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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
mechanism of lipid metabolism endogenous
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
26
Liver regulates ___ of LDL-C
steady stage concentration of LDL-C
27
___ regulates the steady state concentration of LDL-C
Liver
28
mechanism of reverse cholesterol transport
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
who cares about elevated cholesterol biological effect
LDL leads to atherosclerosis
30
who cares about elevated cholesterol epidemiology
high LDL and higher total cholesterol assoc with incr risk of CAD (curvilinear))
31
who cares about elevated cholesterol randomized trials
lower LDL, decr heart disease events and death
32
can we reduce CVD events by reducing cholesterol
yes people at higher risk have greater benefits (2ndary prevention for people already with MI and people with already high cholesterol)
33
what is central to initiation and progression of atherosclerosis
atherogenic liporoproteins LDL, VLDL, IDL, remannts
34
what are atherogenic lipoproteins
LDL VLDL IDL remannts
35
when does atherosclerosis begin
slow progressive start at YOUNG AGE
36
how does cholesterol lowering reduce CV events?
stabilizes plaques b/c acute events occur in unstable plaque
37
AVERT how does aggressive lipid lowering compare to angioplasty
STATIN better at reducing ischemic events than angioplasty after 18 months from baseline LDL 140-150
38
how do statins help stabilize plaques
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
what is normal screening measure for cholesterol
COMPLETE LIPOPROTEIN PROFILE AFTER 8-12 HR FAST every 5 yr after 20 y/o
40
what does complete lipoprotein profile measure?
1) total cholesterol 2) HDL 3) triglycerides
41
how do you calculate LDL in fasted state?
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
majority of CHD occurs with ___ cholesterol
average = 130 mg/dL
43
CHD mostly occurs with average cholesterol but can occur with ___ cholesterol
LOW
44
NCEP ATP III LDL -C goal for
LDL < 160
45
NCEP ATP III LDL -C goal for 2+ factors
< 130
46
NCEP ATP III CAD or CAD risk equiv >20% or diabetes
<70 for HIGH RISK
47
CVD risk factors
1) smoking 2) HTN 3) Low HDL-C < 55 female < 65 4) FHx premature CHD 5) Age male > 45 female > 55
48
new 2013 guidelines on cholesterol
study doesn't support LDL goals but supports treating patients with statins at high risk
49
what are the 4 major statin benefit groups
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
things to treat cholesterol to decr ASCVD risk
1) heart healthy diets - 5-6% sat fat and low trans - decr sodium with HTN 2) exercise 3) no tobacco 4) healthy weight
51
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
dyslipidemia + Age + FHx + smoker + Low HDL-C overweight elev triglycerides sedentary
52
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
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
what is severe hypertriglyceridemia assoc with
acute pancreatitis
54
what is a cause of acute pancreatitis
severe hypertriglyceridemia
55
what is moderate hypertriglyceridemia assoc with
1) risk for ASCVD (unclear if lower triglyceride beneficial though) 2) insulin resistance 3) metabolic syndrome 4) type 2 diabetes
56
biological effect of HDL-C
removes cholesterol from periphery anti-oxidant anti-inflamm
57
does HDL incr affect ASCVD events/death
NO EVIDENCE THAT INCR HDL IS BENEFICIAL
58
___ HDL assoc with incr ASCVD
Low
59
mechanism of chylomicron
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
mechanism of VLDL
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
mechanism of LDL
1) LDL binds to liver via apoB-100 or apoE | 2) LDL absorbed via endocytosis and hydrolyzed --> release cholesterol
62
mechanism of HDL
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
mechanism of CETP
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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