Lipids! Flashcards

1
Q

what is the difference between saturated and unsaturated fatty acids? What are linoleic and linolenic acids? What are the polyunsaturated fatty acids?

A

saturated: no C=C bonds
- usually solids at room temp
unsaturated: one C=C bond (polyunsaturated = more than one C=C bonds; omega fatty acids)
- liquids at RT

linoleic and linolenic acids are fatty acids in plants and must be ingested via diet

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2
Q

triglycerides from plants are what form at room temperature? what about the ones from animal fat?

A

plant = polyunsaturated = oils at RT

animal sources = saturated fatty acids = solids at room temperature

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3
Q

what is the structure of lipoproteins, and how does their size relate to what kind of lipoprotein they are?

A

surface: phospholipids, free cholesterol, and apolipoproteins (proteins)
- amphiphatic

core: hydrophobic cholesterol esters and triglycerides

the bigger the lipoprotein, the more core lipids it is carrying
- eg VLDL and chylomicrons, and even LDL

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4
Q

what kind of apolipoproteins are involved in the different kinds of lipoproteins?

A

APO A I and II: HDL
APO B48: chylomicrons only
APO B100: LDL and VLDL
APO C I - III and APO E: VLDL

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5
Q

where are chylomicrons made, what do they do to plasma, and what is their function?

A

made in intestines

large size scatters light = plasma turbidity and also creamy top layer on plasma

transport dietary lipids (exogenous triglycerides) to both the liver and peripheral cells

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6
Q

where are VLDL molecules made, what is their function, and what can increase their production?

A

made in the liver

transport endogenous (hepatic derived) lipids FROM the liver TO the peripheral cells

excess dietary intake of carbs, saturated fatty acids, and trans fatty acids enhanced the liver to make triglycerides

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7
Q

what are IDLs and what can they cause in excess and why?

A

they’re VLDL remnants, as VLDLs turn into LDLs.

can cause PVD and CAD because these particles are damaging to blood vessels

(also seen in high amounts with people with hyperlipoproteinemia due to abnormal form on APO E)

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8
Q

what causes foam cells?

A

macrophages that have taken up too much LDL (since LDL can filtrate into the extracellular space of the vessel walls)

early precursor to atherosclerotic plaque

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9
Q

what is the function of LDL?

A

takes endogenous cholesterol to the arteries as plaque from the liver

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10
Q

what is the function of HDL? Where is it made?

A

transport cholesterol from the arteries back to the liver via the reverse cholesterol transport pathway

made in both the liver and intestine

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11
Q

during the process of digestion, ________ ______ first turns ________ lipids into more _____ compounds with amphipathic properties by cleaving off ______ _____.

A

pancreatic lipase turns dietary lipids into more polar compounds with properties by cleaving off fatty acids
- triglycerides to mono/di-glycerides
- cholesterol esters to free cholesterol
- phospholipids to lysophospholipids

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12
Q

what happens when the newly formed amphipathic lipids in the intestinal lumen aggregate with bile salts?

A

they turn into micelles, and then lipid absorption occurs when the micelles come into contact with the micro villus membranes of the intestinal mucosal cells

  • cholesterol less good than triglycerides at being absorbed
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13
Q

chylomicrons are first secreted into ______ ______ and the enter circulation via the _____ duct. What do they then interact with on various tissues? What do they become when they are transported back to the liver?

A

first secreted into lymphatic vessels and enter circulation via the thoracic duct

interact with proteoglycans on various tissues

broken down into VLDLs in the liver (which then go to the peripheral cells)

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14
Q

what happens to turn VLDL into LDL?

A

VLDL loses core lipids that will turn it into LDL

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15
Q

what happens when proteoglycans interact with chylomicrons?

A

promotion binding of LPL which hydrolyzes triglycerides on chylomicrons
- free fatty acids used by cells for energy
- excess fatty acids re-esterized for long-term energy storage

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16
Q

HDL can also transfer _________ ______ to chylomicrons and _____ to the liver. The cholesterol on HDL is transferred to ____ and then is excreted into ____

A

can also transfer cholesteryl esterase to chylomicrons and VLDL to the liver.

cholesterol on HDL transferred to LDL and excreted into bile

17
Q

the relationship between heart disease and dyslipidemias is what?

