=26180108 | doi=10.2337/dc15-0303 | pmc=4542267 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26180108 }} </ref>
|-
| bgcolor="Lightblue"| The effectiveness of [[surgery|intraoperative]] [[Intravenous therapy|continuous infusion]] of [[insulin]] with the goal to keep [[blood sugar]] lower than 140 mg/dL in [[patients]] undergoing [[CABG]] is not certain.
|}

===2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery (DO NOT EDIT)<ref name="pmid22064599">{{cite journal| author=Hillis LD, Smith PK, Anderson JL, Bittl JA, Bridges CR, Byrne JG et al.| title=2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2011 | volume= | issue= | pages= | pmid=22064599 | doi=10.1161/CIR.0b013e31823c074e | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22064599 }} </ref>===
{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
|-
| bgcolor="LightGreen"|<nowiki>"</nowiki>'''1.''' Use of continuous intravenous insulin to achieve and maintain an early postoperative blood glucose concentration less than or equal to 180 mg/dL while avoiding [[hypoglycemia]] is indicated to reduce the incidence of adverse events, including deep sternal wound infection, after CABG.<ref name="pmid12771873">{{cite journal |author=Furnary AP, Gao G, Grunkemeier GL, Wu Y, Zerr KJ, Bookin SO, Floten HS, Starr A |title=Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting |journal=[[The Journal of Thoracic and Cardiovascular Surgery]] |volume=125 |issue=5 |pages=1007–21 |year=2003 |month=May |pmid=12771873 |doi=10.1067/mtc.2003.181 |url=http://linkinghub.elsevier.com/retrieve/pii/S0022522303501052 |accessdate=2011-12-14}}</ref><ref name="pmid16608860">{{cite journal |author=Ingels C, Debaveye Y, Milants I, Buelens E, Peeraer A, Devriendt Y, Vanhoutte T, Van Damme A, Schetz M, Wouters PJ, Van den Berghe G |title=Strict blood glucose control with insulin during intensive care after cardiac surgery: impact on 4-years survival, dependency on medical care, and quality-of-life |journal=[[European Heart Journal]] |volume=27 |issue=22 |pages=2716–24 |year=2006 |month=November |pmid=16608860 |doi=10.1093/eurheartj/ehi855 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=16608860 |accessdate=2011-12-14}}</ref><ref name="pmid11794168">{{cite journal |author=van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R |title=Intensive insulin therapy in the critically ill patients |journal=[[The New England Journal of Medicine]] |volume=345 |issue=19 |pages=1359–67 |year=2001 |month=November |pmid=11794168 |doi=10.1056/NEJMoa011300 |url=http://dx.doi.org/10.1056/NEJMoa011300 |accessdate=2011-12-14}}</ref> ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|}

{|class="wikitable"
|-
| colspan="1" style="text-align:center; background:LemonChiffon"|[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]]
|-
|bgcolor="LemonChiffon"|<nowiki>"</nowiki>'''1.''' The use of continuous intravenous insulin designed to achieve a target intraoperative blood glucose concentration less than 140 mg/dL has uncertain effectiveness.<ref name="pmid16256784">{{cite journal |author=Butterworth J, Wagenknecht LE, Legault C, Zaccaro DJ, Kon ND, Hammon JW, Rogers AT, Troost BT, Stump DA, Furberg CD, Coker LH |title=Attempted control of hyperglycemia during cardiopulmonary bypass fails to improve neurologic or neurobehavioral outcomes in patients without diabetes mellitus undergoing coronary artery bypass grafting |journal=[[The Journal of Thoracic and Cardiovascular Surgery]] |volume=130 |issue=5 |pages=1319 |year=2005 |month=November |pmid=16256784 |doi=10.1016/j.jtcvs.2005.02.049 |url=http://linkinghub.elsevier.com/retrieve/pii/S0022-5223(05)00368-5 |accessdate=2011-12-14}}</ref><ref name="pmid20216389">{{cite journal |author=Duncan AE, Abd-Elsayed A, Maheshwari A, Xu M, Soltesz E, Koch CG |title=Role of intraoperative and postoperative blood glucose concentrations in predicting outcomes after cardiac surgery |journal=[[Anesthesiology]] |volume=112 |issue=4 |pages=860–71 |year=2010 |month=April |pmid=20216389 |doi=10.1097/ALN.0b013e3181d3d4b4 |url= |accessdate=2011-12-14}}</ref><ref name="pmid17310047">{{cite journal |author=Gandhi GY, Nuttall GA, Abel MD, Mullany CJ, Schaff HV, O'Brien PC, Johnson MG, Williams AR, Cutshall SM, Mundy LM, Rizza RA, McMahon MM |title=Intensive intraoperative insulin therapy versus conventional glucose management during cardiac surgery: a randomized trial |journal=[[Annals of Internal Medicine]] |volume=146 |issue=4 |pages=233–43 |year=2007 |month=February |pmid=17310047 |doi= |url= |accessdate=2011-12-14}}</ref> ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>
|}

==References==
{{reflist|2}}

{{WH}}
{{WS}}
[[Category:Cardiac surgery]]
[[Category:Cardiology]]
[[Category:Surgery]]