Dyslipidemia and CVD- part 2 Flashcards

1
Q

lifestyle mod for dylipidemia

A
wieght management ( 2-7kg beneficial) and should higher HDL and decrease TG and LDL
- PA ( 1200-2200/week) decrease TG by 4-37%, increase HDL and decrease LDL
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2
Q

dominant factor for diet and serum CH

A

sat fat ( but limitations) - all sat fats not the same and predicts total CH only, not lipid fractions

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3
Q

dietar CH and serum CH

A

we have responders and non- responders (1/3)

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4
Q

100mg/d decrease in dietary CH results in?

A

0.05-0.2 mol/L decrease in total CH

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5
Q

how does dietary CH impact blood cholesterol ?

A

reduced activity of LDL receptors, bc getting CH from the diet and going to the liver, so slow down endogenous making of CH, more in circulation

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6
Q

independent mechanisms of dietary CH

A
  • decreased synth of hepatic LDL receptors,
  • more CH in CM–> more atherogenic
  • more CH in VLDL and LDL–> more atherogenic
  • interferes with ability of HDL to clear CH
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7
Q

high CH foods

A

shrimp, organ, heart, brain, veal, pork

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8
Q

total fat goal

A

25-35% total calories ( too low fat may actually decrease HDL)

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9
Q

excess sat fat intake on blood CH/lipoproteins

A

reduced activity of LDL receptors ( less transcription, alter PL composition (sat fat will link with PL), alter LDL itself (less binding)

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10
Q

goal for sat fat

A

less than 10%

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11
Q

what do sat fats also increase?

A

HDL alongside LDL ( so maybe the ratio isn’t so bad) but replace sat fat with MUFA and PUFA

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12
Q

when 5% of energy from sat fat is replaced with PUFA

A

10% reduction in CVD risk

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13
Q

replace sat fat with carbs?

A

no benefit on CVD

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14
Q

recommendation for sat fat in canada

A

no limit, instead focus on health balanced diet

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15
Q

which SFA increase blood LDL

A

Lauric ( but also increases HDL) myristic, palmitic

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16
Q

MCT effect on serum CH

A

no effect

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17
Q

SFA from dairy?

A

neutral effect, not same as SFA from meat

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18
Q

oils with high SFA

A

coconut oil, butter, palm, beef fat, cocoa butter

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19
Q

Trans FA

A

increase LDL (same as SFA) but also reduce size of LDL ( more atherogenic)

  • reduce HDL
  • may increase inflammation markers and endo damage
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20
Q

EPA and DHA come from

A

18:3w3

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21
Q

effects of omega-6 on blood CH

A
  1. passive LDL lowering effect ( removes the suppressing effect of SFA ) so increase clearance of LDL
  2. may decrease HDL formation ( rare)
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22
Q

goal for omega 6

A

5-10% calories - too much may cause inflammation

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23
Q

sources of omega 6

A

corn, sunflower, walnuts, soybean oils

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24
Q

mechanic of the effects of omega 6 on blood CH

A

inhibition of VLDL production–> less VLDL, less LDL and decrease formation of HDL ( if excess)

