Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOHD3: Exam 2 > Lipid Lowering Drugs (Potthoff) > Flashcards

Lipid Lowering Drugs (Potthoff) Flashcards

1
Q

25% of total cholesterol production occurs where?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HMG CoA –> Mevalonic Acid is the rate-limiting step of choleseterol synthesis. What enzyme is responsible for this conversion?

A

HMG CoA reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what enzyme is required for the esterification of cholesterol, readying it for incorporation into a chylomicron?

A

ACAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

free fatty acids in intestinal cells combine with glycerol to form _____, which are incorporated along with cholesterol esters into chylomicrons that can be transported into the general circulation.

A

triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

enzyme that removes triglycerides from chylomicrons in extrahepatic tissues that are expressing the appropriate Apo receptor

A

lipoprotein lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

True or false: high density lipoproteins are small in size and contain largely triglycerides.

A

False. HDL are small in size but they are most dense because they contain mostly protein (with only about 20% composition attributed to cholesterol).

Generally speaking, the larger the lipoprotein gets (e.g., –> VLDL), the more triglycerides they carry in relation to cholesterol, with chylomicrons being the largest of them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the specific apolipoprotein that is associated with LDL, IDL, and VLDL, which are formed in hepatocytes via the endogenous pathway

A

apo B-100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the specific apolipoprotein that is associated with chylomicrons, which are formed in the intestine via the exogenous pathway

A

apo B-48

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the two fates of FFA that are hydrolized from the chylomicrons by lipoprotein lipase (LPL)?

A
  1. In adipose cells, they can be re-esterified and stored

2. in cardiac/skeletal muscle cells they can be oxidized to form ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 3 fates of chylomicron remnants, that have been disassociated by LPL?

A
  1. can be taken up by endocytosis and re-esterified/stored in hepatocytes as cholesterol
  2. can be used for bile acid synthesis
  3. can be incoporated in hepatic lysozomes to VLDL and transported back into circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

True or false: IDL have more triglycerides than cholesterol esters

A

False. CE have more TG than IDLs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the 2 metabolic fates of IDL?

A

can be taken up by hepatocytes or continue losing TAGs and become LDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

enzyme that esterifies cholesterol in the extrahepatic tissues, allowing it to be “scavenged” by HDL where it can be transported back to the liver or incorporated into IDLs

A

LCAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

lipoprotein that is synthesized by the liver, and can be converted to LDL by hepatic lipase

A

VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

lipoprotein that can be taken up by hepatic or nonhepatic tissues, and in circulation can be taken up by macrophages to produce foam cells, which contribute to atheromatous plaques

A

LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the recommended treatment for borderline or high cholesterol?

A

dietary intervention first, and drug treatment if familal CHD or 2 other risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

which of these is NOT a risk factor associated with hypercholesterolemia?

A. Male
B. Diabetes
C. Smoking
D. Hypertension
E. High HDL
A

E. High HDL is considered to have a protective effect against the development of heart disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do omega 3 fatty acids decrease triglycerides? what is the best source of these?

A

they activate the transcription factor PPARα which promotes upregulation of lipoprotein lipase, ultimately decreasing serum TGs. The best source is fish oil (contains the active form).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

a (supposedly) more potent form of omega 3 fatty acid available by prescription

A

Lovaza

20
Q

which of the following is NOT an approach that is utilized to lower lipid levels?

A. preventing absorption of intestinal cholesterol 
B. decreasing cholesterol synthesis
C. downreglating LDL receptors
D. upregulating lipoprotein lipase
E. inhibiting VLDL secretion
A

C. Downregulating LDL receptors would lower the uptake of circulating LDL and lead to higher lipid levels.

21
Q

Bile acid is made from cholesterol in the ____ and stored in the _____.

A

liver; gall bladder

22
Q

how do bile acid sequestrants work?

A

they bind bile acids and block their reabsorption, causing the liver to produce more to replace those that have been lost. Because the body uses cholesterol to make bile acids, this reduces the amount of LDL cholesterol circulating in the blood

23
Q

name 2 commonly prescribed bile acid sequestrants

A

cholestyramine and colesevelam

24
Q

Which of the following statements regarding bile acid sequestrants is FALSE?

A. They increase the uptake of LDL via upregulation of LDL receptors
B. They increase hepatic production of VLDL (increase TGs) by 15-20%
C. Cholestyramine has fewer side effects than colesevelam
D. Colesevelam reduces hyperglycemia
E. Side effects associated with their use include malabsorption of vitamin K, GI upset, and impaired absorption of other drugs

A

C. Cholestyramine is a 1st generation bile acid sequestrant, and is associated with more side effects than colesevelam, which is why it is no longer as commonly used.

25
Q

water soluble vitamin that inhibits VLDL secretion leading to decreased production of LDL and triglycerides, while increasing HDL and having no effect on bile production

A

niacin

26
Q

Which of these is NOT a toxicity associated with niacin?

