Difference between revisions of "Medical liver disease"

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Medical liver disease (view source)

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==Hepatitis C==
==Hepatitis C==
===General===
{{Main|Hepatitis C}}
*Leads to hepatocellular carcinoma in the setting of cirrhosis.
*Tends to be chronic; the "C" in "hepatitis C" stands for ''chronic''.
*Diagnosis is by serology.
 
Associated pathology:
*[[Membranoproliferative glomerulonephritis]].
*[[Membranous nephropathy]].
*[[Cryoglobulinemia]].
 
===Microscopic===
Features:
*Lobular inflammation - this is non-specific finding.
**Usually Grade 1, rarely Grade 2 and almost never Grade 3 or Grade 4.<ref>STC. 6 December 2010.</ref>
*Periportal steatosis in genotype 3.<ref name=pmid16614743>Yoon EJ, Hu KQ. Hepatitis C virus (HCV) infection and hepatic steatosis. Int J Med Sci. 2006;3(2):53-6. Epub 2006 Apr 1. PMID 16614743. Avialable at: [http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1415843 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1415843]. Accessed on: September 9, 2009.</ref>
**Steatosis in hepatitis C is usually a secondary pathology, i.e. a separate pathologic process.<ref>OA. September 2009.</ref>
 
====Images====
{| class="wikitable sortable"
| [[File:HCV C1 2016 06 22.tif|thumb|Hepatitis C case for Libre Pathology]]
| Metavir activity index 1 (Piecemeal necrosis 0-1, Lobular necrosis 1), Metavir fibrosis stage 2.  Hepatitis C genotype 1a.  Expanded, dark triads (UL blue arrowhead). Focus of spotty necrosis (UR green arrowhead). Reticulin shows occasional, equivocal foci of piecemeal necrosis, with a thin black line possibly encircling a hepatocytes (LL yellow arrowhead); the activity index is unaffected by the difference in piecemeal necrosis score. Trichrome shows portal fibrosis with extension outside area of blood vessels (LR purple arrowhead)  Original oculars UL 2X, UR 20X, LL 40X, LR 40X
|-
| [[File:HCV C2 2016 06 22.tif|thumb|Hepatits C case for Libre Pathology]]
| Metavir activity index 2 (Piecemeal necrosis 2, Lobular necrosis 1). Hepatitis C genotype 3a.    Steatosis, not pan-acinar and dark, expanded triads(UL) with the inset showing a Councilman body. Reticulin collapse, not portal-central (UR green arrowhead). Reticulin with more than focal piecemeal necrosis in some triads/tracts (LL magenta arrowheads) Trichrome stain of a  tract (the entire structure may be a large bridge) with thinner bridges (LR cyan arrowheads). 
Original oculars. UL 4X (inset 40X with higher magnification), UR 20X, LL 40X, LR 10X
|-
| [[File:HCV c1 2016 06 23.tif|thumb|Metavir stage 4 fibrosis in patient with HCV, for Libre Pathology]]
| Metavir activity index 3 (Piecemeal necrosis 2, Lobular necrosis 2), Metavir fibrosis stage 4.  Hepatitis C genotype 1a. Inflamed bands separate hepatocyte regions distorted by steatosis (UL). Bordering tract and acini (UR) lymphocytes, macrophages, eosinophils, and rare neutrophils (black arrowhead) invest both proliferated bile ducts (yellow arrowheads) and hepatocytes, some showing ballooning degeneration (green arrowhead). Reticulin shows hepatocyte cords often two nuclei thick bounded by directionless sinusoids, consistent with a regenerative nodule (LL). Trichrome shows extensive bridging with a potential flattened nodule; although a debate about the presence or absence of definite fibrosis would have existed, with the Metavir scoring system, this is considered fibrosis stage 4 (LR). 
Original oculars UL 4X, UR 40X, LL 20X, LR 10X
|}
 
 
DDx:
*[[Hepatitis B]] (without ground glass hepatocytes).
*[[Autoimmune hepatitis]].
*[[Primary biliary cirrhosis]] without granulomas.
*[[Drug-induced liver disease|Drug reaction]].


