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Pharmacology Exam 3

Total questions: 110

Worksheet time: 1hrs 7mins

Name
Class
Date
1.

Dyslipidemia:

a)

elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein level contributes to the development of atherosclerosis

b)

metabolic disorder characterized by lipoprotein plasma elevation

c)

high blood cholesterol

d)

determined by blood LDL level

2.

Hyperlipidemia (hyperlipoproteinemia):

a)

metabolic disorder characterized by lipoprotein plasma elevation

b)

elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein level contributes to the development of artheroschlerosis

c)

high blood cholesterol

d)

mostly determined by blood LDL level

3.

Hyperlipidemia (hyperlipoproteinemia) 2 major clinical presentations:

a)

acute pancreatitis

b)

atherosclerosis

c)

associated with increased risk of CVD

d)

high blood cholesterol

4.

Hypercholesterolemia:

a)

high blood cholesterol

b)

mostly determined by blood LDL level

c)

associated with increased risk CVD

d)

metabolic disorder characterized by lipoprotein plasma elevation

5.

Hyperlipemia is primarily associated with increased risk of?

a)

pancreatitis

b)

obesity

c)

type 2 diabetes

d)

renal disease

6.

Lipoprotein- proteins that transport plasma lipids (carriers)

a)

large and sparse "fluffy" molecules

b)

outer shell: phospholipid and protein and small amount of free cholesterol

c)

core: esterified cholesterol and triglyceride

7.

Is the core of a lipoprotein hydrophobic?

a)

yes

b)

no

8.

What is an apo-protein?

a)

a protein that binds lipids

b)

a free cholesterol molecule

9.

Which apo-protein is formed in the intestine and found only in chylomicrons?

a)

B-48

b)

B-100

c)

A-1

d)

A-2

10.

Which apo-protein is synthesized in the liver and found mainly in VLDL, LDL?

a)

B-48

b)

B-100

c)

A-1

d)

A-2

11.

Which apo-protein is the principle protein found in HDL?

a)

B-48

b)

B-100

c)

A-1

d)

A-2

12.

Which apo-protein occurs as dimer mainly in HDL?

a)

B-48

b)

B-100

c)

A-1

d)

A-2

13.

What are the functions of apo-proteins?

a)

lipoprotein assembly

b)

structural integrity

c)

enzyme activation

d)

receptor binding

e)

cholesterol transport

14.

Which apo-protein and concentration in plasma (mg/100mL) is paired incorrectly?

a)

A-1: 90-120

b)

A-2: 80-100

c)

B-48: <5

d)

B-100: 80-100

e)

none of them

15.

Where are chylomicrons formed?

a)

intestine

b)

liver

16.

How are chylomicrons transported in the body?

a)

lymphatic system

b)

bloodstream

17.

What do chylomicrons carry?

a)

TGs

b)

un-esterified cholesterol

c)

cholesterol esters

d)

esterified cholesterol

18.

Which is the lowest density, most sparse "fluffy" lipoprotein?

a)

chylomicrons

b)

VLDL

19.

What is Apo C-II?

a)

lipoprotein lipase activator

b)

lipoprotein binder

c)

lipoprotein transporter

20.

Where are VLDLs (very low density lipoproteins) synthesized?

a)

ONLY in the liver

b)

in the liver and intestines

c)

in the liver, intestines, and spleen

21.

What are the components of a VLDL?

a)

Apo B-100

b)

Apo E

c)

Apo C-I

d)

Apo C-II

e)

Apo C-III

22.

In VLDLs, what is Apo B-100 for?

a)

receptor binding

b)

LPL activator

c)

remnant receptor binding

23.

In VLDLs what is Apo C-II for?

a)

receptor binding

b)

LPL activator

c)

remnant receptor binding

24.

In VLDLs what is Apo E for?

a)

receptor binding

b)

LPL activator

c)

remnant receptor binding

25.

What are the functions of VLDLs?

a)

export TGs to peripheral tissues

b)

TGs hydrolyzed from VLDL by LPL (lipoprotein lipase) --> free fatty acids

c)

reverse cholesterol transport

26.

What does familial defective apo-B-100 cause?

a)

hypercholesterolemia

b)

high blood pressure

c)

artheroschlerosis

27.

