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Liver pathology (view source)

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[[Image:Wątroba marska (Ultima Thule).jpg|thumb|right|Drawing of a [[cirrhosis|cirrhotic]] liver. (WC)]]
The '''liver''' is an organ [[pathologist]]s are seeing less of, as [[radiologist]]s (with multimodal imaging and triphasic CT scans) are pretty good at sorting-out many types of liver lesions.
The '''liver''' is an organ [[pathologist]]s are seeing less of, as [[radiologist]]s (with multimodal imaging and triphasic CT scans) are pretty good at sorting-out many types of liver lesions.


This article is an introduction to liver pathology. Liver neoplasms are dealt with in the ''[[liver neoplasms]]'' article.  Medical liver diseases (e.g. viral hepatitis) is dealt with in the ''[[medical liver disease]]'' article.
This article is an introduction to liver pathology. Liver neoplasms are dealt with in the ''[[liver neoplasms]]'' article.  Medical liver diseases (e.g. viral hepatitis) is dealt with in the ''[[medical liver disease]]'' article.
Liver biopsies are quite often non-specific, as the liver has the same appearance for many mechanisms of injury, especially when the injury is marked.
Almost every differential in liver pathology has "drugs" -- if it isn't clearly malignancy.


=Review of liver blood work=
=Review of liver blood work=
===Inflammation activity===
*This is covered in the ''[[Medical_liver_disease#Review_of_liver_blood_work|medical liver disease]]'' article.
*ALT.
*AST.
 
===Cholestatic markers===
*ALP.
*GGT - used to assess whether the ALP is an "honest" value, elevated in cirrhosis.
 
===Cirrhosis/decompensation===
*PLT - low is suggestive of dysfunction.
*INR - high is bad, unless anticoagulated.
 
===Other===
*Bilirubin.
**Direct (AKA conjugated).
**Indirect (AKA unconjugated).
 
A short DDx of elevated:<ref>{{Ref PCPBoD8|441}}</ref>
*Indirect:
**[[Gilbert syndrome]].
**Crigler-Najjar syndrome type 1.
**Crigler-Najjar syndrome type 2.
*Direct:
**Rotor syndrome.
**Dubin-Johnson syndomre.
 
===Viral hepatitis===
*HBV DNA.
*HCV RNA.
*HBs Ag, HBs Ab, HBe Ag, HBe Ab.
*HCV Ab.
 
Others:
*[[Epstein-Barr virus]] (EBV).
*[[Cytomegalovirus]] (CMV) - especially in the immune incompetent.
 
====Hepatitis B====
Meaning & utility of the various [[Hepatitis B]] tests:<ref>URL: [http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/hepatitis-B/ http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/hepatitis-B/]. Accessed on: 16 May 2011.</ref><ref name=lto_hepb>URL: [http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html]. Accessed on: 16 May 2011.</ref>
{| class="wikitable sortable" border="1"
! Test name
! Location
! Positive test
! Negative test
! Usual question
|-
| HBs Ag||Surface||Virus active||No active infection||Active infection?
|-
| HBs Ab||Surface||Exposed OR vaccinated||No exposure OR no vaccine OR loss of Ab||Immunization status?
|-
| HBe Ag||Virus core||Infect. w/ viral replication||No active infection||Active infect. w/ viral replication?
|-
| HBe Ab||Virus core||Exposed to virus||Infect. w/o antibody response OR not exposed||Immune response to infection?
|-
| HBV DNA||-||Active||Not active/no exposure||Viral load/how active?
|-
| HBc Ab||Virus core||Virus active/previous exposure||No exposure||Early active infection?
|}
Notes:
*''HBc Ab'' may test for acute (IgM) or chronic infection - dependent on specific antibody test; it is often used to look for early infection.<ref name=lto_hepb>URL: [http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html http://www.labtestsonline.org/understanding/analytes/hepatitis_b/test.html]. Accessed on: 16 May 2011.</ref>
*''Carriers of hepatitis B'': HBs Ag +ve, HBs Ab -ve, HBc Ag -ve, HBc Ab +ve, HBe Ag -ve, HBe Ab +ve.<ref>URL: [http://labtestsonline.org/understanding/analytes/hepatitis-b/tab/test http://labtestsonline.org/understanding/analytes/hepatitis-b/tab/test]. Accessed on: 3 May 2012.</ref>
 
