Hyperlipidemia Flashcards
What is Hyperlipidemia
abnormal high levels of lipids/ lipoproteins in blood
aquired or genetic
can lead to atherosclerosis
Lipid transport
carried in protein vesicles called lipoproteins
difference between VLDL and LDL
VLDL carries triglycerides
LDL carries Cholesterol
2 types of lipid metabolic pathways
Exogenous and Endogenous pathway
Exogenous pathway
lipids broken down into chylomicrons in intestine
chylomicrons go to peripheral tissue
Triglyceride (TG) broken down by lipoprotein lipase to release fatty acid to be used by muscles
chylomicrons remenants form and taken up by liver to form HDL
endogenous pathway
VLDL formed in liver from TG and cholesterol esters
TG in VLDL metabolised in muscles by lipoprotein lipase to release fatty acid and IDL
IDL metabolised to LDL to use in LDL receptors
atherosclerosis
accumulation of lipids and cholesterol in artery walls
narrows blood vessels so less blood and oxygen reach vital organs
plaque can build up to further narrow vessels
can cause heart attack or stroke
causes of hyperlipidemia
primary: familial/gene mutation affecting TG,HDL and LDL
secondary: lifestyle, diet, diabetes, kidney disease, alchohol/smoking, liver disease
types of hyperlipidemia
hypercholesterolemia- increase in cholesterol
hypertriglyceridemia- increase in TG
combined hyperlipidemia - increase in cholesterol and TG
symptoms of hyperlipidemia
usually no obvious symptoms
can lead to atherosclerosis or stoke
yellow skin lesions made of cholesterol-rich (eruptive) xanthomas appear on skin
high level of LDL/ hypercholesterolemia- xanthomas at multiple joints
high levels of TG/ hypertriglyceridemia- more xanthomas
Xanthelasma- yellow cholesterol plaques around eyelids
phyisical signs of dyslipidemia
-primary: serum total cholesterol>240mg/dL
premature/ family history of cardiovascular disease
-secondary: liver enzymes, urinary protein, fasting glucose
normal levels of lipids(mg/dL)
total cholesterol<200
LDL cholesterol<100
TG<150
HDL>60
familial hypercholesterolemia
genetic disorder(autosomal dominant)
high cholesterol levels
cause by mutation in LDLR which means there is more LDL in circulation than normal
homozygous more severe than heterozygous
5 classes of FH from LDLR
1) no LDLR synthesis
2)no LDLR transport from ER to golgi
3)no LDLR to LDL binding on cell surface
4)no LDLR-LDL internalization
5)no LDLR recycling back to cell surface
mutation in PCSK9 gene
causes gain in function of PCSK9 protein
this causes LDL recptors to be broken down quicker so less recptors to accept LDL which means high cholesterol levels