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GI Exam #2 > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

Liver endothelial cells function

A

Allow for exchange of material between the liver and blood through fenestrations in the PM.

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2
Q

Kupffer cells function

A

Macrophages that protect the liver.

High degree of lysosomes.

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3
Q

Hepatic stellate cells function

A

Serve as a storage site for vitamin A and other lipids.

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4
Q

Pit cells function

A

NK cells of the liver.

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5
Q

Cholangiocytes function

A

Line bile duct. Control bile flow rate and bile pH.

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6
Q

Describe the liver’s unique cicrculation

A

It gets blood from enteric circulataion (portal v.) and from periphery (hepatic a.).
Low portal BP.

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7
Q

What allows the liver to have increased access to the blood?

A

No BM and no tight junctions between hepatocytes and endothelial cells.

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8
Q

How many CoAs (2C) make 1 IPP (5C)?

A

3

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9
Q

IPP can go on to make (3):

A

Steroids
Lipid-soluble vitamins
Prenyl groups (ubiquinone)

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10
Q

How can we generate acetyl CoA? (3)

How is it transported into the cytoplasm?

A

Decarboxylation of pyruvate.
Beta oxidation of FAs.
Breakdown of AAs.

Citrate shuttle.

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11
Q

___ units of IPP form a tetracyclic (4-ring) sterane ring

A

6 units

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12
Q

What is the molecular weight of an allicyclic compound:
How many carbons?
Where is the -OH group?

A

386 g/mol
27 C
-OH at C3

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13
Q

Where can cholesterol be found? (4)

A

PMs
Bile acids/salts
Vit D
Steroid Hs

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14
Q

Recommended daily intake of cholesterol:
Daily production of cholesterol:
Daily excretion of cholesterol:

A

< 300 mg
0.75-1.0 g
5% excreted, 95% reabsorbed

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15
Q

How is biosynthesis of cholesterol related to dietary intake?

A

Inversely proportional

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16
Q

How many acetyl CoA, ATP, NADPH and O2 to create 1 cholesterol?

A

Acetyl CoA - 18
ATP - 18
NADPH - 16
O2 - 4

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17
Q

Phase 1 of cholesterol synthesis:

A

Acetyl CoA —> (acetyl CoA acetyltransferase) acetoacetyl CoA —> (HMG synthase) HMG CoA —> (HMG CoA reductase) mevalonate —> IPP

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18
Q

What is the RLS of cholesterol synthesis?

A

HMG CoA reductase

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19
Q

Phase II of cholesterol synthesis (no enzymes)

A

6 IPP —> Squalene —> Lanosterol —> Cholesterol

20
Q

What is a concern for someone on long-term statin use?

A

Statin-mediated myopathy due to depletion of muscle levels of ubiquinone (CoQ 10).

21
Q

Where is the HMG CoA reductase enzyme located and what’s unique about it?

A

On the ER and has an 8-pass transmembrane component.

22
Q

What sort of inhibitor is a statin against HMG CoA reductase?

A

Competitive inhibitor

23
Q

What is the Ki for statins?

A

5-45 nM

24
Q

What is a direct inhibitor of cholesterol synthesis (HMG CoA reductase)?

A

FFAs
Bile acids
Oxysterols

25
Q

When is HMG CoA reductase active: Phospho or dephosphorylated?

A

Active in dephosphorylated form.

26
Q

Transcriptional Control of cholesterol synthesis

A

Binding of TFs to promoter on HMG CoA reductase gene increases mRNA levels.

27
Q

Mechanism of transcriptional control of cholesterol

A

SREBP-SCAP is usually bound to the ER membrane (to INSIG) when cholesterol is high. When cholesterol is low, it dissociates and goes to golgi where a part of SREBP is cleaved and enters the nucleus to act as a transcription factor to increase HMGR promoter.

28
Q

Antimycotics

A

Inhibit formation of ergosterol (required for PM of fungal cells).
An anti fungal drug.

29
Q

Antiestrogens

A

Prevents conversion of desmosterol to cholesterol.

30
Q

Epileptogenic drugs

A

Inhibit conversion of squalene to lanosterol and impairs cholesterol trafficking.

31
Q

What can antipsychotic drugs induce?

A

Dyslipidemia

32
Q

How is cholesterol eliminated?

A

No enzyme can degrade the sterane ring of cholesterol.

Cholesterol can be converted to bile acids or secreted in feces.

33
Q

What does it mean when we say that bile acids/salts are strong detergents?

A

They help to form micelles which increase SA of lipids increasing their exposure to lipases.

34
Q

What enzyme is responsible for producing chenodeoxycholic acid and colic acid from cholesterol?

A

7a-hydroxycholesterol

35
Q

Conjugation of bile acids

A

Chalice ACOI —> cholyl CoA —> taurocholic acid (add taurine) or glycocholic acid (add glycine)

36
Q

At what pKa is best for the detergent effect (high or low)?

A

Low pKa

37
Q

4 primary conjugated bile acids

A

Glycocholic acid
Taurocholic acid
Glycochenodeoxycholic acid
Taurochenodeoxycholic acid

38
Q

Secondary bile acids (2)

A 
Deoxycholic (from colic acid)
Lithocholic acid (from chenodeoxycholic acid)
39
Q

Cholestryamine

A

A resin that causes a large increase in excretion of bile acids.

40
Q

Effect of 7a-hydroxylase on bile acid synthesis

A

Increased by 7a-hydroxylase

41
Q

Overall, what is the effect of bile acid-binding resins on cholesterol?

A

It lowers plasma cholesterol levels and depletes liver cholesterol pool.

42
Q

What is in a gallstone?

A

Bile supersaturated w/ cholesterol.

43
Q

What can chronic disturbances in bile salt metabolism lead to?

A

Malabsorption (steatorrhea - fat in feces), deficiency of fat soluble vitamins.

44
Q

What is given to reduce cholesterol secretion into bile?

A

Ursodeoxycholic acid

45
Q

Phase I and phase II of detox in the liver

A

Phase I: increase polarity (reduction, oxidation, hydroxylation, hydrolysis)
Phase II: conjugation of functional groups (conjugation, sulfation, methylation, glucuronidation)

46
Q

Inhibiting CYP 450 does what to drug concentrations in plasma?

A

Increases drug conc.

GI Exam #2 (9 decks)

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