===Markers for rare liver diseases===
*Ceruloplasm - low think ''[[Wilson's disease]]''; typical value for Wilson's ~ 0.12 g/L.
**<0.20 g/L is a criteria for Wilson's disease.<ref name=pmid18556333>Diagnostic accuracy of serum ceruloplasmin in Wilson disease: determination of sensitivity and specificity by ROC curve analysis among ATP7B-genotyped subjects. Mak CM, Lam CW, Tam S. Clin Chem. 2008 Aug;54(8):1356-62. Epub 2008 Jun 12. PMID 18556333. URL: [http://www.clinchem.org/cgi/reprint/54/8/1356.pdf http://www.clinchem.org/cgi/reprint/54/8/1356.pdf]. Accessed on: 28 September 2009.</ref>
*Alpha-1 antitrypsin - if low think ''deficiency''.
 
===Hemosiderosis===
*Ferritin - high.
*Iron saturation - high.
 
Causes:
*Hemochromatosis.
*Hemolysis, chronic.
*Cirrhosis.
 
=Medical imaging=
Blood flow:<ref>URL: [http://insidesurgery.com/2010/12/hepatopedal-hepatofugal-flow/ http://insidesurgery.com/2010/12/hepatopedal-hepatofugal-flow/]. Accessed on: 2 December 2011.</ref>
*Hepatopedal flow = normal portal vein flow.
*Hepatofugal flow = reversed portal vein flow.
 
==Interventional measurements==
Wedged to free hepatic venous pressure:<ref name=pmid1864548>{{Cite journal  | last1 = Bion | first1 = E. | last2 = Brenard | first2 = R. | last3 = Pariente | first3 = EA. | last4 = Lebrec | first4 = D. | last5 = Degott | first5 = C. | last6 = Maitre | first6 = F. | last7 = Benhamou | first7 = JP. | title = Sinusoidal portal hypertension in hepatic amyloidosis. | journal = Gut | volume = 32 | issue = 2 | pages = 227-30 | month = Feb | year = 1991 | doi =  | PMID = 1864548 | PMC = 1378815 | URL = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378815/?tool=pubmed }}</ref>
*Normal = 1-4 mmHg.
**Elevated in [[portal hypertension]].


=Normal liver=  
=Normal liver=  
Line 198: Line 112:
=Liver biopsy=
=Liver biopsy=
==Medical liver biopsy adequacy==
==Medical liver biopsy adequacy==
Liver biopsy specimens should be:<ref>{{Ref MacSween|418}}</ref>
*This is covered in the ''[[Medical_liver_disease#Medical_liver_biopsy_adequacy|medical liver disease]]'' article.
*2.0 cm in length and contain 11-15 portal tracts,
*The core should be deeper than 1.0 cm from the liver capsule; specimens close to the capsule may lead to over grading of fibrosis.


==Reporting==
==Reporting==
{{Main|Pathology reports}}
{{Main|Pathology reports}}
<pre>
*This is covered in the ''[[Medical_liver_disease#Reporting|medical liver disease]]'' article.
Specimen, procedure:
- Diagnosis.
</pre>
The diagnosis usually contains grading and staging information, e.g. ''activity 2 /4, Laennec fibrosis stage 1 /4''.
 
In the context of medical liver disease:
*Grade = inflammation/activity.
*Stage = severity of fibrosis/architectural changes.
 
