Lipids Flashcards
Free fatty acids
chains of C w/ terminal carboxyl group
energy, bound to albumin for transport
Triglycerides
3 fatty acids + glycerol
hydrophobic, neutral lipid
Phospholipids
glycerol, 2 fatty acids + phospholipid head group
hydrophilic head, hydrophobic body
1 saturated fatty acid, 1 unsaturated fatty acid
Cholesterol
unsaturated steroid alcohol
free cholesterol & cholesterol esters
Free Cholesterol
hydrophilic at OH group on A ring; rest is hydrophobic
used for hormones, bile acids, 7-dehydrocholesterol (vit D uses this)
Cholesterole esters
fatty acid joined to cholesterol at OH group on ring A
makes hydrophobic, neutral charge
Lipoproteins
various classes
consist of protein, cholesterol esters, cholesterol, triglycerides, & phospholipids
Chylomicrons
type of lipoprotein
carries exogenous triglycerides
SHOULD NOT BE PRESENT IN FASTING SPECIMENS
Apoprotein -48 send remnants to the liver
Lipoprotein Lipase (LPL)
releases fatty acids from chylomicrons to be utilized for energy
VLDL
carries endogenous triglycerides
liver triglycerides made from diet excess
loses triglycerides in circulation via LPL
apoproteins include B-100, E, C’s
LDL
formed in circulation, carries cholesterol & cholesterol esters to cells
from VLDL degradation, apo B-100 stays on the complex
will deliver cholesterol to cells w/ apo B-100 receptors
HDL
collects cholesterol from cells & returns it to the liver
anti-atherogenic lipoprotein ‘reverse cholesterol transport’
APOPROTEIN A-1!
Lipid Metabolism
absorbed fatty acids & lipids are converted into chylomicrons which then enter the circulation Lipoprotein Lipase (LPL) degradation of chylomicrons leads to chylomicron remnants as free fatty acids to be taken up by tissue cells which need apo C-II as co-factor for LPL chylomicron remnants are take up by the liver through receptors liver then makes VLDL & HDL- VLDL is transport for endogenous triglycerides
Atherosclerosis
plague already formed!!!!!
blood vessels partly occluded
Arteriosclerosis
the process by which fatty streaks develop into plauges due to oxidized LDL uptake by macrophages etc fostering the inflammatory process
Hormones that affect cholesterol levels
thyroid, estrogens, insulin
^^ cholesterol levels = low levels of above hormones
overall low levels of cholesterol are better than high levels
Hypercholesterolemia
increase in cholesterol
familia hypercholesterol
hetero- 300-600 mg/dL (statin drugs help)
homo- 800-1000 mg/dL (LDL pheresis)
Hypertriglyceridemia
increased triglyercides
genetic, diabetes, hormone imbalances, renal failure
Hyperlipidemia
increase in both cholesterol & triglycerides
increased risk for CHD- coronary heart disease
Lipoprotein A (LpA)
presence can indicate increase risk for CHD
similar to plasminogen in structure - competes for fibrin binding sites & increases plague formation!!
cholesterol drugs do not help - need niacin & estrogen replacement
measure by immunoassay
independent risk factor for CHD
Enzymatic Cholesterol methods
patient sample has cholesterol esters & cholesterol so in order to measure total cholesterol; must first convert cholesterol esters in serum to free cholesterol
Substrate: cholesterol esters
Enzymes: Cholesterol esterase, cholesterol oxidase, Peroxidase
read colored product
HDL cholesterol methods
various precipitation reagents -> the supernatant analyzed by enzymatic cholesterol method
direct methods for HDL include specific antibody to apo B (APO B is is on all but HDL)
block activity of VLDL, LDL in sample
use alpha-cyclodextrin to select for HDL
Precipitating reagents for HDL analysis
MgCl2 & Dextran Sulfate
Polyethylene Glycol (PEG)
etc
Hyperalphalipoproteinemia
increased HDL ( over 100 mg/dL) very rare & shows decreased risk of CAD
Hypoalphalipoproteinemia
decreased HDL & increased risk for CAD
Tangier’s Disease
absence of HDL w/ low to absent A-I & A-II (need these apoproteins to form HDL)
increased risk of developing atherosclerosis
Triglyceride methods
Substrate: triglycerides (VLDL, LDL, HDLs- mostly VLDL)
Enzymes: bacterial lipase (no interference w/ endogenous lipase), glycerol kinase, glycerolphosphate oxidase, peroxidase
Read: colored product @ 500 nm
NEED FASTING SAMPLES
Triglyceride method glycerol interference
10-20 mg/dL of glycerol in normal samples: can do a ‘glycerol’ blank to subtract interference or most commonly just set calibration to offset
Hyperlipoproteinemias
elevated triglycerides seen secondary to DM, nephrosis, biliary obstruction, endocrine disturbances , fatty liver
Hormone sensitive lipase
lipase that has to do with fat cells & move triglycerides into storage
Calculating LDL
T cholesterol - ( HDL + [Triglycerides/5])
calculation is invalid if triglyceride value is over 500 mg/dL
Measuring LDL
measure apoproteins, apo A-1 & B-100
use antibodies to apo E & A to remove other lipoproteins & measure residual
Additional markers for cardiovascular disease
Lp(a), homocysteine, C-reactive protein, & Hs C reactive protein
