Liver mass pathophysiology: Difference between revisions

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* Bile ductular proliferation  
* Bile ductular proliferation  
* Cells of chronic inflammation
* Cells of chronic inflammation
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|Intrahepatic bileduct cystadenoma
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|Hemangioma
|Hemangioma
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|Lymphangioma
|Lymphangioma
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* Lymphangioma is caused by either sequestration of
** Lymph tissue
** Abnormal budding of lymph vessels
** Lack of fusion with the [[venous]] system,
** Obstruction of lymph vessels.
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**[[Trisomy 13]]
**[[Tirsomy 18]]
**[[Trisomy 21]]
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*[[Turner syndrome]]
*[[Noonan syndrome]]
*[[Down syndrome]]
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*Grey-white mass
*Well circumscribed
*Edematous appearance
*Variable size (may be massive)
*Filled with serous fluid
*Smooth inner lining
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*Thin walled channels lined by [[endothelium]]
|Lymphangiomatosis
*Intraluminal accumulation of [[eosinophilic]] deposits
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*Clusters of intraluminal [[lymphocyte]]s
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*D2-40 +ve
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|Angiomyolipoma
|Angiomyolipoma
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**Nodular or diffusely infiltrative.
**Nodular or diffusely infiltrative.
**Pale in relation to surrounding liver or green.
**Pale in relation to surrounding liver or green.
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|Cholangiocarcinoma
|Cholangiocarcinoma
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*The epithelial cell lining the bile ducts are called cholangiocytes.
*The malignant transformsation of cholangiocytes leads to cholangiocarcinoma.<ref name="FavaLorenzini2012">{{cite journal|last1=Fava|first1=G.|last2=Lorenzini|first2=I.|title=Molecular Pathogenesis of Cholangiocarcinoma|journal=International Journal of Hepatology|volume=2012|year=2012|pages=1–7|issn=2090-3448|doi=10.1155/2012/630543}}</ref>
*Malignant transformation of cholangiocytes into cholangiocarcinoma include following stages:<ref name="targeting">{{cite journal |author=Sirica A |title=Cholangiocarcinoma: molecular targeting strategies for chemoprevention and therapy |journal=Hepatology |volume=41 |issue=1 |pages=5–15 |year=2005 |id=PMID 15690474}}</ref>
*#Hyperplasia
*#Metaplasia
*#Dysplasia
*#Frank carcinoma
*Progression of malignancy is believed to be due to:<ref name="targeting" /><ref>{{cite journal |author=Holzinger F, Z'graggen K, Büchler M |title=Mechanisms of biliary carcinogenesis: a pathogenetic multi-stage cascade towards cholangiocarcinoma |journal=Ann Oncol |volume=10 Suppl 4 |issue= |pages=122-6 |year= |id=PMID 10436802}}</ref><ref>{{cite journal |author=Gores G |title=Cholangiocarcinoma: current concepts and insights |journal=Hepatology |volume=37 |issue=5 |pages=961-9 |year=2003 |id=PMID 12717374}}</ref>
**Inflammation
**Obstruction of bile ducts
**Biliary intraepithelia neoplasia.
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* ARID1A
* BAP1
* BRAF
* FGFR2
* IDH1
* IDH2
* KMT2C
* KRAS
* PBRM1
* PEG3
* PTPN3
* RNF43
* ROBO2
* SMAD4
* TERT
* TP53
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*'''Mass-forming'''
**Nodular lesion or mass in the hepatic parenchyma
**Gray to gray-white, firm and solid carcinoma
*'''Periductal infiltrating'''
**Spreading of the carcinoma along the portal tracts with stricture of the affected bile ducts
**Dilatation of the peripheral bile ducts
*'''Intraductal growth types'''
**Polypoid or papillary tumor within the variably dilated bile duct lumen
**Malignant progression of an intraductal papillary neoplasm of the bile duct
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*Cuboidal or columnar mucin producing cells
*Dense fibrous(desmoplastic) stroma.
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|Hepatic abscess
|Hepatic abscess
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* In patients the [[Reticuloendothelial system|reticuloendothelial cells]] ([[kupffer cells]]) of [[liver]] control the transient portal [[bacteremia]]
* In elderly and [[immunocompromised]] the [[bacteria]] can overwhelm the [[kupffer cells]] and lead to an [[abscess]].<ref name="pmid1863218">{{cite journal| author=Stain SC, Yellin AE, Donovan AJ, Brien HW| title=Pyogenic liver abscess. Modern treatment. | journal=Arch Surg | year= 1991 | volume= 126 | issue= 8 | pages= 991-6 | pmid=1863218 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1863218  }}</ref>
* Development of pyogenic liver abscess is the result of extension of infection from surrounding organs.<ref name="pmid17861705">{{cite journal| author=Munro JC| title=VII. Lymphatic and Hepatic Infections Secondary to Appendicitis. | journal=Ann Surg | year= 1905 | volume= 42 | issue= 5 | pages= 692-734 | pmid=17861705 | doi= | pmc=1425980 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17861705  }}</ref><ref name="pmid8651751">{{cite journal| author=Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL et al.| title=Pyogenic hepatic abscess. Changing trends over 42 years. | journal=Ann Surg | year= 1996 | volume= 223 | issue= 5 | pages= 600-7; discussion 607-9 | pmid=8651751 | doi= | pmc=1235191 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8651751  }}</ref><ref name="pmid15578367">{{cite journal| author=Rahimian J, Wilson T, Oram V, Holzman RS| title=Pyogenic liver abscess: recent trends in etiology and mortality. | journal=Clin Infect Dis | year= 2004 | volume= 39 | issue= 11 | pages= 1654-9 | pmid=15578367 | doi=10.1086/425616 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15578367  }}</ref>
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*Single or multiple cavities, filled with fowl smelling, creamy yellow [[Necrosis|necrotic]] material, usually in [[right lobe of liver]].
*The [[abscess]] may have [[fibrous capsule]] which is a centimeter or more thick and gradually merges into the [[Parenchyma|liver parenchyma]].
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*Multiple [[Neutrophil|neutrophilic]] [[abscesses]] with areas of [[necrosis]] are seen in the [[Parenchyma|liver parencyma]].<ref name="abscess">https://librepathology.org/wiki/Liver_pathology Accessed on February 22, 2017</ref><ref name="pmid11882760">{{cite journal| author=Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin JI, Malech HL et al.| title=Hepatic abscess in patients with chronic granulomatous disease. | journal=Ann Surg | year= 2002 | volume= 235 | issue= 3 | pages= 383-91 | pmid=11882760 | doi= | pmc=1422444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11882760  }}</ref>
*[[Suppuration]], [[liquefaction]]
*Chronic [[Inflammation|inflammatory]] infiltrate consisting of [[lymphocytes]], [[Macrophages|epithelioid macrophages]], [[eosinophils]], and [[neutrophils]].
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|Parasitic cysts
|Parasitic cysts
(Echinococcous)
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*Cysts tend to be:
**Filled with clear fluid
**White appearance
**Solitary
**[[Unilocular hydatid disease|Unilocular]]
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*Cyst wall composed of an acellular laminated external layer and a thin, germinal (nucleated) inner layer
*Brood capsule with protoscoleces inside
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Revision as of 03:17, 4 February 2018

