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MNT Prep > CVD > Flashcards

CVD Flashcards

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1
Q

What is the clinical and point of CAD or CHD?

A

Angina, MI, or sudden-death.

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2
Q

Define mortality.

A

The death rate.

For example, mortality has decreased with statins.

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3
Q

Find morbidity.

A

The amount of people living with the disease. The incidents.

For example, morbidity increases with statins.

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4
Q

What is arteriosclerosis?

A

When artery walls become calcified and lose elasticity and bloodflow decreases

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5
Q

What is atherosclerosis?

A

It is a type of arteriosclerosis. It is one fatty streaks become fibrous plaque and decreased blood flow.

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6
Q

What is a thrombus?

A

Aggregation of platelets and fibrin. Can obstruct a blood vessel.

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7
Q

What is caused by atherosclerosis in the peripheral circulation?

A

Gangrene or intermittent claudication.

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8
Q

Describe the process of oxidative modification of atherosclerosis.

A

Too many saturated fat’s causes LDL to stay in system and become oxidized. Inflammation then causes Macrophages to form foam cells and lipid and cholesterol accumulate to form plaque.

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9
Q

Which lipoproteins are made in the liver?

A

VLDL and HDL.

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10
Q

Which lipoprotein’s are made when their precursor drops off TG?

A

IDL, LDL

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11
Q

Which lipoprotein is made in the intestine?

A

Chylomicron

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12
Q

What lipoprotein’s are considered when triglycerides are high?

A

VLDL and CM.

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13
Q

High CM and high TG means _____ and what isn’t working?

A

Hyperchylomicronemia and C-2 and LPL

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14
Q

What does high LDL and normal TG mean? (High TC, too)

A

Hyperbetalipoproteinemia and the B-100 receptor on the liver is not working. Too much LDL stays in system.

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15
Q

How does the clinical and NCEP process differentiate between dyslipidemias?

A

High TC
High TG
Both

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16
Q

What would a familial heterozygous hypercholesterolemia pt suffer from?

A

Defective (B-100) LDL receptors so:
High TC
High LDL
Normal VLDL

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17
Q

What would a familial homozygous hypercholesterolemia pt suffer from?

A

LDL levels 4x normal levels

Usually MI in childhood.

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18
Q

What would a pt with familial combined hyperlipidemia (FCHL) suffer from?

A 
Too much apo B-100 so: 
High VLDL
High LDL
High TC 
High TG
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19
Q

What is familial dyslipidemia?

A

Rare
Type III
High TC and high TG

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20
Q

What is familial hypertriglyceridemia?

A

Type IV
Very common
Too much VLDL made in liver
High VLDL, high TG

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21
Q

What is familial lipoprotein lipase deficiency?

A

Rare
Less LPL action in all tissues
High VLDL high TG????
Needs to restrict dietary fat to avoid pancreatitis

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22
Q

What do statins do?

A

Blocks the HMG-CoA reductase pathway. Cholesterol production stopped

Lowers LDL and TG, raises HDL

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23
Q

What do bile acid sequestrates do?

A

Called resins
Bile is not recycled back to the liver from the chylomicron. More body cholesterol is needed to produce more bile.

Lowers LDL, raises HDL

Diet: Ca absorption lower, less fat and fat soluble vits absorbed.

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24
Q

What do nicotinic acids do?

Study These Flashcards
A

Best to increase HDL.
Decreases VLDL by less ffa mobilization.
Lowers LDL, lowers TG, higher HDL

