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GIGU > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

What is the liver’s main blood supply?

A

75%- PORTAL VEIN (from GI)

25%- PROPER HEPATIC A

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2
Q

What is a sinusoid?

A

Partitioning of Liver: portal V and proper hepatic A go into, central heaptic V (to IVC) comes out
—> contails bile canaliculus

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3
Q

Hepatocyte

A

metabolic functions of liver, can REGENERATE

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4
Q

Endothelial Cell

A

exchange material between liver and blood

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5
Q

Kupffer Cell

A

MACROPHAGE—helps protect liver, remove RBS, creates cytokines to help immune response via cytokines

—–>lots of lysosomes

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6
Q

Stellate Cell

A

storage for Vitamin A and other lipids

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7
Q

Cholangiocyte

A

lines bile ducts, controls bile flow rate and pH

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8
Q

Pit Cells

A

lymphocytes—> natural killer cells that protect against viruses and tumors

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9
Q

Functions of Liver

A
  • –> primary receiving, distribution, recycling center
  • CARB metabolism
  • LIPID metabolism
  • NUCLEOTIDE metabolism
  • PROTEIN and AA metabolism
  • Removal of nitrogen via urea cycle
  • Synthesis of blood proteins
  • BILIRUBIN metabolism
  • Waste management (xenobiotics)
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10
Q

Highlights of carbohydrate metabolism in liver

A

Liver maintains glucose levels, G6P to release FFA into blood, makes ketone bodies in starvation

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11
Q

What is made during lipid metabolism in liver

A

BILE ACIDS AND SALTS, cholesterol, TAGS, FFA~energy via B-oxidation

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12
Q

What are blood proteins made by liver

A

Albumin, coagulation factors, acute phase response proteins

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13
Q

Major Role of Liver

A
  • monitor, synthesize, recycle, distribute, modify metabolites
  • convert to useful forms or to safe product for excretion
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14
Q

Describe liver circulation and membrane composition

A
  • portal v (GI) and proper hepatic A (periphery) go into liver
  • no basement membrane or tight junctions b/t liver and endothelial cells
  • fenestrations and gaps b/t endothelial cells increase contact between blood and liver
  • good plasma membrane, lots of lysosomes and metabolic enzymes
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15
Q

Bile composition

A

Bile acids, bile salts, cholesterol, phospholipids, FFA, inorganic salts

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16
Q

Function of bile acids and salts

A

emulsify fats in duodenum to increase absorption, eliminate cholesterol and prevent its buildup

  • STRONG DETERGENTS d/t low pKA
  • form micelles around TAGS to increase surface area for lipases to bind and breakdown to FFA
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17
Q

Where are bile acids and salts made?

A

hepatocytes via hepatic cholesterol–> bile canalicuili–> GB–>duodenum in response to food

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18
Q

How do bile acids/salts work?

A

Bile acids (COOH) are converted to bile salts (COO-) in liver–> bind TAG in SI–> micelle–> pancreatic lipase binds to hydrophilic outside of salt–> breakdown to FFA

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19
Q

Synthesis of primary bile acids

A

Hepatic cholesterol–>7 alpha hydroxylase–> 7 alpha hydroycholesterol–> primary bile acids

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20
Q

What are secondary bile acids?

A

cholic acid and chenodeoxycholic acid via 7 alpha dehydroxylase–> deoxycholic acid and lithocholic acid

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21
Q

Why are there primary conjugated bile acids?

A

Bile acids must be conjugated before secretion into duodenum

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22
Q

What are examples of primary bile acids?

A
  • cholic acid

- chenodeoxycholic acid

23
Q

What are examples of primary conjugated bile acids?

