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SPR2015_WEEK4 > atherosclerosis and lipids > Flashcards

atherosclerosis and lipids Flashcards

1
Q

Death from CVD remains high

A

just as many people dying from CVD despite overall death per year same

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2
Q

in older population most deaths due to ___

A

CVD

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3
Q

in younger population most deaths due to ___

A

cancer tied with CVD

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4
Q

1 killer of women ___

A

CVD

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5
Q

atheroma define

A

plaque filled with LDL cholesterol

attracts smooth muscle to cover up lipid deposits

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6
Q

what causes ACS with atherosclerosis

A

plaque rupture attracting platelets

NOT STABLE PLAQUE

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7
Q

How does atherosclerosis affect coronary remodeling?

A

1) with minimal and mod CAD, compensatory expansion maintains constant lumen
2) severe CAD, expansion insufficient and lumen narrows

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8
Q

how does lumen appear in
minimal and mod CAD
vs.
severe CAD

A

minimal and mod CAD = constant lumen due to compensatory expansion

severe CAD = expansion overcome and lumen narrows

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9
Q

Which lesions progress to MI?

A

majority < 50% size of atherosclerosis plaque

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10
Q

Characteristics of plaques prone to rupture

vulnerable vs. stable

A

stable plaque
you have fibrous cap surrounding lipid core fully

vulnerable
lumen can be 70-90% open and fibrous cap overlying lipid core is much thinner

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11
Q

Steps in atherosclerotic process

A

1) LDL enter subendothelium
2) LDL oxidize/glycosylated
3) release of proinflamm cytokine, incr CAM, MCP-1, IL-8
4) monocytes recruited to clean up oxid LDL
5) monocytes phag LDL –> foam cell
6) foam cell + T-lymphocyte cause MMP secretion + activ tissue factor
7) plaque rupture with UNSTABLE LESIONS –> vessel thrombosis

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12
Q

what happens after release of proinflamm cytokines

A

monocytes recruited to clean up oxid LDL

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13
Q

what happens when monocytes phagocytosis LDL

A

become foam cell

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14
Q

what happens after foam cells form?

A

foam cell + t-lymphocyte cause MMP secretion + activ tissue factor

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15
Q

normal fxn of cholesterol

A

1) synthesis + repair of cell membrane and organelle

2) precursor of steroids (vitamin D)

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16
Q

normal fxn of triglycerides

A

1) fuel storage for muscle USE and adipose storage

nonpolar

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17
Q

normal fxn of HDL

A

removes cholesterol from LDL and VLDL and exchange with triglyceride to fill up more cholesterol in HDL so can be cleared by liver

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18
Q

what is generic lipoprotein structure

A

[cholesterol/lipids circulate in lipoproteins]

1) cholesterol/triglycerides = hydrophobic core
2) hydrophilic coat to circulate
3) apoproteins on exterior guide lipoproteins to right receptors for effect (define lipid particle)

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19
Q

define chylomicrons

A

return cholesterol to liver by enterohepatic circulation

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20
Q

what is major component of chylomicrons

A

triglycerides

most triglyceride so most nonpolar
least dense

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21
Q

what is major component of VLDL

A

triglycerides

then cholesterol

made by liver

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22
Q

what is major component of LDL

A

cholesterol

VLDL transformed into LDL
smaller, denser than VLDL

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23
Q

what is major component of HDL

A

protein

phospholipid

cholesterol

most dense
most polar

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24
Q

mechanism of lipid metabolism

exogenous

A

exogenous =

1) dietary fat
2) absorbed into intestine
3) triglyceride/cholesterol packaged into chylomicrons
4) as chylmoicrons dumped into blood stream, body wants fat
5) body sucks out fatty acid from chylomicron
6) LPL (lipoprotein lipase) extracts triglyceride from chylomicron
7) now smaller chylomicron and more cholesterol (REMNANT) –> MISSING C2
8) Remnant taken up by liver

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25
Q

mechanism of lipid metabolism

endogenous

A

1) don’t eat at night
2) liver makes VLDL (B100 important for clearance) to deliver triglycerides to body for fuel
3) LPL then removes triglycerides from VLDL to deliver fatty acids to tissue
4) creates IDL
5) more IDL extracted to create LDL (mostly cholesterol)- has B100 receptor for uptake by liver LDL receptor for clearance of LDL

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26
Q

Liver regulates ___ of LDL-C

A

steady stage concentration of LDL-C

27
Q

___ regulates the steady state concentration of LDL-C

A

Liver

28
Q

mechanism of reverse cholesterol transport

A

LCAT converts nascent HDL into mature HDL with more cholesterol

cholesterol accumulate in mature HDL and cleared via CETP to form VLDL/LDL

if can block CETP (can incr HDL)

29
Q

who cares about elevated cholesterol

biological effect

A

LDL leads to atherosclerosis

30
Q

who cares about elevated cholesterol

epidemiology

A

high LDL and higher total cholesterol assoc with incr risk of CAD
(curvilinear))

31
Q

who cares about elevated cholesterol

randomized trials

A

lower LDL, decr heart disease events and death

32
Q

can we reduce CVD events by reducing cholesterol

A

yes

people at higher risk have greater benefits (2ndary prevention for people already with MI and people with already high cholesterol)

33
Q

what is central to initiation and progression of atherosclerosis

A

atherogenic liporoproteins

LDL, VLDL, IDL, remannts

34
Q

what are atherogenic lipoproteins

A

LDL
VLDL
IDL
remannts

35
Q

when does atherosclerosis begin

A

slow progressive

start at YOUNG AGE

36
Q

how does cholesterol lowering reduce CV events?