Notes:
*The term "acute" is infrequently used in liver pathology.
*In the liver: neutrophils ''is not'' acute -- unlike most elsewhere in the body.<ref>OA. September 2009.</ref>


=Liver injury terms/histologic findings=
=Liver injury terms/histologic findings=
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Image:Von_Meyenburg_complex_low_mag.jpg | Von Meyenburg complex - bile duct hamartoma (WC)
Image:Von_Meyenburg_complex_low_mag.jpg | Von Meyenburg complex - bile duct hamartoma (WC)
Image:Bile_duct_hamartoma_intermed_mag.jpg | Bile duct hamartoma - intermed. mag. (WC)
Image:Bile_duct_hamartoma_intermed_mag.jpg | Bile duct hamartoma - intermed. mag. (WC)
Image:Von_Meyenburg_complex_liver.jpg | Von Meyenburg complex / bile duct hamartoma (WC)
</gallery>
</gallery>
www:
www:
Line 260: Line 161:


===Ballooning degeneration===
===Ballooning degeneration===
*Central nucleus.
{{Main|Ballooning degeneration}}
**"Fat cells" have peripheral nucleus.
*Cytoplasm cleared with "whisps" or cobbwebs.
*Large relative to normal hepatocyte.
**2-3X normal size.<ref>Guindi, M. 16 September 2009.</ref>
 
Notes:
*The term is used only in conjunction with ''[[steatohepatitis]]''.
*''Feathery degeneration'' is the term used in the context of cholestasis.
**It is usually periportal.
 
====Images====
<gallery>
Image:Ballooning_degeneration_high_mag_cropped.jpg | Ballooning degeneration. (WC/Nephron)
</gallery>
www:
*[http://www.uthscsa.edu/hscnews/EnlargePicture.asp?PicName=LiverBeforeTreatment_BODY.jpg Ballooning degeneration (uthscsa.edu)].
*[http://library.med.utah.edu/WebPath/LIVEHTML/LIVER039.html Ballooning degeneration (med.utah.edu)].


===Ground glass hepatocytes===
===Ground glass hepatocytes===
*Eosinophilic dull/hazy, somewhat irregular cytoplasm.
{{Main|Ground glass hepatocyte}}
**Ground glass<ref>URL: [http://en.wikipedia.org/wiki/Ground_glass http://en.wikipedia.org/wiki/Ground_glass]. Accessed on: 7 June 2010.</ref> = glass with a rough/flat finish; glass that is translucent and has a matte finish.
***The term is frequently used in radiology to describe hazy radiodense areas in the lung.<ref>URL: [http://www.healthsystem.virginia.edu/internet/radiology/educ/groundglass.cfm http://www.healthsystem.virginia.edu/internet/radiology/educ/groundglass.cfm]. Accessed on: 7 June 2010.</ref>
*Usually suggests '''chronic''' [[HBV]] infection.
**Pattern NOT seen in acute HBV.
**Caused by virion particles.
 
DDx:
*Pseudo-Lafora bodies in patients on disulfiram (anatabuse) - rare.
 
====Classification====
*GGHs are not routinely classified.
 
Notes:
*Several different types of GGHs are recognized.<ref name=pmid14633616>Wang HC, Wu HC, Chen CF, Fausto N, Lei HY, Su IJ. Different types of ground glass hepatocytes in chronic hepatitis B virus infection contain specific pre-S mutants that may induce endoplasmic reticulum stress. Am J Pathol. 2003 Dec;163(6):2441-9. PMID 14633616. Available at: [http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=14633616 http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=14633616]. Accessed on: September 11, 2009.</ref>
 
Classification:<ref>Wang HC, Wu HC, Chen CF, Fausto N, Lei HY, Su IJ. Different types of ground glass hepatocytes in chronic hepatitis B virus infection contain specific pre-S mutants that may induce endoplasmic reticulum stress. Am J Pathol. 2003 Dec;163(6):2441-9. PMID 14633616. Available at: [http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1892360&rendertype=figure&id=f1
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1892360&rendertype=figure&id=f1]. Accessed on: 17 September 2009.</ref>
*Type I ground glass hepatocytes (GGHs).
**Weak Pre-S2 positive immunostaining; morphology: GGHs scattered singly.
*Type II GGHs.
**Pre-S2 negative immunostaining; morphology: GGHs in clusters.
 
