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DrugCards > AntihyperlipidemicDrugs > Flashcards

AntihyperlipidemicDrugs Flashcards

1
Q

Name the brand version of Atorvastatin

A

Lipitor

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2
Q

Name the brand version of Simvastatin

A

Zocor

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3
Q

Name the brand version of Rosuvastatin

A

Crestor

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4
Q

Name the brand version of Pravastatin

A

Pravachol

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5
Q

Name the brand version of Lovastatin

A

Mevacor

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6
Q

What enzyme metabolizes atorvastatin, simvastatin, and lovastatin?

A

CYP3A4

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7
Q

What enzyme metabolizes fluvastatin and pitavastatin

A

CYP2C9

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8
Q

How is rosuvastatin metabolized?

A

Most of a dose of rosuvastatin will not be extensively metabolized, but some will be metabolized by CYP2C9

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9
Q

How is pravastatin metabolized?

A

Chemical degradation in GI

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10
Q

Which statins are prodrugs?

A

Simvastatin and Lovastatin

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11
Q

What is the formal name of the drug class “statins”?

A

HMG-CoA reductase inhibitors

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12
Q

What are the generic names of the 7 statins we discussed? (bonus points if you also state the brand names)

A
  1. Atorvastatin (Lipitor)
  2. Pitavastatin (Livalo)
  3. Rosuvastatin (Crestor)
  4. Simvastatin (Zocor)
  5. Lovastatin (Mevacor)
  6. Fluvastatin (Lescol)
  7. Pravastatin (Pravachol)
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13
Q

Which enzymes do statins target and why is this desirable in people with hyperlipidemia?

A

They inhibit HMG-CoA reductase, which is the enzyme coordinating the rate limiting step in cholesterol biosynthesis

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14
Q

Which two drugs are PCSK9 inhibitors?

a. Praluent
b. Niacin
c. Alirocumab
d. Colestipol
e. Zetia

A

a and c

  • they are the same drug, Praluent is the brand version of Alirocumab
  • the true 2nd drug is Evolocumab
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15
Q

A person comes in with a UTI, is complaining of muscle spasms, and is exhibiting “flu-like” symptoms. You discover that they were prescribed a new drug to treat their high cholesterol, what type of drug are they most likely being treated with? (bonus points if you can also give drug names)

A

PCSK9 inhibitor
(Alirocumab and Evolocumab)

Side effects of PCSK9 inhibitors include:
-irritation at injection site
-Cold “flu-like” symptoms
Irritation of mucus producing cells/organs
-UTI
-Muscle pain and spasms

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16
Q

Explain the MOA of PCSK9 inhibitors

A

PCSK9 inhibitors are monoclonal antibodies that inhibit PCSK9. This causes receptor levels on the liver to stay constant –> more LDL can be taken up by the liver

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17
Q

A patient comes in complaining of muscle soreness and dark urine. They admit that they are not very active and are concerned because they drink a lot of water and haven’t been doing anything that should cause muscle soreness. They also tell you that they have recently started taking a new medication to help with their high cholesterol. What are they most likely taking? (bonus points if you know the medical terms for their adverse effects)

A 
a statin
(myopathy = muscle pain, myositis w/rhabdomyolysis =muscle tears increase iron in the blood which is filtered out in urine causing a dark-colored urine)
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18
Q

What is the brand version of the Fluvastatin?

A

Lescol

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19
Q

what is the brand of the Pitavastatin?

A

Livalo

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20
Q

All of the structural features are needed for a statin to mimic HMG-CoA except (select all that apply):

a. Unionized carboxylic acid group
b. Acetyl CoA group
c. Ionized carboxylic acid group
d. A 3-methyl group
e. A 7-carbon chain

A

a, b, d

For a statin to mimic HMG-CoA, it must be a 7-C chain with an ionized carboxylic acid group. The 3-methyl group seen on mevalonic acid is not necessary since it doesn’t play a role in binding

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21
Q

What enzyme controls the rate-limiting step in cholesterol synthesis and what is the product of the reaction?

A

Enzyme: HMG-CoA reductase
Product: Mevalonic acid

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22
Q

Lovastatin and Simvastatin are prodrugs that have a ________ ring structure. This structure will need to undergo ______ _______ before the drug can work on its target.

A
  1. Lactone

2. Ester hydrolysis

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23
Q

Hydroxylation at the ___ ________ is the rate limiting step of bile acid formation.

