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Endo > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

LCAT (lecithin cholesterol acyltransferase)

A
  • converts cholesterol into cholesterol esters
  • activated by Apo A
  • important for reverse cholesterol transport (HDL formation)
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2
Q

LPL (lipoprotein lipase)

A
  • hydrolyze the TG in CM and VLDL to glycerol and FFA
  • allow delivery of TG to peripheral tissue
  • activated by Apo C
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3
Q

HL (hepatic lipase)

A
  • hydrolyze TG to glycerol and FFA from CMR in liver
  • key way for liver to extract TG from lipoproteins
  • VLDL and IDL metabolism in liver
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4
Q

ABCA1

A
  • a cholesterol efflux protein

- transfers free cholesterol out of the cell for HDL formation in reverse cholesterol transfer

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5
Q

LDL receptor

A

binds to LDL and facilitates endocytosis

- dysfunction of absence of LDL receptor leads to familial hypercholesterolemia

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6
Q

HMG- CoA reductase

A

rate limiting step in de novo cholesterol syntesis (most cholesterol is produced in liver, not from diet)
- feedback inhibited by cholesterol

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7
Q

Cholesterol- 7-alpha-hydroxylase

A

rate limiting step in bile acid synthesis

  • stimulated by cholesterol
  • suppressed by bile acids
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8
Q

Chylomicrons

A

transport dietary TG and cholesterol from intestine to tissues

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9
Q

VLDL

A

transport TG from liver to tissues

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10
Q

IDL

A

remnant of VLDL that is converted to LDL

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11
Q

LDL

A

deliver cholesterol to peripheral tissues

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12
Q

HDL

A

reverse cholesterol transport

  • delivers cholesterol to liver from peripheral cells via SR-B on liver
  • shuttles Apo C and Apo E
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13
Q

drugs to treat low HDL

A

Fibrate

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14
Q

drugs to treat high LDL

A

statin & bile acid sequestrins (BAS)

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15
Q

How does Fibrate work?

A

promotes HDL formation by activating PPAR receptor and LXR/RXR receptors–> promotes ABCA1 expression in cell membrane–> increases cholesterol effluxed –> promotes reverse cholesterol transport and HDL formation

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16
Q

How does Statin work?

A

blocks de novo cholesterol production by:
statin decreases intracellular cholesterol –> removes suppression of LDL receptor –> receptor is free to move to plasma membrane surface –> LDL receptor on surface clears more plasma cholesterol

17
Q

how does BAS work?

A

BAS binds to bile acid in the intestine so it is secreted in feces–> enterohepatic recycling of bile acid no longer occurs –> intracellular cholesterol is recruited for bile acid synthesis –> frees up LDL receptor in intracellular space –> LDL receptor is free to move to plasma membrane surface –> LDL receptor on surface clears more plasma cholesterol

18
Q

Anti-inflammatory properties of HDL (3)

A
  1. reverse cholesterol transport to remove cholesterol esters from foam cells
  2. inhibit adhesion molecule expression by endothelial cells
  3. reduce oxidation of LDL particles in intima
19
Q

Pathways of homeostasis in Liver (4)

A
  1. disposal via bile acid synthesis (7-alpha-hydroxylase)
  2. storage of cholesterol as cholesterol esters (ACAT)
  3. de novo synthesis of cholesterol (HMG-CoA reductase)
  4. endocytosis of LDL (LDL receptor)
20
Q

MCP-1

A
  • expressed in endothelial cells

- activated by oxidized LDL and causes recruitment of monocytes from the blood

21
Q

foam cell

A

lipid laden macrophage

22
Q

fibrous cap

A

combo of lipid laden foam cells and extracellular matrix of smooth muscle cell that forms on vascular wall to cause atherosclerosis

23
Q

if low HDL where do you worry that cholesterol is being stored?

A

peripheral tissues

24
Q

Apo A

A
  • stimulates LCAT to convert free cholesterol to cholesterol esters
  • required for HDL formation
25
Q

What is risky level for total plasma cholesterol level?

A

> 200 mg/ml

26
Q

What is risky level for LDL cholesterol level?

A

> 100 mg/ml

27
Q

What is risky level for HDL cholesterol level?

A

< 45 mg/ml

28
Q

Apo B

A
  • required for formation and secretion of chylomicron and VLDL
  • binds to LDL receptor and is required for LDL endocytosis
29
Q

Apo C

A
  • activates LPL on endothelial cells to convert TG to FFA and glycerol
  • required for metabolism of CM and VLDL
30
Q

Apo E

A
  • mediates clearance of CMR and IDL by the liver

- ligand for receptor in liver that allows uptake

Endo (2 decks)

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