Liver: Difference between revisions

Line 57:

[[File:Histopathology of congestive hepatopathy.jpg|thumb|Histopathology of congestive hepatopathy, with sinusoidal dilation in zone 3. As the severity of the lesion increases, the sinusoids around the central vein become distended with extravasated red cells and there is adjacent hepatocyte plate atrophy.<ref name=Shah2015>{{cite journal|last1=Shah|first1=Shailja C.|last2=Sass|first2=David A.|title=“Cardiac Hepatopathy”: A Review of Liver Dysfunction in Heart Failure|journal=Liver Research - Open Journal|volume=1|issue=1|year=2015|pages=1–10|issn=23794038|doi=10.17140/LROJ-1-101}}<br>-"This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0),"</ref>]]

~~Congestive hepatopathy appears as dilatation~~ of hepatic ~~sinusoids~~.

*'''Acute hepatic congestion''' shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.<ref>{{cite web|url=http://www.pathwaymedicine.org/acute-hepatic-congestion|title=Acute Hepatic Congestion|website=Pathway Medicine|accessdate=2020-03-06}}</ref>

*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3 ~~of the hepatic acinus~~, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>

*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>

@@ Line 57: / Line 57: @@
 [[File:Histopathology of congestive hepatopathy.jpg|thumb|Histopathology of congestive hepatopathy, with sinusoidal dilation in zone 3. As the severity of the lesion increases, the sinusoids around the central vein become distended with extravasated red cells and there is adjacent hepatocyte plate atrophy.<ref name=Shah2015>{{cite journal|last1=Shah|first1=Shailja C.|last2=Sass|first2=David A.|title=“Cardiac Hepatopathy”: A Review of Liver Dysfunction in Heart Failure|journal=Liver Research - Open Journal|volume=1|issue=1|year=2015|pages=1–10|issn=23794038|doi=10.17140/LROJ-1-101}}<br>-"This is an open access article distributed under the Creative Commons Attribution 4.0 International License (CC BY 4.0),"</ref>]]
-Congestive hepatopathy appears as dilatation of hepatic sinusoids.
+*'''Acute hepatic congestion''' shows dilated sinusoidal capillaries predominantly in zone 3 of the hepatic acinus.<ref>{{cite web|url=http://www.pathwaymedicine.org/acute-hepatic-congestion|title=Acute Hepatic Congestion|website=Pathway Medicine|accessdate=2020-03-06}}</ref>
-*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3 of the hepatic acinus, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>
+*Typical findings of '''chronic hepatic congestion''' are atrophy of hepatocytes in zone 3, perisinusoidal edema, thrombosis and hemorrhage. Chronic congestion typically displays perivenous and perisinusoidal fibrosis, with fibrous septa that bridge central hepatic veins. In contrast, other causes of distortion and cirrhosis typically have fibrous septa predominantly between portal triads. However, nonalcoholic steatohepatitis also may show perisinusoidal fibrosis in early stages; in later stages, the fibrosis tends to be in the portal triad. Cirrhosis develops in the final stages of congestive hepatopathy. Regenerating hepatocytes tend to grow in a sleevelike pattern along portal tracts, resulting in a nodular liver with preserved portal triads and obliterated or fibrosed hepatic veins, a pattern called "reverse lobulation". This pattern can also be seen in venous obstruction due to Budd-Chiari syndrome.<ref name="WellsFenstad2016">{{cite journal|last1=Wells|first1=Michael L.|last2=Fenstad|first2=Eric R.|last3=Poterucha|first3=Joseph T.|last4=Hough|first4=David M.|last5=Young|first5=Phillip M.|last6=Araoz|first6=Philip A.|last7=Ehman|first7=Richard L.|last8=Venkatesh|first8=Sudhakar K.|title=Imaging Findings of Congestive Hepatopathy|journal=RadioGraphics|volume=36|issue=4|year=2016|pages=1024–1037|issn=0271-5333|doi=10.1148/rg.2016150207}}</ref>
 {{Bottom}}

Liver: Difference between revisions

Navigation menu

Search