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PCOL Cardio Questions > PCOL Lipid Pharm > Flashcards

PCOL Lipid Pharm Flashcards

1
Q

What can Hypertriglyceridemia cause?

A

Pancreatitis

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2
Q

What is the Goal to treat Dyslipidemia

A

Decrease LDL, TG, TCE and possibly raise HDL

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3
Q

Lipids (Lipoproteins) are made of what?

A

Phospholipids, Cholesterol and Triglycerides.

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4
Q

What are the different kinds of Apolipoproteins (Apo)?

A 
ApoA
ApoB 48
ApoB 100
ApoE
ApoC
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5
Q

Where is ApoB 48 synthesized?

A

Intestines

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6
Q

What is the function of ApoB 48?

A

Gives structural support to lipoproteins (lipids)

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7
Q

How is ApoB 100 different from ApoB 48 in it’s function?

A

ApoB 100 provides structural support and serves as a ligand for the LDL receptors on liver. Whereas ApoB 48 only gives structural support.

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8
Q

Where is ApoB 100 synthesized in the body?

A

It is synthesized in the liver.

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9
Q 
If ApoB 100 is only synthesized in the liver what molecules will have ApoB 100?    (select all that apply)
A. VLDL
B. Chylomicrons
C. IDL
D. Chylomicron remnants
E. LDL
A

A. VLDL
C. IDL
E. LDL

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10
Q

What is the TG:CE ratio of Chylomicrons?

A

10:1

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11
Q 
Which of these molecules has the highest density?
A. Chylomicron
B. IDL
C. HDL 3
D. LDL
E. HDL 2
A

C. HDL 3

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12
Q 
Which of these molecules has the highest concentration of Cholesterol?
A. Chylomicrons
B. IDL
C. HDL3
D. LDL
E. HDL 2
A

D. LDL

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13
Q

What is the function of Apo C?

A

Allows lipoproteins to bind to LPL.

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14
Q

What does a chylomicron become after it has interacted with an LPL and lost some of it’s Triglycerides?

A

Chylomicron Remnant

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15
Q 
HDL has all of the following Apolipoproteins except: (select all)
A. Apo A
B. Apo B 48
C. Apo C
D. Apo B 100
E. Apo E
A

B. Apo B 48

D. Apo B 100

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16
Q 
LDL has which of the following Apolipoproteins?
A. Apo A
B. Apo B 48
C. Apo C
D. Apo B 100
E. Apo E
A

D. Apo B 100

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17
Q

T/F Smaller amounts of Apo A on the surface of HDL make it more efficient in reverse cholesterol transport

A

False

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18
Q 
Which of the following ligands can bind to LDL receptors in the liver? select all 
A. Apo A
B. Apo B 48 
C. Apo C
D. Apo B 100
E. Apo E
A

D Apo B 100

E. Apo E

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19
Q 
What Apolipoprotein does LDL rely on in order to bind to LDL receptors in the liver?
A. Apo A
B. Apo B 48
C. Apo C
D. Apo B 100 
E. Apo E 
F. Both D and E
A

D. Apo B 100

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20
Q 
If a patient has increased levels of chylomicrons in their blood stream and low amounts of chylomicron remnants what could the patient be lacking? (Select all that apply)
A. Apo C
B. Apo B 48 
C. Apo B 100
D. Apo E
E. LDL receptors 
F. LPL
A

A. Apo C
D. Apo E
E. LDL receptors
F. LPL

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21
Q

What cells is responsible for eliminating oxidized LDL?

A

macrophage

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22
Q 
All of the following are functions of HDL except:
A. Donation and reuptake of Apo E
B. Donation and reuptake of Apo C
C. Donation and reuptake of Apo B 48
D. Reverse cholesterol transport
A

C.

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23
Q

A VLDL remnant is known as ____

A

IDL

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24
Q

What cell does HDL pull cholesterol out of to prevent aetherosclerosis?

A

Foam Cells.

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25
Q

What is the source of chylomicrons?

A

Food/diet

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26
Q

What is a completely assembled chylomicron made out of?

A

Apo B 48
Apo A
Triglycerides
Cholesterol

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27
Q

What will the plasma levels of TGs be in a patient deficient in Apo C and LPL?

A

increased plasma levels of TGs.

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28
Q

T/F HDL will donate Apo E and Apo C to the chylomicron remnants

A

False. It takes them back from the chylomicron remnants since there is little surface area on the remnant to hold the Apo C and E.

