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Therapeutics > Therapy of Dyslipidemias > Flashcards

Therapy of Dyslipidemias Flashcards

1
Q

___ is associated with the development of acute pancreatitis.

A

Hypertriglyceridemia

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2
Q

Initial therapy of lipoprotein disorder is:

A

Life-style modification

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3
Q

What lifestyle modifications can be done for lipoprotein disorders?

A

1) Restricted intake of total and saturated fat and cholesterol
2) Modest increase in unsaturated fat intake (specially mono-unsaturated fat)
3) Regular exercise
4) Smoking cessation
5) Weight reduction

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4
Q

A __ is the drug of choice for patients with hypercholesterolemia

A

Statin

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5
Q

Patients with hypercholesterolemia NOT responding to statin monotherapy may be treated with combination therapy, but should be monitored closely because of:

A

An increased risk for adverse effects and drug interactions

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6
Q

Hypertriglyceridemia usually responds well to:

A

1) Niacin
2) Fibrates

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7
Q

Which drugs are fibrates?

A

1) Gemfibrozil
2) Fenofibrate

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8
Q

How do you treat low HDL-C?

A

1) Life-style modifications
2) Drug therapy with Niacin and Fibrates

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9
Q

Lipoprotein A is formed from:

A

1) LDL
2) Apolipoprotein (a)

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10
Q

Lipoprotein A is homologous with:

A

Plasminogen

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11
Q

Is Lipoprotein A activated by tissue plasminogen activator (TPA)?

A

NO

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12
Q

Lipoprotein A may be found in:

A

Atherosclerotic plaques

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13
Q

Lipoprotein A may contribute to:

A

Coronary disease

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14
Q

How can Lipoprotein A contribute to coronary disease?

A

By inhibiting thrombolysis

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15
Q

Lipoprotein A can be secondarily elevated in patients with:

A

1) Severe nephrosis
2) Some inflammatory states

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16
Q

__ reduces levels of Lipoprotein A in many patients.

A

Niacin

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17
Q

VLDL carries about 10-15% of:

A

1) Serum cholesterol
2) Most fasting triglycerides

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18
Q

High VLDL is a risk factor for:

A

Acute pancreatitis

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19
Q

What are Chylomicrons?

A

Triglyceride-rich particles formed from dietary fat solubilized by bile salts.

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20
Q

What are the secondary causes of Hypercholesterolemia?

A

1) Hypothyroidism
2) Obstructive liver disease
3) Nephrotic syndrome
4) Anorexia nervosa
5) Acute intermittent porphyria
6) Drugs

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21
Q

Which drugs can cause Hypercholesterolemia?

A

1) Progestins
2) Thiazide diuretics
3) Glucocorticoids
4) β-blockers
5) Isotretinoin
6) Protease inhibitors
7) Cyclosporine
8) Sirolimus
9) Mirtazapine

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22
Q

What are the secondary causes of Hypertriglyceridemia?

A

1) Obesity
2) Diabetes mellitus
3) Lipodystrophy
4) Glycogen storage disease
5) Ileal bypass surgery
6) Sepsis
7) Nephrotic syndrome
8) Chronic renal disease
9) Pregnancy
10) Acute hepatitis
11) SLE
12) Monoclonal gammopathy:
a) Multiple myeloma
b) Lymphoma
13) Drugs

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23
Q

Which drugs can cause Hypertriglyceridemia?

A

1) Alcohol
2) Estrogens
3) Isotretinoin
4) Thiazides
5) β-blockers
6) Glucocorticoids
7) Bile-acid binding resins
8) Asparaginase
9) Interferons
10) Azole antifungals
11) Bexarotene
12) Mirtazapine
13) Anabolic steroids
14) Sirolimus

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24
Q

What are the secondary causes of Low HDL?

A

1) Malnutrition
2) Obesity
3) Sedentary life-style
4) Drugs

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25
Q

Which drugs can cause Low HDL?

A

1) Non-ISA β-blockers
2) Anabolic steroids
3) Probucol
4) Isotretinoin
5) Progestins

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26
Q

What are the ultimate goals of dyslipidemia therapy?

A

To reduce the risk of MI, angina, heart failure…etc.

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27
Q

What should be implemented in all patients prior to considering drug therapy for dyslipidemias?

