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| ===Lab findings=== | | ==Physical examination== |
| [[Image:Esophageal varices.jpg|thumb|200px|left|Esophageal varices as seen on Endoscopy]]
| | ==References== |
| | | {{reflist|2}} |
| ===image===
| |
| [[Image:Normal versus Abnormal Barium study of esophagus.jpg|thumb|left|200px|Normal versus Abnormal Barium study of esophagus with varices]]
| |
| '''Radiologic findings:'''
| |
| * Radiologic studies include:<ref name="pmid22357834">{{cite journal |vauthors=Udell JA, Wang CS, Tinmouth J, FitzGerald JM, Ayas NT, Simel DL, Schulzer M, Mak E, Yoshida EM |title=Does this patient with liver disease have cirrhosis? |journal=JAMA |volume=307 |issue=8 |pages=832–42 |year=2012 |pmid=22357834 |doi=10.1001/jama.2012.186 |url=}}</ref>
| |
| ** Abdominal ultrasound
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| ** Computed tomography scan
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| ** Magnetic resonance imaging
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| | |
| * Findings may include:<ref name="pmid3533689">{{cite journal |vauthors=Becker CD, Scheidegger J, Marincek B |title=Hepatic vein occlusion: morphologic features on computed tomography and ultrasonography |journal=Gastrointest Radiol |volume=11 |issue=4 |pages=305–11 |year=1986 |pmid=3533689 |doi= |url=}}</ref><ref name="pmid2526349">{{cite journal |vauthors=Di Lelio A, Cestari C, Lomazzi A, Beretta L |title=Cirrhosis: diagnosis with sonographic study of the liver surface |journal=Radiology |volume=172 |issue=2 |pages=389–92 |year=1989 |pmid=2526349 |doi=10.1148/radiology.172.2.2526349 |url=}}</ref><ref name="pmid3891495">{{cite journal |vauthors=Sanford NL, Walsh P, Matis C, Baddeley H, Powell LW |title=Is ultrasonography useful in the assessment of diffuse parenchymal liver disease? |journal=Gastroenterology |volume=89 |issue=1 |pages=186–91 |year=1985 |pmid=3891495 |doi= |url=}}</ref><ref name="pmid3532188">{{cite journal |vauthors=Giorgio A, Amoroso P, Lettieri G, Fico P, de Stefano G, Finelli L, Scala V, Tarantino L, Pierri P, Pesce G |title=Cirrhosis: value of caudate to right lobe ratio in diagnosis with US |journal=Radiology |volume=161 |issue=2 |pages=443–5 |year=1986 |pmid=3532188 |doi=10.1148/radiology.161.2.3532188 |url=}}</ref><ref name="pmid10341686">{{cite journal |vauthors=Simonovský V |title=The diagnosis of cirrhosis by high resolution ultrasound of the liver surface |journal=Br J Radiol |volume=72 |issue=853 |pages=29–34 |year=1999 |pmid=10341686 |doi=10.1259/bjr.72.853.10341686 |url=}}</ref><ref name="pmid22144108">{{cite journal |vauthors=Trinchet JC, Chaffaut C, Bourcier V, Degos F, Henrion J, Fontaine H, Roulot D, Mallat A, Hillaire S, Cales P, Ollivier I, Vinel JP, Mathurin P, Bronowicki JP, Vilgrain V, N'Kontchou G, Beaugrand M, Chevret S |title=Ultrasonographic surveillance of hepatocellular carcinoma in cirrhosis: a randomized trial comparing 3- and 6-month periodicities |journal=Hepatology |volume=54 |issue=6 |pages=1987–97 |year=2011 |pmid=22144108 |doi=10.1002/hep.24545 |url=}}</ref><ref name="pmid22424438">{{cite journal |vauthors= |title=EASL-EORTC clinical practice guidelines: management of hepatocellular carcinoma |journal=J. Hepatol. |volume=56 |issue=4 |pages=908–43 |year=2012 |pmid=22424438 |doi=10.1016/j.jhep.2011.12.001 |url=}}</ref>
| |
| ** A liver that appears shrunken, irregular, and nodular.
| |
| | |
| * Evidence of Portal HTN:
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| ** varices
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| ** Ascites
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| '''DIAGNOSIS''' —
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| * Abdominal imaging (typically ultrasound) helps:
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| ** Evaluate the liver parenchyma
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| ** Detects extrahepatic manifestations of cirrhosis
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| '''Laboratory tests:'''
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| * AST to platelet ratio index
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| * FibroTest/FibroSure
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| '''Imaging studies:'''
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| * Findings on abdominal imaging are viewed in light of other signs of cirrhosis, such as physical examination or laboratory test findings.
| |
| * In addition to evaluating the liver, abdominal imaging may reveal:
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| ** Hepatocellular carcinoma
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| ** Extrahepatic findings suggestive of cirrhosis:
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| *** Ascites
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| *** Varices
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| *** Splenomegaly
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| *** Hepatic or portal vein thrombosis
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| | |
| * Imaging may indicate etiology of cirrhosis:
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| '''CT'''
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| * Computed tomography (CT) scanning complements ultrasound imaging.
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| * Classical appearances in some diseases:
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| ** Haemochromatosis: where the excess iron deposition causes a dramatic increase in hepatic density.
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| * A hypertrophied caudate lobe discovered on computed tomographic (CT) scanning, for example, suggests Budd-Chiari syndrome.