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25
MUFA goal
no more than 20%
26
compared to PUFA, oleic acid __________ but compared to sat fat oleic does ______
does not lower HDL, does lower LDL ( beneficial to sub for sat fats)
27
advantages of MUFA
doesn't decrease HDL as PUFAs and carbs do, less susebtable to oxidation as PUFA, don't increase TG as carbs do, don't increase cancer risk as PUFA do
28
benefits of OMEGA 3 in hyperlipidemia patients?
decrease TG. and may reduce the risk of mortality in those with CVD
29
effects of omega-3 on blood CH
1. reduce the amount of TG in VLDL 2. prevent coronary thrombosis ( delay proliferation of fibroblasts) 3. reduce plaque formation and growth as they reduce the adhesion molecules 4. don't technically lower LDL but replacing them with sat fat would lower
30
fiber
decrease LDL and total CH
31
excess carb effect on blood CH
1. over production of VLDL-TG (especially if sucrose, fructose) 2. decrease HDL
32
alcohol effects on blood CH
elevates HDL | inhibits acylCoA oxidation in liver: avoid completely if hypertriglyceridemia
33
soy protein
-reduce TC, LDL and TG - no effect on HDL ( optimal level not established, 25g may reduce risk of heart disease)
34
AO
-may inhibit LDL oxidation
35
hyper-homocysteinemia greater than 14 umol/L
increase risk of heart disease ( folate and B12 help )
36
when would supplement folate
patient has high levels or family history of CVD and if B12 def is ruled out)
37
1st target of treatment
lower LDL 1st step: <10% SFA and < 300mg CH 2nd step: <7 % SFA and < 200 mg CH , weight management and increase PA
38
factors that increase HDL
sat fat, CH, alcohol, aerobic excersise, estrogens, female sex
39
factors that decrease HDL levels
simple sugars, high PUFA, obesity, male sex, diabetes, smoking, anabolic steroids
40
portfolio diet
low in sat fats high in phytosterols, soy and soluble fibers and almonds
41
drug treatment for hyperlipidemia
1. statins 2. CH absorption inhibitors 3. BAS 4. PSCK9 5. fibrates 6. Nicotinic acid
42
nicotinic acid
decrease VLDL synthesis and increase LPL activity
43
average reduction for statins
1.8mmol/L LDL-C: 60% decrease in CVD risks
44
side effects of statins
myalgia, myopathy, increased liver enzymes ( so need to monitor these annually)
45
Ezetimibe
decrease intestinal absorption of CH
46
second line recommendation after statins
ezetimibe
47
side effects of ezetimibe
diarrhea, rash, fatigue, muscle weakness or pain
48
BAS
promote sterol excretion ( bind to bile acids in the GI tract so that they will not get reabsorbed) and increase LDL receptors so greater Clarence of VLDL and LDL ( lowers LDL)
49
side effects of BAS
constipations ( big one) | decrease absorption of fat soluble vitamins, Ca, Fe, Zn, aMG
50
PCSK9 inhibitors mechanism
PCSK( is an enzyme that helps degrade LDL receptors so that there are less of them, if inhibitor is introduced than less degradation
51
PCSK9 recommended for
hypercholestrolemia and high LDL-C despite max statin use
52
side effects of PCSK9
diarrhea, muscle or joint pain, bruising
53
when are fibrates used?
only for highly elevated TG it is very strong and will decrease TG by 40-50% ( max at 4 weeks) and increase HDL, however it may also increase LDL, it is not recommended in combo with stations for prevention when target has been reached
54
nicotinic acid
used for primary hypercholesterolemia and hyper tryglyceridemia and hypoalphalipproteinemia
55
what do fibres do? what other medication has the same effect
decrease VLDL synth and enhance LPL activity same as nicotinic acid
56
statin mechanism
block CH synth and increase LDL receptor mediated removal
57
fibrates side effects
GI reactions and muscle toxicity
58
nicotinic acid side effects
** only 50-60% of ppl tolerate nicotinic acid ! | GI distress and skin itching and hepatotoxicity and skin flushing
59
contraindications ( reason to with-hold medication) of nicotinic acid
peptic ulcer, hepatic disease, gout, hyperuricemia
60
contraindications for fibrates
hepatic or renal dysfunction, gallbladder disease
61
some dietary goals for treatment of severe hyperlipidemia
1. ideal body weight 2. decrease fat intake , sat fat ( if high cH) 3. high TG - limit alcohol, sugars, high carbs 4. decrease CH levels
62
dietary recommendations for dyslipidemia
``` sat fat <7% poly FA <10% mono <20% total lipids 20-35% CH < 200mg/d carbs - 50--60% protein 15% sterols 2g/d ```
63
TLC (dietary approach to dyslipidemia)
low sat fat and low CH, increase PA and weight management