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BSI Test 2 > Lecture 25 > Flashcards

Lecture 25 Flashcards

1
Q

Where does cholesterol in the body come from?

A

Diet and is synthesized in the liver.

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2
Q

Cholesterol biosynthesis happens where in the body?

A

Liver

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3
Q

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

A

Lipoproteins

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4
Q

Transports dietary cholesterol and triglycerides to various tissues in body

A

Chylomicrons

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5
Q

Transports mostly triglycerides from liver to adipose tissue

A

VLDL (very low density lipoprotein)

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6
Q

Remnant of VLDL after it delivers triglycerides to tissue; May be cleared from the blood via direct uptake by the liver or remodeled into LDL

A

IDL (intermediate density lipoprotein) also called VLDL remnant

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7
Q
  • Transports mostly cholesterol from liver to various tissues of body
  • Removed from circulation via LDL receptors in the liver
A

LDL (low density lipoprotein)

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8
Q

i. Transports cholesterol from peripheral tissues back to liver where it can be excreted via bile

A

HDL (High density lipoprotein)

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9
Q

This type of lipoprotein is antiatherogenic

A

HDL (High density lipoprotein)

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10
Q

Has:

  • antiinflammatory properties
  • antioxidant properties
  • inhibits LDL oxidation
  • inhibits monocyte migration into subendothelial space
  • Prothrombic properties
A

Antiatherogenic

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11
Q

Unhealthy blood cholesterol levels, high BP, smoking, insulin resistance, diabetes, hyperglycemia, obesity and physical inactivity are risk factors for what disease?

A

Atherosclerosis

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12
Q

This is the space between the basement membrane and the internal elastic lamina where fatty streaks develop

A

Subendothelial space

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13
Q

This type of injury allows LDL to infiltrate into subendothelial space of the artery

A

Endothelial artery

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14
Q

Oxidized LDL (oxLDL) in subendothelial space and altered expression (increase) of adhesion molecules on vessel wall due to endothelial injury cause this to happen.

A

Migration of monocytes and T-cells

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15
Q

When monocytes migrate into subendothelial space, they differentiate into _________ with scavenger receptors.

A

Macrophages

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16
Q

Macrophages endocytose ______ in the subendothelial space

A

oxLDL

17
Q

Foam cell formation and formation of fatty streaks in subendothelial space are casued by what?

A

oxLDL endocytosis by macrophages

18
Q

Release of _____ by foam cells and T cells in subendothelial space cause:

  • smooth muscle migration and proliferation (rapid reproduction)
  • formation of fibrous cap
  • preceipitation of calcium
A

Cytokines

19
Q

Once calcium preciptates into the subendothelial space, this is formed in the artery.

A

Hard plaque

20
Q

Plaque rupture can lead to ___ formation

A

Clot

21
Q

This is when a vessel ruptures due to the weakening of vessel wall leads to dilation or “ballooning”

A

Aneurysm

22
Q

This is turbulent blood flow in regions o curvature or bifurcation which can cause endothelial damage

A

Shear stress

23
Q

Smoking causes carbon monoxide injury to endothelium and _____ rate of LDL oxidation.

A

Increased

24
Q

Causes of endothelial injury

A

Shear stress, hypertension, smoking

25
Q

True or False? When LDL concentration is higher, the LDL molecule circulates longer before it is removed.

A

True

26
Q

The longer the LDL circulates, the the fraction of LDL that will enter the wall and become oxidized increases or decreases?

A

Increases

27
Q

This growth factor normally functions to protect vessels against injury

A

TGF-beta

28
Q

Does LDL enhance or suppress the activity of TGF beta?

A

Suppress

29
Q
  1. Increases vascular smooth muscle cell proliferation
  2. Increases macrophage engulfment of oxLDL
  3. Decreases endothelial nitric oxide production
  4. Increases the production of advanced glycation end-products (AGEs).
A

Role of hyperglycemia in atherosclerosis

30
Q

An ___ is a result of a chain of chemical reactions after an initial non-enzymatic glycation (sugar attachment) of a protein or lipid; this changes the structure and function of proteins and lipids

A

AGE - advanced glycation end-product

31
Q

-Promote cross-linking of proteins in arterial wall leading to trapping of oxLDL molecules

A

AGE

32
Q

-Alters ECM (extracellular matrix) proteins leading to a decrease in vascular compliance

A

AGE

33
Q

-Generate ROS (enhance neutrophil respiratory burst)

A

AGE

34
Q

-Stimulate inflammatory and pro-thrombotic signaling in endothelial cells, macrophages, and vascular smooth muscle cells

A

AGE

35
Q

Pharmacological therapy for atherosclerosis involving HMG CoA Reductase inhibitors

A

Statins

36
Q

Pharmacological therapy for atherosclerosis that a. lowers LDL by blocking intestinal absorption of cholesterol

A

Cholesterol absorption inhibitors

37
Q

Pharmacological therapy for atherosclerosis that decreases VLDL secretion by liver which lowers LDL and decreases catabolism of HDL leading to elevated levels of HDL

A

Niacin

38
Q

Pharmacological therapy for atherosclerosis that increases clearance of triglyceride rich lipoproteins (VLDL, chylomicrons) and increases HDL

A

Fibric acid derivatives

39
Q

Pharmacological therapy for atherosclerosis by lowering LDL by binding bile acids in GI tract leading to increased elimination in stool which forces liver to use cholesterol to synthesize more bile acids. Also, Increases LDL receptor expression in liver which enhances removal of LDL from circulation

A

Bile acid sequestrants

BSI Test 2 (12 decks)

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