A

–> bile acids conjugated with glycine or taurine

from cholic acid:

  • glycocholic acid
  • taurocholic acid

from chenodeoxycholic acid:

  • glycochenodeoxycholic acid
  • taurochenodeoxycholic acid
24
Q

Describe the bile acid/salt pathway

A

1* acid–> 1* conugated acid (COOH) and some bile salt (COO-)–> GB–> duodenum (mainly salt)

  • bacteria deconjugate salts to 1* and 2* bile acids–> absorbed by ILEUM–> either excreted in feces or recycled to liver via portal vein
25
Describe the mechanism of cholesterol-lowering drugs
non-absorbable bile acid binding resins (cholestyramine) INCREASES excretion of bile acids (where normally 95% recycled)--> increases rate of bile acid synthesis and induction of 7alpha hydroxylase--> depletes liver cholesterol pool--> increases hepatic uptake of LDL--> LOWERS PLASMA CHOLESTEROL
26
What are gallstones composed of?
crystals of bile supersaturated with cholesterol
27
How are gallstones formed?
insufficient secretion of bile salts or phospholipids into GB OR excess cholesterol secretion into bile
28
What does chronic cholelithiasis cause?
Malabsorption syndromes (steatorrhea), decreased fat-soluble vitamins
29
Where are metabolites?
components made in the body
30
What are xenobiotics?
ingested materials that have no nutritional value, can be toxic --> pharm, drugs, additives in food
31
Briefly describe the inactivation of xenobiotics
Phase I increases polarity, Phase II conjugated functional groups for safe excretion
32
What is required in Phase I of the inactivation of xenobiotics?
Cytochrome P450
33
Describe Phase I of xenobioitic inactivation
Reduction Oxidation Hydroxylation Hydrolysis xenobiotic--> 1* metabolite
34
Describe Phase II of xenobiotic inactivation
Conjugation Sulfonation Methylation Glucuronidation 1* metabolite--> 2* metabolite--> excretion
35
Describe drug metabolism in liver
increased hydropoilicity corresponds to ability to be excreted - metabolites are normally less active vs drug parent - enzymes have low substrate specificity (can bind to variety of different drugs)
36
What is a prodrug?
A drug that is inactivated when ingested and becomes activated in the body (opposite for metabolites)
37
Which CYP 450 enzymes are involved in phase I of detox pathway?
1, 2, 3
38
How do CYP work?
CYP binds drug with Fe3+--> CYPR releases NADP+ when converting ferric to ferrous--> CYP is now bound to drug with Fe2+--> O2 now OH--> drug hydroxylated and released for phase II--> CYP bound to Fe3+
39
How are CYP enzymes inducible by their substrates in the detox pathway?
- if a drug inhibits CYP--> increases drug levels in plasma - ------------------> citrus juice - if a drug activates CYP--> decreases drug levels in plasma - --------------------> St John's Wart
40
Why can CYP be personalized in drug metabolism?
Many polymorphisms of CYP
41
What is an activator of CYP?
St John's Wart--- decrease drug plasma levels
42
What is an inhibitor of CYP?
Citrus Juice---- increase drug levels in plasma
43
What happens to hepatocytes and sinusoids in diseases of the liver?
Fenestrated BM replaed with increased density collagen between liver and endothelial cells--> increases stiffness and resistance to blood flow through liver--> increases sinusoidal pressure--> decreases free exchange between liver and blood-->PORTAL HTN
44
What is portal HTN?
In diseases of the liver, increased collaged causes fibrosis in the membrane and increases resistance of blood flow in the liver--> increases sinusoidal pressure which increases BP
45
Examples of blood tests to check liver function
Albumin ALT and AST prothrombin time bilirubin, urea, glucose, TAG, cholesterol, alkaline phosphatase
46
Which liver test is more sensitive and why?
ALT, it is cytosolic
47
What happens when there is not enough albumin in blood?
Edema (loss of plasma protein oncotic pressure)
48
What are the normal functions of ALT and AST
transaminases, convert amino acids to keto acids in liver ---SHOULD NOT BE IN BLOOD
49
Does glycine or taurine have the lowest pKA?
Taurine--> better detergent effect
50
Where are secondary bile acids formed?
in intestines--> most recycled via enterohepatic circulation
51
What forces the liver to make new bile acids and prevents recycling?
Bile acid binding resins-->lower plasma cholesterol
52
What are the "F"s of cholelithiasis?
Fat, Fourty, Fair, Female, Fertile
53
What causes cholelithiasis?
excess cholesterol in blood-->gallstones

GIGU (37 decks)

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