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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
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cholestatic pattern of p. 402
For healthy humans, bile usually flows from the liver and into the small intestine, and this is a super important part of digestion and absorption of nutrients.
When there isn’t enough bile flowing between these two, we can say that there’s some sort of cholestasis going on, because chole- means bile and -stasis means inactivity.
This reduction in bile flow can basically be split into two types, hepatocellular cholestasis, where for some reason the hepatocytes aren’t making enough bile, and obstructive cholestasis, where something’s physically blocking bile flow.
For hepatocellular cholestasis, which would be considered a form of intra-hepatic cholestasis since it’s happening inside the liver, a really important culprit is the hormone estrogen.
Estrogen is thought to basically cause the hepatocytes to not be able to pump out bile acids, usually in the form of cholic acid, which is produced when hepatocytes break down cholesterol.
And in this case, hepatocytes literally can’t pump out the cholic acid, because it’s been found that estrogen inhibits the export pump that usually moves the bile acid from the hepatocyte to the bile canaliculi, which leads to the bile ductules and eventually the common hepatic duct.
But bile acids are just one component of bile, right? Wouldn’t the bile still be made, just without the bile acids?
Well, production and secretion of bile acids is a major driving force for the synthesis of bile in the hepatocytes, so when the cells can’t transport the bile acids and so they build up inside the cells, and this is basically a signal to down-regulate bile acid synthesis and excretion of bile altogether, which decreases the total amount of bile production.
When excretion of bile components like conjugated bilirubin are down, but they’re still being conjugated, they also build up along with the bile acids, and eventually, it’s thought that they diffuse or are exocytosed into the interstitial space, where it can access the blood supply.
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