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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
How is a chylomicron remnant created?
The chylomicron particle progressively shrinks in size as the hydrophobic core is hydrolyzed and the hydrophilic lipids and apolipoproteins are transferred to HDL
26
How are chylomicron remnants removed?
Via the liver through a process that requires apoE as a ligand for receptors in the liver
27
Define endogenous pathway of lipoprotein metabolism
The secretion of apoB containing lipoproteins from the liver and the metabolism of TG-rich particles in the peripheral tissue
28
VLDL contain
apoB-100 and higher ratio of cholesterol to triglycerides
29
Where do the VLDL triglycerides come from
Esterification of long-chain fatty acids in the liver
30
MTP activity includeds
Microsomal TG Transfer Protein | Helps with the packaging of TGs with apoB-100 cholesteryl esters, phospholipids and VitE
31
After secretion into the plasma, VLDL does what?
Acquires copies of apoE and apoC from HDL
32
LPL + VLDL =
LPL hydrolyzes TGs of VLDL to form VLDL remnants
33
VLDL remnants becomes
IDL after dissociating from LPL
34
Is IDL removed or kept?
Some is removed via apoE in the liver | 40-60% removed
35
What is done to the IDL that is kept?
Remodeled to form LDL which includes very few TGs, lots of cholesterol and only apoB-100
36
What enzymes is involved in IDL to LDL process?
hepatic lipase
37
Cholesterol in LDL accounts for
1/2 of the plasma cholesterol in most individuals
38
How is LDL cleared
via LDL receptor-mediated endocytosis in the liver
39
Nascent HDL particles are synthesized where?
Intestines and liver
40
What apolipoprotein is used to form discoidal HDL particles and how are these formed?
ApoA-I acquires phospholipids and cholesterol via the ABCA1
41
What do discoidal HDL particles do?
Recruit more cholesterol which is esterfied to cholesteryl esters and moved to the core of HDL
42
What enzymes esterifies HDL cholesterol to cholesteryl esters?
Lecithin-cholesterol acyltransferase (LCAT)
43
What happens as HDL adds more cholesteryl esters?
It becomes more speherical and gains more apolipoproteins and lipids to the surface via chylomicrons and VLDL during lipolysis
44
Cholesteryl esters can be transferred via apoB lipoproteins for TGs via?
Cholesteryl ester transfer protein
45
What happens after the cholesteryl esters are transferred?
They are removed from circulation via LDL receptor mediated endocytosis
46
HDL can be transferred via
direct take up by hepatocytes via scavenger receptor class B1 (SR-B1)
47
SR-B1 does what?
Mediates the selective transfer of lipids to cells
48
Chylomicrons have
lots of TGs which leads to a risk of pancreatitis
49
LDL has
lots of choleserol which leads to high risk of coronary atherosclerosis
50
Primary disorders of lipoproteins metabolism is and examples are?
Abnormalities in lipoproteins | - Familial hypercholestrolemia
51
Secondary disorders of lipoprotein metabolism
``` Obesity DM Thyroid, renal or liver disease Alcohol Estrogen Lysosomal storage disease Cushing's syndrome Drugs ```
52
Which is more common? Primary or secondary?
Secondary
53
Pathogenesis of Familial hypercholesterolemia
Elevated plasma levels of LDL-C with normal TGs, tendon xanthomas and premature coronary atherosclerosis
54
What causes the elevated LDL levels in FH?
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
Total Cholesterol levels in FH
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
Homozygotes have increased risk for?
Accelerated atherosclerosis | Symptomatic coronary athersclerosis before puberty
57
FH symptoms
Can be atypical and sudden death is not uncommon | Don't screen for mutations bc it is rare
58
Homozygotes Diagnosis of FH
Family history Skin biopsy to measure LDL receptor activity Flow cytometry analysis of LDL receptor density on lymphocytes DNA sequencing to find mutations
59
Obesity as a secondary cause
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
Adipose tissue in obese pts
Is metabolically active so lots of hormones produces plus increases regulatory function
61
DM as a secondary cause
Type 1 = without hyperlipidemia if under controll | Ketoacidosis --> high TGs due to increased FFAs from adipose tissue
62
Type II affects on lipids
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
Hypothyroidism as a secondary cause
Elevated LDL due to reduction in hepatic LDL receptor function and delayed clearance of LDL Increased circulating IDL
64
All patients presenting with elevated plasma levels of LDL ,IDL or TGs should be screened for _____.
hypothyroidism
65
Nephrotic syndrome leads to
Hypercholesterolemia or hyperTGs | Increased production and decreased clearance of VLDLs with increased LDL production
66
End Stage Renal Disease leads to
Mild hyperTGs due to accumulation of VLDLs and remnants in the circulation
67
Renal transplants leads to
Increased lipid levels due to effect of the drugs for immunosuppresion and HMG-CoA reductase inhibitors have to be used cautiously
68
Drugs that cause increased lipids?
Cyclosporine and glucocorticoids
69
Hepatitis leads to
Increased VLDL and mild hyperTG
70
Severe hepatitis and liver fialure leads to
decreased plasma cholesterol and TGs
71
Cholestasis leads to
Hypercholesterolemia - free cholesterol coupled with phospholipids (LP-X) can deposit into skin folds and produce lesions (xanthomas)
72
Alcohol can lead to
Increased plasma TGs Increased secretion of VLDLs - Regular daily consumption can increase HDL
73
Screning for Lipoprotein Metabolism disorders
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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