Liver and Gallbladder Flashcards

1
Q

Major Liver Functions

A
  • filtration and storage of blood
  • metabolism of fats/carbs/proteins
  • bile formation
  • vitamin/iron storage
  • coagulation factor formation

Liver buffers circulating blood glucose!

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2
Q

Hydroxylation of Vitamin D

A

occurs in liver and activates!

T4 –> T3

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3
Q

Liver Lobule - Circulation

A

75% portal vein

25% hepatic artery

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4
Q

Hepatocyte

A

epithelial cells that line bile

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5
Q

Kupffer Cells

A

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)

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6
Q

Carbohydrate Metabolism

A
  • glycogen storage
  • gluconeogenesis
  • galactose/fructose to glucose
  • formation of intermediate metabolites
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7
Q

Liver Maintenance of Blood Glucose

A

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)

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8
Q

Protein Metabolism

A
  • 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
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9
Q

Coaggulation Factors

A

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!

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10
Q

Fat Metabolism

A
  • 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)
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11
Q

Cirrhosis

A

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

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12
Q

Steatohepatitis

A

Fatty liver! (fat in hepatocytes)

accompanied by inflammation which leads to scarring of liver and cirrhosis.

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13
Q

Ascites Formation

A

“fluid formation”

  • descreased albumin –> decreased plasma COP = ascites
  • increased resistance –> increased portal pressure –> ascites

Fix? lose fluid by effective intravascular volume and increased renin!

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14
Q

Bilirubin Formation

A

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

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15
Q

Jaundice

A

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

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16
Q

Bile Salts

A

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)

17
Q

Gallbladder

A

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)
18
Q

Feces

A
  1. Melena/Black - upper GI bleed
  2. Maroon - middle GI bleed/Chrohns
  3. Clay - no bile (blocked)
  4. Yellow/Greasy - fat malabsorption/Celiacs
  5. Bright Red - anal bleed