Cirrhosis
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Cirrhosis
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Alcoholic cirrhosis p. 69, 398
cholelithiasis and p. 403
Alcoholism p. 589
cirrhosis and p. 396
Amenorrhea
cirrhosis p. 396
Anemia
cirrhosis p. 396
Anorectal varices
cirrhosis as cause p. 396
Ascites
cirrhosis p. 396
Asterixis p. 80, 533
cirrhosis p. 396
Cirrhosis p. 396
α1-antitrypsin deficiency p. 399
alcoholic p. 69, 398
bacterial peritonitis (spontaneous) p. 397
cholelithiasis and p. 403
cystic fibrosis p. 58
encephalopathy with p. 398
esophageal varices and p. 384
fructose intolerance p. 78
granulomatous disease p. NaN
gynecomastia p. 667
hemochromatosis p. 402
hepatocellular carcinomas p. 399
hyperbilirubinemia in p. 400
loop diuretics for p. 624
non-alcoholic fatty liver disease p. 398
pleural effusion p. 699
portal hypertension p. 396
serum markers for p. 397
Wilson disease p. 402
Edema (generalized)
cirrhosis p. 396
Gynecomastia p. 667
cirrhosis p. 396
Hepatic cirrhosis p. 699
Hepatic encephalopathy p. 398
cirrhosis p. 396
Hepatitis
cirrhosis p. 396
Hepatocellular carcinomas p. 399
cirrhosis and p. 396
“Hobnail” liver in alcoholic cirrhosis p. 398
Hyperbilirubinemia
cirrhosis and p. 396
Hypoalbuminemia
alcoholic cirrhosis as cause p. 398
Hyponatremia p. 609
cirrhosis and p. 396
Jaundice p. 400
alcoholic cirrhosis and p. 399
cirrhosis p. 396
Liver disease
cirrhosis p. 69, 78
Peripheral edema
cirrhosis and p. 396
Petechiae
with cirrhosis p. 396
Portal hypertension p. 396
cirrhosis and p. 396
Purpura
cirrhosis p. 396
Spider angiomas
cirrhosis p. 396
Splenomegaly
cirrhosis p. 396
Testicular atrophy
cirrhosis p. 396
Thrombocytopenia p. 413
cirrhosis p. 396
Transcript
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When cells are injured or damaged and die off, usually that dead tissue that was previously full of living cells becomes fibrotic, meaning it becomes thickened with heaps and heaps of protein and forms scar tissue.
So when your liver is constantly forced to process alcohol like in alcoholic liver disease, or subject to a viral attack for a long time like in HBV, or anything else that causes a long-term or chronic state of liver cell or hepatocyte destruction and inflammation, your liver can become seriously scarred and damaged to the point where it’s no longer reversible, at which point it becomes fibrotic and in the liver we call this process cirrhosis.
Because it’s usually irreversible, cirrhosis is often referred to as “end-stage” or “late-stage” liver damage.
When liver cells are injured, they start to come together and form what are called regenerative nodules. You can think of these as colonies of living liver cells. These are one of the classic signs of cirrhosis and are why a cirrhotic liver is more bumpy as opposed to a smooth, healthy liver.
Also with cirrhotic liver tissue, you’ll see that in between these clumps of cells or nodules, is fibrotic tissue and collagen.
Here’s a classic histology image of cirrhotic tissue, this clump of cells in the middle is the regenerative nodule, and these blue stains surrounding it are the bands of protein from the process of fibrosis.
If we zoom out a bit and look at it with the naked eye, we’ll again see these nodules, which have fibrotic protein bands in between.
How do these bands of fibrotic tissue form though? Well fibrosis is a process mediated by special cells called stellate cells, that sit between the sinusoid and hepatocyte, known as the perisinusoidal space.
Here’s a pretty basic layout of the basic functional unit of the liver, you’ve got the portal vein and hepatic artery that combine into a sinusoid, which then goes into the central vein, and these are all lined with hepatocytes.
Along with these though you’ve also got a bile duct, and all three constitute a portal triad.