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Cardio Exam 2 > Disorders of Lipoprotein Metabolisms > Flashcards

Disorders of Lipoprotein Metabolisms Flashcards

1
Q

Define Lipoproteins

A

Large macromolecular complexes that transport hydrophobic lipisd

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2
Q

Function of lipoproteins

A

Absorption of dietary cholesterol, long-chain fatty acids and fat-soluble vitamins
Transport TGs, cholesterol and vitamins to tissues and cholesterol to the liver

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3
Q

FA are a component of

A

TGs

FA + glycerol = TGs

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4
Q

Cholesterol is produced in

A

the liver and the gut

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5
Q

Define Hydrophobic and give examples

A

Hard to solubulized; cannot enter aqueous fluids

- Cholesteryl esters and TGs

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6
Q

Define Hydrophillic and give examples

A

Easy to solubulized; on the surface of lipoproteins

- Proteins, cholesterol, phospholipids

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7
Q

Can molecules change?

A

Yes some hydrophilic molecules can become hydrophobic molecules

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8
Q

Define Cholesteryl esters

A

Are made from cholesterol and FAs via esterification

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9
Q

Define Hydrolysis

A

Enzyme = lipase

TGs –> FAs

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10
Q

Difference between HDL and LDL

A

HDL: tiny but very dense
LDL: lots of cholesterol and you want low levels in the blood

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11
Q

Clinical evidence says what about LDL

A

Increased levels of LDL leads to atherosclerosis and cardiovascular disease

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12
Q

Chylomicrons are

A

the largest and they are involved in absorption of dietary lipids and carrying the lipids from the gut to other areas

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13
Q

Chylmicron levels

A

Increase after meals

Are almost gone after 24 hours of fasting

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14
Q

Chylomicrons and VLDL carry

A

TGs

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15
Q

Cholesteryl esters, HDL and LDL carry

A

cholesterol

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16
Q

Define Apolipoproteins

A

Act as cofactors in certain chemical reactions

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17
Q

Apo E is

A

the ligand for cell surface receptors

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18
Q

Apo C does what?

A

Activates enzymes important in lipoprotein metabolism

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19
Q

Apo B special property

A

Other apoproteins can exchange lipids and proteins between each other but ApoB cannot

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20
Q

Define Micelles formation

A

Dietary TGs are hydrolyzed by lipases within the intestinal lumen and emulsified with bile acids to form micelles

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21
Q

What is absorbed in the proximal small intestine?

A

Cholesterol, FAs and fat-soluble vitamins

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22
Q

How are chylomicrons made

A

Long chain FAs are incorporated into TGs and packaged with apoB 48, cholesteryl esters, phospholipids and cholesterol to form chylomicrons

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23
Q

Nascent chylomicrons encounter _____ which does ________?

A 
Lipoprotein lipase (LPL)
Hydrolyzes the TGs to FAs and releases the FAs which are taken to be used as energy or stored as TGs
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24
Q

ApoC II does what and comes from where?

A

Transferred to chylomicrons from HDL and acts a a cofactor for LPL

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25
Q

How is a chylomicron remnant created?

A

The chylomicron particle progressively shrinks in size as the hydrophobic core is hydrolyzed and the hydrophilic lipids and apolipoproteins are transferred to HDL

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26
Q

How are chylomicron remnants removed?

A

Via the liver through a process that requires apoE as a ligand for receptors in the liver

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27
Q

Define endogenous pathway of lipoprotein metabolism

A

The secretion of apoB containing lipoproteins from the liver and the metabolism of TG-rich particles in the peripheral tissue

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28
Q

VLDL contain

A

apoB-100 and higher ratio of cholesterol to triglycerides

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29
Q

Where do the VLDL triglycerides come from

A

Esterification of long-chain fatty acids in the liver

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30
Q

MTP activity includeds

A

Microsomal TG Transfer Protein

Helps with the packaging of TGs with apoB-100 cholesteryl esters, phospholipids and VitE

31
Q

After secretion into the plasma, VLDL does what?

A

Acquires copies of apoE and apoC from HDL

32
Q

LPL + VLDL =

A

LPL hydrolyzes TGs of VLDL to form VLDL remnants

33
Q

VLDL remnants becomes

A

IDL after dissociating from LPL

34
Q

Is IDL removed or kept?

A

Some is removed via apoE in the liver

40-60% removed

35
Q

What is done to the IDL that is kept?

A

Remodeled to form LDL which includes very few TGs, lots of cholesterol and only apoB-100

36
Q

What enzymes is involved in IDL to LDL process?

A

hepatic lipase

37
Q

Cholesterol in LDL accounts for

A

1/2 of the plasma cholesterol in most individuals

38
Q

How is LDL cleared

A

via LDL receptor-mediated endocytosis in the liver

39
Q

Nascent HDL particles are synthesized where?

A

Intestines and liver

40
Q

What apolipoprotein is used to form discoidal HDL particles and how are these formed?

A

ApoA-I acquires phospholipids and cholesterol via the ABCA1

41
Q

What do discoidal HDL particles do?

