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Clinical nutrition > Dyslipidemia and Cardiovascular disease > Flashcards

Dyslipidemia and Cardiovascular disease Flashcards

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1
Q

why there was a decrease in mortality regarding CVD

A

improvements in control of CVD risk factors and medical management of patients with CVD

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2
Q

role of the cardiovascular system

A
  • regulate blood flow to tissues
  • thermoregulation
  • hormone transport
  • maintenance of fluid volume
  • regulation of pH
  • gas exchange
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3
Q

what are the major form of cardiovascular disease

A
  • hypertension
  • atherosclerosis
  • coronary heart disease
  • peripheral vascular disease (stroke, deep vein thrombosis)
  • congestive heart failure
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4
Q

what is atherosclerosis

A

it is the thickening of the blood vessel walls caused by the presence of atherosclerotic plaque therefore there is a restriction of blood flow

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5
Q

atherosclerosis is associated with

A
  • myocardial infarction
  • cerebrovascular accident (stroke, CVA)
  • peripheral vascular disease
  • coronary heart disease
  • congestive heart failure
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6
Q

is atherosclerosis symptomatic

A

no it is asymptomatic

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7
Q

how does an atherosclerotic plaque form

A
  1. there is an injury in the endothelium wall due to high blood pressure, chemicals etc
  2. there will have LDL that will enter and then more LDL will come (fatty streak), monocyte -> macrophage and they will die and form foam cells the foam cells will secrete signals that will call more monocyte and the cycle continue.
  3. a fatty streak thickens and form a plaque it will accumulate lipid, smooth muscle cells, connective tissue etc. The smooth muscle layer will cover all of this.
  4. The artery may expand to accommodate plaque. When this occur, the plaque that develops often contain a large lipid core with a thin fibrous covering and is vulnerable to rupture and thrombosis
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8
Q

what are some factors that damage the endothelial wall

A

high blood pressure
chemicals from tabacco
oxidized LDL
glycated proteins (diabetes)
low nitric acid
high angiotensin 2

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9
Q

what is the risk factor for atherosclerosis?

A

there is an additive effect
- family history
- age and sex (>65 years and men)
- genetic
- obesity (associated with dylispedimia, hypertension, physical inactivity, diabetes)
- dyslipidemia
- cigarette
- sleep apnea

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10
Q

what are the lipids that is made with more triglyceride? and cholesterol?

A

chylomicrons and VLDL
LDL and HDL

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11
Q

what is the lipoprotein that does not contain APO B

A

HDL

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12
Q

What is the difference between HDL and LDL

A

LDL contain more cholesterol than HDL which contains more cholesterol

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13
Q

what is the exogenous pathway of cholesterol transport? and the endogenous

A

exogenous: dietary cholesterols -> intestine -> chylomicrons go to lipoprotein lipase becomes chylomicrons remnants it goes to the liver

endogenous: Remnant receptor it will form VLDL pass by the lipoprotein lipase form IDL
and then form LDL with the LDL receptor it can go to extrahepatic tissue an form HDL

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14
Q

between chylo, vldl, ldl and hdl class each one from bigger -> smaller and by density

A

diameter: chylo (bigger)> VLDL> LDL> HDL
density: HDL>LDL> VLDL/Chylo

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15
Q

What does every lipoprotein contain most?

A

Chylo : contain moslty TG
VLDL: contain mostly TG
LDL: Cholesterol Ester
HDL: Apo P and Phospholipid

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16
Q

what are the serum lipid values for
- total cholesterol
- HDL
- LDL
- triglyceride

A

total cholesterol: < 5.2 mmol/L

HDL: men: >1, women : >1.3 and for protection against heart disease needs to be >1.5

LDL: <2.6

TG: < 1.7

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17
Q

How is LDL calculated? and when it is not valid

A

LDL is calculated from the other measures (Total cholesterol, HDL, and TG) and LDL is not valid when TG is greater than 4.5 mmol/l

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18
Q

what are the functions of apoproteins

A
  • synthesis/secretion of specific lipoproteins
  • stabilize surface coat of lipoproteins
  • activate enzymes
  • interact with cell surface receptors
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19
Q

what is the primary determinant of the metabolic fate of lipoproteins

A

apoprotein

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20
Q

true or false
apopotein reflect changes in lipoprotein composition

A

true

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21
Q

true or false
apoprotein levels may be better predictors of heart predictors than lipid levels