| |
| '''MRI'''<ref name="pmid9129412">{{cite journal |vauthors=Ernst O, Sergent G, Bonvarlet P, Canva-Delcambre V, Paris JC, L'Herminé C |title=Hepatic iron overload: diagnosis and quantification with MR imaging |journal=AJR Am J Roentgenol |volume=168 |issue=5 |pages=1205–8 |year=1997 |pmid=9129412 |doi=10.2214/ajr.168.5.9129412 |url=}}</ref><ref name="pmid10405746">{{cite journal |vauthors=Bonkovsky HL, Rubin RB, Cable EE, Davidoff A, Rijcken TH, Stark DD |title=Hepatic iron concentration: noninvasive estimation by means of MR imaging techniques |journal=Radiology |volume=212 |issue=1 |pages=227–34 |year=1999 |pmid=10405746 |doi=10.1148/radiology.212.1.r99jl35227 |url=}}</ref><ref name="pmid7972774">{{cite journal |vauthors=Gandon Y, Guyader D, Heautot JF, Reda MI, Yaouanq J, Buhé T, Brissot P, Carsin M, Deugnier Y |title=Hemochromatosis: diagnosis and quantification of liver iron with gradient-echo MR imaging |journal=Radiology |volume=193 |issue=2 |pages=533–8 |year=1994 |pmid=7972774 |doi=10.1148/radiology.193.2.7972774 |url=}}</ref><ref name="pmid10470885">{{cite journal |vauthors=Ito K, Mitchell DG, Hann HW, Kim Y, Fujita T, Okazaki H, Honjo K, Matsunaga N |title=Viral-induced cirrhosis: grading of severity using MR imaging |journal=AJR Am J Roentgenol |volume=173 |issue=3 |pages=591–6 |year=1999 |pmid=10470885 |doi=10.2214/ajr.173.3.10470885 |url=}}</ref><ref name="pmid10352597">{{cite journal |vauthors=Ito K, Mitchell DG, Gabata T, Hussain SM |title=Expanded gallbladder fossa: simple MR imaging sign of cirrhosis |journal=Radiology |volume=211 |issue=3 |pages=723–6 |year=1999 |pmid=10352597 |doi=10.1148/radiology.211.3.r99ma31723 |url=}}</ref><ref name="pmid9609897">{{cite journal |vauthors=Ito K, Mitchell DG, Hann HW, Outwater EK, Kim Y, Fujita T, Okazaki H, Honjo K, Matsunaga N |title=Progressive viral-induced cirrhosis: serial MR imaging findings and clinical correlation |journal=Radiology |volume=207 |issue=3 |pages=729–35 |year=1998 |pmid=9609897 |doi=10.1148/radiology.207.3.9609897 |url=}}</ref><ref name="pmid8273643">{{cite journal |vauthors=Finn JP, Kane RA, Edelman RR, Jenkins RL, Lewis WD, Muller M, Longmaid HE |title=Imaging of the portal venous system in patients with cirrhosis: MR angiography vs duplex Doppler sonography |journal=AJR Am J Roentgenol |volume=161 |issue=5 |pages=989–94 |year=1993 |pmid=8273643 |doi=10.2214/ajr.161.5.8273643 |url=}}</ref>
| |
| * Magnetic resonance imaging (MRI):<ref name="pmid10405746">{{cite journal |vauthors=Bonkovsky HL, Rubin RB, Cable EE, Davidoff A, Rijcken TH, Stark DD |title=Hepatic iron concentration: noninvasive estimation by means of MR imaging techniques |journal=Radiology |volume=212 |issue=1 |pages=227–34 |year=1999 |pmid=10405746 |doi=10.1148/radiology.212.1.r99jl35227 |url=}}</ref><ref name="pmid10470885">{{cite journal |vauthors=Ito K, Mitchell DG, Hann HW, Kim Y, Fujita T, Okazaki H, Honjo K, Matsunaga N |title=Viral-induced cirrhosis: grading of severity using MR imaging |journal=AJR Am J Roentgenol |volume=173 |issue=3 |pages=591–6 |year=1999 |pmid=10470885 |doi=10.2214/ajr.173.3.10470885 |url=}}</ref><ref name="pmid11584240">{{cite journal |vauthors=Choi D, Kim SH, Lim JH, Cho JM, Lee WJ, Lee SJ, Lim HK |title=Detection of hepatocellular carcinoma: combined T2-weighted and dynamic gadolinium-enhanced MRI versus combined CT during arterial portography and CT hepatic arteriography |journal=J Comput Assist Tomogr |volume=25 |issue=5 |pages=777–85 |year=2001 |pmid=11584240 |doi= |url=}}</ref><ref name="pmid16244259">{{cite journal |vauthors=Qayyum A, Goh JS, Kakar S, Yeh BM, Merriman RB, Coakley FV |title=Accuracy of liver fat quantification at MR imaging: comparison of out-of-phase gradient-echo and fat-saturated fast spin-echo techniques--initial experience |journal=Radiology |volume=237 |issue=2 |pages=507–11 |year=2005 |pmid=16244259 |doi=10.1148/radiol.2372040539 |url=}}</ref>
| |
| ** determines the nature of focal lesions such as hepatic metastases
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| ** nodular regeneration
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| * Decreased signal intensity on magnetic resonance imaging may indicate iron overload from hereditary hemochromatosis.
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| '''Ultrasonography:''' routinely used during the evaluation of cirrhosis
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| * First-line investigation of choice.
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| * The first radiologic study obtained due to easy availability.
| |
| | |
| * Provides information about :
| |
| ** appearance of the liver
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| ** blood flow within the portal circulation
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| | |
| * less expensive than other imaging modalities
| |
| | |
| * No exposure to intravenous contrast or radiation
| |
| | |
| * Noninvasive
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| * cheap
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| * safe
| |
| | |
| * well tolerated
| |
| | |
| * widely available
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| * Ultrasound, particularly with colour Doppler imaging : <ref name="pmid7718281">{{cite journal |vauthors=Zwiebel WJ |title=Sonographic diagnosis of hepatic vascular disorders |journal=Semin. Ultrasound CT MR |volume=16 |issue=1 |pages=34–48 |year=1995 |pmid=7718281 |doi= |url=}}</ref>
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| ** measures changes in blood flow in the presence of portal hypertension
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| ** excludes biliary obstruction in patients who present with jaundice
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| | |
| * Early signs of cirrhosis in B-ultrasonography include:
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| ** inhomogeneity of the hepatic tissue
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| ** Irregularity of the hepatic surface
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| ** enlargement of the caudate lobe
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| ** Splenomegaly due to portal HTN
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| | |
| * The diagnostic evaluation of cirrhosis with ultrasonography is based on the direct relation between the extent of fibrosis and the ultrasonographically determined degree of liver stiffness.
