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BMS150 Post-MT2 > Lipoprotein Physiology and Atherosclerosis > Flashcards

Lipoprotein Physiology and Atherosclerosis Flashcards

1
Q

How are cholesterol and TGs transported through lymph and blood?

A

By lipoproteins

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2
Q

Outer envelope of lipoprotein?

A

Phospholipid bilayer interspersed with apolipoproteins and un-esterified cholesterol

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3
Q

Inner portion of lipoprotein?

A

Cholesterol esters and TGs

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4
Q

Routes for lipid transport through the body? (3)

A
  1. Exogenous pathway
  2. Endogenous pathway
  3. Reverse cholesterol transport
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5
Q

Exogenous pathway?

A

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

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6
Q

Endogenous pathway?

A

Liver builds apolipoproteins and secretes them into the bloodstream

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7
Q

Reverse cholesterol transport?

A

Scavenges cholesterol from peripheral tissues and returns it to the liver

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8
Q

Initial lipoprotein of the exogenous pathway? Where is it synthesized?

A

Chylomicron - synthesized by enterocyte

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9
Q

What do chylomicrons contain? (4)

A
  • Rich in TGs
  • Retinyl esters
  • Phospholipids
  • Vitmain E
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10
Q

What is inserted as a structural protein for the chylomicron?

A

ApoB-48

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11
Q

Where are chylomicrons secreted to be transported to the bloodstream?

A

Into the lymph => travel to thoracic duct

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12
Q

What does HDL transfer to chylomicrons? Why?

A
  • ApoC-II and ApoA-V
  • Allows them to interact with lipoprotein lipase (LPL)
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13
Q

What does LPL do?

A

Cleaves TGs in chylomicrons to FFAs, which are taken up by peripheral tissues

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14
Q

What is the chylomicron after the TGs are lost?

A

Chylomicron remnant

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15
Q

What does HDL transfer to chylomicron so it can be cleared by the liver?

A

ApoE

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16
Q

Initial lipoprotein of endogenous pathway? Where is it synthesized?

A

VLDL - synthesized in the liver

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17
Q

What does VLDL contain? (4)

A
  • Mostly TGs
  • Phospholipids
  • Cholesteryl esters
  • Vitamin E
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18
Q

Why are ApoC-II and ApoA-V important for LPL activity in peripheral tissues?

A

As LPL drains TGs from VLDL, it becomes IDL and LDL

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19
Q

What is the significance of ApoB-100 in VLDL?

A

Major structural protein that allows clearance by the liver

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20
Q

How does the liver clear IDL and LDL?

A

Via the LDL receptor on hepatocytes

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21
Q

What happens if LDL is not cleared?

A

Becomes oxidized => major risk factor for atherosclerosis

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22
Q

Initial lipoprotein of reverse cholesterol transport? Where is it synthesized?

A

HDL - synthesized in both hepatocyte and enterocyte

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23
Q

What are the major structural proteins of HDL?

A

Apo-A1 and Apo-A2

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24
Q

What additional function does Apo-A1 have?

A

Allow HDL to receive cholesterol from the liver or peripheral tissues

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25
Q

What does the enzyme LCAT do?

A

Converts free cholesterol into cholesterol esters

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26
Q

What is the cholesterol-to-ApoA1 transporter?

A

ATP-binding cassette (ABC) protein

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27
Q

How can the liver remove cholesterol esters from HDL?

A

Scavenger receptor B1

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28
Q

Can the unloaded HDL recirculate?

A

Yes

29
Q

How can HDL exchange cholesterol between other lipoproteins (VLDL and LDL)?

A

Via cholesterol ester transfer protein (CETP)

30
Q

What happens when the hepatocytes accumulate excess cholesterol? (3)

A
  • Reduces LDL clearance
  • Secrete more cholesterol in bile
  • Produce less VLDL
31
Q

What does reducing liver cholesterol content result in?

A

Improved clearance of IDL and LDL

32
Q

What protein degrades/removes the LDL-R from the hepatocyte membrane?

A

PCSK9

33
Q

Development of atheromas in a wide range of large and medium-sized arteries?