There is some suggestion that type II GGHs predispose to [[HCC]], based on data in children<ref name=pmid19719772>Pre-S2 deletion mutants of hepatitis B virus could have an important role in hepatocarcinogenesis in Asian children. Abe K, Thung SN, Wu HC, Tran TT, Le Hoang P, Truong KD, Inui A, Jang JJ, Su IJ. Cancer Sci. 2009 Aug 6. [Epub ahead of print] PMID 19719772.</ref> and based on an animal model.<ref name=pmid18505413>Ground glass hepatocytes contain pre-S mutants and represent preneoplastic lesions in chronic hepatitis B virus infection. Su IJ, Wang HC, Wu HC, Huang WY. J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1169-74. Epub 2008 May 26. Review. PMID 18505413.</ref>
 
Micrographs of GGHs:
<gallery>
Image:Ground_glass_hepatocytes_high_mag_cropped_2.jpg | Ground glass hepatocytes. (WC/Nephron)
Image:Ground_glass_hepatocytes_high_mag_cropped.jpg | Ground glass hepatocyte. (WC/Nephron)
</gallery>
www:
*[http://www.consultantlive.com/aids/article/1145619/1363027 Ground glass hepatocytes (consultantlive.com)].
*[http://www.biomedcentral.com/1471-230X/5/36/figure/F1 Ground glass hepatocytes (biomedcentral.com)].
*[http://pathology.osu.edu/paxit/deptbase/Paxit/Images/10534/PAXIT052.JPG Ground glass hepatocyte (pathology.osu.edu)].


===Mallory bodies===
===Mallory bodies===
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*Inflammation disrupts the "limiting plate", i.e. there is disruption of the hepatocytes that separate the portal tracts from the lobules.
*Inflammation disrupts the "limiting plate", i.e. there is disruption of the hepatocytes that separate the portal tracts from the lobules.


Micrograph:
=====Images=====
<gallery>
Image: Interface hepatitis -- high mag.jpg | IH (mild) - high mag. (WC)
Image: Interface hepatitis -- very high mag.jpg | IH (mild) - very high mag. (WC)
</gallery>
www:
*[http://www.pathologyatlas.ro/viral-chronic-moderate-hepatitis.php Interface hepatitis (pathologyatlas.ro)].
*[http://www.pathologyatlas.ro/viral-chronic-moderate-hepatitis.php Interface hepatitis (pathologyatlas.ro)].
*[http://www.nature.com/modpathol/journal/v20/n1s/fig_tab/3800693f1.html#figure-title Interface hepatitis (nature.com)].<ref name=pmid17486049>{{Cite journal | last1 = Theise | first1 = ND. | title = Liver biopsy assessment in chronic viral hepatitis: a personal, practical approach. | journal = Mod Pathol | volume = 20 Suppl 1 | issue = | pages = S3-14 | month = Feb | year = 2007 | doi = 10.1038/modpathol.3800693 | PMID = 17486049 }}</ref>
*[http://www.nature.com/modpathol/journal/v20/n1s/fig_tab/3800693f1.html#figure-title Interface hepatitis (nature.com)].<ref name=pmid17486049>{{cite journal |author=Theise ND |title=Liver biopsy assessment in chronic viral hepatitis: a personal, practical approach |journal=Mod. Pathol. |volume=20 Suppl 1 |issue= |pages=S3-14 |year=2007 |month=February |pmid=17486049 |doi=10.1038/modpathol.3800693 |url=http://www.nature.com/modpathol/journal/v20/n1s/full/3800693a.html}}</ref>