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29
Q 
A lipid molecule floating around in the plasma contains Apo C, Apo E and Apo B 100. Which molecule(s) is it most likely to be? (select all)
A. Chylomicron
B. VLDL
C. HDL
D. IDL 
E. LDL
A

B. VLDL

D. IDL

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30
Q

Which Lipoproteins does HDL donate Apo E and Apo C too?

A

Chylomicrons and VLDL

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31
Q

Which Lipoproteins on an IDL can interact witht he LDL receptors in the liver?

A

Apo B 100 and Apo E

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32
Q

Which lipoproteins does HDL donate Apo E and C to which lipoproteins does it take them from?

A

Gives them to Chylomicrons and VLDL and takes them from chylomicron remnants and VLDL remnants (IDL)

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33
Q

If an IDL has higher amounts of Apo E on it’s surface than Apo C, will it most likely go to the liver or the LPL?

A

Liver

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34
Q

T/F Chylomicrons are only made from your diet.

A

True

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35
Q

How do plant sterols decrease the amount cholesterol and fatty acids entering the intesinal cells?

A

They compete with the NPC1L1 transport channel and this decreases the chances of fatty acids and cholesterol getting into the intestinal cell.

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36
Q

What is the function of the ACAT and DGAT in the ER of the intestinal cells?

A

Esterifies cholesterol and fatty acids.

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37
Q

After esterification of the fatty acids and cholesterol occurs in the ER what happens next?

A

MTP will transport it to a section of the ER that will assemble the TG, Cholesterol and B48 in order to make the chylomicron.

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38
Q

What is the name of the drug that blocks NPC1L1 in the intestine?

A

Ezetimibe

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39
Q

What can you expect when giving ezetimibe?
A. Lower absorption of cholesterol and fatty acids in the intestine
B. Increased breakdown of cholesterol from the liver
C. Increased production of cholesterol from the liver
D. All of the above
E. A & C

A

E. A & C
You wil get an increase in production of cholesterol from the liver because it will compensate for the lack of cholesterol being absorbed in the small intestine.

40
Q

What is the MOA of Colesevelam?

A

It is a very positively charged molecule that will bind to bile acids and prevent them from being absorbed back into the intestine.

41
Q

How does colesevelam lower cholesterol levels?

A

It binds to positively charged bile acids and leads to them being excreted from the body. When the body senses that you have decreased levels of bile acid it will try to make more by using up cholesterol stores, thus lowering cholesterol.

42
Q

How what is the MOA of Lomitapide?

A

Targets MTP and prevents it from transporting esterified cholesterol and fatty acids. As a result they do not get packaged and chylomicron levels are reduced.

43
Q

Why does Lomitapide work in the liver as well?

A

MTP Transporters are in the intestine and the liver. Since VLDL is made in the liver the same way chylomicrons are made in the intestine then inhibiting MTP in the liver will also decrease levels of VLDL produced as well.

44
Q

What kind of side effects does lomitapide have?

A

GI side effects

45
Q 
What drugs are Bile-Acid Sequestrants? (Select All)
A. Cholestyramine
B. Colestipol
C. Ezetimibe 
D. Lovastatin
E. Colesevelam
A

A, B, E

46
Q

The following effects are seen with Bile Acid Sequestrants except:
A. Decreased Heptatic Bile stores
B. Increased Bile acid synthesis
C. Decreased stores of cholesterol
D. Decreases TG synthesis
E. Increased LDL receptors and increased LDL clearance from the body (lowers LDL in blood)

A

D. Taking Bile Acid Sequestrants will actualy cause an increase in TG synthesis.

47
Q

If Bile Acid Sequestrants can cause an increase in TG synthesis what should patients watch out for?

A

Hypertriglyceridemia which can also lead to pancreatitis

48
Q

What are the main adverse drug reactions associated with Bile Acid Sequestrants?

A

Bloating and Constipation. The reason for this is because it prevents fats from being absorbed into the body and keeps it in the intestine.

49
Q

Which drug prevents the assembly of Apo B- containing proteins by blocking the MTP transporter?

A

Lomitapide (Juxtapid)

50
Q

What is Lomitapide given with?

A

Statins and diet change.

51
Q 
What Apolipoprotein on chylomicrons binds to the HL on the liver when it is too big?
A. Apo A
B. Apo B 100
C. Apo B 48
D. Apo E
E. Apo C
A

D. Apo E

52
Q

What molecule in the liver breaks down the chylomicrons?

A

Lysosomes.