A

true

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22
Q

what can apoprotein correlate with heart disease

A

it can correlate with the seerity of the disease

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23
Q

what the geneotype of apo E4/E4 is associated with

A

associated with Alzheimer/dementia

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24
Q

what is the genotype of apo e2/e2 is associated with

A

LDL receptor does not recognice so there is an increase of VLDL

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25
what is the primary classification of dyslipidemia
single or polygenic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia
26
what is the diagnosis of primary dislipidemia based on
- history (age, family members) - physical signs (xanthomas) - lab analysis (lipid profile, apoproteins, LPL activity) - Serum appearance - genetic sequencing
27
what is the secondary dyslipidemia classification
environmental causes and predisposition
28
is the secondary or the primary cause more frequent and which one is more severe
the primary cause is more severe and the secondary is more frequent
29
what are some examples of hypolipoproteinemias ( primary dyslipidemia)
- abetalipoproteinemia - familial hypobetalipoproteinemia - familial alpha-lipoprotein deficiency
30
explain what happens in abetalipoproteinemia
defect in apo B proteins
31
if someone has abetalipoproteinemia what happens to the lipoproteins
there will be no chylo, VLDL, LDL and TAG will accumulate in liver and intestine
32
what happens in familial hypobetalipoproteinemia
LDL concentration is 10-50% of normal but chylomicron formation occurs
33
what happens in familial alpha lipoprotein deficiency
- no hdl - normal ldl, vldl, chylo - moderate tg
34
what are the types of primary hyperlipoproteinemia
1. hyperchylomicronemia 2a. hypercholesterolemia 2b. combined hyperlipoproteinemia 3. dysbetalipoproteinemia 4. hypertriglyceridemia 5. mixed hyperlipidemia
35
what are the most frequent types of hyperlipoproteinemia?
2b. combined hyperlipoproteinemia 4. hypertriglyceridemia
36
explain hyperchylomicronemia * main lipoprotein effect * serum lipids * main symptoms
* high Chylomicron * High Tg, low HDL-c * early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly
37
explain hypercholesterolemia * main lipoprotein effect * serum lipids * main symptoms
* high LDL-c * High LDL * vascular diseases and xanthelasma
38
explain combined hyperlipoproteinemia * main lipoprotein effect * serum lipids * main symptoms
* high LDL, VLDL, APO B * high Cholesterol, high TG, low HDL * variable, vascular disease
39
explain dysbetalipoproteinemia * main lipoprotein effect * serum lipids * main symptoms
* high LDL, VLDL, b VLDL IDL * high cholesterol, TG, low HDL * tuberoeruptive and palmar xanthomas
40
explain hypertriglyceridemia * main lipoprotein effect * serum lipids * main symptoms
* high VDLD * high TG, low HDL * similar to early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly an exacerbated by alcohol and diabetes
41
explain mixed hyperlipidemia * main lipoprotein effect * serum lipids * main symptoms
* high VLDL, chylomicrons * high TG , low HDL * similar to early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly an exacerbated by alcohol and diabetes
42
which types of hyperlipoproteinemia is worst to cause CVD
combined hyperlipoproteinemia and dysbetalipoproteinemia
43
how is the serum color of the 2 most popular hyperlipoproteinemia ( IIB-combined hyperlipoproteinemia IV - hypertriglyceridimia)
IIB - orange clair IV - white
44
what are the major cause OF LIFESTYLE FACTOR of secondary dyslipidemia
- diet ( high in cholesterol, high is sat , high in trans fat and high in sugar) - alcohol - smoking - lack of PA
45
how is the lipoprotein in a diet - high in cholesterol - high in sat fat - high in trans - high in sugar
* CHOL: high in total cholesterol and LDL * SAT: high LDL, HDL and total chol *Trans: High total, sat and low HDL * SUGAR : low HDL
46
how is the lipoprotein in alcohol intake
high HDL. HIGH TG
47
how is the lipoprotein in smoking
low hdl
48
how is the lipoprotein in low PA
low HDL, high TG
49
what are the diseases that cause secondary dyslipidemia
diabetes, hypothyroidism, renal failure, obesity, myelomas, cholestasis etc
50
how is the lipoprotein in diabetes
CHOL HIGH HIGH LDL LOW HDL HIGH TG
51
how is the lipoprotein in renal failure
high chol low hdl high tg
52
how is the lipoprotein in obesity
low hdl high tg
53
what are the medications that can cause dyslipidiemia
- thiazide diuretics - beta blockers - corticosteroids - estrogens - progesterone - benzadiazepine - retinoic acid - antiretroviral
54
which ons of the medicaments has the higher impact on dyslipidemia
corticosteroid it will increase everything
55
what are the 3 main causes of secondary dyslipidemia
* lifestyle * diseases * medications
56
effects of obesity on lipoprotein metabolism
increased substrate flux to liver
57
increased substrate flux to liver is due to what
due to postprandial ( excess calories) and postabsorptive (high adipose tissue and hormone sensitive lipase) it will have more ffa in the circulation because here will be insulin resistance
58
effects of obesity on lipoprotein metabolism
FFA and carbs will go to the liver. There will be an overproduction of VLDL particles that will make VLDL remnant by lipolysis. It will increase VLDL stimulation and it will make LDL
59
Effects of hypertriglyceridemia of obesity metabolism
FFA and carbs come t live there will be an overproduction of VLDL - Triglycerides.
60
Effects of hypercholesterolemia of obesity
overproduction of VLDL there will be an accumulation of VLDL because there will be a lot of VLDL converting to LDL but there is a reduced activity of LDL receptors in the liver so LDL cannot go back to the liver which will increase their amount in the organism
61
what are the possible mechanism for HDL-C lowering in obesity
FFA and carbs will go to the liver and there will be an increased VLDL triglyceride production. VLDL will make LDL and it will go to the organism. HDL will be used to make VLDL and make LDL and the system repeat
62
What is associated with the lowering of HDL
the severity (high BMI) and distribution (abdominal) obesity are associated with low HDL
63
... linear relationship between BMI and HDL
inverse
64
abdominal/visceral fat is associated with what
- associated with HDL - men and post-menopausal women
65
what is the 2 main reasons for a decrease in HDL in obesity
1. higher uptake of HDL2 by adipocytes 2. increase in HDL catabolism by clearance of Apo A1
66
who to screen for dyslipidemia
men and women > 40 years or women postmenopausal
67
is recommended to test lipoprotein at the fasted or the non fasted state
non fasting state
68
when doing the framinghan risk score what we need to do if there is a family member who had a CVD (men less than 55y and women 65y)
we need to multiply the points by 2
69
is statin indicated for poeple in the low risk level?
no
70
what categories people start to take statin
- ldl higher than 5 mmol/l - diabetes patient - chronic kidney disease - atherosclerotic cardiovascular disease

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