Hyperlipidemia Hockerman Exam 3 Flashcards
What macromolecules are found on the surface of lipoproteins? In the core?
Surface: phospholipid, free cholesterol, protein
Core: triglyceride, cholesterol ester
What lipoprotein is responsible for reverse cholesterol transport?
HDL–the good cholesterol
What lipoprotein has the highest cholesterol content?
LDL
What lipoprotein is secreted by the liver as a source of triglycerides?
VLDL
What lipoprotein transports dietary lipids from gut to liver and adipose tissue?
Chylomicrons
What lipoprotein is simply a triglyceride-depleted VLDL?
IDL
What apolipoprotein is the seed crystal for HDL and helps with reverse cholesterol transport?
ApoA-1 (steak sauce!)
What apolipoprotein is produced in the intestine to form chylomicrons?
ApoB-48
What apolipoprotein is produced in the liver and, with HDL, helps with reverse cholesterol transport?
ApoE
What apolipoprotein is produced in the liver and is the LDL receptor ligand–helps internalize LDL into the liver?
ApoB-100
What apolipoprotein inhibits lipoprotein lipase and interferes with ApoB and ApoE binding to hepatic receptors, preventing triglyceride breakdown and inhibiting LDL internalization?
ApoCIII–LOF mutation leads to lower CHD
IDL + cholesterol from HDL =
LDL
What does the liver do with chylomicron remnants?
Packages them into VLDL, which in turn becomes IDL after capillaries.
What enzyme is rate-limiting in cholesterol synthesis?
HMGCoA reductase–forms mevalonate.
True or false: Limiting dietary intake of cholesterol is the best way to lower blood cholesterol.
False–de novo synthesis is the major source of cholesterol, so limiting intake has minor effects.
What TC/HDL ratio is indicative of increased CVD risk?
> 4.5
What can hypertriglyceridemia lead to?
Pancreatitis, xanthomas (fat in skin). Some association wth increased CHD risk.
What are foam cells?
Dead macrophages that look foamy due to the high amount of cholesterol they contain. Make up the necrotic pore of the plaque.
What is the mechanism of action of cholestyramine (Queastran) and colestipol (Colestid)?
These bile acid binding resins inhibit reabsorption of bile acids from the intestine by binding bile acids to form insoluble complex. Inherently decreases cholesterol in body, but also increases excretion of bile acids because loss of negative feedback! They also up-regulate LDL receptors in the liver.
What is the clinical effect do the bile acid binding resins have? What side effects?
~20% reduction LDL, ~5% increase HDL, may increase TG. Take before meals. High constipation and bloating (eating resin! high fiber diet/water helps), drug interactions.
How does ezetimibe function to decrease cholesterol?
It inhibits intestinal absorption of cholesterol from dietary sources and bile acid secretion (NPC1L1 transporter).
How is ezetimibe primarily used in therapy? What SEs?
Usually in conjunction with statins, but lowers LDL 17% by itself. Generally well tolerated, but some liver/skeletal muscle damage.
What are the two ways that statins lower LDL?
They competetively inhibit HMG-CoA reductase (synthesis) and upregulate LDL receptors in the liver (transcription triggered by low cholesterol levels)
What effects do statins have on lipids?
All dependent on dose/choice: 20-60% reduction in LDL, 10-33% reduction TG, 5-10% increase HDL.
