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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
Q

Describe the mechanism of cholesterol-lowering drugs

A

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
Q

What are gallstones composed of?

A

crystals of bile supersaturated with cholesterol

27
Q

How are gallstones formed?

A

insufficient secretion of bile salts or phospholipids into GB OR excess cholesterol secretion into bile

28
Q

What does chronic cholelithiasis cause?

A

Malabsorption syndromes (steatorrhea), decreased fat-soluble vitamins

29
Q

Where are metabolites?

A

components made in the body

30
Q

What are xenobiotics?

A

ingested materials that have no nutritional value, can be toxic

–> pharm, drugs, additives in food

31
Q

Briefly describe the inactivation of xenobiotics

A

Phase I increases polarity, Phase II conjugated functional groups for safe excretion

32
Q

What is required in Phase I of the inactivation of xenobiotics?

A

Cytochrome P450

33
Q

Describe Phase I of xenobioitic inactivation

A

Reduction
Oxidation
Hydroxylation
Hydrolysis

xenobiotic–> 1* metabolite

34
Q

Describe Phase II of xenobiotic inactivation

A

Conjugation
Sulfonation
Methylation
Glucuronidation

1* metabolite–> 2* metabolite–> excretion

35
Q

Describe drug metabolism in liver

A

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
Q

What is a prodrug?

A

A drug that is inactivated when ingested and becomes activated in the body (opposite for metabolites)

37
Q

Which CYP 450 enzymes are involved in phase I of detox pathway?

A

1, 2, 3

38
Q

How do CYP work?

A

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
Q

How are CYP enzymes inducible by their substrates in the detox pathway?

A
  • 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
Q

Why can CYP be personalized in drug metabolism?

A

Many polymorphisms of CYP

41
Q

What is an activator of CYP?

A

St John’s Wart— decrease drug plasma levels

42
Q

What is an inhibitor of CYP?

A

Citrus Juice—- increase drug levels in plasma

43
Q

What happens to hepatocytes and sinusoids in diseases of the liver?

A

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
Q

What is portal HTN?

A

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
Q

Examples of blood tests to check liver function

A

Albumin
ALT and AST
prothrombin time
bilirubin, urea, glucose, TAG, cholesterol, alkaline phosphatase

46
Q

Which liver test is more sensitive and why?

A

ALT, it is cytosolic

47
Q

What happens when there is not enough albumin in blood?

A

Edema (loss of plasma protein oncotic pressure)

48
Q

What are the normal functions of ALT and AST

A

transaminases, convert amino acids to keto acids in liver

—SHOULD NOT BE IN BLOOD

49
Q

Does glycine or taurine have the lowest pKA?

A

Taurine–> better detergent effect

50
Q

Where are secondary bile acids formed?

A

in intestines–> most recycled via enterohepatic circulation

51
Q

What forces the liver to make new bile acids and prevents recycling?

A

Bile acid binding resins–>lower plasma cholesterol

52
Q

What are the “F”s of cholelithiasis?

A

Fat, Fourty, Fair, Female, Fertile

53
Q

What causes cholelithiasis?

A

excess cholesterol in blood–>gallstones

GIGU (37 decks)

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