53
Q

Why does a Apo B100 and LDL receptor deficiency lead to hypercholesterolemia?

A

LDL only has Apo B 100 to bind to LDL receptors so if you have a deficiency in one or both you will have high levels of cholesterol in the blood since LDL cannot be eliminated.

54
Q 
Which of these is the PRIMARY mechanism for LDL removal?
A. Apo E
B. Apo C
C. Apo B 100
D. Apo A
E. LDL receptors
A

E. LDL receptors

55
Q

What is the MOA of Statins?

A

Competitive inhibitor of HMG-CoA reductase.

56
Q

How do statins decrease LDL production? (Select All)
A. Blocks rate-limiting step in cholesterol biosynthesis
B. Prevents reabsorptoin of cholesterol at intestine
C Increases LDL receptor expression
D. Increases clearance of other lipoproteins such as chylomicrons, IDL, VLDL etc.
E. Decreases VLDL production

A

A, B, D, E

57
Q

All of the following are Pleiotropic effects of statins except:
A. Improve vascular endothelium function
B. Increases Anti-oxidant Effects
C. Reduce Platelet Aggregation and increase Plaque stability.
D. Decreases Antiogenesis.
E. Lower LDL and improve lipid profile

A

E. This is a primary effect

58
Q 
All of the following are pleiotropic effects of statins except:
A. Increases Anti-thrombotic activity
B. Increases Anti-inflammatory activity
C. Decreases cholesterol biosynthesis
D. Immunomodulatory effects
E. Preserve endothelial function
A

C. This is a primary effect

59
Q

T/F Chances of Rhabdomyolysis increase with lower doses of statins

A

False.

60
Q

Which drug greatly increases the chances of Rhabdomyolysis occuring with statins?

A

Gemfibrozil. Because it blocks the OATP1B1 transporters. This will keep the statin in the blood and have a higher chance of reaching muscle tissue.

61
Q 
Which factors will increase the chances of statin-induced Rhabdomyolysis?
A. Age
B. Dose
C Renal and hepatic dysfunction
D. CYP3A4 and 2C9 mutations
E. All of the above
A

E. Your welcome lol

62
Q 
Statins decrease cholesterol production in the liver and this causes upregulation of the NPC1L1 receptor. Which drug do we give in combination with the statin to directly counteract this problem?
A. Colesevelam
B. Aspirin
C. Ezetimibe
D. Amlodipine
A

C.

63
Q 
Which of these drugs is an Antisense?
A. Ezetimibe 
B. Mipomersen
C. Alirocumab
D. Fenofibrate
E. Niacin
A

B. Mipomersen

64
Q

What is the MOA of Mipomersen?

A

Targets the production of Apo B 100 in the liver. It binds to mRNA portion that makes Apo B 100 and prevents it from producing the Apo B 100.

65
Q

How does preventing the production of Apo B 100 lower LDL levels?

A

Without Apo B 100 the lipoprotein VLDL cannot be made since it will not have it’s structural component.

66
Q 
Which of the following drugs are Antibodies? (Select All)
A. Mipomersen
B. Lomitapide
C. Alirocumab
D. Cholestyramine
E. Evolocumab
A

C. Alirocumab

E. Evolocumab

67
Q

What is the class of drug of Evolocumab and Alirocumab?

A

monoclonal antibody

68
Q

What is the MOA of Evolocumab and Alirocumab?

A

Binds to proprotein known as PCSK9 and this prevents LDL receptor degredation. This lowers LDL by increasing the LDL receptor expression.

69
Q

What areas of the body is Lipoprotein Lipase located?

A

Adipose Tissue
Skeletal Muscle
Cardiac Muscle
Breast Tissue.

70
Q

What will plasma TG levels look like with deficiencies in Apo C?

A

Elevated TG levels because the TGs are unable to be broken down by the LPL enzyme and stored as free fatty acids.

71
Q

Low levels of Apo C lead to increased levels of serum TGs. What is this condition known as?

A

Hypertriglyceridemia

72
Q

Fibric acid deriviatives such as Gemfibrozil and Fenofibrate are used for which of the following reasons?
A. Patients with sever hypertriglyceridemia
B. Primary treatment prevention of LDL production
C. Type III Hyperlipoproteinemia
D. All of the above
E. A & C only

A

A & C. Statins are used primarily in the treatment of dyslipidemia

73
Q

How do fibric acid derivatives lower blood TG and lipid levels?

