Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical nutrition > Dyslipidemia and Cardiovascular disease > Flashcards

Dyslipidemia and Cardiovascular disease Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

atherosclerosis is associated with

A
  • myocardial infarction
  • cerebrovascular accident (stroke, CVA)
  • peripheral vascular disease
  • coronary heart disease
  • congestive heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

is atherosclerosis symptomatic

A

no it is asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

chylomicrons and VLDL
LDL and HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the lipoprotein that does not contain APO B

A

HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the difference between HDL and LDL

A

LDL contain more cholesterol than HDL which contains more cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the primary determinant of the metabolic fate of lipoproteins

A

apoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

true or false
apopotein reflect changes in lipoprotein composition

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can apoprotein correlate with heart disease

A

it can correlate with the seerity of the disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what the geneotype of apo E4/E4 is associated with

A

associated with Alzheimer/dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the primary classification of dyslipidemia

A

single or polygenic abnormalities affecting lipoprotein function resulting in hyperlipidemia or hypolipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the diagnosis of primary dislipidemia based on

A
  • history (age, family members)
  • physical signs (xanthomas)
  • lab analysis (lipid profile, apoproteins, LPL activity)
  • Serum appearance
  • genetic sequencing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the secondary dyslipidemia classification

A

environmental causes and predisposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

is the secondary or the primary cause more frequent and which one is more severe

A

the primary cause is more severe and the secondary is more frequent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are some examples of hypolipoproteinemias ( primary dyslipidemia)

A
  • abetalipoproteinemia
  • familial hypobetalipoproteinemia
  • familial alpha-lipoprotein deficiency
30
Q

explain what happens in abetalipoproteinemia

A

defect in apo B proteins

31
Q

if someone has abetalipoproteinemia what happens to the lipoproteins

A

there will be no chylo, VLDL, LDL and TAG will accumulate in liver and intestine

32
Q

what happens in familial hypobetalipoproteinemia

A

LDL concentration is 10-50% of normal but chylomicron formation occurs

33
Q

what happens in familial alpha lipoprotein deficiency

A
  • no hdl
  • normal ldl, vldl, chylo
  • moderate tg
34
Q

what are the types of primary hyperlipoproteinemia

A
  1. hyperchylomicronemia
    2a. hypercholesterolemia
    2b. combined hyperlipoproteinemia
  2. dysbetalipoproteinemia
  3. hypertriglyceridemia
  4. mixed hyperlipidemia
35
Q

what are the most frequent types of hyperlipoproteinemia?

A

2b. combined hyperlipoproteinemia
4. hypertriglyceridemia

36
Q

explain hyperchylomicronemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high Chylomicron
  • High Tg, low HDL-c
  • early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly
37
Q

explain hypercholesterolemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high LDL-c
  • High LDL
  • vascular diseases and xanthelasma
38
Q

explain combined hyperlipoproteinemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high LDL, VLDL, APO B
  • high Cholesterol, high TG, low HDL
  • variable, vascular disease
39
Q

explain dysbetalipoproteinemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high LDL, VLDL, b VLDL IDL
  • high cholesterol, TG, low HDL
  • tuberoeruptive and palmar xanthomas
40
Q

explain hypertriglyceridemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high VDLD
  • high TG, low HDL
  • similar to early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly an exacerbated by alcohol and diabetes
41
Q

explain mixed hyperlipidemia
* main lipoprotein effect
* serum lipids
* main symptoms

A
  • high VLDL, chylomicrons
  • high TG , low HDL
  • similar to early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly an exacerbated by alcohol and diabetes
42
Q

which types of hyperlipoproteinemia is worst to cause CVD

A

combined hyperlipoproteinemia and dysbetalipoproteinemia

43
Q

how is the serum color of the 2 most popular hyperlipoproteinemia ( IIB-combined hyperlipoproteinemia IV - hypertriglyceridimia)

A

IIB - orange clair
IV - white

44
Q

what are the major cause OF LIFESTYLE FACTOR of secondary dyslipidemia

A
  • diet ( high in cholesterol, high is sat , high in trans fat and high in sugar)
  • alcohol
  • smoking
  • lack of PA
45
Q

how is the lipoprotein in a diet
- high in cholesterol
- high in sat fat
- high in trans
- high in sugar

A
  • 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
Q

how is the lipoprotein in alcohol intake

A

high HDL. HIGH TG

47
Q

how is the lipoprotein in smoking

A

low hdl

48
Q

how is the lipoprotein in low PA

A

low HDL, high TG

49
Q

what are the diseases that cause secondary dyslipidemia

A

diabetes, hypothyroidism, renal failure, obesity, myelomas, cholestasis etc

50
Q

how is the lipoprotein in diabetes

A

CHOL HIGH
HIGH LDL
LOW HDL
HIGH TG

51
Q

how is the lipoprotein in renal failure

A

high chol
low hdl
high tg

52
Q

how is the lipoprotein in obesity

A

low hdl
high tg

53
Q

what are the medications that can cause dyslipidiemia

A
  • thiazide diuretics
  • beta blockers
  • corticosteroids
  • estrogens
  • progesterone
  • benzadiazepine
  • retinoic acid
  • antiretroviral
54
Q

which ons of the medicaments has the higher impact on dyslipidemia

A

corticosteroid it will increase everything

55
Q

what are the 3 main causes of secondary dyslipidemia

A
  • lifestyle
  • diseases
  • medications
56
Q

effects of obesity on lipoprotein metabolism

A

increased substrate flux to liver

57
Q

increased substrate flux to liver is due to what

A

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
Q

effects of obesity on lipoprotein metabolism

A

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
Q

Effects of hypertriglyceridemia of obesity metabolism

A

FFA and carbs come t live there will be an overproduction of VLDL - Triglycerides.

60
Q

Effects of hypercholesterolemia of obesity

A

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
Q

what are the possible mechanism for HDL-C lowering in obesity

A

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
Q

What is associated with the lowering of HDL

A

the severity (high BMI) and distribution (abdominal) obesity are associated with low HDL

63
Q

… linear relationship between BMI and HDL

A

inverse

64
Q

abdominal/visceral fat is associated with what

A
  • associated with HDL
  • men and post-menopausal women
65
Q

what is the 2 main reasons for a decrease in HDL in obesity

A
  1. higher uptake of HDL2 by adipocytes
  2. increase in HDL catabolism by clearance of Apo A1
66
Q

who to screen for dyslipidemia

A

men and women > 40 years or women postmenopausal

67
Q

is recommended to test lipoprotein at the fasted or the non fasted state

A

non fasting state

68
Q

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)

A

we need to multiply the points by 2

69
Q

is statin indicated for poeple in the low risk level?

A

no

70
Q

what categories people start to take statin

A
  • ldl higher than 5 mmol/l
  • diabetes patient
  • chronic kidney disease
  • atherosclerotic cardiovascular disease

Clinical nutrition (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions