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Clin 1 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

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1
Q

What is the characteristic of apo E-2?

A

does not bind to LDL receptors = increase in VLDL remnants

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2
Q

What are the types of primary hyperlipoproteinemias and the main lipoproteins affected?

A 
I - chylomicrons
IIa - LDL
IIb - LDL - VLDL
III - B-LDL IDL + VLDL + LDL
IV - VLDL
V - VLDL + Chylomicrons
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3
Q

Which types of primary hyperlipoproteinemias have higher CVD risks?

A

IIb + III

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4
Q

What are xanthomas?

A

visible sign of hyperlipoproteinemia

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5
Q

What is the effect of alcohol on lipids profile?

A

it blocks acyl-CoA oxidation so it’s converted to fat

also increases HDL-C

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6
Q

TRUE or FALSE

Lp (a) is very atherogenic

A

true

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7
Q

What affects the variation in serum cholesterol?

A

serum cholesterol = saturated - polyunsaturated + dietary cholesterol
*saturated fats have a bigger impact on serum cholesterol than dietary cholesterol

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8
Q

What are the limitations of the predictive equations for serum cholesterol?

A
  • not all SFA are the same
  • assuming that MUFA and carbohydrates don’t have an effect
  • effect on total cholesterol might not be linear
  • total cholesterol not fractions
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9
Q

What were the findings of the seven countries study?

A

positive linear correlation btwn coronary deaths and serum cholesterol
outliar = crete = mediterranean diet but also other factors
* might have been financed by the sugar industry

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10
Q

TRUE or FALSE

a large decrease in dietary cholesterol (100 mg) results in a significant decrease in serum cholesterol

A

FALSE

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11
Q

What are the effect of dietary cholesterol on lipid metabolism?

A
  • impairs HDL clearance of cholesterol
  • reduce synthesis of LDL receptors
  • increase cholesterol in VLDL, VLDL remnants + chylomicrons
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12
Q

What should be the recommendation to the general population to reduce sat fats?

A

all processed foods, baked goods, pizza and ice cream

not necessarily meat and dairy

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13
Q

What are the medium chain SFAs?

A

caprylic, caproic

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14
Q

What is the intermediate chain SFAs?

A

lauric

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15
Q

What are the long chain SFAs?

A

Myristic
Palmitic
Stearic

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16
Q

Do SFAs from cheese and butter have the same effect?

A

no, cheese less increase in LDL compared to butter

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17
Q

Do SFAs from dairy and meat have the same effects?

A

no dairy products decrease CVD risks

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18
Q

what are dietary sources of linoleic acid?

A

safflower oil, soybean oil, corn oil, sunflower seed oil, walnut

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19
Q

By replacing SFAs with PUFAs what are the effects?

A

reduced CVD risks but not mortality

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20
Q

Is omega-3 supplementation useful to reduce CVD risk?

A

no

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21
Q

What decreases HDL-C?

A
  • high PUFAs intake
  • high sugar intake
  • obesity
  • male sex
  • steroids
  • smoking
  • DM
  • Some anti-hypertensive drugs
  • androgens
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22
Q

What increases HDL-C?

A
  • dietary cholesterol
  • saturated fatty acids
  • moderate alcohol intake
  • female sex
  • estrogens
  • long-term aerobic program
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23
Q

What are the drugs for DLP and CVD prevention?

A
  • HMG-CoA inhibitors
  • Cholesterol absorption inhibitors
  • Bile acid sequestrants
  • PCSK9 inhibitors
  • Fibrates
  • Nicotinic acid slow release
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24
Q

What is ezetimibe?

