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Pathophysiology prev
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Cirrhosis Microchapters |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Meckel
Meckel
References
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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.
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Image
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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[2]
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Histopathology of a pancreatic endocrine tumor (insulinoma). Chromogranin A immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[2]
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Histopathology of a pancreatic endocrine tumor (insulinoma). Insulin immunostain. Source:https://librepathology.org/wiki/Neuroendocrine_tumour_of_the_pancreas[2]
References
- ↑ Arthur MJ (2002). "Reversibility of liver fibrosis and cirrhosis following treatment for hepatitis C". Gastroenterology. 122 (5): 1525–8. PMID 11984538.
- ↑ 2.0 2.1 2.2 Neuroendocrine tumor of the pancreas. Libre Pathology. http://librepathology.org/wiki/index.php/Neuroendocrine_tumour_of_the_pancreas
REFERENCES