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Difference between revisions of "Medical liver disease"
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Medical liver disease (view source)
Revision as of 16:11, 28 December 2016
, 16:11, 28 December 2016→Overlapping Disorders: added case
(→Hepatic sarcoidosis: Added a new section for overlapping disorders like this one) |
(→Overlapping Disorders: added case) |
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{{Main|Hepatic sarcoidosis}} | {{Main|Hepatic sarcoidosis}} | ||
==Overlapping Disorders== | ==Overlapping Disorders== | ||
[[File:1 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:1 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
[[File:2 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:2 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
[[File:3 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:3 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
[[File:4 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:4 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
[[File:5 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:5 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
[[File:6 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | [[File:6 Mixed Disorder 1 680x512px.tif|Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed.]] | ||
Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed. A. Low power shows hepatocytes afflicted by steatosis and an inflamed portal tract | Changes of steatohepatitis and interface hepatitis, with granuloma. Patient with diabetes was ANA, AMA, HCV, HBV negative, without drugs known to produce granulomas or interface hepatitis. This may be a case of AMA negative primary biliary cirrhosis, but studies to determine that with certainty were not performed. A. Low power shows hepatocytes afflicted by steatosis and an inflamed portal tract. B. In a region of fatty change lie cytoplasmic tufts of ballooning degeneration (green arrows) and a lipogranuloma (black arrow). C. At the portal-hepatocyte junction lies interface hepatitis (black arrows), as well as extension of inflammation into the lobule (green arrows). D. Red hepatocytes bounded by inflammation denote piecemeal necrosis [PAS without diastase]. E. Giant cells intermixed with lymphocytes prove a portal granuloma [PAS without diastase]. F. A blue fibrous bridge extends from a triad [Trichrome]. | ||
[[File:4 95599552608917 sl 1.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 2.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 3.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 4.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 5.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 6.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
[[File:4 95599552608917 sl 7.png|Acute obstructive changes and changes of recurrent acute injury]] | |||
Acute obstructive changes and changes of recurrent injury in 46 yo man with Clostridium perfringens positive blood culture, an ERCP that showed duodenal compression by the pancreas with resultant bile duct dilatation. The patient had had and continued to have multiple bouts of acute pancreatitis. At the time of biopsy, decreased platelet count/hemoglobin/albumin, elevated lipase/amylase/PT/PTT, normal alkaline phosphatase, bilirubin, AST/ALT, AMA, hepatitis virus serology, ANA. A. Fragment biopsy shows inflamed triads and bridges. B. Trichrome shows bridges without nodules, evidence of prior injury; the patient subsequently developed multiple episodes of pancreatitis. C. Reticulin shows piecemeal necrosis, with black lines bounding individual hepatocytes at interface (arrows). D. Collapse is shown by closly approximated thick black lines; one cannot call portal-central collapse without seeing a central vein. Note on this and the other reticulin image that regeneration, two cell thick cords, is not prominent. E. PAS D of two portal triads, far nearer than normal, both expanded. Note increased number of ducts/ductules (red arrows), neutrophils, and PAS-D macrophages. F. PAS D shows collapse extending from a triad to a portion of a lobule with steatosis. No feathery degeneration or bile duct plugs were seen. Neither were foci of spotty necrosis or abscess seen. G. Other triads, again edematous, showed more of a chronic inflammatory response, with occasional plasma cells (black arrows). Also present are neutrophils (red arrows). The bile duct (grey arrow) near the artery (brown arrow) shows mildly disturbed nuclei. . Note early proliferated bile ductules (cyan arrows). | |||
=See also= | =See also= | ||