Lipoportein and lipid disorders Flashcards
healthy/risk factor limits
BMI
BP
FBS
BMI <28, >35
BP 120/90, 135/85 (or Rx)
FBS <100, Diabetes
LDL-C >____ = risk for ASCVD
HDL < ____ = risk for ASCVD
Trigs between ____ and ___ > Risk for CAD
(>1000 = pancreatitis)
LDL- C > 100
HDL <40
Trigs 200-499
genetic lipid disorders
Type I
Type IIa
lifestyle or disease driven lipid disorders
Type II B
Type III
Type IV
Type V
Name and common presentation,
Type I
Severe hypertriglyceridemia
childhood with Trigs >2000
Name and common presentation,
Type IIB
Familial Combinded Hyperlipedia
(or with metabolic syndrome)
LDL, VLDL high
(all numbers borderline)
Name and common presentation, Type IIa
Familal Hypercholesterolemia
CAD Age<60,
LDL high
Name and common presentation, Type III
Dysbetaliporoteineima
Premature CAD
excess VLDL, IDL
Name and common presentation, type IV
hypertriglyceridemia
pancreatitis,
VLDL high, Trigs 500-1000
Name and common presentation, type V
Hypertriglyceridemia
pancreatitis, usually diabetic
high VLDL+chylomicrons
Trigs>1000
least well-recognized by LDL receptor in liver, leading to long half life in plasma
B-100
LPL removes ___ from chylomicrons to mobilize fFA
TG
LPL removes TG from ____, leading to fFA and IDL
VLDLs
Pathogenesis of Type I (severe hyperchylomicronia)
LPL, ApoC2, or APO-C3 on chylo dysfunctional so TGs not removed from chylo
pathogenesis type IIA (FH)
LDL-R defective, LDL accumulates
pathogenesis type IIB (Famial combined hyperlipidemia)
Central adipositiy and insulin resistance
(High Trigs, low HDL, increased LDLP)
Trigs drives CETP > moves trigs to LDL and HDL promoting further LPL+HL activitiy
role of Hepatic lipase
remove TG from HDL and LDL to form sdLDL and sdHDL
pathogenesis type III (dysbetalipoproteinemia)
apoE2 on IDL is poorly recognized by LDL-R
Apo E2 overproduction
excess of VLDL and LDL
pathogenesis type IV (Hypertriglyceridemia)
ApoC2 or apoC3 on VLDL do not work > VLDL accumulate
Pathogenesis type V Familail hypertriglyceridemia
ApoC2 or ApoC3 on both VLDL **AND **Chylomicrons don’t work > accumualte
ApoC2 impact on LPL
ApoC3 impact
ApoC2 - activates LPL > TG removal from VLDL/Chylo
ApoC3 - deactivates > particle can now mobilize
inherited loss of LPL or defective apoC2/C3
chylomicrons fill with Trigs at enterocyte but cannot offload to periphery
Type I hyperchylomicronemia
overproduction of VLDL,
commonly seen with insulin resistance, metabolic syndrome, inflammation of visceral adiposity
TRigs 200-500
Type IIb FH
Trigs 500-1000
Large VLDL (poor LPL function)
Type IV hypertriglyceridemia
trigs>1000
excess chylomicrons
Type I severe hypertriglyceridemia
raise HDL via (besides diet)
Aerobic exercise
Alcohol
Estrogens
PCSK9 catabolizes
drug therapy aims:
LDL - receptor
drug targets to increase LDL receptor more often to increase pull from blood
metabolic syndrome causes atherogenic dyslipediamia > ___
increased LDL-P
Increased VLDL remants (which are very atherogenic)
Metabolic syndrome criteria, men
Waist > 40in
Trigs >150
HDL<40
BP 135/85
FPG >100
(wait to have burgers, fatty)
in metabolic syndrome+ type IIb, visceral adiposity and insulin resistance drive ______ leading to ___ push into circulation
the excess ___ promote ongoing LOL activity that reduce HDL and LDL-P, which stay in circulation longer
in metabolic syndrome+ type IIb, visceral adiposity and insulin resistance drive FFA to liver leading to trig-rich VLDL push into circulation
the excess Trigs promote ongoing LOL activity that reduce HDL and LDL-P, which stay in circulation longer
metabolic syndrome “atherogenic dyslipidemia”
high trigs
low HDL
LDL particles > LDL cholesterol
