largest organ weighing around 1500 grams (3 pounds)

composed largely of liver cells (hepatocytes), bile duct components and vascular elements

a dual blood supply

1. excretory

2.metabolic

3.storage

4.synthetic

measured by the release of enzymes within the liver cells when they die. 

include ALT and AST

yellow discoloration of the skin and mucosa caused by hyperbilirubinemia

often first appears in the sclera of eyes (white part)

allow us to tell direct (conjugated) from indirect (non-conjugated).

provides us useful information regarding the cause of jaundice

benign disease. contracted from sewage, contaminated food etc.

NEVER becomes chronic and common in third world countries 

Antigens s(surface), c(core) and e are useful in monitoring of the disease. 

When infected, the antigen is secreted and can be seen in the serum 1 week after onset of infection

the antigen then disappears and the ABy appears (if those patients who do not produce ABy's often develop chronic hepatitis)

acquired by blood transfusion or sexual contact

mild clinical presentation and can progress to chronic hepatitis with cirrhosis 

loss of normal liver structure and function characterized by bands separating lobules and pseudolobular formation. end state liver disease

common agents are Viral hepatitis, especially B and C and chronic alcoholic use

1. Alpha1- antitrypsin deficiency 

2. Biliary cirrhosis

3. bacterial infections of the biliary tree

4. Parasitic infections (Flukes)

5. Autoimmune diseases

6. drugs

increased fluid in the peritoneal cavity due to the result of back pressure and loss of albumin from the liver

leads to renal hypoperfusion with release of aldosterone, Na retention and increased water uptake which makes more fluid released into abdomen

drugs like Tylenol and even tetracycline that produce significant hepatic disease such as the Statins and others.

Toxins are Carbon trichloride as well as mushrooms (amanita species)

we see liver cell necrosis (mallary-wise bodies) and collections of neutrophils and steatosis

some individuals following episodes of alcoholic hepatitis develop fibrosis and end stage cirrhosis

hereditary disease of the liver more in males

intermittent jaundice, elevations of unconjugated bilirubin

no treatment and no complication

believed to be a T-cell mediated destruction of bile ducts (type 4 hypersensitivity reaction) that eventually produces cirrhosis

affect women 9:1

destruction of bile ducts both intra and extrahepatic

perhaps autoimmune and associated with other autoimmune disorders

unknown orgin

bacteria can travel up the common bile duct and into the liver. 

produces high fever and signs of sepsis

very common, many do not produce disease

estimated 20% of people older than 65 have these

75% produced from cholesterol and calcium, other produced from bile breakdown

produce the most disease since they can block the common bile duct leading to the small intestine.

This results in spastic pain in the right upper quadrant and jaundice

any obstruction produces an opportunity for infection to occur and get infected gallbladder, much like an appendix

complications include ascending cholangitis, and rupture with peritonitis 

acute causes called cholecystitis (inflammation) with cholelithiasis (stone) is usually surgery. 

gall bladder is not very important and horses do not even have them. it is important that the common bile duct not be damaged 

look like liver cells and often arise in cirrhotic livers of any organ

may prevent as multi-focal or single tumors

present late and difficult to treat

associated with obstruction of hepatic vein by thrombosis. 

Hepatocellular carcinomas may produce this syndrome

rare malignant tumor of the bile ducts

especially difficult to diagnosis especially when in common duct but now can run small camera into common bile duct to look and get biopsy

arises in gall bladder epithelium and often directly invades adjacent liver tissue

presents late and no really good treatment