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Gastrointestinal system
Biliary atresia
Crigler-Najjar syndrome
Dubin-Johnson syndrome
Gilbert's syndrome
Rotor syndrome
Acute cholecystitis
Ascending cholangitis
Biliary colic
Cholangiocarcinoma
Chronic cholecystitis
Gallbladder cancer
Gallstone ileus
Gallstones
Alcohol-induced liver disease
Alpha 1-antitrypsin deficiency
Autoimmune hepatitis
Benign liver tumors
Budd-Chiari syndrome
Cholestatic liver disease
Cirrhosis
Hemochromatosis
Hepatic encephalopathy
Hepatitis
Hepatocellular adenoma
Hepatocellular carcinoma
Jaundice
Neonatal hepatitis
Non-alcoholic fatty liver disease
Portal hypertension
Primary biliary cirrhosis
Primary sclerosing cholangitis
Reye syndrome
Wilson disease
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Acute pancreatitis
Chronic pancreatitis
Pancreatic cancer
Pancreatic pseudocyst
Bowel obstruction
Gallstone ileus
Intestinal adhesions
Volvulus
Colorectal cancer
Colorectal polyps
Familial adenomatous polyposis
Gardner syndrome
Juvenile polyposis syndrome
Peutz-Jeghers syndrome
Gastroschisis
Hirschsprung disease
Imperforate anus
Intestinal atresia
Intestinal malrotation
Intussusception
Meckel diverticulum
Necrotizing enterocolitis
Omphalocele
Abdominal hernias
Femoral hernia
Inguinal hernia
Crohn disease
Microscopic colitis
Ulcerative colitis
Ischemic colitis
Small bowel ischemia and infarction
Celiac disease
Lactose intolerance
Protein losing enteropathy
Short bowel syndrome (NORD)
Small bowel bacterial overgrowth syndrome
Tropical sprue
Whipple's disease
Carcinoid syndrome
Appendicitis
Diverticulosis and diverticulitis
Gastroenteritis
Irritable bowel syndrome
Anal fissure
Anal fistula
Hemorrhoid
Rectal prolapse
Cleft lip and palate
Congenital diaphragmatic hernia
Esophageal web
Pyloric stenosis
Tracheoesophageal fistula
Achalasia
Barrett esophagus
Boerhaave syndrome
Diffuse esophageal spasm
Eosinophilic esophagitis (NORD)
Esophageal cancer
Gastroesophageal reflux disease (GERD)
Mallory-Weiss syndrome
Plummer-Vinson syndrome
Zenker diverticulum
Cyclic vomiting syndrome
Gastric cancer
Gastric dumping syndrome
Gastritis
Gastroenteritis
Gastroparesis
Peptic ulcer
Aphthous ulcers
Dental abscess
Dental caries disease
Gingivitis and periodontitis
Ludwig angina
Oral cancer
Oral candidiasis
Parotitis
Sialadenitis
Temporomandibular joint dysfunction
Warthin tumor
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
Hepatitis
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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
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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