=Other infections=
=Other infections=
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*[http://www.atlas.or.kr/atlas/include/viewImg.html?uid=645 Hydatid cyst (atlas.or.kr)].
*[http://www.atlas.or.kr/atlas/include/viewImg.html?uid=645 Hydatid cyst (atlas.or.kr)].
*[http://casereports.bmj.com/content/2009/bcr.04.2009.1798.full Hydatid cyst (casereports.bmj.com)].
*[http://casereports.bmj.com/content/2009/bcr.04.2009.1798.full Hydatid cyst (casereports.bmj.com)].
==Abscess==
A. [[File:1 ABS 1 680x512px.tif|A process replaces most of the liver parenchyma (20X).]]
<br>
B. [[File:2 ABS 1 680x512px.tif|Fibrinopurulent exudate apposes granulation tissue (200X).]]
<br>
C. [[File:3 ABS 1 680x512px.tif|Neutrophils lie in widened sinusoids (200X)..]]
<br>
D. [[File:4 ABS 1 680x512px.tif|Trichrome shows collagenization of spaces of Disse. Scarring about an abscess or other mass lesion should not be interpreted as reflective of the liver in general (200X).]]
<br>
Abscess. A. A process replaces most of the liver parenchyma. B. Fibrinopurulent exudate apposes granulation tissue. C. Neutrophils lie in widened sinusoids. D. Trichrome shows collagenization of spaces of Disse. Scarring about an abscess or other mass lesion should not be interpreted as reflective of the liver in general (LR 200X).
==Coccidiomycosis==
A. [[File:Coccidiomycosis - 1 - 40X 680x512px shot.tif|500x500px Granulomas at low power]]
<br>
B. [[File:Coccidiomycosis - 1 - 200X 680x513px shot.tif|500x500px Granulomas with centrally crowded cells & lady slipper macrophage nuclei]]
<br>
C. [[File:Coccidiomycosis - 1 - 400X 1369x1024px shot.tif|500x500px Center of previous granuloma showing pyknotic macrophage nuclei]]
<br>
D. [[File:Coccidiomycosis - 1 - GMS 400X 1369x1024px shot.tif|500x500px Four Coccidiomycotic spherules]]
<br>
Coccidiomycosis. A. Note the granulomas in otherwise undisturbed liver (UL). B. Granuloma with centrally crowded cells & lady slipper macrophage nuclei. C. Center of granuloma with pyknotic macrophage nuclei, "necrotizing". D. Organisms on GMS stain.


=Metabolic and toxic=
=Metabolic and toxic=
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====Images====
====Images====
{| class="wikitable sortable"
 
| [[File:Alcoholic Liver Disease c1 2016 06 23.tif|thumb|Cirrhosis in a patient with a history of alcohol abuse]]
A. [[File:1 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
| Cirrhosis in a person with alcohol abuse. At low power bands separate hepatocyte regions (UL). Higher power at left shows isles of hepatocytes, some ballooned; at right, hepatocytes with many lumens, at lower power perhaps suggesting steatosis, here evidencing regeneration (UL). Focus of spotty necrosis (UR). PAS-D stain showing extensive benign bile duct proliferation, overall localized, with red rimd (LL). Trichrome shows fibrosis about nodules (LR).
<br>
Original oculars UL 4X, UR 20X, LL 40X, LR 10X
B. [[File:2 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
|}
<br>
C. [[File:3 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
<br>
D. [[File:4 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
<br>
E. [[File:5 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
<br>
F. [[File:6 etoh 3 680x512px.tif| Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).]]
<br>
 