===Liver fibrosis===
===Liver fibrosis===
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===Cirrhosis===
===Cirrhosis===
*Cirrhosis ''is'' stage 4 (Laennec).
{{Main|Cirrhosis}}
**The formal Robbins definitions is:<ref name=Ref_PCPBoD8_439>{{Ref PCPBoD8|439}}</ref> (1) bridging fibrosis, (2) nodule formation, and (3) disruption of the hepatic architecture.
*The etiology of late stage fibrosis (cirrhosis), may be impossible to determine.
*Perisinusoidal fibrosis may suggest congestive hepatopathy.<ref>OA. September 15, 2009.</ref>
*In NAFLD portal-to-portal fibrosis (septal/bridging fibrosis) tends to be more common than perivenular fibrosis.<ref name=pmid14991537>Pathologic features associated with fibrosis in nonalcoholic fatty liver disease. Gramlich T, Kleiner DE, McCullough AJ, Matteoni CA, Boparai N, Younossi ZM. Hum Pathol. 2004 Feb;35(2):196-9. PMID 14991537.</ref>
*The classic teaching is that cirrhosis is irreversible; however, there is increasing evidence that it regresses.<ref name=pmid11079009>{{Cite journal  | last1 = Wanless | first1 = IR. | last2 = Nakashima | first2 = E. | last3 = Sherman | first3 = 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 | month = Nov | year = 2000 | doi = 10.1043/0003-9985(2000)1241599:ROHC2.0.CO;2 | PMID = 11079009 }}</ref><ref name=pmid21286337>{{Cite journal  | last1 = Kim | first1 = SU. | last2 = Park | first2 = JY. | last3 = Kim | first3 = do Y. | last4 = Ahn | first4 = SH. | last5 = Choi | first5 = EH. | last6 = Seok | first6 = JY. | last7 = Lee | first7 = JM. | last8 = Park | first8 = YN. | last9 = Chon | first9 = CY. | title = Non-invasive assessment of changes in liver fibrosis via liver stiffness measurement in patients with chronic hepatitis B: impact of antiviral treatment on fibrosis regression. | journal = Hepatol Int | volume = 4 | issue = 4 | pages = 673-80 | month =  | year = 2010 | doi = 10.1007/s12072-010-9201-7 | PMID = 21286337 }}</ref><ref name=pmid24304452>{{Cite journal  | last1 = Casado | first1 = JL. | last2 = Quereda | first2 = C. | last3 = Moreno | first3 = A. | last4 = Pérez-Elías | first4 = MJ. | last5 = Martí-Belda | first5 = P. | last6 = Moreno | first6 = S. | title = Regression of liver fibrosis is progressive after sustained virological response to HCV therapy in patients with hepatitis C and HIV coinfection. | journal = J Viral Hepat | volume = 20 | issue = 12 | pages = 829-37 | month = Dec | year = 2013 | doi = 10.1111/jvh.12108 | PMID = 24304452 }}</ref>


Special types:
===Steatosis===
*Garland cirrhosis ([[AKA]] holly leaf cirrhosis) - see ''[[primary biliary cirrhosis]]''.
{{Main|Steatosis}}
====Gross====
Cirrhosis can be divided (in gross pathology) into:
*Micronodular cirrhosis - classically due to [[alcohol]].
**Uniform, diffuse.
*Macronodular cirrhosis - classically due to viral hepatitis.
**Irregular.
 
Images:
*[http://www.meddean.luc.edu/lumen/MedEd/orfpath/cirhosis.htm Cirrhosis - macronodular & micronodular (meddean.luc.edu)].
<gallery>
Image:Cirrhosis_high_mag.jpg | Cirrhotic liver - trichrome stain. (WC/Nephron)
</gallery>
 
===Steatosis of the liver===
Can be divided into:
#Microvesicular steatosis.
#*Rare.
#*Nucleus is central.<ref>STC. 6 December 2010.</ref>
#Macrovesicular steatosis.
#*Common.
#*Nucleus is eccentric.
 