| |
| | |
| * ultrasonography can rule cirrhosis in or out in over 90% of cases , its findings are less than 100% specific because of occasional in -correct measurements and false-positive findings
| |
| | |
| * Findings:<ref name="pmid2526349">{{cite journal |vauthors=Di Lelio A, Cestari C, Lomazzi A, Beretta L |title=Cirrhosis: diagnosis with sonographic study of the liver surface |journal=Radiology |volume=172 |issue=2 |pages=389–92 |year=1989 |pmid=2526349 |doi=10.1148/radiology.172.2.2526349 |url=}}</ref><ref name="pmid11866220">{{cite journal |vauthors=Martínez-Noguera A, Montserrat E, Torrubia S, Villalba J |title=Doppler in hepatic cirrhosis and chronic hepatitis |journal=Semin. Ultrasound CT MR |volume=23 |issue=1 |pages=19–36 |year=2002 |pmid=11866220 |doi= |url=}}</ref><ref name="pmid12216750">{{cite journal |vauthors=Tchelepi H, Ralls PW, Radin R, Grant E |title=Sonography of diffuse liver disease |journal=J Ultrasound Med |volume=21 |issue=9 |pages=1023–32; quiz 1033–4 |year=2002 |pmid=12216750 |doi= |url=}}</ref><ref name="pmid12202712">{{cite journal |vauthors=Awaya H, Mitchell DG, Kamishima T, Holland G, Ito K, Matsumoto T |title=Cirrhosis: modified caudate-right lobe ratio |journal=Radiology |volume=224 |issue=3 |pages=769–74 |year=2002 |pmid=12202712 |doi=10.1148/radiol.2243011495 |url=}}</ref><ref name="pmid10334257">{{cite journal |vauthors=Albrecht T, Blomley MJ, Cosgrove DO, Taylor-Robinson SD, Jayaram V, Eckersley R, Urbank A, Butler-Barnes J, Patel N |title=Non-invasive diagnosis of hepatic cirrhosis by transit-time analysis of an ultrasound contrast agent |journal=Lancet |volume=353 |issue=9164 |pages=1579–83 |year=1999 |pmid=10334257 |doi=10.1016/S0140-6736(98)06373-9 |url=}}</ref>
| |
| ** Advanced cirrhosis: liver may appear small and nodular
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| ** Surface nodularity and increased echogenicity with irregular appearing areas are consistent with cirrhosis
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| ** Usually atrophy of the right lobe and hypertrophy of the caudate or left lobes.
| |
| | |
| * Ultrasonography may also be used as a screening test for hepatocellular carcinoma :nodules on ultrasonography warrants further evaluation
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| * Findings of portal hypertension:
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| ** increased diameter of the portal vein
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| ** presence of collateral veins
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| ** decreased flow within the portal circulation on Doppler imaging
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| * Ultrasonography is also useful for detecting splenomegaly, ascites, and portal vein thrombosis.
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| '''Computed tomography '''– not routinely used in the diagnosis of cirrhosis
| |
| * It provides similar information to ultrasonography, but at the expense of radiation and contrast exposure.
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| | |
| * CT findings:
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| ** Hepatic nodularity
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| ** Atrophy of the right lobe
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| ** Hypertrophy of the caudate or left lobes
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| ** Ascites
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| ** Varices
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| * CT portal phase imaging:
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| ** Patency of the portal vein can be demonstrated
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| '''Magnetic resonance imaging:'''
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| * The role of magnetic resonance imaging (MRI) in the diagnosis of cirrhosis is unclear.
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| * Use is limited by expense
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| * Poor tolerance of the examination
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| * Ability to obtain information provided by MRI through other means
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| * reveal iron overload and provide an estimate of the hepatic iron concentration
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| * Magnetic resonance angiography (MRA) is more sensitive than ultrasonography for diagnosing complications of cirrhosis:
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| * portal vein thrombosis
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| * CT portal phase imaging, MRA can determine the volume and direction of blood flow in the portal vein.
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| '''Elastography:''' <ref name="pmid18395077">{{cite journal |vauthors=Friedrich-Rust M, Ong MF, Martens S, Sarrazin C, Bojunga J, Zeuzem S, Herrmann E |title=Performance of transient elastography for the staging of liver fibrosis: a meta-analysis |journal=Gastroenterology |volume=134 |issue=4 |pages=960–74 |year=2008 |pmid=18395077 |doi=10.1053/j.gastro.2008.01.034 |url=}}</ref><ref name="pmid15690481">{{cite journal |vauthors=Ziol M, Handra-Luca A, Kettaneh A, Christidis C, Mal F, Kazemi F, de Lédinghen V, Marcellin P, Dhumeaux D, Trinchet JC, Beaugrand M |title=Noninvasive assessment of liver fibrosis by measurement of stiffness in patients with chronic hepatitis C |journal=Hepatology |volume=41 |issue=1 |pages=48–54 |year=2005 |pmid=15690481 |doi=10.1002/hep.20506 |url=}}</ref><ref name="pmid14698338">{{cite journal |vauthors=Sandrin L, Fourquet B, Hasquenoph JM, Yon S, Fournier C, Mal F, Christidis C, Ziol M, Poulet B, Kazemi F, Beaugrand M, Palau R |title=Transient elastography: a new noninvasive method for assessment of hepatic fibrosis |journal=Ultrasound Med Biol |volume=29 |issue=12 |pages=1705–13 |year=2003 |pmid=14698338 |doi= |url=}}</ref><ref name="pmid23558397">{{cite journal |vauthors=Bamber J, Cosgrove D, Dietrich CF, Fromageau J, Bojunga J, Calliada F, Cantisani V, Correas JM, D'Onofrio M, Drakonaki EE, Fink M, Friedrich-Rust M, Gilja OH, Havre RF, Jenssen C, Klauser AS, Ohlinger R, Saftoiu A, Schaefer F, Sporea I, Piscaglia F |title=EFSUMB guidelines and recommendations on the clinical use of ultrasound elastography. Part 1: Basic principles and technology |journal=Ultraschall Med |volume=34 |issue=2 |pages=169–84 |year=2013 |pmid=23558397 |doi=10.1055/s-0033-1335205 |url=}}</ref><ref name="pmid25911335">{{cite journal |vauthors= |title=EASL-ALEH Clinical Practice Guidelines: Non-invasive tests for evaluation of liver disease severity and prognosis |journal=J. Hepatol. |volume=63 |issue=1 |pages=237–64 |year=2015 |pmid=25911335 |doi=10.1016/j.jhep.2015.04.006 |url=}}</ref><ref name="pmid21205132">{{cite journal |vauthors=Castera L, Bedossa P |title=How to assess liver fibrosis in chronic hepatitis C: serum markers or transient elastography vs. liver biopsy? |journal=Liver Int. |volume=31 Suppl 1 |issue= |pages=13–7 |year=2011 |pmid=21205132 |doi=10.1111/j.1478-3231.2010.02380.x |url=}}</ref><ref name="pmid23732714">{{cite journal |vauthors=Chou R, Wasson N |title=Blood tests to diagnose fibrosis or cirrhosis in patients with chronic hepatitis C virus infection: a systematic review |journal=Ann. Intern. Med. |volume=158 |issue=11 |pages=807–20 |year=2013 |pmid=23732714 |doi=10.7326/0003-4819-158-11-201306040-00005 |url=}}</ref><ref name="pmid26779260">{{cite journal |vauthors=Khallafi H, Qureshi K |title=Imaging Based Methods of Liver Fibrosis Assessment in Viral Hepatitis: A Practical Approach |journal=Interdiscip Perspect Infect Dis |volume=2015 |issue= |pages=809289 |year=2015 |pmid=26779260 |pmc=4686715 |doi=10.1155/2015/809289 |url=}}</ref><ref name="pmid23954643">{{cite journal |vauthors=Singh S, Fujii LL, Murad MH, Wang Z, Asrani SK, Ehman RL, Kamath PS, Talwalkar JA |title=Liver stiffness is associated with risk of decompensation, liver cancer, and death in patients with chronic liver diseases: a systematic review and meta-analysis |journal=Clin. Gastroenterol. Hepatol. |volume=11 |issue=12 |pages=1573–84.e1–2; quiz e88–9 |year=2013 |pmid=23954643 |pmc=3900882 |doi=10.1016/j.cgh.2013.07.034 |url=}}</ref>
| |
| * Increasing scarring of the liver is associated with increasing "stiffness" of the tissue.
