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GIGU > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

What is the blood supply to the liver?

A

75 percent from hepatic portal V.

25 percent from proper hepatic A.

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2
Q

What is the main cell type in the liver and what are they responsible for?

A

hepatocytes (80 percent of liver cells)

  • carry out most of the metabolic fxn of the liver
  • can regenerate
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3
Q

What do the endothelial cells of the liver do?

A

-allow exchange of material from liver to blood and vice versa via pores and fenestrations in the plasma membrane

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4
Q

What are characteristics of the Kupffer Cells in the liver?

A
  • within the sinusoids (in the lining)
  • have well-developed endocytic and phagocytic fxn
  • lots of lysosomes in these cells
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5
Q

What is the function of Kupffer Cells in the liver?

A

-macrophages that protect the liver from gut-derived microbes, removed dead RBC, orchestrate immune response, secrete cytokines

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6
Q

What do the hepatic stellate cells do?

A

-serve as storage site for vitamin A and other lipids

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7
Q

What are Pit Cells in the liver?

A
  • lymphocytes and natural killer cells

- protect liver against viruses and tumor cells

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8
Q

What are cholangiocytes?

A

they line the bile ducts and control the rate of bile flow and control the bile pH

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9
Q

What processes are carried out by the liver in regards to carbohydrate metabolism?

A
  • glucostasis = maintains blood glucose levels
  • glycogenesis
  • glycogenolysis
  • gluconeogenesis (d/t presence of G6P-ase)
  • makes ketone bodies during starvation
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10
Q

What processes are carried out by the liver in regards to lipid metabolism?

A
  • synthesis of TAG’s, phospholipids, steroids (cholesterol, bile), lipoproteins (VLDL, LDL, etc)
  • lipolysis (degradation or TAG’s, plasma lipoproteins; beta-oxidation; regulation of FFA metabolism)
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11
Q

True or False: liver conducts nucleotide biosynthesis

A

True

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12
Q

What cycle dealing with amino acid metabolism only occurs in the liver?

A
  • urea cycle (removal of nitrogen)

- impaired clearance of ammonia leads to brain damage

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13
Q

What blood proteins are synthesized by the liver?

A

-albumin, antibodies, apoproteins (for lipid transport), fibrinogen, prothrombin, clotting factors (V, VII, IX and X)

  • acute phase response proteins (C-reactive protein)
  • protease inhibitors (alpha1 antitrypsin)
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14
Q

True or False: liver metabolizes bilirubin

A

True

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15
Q

What is the liver’s role (overall big picture) in waste management?

A

-inactivation, detoxification, and biotransformation of metabolites and xenobiotics

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16
Q

How is the liver’s circulation unique?

A
  • receives blood from enteric circulation via portal V.
  • receives blood from periphery via hepatic A.
  • low portal blood pressure
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17
Q

What major structural adaptation aids the liver in its function?

A
  • lack of basement membrane and absence of tight junctions b/w hepatocytes and endothelial cells
  • pores allow greater access and increased contact b/w liver and blood
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18
Q

What are the cellular adaptations and characteristics of hepatocytes that aid the liver in its function?

A
  • well-developed plasma membrane
  • well-developed ER (smooth and rough)
  • lots of lysosomes
  • lots of metabolic enzymes
19
Q

What are the steps in the synthesis of primary bile acids?

A

–7alpha-hydroxylase changes cholesterol into 7alpha-hydroxycholesterol

–the side chain is snipped and a COOH is added to make chenodeoxycholic acid or cholic acid

20
Q

What must happen to chenodeoxycholic acid and cholic acid prior to being secreted?

A

they must be conjugated

21
Q

How are chenodeoxycholic acid and cholic acid conjugated?

A
  • CoA is added
  • then CoA is removed and replaced by an amino acid
  • -taurine or glycine
  • –taurochenodeoxycholic acid or taurocholic acid
  • –glycochenodeoxycholic acid or glycocholic acid
22
Q

Which primary conjugated bile acid is a better emulsifier?

A

-taurocholic acid with a pKa of 2
versus
–glycocholic acid with a pKa of 4

23
Q

What is the rate-limiting step in bile acid synthesis?

A

the creation of 7alpha-hydroxycholesterol from cholesterol by 7alpha-hydroxylase

24
Q

What is the cofactor used by 7alpha-hydroxylase?