A

7C position

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24
Q

Which of the following is considered to be the “primary” bile salt?

a. Cholic acid
b. Taurocholic acid
c. Cholesterol
d. Glycocholic acid

A

a. Cholic acid

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25
Q

The sodium or potassium salts of which of the following is/are called bile salts?

a. Cholesterol
b. Taurocholic acid
c. Glycocholic acid
d. Cholic acid

A

b. Taurocholic acid

c. Glycocholic acid

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26
Q

Cholic acid undergoes which of the following phase II metabolism reactions? (select all that apply)

a. Aliphatic hydroxylation
b. Taurine conjugation
c. Glucuronidation
d. Sulfation
e. Glycine conjugation

A

b. Taurine conjugation
c. Glucuronidation
d. Glycine conjugation

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27
Q

Statins inhibit HMG-CoA reductase. How does this reduce cholesterol?

A

HMG-CoA reductase moderates the rate limiting step in cholesterol synthesis. Inhibiting it reduces cholesterol synthesis, including the production of isoprenoids needed for lipid modification of proteins.
The decrease of cholesterol in the liver leads to SREBP activation. SREBP activation leads to gene transcription and the upregulation of LDL receptors in liver cells. An increase in LDL receptors means more LDL is taken in and metabolized by the liver.

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28
Q

Statins can have all of the following effects on cholesterol levels except (select all that apply):

a. Increase TG
b. Decrease HDL and increase LDL
c. Increase HDL and decrease LDL
d. Increase CM

A

a, b, and d
-Statins decrease LDL and TG while increasing HDL

  • statins are taken at night before bed so they have no effect on CM since CM are only detectible for up to 2 hrs after meals.
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29
Q

Bile acid sequestrants can have which of the following effects on cholesterol:
a. Decrease TG, decrease LDL, increase HDL
b, Increase TG, decrease LDL, decrease HDL
c. Increase TG, decrease LDL, increase HDL
d. No effect on TG, decrease LDL, increase HDL

A

d. No effect on TG, decrease LDL, increase HDL
- BASs bind to bile acid in the intestines and inhibit bile acid reuptake. This lowers cytosolic cholesterol levels which leads to the activation of SREBP. Activation of SREBP leads to upregulation of LDL receptors in the liver that lowers LDL concentration.

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30
Q

List the 3 bile acid sequestrants discussed in lecture

A

Cholestyramine
Colesevelam
Colestipol

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31
Q

A patient presents with weakness, bloating, dyspepsia, and several symptoms of vitamin deficiency. When you ask about their medication history, the pt tells you they are taking simvastatin and colestipol. What changes, if any, would you make to the pt’s meds? Justify your decision.

A

Keep the statin and add a multivitamin. Either keep the patient on the BAS and prescribe another medication for the bloating and dyspepsia or switch the patient to a PCSK9 inhibitor, a cholesterol uptake inhibitor, a fibrate, or niacin. GI upset is a common side effect of these meds too, but the patient may function better on them.

32
Q

Prescription niacin is available under what trade name?

A

Niaspan

33
Q

If a person has a condition where their ability to process hepatically cleared drugs is compromised, which of the following statins would you recommend? (select 2)

a. Pitavastatin
b. Rosuvastatin
c. Lovastatin
d. Atorvastatin
e. Fluvastatin
f. Pravastatin

A

b. Rosuvastatin and f. Pravastatin

  • Rosuvastatin is not extensively metabolized, although there is a small amount by CYP 2C9
  • Pravastatin is degraded in the GI
34
Q

Which of the following are pleiotropic effects of statins? (select all that apply)

a. Antioxidant properties
b. Inhibition of inflammatory response
c. Lower LDL levels
d. Weight loss
e. Improvement of endothelial dysfunction

A

a, b, and e

  • Statin pleiotropic effects include:
    1. Improvement in endothelial dysfunction
    2. Increased NO bioavailability
    3. Antioxidant properties
    4. Inhibition of inflammatory responses
    5. Stabilization of atherosclerotic plaques
35
Q

Stage I of cholesterol synthesis starts with the 2 step process of turning ______ into _______.

A

Acetyl-CoA into HMG-CoA

36
Q

The rate limiting step of cholesterol synthesis involves turning _______ into ________ using the enzyme ________.

A

HMG-CoA into Mevalonic acid

HMG-CoA reductase

37
Q

Stage II of cholesterol synthesis involves the cyclization of _____________ into ____________.

A

Squalene into lanosterol

38
Q

The 3rd and final stage of cholesterol synthesis involves the conversion of _______________ into _____________.

A

Lanosterol into cholesterol.

39
Q

BAS causes the excretion of bile acids in feces. How does this lead to a decreases in LDL levels?

A

The excretion of bile acids in feces means that liver must do more de novo synthesis of cholesterol (including TGs) to make more bile acids. This leads to a low cytosolic LDL condition that activates the transcription factor SREBP. Activation of SREBP leads to the production and upregulation of LDL-receptors. A small increase in HDL is also generated. As a consequence, plasma LDL levels decrease.

