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Clinical Chemistry > Lipids > Flashcards

Lipids Flashcards

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1
Q

Free fatty acids

A

chains of C w/ terminal carboxyl group

energy, bound to albumin for transport

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2
Q

Triglycerides

A

3 fatty acids + glycerol

hydrophobic, neutral lipid

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3
Q

Phospholipids

A

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

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4
Q

Cholesterol

A

unsaturated steroid alcohol

free cholesterol & cholesterol esters

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5
Q

Free Cholesterol

A

hydrophilic at OH group on A ring; rest is hydrophobic

used for hormones, bile acids, 7-dehydrocholesterol (vit D uses this)

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6
Q

Cholesterole esters

A

fatty acid joined to cholesterol at OH group on ring A

makes hydrophobic, neutral charge

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7
Q

Lipoproteins

A

various classes

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

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8
Q

Chylomicrons

A

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

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9
Q

Lipoprotein Lipase (LPL)

A

releases fatty acids from chylomicrons to be utilized for energy

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10
Q

VLDL

A

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

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11
Q

LDL

A

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

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12
Q

HDL

A

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

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13
Q

Lipid Metabolism

A 
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
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14
Q

Atherosclerosis

A

plague already formed!!!!!

blood vessels partly occluded

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15
Q

Arteriosclerosis

A

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

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16
Q

Hormones that affect cholesterol levels

A

thyroid, estrogens, insulin
^^ cholesterol levels = low levels of above hormones
overall low levels of cholesterol are better than high levels

17
Q

Hypercholesterolemia

A

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

18
Q

Hypertriglyceridemia

A

increased triglyercides

genetic, diabetes, hormone imbalances, renal failure

19
Q

Hyperlipidemia

A

increase in both cholesterol & triglycerides

increased risk for CHD- coronary heart disease

20
Q

Lipoprotein A (LpA)

A

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
Q

Enzymatic Cholesterol methods

A

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
Q

HDL cholesterol methods

A

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
Q

Precipitating reagents for HDL analysis

A

MgCl2 & Dextran Sulfate
Polyethylene Glycol (PEG)
etc

24
Q

Hyperalphalipoproteinemia

A 
increased HDL ( over 100 mg/dL)
very rare & shows decreased risk of CAD
25
Q

Hypoalphalipoproteinemia

A

decreased HDL & increased risk for CAD

26
Q

Tangier’s Disease

A

absence of HDL w/ low to absent A-I & A-II (need these apoproteins to form HDL)
increased risk of developing atherosclerosis

27
Q

Triglyceride methods

A

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
Q

Triglyceride method glycerol interference

A

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
Q

Hyperlipoproteinemias

A

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

30
Q

Hormone sensitive lipase

A

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

31
Q

Calculating LDL

A

T cholesterol - ( HDL + [Triglycerides/5])

calculation is invalid if triglyceride value is over 500 mg/dL

32
Q

Measuring LDL

A

measure apoproteins, apo A-1 & B-100

use antibodies to apo E & A to remove other lipoproteins & measure residual

33
Q

Additional markers for cardiovascular disease

A

Lp(a), homocysteine, C-reactive protein, & Hs C reactive protein

Clinical Chemistry (23 decks)

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