What is the principal protein of LDL and what does it do?

a)

Apo-B-100; receptor binding

b)

Apo C-II; LPL activator

c)

Apo E; remnant receptor binding

28.

LDL particles in the circulation are derived from what?

a)

VLDL

b)

TG

c)

HDL

29.

What is the function of the LDL?

a)

deliver cholesterol to the cells

b)

export TGs to peripheral tissues

30.

How much plasma cholesterol is found in the LDL?

a)

1/3

b)

2/3

c)

the LDL is a summation of all the cholesterol in the plasma

31.

How are LDL clearance particles mediated?

a)

LDL receptors

b)

HDL receptors

c)

negative feedback by TGs

32.

Where are LDL plasma clearance particles mainly (70%) located?

a)

liver

b)

spleen

c)

intestines

33.

What enhances LDL receptor gene expression?

a)

thyroxine

b)

estrogen

c)

levothyroxine

d)

testosterone

34.

What is the principal protein of HDL?

a)

apo-A1

b)

apo-B1

c)

Apo C

d)

Ape E

35.

Which is the most dense lipoprotein?

a)

HDL

b)

LDL

c)

VLDL

36.

What does Apo A1 do in HDLs?

a)

activates lecithin-cholesterol actyltransferase

b)

export TGs to peripheral tissues

37.

What does lecithin-cholesterol acyltransferase (LCAT) do?

a)

convert free cholesterol into cholesteryl ester (more hydrophobic form of cholesterol)

b)

deplete TG supply

38.

What does Apo C do in HDLs?

a)

activate LPL

b)

remnant receptor binding

c)

activates LCAT

39.

What does Apo E do in HDL?

a)

activate LCAT

b)

activate LPL

c)

remnant receptor binding

40.

Is HDL the good or bad cholesterol?

a)

good

b)

bad

41.

Where is HDL secreted?

a)

liver

b)

intestine

c)

heart

d)

spleen

42.

Which gene mutates and causes HDL deficiency?

a)

Apo A1 gene

b)

Apo C gene

c)

Apo E gene

43.

What membrane transporter facilitates the transfer of free cholesterol from cells to the HDL?

a)

ABCA1

b)

CABA1

c)

BACA1

44.

What is HDL involved in?

a)

reverse cholesterol transport

b)

TG export to the peripheral tissues

45.

What forms an Lp(a) lipoprotein?

a)

LDL particle

b)

second apoprotein (a)

c)

disulfide bond

d)

apoB-100

46.

Where is protein (a) found?

a)

atherosclerotic plaque

b)

TGs

c)

LDLs

d)

HDLs

47.

What does protein (a) do?

a)

inhibits thrombolysis

b)

if a higher level it can increase risk of CHD

c)

homologous with plasminogen but not activated by tissue plasminogen activator

d)

causes thrombolysis

48.

What is cholesterol required for?

a)

membrane structural integrity

b)

membrane fluidity

c)

bile acid synthesis

d)

hormone synthesis

49.

Which lipid disorder (primary hypertriglyceridemia/hyperlipemia) has the following characteristics?

-lipoprotein lipase LPL activity deficiency

-Apo-C-II deficiency

a)

primary chylomicronemia

b)

familial hypertriglyceridemia

c)

familial hypercholesterolemia

d)

Lp(a) hyperlipoproteinemia

50.

Which lipid disorder (primary hypertriglyceridemia/hyperlipemia) has the following characteristics?

-impaired removal of TG lipoproteins

-genetic variations

-aggravated by alcohol, obesity and diabetes

a)

primary chylomicronemia

b)

familial hypertriglyceridemia

c)

familial hypercholesterolamia

d)

familial ligand-defective apolipoprotein B-100

51.

Which lipid disorder (primary hypercholesterolemia) has the following characteristic?

-mainly defects of LDL receptors

a)

familial hypercholesterolemia

b)

familial ligand-defective apolipoprotein B-100

c)

Lp(a) lhyperlipoproteinemia

d)

cholesteryl ester storage disease

e)

HDL deficiency

52.

Which lipid disorder (primary hypercholesterolemia) has the following characteristic?