A

stems from deposition of lipids mainly in the form of esterified cholesterol in artery walls. This deposition results in fatty streaks (excess fat in macrophages in the sub endothelial cells) that can turn into plaques later in life
- plaques in legs/arms = peripheral vascular disease

18
Q

lipid deposits in the skin form nodules called _________?

A

xanthomas (usually due to a genetic abnormality)

19
Q

there is a strong correlation between hypercholesterolemia and ____ ____? what is a genetic abnormality that predispose people to have high cholesterol

A

CAD mortality

familial hypercholesterolemia
- heterozygotes more common to see than homozygotes
- can see xanthomas (cholesterol deposits) under tendons or the cornea

20
Q

how do you treat hypercholesterolemia?

A

statin: a HMG-CoA reductase inhibitor, and this adds LDL receptors to liver for removal of LDL from circulation

21
Q

increased cholesterol levels are associated with what four things? what about decreased cholesterol levels?

A

increased: hypothyroidism, liver disease, renal disease, and diabetes

decreased: hyperthyroidism, inherited defects, malabsorption, and impaired liver function

22
Q

what things are associated with increased and decreased HDL?

A

increased: progesterone levels, exercise, and blood pressure medications

decreased: progesterone levels, obesity, smoking, triglyceride increase, and diabetes

23
Q

increased triglycerides is increased in secondary disorders such as?

A

hormonal abnormalities with the pancreas (insulin/glucagon), adrenal glands (ACTH), pituitary (GH), or diabetes mellitus (shunting of glucose into the pentose pathway that increase fatty acid synthesis), or alcohol consumption

can accelerate atherosclerosis process

24
Q

severe hypertryglyceridemia can cause acute and recurrent _________. Usually due to a deficiency of what two things?

A

pancreatitis

due to APO C2 or LPL that will hydrolyze triglycerides for cells for energy

25
Q

what are causes for increase glycerol levels (increased triglycerides)?

A

mannitol infusion, nitroglycerine use, hemodialysis

26
Q

familial combined hyperlipidemia is caused by an increase in what two things? what are these elevations due to?

A

increase in elevated cholesterol, triglycerides, or both. Due in part to excessive hepatic synthesis of apoprotein B (leads to increased VLDL secretion and increased production of LDL from VLDL)

27
Q

familial dysbetalipoproteinemia (hyperlipidemia type III) is due to what?

A

accumulation of cholesterol-rich VLDL and chylomicron remnants (eg IDL) due to defective catabolism of these particles
- increased total cholesterol (200 - 300 mg/dL) and increased triglycerides (300 - 600 mg/dL)
- increased PVD and CAD risk

28
Q

mixed hypertriglyceremia/hypercholesterolemia can be due to what three things?

A

diabetes mellitus, nephrotic syndrome, or familial

29
Q

decreased HDL is assisted with what disease?

A

Tangier’s disease (hypoalphaproteinemia)

30
Q

cholesterol measurement is dependent on ________ for ___ hours

A

fasting for 12 hours

31
Q

what is the most common enzymatic sequence for measuring cholesterol? What things should be avoided during cholesterol analysis?

A

cholesteryl ester hydrolase: cleaves fatty acid residues from cholesteryl esters to make free cholesterol that gets reduced by cholesterol oxidase to make H2O2 to make a color reaction

avoid reducing agents: Vit C and bilirubin
also avoid turbidity

32
Q

HDL analysis uses:

A

ultra centrifugation or selective precipitation

33
Q

what is the friedewald calculation for LDL-C?

A

total cholesterol - HDL - trig/5

where VLDL is trig/5 as long as trig doesn’t exceed 400 mg/dL)

34
Q

how long do you need to fast for triglyceride analysis?

A

12 - 16 hrs

35
Q

what is the reference range for
- total cholesterol
- HDL-C
- LDL-C
- triglycerides
- glucose
(all in mg/dL)

A

total cholesterol: 140 - 200
HDL: 40 - 75
LDL: 50 -130
triglycerides: 60 - 150
glucose: 75 - 100

36
Q

cholesterol can be falsely ______ due to _____ when patient is laying down

A

falsely decreased due to hemodilution (diluted blood)