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| * Transient elastography and the acoustic radiation force impulse (ARFI) technique are now well-established methods for the staging of fibrosis in various liver diseases <ref name="pmid20581229">{{cite journal |vauthors=Castera L, Pinzani M |title=Biopsy and non-invasive methods for the diagnosis of liver fibrosis: does it take two to tango? |journal=Gut |volume=59 |issue=7 |pages=861–6 |year=2010 |pmid=20581229 |doi=10.1136/gut.2010.214650 |url=}}</ref><ref name="pmid22239521">{{cite journal |vauthors=Friedrich-Rust M, Nierhoff J, Lupsor M, Sporea I, Fierbinteanu-Braticevici C, Strobel D, Takahashi H, Yoneda M, Suda T, Zeuzem S, Herrmann E |title=Performance of Acoustic Radiation Force Impulse imaging for the staging of liver fibrosis: a pooled meta-analysis |journal=J. Viral Hepat. |volume=19 |issue=2 |pages=e212–9 |year=2012 |pmid=22239521 |doi=10.1111/j.1365-2893.2011.01537.x |url=}}</ref>
| |
| '''Nuclear studies:'''<ref name="pmid26494949">{{cite journal |vauthors=Nishikawa H, Osaki Y |title=Liver Cirrhosis: Evaluation, Nutritional Status, and Prognosis |journal=Mediators Inflamm. |volume=2015 |issue= |pages=872152 |year=2015 |pmid=26494949 |pmc=4606163 |doi=10.1155/2015/872152 |url=}}</ref>
| |
| | |
| * Radionuclide testing can be useful in suggesting the diagnosis of cirrhosis:<ref name="pmid3995244">{{cite journal |vauthors=McLaren MI, Fleming JS, Walmsley BH, Ackery DM, Taylor I, Karran SJ |title=Dynamic liver scanning in cirrhosis |journal=Br J Surg |volume=72 |issue=5 |pages=394–6 |year=1985 |pmid=3995244 |doi= |url=}}</ref>
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| ** 99mTc sulfur colloid is normally taken up by cells of the reticuloendothelial system
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| ** Cirrhosis: heterogeneity in the uptake of 99mTc sulfur colloid by the liver and increased uptake by the spleen and bone marrow
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| ===EGD===
| |
| EGD<ref name="pmid24328372">{{cite journal |vauthors=Zardi EM, Di Matteo FM, Pacella CM, Sanyal AJ |title=Invasive and non-invasive techniques for detecting portal hypertension and predicting variceal bleeding in cirrhosis: a review |journal=Ann. Med. |volume=46 |issue=1 |pages=8–17 |year=2014 |pmid=24328372 |pmc=4904298 |doi=10.3109/07853890.2013.857831 |url=}}</ref>
| |
| ==== Endoscopic retrograde cholangiopancreatography ====
| |
| * diagnosis of sclerosing cholangitis
| |
| '''Liver biopsy:''' <ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid12865280">{{cite journal |vauthors=Blomley MJ, Lim AK, Harvey CJ, Patel N, Eckersley RJ, Basilico R, Heckemann R, Urbank A, Cosgrove DO, Taylor-Robinson SD |title=Liver microbubble transit time compared with histology and Child-Pugh score in diffuse liver disease: a cross sectional study |journal=Gut |volume=52 |issue=8 |pages=1188–93 |year=2003 |pmid=12865280 |pmc=1773750 |doi= |url=}}</ref><ref name="pmid11211142">{{cite journal |vauthors=Kim CK, Lim JH, Lee WJ |title=Detection of hepatocellular carcinomas and dysplastic nodules in cirrhotic liver: accuracy of ultrasonography in transplant patients |journal=J Ultrasound Med |volume=20 |issue=2 |pages=99–104 |year=2001 |pmid=11211142 |doi= |url=}}</ref><ref name="pmid443970">{{cite journal |vauthors=Abdi W, Millan JC, Mezey E |title=Sampling variability on percutaneous liver biopsy |journal=Arch. Intern. Med. |volume=139 |issue=6 |pages=667–9 |year=1979 |pmid=443970 |doi= |url=}}</ref><ref name="pmid14647056">{{cite journal |vauthors=Bedossa P, Dargère D, Paradis V |title=Sampling variability of liver fibrosis in chronic hepatitis C |journal=Hepatology |volume=38 |issue=6 |pages=1449–57 |year=2003 |pmid=14647056 |doi=10.1016/j.hep.2003.09.022 |url=}}</ref><ref name="pmid12385448">{{cite journal |vauthors=Regev A, Berho M, Jeffers LJ, Milikowski C, Molina EG, Pyrsopoulos NT, Feng ZZ, Reddy KR, Schiff ER |title=Sampling error and intraobserver variation in liver biopsy in patients with chronic HCV infection |journal=Am. J. Gastroenterol. |volume=97 |issue=10 |pages=2614–8 |year=2002 |pmid=12385448 |doi=10.1111/j.1572-0241.2002.06038.x |url=}}</ref><ref name="pmid11172192">{{cite journal |vauthors=Bravo AA, Sheth SG, Chopra S |title=Liver biopsy |journal=N. Engl. J. Med. |volume=344 |issue=7 |pages=495–500 |year=2001 |pmid=11172192 |doi=10.1056/NEJM200102153440706 |url=}}</ref><ref name="pmid19243014">{{cite journal |vauthors=Rockey DC, Caldwell SH, Goodman ZD, Nelson RC, Smith AD |title=Liver biopsy |journal=Hepatology |volume=49 |issue=3 |pages=1017–44 |year=2009 |pmid=19243014 |doi=10.1002/hep.22742 |url=}}</ref>
| |
| * Cirrhosis is primarily a histological diagnosis.