Alcoholic hepatitis with Metavir stage IV fibrosis (advanced fibrosis/cirrhosis).
A. Trichrome shows relatively non-inflamed fibrous bands, as well as [between green dots] nodules. The lack of regeneration throughout might have precluded a diagnosis of cirrhosis, but stage IV fibrosis under the Metavir system is justified. B. Reticulin shows regenerative nodules [left] with mostly two or more nuclei between black lines juxtaposed to non-regenerative hepatocytes on the right, without piecemeal necrosis. C. Regenerative nodules show occasional neutrophils [red arrow] and cytoplasmic tufts of ballooned cells, sometimes possibly Mallory hyalin [green arrows]. D. Triads (note vein [green arrow], artery [yellow arrow], and interlobular bile duct [blue arrow]) generally showed little or no interface hepatitis, even when expanded by fibrosis and inflamed. E. Occasional foci of spotty necrosis were seen.  F. This edge of an inflamed triads shows neutrophils about proliferated bile ducts [red arrows], as well as Mallory-Denk bodies [blue arrows].
<br>
A. [[File:1 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
B. [[File:2 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
C. [[File:3 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
D. [[File:4 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
E. [[File:5 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
F. [[File:6 etoh 4 680x512px.tif| Cirrhosis in an alcoholic.]]
<br>
Definite cirrhosis in an alcoholic. A. Hepatocyte free bands parse tissue, with occasional definite islands [arrows]. B. Trichrome establishes blue fibrosis about isles [arrows]. C. Reticulin stain shows nodules with regeneration, wherein a large proportion of them are at least two nuclei thick [arrows]. D. Bile duct proliferation can be difficult, sometimes mimicking cholangiocarcinoma. Follow the double headed arrows to see how the ductules can be seen to proliferate from a single sources, with all ducts being complete, without necrotic epithelial cells. E. PAS with distase can help, as cholangiocarcinoma generally lacks the red rim of proliferating bile ductules [arrows]; again note the connections that can be made between the ductule openings by the blue double headed arrows. The cyan double headed arrows show general parallelism, consistent with uniform directionality induced by extrinsic force, not a neoplastic spread. F. Trichrome shows the most difficult focus. Double headed arrows display the connectivity seen before of the proliferated bile ductules. Note that numerous pairs of adjacent perpendicular glands without a head to foot appearance are not seen that would indicate the disorderly spread of cholangiocarcinoma.
<br>
A. [[File:1 ALC 2 680x512px.tif|Expanded, inflamed triads with increased bile duct/vascular openings. Mild steatosis (40X).]]
<br>
B. [[File:2 ALC 2 680x512px.tif|Trichrome stain shows periportal fibrosis [red arrowheads] (200X).]]
<br>
C. [[File:3 ALC 2 680x512px.tif|PAS with diastase stain shows proliferated bile ductules [blue arrowheads] in stroma with mixed inflammatory infiltrate (400X)]]
<br>
D. [[File:4 ALC 2 680x512px.tif|Neutrophils about ballooned hepatocyte (satellitosis) [yellow arrowheads]. Councilman bodies [green arrowheads] (400X).]]
<br>
Alcoholic hepatitis without cirrhosis. No history of viral disease. AMA negative. A. Expanded, inflamed triads with increased bile duct/vascular openings. Mild steatosis. B. Trichrome stain shows periportal fibrosis [red arrowheads]. C. PAS with diastase stain shows proliferated bile ductules [blue arrowheads] in stroma with mixed inflammatory infiltrate. D. Neutrophils about ballooned hepatocyte (satellitosis) [yellow arrowheads]. Councilman bodies [green arrowheads].


Notes:
Notes:
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*Abbreviated PBC.
*Abbreviated PBC.
{{Main|Primary biliary cirrhosis}}
{{Main|Primary biliary cirrhosis}}
==Autoimmune hepatitis with obstruction - combined changes==
A. [[File:1 AIH OBS 1.tif|Low power shows inflammation; portal triads, lobules, central veins cannot be distinguished (40X).]]
<br>
B. [[File:2 AIH OBS 1.tif|Trichrome shows central venous sclerosis (red arrowhead), periportal fibrosis (green arrowhead), & space of Disse collagenization (yellow arrowhead); juxtaposition of central vein & portal tract indicates collapse, no definite bridging was seen (100X)]]
<br>
C. [[File:3 AIH OBS 1.tif|Central vein is inflamed with a rare plasma cell (cyan arrowhead) (400X).]]
<br>
D. [[File:4 AIH OBS 1.tif|Interface hepatitis with plasma cells (yellow arrows) and ballooned hepatocytes (red arrows).  Lobule is disorganized (400X).]]
<br>
E. [[File:5 AIH OBS 1.tif|Proliferating bile ductules (blue arrows) with occasional neutrophils (fucsia arrows), indicative of obstruction, but not acute cholangitis, which requires inflamed bile duct itself, best diagnosed with associated blood vessel (400X).]]
<br>
F. [[File:6 AIH OBS 1.tif|Rare distorted rosettes with greenish brown strands of bile (left arrow) or bile plugs (right arrow) (400X).]]
<br>
Patient with SLE and obstructive jaundice that resolved with apparent passage of stone. A. Low power shows inflammation; portal triads, lobules, central veins cannot be distinguished. B. Trichrome shows central venous sclerosis (red arrowhead), periportal fibrosis (green arrowhead), & space of Disse collagenization (yellow arrowhead); juxtaposition of central vein & portal tract indicates collapse, no definite bridging was seen. C. Central vein is inflamed with a rare plasma cell (cyan arrowhead). D. Interface hepatitis with plasma cells (yellow arrows) and ballooned hepatocytes (red arrows). Lobule is disorganized. E. Proliferating bile ductules (blue arrows) with occasional neutrophils (fucsia arrows), indicative of obstruction, but not acute cholangitis, which requires inflamed bile duct itself, best diagnosed with associated blood vessel. F. Rare distorted rosettes with greenish brown strands of bile (left arrow) or bile plugs (right arrow).


