Major Liver Functions
- filtration and storage of blood
- metabolism of fats/carbs/proteins
- bile formation
- vitamin/iron storage
- coagulation factor formation
Liver buffers circulating blood glucose!
Hydroxylation of Vitamin D
occurs in liver and activates!
T4 –> T3
Liver Lobule - Circulation
75% portal vein
25% hepatic artery
Hepatocyte
epithelial cells that line bile
Kupffer Cells
phagocytes (tissue macrophage) located in liver sinusoids
Main cell system for removal of microbes (removes 99% of bacteria from gut that flows to liver through portal system)
Carbohydrate Metabolism
- glycogen storage
- gluconeogenesis
- galactose/fructose to glucose
- formation of intermediate metabolites
Liver Maintenance of Blood Glucose
glycogenesis: excess glucose converted to glycogen
glycogenolysis: depolymerization of glycogen to increase blood glucose
gluconeogenesis: glucose prodution from AAs and non-hexose sugars
Cori Cycle: increases glucose to make glycogen (liver does this via de novo synth)
Protein Metabolism
- deamination of AAs
- removal of ammonia via kidney/liver by making urea (degrade amines, AAs, purine and urea in gut)
- formation of plasma proteins
- synthesis of non-essential AAs
Coaggulation Factors
Vitamin K = cofactor in liver to make clotting factors
(liver actually makes the factor)
liver disease or vitamin K deficiencies lead to bleeding abnormalities (liver requires Vitamin K to make prothrombin and factors 7, 9, 10)
Fibrinogen and accelerator globulin!
Fat Metabolism
- conversion of carbs/proteins –> fat
- Beta oxidation of fatty acids (FA move into mitochondria and then turn to acetyl CoA)
- synthesis of lipoproteins, cholesterol (to make bile salts) and phospholipids (cell membrane)
Cirrhosis
chronic liver disease
normal liver cells are damaged and replaced by scar tissue
* NOT just alcoholics however alcohol intake is most common casuse as it leads to accumulation of fat within hepatocytes
Steatohepatitis
Fatty liver! (fat in hepatocytes)
accompanied by inflammation which leads to scarring of liver and cirrhosis.
Ascites Formation
“fluid formation”
- descreased albumin –> decreased plasma COP = ascites
- increased resistance –> increased portal pressure –> ascites
Fix? lose fluid by effective intravascular volume and increased renin!
Bilirubin Formation
urobiligen = VERY soluble which means it has choices. . . can be reabsorbed, oxidized or excreted
1) Phagocyte (RBC) breaksdown to release bilirubin
2) bilirubin enters hepatocyte via albumin
3) free bilrubin is taken up by hepatocyte and is conjugated and excreted into bile
Jaundice
too much unconjugated bilirubin!!! (system becomes backed up and can’t excrete)
Hemolysis - unconjugated bilirubin overproduction
Neonatal Jaundice - defective conjugation
Cirrhosis/Hepatits - defectiv excretion of all bilirubin
Cancer/Gallstones - obstruction of excretion pathway of all bilirubin
Bile Salts
Most abundant solute in bile = bile salts
calcium cannot be absorbed because bile salts are amphipathic!
–> cholic acid (phobic) + glycine (philic) =
glycocholic acid (amphipathic bile salt)
Gallbladder
CCK + peristalsis = emptying
emptys through cystic duct when food (especially fatty food) enters duodenum
- CCK sense fat in the duodenum - contracts gallbladder and relaxes sphincter of Oddi
- Duodenal peristaltic waves occur! MOST IMPORTANT
- vagus + enteric (minor role)
Feces
- Melena/Black - upper GI bleed
- Maroon - middle GI bleed/Chrohns
- Clay - no bile (blocked)
- Yellow/Greasy - fat malabsorption/Celiacs
- Bright Red - anal bleed
