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Pharma2 MCQs > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Which of the following lipids are included in the category of hyperlipidemia?
a. Cholesterol and phospholipids
b. Triglycerides and phospholipids
c. Cholesterol and triglycerides
d. Fatty acids and phospholipids

A

c. Cholesterol and triglycerides

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2
Q

Why do lipids need a transporter to move around the body?
a. Because they are water-soluble
b. Because they are water-insoluble
c. Because they are water-insoluble
d. Because they are too large

A

c. Because they are water-insoluble

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3
Q

What are lipoproteins composed of?
a. Protein and carbohydrate
b. Lipid and carbohydrate
c. Lipid and apolipoprotein
d. Protein and nucleic acid

A

c. Lipid and apolipoprotein

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4
Q

Which type of lipoprotein is secreted from the intestine to carry exogenous triglycerides and cholesterol?
a. VLDL
b. Chylomicron
c. LDL
d. HDL

A

b. Chylomicron

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5
Q

VLDL is secreted from the liver to carry which type of triglycerides?
a. Endogenous
b. Exogenous
c. Dietary
d. Peripheral

A

a. Endogenous

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6
Q

LDL is secreted from the liver to carry which type of cholesterol?
a. Exogenous
b. Endogenous
c. Dietary
d. Peripheral

A

b. Endogenous

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7
Q

What is the primary function of HDL?
a. Carry exogenous triglycerides from the GIT to blood circulation
b. Carry endogenous triglycerides from the liver to blood circulation
c. Carry cholesterol from peripheral tissues and blood circulation to the liver for metabolism and/or secretion
d. Carry endogenous cholesterol from the liver to blood circulation

A

c. Carry cholesterol from peripheral tissues and blood circulation to the liver for metabolism and/or secretion

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8
Q

Coronary heart disease (CHD) is correlated with which of the following lipid profiles?
a. Low levels of low-density lipoprotein cholesterol (LDL-C)
b. Low levels of triglycerides
c. Elevated levels of low-density lipoprotein cholesterol (LDL-C)
d. High levels of high-density lipoprotein cholesterol (HDL-C)

A

c. Elevated levels of low-density lipoprotein cholesterol (LDL-C)

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9
Q

Elevated levels of which lipid are associated with an increased risk of coronary heart disease (CHD)?
a. Triglycerides
b. High-density lipoprotein cholesterol (HDL-C)
c. Apolipoproteins
d. Phospholipids

A

a. Triglycerides

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10
Q

Low levels of which type of cholesterol are correlated with coronary heart disease (CHD)?
a. Low-density lipoprotein cholesterol (LDL-C)
b. High-density lipoprotein cholesterol (HDL-C)
c. Triglycerides
d. Apolipoproteins

A

b. High-density lipoprotein cholesterol (HDL-C)

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11
Q

Plasma lipids primarily consist of which of the following?
a. Carbohydrates and proteins
b. Lipoproteins
c. Nucleic acids and lipids
d. Amino acids and cholesterol

A

b. Lipoproteins

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12
Q

Lipoprotein is a combination of which components?
a. Phospholipid and protein
b. Triglyceride or cholesterol with apoprotein
c. Cholesterol and carbohydrate
d. Triglyceride and carbohydrate

A

b. Triglyceride or cholesterol with apoprotein

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13
Q

Which lipoprotein has the highest atherogenicity?
a. HDL
b. VLDL
c. LDL
d. Chylomicrons

A

c. LDL

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14
Q

What is the correct order of clinically important lipoproteins in decreasing order of atherogenicity?
a. VLDL > LDL > HDL > Chylomicrons
b. LDL > VLDL > Chylomicrons > HDL
c. HDL > LDL > VLDL > Chylomicrons
d. Chylomicrons > LDL > VLDL > HDL

A

b. LDL > VLDL > Chylomicrons > HDL

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15
Q

What do HMG CoA reductase inhibitors primarily lower?
a. HDL cholesterol
b. Triglycerides
c. LDL cholesterol
d. Total cholesterol

