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D1 Spring > Pharmacology - Lipid-Lowering Drugs (Exam 4) > Flashcards

Pharmacology - Lipid-Lowering Drugs (Exam 4) Flashcards

1
Q

T/F Lipids can be present in the blood without being bound to something

A

FALSE

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2
Q

How are lipids transported in the blood?

A

As protein-lipid complexes

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3
Q

What do protein-lipid complexes minimize?

A

Unfavorable hydrophobic-hydrophilic interactions

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4
Q

How are fatty acids transported in the blood?

A

Bound to albumin

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5
Q

Triglycerides derived from the diet are transported in what?

A

Lipoproteins

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6
Q

Large macromolecular complexed with proteins, triglycerides, and cholesterol

A

Lipoproteins

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7
Q

List the lipoproteins from biggest/least dense to smallest/most dense

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
  6. Free fatty acid-albumin complex
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8
Q

Largest, high % of triglycerides, lowest in density

A

Chylomicrons

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9
Q

2nd highest in triglycerides as a % of weight

A

VLDL

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10
Q

Highest in cholesterol esters as % weight

A

LDL

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11
Q

Highest in density due to high protein:lipid ratio

A

HDL

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12
Q

What are lipoproteins classified by?

A

Density

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13
Q

Fat ________
Protein ________
Cholesterol is ___________

A

Fat floats
Protein sinks
Cholesterol is in between

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14
Q

What is the essential component of cell membranes?

A

Cholesterol

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15
Q

What is the precursor of steroid hormones and bile acids?

A

Cholesterol

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16
Q

What does cholesterol play a role in?

A

Triglyceride transport

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17
Q

What is total cholesterol a combination of?

A

Cholesterol in VLDL, LDL, and HDL

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18
Q

What can shorten lifespan?

A

High blood cholesterol levels

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19
Q

What is the defining feature of atherosclerosis?

A

Deposition of cholesterol in arteries

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20
Q

What is the primary cause of premature death in the US?

A

Atherosclerosis

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21
Q

A type of fat that is carried in the blood and stored in fat cells throughout the body

A

Triglycerides

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22
Q

What are excess calories, sugar, and alcohol converted into?

A

Triglycerides

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23
Q

What is the building block of complex lipids?

A

Triglycerides

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24
Q

What can triglycerides be hydrolyzed to generate?

A

Fatty acids

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25
Q

What are the causes of high triglycerides in the general population?

A

Obesity
Inactivity
Smoking
Excess alcohol
High carb diets
Other disease (diabetes, renal failure)
Drugs (steroids, estrogen, etc)
Genetics

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26
Q

A triglyceride score of ______ or higher puts you at risk for metabolic syndrome

A

150

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27
Q

Metabolic syndrome is a clinical diagnosis that requires more than 3 of which risk factors?

A

Abdominal obesity
Elevated triglycerides
Reduced HDL cholesterol
Hypertension
Impaired fasting glucose

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28
Q

Atherosclerosis is caused from a development of what?

A

Fatty streaks and plaques in arteries

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29
Q

What happens when fatty streaks and plaques start developing in arteries? (ON EXAM)

A

Obstruct blood flow and weaken vessels

Macrophages invade injured endothelium -> become foam cells that die -> become part of plaque

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30
Q

T/F exogenous lipoprotein metabolism is from the diet

A

True

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31
Q

List the steps of exogenous lipoprotein metabolism

A
  1. Chylomicrons form in intestinal cells -> transport dietary cholesterol and triglycerides
  2. Enter circulation via intestinal lymph system
  3. Go to capillary endothelium of muscle and adipose tissue -> degraded to fatty acids, glycerol, monoglycerides by lipoprotein lipase
  4. Chylomicron remnants are depleted of triglycerides, but are enriched in cholesterol
  5. Chylomicron remnants enter liver -> bind to LDL receptor on hepatocytes -> taken up and metabolized to make more lipids
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32
Q

List the steps of endogenous lipoprotein metabolism

A
  1. VLDL synthesis in ER of hepatocytes
  2. VLDL secreted by liver into circulation
  3. Lipoprotein lipase degrades triglycerides to form IDL particles depleted of triglycerides
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33
Q

What are the 2 fates of IDL particles in endogenous lipoprotein metabolism?