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| * Percutaneous liver biopsy remains the cornerstone of diagnosis.
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| * quick and simple to perform in a cooperative patient with a normal INR and platelet count.
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| * The gold standard for diagnosing cirrhosis is:
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| ** Examination of an explanted liver, either at autopsy or following liver transplantation, because the architecture of the entire liver can be appreciated.
| |
| | |
| * Cirrhosis is diagnosed with a liver biopsy <ref name="pmid22833761">{{cite journal |vauthors=Tannapfel A, Dienes HP, Lohse AW |title=The indications for liver biopsy |journal=Dtsch Arztebl Int |volume=109 |issue=27-28 |pages=477–83 |year=2012 |pmid=22833761 |pmc=3402072 |doi=10.3238/arztebl.2012.0477 |url=}}</ref><ref name="pmid15278290">{{cite journal |vauthors=Schirmacher P, Fleig WE, Tannapfel A, Langner C, Dries V, Terracciano L, Denk H, Dienes HP |title=[Bioptic diagnosis of chronic hepatitis. Results of an evidence-based consensus conference of the German Society of Pathology, of the German Society for Digestive and Metabolic Diseases and of Compensated Hepatitis (HepNet)] |language=German |journal=Pathologe |volume=25 |issue=5 |pages=337–48 |year=2004 |pmid=15278290 |doi=10.1007/s00292-004-0692-7 |url=}}</ref>
| |
| | |
| * Sample of the liver is obtained by:<ref name="pmid16636018">{{cite journal |vauthors=Cholongitas E, Quaglia A, Samonakis D, Senzolo M, Triantos C, Patch D, Leandro G, Dhillon AP, Burroughs AK |title=Transjugular liver biopsy: how good is it for accurate histological interpretation? |journal=Gut |volume=55 |issue=12 |pages=1789–94 |year=2006 |pmid=16636018 |pmc=1856467 |doi=10.1136/gut.2005.090415 |url=}}</ref>
| |
| ** Percutaneous
| |
| ** Transjugular
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| ** Laparoscopic radiographically-guided fine-needle approach.
| |
| | |
| * Liver biopsy is not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and if the results would not alter the patient's management.
| |
| | |
| * Patient with a history of heavy alcohol use who has ascites, severe coagulopathy, and a shrunken, nodular-appearing liver on ultrasonography.
| |
| | |
| * Liver biopsy may be suggestive of etiology:
| |
| * Metabolic causes of cirrhosis include:
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| ** Hereditary hemochromatosis
| |
| ** Nonalcoholic steatohepatitis
| |
| ** Wilson disease
| |
| ** Alpha-1 antitrypsin deficiency
| |
| | |
| * Risks:
| |
| ** haemorrhage
| |
| ** biliary peritonitis
| |
| ** haematoma
| |
| ** perforation of other viscera
| |
| ** mortality rates of between 0.01% and 0.1%
| |
| | |
| * Percutaneous biopsy of focal lesions may be performed in combination with either ultrasound or CT imaging.
| |
| | |
| * Prerequisites:
| |
| ** normal INR and platelet count.
| |
| | |
| * May be performed in combination with either ultrasound or CT.
| |
| * Patients with moderate coagulopathy:
| |
| ** Plugged liver biopsy : injection of gelatin sponges or metal coils down the tract after biopsy
| |
| ** Laparoscopic liver biopsy performed on a sedated patient with moderate coagulopathy
| |
| *** Advantage: allows direct visualisation of the liver
| |
| | |
| * Patients with severe clotting disorders:
| |
| * Transjugular liver biopsy :
| |
| ** risk of intraperitoneal bleed is less
| |
| ** Disadvantages:
| |
| *** biopsies are small: multiple biopsies required
| |
| *** taken 'blindly'
| |
| | |
| ===rough===
| |
|
| |
|
| | {{WH}} |
| | {{WS}} |
|
| |
|
| | ==References== |
| | {{Reflist|2}} |
|
| |
|
| ==Physical Examination==
| |
| [[Image: Normal versus Abnormal Barium study of esophagus.jpg|thumb|left|200px|Normal versus Abnormal Barium study of esophagus with varices]]
| |
|
| |
|
| | | ===Pathophysiology prev=== |
| ===GIF maker=== | | <div style="-webkit-user-select: none;"> |
| | | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| [[File:Cirrhosis baba gif.gif|500px|right|thumb|Liver Cirhhosis <br> Source:Wikimedia commons<ref name="urlCategory:Histopathology of cirrhosis - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/Category:Histopathology_of_cirrhosis#/media/File:Cirrhosis_high_mag.jpg |title=Category:Histopathology of cirrhosis - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
| |
| | |
| | |
| | |
| [[File:Spider angioma p.jpg|500px|center|thumb|Spider angiomata <br> Source:Wikimedia commons ]]
| |
| [[File:Output OBujt7.gif|500px|left|thumb|Spider angiomata <br> Source:Wikimedia commons]]
| |
| | |
| | |
| | |
| ==Physical Examination==
| |
| | |
| *Physical examination of [[Patient|patients]] with [[cirrhosis]] is usually remarkable for: [[jaundice]], [[Spider angioma|spider angiomata]], [[ascites]], [[asterixis]], [[Splenomegaly|spleenomegaly]] and [[palmar erythema]].
| |
| | |
| ===Appearance of the Patient===
| |
| | |
| *[[Patient|Patients]] with [[cirrhosis]] usually appear weak due to constitutional [[Symptom|symptoms]] such as [[weight loss]], [[anorexia]] and [[muscle atrophy]]. Yellowish discoloration of [[skin]] and [[abdominal distension]] may also be present due to [[ascites]].
| |
| | |
| *Normal/low [[blood pressure]] with normal [[pulse pressure]].
| |
| | |
| ===Skin===
| |
| *[[Jaundice]] : yellow discoloration of the skin, eyes, and mucus membranes due to increased [[bilirubin]] (at least 2-3 mg/dL or 30 mmol/L). Urine may also appear dark.