Microvescicular is considered potentially life threatening.<ref name=pmid15503661>{{Cite journal  | last1 = Jolly | first1 = RA. | last2 = Ciurlionis | first2 = R. | last3 = Morfitt | first3 = D. | last4 = Helgren | first4 = M. | last5 = Patterson | first5 = R. | last6 = Ulrich | first6 = RG. | last7 = Waring | first7 = JF. | title = Microvesicular steatosis induced by a short chain fatty acid: effects on mitochondrial function and correlation with gene expression. | journal = Toxicol Pathol | volume = 32 Suppl 2 | issue =  | pages = 19-25 | month =  | year =  | doi =  | PMID = 15503661 | URL = http://tpx.sagepub.com/cgi/pmidlookup?view=long&pmid=15503661 }}</ref>
 
Quantity of fat is usually given as a percentage and graded ''mild'', ''moderate'', or ''marked''.
*Mild <33%, moderate >33% & <66%, marked >66%.<ref>Guindi, M. September 17, 2009.</ref>
 
Notes:
*It is considered technically incorrect to say the liver, in steatosis/steatohepatitis, contains ''adipocytes''; they are ''lipid-laden hepatocytes'',<ref>Guindi, M. September 2009.</ref> despite that:
**Histologically, these cells look like adipocytes.
**Lipid-laden hepatocytes have gene activations suggestive of adipogenic-like transformation.<ref>URL: [http://www.jci.org/articles/view/20513/version/1 http://www.jci.org/articles/view/20513/version/1]. Accessed on: 23 September 2009.</ref>
 
====Microvesicular steatosis====
Microvesicular steatosis DDx:<ref name=pmid2177300>{{cite journal |author=Hautekeete ML, Degott C, Benhamou JP |title=Microvesicular steatosis of the liver |journal=Acta Clin Belg |volume=45 |issue=5 |pages=311–26 |year=1990 |pmid=2177300 |doi= |url=}}</ref>
*Acute fatty liver of pregnancy,
*Reye's syndrome.
*Drug toxicity:
**Sodium valproate toxicity.
**High-dose tetracycline toxicity.
*Jamaican vomiting sickness.
*Congenital defects of urea cycle enzymes.
 
Less common causes:
*Alcoholism.
*Hepatitis D.
*Weird stuff:
**Congenital defects of fatty acid beta oxidation,
**Cholesterol ester storage disease,
**Wolman disease and Alpers syndrome.
 
The classic causes of microvesicular steatosis are:<ref>[http://www.mailman.srv.ualberta.ca/pipermail/patho-l/1996-June/001788.html http://www.mailman.srv.ualberta.ca/pipermail/patho-l/1996-June/001788.html]</ref>
*Fatty liver of pregnancy.
*Aspirin (Reye's syndrome).
*Tetracycline.
It was once thought that all other causes of fatty liver produce macrovesicular steatosis.
 
====Macrovesicular steatosis====
Can sometimes be divided into ''centrilobular'' predominant and ''periportal'' predominant.<ref name=pcddx_steatosis>Steatosis. pathconsultddx.com. URL: [http://www.pathconsultddx.com/pathCon/diagnosis?pii=S1559-8675%2806%2970840-3 http://www.pathconsultddx.com/pathCon/diagnosis?pii=S1559-8675%2806%2970840-3]. Accessed on: 2 Sep 2009.</ref>
 
Centrilobular predominant (zone III) - ''DOA'':<ref name=pcddx_steatosis/>
*[[Diabetes mellitus]].
*Obesity, non-alcoholic steatohepatitis (NASH).
*Alcoholic liver disease, alcoholic steatohepatitis (ASH).
 
