00:00 / 00:00
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Benign liver tumors
Cholestatic liver disease
Non-alcoholic fatty liver disease
Primary biliary cirrhosis
Primary sclerosing cholangitis
Pancreatic neuroendocrine neoplasms
Familial adenomatous polyposis
Juvenile polyposis syndrome
Small bowel ischemia and infarction
Protein losing enteropathy
Short bowel syndrome (NORD)
Small bowel bacterial overgrowth syndrome
Diverticulosis and diverticulitis
Irritable bowel syndrome
Cleft lip and palate
Congenital diaphragmatic hernia
Diffuse esophageal spasm
Eosinophilic esophagitis (NORD)
Gastroesophageal reflux disease (GERD)
Cyclic vomiting syndrome
Gastric dumping syndrome
Dental caries disease
Gingivitis and periodontitis
Temporomandibular joint dysfunction
Appendicitis: Pathology review
Cirrhosis: Pathology review
Colorectal polyps and cancer: Pathology review
Congenital gastrointestinal disorders: Pathology review
Diverticular disease: Pathology review
Esophageal disorders: Pathology review
Gallbladder disorders: Pathology review
Gastrointestinal bleeding: Pathology review
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Inflammatory bowel disease: Pathology review
Jaundice: Pathology review
Malabsorption syndromes: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Pancreatitis: Pathology review
Viral hepatitis: Pathology review
0 / 12 complete
0 / 16 complete
Cirrhosis - Patient Stories
Complications of Cirrhosis
Nonalcoholic Fatty Liver Disease
Cirrhosis - Pathogenesis & Clinical Manifestations
cholelithiasis and p. 403
cirrhosis and p. 396
cirrhosis p. 396
cirrhosis as cause p. 396
α1-antitrypsin deficiency p. 399
alcoholic p. 69, 398
bacterial peritonitis (spontaneous) p. 397
cystic fibrosis p. 58
encephalopathy with p. 398
esophageal varices and p. 384
fructose intolerance p. 78
granulomatous disease p. NaN
gynecomastia p. 669
hemochromatosis p. 402
hepatocellular carcinomas p. 399
hyperbilirubinemia in p. 400
loop diuretics for p. 628
non-alcoholic fatty liver disease p. 398
pleural effusion p. 701
portal hypertension p. 396
serum markers for p. 397
Wilson disease p. 402
alcoholic cirrhosis as cause p. 398
alcoholic cirrhosis and p. 399
cirrhosis p. 69, 78
with cirrhosis p. 396
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.
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