Liver Mass Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Overview

Pathophysiology

Genetics

Associated Conditions

Gross Pathology

Pathogeneis Genetics Associated conditions Gross Pathology Microscopic Pathology
Hepatocellular adenoma
  • Estrogens cause the transformation of hepatocytes via steroid receptors
  • Results in generalized vascular ectasia
  • Transcription factor 1 gene (TCF1)
  • Interleukin 6 signal transducer gene (IL6ST)
  • β catenin-1 gene (CTNNB1)
  • Glycogen storage disease types Ia and III
  • Fanconi anemia
  • Thalassemia
  • Familial adenomatous polyposis
  • Familial diabetes mellitus
  • Hurler disease
  • Galactosemia
  • Well circumscribed
  • Nonlobulated
  • Smooth and soft
  • White to yellow to brown lesions
  • Cords of hepatocytes that have a high glycogen and fat content
  • Lack of normal hepatic parenchymal architecture
  • Absence of portal tracts and hepatic veins
Focal nodular hyperplasia
  • Develop around a preexisting arterial malformation
  • Production of growth factors promote growth of small arteries 
  • Increased perfusion of the adjacent tissue results in peritumoral hyperplasia.
  • β-catenin gene (CTNNB1)
  • TP53
  • APC or HNF1α
  • Klippel-Trénaunay-Weber syndrome
  • Well-circumscribed
  • Non-encapsulated
  • Central fibrous scar
  • Hepatic parenchyma arranged in incomplete nodules
  • Fibrous tissue with thick-walled vessels
  • Bile ductular proliferation
  • Cells of chronic inflammation
Hemangioma
  • Congenital disorder
  • Vascular malformations that enlarge by ectasia 
  • Estrogen and progesterone influence over tumor growth
  • More common in females
  • Von Hippel Lindau disease
  • Well-circumscribed
  • Appear red-brown
  • Solitary nodules
  • Less than 5cms
  • Large cystically dilated vessels
  • Thin walls
  • Intravascular thrombosis
  • Calcifications
Hepatic Cyst
  • Von Meyenburg complexes separate from biliary tree and dilate to form cyst
  • Single, unilocular cyst
  • Variable amounts of clear amber fluid (may contain blood, bile, mucus, pus)
  • Lined by flat / cuboidal epithelium
  • Epithelium rests on thin collagenous wall without spindle cell stroma
  • Degenerative changes include epithelial desquamation, multiloculation, calcification
Lymphangioma
  • Lymphangioma is caused by either sequestration of
    • Lymph tissue
    • Abnormal budding of lymph vessels
    • Lack of fusion with the venous system,
    • Obstruction of lymph vessels.
  • Grey-white mass
  • Well circumscribed
  • Edematous appearance
  • Variable size (may be massive)
  • Filled with serous fluid
  • Smooth inner lining
Angiomyolipoma
  • Well circumscribed
  • Uniform yellow mass
HCC
  • Arises from precancerous lesions.
    • Nodular or diffusely infiltrative.
    • Pale in relation to surrounding liver or green.
  • Large polygonal tumours cells
  • Graunular eosinophilic cytoplasm
  • Layered dense collagen bundles
Cholangiocarcinoma
  • The epithelial cell lining the bile ducts are called cholangiocytes.
  • The malignant transformsation of cholangiocytes leads to cholangiocarcinoma.[1]
  • Malignant transformation of cholangiocytes into cholangiocarcinoma include following stages:[2]
    1. Hyperplasia
    2. Metaplasia
    3. Dysplasia
    4. Frank carcinoma
  • Progression of malignancy is believed to be due to:[2][3][4]
    • Inflammation
    • Obstruction of bile ducts
    • Biliary intraepithelia neoplasia.
  • ARID1A
  • BAP1
  • BRAF
  • FGFR2
  • IDH1
  • IDH2
  • KMT2C
  • KRAS
  • PBRM1
  • PEG3
  • PTPN3
  • RNF43
  • ROBO2
  • SMAD4
  • TERT
  • TP53
  • Mass-forming
    • Nodular lesion or mass in the hepatic parenchyma
    • Gray to gray-white, firm and solid carcinoma
  • Periductal infiltrating
    • Spreading of the carcinoma along the portal tracts with stricture of the affected bile ducts
    • Dilatation of the peripheral bile ducts
  • Intraductal growth types
    • Polypoid or papillary tumor within the variably dilated bile duct lumen
    • Malignant progression of an intraductal papillary neoplasm of the bile duct
  • Cuboidal or columnar mucin producing cells
  • Dense fibrous(desmoplastic) stroma.
Hepatic abscess
Parasitic cysts

