24 hyperlipidemia Flashcards
metabolic consequences of hyperlipidemia
more FFA
more VLDL produced
more TG offloaded into LDL/HDL
more TG hydrolyzed by HTGL
SMALLER, MORE DENSE LDL/HDL
- get into endothelium easier
- dont bind LDLR as well(more in plasma)
HDL/LDL content at birth
about equal 34/30
apoB
found on non-HDL atherogenic molecules
- LDL
- IDL
- VLDL/VLDL remnants
- chylomicrons
Lipoprotein lipase
hydrolyzes TG into FFAs so that they can be taken up by the muscle/heart/adipose tissue
PCSK9
targets the LDLR for degradation
familial hypercholesterolemia signs
corneal arcus
xanthelasma
tendon and cutaneous xanthomas
familial hypercholesterolemia is an increase in what
LDL
familial combined hyperlipidemia
overproduction of apoB
increased LDL/VLDL and or TG
type III hyperlipidemia
homozygosity for apo-E2
**PLUS** metabolic abnormality (e.g, T2DM).
excess remnant particles
high cholesterol and TG levels;
yellow streaks in the palmer creases and/or xanthomas
why is high fasting TG in blood a bad sign?
TG themselves are not atherogenic but are markers for excess remnant particles(cholesterol rich) which ARE atherogenic
lots of TG means remnant particles are not being taken up by liver properly which is BAD; high cholesterol; increased atherogenicity
metabolic consequence of hypertrigliceryidemia
small dense LDLs which dont get taken up as easily by LDLR(more in blood)
and
can get between endothelial wall more easily to start a fatty streak
normal fasting triglycerides
high?
<150 mg/dL
high is 200+
causes of hypertriglyceridemia
comes with excess production of TG rich particles(high fat diet, cholesterolemia) or lack up their uptake
signs of very high triglycerides
milky layer on blood
cream colored retinal vessels
palmar crease is yellow
fat deposits(xanthomas)