==Autoimmune hepatitis-primary biliary cirrhosis overlap syndrome==
==Autoimmune hepatitis-primary biliary cirrhosis overlap syndrome==
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===Microscopic===
===Microscopic===
:See: ''[[autoimmune hepatitis]]'' and ''[[primary biliary cirrhosis]]''.
:See: ''[[autoimmune hepatitis]]'' and ''[[primary biliary cirrhosis]]''.
A. [[File:1 AIH PBC 1 680x512px.tif|Expanded portal tracts with fuzzy edges (40X).]]
<br>
B. [[File:2 AIH PBC 1 680x512px.tif|Interface hepatitis with plasma cells (400X).]]
<br>
C. [[File:3 AIH PBC 1 680x512px.tif|Loose granuloma (400X).]]
<br>
D. [[File:4 AIH PBC 1 680x512px.tif|Damaged bile duct (400X).]]
<br>
AIH/PBC overlap. AMA & ANA positive with Alkaline phosphatase > 2 upper limit of normal & one ALT > 5 times upper limit of normal. A. Expanded portal tracts with fuzzy edges. B. Interface hepatitis with plasma cells. C. Loose granuloma. D. Damaged bile duct.


==Primary sclerosing cholangitis==
==Primary sclerosing cholangitis==
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=Other=
=Other=
==Primary Systemic Sclerosis==
[[File:5 05168051 sl 1.png |Primary systemic sclerosis in the liver]]
[[File:5 05168051 sl 2.png |Primary systemic sclerosis in the liver]]
[[File:5 05168051 sl 3.png |Primary systemic sclerosis in the liver]]
[[File:5 05168051 sl 4.png |Primary systemic sclerosis in the liver]]
[[File:5 05168051 sl 5.png |Primary systemic sclerosis in the liver]]
[[File:5 05168051 sl 6.png |Primary systemic sclerosis in the liver]]
<br>
Primary systemic sclerosis in a 67 year old White, non-Hispanic man who had undergone renal transplantation for idiopathic nodular glomerusclerosis, which had recurred in 2013. He had been scheduled to receive a second transplantation, but had not yet received one.  The patient had a positive anti-nuclear antigen study, with a positive scleroderma antibody (SCL-70), a high SCL-70 antibody index of 3.9, and negative DNA, Chromatin, Anti-Riboscomal P, SS-A, SS-B, anti Smith, RNP, JO-1, anticentromere antibody and rheumatoid factor serologic studies.  Hepatitis A, B, and C serologic studies were negative. Liver function tests showed normal albumin and total bilirubin levels with alkaline phosphatase of 712 IU/L (35-129 normal range), alanine aminotransferase 59 IU/L (5-41 normal range), and aspartate aminotransferase 68 IU/L (5-37 normal range). This case provisions many of the features known to be present in primary systemic sclerosis as seen in the skin. A. At low power, triads appear almost as white ghosts against a relatively normal set of hepatocyte lobules. B. Closer examination reveals some triads to be expanded, with peripheral bile ductular proliferation and modest associated chronic inflammation without interface hepatitis. C. Portal arterioles had thick walls; inflammation included lymphocytes and occasional plasma cells. D. Trichrome failed to stain the material in the triads blue, but did show space of Disse collagenization. E. PAS with diastase showed positive staining of the material with emphasis on the arteriole walls. F. Hemosiderosis was seen on iron stain.
==Budd-Chiari syndrome==
==Budd-Chiari syndrome==
*[[AKA]] ''hepatic vein obstruction''.
*[[AKA]] ''hepatic vein obstruction''.
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*[[CK7]] -ve.
*[[CK7]] -ve.
**Marks bile ducts.
**Marks bile ducts.
==Hepatic Graft versus Host Disease (L-GVHD)==
[[File:3 579232643 sl 1.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 2.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 3.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 4.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 5.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 6.png| Hepatic graft versus host disease (L-GVHD)]]
[[File:3 579232643 sl 7.png| Hepatic graft versus host disease (L-GVHD)]]
<br>