A

Therapeutic life-style modification

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28
Q

What are the therapeutic life-style modifications followed for dyslipidemia?

A

1) Reduced intakes of saturated fats, cholesterol, and total fat
2) Use of dietary options to reduce LDL-C
3) Physical activity of moderate intensity 30 minutes per day for most days of the week
4) Restriction of alcohol drinking
5) Weight reduction in overweight
6) Stop smoking
7) Control hypertension

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29
Q

What dietary options can reduce LDL-C?

A

1) Plant phytosterols
2) Increased soluble fiber intake
3) Weight reduction
4) Increased physical activity

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30
Q

___ are structurally similar to cholesterol, and compete for its intestinal absorption.

A

Plant phytosterols

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31
Q

How do Plant phytosterols decrease LDL-C?

A

1) Competing for cholesterol absorption
2) Reduce bile acid absorption = Cholesterol is degraded into bile acids

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32
Q

What are some food sources of phytosterols?

A

1) Cereals (oat, wheat, brown rice)
2) Legumes (peas, beans, lentils)
3) Nuts and Seeds (peanuts, almonds, sunflower seeds, pumpkin seeds, sesame seeds)
4) Fruits and vegetables (broccoli, cauliflower, apples, avocados, tomato, blueberries)

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33
Q

___ + ___ raises HDL and reduces non-HDL cholesterol.

A

Weight control + Increased physical activity

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34
Q

______ can result in useful adjunctive reductions in total and LDL cholesterol.

A

Increased intake of soluble fiber

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35
Q

What are some examples of soluble fibers?

A

1) Oat bran
2) Pectins
3) Psyllium products

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36
Q

Which supplement can be used in hyperlipidemia?

A

Omega-3 fatty acids

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37
Q

How do Omega-3 fatty acids work?

A

1) Activate peroxisome proliferator-activated receptor-alpha (PPAR-α)
2) Alters synthesis of prostanoids = synthesis of vasodilator prostaglandins and inhibitors of platelet aggregation

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38
Q

What do Omega-3 fatty acids do?

A

1) Reduce triglycerides in VLDL
2) Increase both HDL and LDL

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39
Q

Adverse reactions of Omega-3 fatty acids?

A

1) Thrombocytopenia
2) Bleeding disorders

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40
Q

What are the Omega-3 fatty acids?

A

1) Eicosapentaenoic acid
2) Docosahexaenoic acid

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41
Q

Other effects of omega-3 fatty acids include:

A

1) Changes in immune function and cellular proliferation
2) Antioxidant actions
3) Anti-inflammatory actions
4) Antiarrhythmic activities

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42
Q

Which lipid lowering drug is useful for ALL lipoprotein disorders?

A

NONE

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43
Q

What is Type 1 Hyperlipoproteinemia?

A

Elevated Chylomicrons

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44
Q

What is Type 2a Hyperlipoproteinemia?

A

Elevated LDL

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45
Q

What is Type 2b Hyperlipoproteinemia?

A

Elevated LDL + VLDL

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46
Q

What is Type 3 Hyperlipoproteinemia?

A

Elevated IDL

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47
Q

What is Type 4 Hyperlipoproteinemia?

A

Elevated VLDL

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48
Q

What is Type 5 Hyperlipoproteinemia?

A

Elevated VLDL + Chylomicrons

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49
Q

What is the drug of choice for Type 1 Hyperlipoproteinemia?

A

None

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50
Q

What is the drug of choice for Type 2a Hyperlipoproteinemia?

A

1) Statins!!!!!
2) Bile acid binding resins
3) Niacin

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51
Q

What is the drug of choice for Type 2b Hyperlipoproteinemia?

A

1) Statins!!!!!
2) Fibrates
3) Niacin

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52
Q

What is the drug of choice for Type 3 Hyperlipoproteinemia?

A

1) Fibrates
2) Niacin

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53
Q

What is the drug of choice for Type 4 Hyperlipoproteinemia?

A

1) Fibrates
2) Niacin

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54
Q

What is the drug of choice for Type 5 Hyperlipoproteinemia?

A

1) Fibrates
2) Niacin

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55
Q

Treatment of type I hyperlipoproteinemia is directed towards:

A

Reduction of chylomicrons derived from dietary fat with the subsequent reduction in plasma triglycerides.