A

stabilizes plaques
b/c
acute events occur in unstable plaque

37
Q

AVERT

how does aggressive lipid lowering compare to angioplasty

A

STATIN better at reducing ischemic events than angioplasty after 18 months

from baseline LDL 140-150

38
Q

how do statins help stabilize plaques

A

1) decr lipids in atheroma plaque core
2) decr inflamm cells (macs + T-lymph)
3) decr MMP + tissue factor activ (incr smooth muscle prolif)
4) decr plaque rupture
5) decr thormbogenesis

39
Q

what is normal screening measure for cholesterol

A

COMPLETE LIPOPROTEIN PROFILE AFTER 8-12 HR FAST every 5 yr after 20 y/o

40
Q

what does complete lipoprotein profile measure?

A

1) total cholesterol
2) HDL
3) triglycerides

41
Q

how do you calculate LDL in fasted state?

A

FRIEDEWALD (TG must be below 400 if higher then have chylomicrons circulating)

Total = LDL + HDL + VLDL 
VLDL = TG/5 when TG < 400

LDL = total cholest - HDL - (TG/5)

42
Q

majority of CHD occurs with ___ cholesterol

A

average = 130 mg/dL

43
Q

CHD mostly occurs with average cholesterol but can occur with ___ cholesterol

A

LOW

44
Q

NCEP ATP III

LDL -C goal for <or 1 risk factor

A

LDL < 160

45
Q

NCEP ATP III

LDL -C goal for 2+ factors

A

< 130

46
Q

NCEP ATP III

CAD or CAD risk equiv >20% or diabetes

A

<70 for HIGH RISK

47
Q

CVD risk factors

A

1) smoking
2) HTN

3) Low HDL-C < 55
female < 65

4) FHx premature CHD

5) Age
male > 45
female > 55

48
Q

new 2013 guidelines on cholesterol

A

study doesn’t support LDL goals

but supports treating patients with statins at high risk

49
Q

what are the 4 major statin benefit groups

A

1) known clinical ASCVD (MI, stroke, PAD)
2) LDL > 190 (usu genetics)
3) diabetes 1 or 2 (>40 y/o + LDL >70)
4) individuals who have 10 yr risk > 7.5% using risk calculator

50
Q

things to treat cholesterol to decr ASCVD risk

A

1) heart healthy diets
- 5-6% sat fat and low trans
- decr sodium with HTN

2) exercise
3) no tobacco
4) healthy weight

51
Q

what does he have?

Case 1 
55 y/o male overweight sedentary
- no other meds
- Fhx of premature CHD
- no exercise
- prior smoker
- drinks alcohol occassionally

BP 129/80, Wt 188, BMI 27, waist = 39
Glu 92
AST 12
ALT 16

A

dyslipidemia

+ Age
+ FHx
+ smoker
+ Low HDL-C

overweight
elev triglycerides
sedentary

52
Q

how do you treat?

Case 1 
55 y/o male overweight sedentary
- no other meds
- Fhx of premature CHD
- no exercise
- prior smoker
- drinks alcohol occassionally

BP 129/80, Wt 188, BMI 27, waist = 39
Glu 92
AST 12
ALT 16

A

hypercholesterolemia
No known ASCVD or diabetes and LDL high intensity due to family history)

Smoking = smoking cessation

Overweight = weight maintenance to weight loss

Sedentary = incr physical activity l

53
Q

what is severe hypertriglyceridemia assoc with

A

acute pancreatitis

54
Q

what is a cause of acute pancreatitis

A

severe hypertriglyceridemia

55
Q

what is moderate hypertriglyceridemia assoc with

A

1) risk for ASCVD (unclear if lower triglyceride beneficial though)
2) insulin resistance
3) metabolic syndrome
4) type 2 diabetes

56
Q

biological effect of HDL-C

A

removes cholesterol from periphery

anti-oxidant

anti-inflamm

57
Q

does HDL incr affect ASCVD events/death

A

NO EVIDENCE THAT INCR HDL IS BENEFICIAL

58
Q

___ HDL assoc with incr ASCVD

A

Low

59
Q

mechanism of chylomicron

A

1) eat fat
2) intestine release fat into blood as chylomicron
3) as chylomicron pass thru capillaries of muscle/fat, lipoprotein act on triglyceride –> form remnants and IDL
4) go to liver –> endocytosis of chylomicron remnants
5) hydrolized to release fatty acid for energy and cholesterol into VLDL pool

60
Q

mechanism of VLDL

A

1) triglyceride + cholesterol + apoB-100 into VLDL
2) nascent VLDL released into blood
3) apoC-11 receptor on VLDL activ lipoprotein lipase –> hydrolyze VLDL –> release fatty acids, remnants, IDL
4) abs by muscles, fat
5) remnants interact with apoE and aborb by liver and hydrolyzed
6) hydrolyzed remnants –> form LDL (high cholesterol)

61
Q

mechanism of LDL

A

1) LDL binds to liver via apoB-100 or apoE

2) LDL absorbed via endocytosis and hydrolyzed –> release cholesterol

62
Q

mechanism of HDL

A

1) HDL pick up cholesterol
2) LCAT convert fee cholesterol into ester sequestered in lipoprotein core –> form HDL
3) accum more cholest as circulate
4) HDL transport cholesterol to liver
5) HDL removed by HDL receptors (scavenger)

63
Q

mechanism of CETP

A

1) CETP exchanges triglycerides of VLDL for HDL
2) VLDL convert to LDL –> removed by LDL pathway
3) triglyceride in HDL not stable so degraded by liver and leave HDL
4) excrete into bile

SPR2015_WEEK4 (14 decks)

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