A

c. LDL cholesterol

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16
Q

HMG CoA reductase inhibitors are commonly known as:
a. Beta-blockers
b. Statins
c. ACE inhibitors
d. Diuretics

A

b. Statins

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17
Q

Which of the following is not a statin?
a. Lovastatin
b. Simvastatin
c. Pravastatin
d. Lisinopril

A

d. Lisinopril

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18
Q

What is the primary mechanism of action of statins?
a. Increase triglyceride synthesis
b. Inhibit the rate-limiting step in cholesterol synthesis
c. Block absorption of dietary cholesterol
d. Increase HDL cholesterol synthesis

A

b. Inhibit the rate-limiting step in cholesterol synthesis

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19
Q

By depleting intracellular cholesterol, statins cause cells to:
a. Decrease the number of cell surface LDL receptors
b. Decrease LDL catabolism
c. Increase the number of cell surface LDL receptors
d. Increase intracellular cholesterol synthesis

A

c. Increase the number of cell surface LDL receptors

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20
Q

Statins result in an increased number of LDL receptors, leading to:
a. Decreased HDL levels
b. Decreased triglyceride levels
c. Increased LDL catabolism
d. Increased intracellular cholesterol

A

c. Increased LDL catabolism

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21
Q

In addition to lowering LDL-C, HMG CoA reductase inhibitors also:
a. Decrease triglyceride levels
b. Decrease HDL levels
c. Increase LDL synthesis
d. Increase triglyceride synthesis

A

a. Decrease triglyceride levels

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22
Q

Statins can increase which cholesterol level in some patients?
a. LDL cholesterol
b. HDL cholesterol
c. Total cholesterol
d. Triglycerides

A

b. HDL cholesterol

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23
Q

Which of the following is considered the most effective statin?
a. Lovastatin
b. Simvastatin
c. Rosuvastatin
d. Fluvastatin

A

c. Rosuvastatin

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24
Q

Statins are considered the primary treatment option for which condition?
a. Hypertension
b. Hypercholesterolemia
c. Diabetes
d. Hyperglycemia

A

b. Hypercholesterolemia

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25
Q

Statins are considered first-line treatment for patients with elevated risk of which disease?
a. Chronic Obstructive Pulmonary Disease (COPD)
b. Chronic Kidney Disease (CKD)
c. Atherosclerotic Cardiovascular Disease (ASCVD)
d. Congestive Heart Failure (CHF)

A

c. Atherosclerotic Cardiovascular Disease (ASCVD)

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26
Q

When should statins be administered for maximum effectiveness?
a. In the morning
b. In the evening
c. At noon
d. Before bedtime

A

b. In the evening

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27
Q

Which of the following is a common adverse effect of statins?
a. Elevated liver enzymes
b. Hypoglycemia
c. Hypertension
d. Anemia

A

a. Elevated liver enzymes

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28
Q

Myopathy and rhabdomyolysis associated with statins involve:
a. Liver damage
b. Muscle pain and muscle fiber destruction
c. Kidney failure
d. Nervous system damage

A

b. Muscle pain and muscle fiber destruction

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29
Q

Statins may increase the effect of which anticoagulant by inhibiting its metabolism?
a. Heparin
b. Warfarin
c. Aspirin
d. Clopidogrel

A

b. Warfarin

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30
Q

Why are statins contraindicated during pregnancy and lactation?
a. Due to potential adverse effects on the fetus or infant
b. Because they are ineffective during pregnancy
c. Because they increase blood pressure
d. Due to increased risk of gestational diabetes

A

a. Due to potential adverse effects on the fetus or infant

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31
Q

Statins are effective in lowering plasma cholesterol levels in which types of hyperlipidemias?
a. All types of hyperlipidemias
b. Only in familial hypercholesterolemia
c. Only in dietary-induced hyperlipidemia
d. Only in secondary hyperlipidemia