(Echinococcous)

  • Cysts tend to be:
    • Filled with clear fluid
    • White appearance
    • Solitary
    • Unilocular
  • Cyst wall composed of an acellular laminated external layer and a thin, germinal (nucleated) inner layer
  • Brood capsule with protoscoleces inside

Microscopic Pathology

References

  1. ↑ Fava, G.; Lorenzini, I. (2012). "Molecular Pathogenesis of Cholangiocarcinoma". International Journal of Hepatology. 2012: 1–7. doi:10.1155/2012/630543. ISSN 2090-3448.
  2. ↑ 2.0 2.1 Sirica A (2005). "Cholangiocarcinoma: molecular targeting strategies for chemoprevention and therapy". Hepatology. 41 (1): 5–15. PMID 15690474.
  3. ↑ Holzinger F, Z'graggen K, Büchler M. "Mechanisms of biliary carcinogenesis: a pathogenetic multi-stage cascade towards cholangiocarcinoma". Ann Oncol. 10 Suppl 4: 122–6. PMID 10436802.
  4. ↑ Gores G (2003). "Cholangiocarcinoma: current concepts and insights". Hepatology. 37 (5): 961–9. PMID 12717374.
  5. ↑ Stain SC, Yellin AE, Donovan AJ, Brien HW (1991). "Pyogenic liver abscess. Modern treatment". Arch Surg. 126 (8): 991–6. PMID 1863218.
  6. ↑ Munro JC (1905). "VII. Lymphatic and Hepatic Infections Secondary to Appendicitis". Ann Surg. 42 (5): 692–734. PMC 1425980. PMID 17861705.
  7. ↑ Huang CJ, Pitt HA, Lipsett PA, Osterman FA, Lillemoe KD, Cameron JL; et al. (1996). "Pyogenic hepatic abscess. Changing trends over 42 years". Ann Surg. 223 (5): 600–7, discussion 607-9. PMC 1235191. PMID 8651751.
  8. ↑ Rahimian J, Wilson T, Oram V, Holzman RS (2004). "Pyogenic liver abscess: recent trends in etiology and mortality". Clin Infect Dis. 39 (11): 1654–9. doi:10.1086/425616. PMID 15578367.
  9. ↑ https://librepathology.org/wiki/Liver_pathology Accessed on February 22, 2017
  10. ↑ Lublin M, Bartlett DL, Danforth DN, Kauffman H, Gallin JI, Malech HL; et al. (2002). "Hepatic abscess in patients with chronic granulomatous disease". Ann Surg. 235 (3): 383–91. PMC 1422444. PMID 11882760.

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