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56
Q

Niacin is __(oxidized/reduced) in the body to the amide which is incorporated into:

A

Reduced; NAD = Energy metabolism

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57
Q

Pharmacodynamics of Niacin?

A

1) Inhibits VLDL secretion from the liver and thus LDL production
2) Raises HDL cholesterol
3) Reduces the level of LP(a)
4) Reduces fibrinogen levels
5) Increases tissue plasminogen activator (TPA)

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58
Q

How does Niacin raise HDL cholesterol?

A

By decreasing its catabolism

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59
Q

Adverse reactions of Niacin?

A

1) Acanthosis nigricans
2) Elevation of liver function tests
3) Prostaglandin-mediated cutaneous flushing and itching
4) Hyperuricemia
5) Hyperglycemia

60
Q

Niacin is contraindicated in those with:

A

Active liver disease

61
Q

How can you prevent the flushing and itching associated with Niacin?

A

By giving Aspirin 325 mg shortly before Niacin

62
Q

____ may mediate niacin-induced vasodilation.

A

Prostaglandin D receptor subtype 1 (DP1)

63
Q

What is Laropiprant?

A

A selective antagonist of Prostaglandin D receptor subtype 1 (DP1)

64
Q

Why might we give Laropiprant with Niacin?

A

To lower flushing and itching symptoms

65
Q

What should be avoided at the time of ingestion of Niacin?

A

1) Alcohol
2) Hot drinks

66
Q

Why should alcohol and hot drinks be avoided with Niacin?

A

They may magnify flushing and pruritus

67
Q

Niacin increases risk of ___ when given with Statins.

A

Myopathy

68
Q

Niacin increases risk of myopathy when given with ___.

A

Statins

69
Q

Fibric acid derivatives include:

A

1) Phenofibate
2) Gemfibrozil

70
Q

What do Fibric acid derivatives do?

A

Enhance hydrolysis of VLDL and chylomicron triglycerides in the circulation by lipoprotein lipase.

71
Q

Fibric acid derivatives stimulate:

A

Cellular fatty acid uptake

72
Q

A major effect of Fibric acid derivatives is an increase in:

A

Oxidation of fatty acids in liver and striated muscle

73
Q

ALL effects of Fibric acid derivatives?

A

1) Reduction of VLDL
2) Modest decrease in LDL
3) Elevation of HDL

74
Q

Fibric acid derivatives may increase LDL in which patients?

A

With hypertriglyceridemia, as triglycerides are reduced.

75
Q

How do Fibric acid derivatives increase HDL?

A

By increasing the production of apo-A1 and apoAII in the liver

76
Q

Adverse effects of Fibric acid derivatives?

A

1) Gallstones
2) May potentiate the effects of oral anticoagulants
3) Reduce platelet activity
4) Hypokalemia and cardiac arrhythmias
5) Myositis and elevations in creatine phosphokinase
6) Elevation of liver enzymes
7) Reduce WBCs and hematocrit

77
Q

Why might Fibric acid derivatives cause gallstones?

A

Due to an increase in the lithogenicity of bile

78
Q

What should you monitor in a patient taking both Fibric acid derivatives and oral coagulants?

A

INR

79
Q

Fibric acid derivatives should be avoided in which patients?

A

1) Hepatic dysfunction
2) Renal dysfunction

80
Q

Primary hypercholesterolemia may be treated with:

A

1) Statins! (1st choice!)
2) Bile acid binding resins
3) Niacin
4) Ezetimibe

81
Q

Which drugs are Bile acid binding resins?

A

1) Colestipol
2) Cholestyramine
3) Colesevelam

82
Q

What are Statins mode of action?

A

HMG Co-A reductase inhibitors

83
Q

HMG CoA Reductase inhibition leads to reduced cholesterol content of hepatocytes =

A

Increased LDL receptor synthesis (Breakdown of LDL and its precursors)

84
Q

Other actions of Statins include:

A

1) Reduce oxidative stress
2) Reduce vascular inflammation
3) Stabilize atherosclerotic lesions
4) Improve the microcirculation
5) Inhibit proliferation of arterial wall smooth muscle
6) Improve endothelial cell function

85
Q

Which drugs are Statins?