A

Recruit more cholesterol which is esterfied to cholesteryl esters and moved to the core of HDL

42
Q

What enzymes esterifies HDL cholesterol to cholesteryl esters?

A

Lecithin-cholesterol acyltransferase (LCAT)

43
Q

What happens as HDL adds more cholesteryl esters?

A

It becomes more speherical and gains more apolipoproteins and lipids to the surface via chylomicrons and VLDL during lipolysis

44
Q

Cholesteryl esters can be transferred via apoB lipoproteins for TGs via?

A

Cholesteryl ester transfer protein

45
Q

What happens after the cholesteryl esters are transferred?

A

They are removed from circulation via LDL receptor mediated endocytosis

46
Q

HDL can be transferred via

A

direct take up by hepatocytes via scavenger receptor class B1 (SR-B1)

47
Q

SR-B1 does what?

A

Mediates the selective transfer of lipids to cells

48
Q

Chylomicrons have

A

lots of TGs which leads to a risk of pancreatitis

49
Q

LDL has

A

lots of choleserol which leads to high risk of coronary atherosclerosis

50
Q

Primary disorders of lipoproteins metabolism is and examples are?

A

Abnormalities in lipoproteins

- Familial hypercholestrolemia

51
Q

Secondary disorders of lipoprotein metabolism

A 
Obesity
DM
Thyroid, renal or liver disease
Alcohol
Estrogen
Lysosomal storage disease
Cushing's syndrome
Drugs
52
Q

Which is more common? Primary or secondary?

A

Secondary

53
Q

Pathogenesis of Familial hypercholesterolemia

A

Elevated plasma levels of LDL-C with normal TGs, tendon xanthomas and premature coronary atherosclerosis

54
Q

What causes the elevated LDL levels in FH?

A

Increased production of LDL from IDL (bc normally IDL is removed by LDL receptor mediated endocytosis and receptors are mutated) and a delayed removal of LDL from the blood

55
Q

Total Cholesterol levels in FH

A

500-1000 mg/dL (homo)
200-400 mg/dL (hetero)
So there is a direct link between the genes and the level of cholesterol

56
Q

Homozygotes have increased risk for?

A

Accelerated atherosclerosis

Symptomatic coronary athersclerosis before puberty

57
Q

FH symptoms

A

Can be atypical and sudden death is not uncommon

Don’t screen for mutations bc it is rare

58
Q

Homozygotes Diagnosis of FH

A

Family history
Skin biopsy to measure LDL receptor activity
Flow cytometry analysis of LDL receptor density on lymphocytes
DNA sequencing to find mutations

59
Q

Obesity as a secondary cause

A

Increased mass of adipose tissue
Increased amounts of FFA are deliverd to the liver form adipose tissue –> Increased VLDL
Typically have insulin resistance which promotes FA synthesis in the liver

60
Q

Adipose tissue in obese pts

A

Is metabolically active so lots of hormones produces plus increases regulatory function

61
Q

DM as a secondary cause

A

Type 1 = without hyperlipidemia if under controll

Ketoacidosis –> high TGs due to increased FFAs from adipose tissue

62
Q

Type II affects on lipids

A

High insulin due to insuline resistance leads to:

  • decreased LPL
  • Increased release of FAs
  • Increased synthesis of FAs
  • Increased production of VLDLS
  • Elevated TGs from LVLDL
  • Increased LDL
  • Decreased HDL
63
Q

Hypothyroidism as a secondary cause

A

Elevated LDL due to reduction in hepatic LDL receptor function and delayed clearance of LDL
Increased circulating IDL

64
Q

All patients presenting with elevated plasma levels of LDL ,IDL or TGs should be screened for _____.

A

hypothyroidism

65
Q

Nephrotic syndrome leads to

A

Hypercholesterolemia or hyperTGs

Increased production and decreased clearance of VLDLs with increased LDL production

66
Q

End Stage Renal Disease leads to

A

Mild hyperTGs due to accumulation of VLDLs and remnants in the circulation

67
Q

Renal transplants leads to

A

Increased lipid levels due to effect of the drugs for immunosuppresion and HMG-CoA reductase inhibitors have to be used cautiously

68
Q

Drugs that cause increased lipids?

A

Cyclosporine and glucocorticoids

69
Q

Hepatitis leads to

A

Increased VLDL and mild hyperTG

70
Q

Severe hepatitis and liver fialure leads to

A

decreased plasma cholesterol and TGs

71
Q

Cholestasis leads to

A

Hypercholesterolemia - free cholesterol coupled with phospholipids (LP-X) can deposit into skin folds and produce lesions (xanthomas)

72
Q

Alcohol can lead to

A

Increased plasma TGs
Increased secretion of VLDLs
- Regular daily consumption can increase HDL

73
Q

Screning for Lipoprotein Metabolism disorders

A

Age 20 + should have plasma levels of cholesterol, TGs, LDL, HDL measured after a 12 hour overnight fast

Cardio Exam 2 (10 decks)

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