-defect in the domain of B-100

a)

familial hypercholesterolemia

b)

familial ligand-defective apolipoprotein B-100

c)

Lp(a) hyperlipoproteinemia

d)

cholesteryl ester storage disease

e)

HDL deficiency

53.

Which lipid disorder (primary hypercholesterolemia) has the following characteristic?

-increase the production of Lp(a)

a)

familial hypercholesterolemia

b)

familial ligand-defective apolipoprotein B-100

c)

Lp(a) hyperlipoproteinemia

d)

cholesteryl ester storage disease

e)

HDL deficiency

54.

Which lipid disorder (primary hypercholesterolemia) has the following characteristic?

-lacking of lysosomal acid lipase (LAL)

a)

familial hypercholesterolemia

b)

familial ligand-defective apolipoprotein B-100

c)

Lp(a) hyperlipoproteinemia

d)

cholesteryl ester storage disease

e)

HDL deficiency

55.

Which lipid disorder (primary hypercholesterolemia) has the following characteristic?

-rare genetic disorder

-associated with extremely low levels of HDL

a)

familial hypercholesterolemia

b)

familial ligand-defective apolipoprotein B-100

c)

Lp(a) hyperlipoproteinemia

d)

cholesteryl ester storage disease

e)

HDL deficiency

56.

Which conditions are common causes of secondary hyperlipidemia?

a)

alcohol excess

b)

excess weight

c)

hypothyroidism

d)

pregnancy

e)

breastfeeding

57.

Which drug classes are common causes of secondary hyperlipidemia?

a)

beta-blockers

b)

corticosteroids

c)

alpha 2 antagonists

d)

highly active antiretroviral therapy (HAART)

e)

loop diuretics

58.

Which drug classes are common causes of secondary hyperlipidemia?

a)

hormone replacement therapy (HRT)

b)

oral contraceptives

c)

thiazide diuretics

d)

androgens

e)

ACE inhibitors

59.

Which of the following are characteristics of the bile acid-sequestering resins?

a)

inhibition of the re-absorption of bile acid enhances its production from cholesterol via 7a-hydroxylation

b)

negative feedback loop

c)

bind negatively charged bile acids in the intestinal lumen and prevent their reabsorption

d)

forcing elimination of bile acids- increases the conversion of cholesterol to bile acid

e)

inhibiting the transport protein NPC1L1 in the jejunal enterocytes

60.

Which of the following are bile acid-sequestering resins?

a)

cholestyramine

b)

colesevelam

c)

colestipol

d)

simvastatin

e)

ezetimibe

61.

What is the PK of the bile acid-sequestering resins?

a)

highly positively charged

b)

water soluble vitamin

c)

highly water insoluble (lipophilic)

d)

readily absorbed

62.

What is the MOA of the bile acid-sequestering resins?

a)

bind negatively charged bile acids in the intestinal lumen and prevent their reabsorption

b)

forcing elimination of bile acids- increases the conversion of cholesterol to bile acids

c)

inhibits the lipolysis or TGs by hormone-sensitive lipase

d)

inhibits TG synthesis by inhibition of esterification and synthesis of fatty acids

63.

What are the benefits of the bile acid-sequestering resins?

a)

reduce plasma LDL- dose dependent

b)

slightly increase HDL levels

c)

strong safety record

d)

DOC: lipid-lowering agents in children and in pregnant or breastfeeding women

64.

What are the side effects of the bile acid-sequestering resins?

a)

constipation

b)

bloating, abdominal fullness, flatulence

c)

increase TGs

d)

reduced absorption of other drugs in the GI tract (administer 1 hour before or 4-6 hours after concurrent medications)

e)

diarrhea

65.

Which drug is a cholesterol absorption blocker?

a)

ezetimibe

b)

simvastatin

c)

atorvastatin

d)

colesevelam

66.

Which drug has the following MOA: inhibiting the transport protein NPC1L1 in the jejunal enterocytes

-inhibits cholesterol uptake

-decreases LDL and chylomicrons

-no effect on the intestinal TG absorption

-targeting both endogenous and exogenous cholesterol

a)

ezetimibe

b)

cholestyramine

c)

atorvastatin

67.

