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mnt prep > CVD > Flashcards

CVD Flashcards

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?

A

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

25
Q

What do fibrates do?

A

Increase transcription factor for apo-A and LPL.

Lowers TG (main purpose), lowers LDL, raise HDL

26
Q

What does Zetia do?

A

Used with statins

Stops absorption of cholesterol at brush border. Decreases cholesterol delivery from intestine to liver.

27
Q

What diseases do CVD include?

A

Hypertension, cerebrovascular disease, peripheral vascular disease, congestive heart failure or, coronary artery disease, congenital heart defects

28
Q

What cofactors does LPL need to break down TG into FA?

A

Insulin and C-two

29
Q

What is the consequence of CM are not having B48?

A

CMR cannot go back to liver

30
Q

What does B 48 represent? What does C2 represent?

A

B48 signals that CM is from enterocyte.

C-2 signals that it can work with LPL

31
Q

Where are the TG’s located when we take our TG measurement?

A

Not in the CMR because we are fasted.

In the TC, LDL, TG, and HDL.

32
Q

What does a high saturated fat diet cause?

A

Down regulation of apo-B 100 receptor. LDL stays in circulation longer

33
Q

Where does pancreatic lipase Cleave?

Where do lingual and gastric lipases cleave?

A

Sn-1 and Sn-3

Sn-3 only

34
Q

What stimulates Bile release?

Where is the main site of lipid digestion?

A

CCK

Duodenum with pancreatic lipase

35
Q

What does high TG usually elude to?

A

CII problem or LPL problem.

Too much VLDL.

36
Q

ATP III characteristics

A 
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
Q

ATP IV characteristics

A

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
Q

2 times to use “high-intensity” statins. (ATP IV)

A

Already has ASCVD (2nd prevention)
If LDL is over 190mg/dL due to genetics

Can expect LDL to lower by 50%

39
Q

2 times to use moderate intensity statin treatments. (ATP IV)

A

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
Q

What are the ATP IV lifestyle recommendations?

A

Dietary patterns (med, DASH, MyPlate, AHA)
Fats, Na, K
40 min PA 3-4 days per week
Weight loss and maintain

41
Q

What are ATP IV diet recs?

A

6-7% SFA

2400 Na but want 1500. (Goal to lower current by 1000)

42
Q

What are saturated fat and cholesterol recommendations based on TLC? Are they the same macronutrient distribution’s as the AMDR?

A

Less than 7% total kcals from SFA
Less than 200mg cholesterol per day
Different than AMDR because TLC is older

43
Q

What are the effects of saturated fat on lipid profile?

A

Increased LDL
Increased TC
Increased HDL

44
Q

What are the main sources of saturated fat’s? What is the most prevalent saturated fat?

A

Animal fats (dairy and meat), coconut and palm oils

Palmitic acid is 60% of what we eat.

45
Q

What’s the order of saturated fats from worst for raising LDL to least effective?

A 
Myristic acid (14:0)
Palmitic acid (16:0)
Lauric acid (12:0) 
Stearic acid (18:0)
46
Q

What are the daily cholesterol guidelines for ATP three, TLC, AHA, and DG?

A

Less than 200mg for ATP3 and TLC

Less than 300mg for AHA and DG

47
Q

What is the most prevalent MUFA?

A

Oleic acid (18:1 w-9)

48
Q

What effect do MUFA have on the lipid profile?

A

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
Q

What is the common name for MUFAs? What are examples of sources?

A

Omega-9 FAs

Olive, canola, peanut, rice, hazelnut, avocado

50
Q

What effect does PUFA have on the lipid profile?

A

Replace CHO- decrease LDL, increase HDL
Replace SFA- decreases LDL, HDL, and TC
Too much makes LDL oxidation cascade

51
Q

What is the common name for 18:2 w-6? What are some sources?

A

Omega-6’s
LA- linoleic acid

Veggie oils: corn, safflower, soybean, sunflower

52
Q

What is the common name for 18:3 w-3? What are the best sources?

A

Omega 3 FA
ALA- linolenic acid

Fish oils, walnuts, egg lands best eggs, flax seeds

53
Q

What is the effect of omega 3 FAs on lipid profile?

A

Decreases TG!!!!!
Increases LDL
Decrease blood clot time and decrease BP

54
Q

What source of fat is soybean oil and what can it be modified to?

A

It is linoleic acid (omega6) but can be GMO to stearidonic acid (18:4 w-3)

55
Q

What effect does TFA have on lipid profile?

A

Increase LDL as much as SFA

56
Q

What effect does alcohol have on lipid profile?

A

According to ATP3, moderate levels increase HDL, increase TG, and don’t change LDL

57
Q

What is linoleic converted into (18:2 w-6)? What bodily effects does it have?

A

Made into aracadonic acid (20:4 w-6 or ARA)

Pro-inflame and pro-coagulant

58
Q

What enzyme do both LA and ALA compete for?

A

Delta-6 desaturase

59
Q

What is ALA converted into (18:3 w-3)? What bodily effects do these have?

A

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)

mnt prep (27 decks)

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