Hepatic graft versus host disease (L-GVHD) in a 22 yo man who underwent bone marrow transplantation after developing ALL. A. Low power view shows brownish discoloration in triad, but is otherwise of little interest. B. Arterioles in triads were accompanied by bile ducts in only 30% of cases; this image shows an arteriole without a bile duct. Note the pigment and the accompanying macrophage/lymphocyte inflammation, not extreme. The added chronic inflammation is a feature of chronic L-GVHD. C. Bile ducts, when shown, showed extensive damage, here seen as loss of cytoplasm,  and nuclear pleomorphism and hyperchromasia (other degenerative changes, not seen here, include nuclear dropout or necrosis, cytoplasmic eosinophilia, loss of duct lumen). Lymphocytosis into the ducts was not seen. D. Ballooned hepatocytes and dilated canaliculi were seen. E. Pigment was present, but mostly in Kupffer cells, not hepatocytes or as bile plugs. F. Up to two foci of spotty necrosis were seen in a 100X field (field shown is 200X); not shown are rare apoptotic hepatocytes. G. An iron stain showed the pigment represented extemsive iron deposition, with emphasis on Kupffer cells and portal triad macrophages, frustrating definite assessment of bile plugs in canaliculi. The hemosiderosis resulted from the many blood transfusions the patient had received.
==Extrahepatic biliary obstruction==
A. [[File:1 OBS 3 680x512px.tif|Sinusoidal dilatation, circular spaces of hepatocytes, small portal triads(40X).]]
<br>
B. [[File:2 OBS 3 680x512px.tif|Bile in hepatocytes about central vein & in plugs in canaliculi [yellow arrowhead] (400X).]]
<br>
C. [[File:3 OBS 3 680x512px.tif|Trichrome shows fibrosis about central vein (400X).]]
<br>
D. [[File:4 OBS 3 680x512px.tif|PAS with diastase shows portal triads with mild edema and chronic inflammation, without tortuous bile duct (400X).]]
<br>
Early extrahepatic biliary obstruction, demonstrated radiographically, transient, with rise in bilirubin, alkaline phosphatase, and transaminases. Pure canalicular cholestasis near terminal hepatic venules also seen in acute hepatitis, drug reactions, benign recurrent cholestasis, pregnancy, sepsis, & lymphomas. A. Sinusoidal dilatation, circular spaces of hepatocytes, small portal triads. B. Bile in hepatocytes about central vein & in plugs in canaliculi [yellow arrowhead]. C. Trichrome shows fibrosis about central vein. D. PAS with diastase shows portal triads with mild edema and chronic inflammation, without tortuous bile duct.
<br>
A. [[File:1 OBS 2 680x512px.tif|Expanded inflamed portal triads, swollen hepatocytes (40X)]]
<br>
B. [[File:2 OBS 2 680x512px.tif|Edematous stroma, proliferating ductules [yellow arrowheads], PAS-D macrophages [red arrowhead] (PAS with diastasse, 200X)]]
<br>
C. [[File:3 OBS 2 680x512px.tif|Disordered, often swollen hepatocytes,some with feathery degeneration (net like spaces in cytoplasm [blue arrowhead], rare Councilman body [green arrowhead] (400X)]]
<br>
D. [[File:4 OBS 2 1360x1024px.tif|Bile in hepatocytes [cyan arrrowhead] & in canaliculi [purple arrowheads]. Empty acinar spaces bounded by hepatocytes [orange arrowhead] (400X, higher pixel),]]
<br>
Changes of extrahepatic biliary obstruction, months duration. A. Expanded inflamed portal triads, swollen hepatocytes. B. Edematous stroma, proliferating ductules [yellow arrowheads], PAS-D macrophages [red arrowhead]. C. Disordered, often swollen hepatocytes,some with feathery degeneration (net like spaces in cytoplasm)  [blue arrowhead], rare Councilman body [green arrowhead]. D. Bile in hepatocytes [cyan arrrowhead] & in canaliculi [purple arrowheads]. Empty acinar spaces bounded by hepatocytes [orange arrowhead].
<br>
A. [[File:1 Bd obs 4 680x512px.tif|Expanded, light colored portal triads (arrows)(20X).]]
<br>
B. [[File:2 Bd obs 4 680x512px.tif|Proliferating bile ductules (cyan arrows) with neutrophils (yellow arrows), not specific for acute cholangitis, of assistance with large bile duct obstruction (400X)..]]
<br>
C. [[File:3 Bd obs 4 680x512px.tif|Uninflamed interlobular duct (yellow arrow) with, accompanying blood vessel (red arrow) (400X)]]
<br>
D. [[File:4 Bd obs 4 680x512px.tif|Bile infarct with pyknotic nuclei (arrows)(400X).]]
<br>
E. [[File:5 Bd obs 4 680x512px.tif|Bile (arrow) in interlobular bile duct with disordered nuclei (400X).]]
<br>
F. [[File:6 Bd obs 4 680x512px.tif|Bile plugs in cannaliculi (red arrows), feathery degeneration producing foamy macrophage like hepatocytes (yellow arrows)(400X).]]
<br>
Large bile duct obstruction. A. Expanded, light colored portal triads (arrows). B. Proliferating bile ductules (cyan arrows) with neutrophils (yellow arrows), not specific for acute cholangitis, of assistance with large bile duct obstruction. C. Uninflamed interlobular duct (yellow arrow) with, accompanying blood vessel (red arrow). D. Bile infarct with pyknotic nuclei (arrows). E. Bile (arrow) in interlobular bile duct with disordered nuclei. F. Bile plugs in cannaliculi (red arrows), feathery degeneration producing foamy macrophage-like hepatocytes (yellow arrows).