A

a. All types of hyperlipidemias

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32
Q

Niacin (nicotinic acid) reduces LDL-C by:
a. 10%
b. 15%
c. 20%
d. 25%

A

c. 20%

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33
Q

Niacin lowers triglycerides by:
a. 20%
b. 25%
c. 35%
d. 40%

A

c. 35%

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34
Q

Which of the following is the most effective agent for increasing HDL-C?
a. Statins
b. Fibrates
c. Bile acid sequestrants
d. Niacin (nicotinic acid)

A

d. Niacin (nicotinic acid)

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35
Q

Niacin’s mechanism of action includes inhibiting:
a. Cholesterol absorption
b. Lipolysis in adipose tissue
c. VLDL production in the liver
d. LDL receptor activity

A

b. Lipolysis in adipose tissue

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36
Q

By inhibiting lipolysis in adipose tissue, niacin reduces the production of:
a. Cholesterol
b. HDL
c. VLDL
d. Free fatty acids

A

d. Free fatty acids

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37
Q

The liver uses circulating free fatty acids as a major precursor for:
a. Triglyceride synthesis
b. HDL synthesis
c. Cholesterol synthesis
d. Protein synthesis

A

a. Triglyceride synthesis

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38
Q

Reduced liver triglyceride levels due to niacin lead to decreased production of:
a. HDL
b. VLDL
c. LDL receptors
d. Apolipoproteins

A

b. VLDL

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39
Q

Decreased hepatic VLDL production by niacin ultimately reduces:
a. HDL plasma concentrations
b. Free fatty acid plasma concentrations
c. LDL-C plasma concentrations
d. Total cholesterol plasma concentrations

A

c. LDL-C plasma concentrations

40
Q

Niacin lowers plasma levels of both cholesterol and:
a. LDL
b. HDL
c. Triglycerides
d. Free fatty acids

A

c. Triglycerides

41
Q

Niacin is useful in the treatment of:
a. Hypertension
b. Familial hyperlipidemias
c. Diabetes
d. Osteoporosis

A

b. Familial hyperlipidemias

42
Q

The most common side effect of niacin is:
a. Headache
b. Nausea
c. Intense cutaneous flush and pruritus
d. Diarrhea

A

c. Intense cutaneous flush and pruritus

43
Q

What is the primary cause of the intense cutaneous flush and pruritus associated with niacin?
a. Histamine release
b. Production of prostaglandins
c. Increased blood flow
d. Decreased uric acid

A

b. Production of prostaglandins

44
Q

To reduce the side effect of flushing when taking niacin, it is recommended to:
a. Take it in the morning
b. Take NSAIDs before administering niacin and take it at night
c. Increase water intake
d. Avoid fatty foods

A

b. Take NSAIDs before administering niacin and take it at night

45
Q

Niacin inhibits the tubular secretion of which substance, predisposing patients to hyperuricemia and gout?
a. Sodium
b. Uric acid
c. Potassium
d. Creatinine

A

b. Uric acid

46
Q

Which of the following adverse effects has been reported with niacin use?
a. Nephrotoxicity
b. Cardiotoxicity
c. Hepatotoxicity
d. Neurotoxicity

A

c. Hepatotoxicity

47
Q

Due to the risk of hepatotoxicity, niacin should be avoided in patients with:
a. Hepatic disease
b. Renal disease
c. Cardiovascular disease
d. Respiratory disease

A

a. Hepatic disease

48
Q

Caution should be exercised when niacin is administered with:
a. Statins
b. ACE inhibitors
c. Diuretics
d. Beta-blockers

A

a. Statins

49
Q

Fenofibrate and gemfibrozil are derivatives of which acid?
a. Acetic acid
b. Nicotinic acid
c. Fibric acid
d. Citric acid

A

c. Fibric acid

50
Q

What effect do fibrates have on serum triglycerides and HDL levels?
a. Lower serum triglycerides and increase HDL levels
b. Lower serum triglycerides and decrease HDL levels
c. Increase serum triglycerides and increase HDL levels
d. Increase serum triglycerides and decrease HDL levels

