Dyslipidemia and Cardiovascular disease Flashcards by gabriela mena

why there was a decrease in mortality regarding CVD

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

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role of the cardiovascular system

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

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what are the major form of cardiovascular disease

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

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what is atherosclerosis

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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atherosclerosis is associated with

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

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is atherosclerosis symptomatic

no it is asymptomatic

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how does an atherosclerotic plaque form

there is an injury in the endothelium wall due to high blood pressure, chemicals etc
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.
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.
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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what are some factors that damage the endothelial wall

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

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what is the risk factor for atherosclerosis?

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

chylomicrons and VLDL
LDL and HDL

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what is the lipoprotein that does not contain APO B

HDL

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What is the difference between HDL and LDL

LDL contain more cholesterol than HDL which contains more cholesterol

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

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

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

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What does every lipoprotein contain most?

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

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

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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How is LDL calculated? and when it is not valid

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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what are the functions of apoproteins

synthesis/secretion of specific lipoproteins
stabilize surface coat of lipoproteins
activate enzymes
interact with cell surface receptors

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what is the primary determinant of the metabolic fate of lipoproteins

apoprotein

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true or false
apopotein reflect changes in lipoprotein composition

true

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

true

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what can apoprotein correlate with heart disease

it can correlate with the seerity of the disease

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what the geneotype of apo E4/E4 is associated with

associated with Alzheimer/dementia

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

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

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what is the primary classification of dyslipidemia

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

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

what is the secondary dyslipidemia classification

environmental causes and predisposition

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

what are some examples of hypolipoproteinemias ( primary dyslipidemia)

- abetalipoproteinemia - familial hypobetalipoproteinemia - familial alpha-lipoprotein deficiency

explain what happens in abetalipoproteinemia

defect in apo B proteins

if someone has abetalipoproteinemia what happens to the lipoproteins

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

what happens in familial hypobetalipoproteinemia

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

what happens in familial alpha lipoprotein deficiency

- no hdl - normal ldl, vldl, chylo - moderate tg

what are the types of primary hyperlipoproteinemia

1. hyperchylomicronemia 2a. hypercholesterolemia 2b. combined hyperlipoproteinemia 3. dysbetalipoproteinemia 4. hypertriglyceridemia 5. mixed hyperlipidemia

what are the most frequent types of hyperlipoproteinemia?

2b. combined hyperlipoproteinemia 4. hypertriglyceridemia

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

* high Chylomicron * High Tg, low HDL-c * early, skin xanthomas, pancreatitis, lipemia retinalis, hepatosplenomegaly

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

* high LDL-c * High LDL * vascular diseases and xanthelasma

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

* high LDL, VLDL, APO B * high Cholesterol, high TG, low HDL * variable, vascular disease

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

* high LDL, VLDL, b VLDL IDL * high cholesterol, TG, low HDL * tuberoeruptive and palmar xanthomas

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

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

which types of hyperlipoproteinemia is worst to cause CVD

combined hyperlipoproteinemia and dysbetalipoproteinemia

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

IIB - orange clair IV - white

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

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

how is the lipoprotein in alcohol intake

high HDL. HIGH TG

how is the lipoprotein in smoking

low hdl

how is the lipoprotein in low PA

low HDL, high TG

what are the diseases that cause secondary dyslipidemia

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

how is the lipoprotein in diabetes

CHOL HIGH HIGH LDL LOW HDL HIGH TG

how is the lipoprotein in renal failure

high chol low hdl high tg

how is the lipoprotein in obesity

low hdl high tg

what are the medications that can cause dyslipidiemia

- thiazide diuretics - beta blockers - corticosteroids - estrogens - progesterone - benzadiazepine - retinoic acid - antiretroviral

which ons of the medicaments has the higher impact on dyslipidemia

corticosteroid it will increase everything

what are the 3 main causes of secondary dyslipidemia

* lifestyle * diseases * medications

effects of obesity on lipoprotein metabolism

increased substrate flux to liver

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

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

Effects of hypertriglyceridemia of obesity metabolism

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

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

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

What is associated with the lowering of HDL

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

... linear relationship between BMI and HDL

inverse

abdominal/visceral fat is associated with what

- associated with HDL - men and post-menopausal women

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

who to screen for dyslipidemia

men and women > 40 years or women postmenopausal

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

non fasting state

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

is statin indicated for poeple in the low risk level?

what categories people start to take statin

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