| |
| *[[Pallor]]
| |
| *[[Bruise|Bruises]]
| |
| *[[Palmar erythema]] on the [[Thenar eminence|thenar]] and [[Hypothenar eminence|hypothenar eminences]], due to altered sex hormone metabolism.
| |
| *[[Spider angioma|Spider angiomata]]: Increased estradiol levels lead to the formation of vascular lesions consisting of central arterioles surrounded by smaller vessels <ref name="pmid10423070">{{cite journal |author=Li CP, Lee FY, Hwang SJ, ''et al'' |title=Spider angiomas in patients with liver cirrhosis: role of alcoholism and impaired liver function|journal=Scand. J. Gastroenterol. |volume=34 |issue=5 |pages=520-3 |year=1999 |pmid=10423070 |doi=}}</ref>
| |
| *'''[[Telangiectasia|Telangiectasias]]''' or '''spider veins:''' small dilated [[blood vessel]]s near the surface of the [[skin]].
| |
| | |
| ===HEENT===
| |
| * Abnormalities of the head/hair may include thinning of hair on the scalp due to [[hyperestrogenism]]
| |
| * '''[[Kayser-Fleischer ring]]s''' : dark rings that appear to encircle the [[iris (anatomy)|iris]] of the [[eye]] in [[Patient|patients]] with [[Wilson's disease]].
| |
| * [[Parotid gland]] enlargement
| |
| * [[Fetor hepaticus]]: severe portal-systemic shunting leads to increased levels of [[dimethyl sulfide]] leads to a sweet pungent smell in the breath
| |
| | |
| ===Abdomen===
| |
| * Inspection:
| |
| ** [[Abdominal distension]]
| |
| ** [[Caput medusae]]
| |
| | |
| * Palpation:
| |
| ** Fluid wave
| |
| ** [[Hepatomegaly]] may be present in initial stages. The liver may also be normal or shrunken.
| |
| ** [[Splenomegaly|Spleenomegaly]] may be present in patients with [[cirrhosis]] from nonalcoholic etiologies, due to portal hypertension
| |
| | |
| * Percussion:
| |
| ** Flank dullness may be present due to [[ascites]] (needs approximately 1500ml for detection)
| |
| | |
| * Auscultation:
| |
| ** [[Cruveilhier-Baumgarten murmur]]: venous hum that may be present in patients with [[portal hypertension]].
| |
| *** Mechanism: due to collateral connections between remnant of the [[umbilical vein]] and the [[Portal venous system|portal system]]
| |
| *** Location: [[Epigastrium]]
| |
| *** Exacerbating factors: [[Valsalva maneuver]]
| |
| *** Diminished by: application of [[pressure]] on the [[skin]] above the [[Navel|umbilicus]]
| |
| | |
| ===Genitourinary===
| |
| *[[Testicular atrophy]]
| |
| *Inversion of the normal male [[pubic hair]] pattern
| |
| ===Neuromuscular===
| |
| * [[Hepatic encephalopathy]] may have signs of:
| |
| ** Alteration of [[Mental status examination|mental status]]
| |
| ** [[Confusion]]
| |
| ** [[Coma]]
| |
| * [[Asterixis]] (bilateral but asynchronous flapping motions of outstretched, dorsiflexed hands) is seen in patients with [[hepatic encephalopathy]].
| |
| | |
| ===Extremities===
| |
| *[[edema]] of the lower extremities
| |
| *[[Muscle atrophy]]
| |
| *Nail changes:
| |
| **Muehrcke nails: paired horizontal white bands separated by normal color due to [[hypoalbuminemia]]
| |
| **Terry nails: the proximal two-thirds of the nail plate appears white, whereas the distal one-third is red due to [[hypoalbuminemia]]
| |
| ** [[Clubbing]]: the angle between the nail plate and proximal nail fold is greater than 180 degrees
| |
| **Severe [[clubbing]]:
| |
| ***"Drum stick" appearance of distal fingers
| |
| ***[[Hypertrophic pulmonary osteoarthropathy|Hypertrophic osteoarthropathy]]: chronic proliferative [[periostitis]] of the [[long bones]]
| |
| **[[Dupuytrens contracture|Dupuytren's contracture]] may cause flexion deformities of the fingers: This occurs due to shortening and thickening of the palmar fascia, due to collagen deposition and fibroblastic proliferation.
| |
| **[[Asterixis]] in cases with [[hepatic encephalopathy]]
| |
| | |
| === Chest findings ===
| |
| * [[Gynecomastia]]: due to increased estradiol levels
| |
| * Loss of chest or [[Underarm hair|axillary hair]]
| |
| ===Other findings===
| |
| * [[Hemorrhoids]]
| |
| * [[Hematemesis]]
| |
| * [[Melena]]
| |
| | |
| ==History==
| |
| | |
| === Psychosocial history ===
| |
| *Past history of abuse
| |
| | |
| === Past Medical history ===
| |
| *History of
| |
| | |
| === Menstrual history ===
| |
| *History of
| |
| | |
| === Family history ===
| |
| *[[Family history]] of:
| |
| **
| |
| | |
| === Medication history ===
| |
| *History of [[medication]] use should be obtained as many [[:Category:Drugs|drugs]] such as [[Opioid|opioids]] cause [[constipation]] as a side effect.
| |
| | |
| ===Causes===
| |
| {| class="wikitable" | |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Drugs and Toxins
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Infections
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Autoimmune
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Metabolic
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Biliary obstruction(Secondary bilary cirrhosis)
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Vascular
| |
| ! style="background:#4479BA; color: #FFFFFF;" align="center" + |Miscellaneous
| |
| |- | | |- |
| |Alcohol | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
| |Hepatitis B | |
| |Primary Biliary Cirrhosis | |
| |Wilson's disease
| |
| |Cystic fibrosis
| |
| |Chronic RHF
| |
| |Sarcoidosis
| |
| |- | | |- |
| |Methotrexate | | |} |
| |Hepatitis C
| | __NOTOC__ |
| |Autoimmune hepatitis
| | {{Cirrhosis}} |
| |Hemochromatosis
| | {{CMG}} {{AE}} |
| |Biliary atresia
| |
| |Budd-Chiari syndrome
| |
| |Intestinal
| |
|
| |
|
| bypass operations for obesity
| | |
| | ===Pathophysiology prev=== |
| | <div style="-webkit-user-select: none;"> |
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| |- | | |- |
| |Isoniazid | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
| |Schistosoma japonicum | |
| |Primary Sclerosing Cholangitis
| |
| |Alpha-1 antitrypsin deficiency
| |
| |Bile duct strictures
| |
| |Veno-occlusive disease
| |
| |Cryptogenic: unknown | |
| |- | | |- |
| |Methyldopa
| |
| |
| |
| |
| |
| |Porphyria
| |
| |Gallstones
| |
| |
| |
| |
| |
| |-
| |
| |
| |
| |
| |
| |
| |
| |Glycogen storage diseases (such as Galactosaemia, Abetalipoproteinaemia)
| |
| |
| |
| |
| |
| |
| |
| |} | | |} |
| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
|
| |
|
| ===Cirrhosis=== | | == History and Symptoms == |
|
| |
|
| Pathophysiology <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>
| | * History should include: |
| * When an injured issue is replaced by a collagenous scar, it is termed as fibrosis.