A

vitamin C

25
Q

How are primary conjugated bile acids changed into secondary bile acids?

A

by gut bacteria that deconjugate and dehydroxylate

26
Q

What are the secondary bile acids?

A
  • deoxycholic acid from cholic acid

- lithocholic acid from chenodeoxycholic acid

27
Q

Once the bile acids are released, what happens to them?

A
  • 95 percent is absorbed by the ileum and recycled by the liver
  • 5 percent is excreted in the feces
28
Q

How do bile acids and bile salts emulsify fats?

A
  • the hydrophobic surfaces of bile salts associate with TAG’s and form a micelle
  • hydrophilic surface of bile salts faces outward, allowing interaction w/ pancreatic lipase
29
Q

What is the mechanism of digestion by pancreatic lipases?

A

pancreatic lipases free fatty acids from large micelles in to a smaller micelle that can be absorbed through intestinal mucosa

30
Q

Clinical Correlation: Gallstones

A
  • result from supersaturation of bile /cholesterol

- cholesterol crystals form

31
Q

What is are the causes of cholelithiasis?

A
  • insufficient secretion of bile salts that are required for the cholesterol to stay in solution
  • excess cholesterol secretion into bile
32
Q

What are some consequences of chronic disturbance in bile salt metabolism?

A
  • malabsorption syndromes
  • steatorrhea (fat in feces)
  • deficiency in fat-soluble vitamins
33
Q

What is the mechanism behind how cholesterol-lowering drugs such as cholestyramine work?

A

-bind to bile acids and prevent it from being reabsorbed
–bile is excreted
-decreased inhibition of 7alpha-hydroxylase
(bile normally inhibits 7alpha-hydroxylase)
-bile must be synthesized using up more cholesterol

34
Q

What is a difference between hepatic metabolic enzymes versus others?

A

-low substrate specificity b/c they have to be able to deal w/ an infinite range of molecules

35
Q

What are the phases of inactivation of xenobiotics?

A

Phase I - reduction, oxidation, hydroxylation, or hydrolysis increases the polarity (catalyzed by CYPs)

Phase II - conjugation, sulfation, methylation, glucuronidation makes them soluble enough to excrete

36
Q

What is the rate-limiting enzyme in metabolism catalyzed by CYPs (most commonly CYP1, CYP2, and CYP3)?

A

CYPR

cytochrome P450 reductase

37
Q

Name a couple things that inhibit CYPs and the result of inhibition.

A
  • itraconozole and citrus juice

- increase in drug plasma levels

38
Q

Name a couple things that stimulate CYPs and the result of stimulation.

A
  • rifampicin and St. John’s Wort

- decrease in plasma drug levels

39
Q

How does “personalized medicine” play into drug metabolism?

A
  • there are many polymorphisms of CYPs
  • -influences the way drugs are metabolized

-the CYPs of an individual patient can be genotyped

40
Q

Clinical Correlation: Tylenol Toxicity

A
  • normally conjugated with glucuronic acid or sulfate
  • in overdose, capacity for conjugation is overwhelmed
  • excess Tylenol oxidized by CYP3A4 into NABQ1
  • -a free radical that causes hepatic failure and death
  • tx by glutathione or N-acetyl cysteine
41
Q

What are the mechanisms of liver disease?

A
  • endothelial cells pack more tightly together
  • membrane contains collagen
  • stiff hepatic vasculature resists free flow of blood
  • impairs exchange of material bw hepatocytes and liver
42
Q

How can liver fxn be assessed using blood albumin levels?

A
  • lack of albumin causes edema
  • albumin provides the osmotic pressure
  • low albumin means the liver isn’t making enough
43
Q

How can liver fxn be assessed using AST and ALT levels?

A
  • they’re normally in hepatocytes, NOT blood
  • damaged hepatocytes release AST/ALT into blood
  • ALT is more sensitive b/c it’s cytosolic
  • ALT and AST are both in hepatocyte mitochondria
  • req’d for conversion of amino acids into ketoacids
44
Q

How can liver fxn be assessed using prothrombin time (PT)?

A
  • liver makes prothrombin

- increased prothrombin time means liver isn’t making enough prothrombin

GIGU (9 decks)

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