A
  1. Bind to LDL receptor on hepatocytes -> get taken up and metabolized to make more lipids
  2. Metabolized by hepatic lipase on surface of hepatocytes -> form LDL -> LDL put into circulation -> taken up and metabolized by cells to make cholesterol
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34
Q

What is the suffix of lipid lowering drugs?

A

“-statin”

35
Q

What is the class of lipid lowering drugs that we need to know?

A

HMG CoA reductase inhibitors (statins)

36
Q

What are statins used for?

A

Hypercholesterolemia - caused by elevated LDL concentrations in people that have not responded to dietary modifications

37
Q

What are statins ineffective in?

A

Familial hypercholesterolemia
Homozygous for defective LDL receptor gene

38
Q

What is the mechanism of action of statins? (ON EXAM)

A

Competitively inhibit HMG CoA reductase, which is the rate-limiting step in endogenous cholesterol synthesis

39
Q

Statins can decrease ___________ levels and increase _______________ levels

A

triglyceride; HDL cholesterol

40
Q

Where are statins metabolized?

41
Q

How are statins excreted?

A

Bile and feces

(some urinary elimination also)

42
Q

What can statins cause?

A

Elevated liver enzymes

(liver function is often evaluated prior to tx)

43
Q

What is used to make cortisol, estradiol, testosterone, aldosterone, vitamin D, etc?

A

Cholesterol

44
Q

What are the adverse effects of statins?

A

Liver failure
Myopathy Rhabdomyolysis (skeletal muscle injury)

45
Q

Who cannot use statins?

A

Pregnant women

46
Q

What can statins increase the effects of?

47
Q

Fibrates are derivates of _______ ________

A

fibric acid

48
Q

What are fibrates used for?

A

Hypertriglyceridemias

49
Q

What do fibrates lower?

A

Serium triglycerides

50
Q

What do fibrates increase?

51
Q

What is the possible mechanism of fibrates?

A

Activates ligands for PPAR-alpha, which is a transcription factor that regulates genes for lipid and glucose homeostasis

52
Q

Which drug can increase incidence of Rhabdomyolysis if used in combination with statins?

53
Q

What does nicotinic acid (niacin) increase and decrease?

A

Increase HDL and lipoprotein lipase
Decrease VLDL and LDL

54
Q

What is the mechanism of nicotinic acid (niacin)?

A

Inhibit VLDL synthesis by stopping adipose tissue lypolysis and delivery of fatty acids to the liver

55
Q

T/F nicotinic acid (niacin) has a long half life

A

FALSE, it has a very short half life

56
Q

What does nicotinic acid (niacin) cause in 50% of people?

A

Flushing and GI distress

57
Q

What can nicotinic acid (niacin) worsen in diabetic patients?

A

Insulin resistance
Hyperglycemia

58
Q

Bile acid sequestrants are __________ in water

59
Q

Which drug is available as a dry resin that is mixed w/ juice and drank as a slurry?

A

Bile acid sequestrants

60
Q

What do bile acid sequestrants decrease?

A

Decrease plasma cholesterol and LDL levels

61
Q

What are bile acid sequestrants?

A

Anion exchange resins

62
Q

What do bile acid sequestrants bind to?

A

Bile acids in the intestinal lumen

63
Q

What are bile acids made from in the liver?

A

Cholesterol

64
Q

What patients cannot take bile acid sequestrants?

A

Patients w/ homozygous familial hypercholesterolemia

(they do not have functional LDL receptors)

65
Q

T/F bile acid sequestrants are absorbed

A

FALSE, they are NOT absorbed, so there are very few side-effects other than GI issues

66
Q

What are some side effects of bile acid sequestrants?