25
What do fibrates do?
Increase transcription factor for apo-A and LPL. Lowers TG (main purpose), lowers LDL, raise HDL
26
What does Zetia do?
Used with statins | Stops absorption of cholesterol at brush border. Decreases cholesterol delivery from intestine to liver.
27
What diseases do CVD include?
Hypertension, cerebrovascular disease, peripheral vascular disease, congestive heart failure or, coronary artery disease, congenital heart defects
28
What cofactors does LPL need to break down TG into FA?
Insulin and C-two
29
What is the consequence of CM are not having B48?
CMR cannot go back to liver
30
What does B 48 represent? What does C2 represent?
B48 signals that CM is from enterocyte. | C-2 signals that it can work with LPL
31
Where are the TG's located when we take our TG measurement?
Not in the CMR because we are fasted. In the TC, LDL, TG, and HDL.
32
What does a high saturated fat diet cause?
Down regulation of apo-B 100 receptor. LDL stays in circulation longer
33
Where does pancreatic lipase Cleave? Where do lingual and gastric lipases cleave?
Sn-1 and Sn-3 Sn-3 only
34
What stimulates Bile release? Where is the main site of lipid digestion?
CCK Duodenum with pancreatic lipase
35
What does high TG usually elude to?
CII problem or LPL problem. Too much VLDL.
36
ATP III characteristics
``` 2001 Drugs if 10 year risk over 10% Seeks MI risk only Framingham risk assessment People even under 40 yo Based on LDL target levels ```
37
ATP IV characteristics
2013 Drugs if 10 yr risk factor is equal or above 7.5% Evaluates risk of MI, CVD, stroke and deaths (ASCVD) Not based on LDL target, based on statins intensity Only calculated risk for 40-79 yo
38
2 times to use "high-intensity" statins. (ATP IV)
Already has ASCVD (2nd prevention) If LDL is over 190mg/dL due to genetics Can expect LDL to lower by 50%
39
2 times to use moderate intensity statin treatments. (ATP IV)
Pt 40-75 with DM and LDL less than 190mg/dL | Pt 40-75 w/o DM but global 10-yr risk of over 7.5% (1 prevention)
40
What are the ATP IV lifestyle recommendations?
Dietary patterns (med, DASH, MyPlate, AHA) Fats, Na, K 40 min PA 3-4 days per week Weight loss and maintain
41
What are ATP IV diet recs?
6-7% SFA | 2400 Na but want 1500. (Goal to lower current by 1000)
42
What are saturated fat and cholesterol recommendations based on TLC? Are they the same macronutrient distribution's as the AMDR?
Less than 7% total kcals from SFA Less than 200mg cholesterol per day Different than AMDR because TLC is older
43
What are the effects of saturated fat on lipid profile?
Increased LDL Increased TC Increased HDL
44
What are the main sources of saturated fat's? What is the most prevalent saturated fat?
Animal fats (dairy and meat), coconut and palm oils Palmitic acid is 60% of what we eat.
45
What's the order of saturated fats from worst for raising LDL to least effective?
``` Myristic acid (14:0) Palmitic acid (16:0) Lauric acid (12:0) Stearic acid (18:0) ```
46
What are the daily cholesterol guidelines for ATP three, TLC, AHA, and DG?
Less than 200mg for ATP3 and TLC | Less than 300mg for AHA and DG
47
What is the most prevalent MUFA?
Oleic acid (18:1 w-9)
48
What effect do MUFA have on the lipid profile?
Sub for CHO- no change Sub for SFA- decreases TC, TG, and LDL (Will lower HDL if total fat kcals are less than 30%
49
What is the common name for MUFAs? What are examples of sources?
Omega-9 FAs | Olive, canola, peanut, rice, hazelnut, avocado
50
What effect does PUFA have on the lipid profile?
Replace CHO- decrease LDL, increase HDL Replace SFA- decreases LDL, HDL, and TC Too much makes LDL oxidation cascade
51
What is the common name for 18:2 w-6? What are some sources?
Omega-6's LA- linoleic acid Veggie oils: corn, safflower, soybean, sunflower
52
What is the common name for 18:3 w-3? What are the best sources?
Omega 3 FA ALA- linolenic acid Fish oils, walnuts, egg lands best eggs, flax seeds
53
What is the effect of omega 3 FAs on lipid profile?
Decreases TG!!!!! Increases LDL Decrease blood clot time and decrease BP
54
What source of fat is soybean oil and what can it be modified to?
It is linoleic acid (omega6) but can be GMO to stearidonic acid (18:4 w-3)
55
What effect does TFA have on lipid profile?
Increase LDL as much as SFA
56
What effect does alcohol have on lipid profile?
According to ATP3, moderate levels increase HDL, increase TG, and don't change LDL
57
What is linoleic converted into (18:2 w-6)? What bodily effects does it have?
Made into aracadonic acid (20:4 w-6 or ARA) Pro-inflame and pro-coagulant
58
What enzyme do both LA and ALA compete for?
Delta-6 desaturase
59
What is ALA converted into (18:3 w-3)? What bodily effects do these have?
Made into eicosopentanoic acid (EPA or 20:5 w-3) which is then made into docosahexanoic acid (DHA or 22:6w-3). These are anticoagulant and anti-inflammatory. (Beware of people taking fish oil and warfarin)

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