A

1) Lovastatin
2) Simvastatin
3) Atorvastatin
4) Rosuvastatin

86
Q

Ezetimibe moa?

A

Inhibits cholesterol absorption through the gut

87
Q

Adverse effects of Statins?

A

1) Elevation of serum ALT
2) Serious muscle toxicity (myopathy)
3) Elevated serum CPK
4) Rhabdomyolysis
5) Myoglobinuria
6) Renal shutdown
3) Teratogenicity

88
Q

Can you take Statins during pregnancy & Lactation?

A

NO

89
Q

Myopathy associated with Statins increases in severity if co-administered with:

A

1) Nicotinic acid
2) Fibrates
3) Ketoconazole
4) Cyclosporine
5) Erythromycin
6) Verapamil
7) Cimetidine
8) Metronidazole
9) Amiodarone
10) Grapefruit juice
11) Protease inhibitors (anti-HIV)

90
Q

Bile Acid Binding Resins moa?

A

They exchange Cl- for the negatively charged bile acids = preventing negative feedback = enhancing of cholesterol breakdown = increases LDL receptors

91
Q

Loss of bile acids also reduces __ and ___ absorption from GIT.

A

Fat and cholesterol

92
Q

When might the VLDL be increased during treatment with Bild Acid Binding Resins?

A

In patients with combined hyperlipidemia (2b)(hypertriglyceridemia and
hypercholesterolemia)

93
Q

Bile Acid Binding Resins are ONLY useful for:

A

Isolated increases in LDL

94
Q

Adverse effects of Bile Acid Binding Resins?

A

1) GI complaints of gritty taste,
constipation, bloating (epigastric fullness), nausea, flatulence, and GIT obstruction.
2) Impaired absorption of fat-soluble vitamins A, D, E, and K.
3) Hypernatremia
4) Hyperchloremic metabolic acidosis

95
Q

Bile Acid Binding Resins can reduce the bioavailability of which drugs?

A

1) Coumarin anticoagulants
2) Nicotinic acid
3) Thyroxine
4) Acetaminophen
5) Hydrocortisone
6) Hydrochlorothiazide
7) Iron

96
Q

How can you avoid drug interactions when giving Bile Acid Binding Resins?

A

By spacing administration by 6 hours between the bile acid resin and other drugs.

97
Q

Both the statins and the resins are NOT effective in patients lacking:

A

LDL receptors

98
Q

Which patients may lack LDL receptors?

A

Those with Familial Homozygous Hypercholesterolemia

99
Q

Severe forms of hypercholesterolemia may
require:

A

More intensive combination therapy

100
Q

Ezetimibe moa?

A

1) Inhibits intestinal cholesterol absorption = reduces LDL
2) Inhibits phytosterol absorption

101
Q

Why is Ezetimibe effective even in the absence of dietary
cholesterol?

A

Because it inhibits reabsorption of cholesterol excreted in bile

102
Q

Ezetimibe could be used in combination therapy, synergistic with ___.

A

Statins

103
Q

Ezetimibe could be used in combination therapy in which type?

A

2b

104
Q

Plasma concentration of Ezetimibe is ___(decreased/increased) when
co-administered with fibrates and ___(increased/decreased) when given with resins.

A

Increased; Decreased

105
Q

Adverse effects of Ezetimibe?

A

1) Muscle pain and weakness
2) Hepatitis and jaundice
3) Pancreatitis and elevation of amylase

106
Q

Plasma concentration of Ezetimibe is increased when co-administered with __ and reduced when given with __.

A

Fibrates; Resins

107
Q

Can combined hyperlipoproteinemia (type IIb)
be treated with statins, niacin, or gemfibrozil combinations to lower LDL cholesterol WITHOUT
elevating VLDL and triglycerides?

A

YES

108
Q

Fibric acid (gemfibrozil, fenofibrate) monotherapy is effective in reducing __, but
may increase __.

A

VLDL; LDL

109
Q

Low HDL Cholesterol (<40 mg/dL) may be a consequence of:

A

1) Insulin resistance
2) Physical inactivity
3) Type 2 diabetes
4) Cigarette smoking
5) Very high carbohydrate intake
6) Certain drugs

110
Q

Drugs of choice for Low HDL Cholesterol (<40 mg/dL)?