Image:
<gallery>
Image:Non-alcoholic_fatty_liver_disease1.jpg | Centrilobular steatosis. (WC/Nephron)
</gallery>
 
Periportal predominant (zone I) - ''TAPES'':<ref name=pcddx_steatosis/>
*Total parenteral nutrition (TPN).
*AIDS.
*Phosphorus poisoning.
*Exogenous steroids.
*[[Starvation]].<ref name=pmid10600264>{{Cite journal  | last1 = Nagy | first1 = I. | last2 = Németh | first2 = J. | last3 = Lászik | first3 = Z. | title = Effect of L-aminocarnitine, an inhibitor of mitochondrial fatty acid oxidation, on the exocrine pancreas and liver in fasted rats. | journal = Pharmacol Res | volume = 41 | issue = 1 | pages = 9-17 | month = Jan | year = 2000 | doi = 10.1006/phrs.1999.0565 | PMID = 10600264 }}</ref>
 
Notes:
*HCV genotype 3 is reported to cause periportal steatosis.<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>
*Donor livers with more ''macrovescicular steatosis'' = worse outcome.
**More than 30% means the liver is undesirable for [[Liver transplantation pathology|transplantation]].<ref>STC. 6 December 2010.</ref>
 
Image:
<gallery>
Image:Periportal_hepatosteatosis_intermed_mag.jpg | Periportal steatosis. (WC/Nephron)
</gallery>


===Cholestasis===
===Cholestasis===
:''Cholestatic [[hepatitis]]'' redirects here.
{{Main|Cholestasis}}
====General====
Clinical - classic:<ref>URL: [http://www.patient.co.uk/doctor/cholestasis http://www.patient.co.uk/doctor/cholestasis]. Accessed on: 28 November 2013.</ref>
*Dark urine and light stools.
 
Short DDx - by etiology:
*Congenital: Bile duct cyst, biliary atresia, liver cysts.
*Infectious: Worm.
*Tumour: pancreas, bile duct, liver.
*Endocrine: cholestasis of pregnancy.
*Trauma -> sepsis.
*Autoimmune: PSC, PBC.
*Toxins: alcohol -> cirrhosis.
*Everything else: drugs, e.g. [[NSAID]]s.
 
Short DDx - structural:
*Obstruction - large duct:
**Tumour.
**Gallstone.
**Worm.
**PSC.
*Small duct - autoimmune:
**PBC.
*Other:
**Rx.
**Toxins.
**Cholestasis of pregnancy.
 
====Microscopic====
Appearance of bile:
*Smooth/homogenous.
*Brown/yellow.
*Globule/droplet - that is larger than an iron granule.
 
Note:
*Iron in bile ducts or endothelial cell = non-specific, used to be thought to be specific for [[hereditary hemochromatosis]].
 
=====Brown/yellow cytoplasmic inclusions=====
Comparison of brown/yellow cytoplasmic inclusions:<ref>Guindi, M. September 2009.</ref>
{| class="wikitable sortable" border="1"
! Finding
! Colour
! Granularity
! Refractile
! Usual location
! Association
! Stain
! Image
|-
| Iron||Brown||Coarse granules||Yes - shinny||Periportal<br>(zone I)||Hemolysis, hereditary hemochromatosis || [[Prussian blue stain|Prussian blue]] +ve || [[Image:Sickle_cell_disease_and_cirrhosis_-_very_high_mag.jpg|thumb|center|100px|Iron and bile. (WC)]]
|-
| Bile||Brown - coffee stained||Not granular||No - dull||Portal||Duct injury/obstruction
| None || [[Image:Cholestasis_high_mag.jpg|thumb|100px|center|Bile. (WC)]]
|-
| Lipofuscin||Yellow||Fine granules||No||Centrilobular<br>(zone III)||Advanced age || [[PAS stain]] +ve || [[Image:Ground_glass_hepatocytes_high_mag_cropped.jpg|thumb|100px|center|Lipofuscin. (WC)]]
|-
|}
 