A. irreverisble elevations in liver function test
B. insulin resistance with long-term use
C. prostaglandin mediated vasodilation (flushing)
D. hyperuricemia
E. acute hepatic necrosis

A

A. While niacin use is associated with an elevated liver function test, this is a reversible toxicity.

27
Q

lovastatin, simvastatin and atorvastatin are all metabolized by which CYP?

A

CYP3A4

28
Q

fluvastatin and rosuvastatin are metabolized by which CYP?

A

CYP2C9

29
Q

why is it recommended that HMG CoA reductase inhibitors be taken at night?

A

this is when cholesterol synthesis is mainly happening, and the inhibitors have varying half lives, some as short as 1-3 hours (lovastatin)

30
Q

statins that are CYP3A4 substrates have ____ drug levels in the presence of CYP3A4 inhibitors and _____ drug levels in the presence of CYP3A4 inducers (e.g., barbiturates)

A

increased; decreased

31
Q

what is a major toxicity associated with increased levels of statins, as seen in drug-drug interactions that inhibit CYP3A4?

A

myopathy. grapefruit juice is also an inhibitor of CYP3A4, and this toxicity is seen in patients who drink more than 1 L of grapefruit juice per day (ummm, who does this)

32
Q

class of drugs that act as ligands for PPARα, a transcription factor which promotes the upregulation of lipoprotein lipase and ultimately decreases TGs

A

fibric acids (gemfibrozil, clofibrate, fenofibrate)

33
Q

name 3 fibric acids

A

gemfibrozil, clofibrate, fenofibrate

34
Q

which of these statements regarding fibric acids is FALSE?

A. serve as ligands for a transcription factor that upregulates lipoprotein lipase
B. lowers triglycerides and HDL cholesterol
C. decreases VLDL and LDL
D. clear chylomicrons quickly from circulation
E. primary useful for treating hypertriglyceridemia

A

B. Fibric acids lead to a decrease in triglycerides but actually raise HDL.

35
Q

risk of myopathy with use of fibric acids is increased when they are combined with what other class of drugs?

A

statins

36
Q

drug that impairs the intestinal absorption of cholesterol by inhibiting the transporter NPC1L1

A

ezetimibe

37
Q 
All of the following classes of drugs have a moderate to great impact on reducing serum LDL cholesterol EXCEPT:
A. Bile acid sequestrants
B. Nictonic acid (niacin)
C. HMG CoA reductase inhibitors
D. Cholesterol absorption inhibitors
E. Fibric acids
A

E

38
Q

Which class of drugs has the greatest effect on increasing HDL?

A. Bile acid sequestrants
B. Nictonic acid (niacin)
C. HMG CoA reductase inhibitors
D. Cholesterol absorption inhibitors
E. Fibric acids
A

B

39
Q

Which class of drugs has the greatest effect on decreasing serum triglycerides?

A. Bile acid sequestrants
B. Nictonic acid (niacin)
C. HMG CoA reductase inhibitors
D. Cholesterol absorption inhibitors
E. Fibric acids
A

E. Omega 3 fatty acids are also shown to have a great effect on decreasing serum TGs.

40
Q

Which class of drugs shows no effect on serum triglyceride levels?

A. Bile acid sequestrants
B. Nictonic acid (niacin)
C. HMG CoA reductase inhibitors
D. Cholesterol absorption inhibitors
E. Fibric acids
A

A.

41
Q

What would be the most effective treatment plan for a patient who presents with high LDL cholesterol and high triglycerides?

A. Dietary intervention + Clofibrate + Niacin
B. Dietary intervention + Simvastatin + Gemfibrozil
C. Dietary intervention + Niacin + Colesevelam
D. Dietary intervention + Neomycin + Cholestyramine
E. Dietary intervention only

A

C. The best treatment plan would include dietary intervention, followed by niacin or a fibrate for their TG lowering capabilities, and then a bile sequestrant or HMG CoA reductase inhibitor for the high LDL.

In this example, C is better than B because you can avoid the drug-drug interaction (myopathy) of mixing a statin with a fibrate.

42
Q

True or false: the best treatment plan for a person with high triglycerides and normal LDL is dietary intervention + a statin.

A

False. Recommended treatment includes dietary intervention + a fibrate or niacin.

43
Q

Which of the following is the LEAST effective treatment for a patient presenting with high LDL whose triglycerides are normal?

A. Dietary intervention
B. Fibric acid
C. Nicotinic acid
D. HMG CoA reductase inhibitor
E. Bile acid sequestrants
A

B. Fibric acids have very little effect on lowering LDL.

44
Q

True or false: the best treatment for improving a low HDL is diet, exercise and smoking cessation.

A

True. A fibrate or niacin may also be used, though no studies have shown a clear cardiovascular benefit to increasing serum HDL.

45
Q

True or false: statins and bile acid resins are most effective when used in combination.

A

True. In combination, statins and resins cause a greater increase in HDL and greater decrease in LDL levels.

46
Q

This class of drugs decreases cholesterol synthesis, increases LDL receptors, and increases LDL uptake from the blood

A

statins (HMG CoA reductase inhibitors)

MOHD3: Exam 2 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions