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Advanced Pharmacology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Chylomicrons carry fats absorbed in the ____

A

Diet

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2
Q

VLDL carries fats from the ____

A

Liver

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3
Q

LDL is “___” cholesterol

A

Bad

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4
Q

HDL is the “____” cholesterol

A

Good

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5
Q

Lipoproteins are spherical particles that transport ____ molecules, principally cholesterol and triglycerides

A

Hydrophobic

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6
Q

The surface of chylomicrons is composed of a monolayer of ____ and unesterified cholesterol molecules

A

Phospholipid

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7
Q

Apolipoprotein B-100 carries ____ to tissues

A

Cholesterol

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8
Q

The goal for apolipoprotein B-100 is < ____ mg/dl for high-risk individuals

A

80

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9
Q

Apolipoprotein B-100 levels may be a better indicator of ____ ____ risk than total cholesterol or LDL

A

Cardiac disease

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10
Q

Exogenous cholesterol and triglycerides are simultaneously absorbed from the ____ ____ by different mechanisms

A

Intestinal lumen

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11
Q

Cholesterol is taken up from micelles across a regulatory channel named ____

A

NPC1L1

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12
Q

A fraction of the cholesterol is pumped back into the lumen by ____, a heterodimeric ATP-dependent plasma membrane protein

A

ABCG5/G8

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13
Q

The remainder of cholesterol is converted to cholesteryl esters by ____

A

ACAT

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14
Q

Triglycerides are taken up as ___ ___ and ____, which are re-esterified by DGAT

A

Fatty acids, monoglycerides

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15
Q

Formation of ____ occurs when IDL particles interact with hepatic lipase to become denser and cholesteryl ester-enriched

A

LDL

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16
Q

When LDL is formed, both ___ and ____ lose affinity for the particle and are transferred to HDL, leaving only apoB1000

A

apoE and apoCII

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17
Q

The binding of apolipoprotein B100 to LDL receptors on hepatocytes or other cell types promotes LDL internalization into endocytic vesicles and fusion of the vesicles with ____

A

Lysosomes

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18
Q

LDL receptors are recycled to the cell surface, whereas lipoprotein particles are hydrolyzed into amino acids, releasing free _____

A

Cholesterol

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19
Q

Intracellular cholesterol has what 3 regulator effects on the cell?

A

-Cholesterol decreases the activity of HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis
-Cholesterol activates acetyl CoA: cholesterol acyltransferase (ACAT), an enzyme that esterifies free cholesterol into cholesteryl esters for intracellular storage or export
-Cholesterol inhibits the transcription of the gene encoding the LDL receptor, and, thereby, decreases further uptake of cholesterol by the cell

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20
Q

Elevated LDL is a major risk factor for the development of _____

A

Atheroscleorosis

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21
Q

Native LDL that migrates into the subendothelial space can under chemical transformation to oxidized LDL via lipid peroxidation and fragmentation of _____

A

apoB100

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22
Q

Oxidized LDL has a number of deleterious effects on _____ function

A

Vascular

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23
Q

Oxidized LDL promotes monocytes chemotaxis to the ____ space and inhibits monocyte egress from that space

A

Subendothelial

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24
Q

Resident monocyte:macrophages bind to oxidized LDL via a scavenger receptor, resulting in the formation of lipid-laden ___ ___

A

Foam cells

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25
Q

Oxidized LDL can directly injure endothelial cells and cause endothelial _____

A

Dysfunction

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26
Q

Oxidized LDL can also cause foam cell ____, with a release of numerous proteolytic enzymes

A

Necrosis

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27
Q

Within a hepatocyte, a portion of cholesterol is concerted to ____ ____

A

Bile acids

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28
Q

The process of converting cholesterol to bile acids is rate-limited by ____ _____, which is expressed only in hepatocytes

A

Cholesterol 7a-hydroxylase

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29
Q

____ is the most abundant bile salt synthesized by the human liver

A

Cholate

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30
Q

What are some non-pharmacological treatments of dyslipidemia?

A

-Lifestyle and diet habits
-Low cholesterol, low-fat diet (12 weeks before starting drug treatment and continued thereafter)
-Weight loss program
-Exercising
-Evaluate for alcoholism (may be the cause of hyperlipidemia)

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31
Q

Options for the pharmacological treatment of dyslipidemia:

A

Inhibitors of HGM-CoA Reductase (statins):
-Lovastatin
-Simvastatin
-Fluvastatin
-Atorvastatin
-Pravastatin
-Rosuvastatin
-Pitavastatin

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32
Q

Adjuncts to hypertension treatment with dyslipidemia are based on patient cardiovascular risk:

A

-High-intensity statin
-Moderate-intensity statin
-Move away from LDL goals
-Move away from non-statins if patient can’t tolerate statin

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33
Q

What are high-intensity statins?

A

-Atorvastatin 40-80 mg
-Rosuvastatin 20-40 mg

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34
Q

What are examples of moderate-intensity statins?

A

-Simvastatin 20-40 mg
-Atorvastatin 10-20 mg
-Rosuvastatin 5-10 mg
-Lovastatin 40 mg
-Pravastatin 40-80 mg
-Pitavastatin 2-4 mg
-Fluvastatin 80 mg

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35
Q

Mechanism of action of statins:

A

-Block the rate-limiting step in the synthesis of cholesterol
-Molecular site of action: bind to and inhibit the enzyme HMG Co-A reductase, the rate-limiting enzyme in the synthesis of cholesterol by the hepatocytes

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36
Q

Statins competitively inhibit HMG-CoA reductase, the enzyme that catalyzes the rate limiting synthesis in ____ biosynthesis

A

Cholesterol

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37
Q

Decreased cellular cholesterol concentrations lead to _____ activation and cleavage of the sterol regulatory element binding protein, which is a transcription factor that normally resides in the cytoplasm

A

Protease

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38
Q

The cleaved sterol regulatory element binding protein diffuses into the nucleus, where it binds to sterol response elements, leading to up-regulation of ___-____ gene transcription

A

LDL-receptor

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39
Q

Up-regulation of LDL-receptor leads to ____ cellular LDL-receptor expression

A

Increased

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40
Q

The increased LDL receptor expression promotes uptake of LDL particles and results in reduced _____ concentrations in the plasma

A

LDL-cholesterol

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41
Q

The liver compensates for the reduced ability to synthesize cholesterol by ____ ___ cholesterol circulating in the blood in

A

Taking up

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42
Q

The reduction in the cholesterol concentration in the liver leads to an ____ in the number of LDL receptors inserted in the hepatocyte membrane

A

Increase

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43
Q

The goal for treatment of dyslipidemia is to increase the hepatic uptake of ____, which decreases the amount in circulation

A

LDL

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44
Q

Statins reduce LDL by ___-___%

A

20-55

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45
Q

Potency differs between statins; what is the most potent to least potent statin?

A

Ruvostatin > Atorvastatin > Simvastatin > Pravastatin (in ability to reduce LDL per equal dose)

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46
Q

Adverse effects of statins?

A

-Liver toxicity (low incidence, but would need to d/c drug)
-Myotoxicity
-Rhabdomyolysis
-Abdominal pain
-Nausea
-Headache
-Photosensitivity

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47
Q

How is liver toxicity evidenced by statins?

A

Increase in blood transaminase, an enzyme that is released from the liver when hepatocytes are damaged

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48
Q

Myotoxicity results from damage to ____ muscle cells and ranges from symptoms of myalgia (muscle pain) to rhabdomyolysis (deterioration and death of skeletal muscle cells)

A

Skeletal

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49
Q

Myotoxicity can be monitored by measuring blood levels of ____ ____, which is an enzyme that is released from damaged skeletal muscle cells

A

Creatine phosphokinase

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50
Q

____ is a syndrome characterized by muscle necrosis that causes intracellular constituents of the affected skeletal muscle to be released into the circulation

A

Rhabdomyolysis

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51
Q

The severity of rhabdomyolysis ranges from asymptomatic elevations of muscle enzymes in blood to a life-threatening condition that leads to…

A

-Extreme increases in muscle enzymes in the blood
-Electrolyte imbalances
-Acute renal failure (liver function tests are recommended before start (or increase of dose) and 12 weeks after to monitor for problems)

52
Q

Warnings/precautions for statins:

A

-Pregnancy category X
-Report unexplained muscle pain to doctor

53
Q

What statins are metabolized by the 2C9 CYP pathway?

A

-Fluvastatin
-Rosuvastatin (also 2C19)

54
Q

What statin is not metabolized by any CYP450 enzymes?

A

Pravastatin

55
Q

What 3 statins are metabolized by the 3A4 enzyme of CYP?

A

-Lovastatin
-Simvastatin
-Atorvastatin

56
Q

What are two statin drugs that are not lipophilic?

A

-Rosuvastatin
-Pravastatin

57
Q

What two statin drugs have no active metabolites?

A

-Fluvastatin
-Pravastatin

58
Q

What statin drug has the highest half-life?

A

Rosuvastatin

59
Q

What drug class is contraindicated for someone on a statin drug?

A

Fibrates (Gemfibrozil)

60
Q

What other drug classes are contraindicated with some statin drugs?