A

Act as an agonist to the PPAR-a (Peroxisome Proliferator Activated Receptors) and increases LPL function and expression. It can also slightly enhance HDL levels

74
Q 
Where is the primary site of action of Fibric Acid?
A. Liver
B. Intestine
C. Periphery
D. ER
A

C. Periphery. It does act at the liver as well however, it is only a secondary function (a bonus effect)

75
Q

What is the function of fibric acid at the liver?

A

Decreases free fatty acid production in the liver thus lowering the amount of TGs produced and lowering the production of VLDL and LDL as a result. This is a secondary bonus effect however.

76
Q

What additional secondary effects does Fibric Acid have?

A

Increases fatty acid oxidation, Increases Apo A expression (which is why fibric acid derivatives increase HDL) and reduces LDL receptor clearance.

77
Q

Boostaphilus love males boostaphilus more. True or False

A

Twue, because yeah!

78
Q

What possible side effects can Fibric acid have when administered with a statin?

A

Rhabdomyolysis and myopathy. This is more common with Gemfibrozil however which is why it is contraindicated to give Statins with Gemfibrozil

79
Q 
Which of the following are effects of Fibric acid derivatives? (Select All)
A. Decreased levels of LDL
B. Increased levels of VLDL
C. Decreased levels of VLDL
D. Increased levels of HDL
E. Decreased levels of TGs
A

A,C, D, E

HOWEVER. for some unknown reason gemfibrozil can actually increase LDL levels

80
Q

What is the primary effect of Niacin?

A

Primary site of action is the liver by esterifying the fatty acids in order to stop the conversion of Fatty Acids to TGs in the Liver. This causes a lower production of VLDL and that leads to a lower production of LDL as a result.

81
Q

What is the Secondary (minor) Effect of Niacin?

A

It prevents the breakdown of TGs to free fatty acids in adipose tissue by binding to GPCR109A which is a Gi subunit. This inhibits lipolysis.

82
Q

What are the two main side effects of Niacin? How should you tell the patient to take the medication?

A

Flushing and Dyspepsia. Tell the patient to take the medication with cool beverages and NOT HOT BEVERAGES OR ALCOHOL.

83
Q

Why does Niacin cause flushing

A

It increases Prostaglandin Synthesis which leads to vasodilation and skin flushing.

84
Q

Niacin Lowers LDL, VLDL and TG while increasing HDL. If this is the case then why don’t we take it to treat dyslipidemia as often as statins?

A

In order to get these effects you must take the medication at much higher doses and this will lead to more side effects.

85
Q

What kind of effects will you see with omega-3-fatty acids?

A

Anti-inflammatory and vasodilatory effects. Always better. Omega-3 competes with Omega-6 (which has vasoconstriction and inflammatory effects)

86
Q

What are Omega-3 Fatty acids primariliy used for?

A

Cardiovascular Risk Reduction. This includes Hypertriglyceridemia, HTN, Angina and Atherosclerosis

87
Q

Why is it preferred to consume fish rather than Omega supplements?

A

In order to get the same amount of Ecosanoid (EPA) and DHA you would need to consume large amounts of the suplement.

88
Q

What kind of toxicity could you get with Omega-3-fatty acid supplements?

A

Vitamin A toxicity since most Omega-3-fatty acid supplements contain vitamin A as well.

89
Q 
What is the major Apolipoprotein of HDL?
A. Apo B
B. Apo C
C. Apo E
D. Apo A
A

D. Apo A

It is needed for the normal function of HDL

90
Q

What are the 3 types of HDL and where can HDL be synthesized?

A

Pre-HDL, HDL 3, HDL 2. It can be synthesized by the liver and intestine.

91
Q

What are the 3 key functions of HDL?

A

Donates Apo C and Apo E
HDL Maturation: scavenges Apoproteins and phospholipids
Reverse Cholesterol transport (Biggest function)

92
Q

What transporter does Apo A bind to in order to do reverse cholesterol transport?

A

ABCA1 and ABCG1.

93
Q

Once the HDL has been docked to the macrophage vwhat does it use to take the cholesterol back from the foam cell?

A

Lecithin Cholesterol Acyltransferase (LCAT).

94
Q

What is the purpose of the LCAT in the reverse cholesterol transport process?

A

It esterifies the cholesterol in the foam cell in order to remove it from the cell.

95
Q

What enzyme is responsible for the exchange of TGs for cholesterol?

A

Cholesteryl Ester Transferase Protein (CETP)

PCOL Cardio Questions (4 decks)

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