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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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Complications of Cirrhosis
Nonalcoholic Fatty Liver Disease
Primary Biliary Cholangitis (Primary Biliary Cirrhosis)
Primary Biliary Cholangitis (Primary Biliary Cirrhosis) Diagnosis and Treatment
Primary Sclerosing Cholangitis Labs and Treatment
Primary Sclerosing Cholangitis Mechanisms
At the family medicine clinic, a 52- year- old male immigrant from Africa, named Jamar, came in for a checkup for the first time in a decade. On questioning, he admits to an extensive history of alcohol abuse. Physical examination reveals gynecomastia, palmar erythema and spider angiomata, as well as a palpable spleen.
Next, a 70- year- old Caucasian female, named Eleanor, with a history of chronic hepatitis C infection, is brought to the emergency department by paramedics due to altered mental status. She is completely disoriented and unable to provide an adequate history. Neurologic examination also reveals asterixis.
Lab tests of both show increased aspartate aminotransferase, or AST, and alanine aminotransferase or ALT. There’s also decreased albumin and increased prothrombin time. The difference is that Jamar has an AST level twice as high as ALT, in contrast with Eleanor, who has an ALT higher than AST. Eleanor, in particular, also has high serum levels of ammonia.
Both Jamar and Eleanor have cirrhosis. This is when chronic inflammation damages the liver causing it to become fibrotic. Normally, the liver is highly regenerative but scar tissue can replace liver cells which prevents regeneration and when this goes on for too long, it reaches the point where the damage is no longer reversible. If enough of the liver is replaced by scar tissue in advanced cirrhosis, a liver transplant might be needed. . Now, if we zoom into a hepatic lobule, we can see that it’s made of sheets of hepatocytes with sinusoids between them. The sinusoids are made of branches of the portal vein and hepatic artery, and together with the bile duct, form the portal triad which runs towards the central vein.
Now, there’s a space around each sinusoid, called the perisinusoidal space which contains stellate cells. When the hepatocytes are injured, they cluster together and form regenerative nodules. Here, they secrete paracrine factors that activate the stellate cells, which then proliferate, and start secreting transforming growth factor beta1, or TGF-beta. This causes them to produce collagen. The collagen builds up around the nodules and helps form scar tissue, leading to fibrosis.
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