A

-Azole antifungals
-Macrolide antibiotics
-Calcium channel blockers
-Amiodarone
-Cyclosporine
-Protease inhibitors
-Antidepressants

61
Q

Ezetimibe (ZETIA) is a drug that interferes with the absorption of ____ ____

A

Dietary cholesterol

62
Q

Ezetimibe inhibits the absorption of dietary cholesterol in the ___ ___

A

Small intestine

63
Q

Ezetimibe (ZETIA) binds to and inhibits the transport protein that assists the transport of dietary cholesterol through the ____ _____ (NCP1L1) across the cell membrane of the columnar epithelial cells of the brush border of the small intestine

A

Sterol transporter

64
Q

The net effects of Ezetimibe (ZETIA) is that less cholesterol from the diet is _____ and delivered to the liver

A

Absorbed

65
Q

Ezetimibe has no effect on cholesterol synthesized by the _____

A

Liver

66
Q

The amount of cholesterol absorbed from the diet that enters the blood and is delivered to the liver is ____ when on Ezetimibe

A

Decreased

67
Q

Ezetimibe reduces LDL cholesterol by approximately ____%

A

18

68
Q

Clinical uses of Ezetimibe:

A

-With statin to further enhance the lowering of LDL
-To permit a lowering of stain dosage to avoid statin-related complications
-To treat hypercholesterolemia when statin use cannot be tolerated or is contraindicated

69
Q

Adverse effects of Ezetimibe:

A

-Arthralgia
-Dizziness
-Diarrhea
-Sinusitis
-Increased liver enzymes when added to statins

70
Q

Ezetimibe is pregnancy category ____

A

C

71
Q

What are four drug-drug interactions with Ezetimibe?

A

-Cyclosporine (increases the concentration of both drugs)
-Fenobirate (may lead to cholelithiasis)
-Cholestyramine (can decrease ezetimibe concentration by 55%)
-Coumadin (monitor INR)

72
Q

Alirocumab (Praluent) is a monoclonal antibody indicated for ____ ____ and ____ ____ _____, and needs additional decrease in lipids

A

Familial hypercholesterolemia and coronary artery disease

73
Q

Alirocumab (Praluent) inhibits _____, which normally reduces the number of receptors that remove LDL from the bloodstream

A

PCSK9

74
Q

Alirocumab (Praluent) causes a significant decrease in ____, but the long-term effects on cardiovascular morbidity and mortality is yet to be determined

A

LDL

75
Q

_____, a water-soluble B complex vitamin, was first described as a lipid-lowering agent around 1955

A

Niacin

76
Q

The effectiveness of niacin as a lipid-lowering agent is unrelated to its vitamin effects and requires a much _____ dose

A

Higher

77
Q

Niacin decreases hepatic production and secretion of _____ and _____

A

LDL and VLDL

78
Q

The effect niacin has on LDL and VLDL is secondary to the inhibition of _____ is adipose tissue (intracellular lipase system)

A

Lipolysis

79
Q

Niacin/nicotinic acid acts on the nicotinic acid receptor that is expressed by ____ ____ and present in the cellular membrane of the adipocyte

A

Adipose tissue

80
Q

Niacin causes less free ____ ____ to be formed, and as a result, there are less in the plasma

A

Fatty acids

81
Q

Since niacin causes a decrease in the free fatty acid concentration, the liver has less available substrate to form _____

A

Triglycerides

82
Q

Reduced synthesis of triglycerides in the liver results in a _____ in the formation of VLDL triglycerides and therefore, the circulation triglyceride levels

A

Decrease

83
Q

With less VLDL produced, there is a drop in the formation of ____

A

LDL

84
Q

Niacin lowers ____ and ____ levels, which increases HDL levels

A

LDL and triglycerides

85
Q

Niacin’s effects on lipoprotein levels:

A

-Decrease in VLDL and LDL
-Decrease in triglycerides by 25-30%
-Decrease in LDL by 10-25%
-Increase in HDL by 15-35%

86
Q

Adverse effects of niacin:

A

-Flushing of the face and upper extremities
-Gastrointestinal effects include dyspepsia, nausea, and vomiting
-May cause ulcers and is therefore contraindicated in individuals with a history of ulcers

87
Q

What are three examples of fibric acid derivatives used for the treatment of dyslipidemia?

