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Lecture 25 Flashcards

1
Q

Cholesterol comes from diet and also is synthesized in the ____

A

liver.

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2
Q

What is the rate limiting enzyme in the synthesis of cholesterol?

A

HMG-CoA reductase

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3
Q

________ are spherical structures with an outer wall made of phospholipids, cholesterol, and proteins (apolipoproteins) which carry cholesterol and triglycerides (TAG) within the body.

A

Lipoproteins

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4
Q

What does acetyl-CoA and acetoacetyl-CoA combine to form?

A

HMG-CoA

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5
Q

HMG-CoA together with (2)NADPH and the rate limiting enzyme, forms ________.

A

Mevalonate

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6
Q

What are the next 3 products that are formed after Mevalonate and before Squalene?

A

Isopentenyl Pyrophosphate then Geranyl Pyrophosphate, then Farnesyl Pyrophosphate.

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7
Q

After Squalene is formed, what is the next molecule that is formed before Cholesterol?

A

Lanosterol

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8
Q

Heme A, dolichol, ubiquinone (Co-enzyme Q) and prenylated proteins are formed from ________

A

Farnesyl Pyrophosphate

note prenylated proteins can be formed from Geranyl Pyrophosphate

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9
Q

T or F? Bile salts and steroids are made from Cholesterol.

A

True

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10
Q

What are types of lipoproteins?

A 
Chylomicrons
VLDL (very low-density lipoprotein)
IDL (intermediate density lipoprotein)
LDL (low-density lipoprotein)
HDL (high-density lipoprotein)
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11
Q

Why are apoproteins import?

A

They have very specific functions in cell signaling.

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12
Q

Which lipoprotein transports dietary cholesterol and triglycerides from the GI tract to various tissues in the body?

A

Chylomicrons

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13
Q

Which lipoprotein transports mostly triglycerides from liver to adipose tissue?

A

VLDL

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14
Q

Which lipoprotein is a remnant of VLDL after it delivers triglycerides to tissue and may be cleared from the blood via direct uptake by the liver or remodeled into LDL?

A

IDL

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15
Q

Which lipoprotein transports mostly cholesterol from the liver to various tissues of the body?

A

LDL. (Removed from circulation via LDL receptors in the liver)

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16
Q

Which lipoprotein is antiantherogenic and transports cholesterol from peripheral tissues back to the liver where it can be excreted via bile?

A

HDL. (good cholesterol)

17
Q

What are the properties of antiatherogenic?

A
  1. Antiinflammatory properties
  2. Antioxidant properties
  3. Inhibits oxidation of LDL
  4. Inhibits monocyte migration into subendothelial space
  5. Prothrombolytic properties
18
Q

T or F? HDL takes excess cholesterol from the cells to the liver and then is taken in via receptor-mediated endocytosis into the liver.

A

False, only the uptake of VLDL, LDL, and cholesterol to cells are via receptor-mediated endocytosis.

19
Q

What are the risk factors of atherosclerosis?

A
  1. Unhealthy blood cholesterol levels
  2. High blood pressure
  3. Smoking
  4. Insulin resistance, diabetes, hyperglycemia
  5. Obesity
  6. Physical inactivity
20
Q

What is the subendothelial space where fatty streak develope?

A

It is the space between the basement membrane and the internal elastic lamina.

21
Q

How does atherosclerosis alter blood flow?

A
  1. Narrowing of artery can cause ischemia
  2. Plaque rupture can lead to clot formation (Obstruct flow of vessel or clot can break off and lodge in smaller vessels)
  3. Aneurysm
22
Q

What is an aneurysm?

A

The weakening of vessel wall leads to dilation or “ballooning” and can rupture.

23
Q

What causes the initial endothelial injury?

A

Shear stress
Hypertension
Smoking

24
Q

How can shear stress cause endothelial injury?

A

Blood flow is turbulent in regions of curvature or bifurcation
Turbulent flow can cause endothelial damage

25
Atherosclerosis is more like to happen in arteries than veins, why?
Arteries are less compliant and at higher pressure which increases the chances for endothelium damage.
26
How does hypertension cause endothelial injury?
Increases shear stress on vessel walls
27
How does smoking cause endothelial injury?
1. Carbon monoxide can injure endothelium | 2. Increases rate of LDL oxidation
28
Why are LDL in hypercholesterolemia bad?
1. The longer LDL circulates, the greater the fraction of LDL will enter wall and become oxidized 2. LDL suppresses activity of TGF-beta (transforming growth factor-beta) which normally functions to protect vessels against injury
29
The activity of _________ normally functions to protect vessels against injury.
TGF-beta (transforming growth factor-beta)
30
What are the roles of hyperglycemia in atherosclerosis?
1. Increases vascular smooth muscle cell proliferation (makes it stiff) 2. Increases macrophage engulfment of oxLDL 3. Decreases endothelial nitric oxide production 4. Increases the production of advanced glycation end-products (AGEs).
31
What are advanced glycation end-products (AGEs)?
An AGE is a result of a chain of chemical reactions after an initial non-enzymatic glycation (sugar attachment) of a protein or lipid. This process and formation of AGE changes the structure and function of proteins and lipids
32
How does the increase in the production of advanced glycation end-products (AGEs) contribute to atherosclerosis?
1. Promote cross-linking of proteins in arterial wall leading to trapping of oxLDL molecules 2. Alters ECM (extracellular matrix) proteins (making the stiffer) 3. AGEs generate reactive nitrogen species (ROS) 4. AGEs stimulate inflammatory and pro-thrombotic signaling in endothelial cells, macrophages, and vascular smooth muscle cells
33
How does a decrease in nitric oxide contribute to atherosclerosis?
The decrease in nitric oxide reduces vasodilation, making vessels less compliant and increase the shear stress.
34
How does statins treat atherosclerosis?
Statins are an HMG-CoA Reductase inhibitors, which will ultimately reduce the production of cholesterol.
35
How does cholesterol absorption inhibitors lower LDL?
Cholesterol absorption inhibitors lower LDL by blocking intestinal absorption of cholesterol.
36
How does Niacin work as therapy for hypercholesteremia?
1. It decreases triglyceride synthesis in the liver which decreases VLDL secretion by liver which lowers LDL production 2. Decreases catabolism of HDL leading to elevated levels of HDL
37
How does fibric acid derivatives work as therapy for hypercholesteremia?
It increases clearance of triglyceride rich lipoproteins (VLDL, chylomicrons) and increases HDL
38
How does bile acid sequestrants work as therapy for hypercholesteremia?
1. Lowers LDL by binding bile acids in GI tract leading to increased elimination in stool (forces liver to use cholesterol to synthesize more bile acids) 2. Increases LDL receptor expression in liver which enhances removal of LDL from circulation

BSI 2 (22 decks)

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