A
  1. Binds to anionic drugs and decreases their absorption (ex: warfarin)
  2. Hyperchloremic acidosis
  3. Bad taste
67
Q

What drug is a cholesterol absorption inhibitor?

68
Q

What is the mechanism of Ezetimibe?

A

Blocks NPC1L1 to prevent lipid transport
Blocks cholesterol uptake in intesine

69
Q

T/F Ezetimibe is effective at lowering lipid levels

A

FALSE, they are NOT very effective because they aren’t affecting endogenous lipid metabolism

70
Q

T/F most cholesterol comes from the endogenous lipid pathway

71
Q

Which patients cannot use Ezetimibe?

A

Patients with liver failure

72
Q

T/F most patients are on a cocktail (combination) of lipid lowering drugs

73
Q

What is the mechanism of omega-3 polyunsaturated fatty acids (fish oil)?

A

Decrease triglycerides
Inhibit synthesis of VLDL triglycerides and apolipoprotein B
Alter plasma cholesterol
Increase HDL

74
Q

Which type of lipoprotein is the largest particle of low density, and who’s main function is to transport dietary lipids to tissues for use and storage?

A. LDLs
B. HDLs
C. Chylomicrons
D. IDLs
E. VLDLs

A

C. Chylomicrons

75
Q

Which lipoprotein is considered a scavenger for cholesterol?

A. HDLs
B. LDLs
C. VLDLS
D. Chylomicrons
E. IDLs

76
Q

What is the function and location of lipoprotein lipase? (ON EXAM)

A. Transfer of cholesteryl esters from HDL to LDL and VLDL - Plasma
B. Hydrolysis of triglycerides in HDL and IDL - Liver
C. Esterification of free cholesterol to cholesteryl esters - Plasma
D. Hydrolysis of chylomicrons and VLDL triglycerides - Capillary Endothelium
E. Conversion of LDL into HDL – Intestinal epithelium

A

D. Hydrolysis of chylomicrons and VLDL triglycerides - Capillary Endothelium

77
Q

What type of cells do macrophages become as they engulf more and more cholesterol, becoming large and vacuolated? (ON EXAM)

A. Plasma Cells.
B. Neutrophils.
C. Super macrophages.
D. Foam Cells.
E. Hepatocytes

A

D. Foam Cells.

78
Q

How do the Bile Acid-Binding Resins (Cholestyramine, Colestipol, and Colesevelam) function?

A. By binding LDLs and removing them from circulation
B. By directly increasing HDL synthesis
C. By attacking the plaque directly
D. By binding bile acids
E. By inducing triglyceride metabolism

A

D. By binding bile acids

79
Q

What type of individual would not benefit from the bile acid binding resins?

A. Hemophiliacs
B. Patients suffering from gout
C. Patients genetically deficient in functional LDL receptors
D. Patients with a fever
E. Patients in renal failure

A

C. Patients genetically deficient in functional LDL receptors

80
Q

Which drugs are competitive inhibitors of hepatic HMG CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis? (ON EXAM)

A. Statins
B. Ezetimibe
C. Fibric acid derivatives
D. Bile acid-binding resins
E. Niacin

A

A. Statins

81
Q

What drugs act as act as PPARalpha ligands ultimately resulting in increased lipases and therefore increased lipid degradation?

A. Statins
B. Ezetimibe
C. Fibric acid derivatives
D. Bile acid-binding resins
E. Niacin

A

C. Fibric acid derivatives

82
Q

What drug class when used alone can have a side-effect of breakdown of muscle proteins that leads to renal toxicity with symptoms that include muscle pain and weakness and dark
urine?

A. Statins
B. Ezetimibe
C. docosahexaenoic acid
D. Bile acid-binding resins
E. Fibric acid derivatives

A

A. Statins

83
Q

Which lipid lowering drug acts by inhibiting endogenous cholesterol synthesis?

A. Colesevelam
B. Ezetimibe
C. Fenofibrate
D. Fluvastatin
E. Niacin

A

D. Fluvastatin

D1 Spring (47 decks)

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