A

-Clofibrate (original, not used anymore)
-Gemfibrozil (LOPID)
-Fenofibrate (TRICOR)

88
Q

Fenofibrate and Gemfibrozil bind to and stimulate the ____ ____ ____ ____

A

Peroxisome proliferator-activated receptor alpha

89
Q

Fenofibrate and Gemfibrozil cause _____ expression of lipoprotein lipase

A

Increased

90
Q

Thus, Fenofibrate and Gemfibrozil have the capacity to reduce circulating triglyceride levels by ____-____% (they may also lower LDL levels 6-20%, or slightly raise levels)

A

35-53

91
Q

Fibric acid derivatives like Fenofibrate or Genfibrozil can be used alone or in combination with ____ (used in combination can increase risk of myopathy)

A

Statins

92
Q

Adverse effects of fibric acid derivates:

A

-Rash
-N/V/D
-Myalgia

93
Q

Firbic acid derivatives are pregnancy category ____

A

C

94
Q

Kinetics of Fenofibrate:

A

-Well absorbed from GI
-Food increases absorption
-Highly protein bound (99%)
-Half-life: 20 hours
-Hepatic metabolism
-Renal excretion

95
Q

When would Fenofibrate be contraindicated?

A

-Hepatic or severe renal dysfunction
-Gallbladder disease

96
Q

Adverse effects of Fenofibrate:

A

-Pancreatitis
-Hepatotoxicity
-Rhabdomyolysis

97
Q

Kinetics of Gemfibrozil:

A

-Well absorbed from the GI tract
-Hepatic metabolism
-Renal excretion

98
Q

When would Gemfibrozil be contraindicated?

A

-Hepatic or severe renal dysfunction
-Gallbladder disease

99
Q

Adverse effects of Gemfibrozil:

A

-Rhabdomyolysis
-Hyperglycemic effects (monitor diabetic patients)

100
Q

What are three examples of Bile Acid Binding Resin?

A

-Cholestyramine (Questran)
-Colestipol (Colestid)
-Colesevelam (Welchol)

101
Q

Ion-exchange resins are not ____

A

Absorbed

102
Q

Bile acid binding resins bind to bile salts in the intestine in exchange for ____ ____

A

Chloride ions

103
Q

Under normal circumstances, the liver secretes bile acids and ____% are recycled by being reabsorbed

A

97

104
Q

However, bile salts that are bound to resin are lost in the ____

A

Feces

105
Q

The liver compensated by forming more ___ ___ from cholesterol

A

Bile salts

106
Q

Bile acid binding resins increase the liver’s need for _____ as a substrate; there is compensatory increase in LDL receptors inserted into the hepatocyte membranes in order to retrieve cholesterol from the LDL

A

Cholesterol

107
Q

Bile acid binding resins decrease LDL levels by ___-___%

A

10-30

108
Q

Adverse effects of all bile acid binding resins:

A

-Constipation (can be severe and lead to impaction)
-GI bleed
-Belthcing
-Bloating
-Flatulence
-N/V
-Indigestion
-Anorexia

109
Q

Additional adverse effects of Cholestyramine:

A

-Vitamin K deficiencies (from bleeding)
-Headache
-Impaired absorption of fat-soluble vitamins (A, D, E, K)
-Hyperchloremic acidosis

110
Q

Additional adverse effects of Colestipol:

A

-Dizziness
-Anxiety
-Vertigo
-Fatigue

111
Q

Lovaza is a prescription ____ _____ _____

A

Omega-3 fatty acid

112
Q

Lovaza decreases synthesis of ____ in the liver because DHA and EPA are poor substrates for enzymes to convert to triglycerides

A

Triglycerides

113
Q

Lovaza decreases triglycerides by ____% and increases HDL by ____

A

45%; 9%

114
Q

Lovaza also decreases other cholesterols by ___%

A

14

115
Q

Side effects of Lovaza:

A

-Infection
-Weird taste
-Back pain

116
Q

Omega-3s and fish oils have no _____ effects and better manufacturing decreases exposure to mercury

A

Antithrombotic

117
Q

Fish oils are not equal to prescription omega-3s (Lovaza) due to…

A

-Ratio of DHA and EPA
-Products being unregulated

118
Q

Fish oils can be taken with ____ and ____

A

Niacin and Statin

119
Q

Fish oils have what cardio effects that complement statin?

A

-Antithrombic effects
-Endothelial relaxation
-Anti-inflammatory effects

120
Q

Soluble fiber decreases LDL by ___%

A

7

121
Q

Phytosterols and plant sterols decrease LDL by 15% by competing with cholesterol for absorption sites in the ____

A

Intestine

122
Q

Soy protein can decrease LDL by 3%, but you would need to get ___ grams which is hard to get

A

25

123
Q

Red yeast rice can decrease LDL by ____ mg/dl by blocking cholesterol production in the liver

A

35

124
Q

Red yeast rice is a natural form of _____ (you must test LFTs)

A

Lovastatin

125
Q

Flaxseed can also be used to treat dyslipidemia as it a plant source of _____

A

Omega-3

126
Q

____ can also lower lipid levels

A

CoQ10

Advanced Pharmacology (10 decks)

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