40
Q

True or false:

BAS are large polymers with a positive charge used to form an ionic interaction with a bile salt

A

True

  • BAS are:
    1. large polymers
    2. cationic at intestinal pH
    3. contain quaternary salt, secondary/ tertiary amines
41
Q

how are BASs commonly taken ?

A

PO with meals

42
Q

True or False:

Fibrates are generally recommended in patients with hypercholesterolemia that are under 25 yo.

A

False

-BAS are generally used in conjunction with a statin if statin therapy is insufficient or in patients with hypercholesterolemia that are under 25 yo.

43
Q

What is the brand of Ezetimibe

A

Zetia

44
Q

How does the cholesterol absorption inhibitor _________ (we only learned 1) lead to an increased expression of LDL receptors?

A

Ezetimibe (Zetia) blocks the receptor NCP1L1 in epithelial cells in the small intestine. This reduces cholesterol absorption. This means no CM synthesis and leads to decreased cytosolic cholesterol levels. This causes the liver to work harder to make VLDL. Decreased cytosolic cholesterol leads to upregulation of SREBP –> more LDL receptors and lower LDL.

45
Q

Cholesterol absorption inhibitors are considered superior to BASs because cholesterol absorption inhibitors do not affect the absorption of ______ or _____________________.

A

Cholesterol absorption inhibitors do not affect the absorption of TGs or fat soluble vitamins.

46
Q

The ionization state of zetia is:

a. cationic
b. anionic
c. neutral

A

Neutral

47
Q

What are the major side effects of zetia?

A

GI upset, dyspepsia, loose & fatty stool

rarely: myopathy

48
Q

Which drug acts as a combination of simvastatin and ezetimibe?

a. Cholestyramine
b. Niacin
c. Mevachol
d. Zetia
e. Vytorin

A

e. Vytorin

49
Q

The two fibrates available in the US are: (select 2)

a. Lipitor
b. Lopid
c. Tricor
d. Cholestipol
e. Alirocumab

A

b. Lopid and d. Tricore

50
Q

Tricor is the brand name of the fibrate __________.

A

Fenofibrate

51
Q

Lopid is the brand name of the fibrate __________.

A

Gemfibrozil

52
Q

Fibrates are agonists of what receptor?

A

PPARalpha

53
Q

Fibrates main lipid effect is to reduce which of the following?:

a. LDL
b. vLDL
c. TGs
d. HDL
e. CM

A

c. Triglycerides

- specifically plasma TGs

54
Q

Which is a secondary effect of fibrates?

a. Reduce inflammation which decreases chances that atherosclerotic plaques will rupture
b. Decreased cholesterol absorption in the small intestine
c. Increases NO bioavailability
d. Reduced plasma TGs are a result of PPARa agonism.
e. Heart arrhythmias

A

a. Reduce inflammation which decreases chances that atherosclerotic plaques will rupture

  • b. is the a consequence of cholesterol absorption inhibitors
  • c. is a pleiotropic effect of statins
  • d. is the main lipid effect of fibrates
  • e. is a side effect of fibrates
55
Q

A patient comes into to your clinic complaining of chest discomfort and has an irregular heart rhythm. You see that the patient is taking a statin and was recently prescribed another medication for hypercholesterolemia. The patient also has no history of heart issues. Assuming the 2nd medication is contributing to the cardiac symptoms, what type of drug is the patient most likely taking?

A

A fibrate

-Other side effects include GI discomfort and (rarely) myopathy

56
Q

Which of the 2 fibrates is a prodrug?

A

Fenofibrate (Tricore)

57
Q

How do fibrates increase HDL numbers?

A

The agonism of PPARa increases apoA-I and apoA-II synthesis in hepatocytes which increases plasma HDL

58
Q

PPARa activation by fibrates decreases plasma TGs through 2 different mechanisms. Describe one.

A
  1. PPARa activation –> decreased apoC-III synthesis in hepatocytes and increased LPL expression in muscle vascular beds –> Increased fatty acid uptake in muscle cells and increased fatty acid oxidation in muscle cells –> decreased plasma TGs
  2. PPARa activation –> increased fatty acid oxidation in hepatocytes –> decreased TG synthesis –> decreased plasma TGs
59
Q

True or false:

Fibrates are only prescribed in conjunction with statin therapy.

A

False

- Fibrates can be prescribed to treat patients who only have high TG levels.