A

Atherosclerosis

34
Q

What causes endothelial injury in atherosclerosis? (4)

A
  • Inflammation
  • HTN
  • Toxins
  • Hyperlipidemia
35
Q

What does endothelial injury cause in atherosclerosis? (3)

A
  • Increased vascular permeability
  • Leukocyte adhesion
  • Thrombosis
36
Q

What does accumulation of lipoproteins in the vessel wall cause? (2)

A
  • Increase free radical production
  • Activates macrophages
37
Q

Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into _______and _______

A

Macrophages and foam cells

38
Q

What happens while the LDL is bound weakly to the ECM of the intima for a variable period of time?

A

They become oxidized (ox-LDL) and are hidden from antioxidants in the plasma

39
Q

What may increase the binding of LDL to the matrix?

A

AGEs

40
Q

As the plaque grows and the overlying endothelium becomes more dysfunctional → ___________

A

Platelet adhesion

41
Q

Lipid-filled macrophages + smooth muscle cells = ________

A

Foam cells

42
Q

Emerging risk factors for atherosclerosis?

A
  • Lipoprotein (a)
  • Pro-thrombotic factors
  • Pro-inflammatory factors
43
Q

Primary care lipid measurements?

A

TC, LDL, HDL, TGs

44
Q

When do you screen with full fasting profile q1-3 year?

A
  • Males > 40 yo
  • Females > 50 yo in menopause
  • any age for adults with additional RF
45
Q

________ is linked to the development, enlargement, and rupture of atheromas

A

Inflammation

46
Q

What are the best markers for systemic inflammation pertaining to atherosclerosis?

A
  • hsCRP (best)
  • CRP
47
Q

What is hsCRP?

A

Independent risk factor for development of MI and stroke

48
Q

What does CRP do with regards to atherosclerosis?

A

Increased adhesion of leukocytes to atherosclerotic endothelium

49
Q

What is metabolic syndrome?

A

A combination of physical exam and lab findings conferring a higher risk for coronary heart disease, diabetes, fatty liver, and cancer

50
Q

Is metabolic syndrome common?

A

Common in NA - prev ranges from 20-30%

51
Q

How do you recognize metabolic syndrome?

A

Must have 3/5:
- Elevated fasting glucose
- BP > 130/85
- Hypertriglyceridemia
- Lowered HDL-C
- Increased waist circumferance

52
Q

Cardiac consequences of atherosclerosis?

A
  • Myocardial infarction (heart attack)
  • Heart failure
53
Q

Neurologic consequences of atherosclerosis?

A
  • Ischemic strokes
54
Q

Peripheral vascular disease consequences of atherosclerosis?

A
  • Impaired circulation to the extremities (esp. lower)
  • Impaired circulation to the kidneys due to renal artery stenosis
55
Q

Aneurysm formation as a consequence of atherosclerosis?

A
  • Usually in abdominal aorta
56
Q

Acute plaque changes fall under 3 categories…?

A
  • Rupture/fissuring = exposure of highly thrombogenic plaque constituents
  • Erosion/ulceration = exposure of the thrombogenic subendothelial basement membrane to blood
  • Hemorrhage into the atheroma = enlargement of atheroma
57
Q

What is plaque stability strongly affected by? (3)

A
  • Hemodynamic disturbances
  • Increased inflammation
  • Factors that increase clot formation
58
Q

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

A

Atheroembolism

59
Q

What can an atheroembolism cause?

A

Stroke or MI

60
Q

Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue → weakness resulting in aneurysmal dilation and potential rupture?

A

Aneurysm formation

61
Q

Often the thrombosis migrates “downstream” to cause more complete occlusion of a smaller vessel when this happens?

A

Rupture, ulceration, or erosion

62
Q

What will ruptures, ulcerations, or erosions cause?

A

Stroke or MI

63
Q

Rupture of the overlying fibrous cap, or of the thin walled vessels in the areas of neovascularization, can cause?

A

Hemorrhage into a plaque

64
Q

What might a hemorrhage into a plaque cause? (2)

A
  • Make aneurysm worse
  • Cause acute ischemic insult
65
Q

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?

A

Aneurysm

66
Q

True aneurysm?

A

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

67
Q

False aneurysm?

A

Defect in the vascular wall → extravascular hematoma

68
Q

Blood exits the lumen and enters the wall of the vessel?

A

Dissection

BMS150 Post-MT2 (17 decks)

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