A

a. Lower serum triglycerides and increase HDL levels

51
Q

Which two agents are most efficacious in lowering triglycerides?
a. Statins and bile acid sequestrants
b. Niacin and statins
c. Bile acid sequestrants and fibrates
d. Niacin and fibric acid derivatives

A

d. Niacin and fibric acid derivatives

52
Q

Peroxisome proliferator-activated receptors (PPARs) are part of which receptor family?
a. G-protein-coupled receptors
b. Tyrosine kinase receptors
c. Nuclear receptor family
d. Ion channel receptors

A

c. Nuclear receptor family

53
Q

Fenofibrate and gemfibrozil activate which intracellular receptor?
a. LDL receptor
b. PPARs
c. HDL receptor
d. VLDL receptor

A

b. PPARs

54
Q

Activation of PPARs by fibrates leads to:
a. Decreased triglyceride concentrations through increased expression of lipoprotein lipase
b. Increased triglyceride concentrations through decreased expression of lipoprotein lipase
c. Increased cholesterol synthesis
d. Decreased HDL levels

A

a. Decreased triglyceride concentrations through increased expression of lipoprotein lipase

55
Q

What enzyme’s expression is increased by fibrates, aiding in the breakdown of triglycerides?
a. HMG CoA reductase
b. Lipoprotein lipase
c. Acetyl-CoA carboxylase
d. Cholesterol esterase

A

b. Lipoprotein lipase

56
Q

Fibrates are primarily used in the treatment of:
a. Hypercholesterolemia
b. Hypertension
c. Hypertriglyceridemias
d. Hyperglycemia

A

c. Hypertriglyceridemias

57
Q

The most common adverse effects of fibrates are:
a. Severe headaches
b. Mild gastrointestinal (GI) disturbances
c. Skin rashes
d. Hypertension

A

b. Mild gastrointestinal (GI) disturbances

58
Q

Fibrates increase the excretion of which substance, leading to a predisposition to form gallstones?
a. Uric acid
b. Calcium
c. Phosphates
d. Biliary cholesterol

A

d. Biliary cholesterol

59
Q

Patients taking gemfibrozil and statins together may experience which adverse effects?
a. Hepatotoxicity and nephrotoxicity
b. Myopathy and rhabdomyolysis
c. Anemia and leukopenia
d. Hypoglycemia and hyperglycemia

A

b. Myopathy and rhabdomyolysis

60
Q

What is the primary reason fibrates predispose patients to gallstone formation?
a. Increased calcium absorption
b. Increased biliary cholesterol excretion
c. Decreased bile production
d. Increased bile acid production

A

b. Increased biliary cholesterol excretion

61
Q

Which combination of drugs increases the risk of myopathy and rhabdomyolysis?
a. Niacin and statins
b. Gemfibrozil and statins
c. Fibrates and beta-blockers
d. Statins and ACE inhibitors

A

b. Gemfibrozil and statins

62
Q

Bile acid sequestrants (resins) primarily lower which type of cholesterol?
a. LDL cholesterol
b. HDL cholesterol
c. Total cholesterol
d. Triglycerides

A

a. LDL cholesterol

63
Q

The benefits of bile acid sequestrants are:
a. Greater than those observed with statins
b. Equal to those observed with statins
c. Less than those observed with statins
d. Not comparable to those observed with statins

A

c. Less than those observed with statins

64
Q

Which of the following drugs bind to bile acids and bile salts in the small intestine?
a. Atorvastatin, simvastatin, and rosuvastatin
b. Cholestyramine, colestipol, and colesevelam
c. Gemfibrozil, fenofibrate, and clofibrate
d. Niacin, ezetimibe, and omega-3 fatty acids

A

b. Cholestyramine, colestipol, and colesevelam

65
Q

What happens to the resin/bile acid complex formed by bile acid sequestrants?
a. It is reabsorbed in the bloodstream
b. It is metabolized in the liver
c. It is excreted in the feces
d. It is stored in the gallbladder

