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Flashcards in Lipids Deck (33)
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1

Free fatty acids

chains of C w/ terminal carboxyl group
energy, bound to albumin for transport

2

Triglycerides

3 fatty acids + glycerol
hydrophobic, neutral lipid

3

Phospholipids

glycerol, 2 fatty acids + phospholipid head group
hydrophilic head, hydrophobic body
1 saturated fatty acid, 1 unsaturated fatty acid

4

Cholesterol

unsaturated steroid alcohol
free cholesterol & cholesterol esters

5

Free Cholesterol

hydrophilic at OH group on A ring; rest is hydrophobic
used for hormones, bile acids, 7-dehydrocholesterol (vit D uses this)

6

Cholesterole esters

fatty acid joined to cholesterol at OH group on ring A
makes hydrophobic, neutral charge

7

Lipoproteins

various classes
consist of protein, cholesterol esters, cholesterol, triglycerides, & phospholipids

8

Chylomicrons

type of lipoprotein
carries exogenous triglycerides
SHOULD NOT BE PRESENT IN FASTING SPECIMENS
Apoprotein -48 send remnants to the liver

9

Lipoprotein Lipase (LPL)

releases fatty acids from chylomicrons to be utilized for energy

10

VLDL

carries endogenous triglycerides
liver triglycerides made from diet excess
loses triglycerides in circulation via LPL
apoproteins include B-100, E, C's

11

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

12

HDL

collects cholesterol from cells & returns it to the liver
anti-atherogenic lipoprotein 'reverse cholesterol transport'
APOPROTEIN A-1!

13

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

14

Atherosclerosis

plague already formed!!!!!
blood vessels partly occluded

15

Arteriosclerosis

the process by which fatty streaks develop into plauges due to oxidized LDL uptake by macrophages etc fostering the inflammatory process

16

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

17

Hypercholesterolemia

increase in cholesterol
familia hypercholesterol
hetero- 300-600 mg/dL (statin drugs help)
homo- 800-1000 mg/dL (LDL pheresis)

18

Hypertriglyceridemia

increased triglyercides
genetic, diabetes, hormone imbalances, renal failure

19

Hyperlipidemia

increase in both cholesterol & triglycerides
increased risk for CHD- coronary heart disease

20

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

21

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

22

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

23

Precipitating reagents for HDL analysis

MgCl2 & Dextran Sulfate
Polyethylene Glycol (PEG)
etc

24

Hyperalphalipoproteinemia

increased HDL ( over 100 mg/dL)
very rare & shows decreased risk of CAD

25

Hypoalphalipoproteinemia

decreased HDL & increased risk for CAD

26

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

27

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

28

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

29

Hyperlipoproteinemias

elevated triglycerides seen secondary to DM, nephrosis, biliary obstruction, endocrine disturbances , fatty liver

30

Hormone sensitive lipase

lipase that has to do with fat cells & move triglycerides into storage