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
statin
- # 1 class for dyslipidemia
- HMGcoa reductase inhibitor
- put on it d/t high cholesterol and MI
- statin increase PCSK9
not for pregnant women
baby needs cholesterol and mom needs it to make breast milk
Side effects of statin
CK elevation
muscle pain/weakness-most common reason why people stop drug
Niacin
- AKA Vit. B3
- prevents VLDL from turning into LDL
Niacin side effects
cutaneous vasodilation which causes flushing
fibrates
- increase breakdown of fat. This decreases VLDL
fibrate examples
-fib-
gemfibrozil
fenofibrate
examples of bile acid bind resin BABR
Choles-
Cholestyramine
Cholestipol
Absorption inhibitor MOA
block NPC1L1 transporter from transporting cholesterol from the bile acid into the body
Absorption inhibitor example
Ezetimibe
side effects of Absorption inhibitor
possible atrial wall thickening?
MAB- PCSK 9 inhibitors are never given
alone, always with a statin
Lowers LDL by 65% if given with statin
side effects of MAB- PCSK 9 inhibitor
Risk of hypocholesterolemia
PCSK9 pathway
- PCSK9 binds to LDL-r. Goes into clatherin coated pit. Receptor is now marked for destruction by the lysosome.
This leads to a decrease in LDL-r
less cholesterol being taken in d/t limited receptors=more in bloodstream
statin increase PCSK9
PCSK9 example
Evolocumab
risks of low cholesterol
cancer
hemorrhage stroke
preterm and low birthweight
decrease wound healing