What's the PK of ezetimibe?

a)

highly lipophilic

b)

readily absorbed

c)

glucuronidated in the intestinal epithelium and absorbed

d)

highly hydrophobic

68.

What drug class should ezetimibe not be given with and why?

a)

bile acid-sequestering resins

b)

HMG-CoA reductase inhibitors

c)

bile acid-sequestering resins inhibit absorption of ezetimibe

d)

ezetimibe inhibits absorption of bile acid-sequestering resins

69.

What are the benefits of high doses (2-6 gm/day) of Niacin (nicotinic acid)?

a)

lowers TGs and LDL

b)

raises HDL more than any other lipid-lowering agent

c)

lowers LDL

d)

blocks Apo B-100

70.

Which drug has the following MOA?

-in adipose tissues: inhibits the lipolysis of TGs by hormone-sensitive lipase. Reduces transport of free fatty acids to the liver; decrease hepatic TG synthesis

-in the liver: inhibits TG synthesis by inhibition of esterification and synthesis of fatty acids; increases apoB degradation; reduces overall VLDL production, enhances LPL activity (promotes the clearance of chylomicrons and VLDL TGs); decreasing the fractional clearance of apo A-1 in HDL rather than by enhancing HDL synthesis (raises HDL-C levels)

a)

niacin

b)

ezetimibe

c)

colestipol

d)

cholestyramine

71.

What is the PK of niacin?

a)

water soluble vitamin

b)

half life is about 60 minutes- dosed 2-3 times daily

c)

fat soluble vitamin

d)

half life is about 12 hours- dosed daily

72.

What are the side effects of niacin?

a)

flushing

b)

pruritus- taking an asa each day can alleviate the flushing in many patients

c)

dry skin

d)

anticholinergic effects

73.

Which forms of niacin are the main culprits of hepatotoxic effects?

a)

immediate release

b)

sustained release

c)

extended release (niaspan)

74.

Niacin can reactivate ulcer disease.

a)

true

b)

false

75.

Niacin can cause hyperuricemia (precipitate gout).

a)

true

b)

false

76.

Which drugs are fibrates (fibric acid derivatives)?

a)

fenofibrate

b)

gemfibrozil

c)

clofibrate

d)

bezafibrate

e)

ciprofibrate

77.

What are the PK characteristics of fibrates?

a)

all are absorbed rapidly and efficiently (>90%)

b)

food enhances absorption

c)

highly bound to plasma proteins > 95%

d)

60-90% of an oral dose is excreted in the urine (impaired in renal failure)

e)

not good oral bioavailability

78.

What is the MOA of fibrates?

a)

the bind to and activate PPARα

b)

inhibits TG synthesis by inhibition of esterification and synthesis of fatty acids

c)

inhibits the lipolysis of TGs by hormone-sensitive lipase

d)

inhibiting the transport protein NPC1L1 in the jejunal enterocytes

79.

Where is PPARα expressed primarily?

a)

liver

b)

brown adipose tissue

c)

intestine

d)

spleen

80.

What does PPARα do?

a)

mediates stimulation of fatty acid oxidation (inhibition of TG synthesis)

b)

increases LPL synthesis (enhances the clearance of TG-rich lipoproteins)

c)

inhibits TG synthesis by inhibition of esterification and synthesis of fatty acids

81.

Which apo has reduced expression in PPARα? What does that affect?

a)

apoC-III

b)

apoA-I

c)

apo-A-II

d)

enhance the clearance of VLDL

e)

increase HDL levels

82.

Which apo(s) is/are expressed more frequently due to stimulation from PPARα? What does this cause?

a)

apoC-III

b)

apoA-I

c)

apoA-II

d)

enhance the clearance of VLDL

e)

increase HDL levels

83.

When a fibrate drug binds to and activates PPARα, what gets inhibited?

a)

lipolysis

b)

the re-absorption of bile acid

84.

Which fibrates have the side effect of myopathy?

a)

clofibrate

b)

fenofibrate

c)

gemfibrozil

d)

bezafibrate

e)

ciprofibrate

85.

Can fibrates be used by children or pregnant women?

a)

yes

b)

no

86.