A

c. It is excreted in the feces

66
Q

The excretion of the resin/bile acid complex leads to a decrease in:
a. LDL receptor activity
b. Bile acid concentration in the intestine
c. HDL synthesis
d. Triglyceride synthesis

A

b. Bile acid concentration in the intestine

67
Q

As a result of bile acid sequestrants, hepatocytes increase the conversion of:
a. HDL to LDL
b. Triglycerides to free fatty acids
c. Cholesterol to bile acids
d. Bile acids to cholesterol

A

c. Cholesterol to bile acids

68
Q

The increased conversion of cholesterol to bile acids causes intracellular cholesterol concentrations to:
a. Increase
b. Decrease
c. Remain the same
d. Fluctuate

A

b. Decrease

69
Q

Bile acid-binding resins are often used in combination with diet or niacin for treating which types of hyperlipidemias?
a. Type I and type IIA
b. Type IIA and type IIB
c. Type I and type IIB
d. Type IIB and type III

A

b. Type IIA and type IIB

70
Q

Colesevelam is also indicated for which condition due to its glucose-lowering effects?
a. Type 1 diabetes
b. Type 2 diabetes
c. Gestational diabetes
d. Prediabetes

A

b. Type 2 diabetes

71
Q

Bile acid sequestrants are insoluble in which substance?
a. Water
b. Blood
c. Alcohol
d. Oil

A

a. Water

72
Q

Bile acid sequestrants have what characteristic molecular weight?
a. Low
b. Large
c. Medium
d. Small

A

b. Large

73
Q

After oral administration, bile acid sequestrants are:
a. Partially absorbed and metabolized by the intestine
b. Neither absorbed nor metabolically altered by the intestine
c. Fully absorbed by the intestine
d. Metabolized by the liver

A

b. Neither absorbed nor metabolically altered by the intestine

74
Q

What happens to bile acid sequestrants after they are administered orally?
a. They are stored in the liver
b. They are totally excreted in feces
c. They are metabolized by intestinal bacteria
d. They are absorbed into the bloodstream

A

b. They are totally excreted in feces

75
Q

The most common side effects of bile acid-binding resins are:
a. Headaches and dizziness
b. GI disturbances such as constipation, nausea, and flatulence
c. Skin rashes and itching
d. Muscle pain and weakness

A

b. GI disturbances such as constipation, nausea, and flatulence

76
Q

Bile acid-binding resins may impair the absorption of which types of vitamins?
a. Water-soluble vitamins (B and C)
b. Fat-soluble vitamins (A, D, E, and K)
c. All vitamins
d. Minerals

A

b. Fat-soluble vitamins (A, D, E, and K)

77
Q

Bile acid-binding resins can interfere with the absorption of:
a. Proteins
b. Carbohydrates
c. Many drugs
d. Electrolytes

A

c. Many drugs

78
Q

These agents may raise levels of which lipid, making them contraindicated in patients with significant hypertriglyceridemia?
a. HDL
b. LDL
c. Triglycerides
d. Total cholesterol

A

c. Triglycerides

79
Q

Bile acid-binding resins are contraindicated in patients with:
a. Hypercholesterolemia
b. Significant hypertriglyceridemia
c. Hypertension
d. Type 2 diabetes

A

b. Significant hypertriglyceridemia

80
Q

The mechanism through which bile acid-binding resins impair the absorption of fat-soluble vitamins involves:
a. Binding to bile acids and preventing their reabsorption
b. Directly inhibiting the vitamin receptors
c. Increasing the excretion of water-soluble vitamins
d. Enhancing the metabolism of vitamins in the liver

A

a. Binding to bile acids and preventing their reabsorption

81
Q

Ezetimibe selectively inhibits the absorption of cholesterol in which part of the body?
a. Stomach
b. Small intestine
c. Large intestine
d. Liver

A

b. Small intestine

82
Q

Ezetimibe decreases the delivery of intestinal cholesterol to:
a. The kidneys
b. The liver
c. The pancreas
d. The gallbladder

