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Cleft lip and palate
Congenital diaphragmatic hernia
Temporomandibular joint dysfunction
Gingivitis and periodontitis
Dental caries disease
Eosinophilic esophagitis (NORD)
Diffuse esophageal spasm
Gastroesophageal reflux disease (GERD)
Gastric dumping syndrome
Cyclic vomiting syndrome
Small bowel bacterial overgrowth syndrome
Short bowel syndrome (NORD)
Protein losing enteropathy
Small bowel ischemia and infarction
Familial adenomatous polyposis
Juvenile polyposis syndrome
Irritable bowel syndrome
Diverticulosis and diverticulitis
Non-alcoholic fatty liver disease
Cholestatic liver disease
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Primary biliary cirrhosis
Primary sclerosing cholangitis
Benign liver tumors
Pancreatic neuroendocrine neoplasms
Congenital gastrointestinal disorders: Pathology review
Esophageal disorders: Pathology review
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Inflammatory bowel disease: Pathology review
Malabsorption syndromes: Pathology review
Diverticular disease: Pathology review
Appendicitis: Pathology review
Gastrointestinal bleeding: Pathology review
Colorectal polyps and cancer: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Pancreatitis: Pathology review
Gallbladder disorders: Pathology review
Jaundice: Pathology review
Viral hepatitis: Pathology review
Cirrhosis: Pathology review
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0 / 21 complete
hepatitis C p. 171
characteristics of p. NaN
extrahepatic manifestations p. 170
flaviviruses p. 164
hepatocellular carcinoma and p. 401
lichen planus p. 496
as oncogenic microbe p. 223
therapy for p. 201
hepatitis C p. 170
hepatitis C p. 170
hepatitis C p. 201
Tanner Marshall, MS
Hepatitis, meaning like this inflammation, of the liver, most commonly comes about because of a virus.
These viruses tend to target the cells in the liver, and when they get in and infect these cells, they tend to cause them to present these weird and abnormal proteins via their MHC class 1 molecules, and at the same time, you’ve also got these immune cells infiltrating the liver and trying to figure out what’s going on, and so the CD8 positive T cells recognize these abnormal proteins as a sign that the cells are pretty much toast, and the hepatocytes go through cytotoxic killing by the T cells and apoptosis.
Hepatocytes undergoing apoptosis are sometimes referred to as Councilman bodies, shown on histology here, and this typically takes place in the portal tracts and lobules of the liver.
This cytotoxic killing of hepatocytes is the main mechanism behind inflammation of the liver, and eventual liver damage in viral hepatitis!
As someone’s hepatitis progresses, we’ll see a couple classic symptoms related to your immune system mounting an attack, like fever, malaise, and nausea.
Additionally though, patients might have hepatomegaly, where their liver is abnormally large from inflammation, which might cause some pain.
Also, as more and more damage is done to the liver, the amount of transaminases in their blood will increase.
Your liver has these transaminase enzymes so it can do its job of breaking down various amino acids.
Typically the serum amino transaminase, or the amount in your blood, is pretty low, but when your hepatocytes start getting damaged they start leaking these into the blood, so a common sign is a greater amount of both alanine aminotransferase, or ALT, and aspartate aminotransferase, or AST, typically even though both are elevated, ALT will be greater than AST in viral hepatitis and will also be the last of the two liver enzymes to return to normal.
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