Fibrates can potentiate the action of oral anticoagulant warfarin. What does this mean?

a)

fibrates displace warfarin from their binding sites on albumin

b)

fibrates act as an inducer, metabolizing warfarin faster (dose must be adjusted)

87.

What is the MOA of statins?

a)

competitive inhibitors of HMG-CoA reductase enzyme- rate limiting enzyme in cholesterol synthesis

b)

structural analogs of HMG-CoA

c)

inhibit the first step in sterol synthesis

d)

bind to and activate PPARα

88.

What do statins reduce?

a)

VLDL

b)

LDL

c)

HDL

89.

What do statins increase expression of?

a)

LDL receptors

b)

HDL receptors

c)

VLDL receptors

90.

What are the potential cardioprotective effects of statins?

a)

reduce platelet aggregation and reduce platelet thrombi deposition

b)

anti-inflammatory role

c)

modulate the cellularity of the artery wall

91.

Which 2 statin drugs are prodrugs?

a)

simvastatin

b)

lovastatin

c)

pravastatin

d)

fluvastatin

92.

Intestinal absorption of statins is variable (30-85%). Is absorption enhanced or decreased by food?

a)

enhanced

b)

decreased

93.

Which statin is almost completely absorbed?

a)

atorvastatin

b)

rosuvastatin

c)

simvastatin

d)

fluvastatin

94.

Which statin is only 50% protein bound vs the other statins which are >95% protein bound?

a)

pravastatin

b)

lovastatin

c)

simvastatin

d)

atorvastatin

95.

How are statins excreted?

a)

liver

b)

kidneys

96.

Metabolized mainly by CYP3A4

a)

simvastatin

b)

atorvastatin

c)

lovastatin

d)

fluvastatin

e)

rosuvastatin

97.

Metabolized mainly by CYP2C9

a)

fluvastatin

b)

rosuvastatin

c)

pravastatin

d)

simvastatin

e)

atorvastatin

98.

Which statin is not metabolized by CYP450 enzymes?

a)

atorvastatin

b)

simvastatin

c)

lovastatin

d)

pravastatin

99.

Doubling the dose of a statin will further reduce the LDL-c level by how much?

a)

6%

b)

12%

c)

3%

d)

4%

100.

Which CYP families should be avoided in statin use?

a)

CYP3A4

b)

CYP2C9

c)

CYP2D6

101.

What are the major side effects of statins?

a)

hepatotoxicity (ALT for baseline then monitor)

b)

myopathy (muscle ache/myalgia, weakness, stiffness, cramps, serum CK may vary)

c)

rhabdomyolysis (serum CK elevated)

d)

GI upset

102.

Factors that may aggravate myopathic effects of statins?

a)

age >80 years

b)

alcohol abuse

c)

excessive grapefruit juice intake

d)

high statin dose

e)

low physical activity

103.

Which lipid lowering drug class in contraindicated (rating X) in pregnancy?

a)

ezetimibe

b)

niacin

c)

fibrates

d)

bile acid-sequestering resins

e)

statins

104.

Why should concurrent use of gemfibrozil be avoided when taking simvastatin, atorvastatin, or lovastatin?

a)

gemfibrozil is a CYP3A4 inhibitor

b)

gemfibrozil is a CYP3A4 inducer

105.

CYP3A4 inhibitors?

a)

amiodarone

b)

azoles

c)

cyclosporine

d)

grapefruit juice

e)

macrolide antibiotics

106.

CYP3A4 activators?

a)

phenytoin

b)

barbituates

c)

rifampin

d)

amiodarone

e)

macrolide antibiotics

107.

Which drug is both a CYP3A4 and CYP2C9 inhibitor?

a)

amiodarone

b)

ketoconazole

c)

phenytoin

d)

cyclosporine

108.

CYP2C9 inhibitors

a)

ketoconazole

b)

fluconazole

c)

fluoxetine

d)

fluvoxamine

e)

metronidazole

109.

Why are most statins given in the evening?

a)

cholesterol synthesis occurs predominantly at night

b)

cholesterol synthesis has already occurred, so this will prevent any additional overnight synthesis

110.

Which statins can be dosed at any time?

a)

atorvastatin

b)

pravastatin

c)

rosuvastatin

d)

pitavastatin

e)

fluvastatin

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