| | ** Appearance of bowel movements |
| * When fibrosis of the liver reaches an advanced stage where distortion of the hepatic vasculature also occurs, it is termed as cirrhosis of the liver. | | ** Travel history |
| * The cellular mechanisms responsible for cirrhosis are similar regardless of the type of initial insult and site of injury within the liver lobule. | | ** Associated symptoms |
| * Viral hepatitis involves the periportal region, whereas involvement in alcoholic liver disease is largely pericentral.
| | ** Immune status |
| * If the damage progresses, panlobular cirrhosis may result.
| | ** Woodland exposure |
| * 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>
| | ==References== |
| ** Inflammation
| | {{reflist|2}} |
| ** Hepatic stellate cell activation
| | |
| ** Angiogenesis
| | {{WH}} |
| ** Fibrogenesis | | {{WS}} |
| * Kupffer cells are hepatic macrophages responsible for Hepatic Stellate cell activation during injury.
| |
| * The hepatic stellate cell (also known as the perisinusoidal cell or Ito cell) plays a key role in the pathogenesis of liver fibrosis/cirrhosis. | |
| * Hepatic stellate cells(HSC) are usually located in the subendothelial space of Disse and become activated to a myofibroblast-like phenotype in areas of liver injury. | |
| * Collagen and non collagenous matrix proteins responsible for fibrosis are produced by the activated Hepatic Stellate Cells(HSC). | |
| * Hepatocyte damage causes the release of lipid peroxidases from injured cell membranes leading to necrosis of parenchymal cells. | |
| * Activated HSC produce numerous cytokines and their receptors, such as PDGF and TGF-f31 which are responsible for fibrogenesis. | |
| * The matrix formed due to HSC activation is deposited in the space of Disse and leads to loss of fenestrations of endothelial cells, which is a process called capillarization. | |
| * Cirrhosis leads to 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 hepatic shunts (due to angiogenesis and loss of parenchymal cells)
| |
| ** hepatic endothelial dysfunction
| |
| * The 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 vasodilators, such as nitric oxide due to oxidative stress
| |
| ** increased production of vasoconstrictors (mainly adrenergic stimulation and activation of endothelins and RAAS)
| |
| * Fibrosis eventually leads to formation of septae that grossly distort the liver architecture which includes both the liver parenchyma and the vasculature. A cirrhotic liver compromises hepatic sinusoidal exchange by shunting arterial and portal blood directly into the central veins (hepatic outflow). Vascularized fibrous septa connect central veins with portal tracts leading to islands of hepatocytes surrounded by fibrous bands without 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>
| |
| * The formation of fibrotic bands is accompanied by regenerative nodule formation in the hepatic parenchyma.
| |
| * Advancement of cirrhosis may lead to parenchymal dysfunction and development of portal hypertension.
| |
| * Portal HTN results from the combination of the following:
| |
| ** Structural disturbances associated with advanced liver disease account for 70% of total hepatic vascular resistance.
| |
| ** Functional abnormalities such as endothelial dysfunction and increased hepatic vascular tone account for 30% of total hepatic vascular resistance.
| |
|
| |
|
| Pathogenesis of Cirrhosis due to Alcohol:
| | ==Other Imaging Findings== |
| * More than 66 percent of all American adults consume alcohol.
| | * [[Endoscopy]] |
| * Cirrhosis due to alcohol accounts for approximately forty percent of mortality rates due to cirrhosis.
| | * [[Barium enema]] |
| * Mechanisms of alcohol-induced damage include:
| | * [[Colonoscopy]] |
| ** Impaired protein synthesis, secretion, glycosylation
| | * [[Sigmoidoscopy]] |
| * Ethanol intake leads to elevated accumulation of intracellular triglycerides by:
| |
| ** Lipoprotein secretion
| |
| ** Decreased fatty acid 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 by:
| |
| ** Trafficking of hepatic proteins
| |
| ** Interrupting microtubule formation
| |
| ** Interfering with enzyme activities
| |
| * Damage of hepatocytes leads to the formation of reactive oxygen species that activate 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 cytokines that stimulates stellate cells.
| |
| *Stellate cell activation leads to the production of extracellular matrix and collagen.
| |
| * Portal triads develop connections with central veins due to connective tissue formation in pericentral and periportal zones, leading to the formation of regenerative nodules. | |
| * Shrinkage of the liver occurs over years due to repeated insults that lead to: | |
| ** Loss of hepatocytes | |
| ** Increased production and deposition of collagen | |
|
| |
|
| | ==Other diagnostic studies== |
| | == Other Diagnostic Studies == |
|
| |
|
| Pathology
| | * Breath hydrogen test |
| * There are four stages of Cirrhosis as it progresses: | |
| ** Chronic nonsuppurative destructive cholangitis - inflammation and necrosis of portal tracts with lymphocyte infiltration leading 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 leading to regenerative nodule formation.
| |
|
| |
|
| ===Classification=== | | * [[HIV test]]ing for those patients suspected of having HIV |
| __NOTOC__
| | |
| {{Cirrhosis}}
| | == |
| {{CMG}} {{AE}} {{CP}}
| |
|
| |
|
| ==Overview== | | ==Overview== |
| Cirrhosis of the [[liver]] can be classified using two methods; classification based on [[etiology]], and classification based on [[morphology]]. Currently, classifying cirrhosis based on morphology is not used, as it requires an invasive procedure to examine the gross appearance of the liver, and it provides little diagnostic value. Classifying cirrhosis according to etiology is a more accepted form of classification, as it can be attained through non-invasive laboratory testing, and has a higher diagnostic value.
