Dyslipidemia Flashcards
increase in serum cholesterol leads to what
increased risk for CHD
greatest risk factor for CHD
low HDL’s and normal to elevated LDL’s
what increases with exercise
HDL’s
most dangerous LDLs
small and dense (TG rich)
dumptrucks and scavenge the cholesterol out of serum
HDL’s
4 broad and main steps of atherosclerosis
- endothelial dysfuntion
- LDL comes in and becomes oxidized (oxLDL)
- macrophages engulf particles but can’t break them down
- foam cells; more macrophages attract others to come in and overtime buildup of foam cells
occurs when foam cells continue to build up inside endothelial cells of vessel; reversible
fatty streak
total cholesterol=
HDL + LDL + VLDL
VLDL=
TG/5
primary treatment for all lipid related disorders
diet and exercise
_____ comes from excess caloric intake and lack of exercise
excess cholesterol
drug that also helps upregulate LDLR on liver membrane to bring in more LDL from blood
statins
Ezetimibe + statins=
block cholesterol and upregulate LDLR
elevated level of lipids in blood
hyperlipidemia
imbalance of lipids in blood
dyslipidemia
hypertriglyceridemia
TG>150
hypercholesteremia
TC>200
Dyslipidemia
HDL <40(male) <50 (female)
TG>150
lipids appear normal
FH of heart attack in 20s
G5 and G8 disruption (plant sterols in blood)
Sitosterolemia
to Rx sitosterolemia
Ezetimibe
no beta band (no LDL)
TG in gut can’t get out and baby is gassy (likes fruit juice)
TG stays in liver and can lead to cirrhosis
Abetalipoproteinemia
main cause of abetalipoproteinemia
no MTP
due to absence of LPL lipase or apoC2
rare; recessive
TG’s>1000
presents in childhood
familial hypertriglyceridemia (type I)
familial hypertriglyceridemia can lead to what
pancreatitis
to Rx familial hypertriglyceridemia
fasting
low HDL; high small dense LDL (TG rich LDL’s)
elevated remnants
metabolic dyslipidemia (metabolic syndrome) type II
abnormal band dis beta (remnants)
uncommon
abnormal apoE2 (VLDL and chylomicrons accumulate—elevated TG’s)
Familial Dysbetalipoproteinemia (type III)
1 sign of familial dysbetalipoproteinemia on palms
palmar xanthomas
another sign of familial dysbetalipoproteinemia on elbows and knees
tuberoeruptive xanthomas
decrease in what leads to elevated TG’s
chylomicron apoproteins
uncommon
TG’s -500-5000
VLDL and chylomicron defect
overproduction and impaired clearance of TGs
rarely seen in childhood
Familial hyperlipoproteinemia
sign of Familial hyperlipoproteinemia on glutes
eruptive xanthomas
elevated LDL
1/5 adults
primary hypercholesterolemia
defect in LDLR
FH of premature CHD
corneal arcus, xanthelasma, tendon xanthomas
Familial hypercholesterolemia
corneal arcus (familial hypercholesterolemia)
Xanthelasma (familial hypercholesterolemia)
tendon xanthomas (Familial hypercholesterolemia)
tendon xanthomas (Familial hypercholesterolemia)
TC: 270-370
AD
xanthomas less frequent
LDL accumulates in blood
Familial defective apoB100
LDLR recycling defective (less LDLR)
Familial PCSK-9
blocks PCSK9 and reduces LDL in plasma dramatically
specific antibodies
overproduction of apoB100
variable lipoprotein pattern
elevated LDL, TC, TG, low HDL
Familial combined hyperlipidemia
1/4 american adults
due to multiple faulty genes leading to elevated TC and LDL
Polygenic hypercholesterolemia
less LDLR, more LDL
associated with Alzheimers
apoE4 isoforms
has high affinity for apoER (remnants not being taken up)
E4
abnormal protein attached to LDL
has clotting effects
found elevated when you run tests (genetic)
Lpa
good or bad low HDL <40 or <50
BAD
apoproteins that produce HDL
A1 and E
HDL to cholesterol ester
LCAT
HDL can do 2 things when it picks up cholesterol
- exchange to cholesterol ester
- pick up apoE and take to liver to be cleared
decrease HDL=increase
cholesterol in artery wall