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BMS 150 Final > Lipoprotein Physiology and Atherosclerosis > Flashcards

Lipoprotein Physiology and Atherosclerosis Flashcards

1
Q

Cholesterol and triglycerides are transported through lymph and blood by a sub-cellular body known as a

A

lipoprotein

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2
Q

Lipids are transported through the body via lipoproteins along three major routes:

A
  • exogenous pathway
  • endogenous pathway
  • reverse cholesterol transport
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3
Q

what is the exogenous pathway

A

gathers lipids from the digestive tract and distributes them throughout the body after a meal

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4
Q

what is the endogenous pathway

A

the liver builds apoliproteins and secretes them into the bloodstream – also distributes lipids throughout the body

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5
Q

what is the reverse cholesterol transport

A

scavenges cholesterol from peripheral tissues and returns it to the liver

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6
Q

? are synthesized by the enterocyte

A

chylomicrons

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7
Q

what is inserted as a structural protein for the chylomicron during the exogenous pathway

A

ApoB-48

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8
Q

HDL particles transfer ? and ? to the chylomicrons

A

ApoC-II and ApoA-V

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9
Q

ApoC-II and ApoA-V allow the chylomicron to ?

A

interact with lipoprotein lipase (LPL)

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10
Q

LPL on the endothelial cells of capillaries do what to the chylomicrons?

A

cleaves TGs in chylomicrons to FFAs

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11
Q

after TGs are lost, the chylomicron becomes a ?

A

chylomicron remnant

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12
Q

HDL also transfers ? to the chylomicron so that the chylomicron remnant can be ?

A

ApoE
cleared by the liver

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13
Q

Chylomicron remnants are cleared by the liver via an ?

A

ApoE-dependent mechanism (LDL receptor)

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14
Q

what is the function of the exogenous pathway

A

carry dietary lipids to most cells but especially liver

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15
Q

what is the initial lipoprotein and intermediate lipoprotein of the exogenous pathway

A

chylomicron and chylomicron remnants

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16
Q

VLDL is synthesized by the ?

A

liver

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17
Q

VLDL contains what apoproteins

A

ApoC-II, ApoA-V and ApoB-100

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18
Q

As LPL “drains” triglycerides from VLDL, it becomes ? and then ?

A

IDL and LDL

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19
Q

IDL that loses TGs and becomes more and more cholesterol-rich becomes ?

A

LDL

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20
Q

Liver clears IDL and LDL via the ?

A

LDL receptor on hepatocytes

21
Q

If LDL is not cleared, it can become oxidized and becomes a major risk factor for the development of

A

atherosclerosis

22
Q

HDL is synthesized by ?

A

both hepatocytes and enterocytes

23
Q

what is LCAT?

A

Lecithin-cholesterol acyltransferase

24
Q

what does LCAT do?

A

aids the process of HDL receiving cholesterol by converting free cholesterol into cholesterol esters

25
Q

HDL can help remove cholesterol from peripheral tissues via what?

A

LCAT-ApoA-1-ABC interactions

26
Q

Once hepatocytes in the liver accumulate excess cholesterol, they downregulate the ?, which reduces ?

A

LDL receptor
LDL clearance

27
Q

reducing liver cholesterol content will result in ?

A

improved clearance of IDL and LDL

28
Q

what is atherosclerosis?

A

the development of atheromas in a wide range of large and medium-sized arteries

29
Q

atherosclerosis will lead to ?

A
  • endothelial injury
  • accumulation of lipoproteins in the vessel wall
30
Q

what is the LDL level for low risk of cardiac risk

A

< 2.59 mmol/L

31
Q

what is the LDL level for good level to not have cardiac risk

A

2.59-3.34 mmol/L

32
Q

what is the LDL level for borderline high of cardiac risk

A

3.37-4.11

33
Q

what is the LDL level for bad level to have cardiac risk

A

> 4.14

34
Q

what is the normal range of triglycerides in a human

A

0.45-1.71 mmol/L

35
Q

what is the HDL for low risk of cardiac risk

A

> 1.55 mmol/L

36
Q

what is the HDL level for high risk of cardiac risk

A

<1.04 mmol/L

37
Q

what is normal for total cholesterol in a human

A

< 5.2 mmol/L

38
Q

what is the goal when calculating TC:HDL ratio to calculate cardiac risk from atheroschlerosis?

A

<3.5

39
Q

framingham risk score for risk (low, intermediate, and high)

A

low risk : <10 %
intermediate risk 10-20%
high risk > 20%

40
Q

what is one of the best markers of systemic inflammation as it pertains to atherosclerosis

A

hsCRP

41
Q

what is a constellation of physical exam and laboratory findings that confer a higher risk for coronary heart disease, diabetes, fatty liver, cancer

A

the metabolic syndrome

42
Q

Atherosclerosis - acute plaque changes
Fall under three general categories which are?

A
  • rupture/fissuring
  • erosion/ulceration
  • hemorrhage into the atheroma
43
Q

plaque stability tends to be most strongly affected by?

A
  • hemodynamic disturbances (increases in blood pressure)
  • increased inflammation (disruption of the extracellular matrix of the atheroma)
  • Factors that increase clot formation (i.e. platelet activation)
44
Q

what is atheroembolism

A

Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli

45
Q

rupture, ulceration or erosion of these plaques may result in

A

stroke or MI

46
Q

what is a true aneurysm

A

an “intact” attenuated arterial wall or thinned ventricular wall of the heart

46
Q

what is an aneurysm

A

abnormal stretching (dilation or dilatation) in the wall of an artery, a vein, or the heart with a diameter that is at least 50% greater than normal

47
Q

what is a false aneurysm

A

defect in the vascular wall -> extravascular hematoma

48
Q

what is a dissection?

A

blood exits the lumen and enters the wall of the vessel

BMS 150 Final (17 decks)

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