Cholesterol and Atheroma Flashcards

1
Q

what are the 4 types of lipoproteins?

A

high density lipoprotein (apoA I and apoA II)
low density lipoprotein (apoB-100)
Very low density lipoprotein (apoB-100)
chylomicrons (apoB-48)

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2
Q

basic structure of lipoproteins

A

hydrophobic core

hydrophilic coat layered with apoproteins

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3
Q

where do ApoB containing lipoproteins deliver TAGs for ATP biogenesis?

A

Muscle cells

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4
Q

where do ApoB containing lipoproteins deliver TAGs for storage?

A

adipocytes

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5
Q

where are apoB-100 lipoproteins made?

A

liver

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6
Q

where are apoB-48 lipoproteins made?

A

intestine

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7
Q

what happens to some LDL in the artery?

A

it is oxidised into OXLDL

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8
Q

what do macrophages do to OXLDL?

A

convert it to cholesterol- laden foam cells

which forms fatty streaks

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9
Q

what occurs due to the presence of fatty streaks in the artery?

A

inflammatory substances are released from various cells and this causes proliferation of smooth muscle cells and causes the deposition of collagen

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10
Q

what does a atheromatous plaque contain?

A

fibrous cap and lipid core

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11
Q

where is HDL produced and where does it mature?

A

it is made in the liver (initially as ApoA-I), then matures in the plasma

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12
Q

what do simvastatin and atorvastatin act as?

A

competitive inhibitors of HMG-CoA reductase

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13
Q

why is HMG-CoA important in the synthesis of cholesterol?

A

it is important in the rate limiting step

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14
Q

give one example when statins are useless

A

if the patient has homozygous familial hypercholesterolaemia

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15
Q

what other positive effects do statins have?

A

decreased inflammation, reversal of endothelial dysfunction, decreased thrombosis, stabilisation of atherosclerotic plaques

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16
Q

how should patients take statins?

A

orally

at night

17
Q

what is the function of fibrates?

A

decrease in TGAs

first line in patients with very high TGA levels

18
Q

give an example of a drug that inhibits cholesterol absorption?

A

Ezatimbe

19
Q

pathogenesis of atheroma

A
  • Primary endothelial injury
  • Accumulation of Lipids and Macrophages
  • Migration of smooth muscle cells (from tunica media)
  • Increase in size and gets fibrous gap