==Congestive hepatopathy==
==Congestive hepatopathy==
===General===
{{Main|Congestive hepatopathy}}
*Liver failure due to (right) heart failure.
*AKA ''cardiac cirrhosis'' - a term used by clinicians.
**Generally, it does not satisfy pathologic criteria for cirrhosis.<ref>URL: [http://emedicine.medscape.com/article/151792-overview http://emedicine.medscape.com/article/151792-overview]. Accessed on: 17 June 2010.</ref>
 
===Gross===
*"Nutmeg" liver - yellow spotted appearance.
 
===Microscopic===
Features:<ref>URL: [http://emedicine.medscape.com/article/151792-diagnosis http://emedicine.medscape.com/article/151792-diagnosis]. Accessed on: 17 June 2010.</ref>
*Zone III atrophy.
*Portal venule (central vein) distension.
*Perisinusoidal fibrosis - progresses to centrilobular fibrosis and then diffuse fibrosis.
*Dilation of sinusoids in ''all'' zone III areas - '''key feature'''.<ref>Suggested by OA. September 2009.</ref>
 
DDx:
*[[Hemangioma of the liver]] - should be focal lesion.
 
====Images====
<gallery>
Image:Congestive_hepatopathy_high_mag.jpg | Mild congestive hepatopathy. (WC)
</gallery>


==Drug-induced liver disease==
==Drug-induced liver disease==
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*No thrombosis.
*No thrombosis.


==Ascending Cholangitis==
==Ascending Cholangitis (Acute Cholangitis)==
===General===
===General===
*Term for infection of bile ducts, usually due to obstruction
*Term for infection of bile ducts, usually due to obstruction
Line 467: Line 547:
===Microscopic===
===Microscopic===
====Images====
====Images====
{| class="wikitable sortable"
 