A

b. The liver

83
Q

What effect does ezetimibe have on LDL cholesterol levels?
a. It increases LDL cholesterol
b. It lowers LDL cholesterol
c. It has no effect on LDL cholesterol
d. It stabilizes LDL cholesterol

A

b. It lowers LDL cholesterol

84
Q

Ezetimibe increases HDL cholesterol by:
a. Reducing HDL catabolism
b. Increasing the clearance of cholesterol from blood
c. Enhancing HDL synthesis
d. Inhibiting HDL uptake

A

b. Increasing the clearance of cholesterol from blood

85
Q

The commonality of adverse effects with the use of ezetimibe is:
a. Very high
b. Moderate
c. Uncommon
d. Frequent

A

c. Uncommon

86
Q

Ezetimibe inhibits the absorption of which types of cholesterol?
a. Dietary cholesterol only
b. Biliary cholesterol only
c. Both dietary and biliary cholesterol
d. Endogenous cholesterol only

A

c. Both dietary and biliary cholesterol

87
Q

Ezetimibe’s primary therapeutic effect is to:
a. Lower LDL cholesterol and increase HDL cholesterol
b. Increase LDL cholesterol and decrease HDL cholesterol
c. Lower HDL cholesterol and increase LDL cholesterol
d. Stabilize both LDL and HDL cholesterol levels

A

a. Lower LDL cholesterol and increase HDL cholesterol

88
Q

What is the mechanism by which ezetimibe lowers cholesterol levels?
a. Inhibiting cholesterol synthesis in the liver
b. Inhibiting absorption of dietary and biliary cholesterol in the small intestine
c. Enhancing cholesterol excretion through the kidneys
d. Increasing the metabolism of cholesterol in the liver

A

b. Inhibiting absorption of dietary and biliary cholesterol in the small intestine

89
Q

Omega-3 polyunsaturated fatty acids (PUFAs) are essential fatty acids used for:
a. Triglyceride lowering
b. LDL cholesterol lowering
c. HDL cholesterol lowering
d. Total cholesterol lowering

A

a. Triglyceride lowering

90
Q

Omega-3 fatty acids may have what effect on LDL cholesterol?
a. Lower LDL cholesterol
b. Raise LDL cholesterol
c. Have no effect on LDL cholesterol
d. Stabilize LDL cholesterol

A

b. Raise LDL cholesterol

91
Q

Essential fatty acids inhibit the synthesis of which substances in the liver?
a. HDL and LDL
b. Cholesterol and triglycerides
c. VLDL and triglycerides
d. Bile acids and cholesterol

A

c. VLDL and triglycerides

92
Q

The omega-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are primarily found in which sources?
a. Plant sources such as flaxseed and chia
b. Animal sources such as beef and pork
c. Marine sources such as tuna, halibut, and salmon
d. Dairy sources such as milk and cheese

A

c. Marine sources such as tuna, halibut, and salmon

93
Q

The most common side effects of omega-3 PUFAs include:
a. Headaches and dizziness
b. GI effects (abdominal pain, nausea, diarrhea) and a fishy aftertaste
c. Skin rashes and itching
d. Muscle pain and weakness

A

b. GI effects (abdominal pain, nausea, diarrhea) and a fishy aftertaste

94
Q

What can increase the bleeding risk in patients taking omega-3 PUFAs?
a. Concurrent use of beta-blockers
b. Concurrent use of ACE inhibitors
c. Concurrent use of diuretics
d. Concurrent use of anticoagulants or antiplatelets

A

d. Concurrent use of anticoagulants or antiplatelets

95
Q

Omega-3 fatty acids are most effective in lowering which lipid?
a. HDL cholesterol
b. LDL cholesterol
c. Triglycerides
d. Total cholesterol

A

c. Triglycerides

96
Q

The presence of which aftertaste is a common side effect of omega-3 PUFAs?
a. Fishy aftertaste
b. Bitter aftertaste
c. Metallic aftertaste
d. Sweet aftertaste

A

a. Fishy aftertaste

Pharma2 MCQs (6 decks)

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