Liver and GB part I covered in Exam II Flashcards
liver blood supplies
hepatic artery
hepatic portal vein: from GI to the liver
hepatic vein: from liver to inferior vena cava to the heart
bilirubin formation
RBCs -> heme -> biliverdin
-> uncong. bilirubin + albumin (in serum) -> conjugation in the liver to produce conjugated bilirubin -> intestinal bacteria -> urobilinogen -> feces and urine
circumstances with an increased urinary urobilinogen excretion
Excessive bilirubin production seen in hemolytic anemia
Inefficient hepatic clearance of the absorbed urobilinogen through enterohepatic circulation seen in cirrhosis or hepatitis
Excessive exposure of bilirubin to intestinal bacteria seen in constipation
circumstances with a decreased urinary urobilinogen excretion
biliary obstruction seen in tumors
mechanisms to protect against increased bilirubin
binding to plasma albumin
rapid uptake
conjugation
clearance
potential health benefit of bilirubin
acts as an antioxidant like glutathione
what type of bilirubin (conj or unconj) can be caused by excessive hemolysis
unconj bc the conjugation system becomes overwhelmed
what type of bilirubin (conj or unconj) can be caused by abnormalities in the liver
it depends: the conj system is normal but clearance is abnormal or vise versa, we might have a mix of conj and unconj
what type of bilirubin (conj or unconj) can be caused by the mechanical obstruction of bile flow after its formation
conj
etiologies of increased unconj bilirubin in newborns
Increased in number of RBCs
Decreased RBCs’ life span
Decreased bilirubin clearance
what cells send mitotic signals in the liver regeneration
Macrophages
Hepatic stellate cells
Liver endothelial cells
etiologies of acute liver failure
acetaminophen, HAV, HBV, HCV
clinical characteristics of acute liver failure
severe acute liver injury
hepatic encephalopathy
prolonged prothrombin time/INR
pathophys of hepatic encephalopathy in acute liver failure
increased ammonia in the systemic circulation that crosses the BBB
in astrocytes, ammonia gets metabolized to glutamate -> astrocyte swelling -> increased ROS -> increased ICP
*watch for brain herniation
pathophys of acetaminophen-induced liver injury
acetaminophen overdose: gluthotion storage gets depleted -> it gets metabolized by CYP450 -> formation of free NAPQI -> NAPQI binds to the liver proteins -> cells damage and death