60
Q

The effects of niacin are mediated through which receptor type of receptor:

a. Gai-GPCR
b. NCP1L1
c. PCSK9
d. SREBP
e. PPARa

A

Answer: a. Gai-GPCR

  • NCP1L1 is the target of the cholesterol absorption inhibitor Zetia
  • PCSK9 is the target of PCSK9 inhibitors Alirocumab and Evolocumab
  • SREBP is a transcription factor activated by low cytosolic cholesterol levels and leads to increased expression of LPL receptors
  • PPARa is activated by the fibrates Gemfibrozil(Lopid) and Fenofibrate (Tricor)
61
Q

Which of the following are key components of niacin’s MOA? (select all that apply)

a. Increased cholesterol excretion in bile
b. Increased HDL levels by reducing ApoA-I clearance
c. Decreased bile reabsorption
d. Decreased cholesterol absorption in the small intestine
e. Decreased de novo synthesis of TGs

A

Answer: a, b, e
Niacin binds Gai-CPR on adipose tissue –> decreases synthesis of hormone-sensitive lipase –> decreased plasma FFA –> decreased TG synthesis —> decreased plasma VLDL —> decreased IDL —> decreased LDL —> decreased cholesterol delivery to peripheral cells –> increased cholesterol removal from cells + decreased apoA-I clearance(from niacin) –> increased cholesterol delivery to liver —> increased excretion of cholesterol in bile

  • The MOA of BAS is decreased bile reabsorption
  • The MOA of cholesterol absorption inhibitors leads to decreased cholesterol absorption in the small intestine
62
Q

While doing rounds in a hospital, you notice that one of your patients looks very flushed. They also complain to you about an itchy skin. You know that they are taking a statin and another medication for high cholesterol. What is the other medication and how can you advise the patient so that they can avoid this issue in the future?

A

Answer: Niacin

  • Flushing decreases over time. To avoid it, the patient can:
    1. Take niacin at night
    2. Take an extended release version
63
Q

Which types of drugs cause an increase in liver LDL receptors by creating a condition of low liver cytosolic cholesterol?

a. Fibrate, BAS, and PCSK9 inhibitors
b. Fibrate, and niacin
c. Statin, Zetia, and BAS
d. Niacin and Zetia

A

c. Statins, BAS, and Zetia

64
Q

Which 2 drugs are best for patients with low HDL levels?

A

Fibrates and Niacin

65
Q

Of all the natural products people take to help lower their cholesterol, only ____________ has been shown to be effective.

A

Omega-3 fatty acids

66
Q

There are 2 prescription strength omega-3 fatty acids. They are _________ and _____________. Both are generally used to treat patients with levels of _________ over _____ mg/dL.

A

Lovaza and Vascepa

TGs over 500mg/dL

67
Q

True or false:

Omega-3 fatty acids work like combination statin and fibrate.

A

True

  • The MOA is through PPARa and SREBPs. They reduce de novo synthesis of TG.
68
Q

Increased LDL levels are associated with:

a. cardiovascular disease
b. arthrosclerosis
c. DM2
d. all of the above
e. none of the above

A

all of the above

69
Q

The major contributors to hyperlipidemia include:

a. Western diet
b. Sedentary lifestyle
c. Obesity
d. all of the above
e. a and b only

A

e. a and b only
- Genetics is also a major contributor
- Obesity is technically incorrect because a and b are the major factors that contribute to obesity

70
Q

VLDL made in liver contain which of the following: (select all that apply)

a. TGs
b. cholesterol
c. ApoB48
d. ApoE
e. ApoC

A

Answer: a, b, d, and e

-CM contain ApoB48, VLDL contains ApoB100

71
Q

__________________________________________ creates an ester bond btw cholesterol and TGs, allowing them to be packed together tightly.

A

AcetylcoenzymeA:cholesterol acyltransferase type 2

72
Q

________________________ is a cholesterol transporter in the small intestine.

A

Niemann-Pick C1 like protein NCP1L1

73
Q

True or false:

Exogenous lipids are produced in the liver

A

False

  • Exogenous lipids come from the diet
  • Endogenous lipids are produced in the liver
74
Q

Omega 3 fatty acids have which of the following effects on lipid levels:

a. Lowers TG, Lowers LDL, Lowers HDL
b. Lowers TG, Lowers LDL, Raises HDL
c. No effect on TG, Lowers LDL, Raises HDL
d. No effect on TG, Lowers LDL, No effect on HDL
e. No effect, natural products don’t work

A

b. Lowers TG and LDL, increases HDL

75
Q

Omega 3 fatty acids act like a fibrate + statin because they:

a. Increase HDL
b. Activates PPARa and SREBP
c. Inhibit cholesterol uptake
d. Bind to bile acid and prevent cholesterol uptake

A

b. Activates PPARa and SREBP

  • Increasing HDL is accomplished by omega 3 fatty acids in high doses but it is not a MOA
  • Inhibiting cholesterol uptake is your MOA for cholesterol uptake inhibitors
  • BAS bind bile acid and cholesterol uptake inhibitor

DrugCards (7 decks)

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