Lipids (1) Flashcards

1
Q

What are lipids?

A

Fatty or oily compounds soluble in organic solvents, including lipoproteins, cholesterol, apolipoproteins, and phospholipids.

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2
Q

What are lipoproteins?

A

Complex compounds with a central hydrophobic core containing cholesterol esters and triglycerides, surrounded by free cholesterol, phospholipids, and apolipoproteins.

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3
Q

How are lipoproteins classified?

A

Based on size, lipid composition, and apolipoprotein type, including Chylomicrons, VLDL, IDL, LDL, HDL, and Lp(a).

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4
Q

What is the function of apolipoproteins?

A

They facilitate the carriage of lipids and cholesterol in the blood, serve as ligands for receptors, guide lipoprotein formation, and activate or inhibit enzymes.

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5
Q

What are the two major metabolic pathways of lipoproteins?

A

Endogenous (synthesis by the liver) and exogenous (from diet).

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6
Q

What begins the endogenous lipoprotein pathway?

A

Formation of VLDL in the liver.

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7
Q

What happens to triglycerides in the endogenous pathway?

A

Lipoprotein lipase metabolizes them to form free fatty acids and IDL.

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8
Q

What is a key function of HDL in cholesterol transport?

A

It transports cholesterol directly to the liver or indirectly transfers it to VLDL or LDL.

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9
Q

What initiates the exogenous lipoprotein pathway?

A

Incorporation of dietary lipids into chylomicrons in the intestine.

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10
Q

What are the pro-atherogenic lipoproteins?

A

Chylomicron remnants, VLDL, IDL, LDL, and Lp(a).

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11
Q

What is the primary risk factor for atherosclerosis?

A

High levels of LDL and apolipoprotein B (apoB100).

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12
Q

What is atherogenesis?

A

The process of atherosclerotic plaque formation, a major cause of coronary artery heart disease.

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13
Q

Which immune cells are involved in atherogenesis?

A

T and B cells, monocytes, and macrophages.

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14
Q

What does chronic inflammation lead to in atherosclerosis?

A

Formation of a necrotic core made up of dead smooth muscle cells and macrophages.

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15
Q

What is Lp(a)?

A

An independent risk factor for atherothrombotic events, consisting of an LDL particle linked to apo(a).

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16
Q

What is dyslipidemia?

A

An imbalance of lipids such as cholesterol, LDL, triglycerides, and HDL.

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17
Q

What is hyperlipidemia?

A

A condition with elevated lipid levels in the body, often associated with high cholesterol.

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18
Q

What defines hyperlipidemia in terms of percentile levels?

A

LDL, total cholesterol, triglycerides above the 90th percentile or HDL below the 10th percentile.

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19
Q

What role does HDL cholesterol play?

A

It helps regulate cholesterol levels to prevent atherogenic imbalances.

20
Q

What is the effect of oxidation on lipoproteins?

A

The outer shell of lipoproteins is highly susceptible to oxidation by free radical species.

21
Q

What do statins inhibit?

A

The enzyme HMG-CoA reductase, which catalyzes the conversion of HMG-CoA to mevalonate.

22
Q

What is the primary therapeutic use of statins?

A

To reduce triglyceride levels and treat dyslipidemia.

23
Q

What do bile acid sequestrants (BAS) do?

A

Reduce plasma LDL cholesterol by interrupting entero-hepatic circulation of bile acids.

24
Q

What is the multifaceted effect of nicotinic acid (niacin) on lipoproteins?

A

Increases HDL cholesterol, decreases LDL cholesterol and triglycerides.

25
Fill in the blank: Elevated levels of LDL cholesterol increases the risk of developing _______.
atherosclerotic plaques.
26
True or False: HDL cholesterol is known as 'bad' cholesterol.
False.
27
What is HDL cholesterol known as?
The 'good' cholesterol ## Footnote HDL cholesterol absorbs cholesterol in the blood and carries it back to the liver for elimination.
28
What is the effect of elevated HDL cholesterol levels?
Reduces the risk for heart disease and stroke.
29
What effect does niacin have on lipoprotein(a)?
Reduces lipoprotein(a) by about 25%.
30
What are fibric acid derivatives also known as?
Fibrates.
31
How do fibrates affect blood triglyceride levels?
They attenuate levels by decreasing hepatic production of VLDL.
32
What is one benefit of fibrates concerning HDL cholesterol?
They enhance the production of apoA-I, increasing levels of higher HDL cholesterol.
33
What conditions are fibrates used to treat?
Primary hypercholesterolemia and mixed dyslipidemia.
34
What are some collateral effects of fibrates?
Gastrointestinal tract problems, increased hepatic transaminase activity, and myopathy.
35
Are fibrates recommended for use with statins?
No, they are not recommended for use together.
36
What is the primary function of ezetimibe?
Inhibits intestinal cholesterol absorption.
37
What is the most common use of ezetimibe?
To lower levels of LDL cholesterol.
38
What conditions is ezetimibe used to treat?
Primary hyperlipidemia, mixed hyperlipidemia, familial hypercholesterolemia (HoFH), and homozygous sitosterolemia.
39
What is LDL apheresis?
A technique that uses a machine to remove unwanted LDL cholesterol from the blood.
40
How frequently is LDL apheresis performed?
Every two to three weeks.
41
What is the effect of LDL apheresis on Lp(a)?
It is effective for lowering Lp(a) in individuals with elevated levels.
42
What do PCSK9 monoclonal antibodies do?
Significantly reduce Lp(a) by around 30% and LDL cholesterol by 30-50%.
43
What is mipomersen used to treat?
Homozygous familial hypercholesterolemia.
44
What is the mechanism of action of mipomersen?
Inhibits apolipoprotein B (apoB) synthesis.
45
What are some antioxidants that may reduce lipoprotein oxidative stress?
* Ascorbate (vitamin C) * Alpha-tocopherol (vitamin E) * Urate * Glutathione peroxidases * Peroxiredoxins * Catalase * Superoxide dismutase * Bilirubin.