| [[File:Asc cholang c1 2016 06 22.tif|thumb|Ascending cholangitis case for Libre Pathology]]
A. [[File:1 asc chol 1 680x512px.tif|Rounded, clear (edematous) portal tracts (arrows) separated by hepatocytes with dilated sinusoids (Row 1 Left 40X).]]
| Ascending cholangitis. Edematous triads, leukocyte speckled (UL), are expanded amid relatively undisturbed hepatocytes. Neutrophils lie within epithelium of proliferated bile ducts (UR). LL Acute inflammation spills out from some triads into the acini (LL). PAS with diastase stain (LR) better shows bile duct damage, with partial loss of the red line surrounding ducts & disorder of nuclei, as well as highlighting intra-epithelial neutrophils.  
<br>
Original oculars.  
B. [[File:2 asc chol 1 680x512px.tif|Neutrophils about hepatocytes (arrows) have spilled into the lobule from a portal tract (Row 1 Right 200X).]]
UL 4X, UR 40X, LL 40X, LR 40X
<br>
|}
C. [[File:3 asc chol 1 680x512px.tif|Proliferated bile ductules (arrows) bearing neutrophils within epithelium and lumens are features of obstruction that should prompt a search for interlobular ducts with acute inflammation (Row 2 Left 400X).]]
<br>
D. [[File:4 asc chol 1 680x512px.tif|The epithelium of the ducts can be severely degenerated. Neutrophils (cyan arrows) invade epithelium of an interlobular duct that are recognizable mainly as a circle of rounded nuclei; the associated arteriole (red arrow) should be identified to ensure an interlobular duct is being evaluated. Note the proliferated bile ductules (blue arrows)  (Row 2 Right 400X).]]
<br>
E. [[File:5 asc chol 1 680x512px.tif|A PAS without diastase stain colors the arteriole (blue arrow), as well as the rim of the interlobular duct within which lies a neutrophil (cyan arrow) (Row 2 Right 400X). .]]
<br>
F. [[File:6 asc chol 1 680x512px.tif|A PAS with diastase stain colors the arteriole (red arrow), as well as the rim of the interlobular duct within which lies a neutrophil (cyan arrow) (Row 1 Right 400X)]]
<br>
Acute cholangitis in a patient with multiple bile duct procedures. After the biopsy, removal of bile duct stones released pus. A. Rounded, clear (edematous) portal tracts (arrows) separated by hepatocytes with dilated sinusoids. B. Neutrophils about hepatocytes (arrows) have spilled into the lobule from a portal tract. C, Proliferated bile ductules (arrows) bearing neutrophils within epithelium and lumens are features of obstruction that should prompt a search for interlobular ducts with acute inflammation. D. The epithelium of the ducts can be severely degenerated. Neutrophils (cyan arrows) invade epithelium of an interlobular duct that are recognizable mainly as a circle of rounded nuclei; the associated arteriole (red arrow) should be identified to ensure an interlobular duct is being evaluated. Note the proliferated bile ductules (blue arrows). E. A PAS without diastase stain colors the arteriole (blue arrow), as well as the rim of the interlobular duct within which lies a neutrophil (cyan arrow). F. A PAS with diastase stain colors the arteriole (red arrow), as well as the rim of the interlobular duct within which lies a neutrophil (cyan arrow).
 
A.[[File:1 Sep Acu Cho 1 680x512px.tif|Low power shows variably sized inflamed portal tracts (40X)]]
<br>
B. [[File:2 Sep Acu Cho 1 680x512px.tif|Trichrome shows dilated sinusoids and space of Disse collagenization (200X)]]
<br>
C. [[File:3 Sep Acu Cho 1 680x512px.tif|Inflammatory focus with macrophages and neutrophils (400X).]]
<br>
D. [[File:4 Sep Acu Cho 1 680x512px.tif|PAS with diastase shows proliferated bile ductules at edge of triad with neutrophils, which should not be used to make a definite diagnosis of acute cholangitis (400X).]]
<br>
E. [[File:5 Sep Acu Cho 1 680x512px.tif|PAS without diastase showing acutely inflamed bile duct, with accompanying blood vessel of similar size, diagnostic of acute cholangitis (400X).]]
<br>
F. [[File:6 Sep Acu Cho 1 680x512px.tif|PAS with diastase showing neutrophil in bille duct lumen, diagnostic of acute cholangitis (400X).]]
<br>
Patient with sepsis and acute cholangitis. A. Low power shows variably sized inflamed portal tracts. B. Trichrome shows dilated sinusoids and space of Disse collagenization. C. Inflammatory focus with macrophages and neutrophils. D. PAS with diastase shows proliferated bile ductules at edge of triad with neutrophils, which should not be used to make a definite diagnosis of acute cholangitis. E. PAS without diastase showing acutely inflamed bile duct, with accompanying blood vessel of similar size, diagnostic of acute cholangitis. F. PAS with diastase showing neutrophil in bille duct lumen, diagnostic of acute cholangitis.


