Dyslipidemia Flashcards
atherogenesis pathway
- excess LDL gets sequestered underneath the intima of the artery
- WBC come in
- differentiate into macrophages (proinflammatory)
- Swallow up LDL
- proinflammatory-> releases things to oxidase LDL
- now oxidized LDL enters blood stream and antibodies are formed against it.
- Macrophage itself can’t break down cholesterol so macrophages build up. Called foam cells
- crystallization of the cholesterol inside of the foam cell makes them rupture
- INFLAMMATION= positive feed back
- when they all die it forms a calcified plaque
cholesterol vs triglyceride
cholesterol is sterile molecule that is a precursor to- steroid hormones, cell membranes, vit. D
triglyceride form adipose tissue
Denovo synthesis
decreased cholesterol in diet makes the liver compensate by increasing cholesterol
bc it is accustomed to high levels
2 sources of cholesterol
80% liver
20% diet
mevalonate pathway
precursor HMGcoa is turned into mevalonate molecule by HMGcoa reductase=Cholesterol after a series of steps
Done in the liver
Statins block HMGcoa reductase
What are the different types of lipoproteins and their function?
- VLDL- turns into LDL
- LDL-bad; Transporter: excess gets stuck in arteries
- HDL-good; Scavenger of cholesterol to bring down cholesterol levels.
Calculate the cholesterol risk ratio using the LDL:HDL ratio
LDL/HDL
target level of LDL
<130
target level of total cholesterol
<200
target level of HDL in men
> 40
target level of HDL in women
> 50
target level of triglycerides is
<120
familial hypercholesterolemia is the most common(primary) cause of
hyper cholesterol
secondary causes of hypercholesterolemia
things that cause increases in cholesterol: diabetes, alcohol etc.
primary is familial
omega 3 fatty acids are good for
lowering cholesterol