=====Large duct obstruction=====
Histologic findings of large-duct obstruction:<ref>{{Ref MacSween|565}}</ref>
#Perivenular bilirubinostasis.
#Portal tract edema & inflammation (neutrophils & macrophages).
#Large bile plugs.
#Bile duct proliferation.<ref name=pmid7439807>{{cite journal |author=Chapman RW, Arborgh BA, Rhodes JM, ''et al.'' |title=Primary sclerosing cholangitis: a review of its clinical features, cholangiography, and hepatic histology |journal=Gut |volume=21 |issue=10 |pages=870–7 |year=1980 |month=October |pmid=7439807 |pmc=1419383 |doi= |url=}}</ref><ref name=pmid14594129>{{cite journal |author=Leuschner U |title=Primary biliary cirrhosis--presentation and diagnosis |journal=Clin Liver Dis |volume=7 |issue=4 |pages=741–58 |year=2003 |month=November |pmid=14594129 |doi= |url=}}</ref>
 
Note:
*''Ductular reaction'' = increased number of ducts + [[neutrophil]]s.<ref name=pmid9845427>{{Cite journal  | last1 = Roskams | first1 = T. | last2 = Desmet | first2 = V. | title = Ductular reaction and its diagnostic significance. | journal = Semin Diagn Pathol | volume = 15 | issue = 4 | pages = 259-69 | month = Nov | year = 1998 | doi =  | PMID = 9845427 }}</ref>
 
=====Small duct obstruction=====
Small-duct obstruction:
*Abnormal liver plate architecture. (???)
 
======Images======
<gallery>
Image:Cholestasis_high_mag.jpg | Cholestasis. (WC/Nephron)
</gallery>
www:
*[http://www.humpath.com/spip.php?article4340&id_document=20040 Centrilobular cholestasis (humpath.com)].
 
====Sign out====
<pre>
LIVER, CORE BIOPSY:
- CENTRILOBULAR CHOLESTATSIS (MILD), SEE MICROSCOPIC DESCRIPTION AND COMMENT.
- NEGATIVE FOR FIBROSIS.
 
COMMENT:
There is no apparent feathery degeneration. There is no bile ductular proliferation. No
definite onion-skin lesions are identified.
 
The centrilobular distribution of the bile favours a large duct obstruction. Possible
causes include gallstones, other obstructing lesions, herbals and drugs.
 
Clinical and radiologic correlation is suggested.
</pre>


=Diseases=
=Diseases=
Line 655: Line 328:
*[[Hydatid cyst]].
*[[Hydatid cyst]].
**Images: [http://pathmicro.med.sc.edu/parasitology/hydatid-hist1.jpg Hydatid cyst (med.sc.edu)] [http://www.atlas.or.kr/atlas/include/viewImg.html?uid=645 Hydatid cyst (atlas.or.kr)] [http://cal.vet.upenn.edu/projects/paraav/images/lab7-14.jpg]
**Images: [http://pathmicro.med.sc.edu/parasitology/hydatid-hist1.jpg Hydatid cyst (med.sc.edu)] [http://www.atlas.or.kr/atlas/include/viewImg.html?uid=645 Hydatid cyst (atlas.or.kr)] [http://cal.vet.upenn.edu/projects/paraav/images/lab7-14.jpg]
*[[Hemangioma]].
*[[Liver hemangioma]].
**Images: [http://www.pathguy.com/lectures/cavernous_hemangioma.jpg Hemangioma (pathguy.com)] [http://www.ikp.unibe.ch/lab2/Hemang.jpg Hemangioma (ikp.unibe.ch)]
**Images: [http://www.pathguy.com/lectures/cavernous_hemangioma.jpg Hemangioma (pathguy.com)] [http://www.ikp.unibe.ch/lab2/Hemang.jpg Hemangioma (ikp.unibe.ch)]
*[[Hepatic adenoma]].
*[[Hepatic adenoma]].
Mark
110

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