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==Overview== | ==Overview== | ||
Meckel | |||
==Meckel== | ==Meckel== | ||
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Revision as of 17:25, 8 January 2018
Pathophysiology prev
| https://https://www.youtube.com/watch?v=5szNmKtyBW4%7C350}} |
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Cirrhosis Microchapters |
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Diagnosis |
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Treatment |
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Case studies |
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Sandbox:Cherry On the Web |
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American Roentgen Ray Society Images of Sandbox:Cherry |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Meckel
Meckel
References
the end
-
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:
- More than 66 percent of all American adults consume alcohol.
- Cirrhosis due to alcohol accounts for approximately forty percent of mortality rates due to cirrhosis.
- Mechanisms of alcohol-induced damage include:
- Impaired protein synthesis, secretion, glycosylation
- 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.[1]
- 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
Pathology
- 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.
Causes
| Drugs and Toxins | Infections | Autoimmune | Metabolic | Biliary obstruction(Secondary bilary cirrhosis) | Vascular | Miscellaneous |
|---|---|---|---|---|---|---|
| Alcohol | Hepatitis B | Primary Biliary Cirrhosis | Wilson's disease | Cystic fibrosis | Chronic RHF | Sarcoidosis |
| Methotrexate | Hepatitis C | Autoimmune hepatitis | Hemochromatosis | Biliary atresia | Budd-Chiari syndrome | Intestinal
bypass operations for obesity |
| Isoniazid | 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) |
Cirrhosis
Pathophysiology [2][3][4][5][6][1]
- When an injured issue is replaced by a collagenous scar, it is termed as fibrosis.
- 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.
- The cellular mechanisms responsible for cirrhosis are similar regardless of the type of initial insult and site of injury within the liver lobule.
- Viral hepatitis involves the periportal region, whereas involvement in alcoholic liver disease is largely pericentral.
- If the damage progresses, panlobular cirrhosis may result.
- Cirrhosis involves the following steps: [7]
- Inflammation
- Hepatic stellate cell activation
- Angiogenesis
- Fibrogenesis
- 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 [8]
- formation of intra hepatic shunts (due to angiogenesis and loss of parenchymal cells)
- hepatic endothelial dysfunction
- The endothelial dysfunction is characterised by [9]
- 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.[10][11][12]
- 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:
- More than 66 percent of all American adults consume alcohol.
- Cirrhosis due to alcohol accounts for approximately forty percent of mortality rates due to cirrhosis.
- Mechanisms of alcohol-induced damage include:
- Impaired protein synthesis, secretion, glycosylation
- 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.[1]
- 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
Pathology
- 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.
Video codes
Normal video
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Video in table
{{#ev:youtube|5ucSlgqGAno}}
Floating video
| Title |
| https://https://www.youtube.com/watch?v=ypYI_lmLD7g%7C350}} |
Redirect
- REDIRECTEsophageal web
synonym website
https://mq.b2i.sg/snow-owl/#!terminology/snomed/10743008
Image
Image to the right
 |
Image and text to the right
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Gallery
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![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]](/images/2/2f/Pancreatic_insulinoma_histology_2.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]
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![Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]](/images/a/a3/Pancreatic_insulinoma_histopathology_3.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]
-
![Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]](/images/d/d5/Pancreatic_insulinoma_histology_4.JPG)
Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]
![Histopathology of a pancreatic endocrine tumor (insulinoma). Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[13]](/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[13]](/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[13]](/index.php/File:Pancreatic_insulinoma_histology_4.JPG)
References
- ↑ 1.0 1.1 1.2 Arthur MJ (2002). "Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C". Gastroenterology. 122 (5): 1525–8. PMID 11984538.
- ↑ Arthur MJ, Iredale JP (1994). "Hepatic lipocytes, TIMP-1 and liver fibrosis". J R Coll Physicians Lond. 28 (3): 200–8. PMID 7932316.
- ↑ Friedman SL (1993). "Seminars in medicine of the Beth Israel Hospital, Boston. The cellular basis of hepatic fibrosis. Mechanisms and treatment strategies". N. Engl. J. Med. 328 (25): 1828–35. doi:10.1056/NEJM199306243282508. PMID 8502273.
- ↑ Iredale JP (1996). "Matrix turnover in fibrogenesis". Hepatogastroenterology. 43 (7): 56–71. PMID 8682489.
- ↑ Gressner AM (1994). "Perisinusoidal lipocytes and fibrogenesis". Gut. 35 (10): 1331–3. PMC 1374996. PMID 7959178.
- ↑ Iredale JP (2007). "Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ". J. Clin. Invest. 117 (3): 539–48. doi:10.1172/JCI30542. PMC 1804370. PMID 17332881.
- ↑ Wanless IR, Wong F, Blendis LM, Greig P, Heathcote EJ, Levy G (1995). "Hepatic and portal vein thrombosis in cirrhosis: possible role in development of parenchymal extinction and portal hypertension". Hepatology. 21 (5): 1238–47. PMID 7737629.
- ↑ Fernández M, Semela D, Bruix J, Colle I, Pinzani M, Bosch J (2009). "Angiogenesis in liver disease". J. Hepatol. 50 (3): 604–20. doi:10.1016/j.jhep.2008.12.011. PMID 19157625.
- ↑ García-Pagán JC, Gracia-Sancho J, Bosch J (2012). "Functional aspects on the pathophysiology of portal hypertension in cirrhosis". J. Hepatol. 57 (2): 458–61. doi:10.1016/j.jhep.2012.03.007. PMID 22504334.
- ↑ Schuppan D, Afdhal NH (2008). "Liver cirrhosis". Lancet. 371 (9615): 838–51. doi:10.1016/S0140-6736(08)60383-9. PMC 2271178. PMID 18328931.
- ↑ Desmet VJ, Roskams T (2004). "Cirrhosis reversal: a duel between dogma and myth". J. Hepatol. 40 (5): 860–7. doi:10.1016/j.jhep.2004.03.007. PMID 15094237.
- ↑ Wanless IR, Nakashima E, Sherman M (2000). "Regression of human cirrhosis. Morphologic features and the genesis of incomplete septal cirrhosis". Arch. Pathol. Lab. Med. 124 (11): 1599–607. doi:10.1043/0003-9985(2000)124<1599:ROHC>2.0.CO;2. PMID 11079009.
- ↑ 13.0 13.1 13.2 Neuroendocrine tumor of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas
REFERENCES