Lipoprotein Physiology Flashcards
Cholesterol and triglycerides are transported through lymph and blood by a sub-cellular body known as a
lipoprotein
Lipids are transported through the body via lipoproteins along three major routes:
- exogenous pathway
- endogenous pathway
- reverse cholesterol transport
what is the exogenous pathway
gathers lipids from the digestive tract and distributes them throughout the body after a meal
what is the endogenous pathway
the liver builds apoliproteins and secretes them into the bloodstream – also distributes lipids throughout the body
what is the reverse cholesterol transport
scavenges cholesterol from peripheral tissues and returns it to the liver
? are synthesized by the enterocyte
chylomicrons
what is inserted as a structural protein for the chylomicron during the exogenous pathway
ApoB-48
HDL particles transfer ? and ? to the chylomicrons
ApoC-II and ApoA-V
ApoC-II and ApoA-V allow the chylomicron to ?
interact with lipoprotein lipase (LPL)
LPL on the endothelial cells of capillaries do what to the chylomicrons?
cleaves TGs in chylomicrons to FFAs
after TGs are lost, the chylomicron becomes a ?
chylomicron remnant
HDL also transfers ? to the chylomicron so that the chylomicron remnant can be ?
ApoE
cleared by the liver
Chylomicron remnants are cleared by the liver via an ?
ApoE-dependent mechanism (LDL receptor)
what is the function of the exogenous pathway
carry dietary lipids to most cells but especially liver
what is the initial lipoprotein and intermediate lipoprotein of the exogenous pathway
chylomicron and chylomicron remnants
VLDL is synthesized by the ?
liver
VLDL contains what apoproteins
ApoC-II, ApoA-V and ApoB-100
As LPL “drains” triglycerides from VLDL, it becomes ? and then ?
IDL and LDL
IDL that loses TGs and becomes more and more cholesterol-rich becomes ?
LDL
Liver clears IDL and LDL via the ?
LDL receptor on hepatocytes
If LDL is not cleared, it can become oxidized and becomes a major risk factor for the development of
atherosclerosis
HDL is synthesized by ?
both hepatocytes and enterocytes
what is LCAT?
Lecithin-cholesterol acyltransferase
what does LCAT do?
aids the process of HDL receiving cholesterol by converting free cholesterol into cholesterol esters
HDL can help remove cholesterol from peripheral tissues via what?
LCAT-ApoA-1-ABC interactions
Once hepatocytes in the liver accumulate excess cholesterol, they downregulate the ?, which reduces ?
LDL receptor
LDL clearance
reducing liver cholesterol content will result in ?
improved clearance of IDL and LDL
what is atherosclerosis?
the development of atheromas in a wide range of large and medium-sized arteries
atherosclerosis will lead to ?
- endothelial injury
- accumulation of lipoproteins in the vessel wall
what is the LDL level for low risk of cardiac risk
< 2.59 mmol/L
what is the LDL level for good level to not have cardiac risk
2.59-3.34 mmol/L
what is the LDL level for borderline high of cardiac risk
3.37-4.11
what is the LDL level for bad level to have cardiac risk
> 4.14
what is the normal range of triglycerides in a human
0.45-1.71 mmol/L
what is the HDL for low risk of cardiac risk
> 1.55 mmol/L
what is the HDL level for high risk of cardiac risk
<1.04 mmol/L
what is normal for total cholesterol in a human
< 5.2 mmol/L
what is the goal when calculating TC:HDL ratio to calculate cardiac risk from atheroschlerosis?
<3.5
framingham risk score for risk (low, intermediate, and high)
low risk : <10 %
intermediate risk 10-20%
high risk > 20%
what is one of the best markers of systemic inflammation as it pertains to atherosclerosis
hsCRP
what is a constellation of physical exam and laboratory findings that confer a higher risk for coronary heart disease, diabetes, fatty liver, cancer
the metabolic syndrome
Atherosclerosis - acute plaque changes
Fall under three general categories which are?
- rupture/fissuring
- erosion/ulceration
- hemorrhage into the atheroma
plaque stability tends to be most strongly affected by?
- hemodynamic disturbances (increases in blood pressure)
- increased inflammation (disruption of the extracellular matrix of the atheroma)
- Factors that increase clot formation (i.e. platelet activation)
what is atheroembolism
Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli
rupture, ulceration or erosion of these plaques may result in
stroke or MI
what is a true aneurysm
an “intact” attenuated arterial wall or thinned ventricular wall of the heart
what is an aneurysm
abnormal stretching (dilation or dilatation) in the wall of an artery, a vein, or the heart with a diameter that is at least 50% greater than normal
what is a false aneurysm
defect in the vascular wall -> extravascular hematoma
what is a dissection?
blood exits the lumen and enters the wall of the vessel
