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Clinical Nutrition > Dyslipidemia and CVD- part 2 > Flashcards

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
Q

MUFA goal

A

no more than 20%

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26
Q

compared to PUFA, oleic acid __________ but compared to sat fat oleic does ______

A

does not lower HDL, does lower LDL ( beneficial to sub for sat fats)

27
Q

advantages of MUFA

A

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
Q

benefits of OMEGA 3 in hyperlipidemia patients?

A

decrease TG. and may reduce the risk of mortality in those with CVD

29
Q

effects of omega-3 on blood CH

A
  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
Q

fiber

A

decrease LDL and total CH

31
Q

excess carb effect on blood CH

A
  1. over production of VLDL-TG (especially if sucrose, fructose)
  2. decrease HDL
32
Q

alcohol effects on blood CH

A

elevates HDL

inhibits acylCoA oxidation in liver: avoid completely if hypertriglyceridemia

33
Q

soy protein

A

-reduce TC, LDL and TG
- no effect on HDL
( optimal level not established, 25g may reduce risk of heart disease)

34
Q

AO

A

-may inhibit LDL oxidation

35
Q

hyper-homocysteinemia

greater than 14 umol/L

A

increase risk of heart disease ( folate and B12 help )

36
Q

when would supplement folate

A

patient has high levels or family history of CVD and if B12 def is ruled out)

37
Q

1st target of treatment

A

lower LDL
1st step: <10% SFA and < 300mg CH
2nd step: <7 % SFA and < 200 mg CH , weight management and increase PA

38
Q

factors that increase HDL

A

sat fat, CH, alcohol, aerobic excersise, estrogens, female sex

39
Q

factors that decrease HDL levels

A

simple sugars, high PUFA, obesity, male sex, diabetes, smoking, anabolic steroids

40
Q

portfolio diet

A

low in sat fats high in phytosterols, soy and soluble fibers and almonds

41
Q

drug treatment for hyperlipidemia

A
  1. statins
  2. CH absorption inhibitors
  3. BAS
  4. PSCK9
  5. fibrates
  6. Nicotinic acid
42
Q

nicotinic acid

A

decrease VLDL synthesis and increase LPL activity

43
Q

average reduction for statins

A

1.8mmol/L LDL-C: 60% decrease in CVD risks

44
Q

side effects of statins

A

myalgia, myopathy, increased liver enzymes ( so need to monitor these annually)

45
Q

Ezetimibe

A

decrease intestinal absorption of CH

46
Q

second line recommendation after statins

A

ezetimibe

47
Q

side effects of ezetimibe

A

diarrhea, rash, fatigue, muscle weakness or pain

48
Q

BAS

A

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
Q

side effects of BAS

A

constipations ( big one)

decrease absorption of fat soluble vitamins, Ca, Fe, Zn, aMG

50
Q

PCSK9 inhibitors mechanism

A

PCSK( is an enzyme that helps degrade LDL receptors so that there are less of them, if inhibitor is introduced than less degradation

51
Q

PCSK9 recommended for

A

hypercholestrolemia and high LDL-C despite max statin use

52
Q

side effects of PCSK9

A

diarrhea, muscle or joint pain, bruising

53
Q

when are fibrates used?

A

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
Q

nicotinic acid

A

used for primary hypercholesterolemia and hyper tryglyceridemia and hypoalphalipproteinemia

55
Q

what do fibres do? what other medication has the same effect

A

decrease VLDL synth and enhance LPL activity

same as nicotinic acid

56
Q

statin mechanism

A

block CH synth and increase LDL receptor mediated removal

57
Q

fibrates side effects

A

GI reactions and muscle toxicity

58
Q

nicotinic acid side effects

A

** only 50-60% of ppl tolerate nicotinic acid !

GI distress and skin itching and hepatotoxicity and skin flushing

59
Q

contraindications ( reason to with-hold medication) of nicotinic acid

A

peptic ulcer, hepatic disease, gout, hyperuricemia

60
Q

contraindications for fibrates

A

hepatic or renal dysfunction, gallbladder disease

61
Q

some dietary goals for treatment of severe hyperlipidemia

A
  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
Q

dietary recommendations for dyslipidemia

A 
sat fat <7%
poly FA <10%
mono <20%
total lipids 20-35% 
CH < 200mg/d
carbs - 50--60%
protein 15%
sterols 2g/d
63
Q

TLC (dietary approach to dyslipidemia)

A

low sat fat and low CH, increase PA and weight management

Clinical Nutrition (25 decks)

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