| |
|
| |
|
| ==Classification Based on Etiology== | | ==References== |
| Cirrhosis can be classified by its etiology. This is the most widely accepted method of [[classification]].
| | {{reflist|2}} |
| ===Alcoholic Cirrhosis===
| |
| This is the most common cause of cirrhosis, and is caused by continuous and prolonged [[alcohol abuse]]. The American Academy of Family Physicians estimate that 60-70 percent of all cases of cirrhosis are a result of [[alcohol abuse]].
| |
| ===Post-Necrotic Cirrhosis===
| |
| This type of cirrhosis occurs after a massive event causes liver [[cell death]]. [[Viral hepatitis]] is the most common cause for this type of cirrhosis. Agents that are [[toxic]] to the liver can also cause this type of cirrhosis, as well as certain types of [[carcinomas]].
| |
|
| |
|
| ===Biliary Cirrhosis===
| | {{WH}} |
| This type of cirrhosis results from any diseases that cause [[biliary obstruction]]. There is usually a blockage in the [[bile duct]] and there may also be [[inflammation]]. The excess [[bile]] in the liver causes tissue destruction. It commonly results in [[jaundice]].
| | {{WS}} |
| ===Cardiac Cirrhosis===
| |
| This type of cirrhosis is caused by [[congestive heart failure]] causing poor circulation of [[oxygenated blood]] to the liver. This results in liver cell death, and the subsequent replacement of dead cells by [[fibrous tissue]].
| |
| ===Genetic Disorder===
| |
| This is when the cirrhosis is caused by a [[genetic disorder]] such as [[hemochromatosis]], [[Wilson's disease]], or [[alpha-1 antitrypsin deficiency]].
| |
| ===Malnutrition===
| |
| This category contains cirrhosis caused by various forms of [[malnutrition]], particularly chronic starvation.
| |
| | |
| ==Classification Based on Morphology==
| |
| [[Cirrhosis]] has historically been classified upon the [[Nodule (medicine)|nodular]] morphology that is seen on upon the gross appearance of the [[liver]]. Accurate assessment of the [[liver]] morphology can only be obtained through [[surgery]], [[biopsy]], or [[autopsy]], therefore more recently, more non-invasive means of classifying and determining the causes of [[cirrhosis]] are used.
| |
|
| |
|
| {| class="wikitable" | | ===Pathophysiology prev=== |
| ! style="background:#4479BA; color: #FFFFFF;" |Micronodular
| | <div style="-webkit-user-select: none;"> |
| ! style="background:#4479BA; color: #FFFFFF;" |Macronodular
| | {| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;" |
| ! style="background:#4479BA; color: #FFFFFF;" |Mixed
| |
| |- | | |- |
| |Micronodular [[cirrhosis]] is characterized by [[Nodule (medicine)|nodules]] that are less than 3mm in diameter | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=5szNmKtyBW4|350}} |
| |Macronodular [[cirrhosis]] is characterized by [[Nodule (medicine)|nodules]] that are more than 3mm in diameter
| |
| |Micronodular [[cirrhosis]] can often progress into macronodular [[Cirrhosis|cirrhosis.]] During this transformation, a mixed form of [[cirrhosis]] may be seen.<ref name="pmid6629323">{{cite journal| author=Fauerholdt L, Schlichting P, Christensen E, Poulsen H, Tygstrup N, Juhl E| title=Conversion of micronodular cirrhosis into macronodular cirrhosis. | journal=Hepatology | year= 1983 | volume= 3 | issue= 6 | pages= 928-31 | pmid=6629323 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6629323 }} </ref>
| |
| |- | | |- |
| |Causes:
| |
| *[[Alcohol]]
| |
| *[[Hemochromatosis]]
| |
| *[[Cholestasis|Cholestatic]] causes of [[cirrhosis]]
| |
| *Hepatic venous outflow obstruction
| |
| *[[Nutrition|Nutritional]] causes of [[cirrhosis]]
| |
| |
| |
| Causes:
| |
| *Chronic [[viral hepatitis]]
| |
| *[[Hemochromatosis]]
| |
| *[[Wilson's disease]]
| |
| *Post-necrotic [[cirrhosis]]
| |
| |Mixed nodular [[cirrhosis]] is also seen in Indian childhood [[cirrhosis]]. <ref name="pmid47794">{{cite journal| author=Nayak NC, Ramalingaswami V| title=Indian childhood cirrhosis. | journal=Clin Gastroenterol | year= 1975 | volume= 4 | issue= 2 | pages= 333-49 | pmid=47794 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=47794 }} </ref>
| |
| |} | | |} |
| | __NOTOC__ |
| | {{Cirrhosis}} |
| | {{CMG}} {{AE}} |
|
| |
|
| ==Video codes== | | ==Video codes== |
| Line 453: |
Line 85: |
| ===Normal video=== | | ===Normal video=== |
| {{#ev:youtube|x6e9Pk6inYI}} | | {{#ev:youtube|x6e9Pk6inYI}} |
| | {{#ev:youtube|4uSSvD1BAHg}} |
| | {{#ev:youtube|PQXb5D-5UZw}} |
| | {{#ev:youtube|UVJYQlUm2A8}} |
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| ===Video in table=== | | ===Video in table=== |
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| ===Image and text to the right=== | | ===Image and text to the right=== |
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| <figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline>[[File:Global distribution of leptospirosis.jpg|577x577px]]</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017. | | <figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline>[[File:Global distribution of leptospirosis.jpg|577x577px]]</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017. |
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| ===Gallery=== | | ===Gallery=== |
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
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| [[Category:Gastroenterology]]
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| [[Category:Hepatology]]
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| {{WS}} | | {{WS}} |
| {{WH}} | | {{WH}} |
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| REFERENCES | | REFERENCES |
| <references /> | | <references /> |
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| | [[Category:Gastroenterology]] |
| | [[Category:Needs overview]] |
| | [[Category:Hepatology]] |
| | [[Category:Disease]] |
</figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> Recent out break of leptospirosis is reported in Bronx, New York and found 3 cases in the months January and February, 2017.
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/2/2f/Pancreatic_insulinoma_histology_2.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/a/a3/Pancreatic_insulinoma_histopathology_3.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/images/d/d5/Pancreatic_insulinoma_histology_4.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_2.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histopathology_3.JPG)
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[1]](/index.php/File:Pancreatic_insulinoma_histology_4.JPG)