A

1) Niacin
2) Fibric acid derivatives

111
Q

Diabetic dyslipidemia is characterized by:

A

1) Hypertriglyceridemia
2) Low HDL
3) Minimal elevation of LDL

112
Q

Most patients with Diabetic dyslipidemia will require:

A

1) Therapeutic life-style modification
2) Drug therapy

113
Q

What should you do when LDL-C is high?

A

1) Intensify glycemic control
2) Add fibric acid derivatives or Niacin
3) Intensify LDL-C-lowering therapy using statins

114
Q

Which patients are more susceptible to adverse effects of lipid-lowering drugs?

A

The elderly

115
Q

The elderly are more likely to have which Bile Acid Resin adverse effect?

A

Constipation

116
Q

The elderly are more likely to have which Niacin adverse effects?

A

1) Skin and eye changes
2) Gout

117
Q

The elderly are more likely to have which Fibric Acid Derivatives adverse effects?

A

1) Gallstones
2) Bone/joint disorders

118
Q

The elderly are more likely to have which Statin adverse effect?

A

Bone/joint disorders

119
Q

How should therapy in the elderly be started?

A

With lower doses and titrated up slowly to minimize adverse effects.

120
Q

__ may be a more important predictor of disease in women.

A

HDL

121
Q

___ and ___ levels rise progressively throughout pregnancy.

A

Cholesterol and triglyceride

122
Q

Which dyslipidemia drugs are given during pregnancy?

A

NONE!!!

123
Q

How do you treat dyslipidemias in pregnant women?

A

Dietary therapy, with emphasis on maintaining a nutritionally balanced diet.

124
Q

Which dyslipidemia drug may be considered in pregnant women if there is a VERY high risk?

A

A Bile Acid Resin

125
Q

___ are Category X and are contraindicated in pregnant women.

A

Statins

126
Q

___ is a pregnancy Category C drug.

A

Ezetimibe

127
Q

Statins are Category _ in pregnancy.

A

X

128
Q

Dyslipidemia drug therapy in children is NOT recommended until the age of _ years or older

A

8

129
Q

Younger children are generally managed with therapeutic life-style changes until after the age of:

A

2 years

130
Q

___ may be safe and are effective in children.

A

Statins

131
Q

What is Mipomersen?

A

Antisense oligonucleotide

132
Q

Mipomersen moa?

A

Specifically binds to the apolipoprotein B-100 mRNA = blocks translation of the gene product

133
Q

The reduction in production of apo B-100 results in:

A

Reduced hepatic production of:
1) VLDL
2) IDL
3) LDL
4) Lipoprotein(a)

134
Q

Mipomersen is indicated in which patients?

A

Those with homozygous familial hypercholesterolemia as an adjunct to diet and other lipid-lowering medications

135
Q

Why is the use of Mipomersen restricted?

A

Because it is hepatotoxic

136
Q

How is Mipomersen given?

A

Subcutaneous injection

137
Q

Lomitapide inhibits:

A

1) Microsomal triglyceride transfer protein (MTP)
2) CYP3A4
3) P-Glycoprotein

138
Q

What is Microsomal triglyceride transfer protein (MTP) responsible for?

A

Absorbing dietary lipids and transferring triglycerides onto apolipoprotein B (apo-B) in the assembly of VLDL

139
Q

What happens if Microsomal triglyceride transfer protein (MTP) is inhibited?

A

Transfer of lipid to apo-B is blocked = ApoB destruction and inhibition of lipoprotein secretion

140
Q

What is Lomitapide given for?

A

Familial hypercholesterolemia

141
Q

Adverse effects of Lomitapide?

A

1) Elevation of serum aminotransferase
2) Increased hepatic fat (steatohepatitis) and hepatic fibrosis

142
Q

What does PCSK9 do?

A

Binds to LDL receptors on hepatocytes = LDLR degradation = Elevates LDL-C blood levels

143
Q

What does Alirocumab do?

A

Inhibits the binding of PCSK9 to
LDL receptors = Reduces LDL-C levels

144
Q

How is Alirocumab given?

A

Subcutaneous injection

145
Q

Which drug is similar to Alirocumab?

A

Evolocumab

146
Q

What is Alirocumab given for?

A

Heterozygous familial hypercholesterolemia

Therapeutics (23 decks)

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