A

cholesterol absorption inhibitor

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25
What are cholestyramine and colestipol?
bile acid sequestrants | promote sterol excretion and increase LDL R
26
What are statins?
HMG-CoA inhibitors decreased VLDL synthesis and conversion to LDL increase VLDL clearance by increasing LDL R activity
27
What are gemifibril + fenofibrate?
fibrates decrease VLDL synthesis increase LPL activity
28
What are evolucumab and alirocumab?
PCSK9 inhibitors prevent LDL R catabolism only for ppl with familial DLP expensive
29
Why the Framingham Risk Scores is not available for 80 yo?
because there are not many benefits to change lifestyle and nutrition at 80 yo may lead to malnutrition
30
What is the link btw estrogen and CVD?
estrogen keeps the blood vessels flexible
31
Can estrogen be used as replacement therapy to prevent CVD?
NO
32
What are the changes related to lipid profile after menopause?
Increase in LDL-C Decrease or no change in HDL-C TGs increase BP increase
33
What are the signs and symptoms of MI?
- Chest pain - Dizziness, light-headed - Jaw, neck and back pain - Arm or shoulder pain - Nausea & vomiting - Shortness of breath
34
What are the types of ACS?
Stable Angina = plaque but no occlusion, vessel unable to dilate enough to allow adequate blood flow to myocardial demand Unstable Angina = partial occlusion NSTEMI = results in an injury and infract to the myocardium STEMI = complete occlusion
35
What are the biomarkers for MI?
- troponin (most specific) - CK MB (specific if no skeletal muscle damage) - LDH (lactate dehydrogenase)
36
What is a cardiac cath?
passing a catheter via arm, groin or neck for visualization, angiogram
37
What is angioplasty?
catheter to place a stent or a balloon
38
What is CABG?
Coronary Artery Bypass Graft By passing where artery is blocked Taking a vessel from leg and inserting to aorta and below the blockage Blood pass the blockage point Can have from 1 to 5 depending on the blockage points
39
What is the diet suggested post MI?
NPO and progress to clear liquids w/o caffeine | want to maximize blood flow to heart
40
What are the key points for secondary prevention?
- take meds - follow up with doctor - manage the risks - get support - participate to cardiac rehab (fitness + improving stress)
41
What is A-fib?
Atrial fibrillation = irregular heart beat = disrupts the blood flow to heart need anti-coagulant (warfarin) = need constant intake of vit K
42
What are the drugs to treat MI?
- Statins - Anti-platelets agent (ASA) - Beta-blockers, ACE-inhibitors - Nitrates - NTG - Anti-coagulants - Meds to protect stomach
43
What are the precautions to take when high TGs?
- avoid sugar - no alcohol - healthy weight - follow heart healthy guidelines
44
What are the considerations when taking warfarin?
- need consistent vit K intake - pay attention to vit A + E that can have an impact on clotting time - asians need lower dose
45
What are the complications of a stroke?
- weakness/paralysis - limited mobility - dysphagia
46
What are the signs of HF?
- coughing - ascites - edema in lower leg - pulmonary edema - heart hypertrophy - pleural effusion
47
What is the left ventricular ejection fraction?
blood pumped out/blood in chamber 50-70% is normal 41-49% is borderline < 40% is reduced
48
What are the consequences of left-side HF?
back up of blood in lungs = increase pressure = edema
49
What are the consequences of right-side HF?
back up of blood in vena cava and body = ascites and leg edema
50
Why the BP decrease, Heart Rate increase and respiration also increases when HF?
BP decreases bc lower blood volume pumped out so heart pumped more often to deliver the same amount of blood (increased HR) and increase respiration for more O to cells
51
What is BNP?
B-type natriuretic peptide used to diagnose HF because it is released when muscle fibers of left ventricle are stretched
52
What are the three main nutritional concerns for patients with HF?
- sodium intake - fluid intake - nutritional adequacy
53
What are the nutritional recommendations for HF?
- 2,000 mg of sodium - fluid restriction 1-2 L or 1-1.5 for more severe - limit alcohol or none if cause of HF
54
What are the effects of fibers on lipid profile?
decreased LDL-C and total cholesterol
55
What are the effects of high carbs on lipid profile?
decreased HDL-C | increased VLDL-TG (sucrose + fructose)
56
What are the effects of alcohol on lipid profile?
increase HDL-C may inhibit oxidation of lipoproteins inhibits acyl-CoA oxidation = increase TGs
57
What are the effects of soy prot on lipid profile?
no effect on HDL-C | decreased TG, LDL-C, cholesterol
58
What are the effects of antioxidants on lipid profile?
may inhibit LDL oxidation
59
What are the effects of phytosterol on lipid profile?
decreased LDL-C | increased cholesterol excretion
60
What are the effects of homocysteine on lipid profile?
increased CVD risk | linked with B6 and folate deficiency
61
What are the effects of nuts on lipid profile?
high intake = decreased CVD risk | moderate intake = decreased LDL-C
62
What are the most prevalent primary hyperlipoproteinemias?
IIb + IV
63
Which med is used for second line of treatment?
Ezetimibe (Cholesterol absorption inhibitor)
64
When does fibrates are used?
For familial hyerTG | Not recommended to add to statins
65
When does PSCK9 are used
To treat familial hypercholesterolemia with high LDL-C
66
When does nicotic acid is used?
HyperTG, hypercholesterolemia or hypoalphalipoproteinemia
67
What are the consequences of obesity on lipid metabolism?
1. excess flux of FAAs to the liver from excess cal intake + hormone-sensitive lipase activity (from insulin resistance) 2. decrease HDL from CETP activity (CE to VLDL and LDL) + uptake by the liver and increase clearance of ApoA = HDL catabolism 3. decrease in LDL receptors 4. increase in TGs from decrease lipolytic effect = more VLDL also from excess cal
68
What are the normal lipid values?
Cholesterol: <5.2 mmol/L HDL-C: 1.0-1.5 mmol/L (1.0 for men and 1.3 for women) LDL-C: <2.6 mmol/L TGs: <1.7 mmol/L
69
Which SFAs increases LDL-C?
palmitic, myristic, lauric
70
What is the effect of trans fat on lipid metabolism?
decreased HDL and increased LDL-C increased CETP activity decreased LDL-R activity clearance of ApoA and decreased catabolism of ApoB
71
What is the effect of cholesterol on lipid metabolism?
increased cholesterol in VLDL remnants and chylo
72
What is the effect of sat fat on lipid metabolism?
increase LDL-C and decreased size, increase HDL-C | decreased synthesis and activity of LDL-R
73
what are the effects of polyunsaturated fats on lipid metabolism?
linolenic acid: decreases TG for hyperlipidemic people decreased risk of mortality for ppl w/ CVD linoleic acid: may decrease LDL-C (passive bc replacing sat fats) but oxidative damage to LDL decreased HDL-C synthesis by the liver may decrease VLDL-C synthesis thus LDL-C

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