==Polycystic kidney disease and the liver==
==Polycystic kidney disease and the liver==
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==Peliosis hepatis==
==Peliosis hepatis==
===General===
{{Main|Peliosis hepatis}}
*Associated with:
**Infections.
**Malignancy.
**Other stuff.
*Rarely biopsied.
 
===Microscopic===
Features:
*Cyst lined by endothelium.
**Usu. incomplete.
*Blood.


==Total parenteral nutrition==
==Total parenteral nutrition==
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Image:Hepatic_amyloidosis_-_very_high_mag.jpg | Amyloidosis of the liver - very high mag. (WC)
Image:Hepatic_amyloidosis_-_very_high_mag.jpg | Amyloidosis of the liver - very high mag. (WC)
</gallery>
</gallery>
A. [[File:1 AMY 1 680x512px.tif|Amorphous material replaces hepatic parenchyma [4X]]]
<br>
B. [[File:2 AMY 1 680x512px.tif|Material barely stains blue on trichrome [10X]]]
<br>
C. [[File:3 AMY 1 680x512px.tif|Material stains red on unpolarized Congo Red [40X]]]
<br>
D. [[File:4 AMY 1 680x512px.tif|Material stains apple green on polarized Congo Red [40X]]]
<br>
Amyloidosis. A. Amorphous material replaces hepatic parenchyma. B. Material barely stains blue on trichrome. C. Material stains red on unpolarized Congo Red. D. Material stains apple green on polarized Congo Red.


===Stains===
===Stains===
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==Fulminant hepatic necrosis==
==Fulminant hepatic necrosis==
===General===
{{Main|Fulminant hepatic necrosis}}
Etiology:
*Viral, i.e. [[Hepatitis A]], [[Hepatitis B]]; [[Hepatitis C]] - extremely rare.
*Trauma.
*Shock.
 
===Microscopic===
Features:
*Hepatocyte [[necrosis]].
*Bile duct proliferation.
 
DDx:
*[[Cholangiocarcinoma]].
*[[Angiosarcoma]].


==Secondary hemochromatosis==
==Secondary hemochromatosis==
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==Hepatic sarcoidosis==
==Hepatic sarcoidosis==
{{Main|Hepatic sarcoidosis}}
{{Main|Hepatic sarcoidosis}}
==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: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: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: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.]]<br>
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]]<br>
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).
[[File:6 17281676469188 sl 1.png| Hepatitis B virus with steatohepatitis]]
[[File:6 17281676469188 sl 2.png| Hepatitis B virus with steatohepatitis]]
[[File:6 17281676469188 sl 3.png| Hepatitis B virus with steatohepatitis]]
[[File:6 17281676469188 sl 4.png| Hepatitis B virus with steatohepatitis]]
[[File:6 17281676469188 sl 5.png| Hepatitis B virus with steatohepatitis]]
[[File:6 17281676469188 sl 6.png| Hepatitis B virus with steatohepatitis]]<br>
Hepatitis B virus with steatohepatitis in a 36 year old man with hepatitis B surface antigen and hepatitis Be antigen positivity, Hepatitis be QTPC of 1750 cop/mL, an occasionally mildly elevated (42) ALT, and  normal glucose, alkaline phosphatase, bilirubin, and other transaminases. He had a history of alcohol abuse, which became controlled.  A. Triads show scant inflammation without definite interface hepatitis. About one-fourth of the lobule, not pan-acinar, is afflicted by steatosis. B. Occasional tufts are seen (arrow), indicating focal ballooning sufficient for a diagnosis of steatohepatitis. C. Glycogenated nuclei (black arrows) and hepatocytes with feathery degeneration (red arrows) are seen.  D. Very rare foci of spotty necrosis were seen. E. Apart from this triad and the one in the trichrome stain in F, which had moderate inflammation comprising lymphocytes and macrophages, all triads were small, most without any inflammation at all. Neither collapse nor piecemeal necrosis were seen on reticulin stain.  F. Trichrome stain showed only portal fibrosis. The interhepatocyte fibrosis required for brunt fibrosis stage I was not seen. Hence, one would grade this as follows: A) Chronic hepatitis (history of hepatitis B), Metavir activity index 1, Piecemeal necrosis 0, Lobular necrosis 1, Metavir fibrosis stage 1, B) Steatohepaitits, Brunt necroinflammatory grade 1, Brunt fibrosis stage 0.


=See also=
=See also=
Michael
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