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Term 2: Metabolism > Reddy's Lipid Metabolism > Flashcards

Reddy's Lipid Metabolism Flashcards

1
Q

What makes up the outer layer of plasma lipid particles (LDL, chylomicrons, etc)?

A
  • amphipathic phospholipids
  • unesterified cholesterol
  • Apolipoproteins
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2
Q

What makes up the core of plasma lipid particles (LDL, chylomicrons, etc)?

A
  • Triglycerides

- cholesterol esters

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3
Q

What are the lipoprotein risk factors for coronary heart disease?

A
  • High LDL

- Low HDL

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4
Q

All of the following plasma lipid particles contain cholesterol. Which cholesterol is considered ‘HEALTHY / GOOD’ cholesterol?

A. Chylomicrons
B. VLDL (Very Low Density Lipoprotein)
C. HDL (High Density Lipoprotein)
D. IDL (Intermediate Density Lipoprotein)
E. LDL (Low Density Lipoprotein)
A

C. HDL

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5
Q

What are the major functions of cholesterol?

A
  • alters fluidity of cell membranes
  • starting material for bile acids
  • starting material for steroid hormones
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6
Q

Where is the unsaturated fatty acid located on glycerol of a TAG?

A

-second carbon

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7
Q

What does phospholipase A2 do?

A
  • releases arachidonic acid from cell membranes

- inhibited by steroids

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8
Q

What does the drug Orlistat do?

A
  • inhibits intestinal lipases

- more lipids end up in feces instead of entering body

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9
Q

What does the drug Ezetimibe do?

A
  • prevents cholesterol absorption in the intestine

- Can be used with other drugs to help lower cholesterol

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10
Q

What type of fatty acids are essential? What do we need them for?

A
  • cis-polyunsaturated fatty acids

- needed to make local hormones and increase cell membrane fluiditiy

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11
Q

How are Trans-fats formed?

A
  • artificially
  • hydrogenation of oils
  • cooking for a long time at high temperatures
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12
Q

What do apolipoproteins do?

A

-help in packaging, transport, binding to receptors of enzymes for chylomicrons etc.

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13
Q

What particle adds apolipoproteins to chylomicrons?

A

-HDL

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14
Q

What does apolipoprotein C do?

A

-helps in docking VLDL and chylomicrons in tissues and activating lipoprotein lipase

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15
Q

What does apolipoprotein E do?

A

-recognizes receptors and helps in lipid particle uptake by the liver

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16
Q

What does HDL do?

A
  • adds lipoproteins to lipid particles
  • picks up cholesterol from periphery and delivers to liver for elimination
  • transfers fatty acids from VLDL to liver
17
Q

HDL cholesterol is considered ‘HEALTHY / GOOD’ cholesterol.
The reason is:

A. HDL is small in size and has high density

B. HDL tags Zip codes, thus help remove lipids from plasma

C. HDL is made both in liver and intestine while VLDL is made only
in liver

D. HDL transfers cholesterol from peripheral tissues (via plasma)
to liver for excretion / reuse

E. HDL contains Apolipoproteins

TWO correct answers

A

-

18
Q

What does LDL do?

A

-delivers cholesterol to the peripheral tissues and liver

19
Q

What do VLDLs do?

A

-deliver de novo TAG to peripheral tissues

20
Q

What is the effect of lower concentration of choleterol in cells on LDL receptors?

A
  • leads to more LDL receptors so that more LDL from plasma can be taken up and increase cellular cholesterol levels
  • more LDL receptors is good because plasma cholesterol levels will go down
21
Q

Where does the liver get its cholesterol?

A
  • makes it from acetate

- picks up from plasma (LDLs etc)

22
Q

How do LDLs lead to atherosclerosis?

A
  • damaged endothelial wall allows cholesterol-rich LDL to inflitrate wall
  • macrophages in the intima take up cholesterol and fibroblasts proliferate = wound response
  • macrophages release cytokines, leukocytes are recruited
  • ulceration of the plaque area promotes thrombosis formation leading to obstruction and infarction
23
Q

What is the main contributor to plaque in the arteries?

A

-circulating LDL

24
Q

What are the two ways in which we excrete cholesterol?

A
  • Free cholesterol with feces

- bile acids lost in feces

25
Q

What is sistosterol?

A
  • methylated cholesterol made in plants

- inhibits the absorption of cholesterol in the intestine

26
Q

Which one of these is likely to decrease obesity?

A.  Cannabinoids (Marijuana)
B.  Orlistat (Alli)
C.  Ghrelin (Growth Hormone-releasing peptide)
D.  Neuropeptide Y
E.  Leptin blockers
A

B. Orlistat (Alli)

27
Q

How do orally given bile acid binding resins lower LDL levels?

A
  • prevent bile (cholesterol) reabsorption, so it is pooped out
  • must use more cholesterol to create more bile acids
28
Q

How do statins reduce cholesterol?

A
  • competitive inhibitor of HMG-CoA reductase, thus inhibiting cholesterol production
  • Increases number of LDL receoptors, so plasma LDL will go down
29
Q

Statin class of drugs are commonly used to reduce
plasma cholesterol levels. Beneficial effects of Statins can
be explained in part, by which of the following?

A. Activation of Hormone-sensitive lipase

B. Activation of HMG-CoA reductase

C. Inhibition of cholesterol absorption in the GI tract

D. Decreased oxidation of LDL cholesterol in the plasma

E. Increasing LDL receptors, thus decreasing plasma LDL

A

E. Increasing LDL receptors, thus decreasing plasma LDL

30
Q

How does Niacin influence hormone sensitive lipase?

A

-it inhibits it so fat stays in the adipose tissue

31
Q

What do Fibrates do?

A

-activate endothelial cell lipase so fat leaves the blood

32
Q

What does Probucol do?

A
  • inhibits oxidation of cholesterol

- this is good because oxidized cholesterol leads to the formation of plaques

33
Q

How do Omega-3 fatty acid supplements work?

A
  • not really sure
  • probably by regulating nuclear transcription to cause decrease in fatty acid synthesis and an increase of beta oxidation of fatty acids
34
Q

What are the beneficial effects of moderate alcohol consumption?

A
  • LDL goes down
  • HDL up
  • CV incidents go down
35
Q

One of your patients has moderately high levels of cholesterol.
Diet and exercise alone did not lower the cholesterol levels
sufficiently. You decide to prescribe Lovastatin.

Treatment with Lovastatin results in:

A. Decreased synthesis of HMG-CoA messenger RNA

B. Increased HMG-CoA reductase enzyme activity

C. Increased ACAT (Liver CAT) activity

D. Increased cholesterol synthesis

E. Increased number of LDL receptors

A

E. Increased number of LDL receptors

Term 2: Metabolism (5 decks)

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