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Gupta ppt 2

Total questions: 78

Worksheet time: 48mins

Name
Class
Date
1.

Degenerative disease-artery wall thickens due to build-up of lipids

The deposits or plaques decrease the lumen of artery, reduce its elasticity and may create subsequent occlusion in the blood vessel

a)

Atherosclerosis

b)

Hyperlipidemia

c)

Hyperlipoproteinemia

2.

Elevated levels of lipids in plasma - Most prevalent indicator for susceptibility to atherosclerotic heart disease

a)

hyperlipidemia

b)

hyperlipoproteinemia

3.

Hyperlipidemia results in an increased concentration of these transport molecules, condition is called

a)

hyperlipidemia

b)

hyperlipoproteinemia

4.

primary disturbances cause of hyperlipidemia

a)

Genetic conditions involving mutations in apolipoproteins, their receptors, transport mechanisms, and lipid-metabolizing enzymes

b)

Western diet

Endocrine conditions

Diseases of the liver or kidneys

5.

secondary disturbance cause of hyperlipidemia

a)

Genetic conditions involving mutations in apolipoproteins, their receptors, transport mechanisms, and lipid-metabolizing enzym

b)

Western diet

Endocrine conditions

Diseases of the liver or kidneys

6.

dyslipidemia is cause by

a)

Total cholesterol or

b)

↓  HDL

c)

↑ LDL 

d)

↓  HDL

e)

or combination of these abnormalities

7.

Cholesterol transport inhibitor affect cholesterol absorption

a)

Ezetimibe

b)

Statins

8.

drug that cause inhibition HMG-CoA reductase affect the Endogenous  cholesterol biosynthesis by inhibit

a)

ezetimibe

b)

statins

9.

Affect Endogenous  lipoprotein and cholesterol metabolism

a)

Bile acid sequestrants

b)

Peroxisome proliferator-activated receptors (PPARα) activators

c)

Omega-3 fatty acids

d)

Lipolysis inhibitors

10.

NPC1L1 receptor blocker

a)

Ezetimibe

b)

Lomitapide

c)

Mipomersan

d)

Alirocumab and Evolocumab

11.

inhibits MTTP

a)

Lomitapide

b)

Ezetimibe

c)

Alirocumab and Evolocumab

d)

Mipomersan

12.

inhibits mRNA responsible for production of ApoB100. Less ApoB100 leads to decreased LDL and VLDL

a)

Ezetimibe

b)

Alirocumab and Evolocumab

c)

Mipomersan

d)

Lomitapide

13.

are approved for familial hypercholesterolemia. These drugs increases recycling of LDL-R helping in removal of LDL from circulation.

Inhibitors of PCSK9

a)

Alirocumab and Evolocumab

b)

Ezetimibe

c)

Mipomersan

d)

Lomitapide

14.

ezetimibe

a)

↑ Risk of hepatotoxicity when combined with statins

b)

• Primarily excreted in feces

c)

•Active Glucuronide Metabolite

d)

• ↑ LDL receptors on liver

e)
15.

Lomitapide (Juxtapid®) 

a)

reduce LDL, total cholesterol, apolipoprotein B, and non-HD cholesterol in patients with homozygous familial hypercholesterolemia (HoFH)

b)

Fatty liver-accumulation of triglycerides in the liver and elevations in transaminases.

c)
16.

Mipomersen

a)

A synthetic (unnatural) phosphorothioate oligonucleotide

b)

Resistant to degradation by nucleases

c)

20 nucleotides in length

d)

Side Effects: Mild to moderate injection site reactions and flu-like symptoms can occur.

17.

Liver compensates by ↑ LDLRs

but cannot Clears LDL and VLDL from blood

a)

true

b)

false

18.

HMG-COA Reductase Inhibitors (HMGRIs) statins

a)

Lower plasma cholesterol by:

b)

↑ in LDL receptors leading to

c)

↑ LDL uptake in liver

d)

↓ VLDL precursors

e)

↓ liver cholesterol biosynthesis

19.
a)

•3,5-Dihydroxy acid represents pharmacophore

b)

•Lactones represents prodrugs

c)

•3R and 5R stereochemistry required

d)

•3,5-Dihydroxy acid represents product drugs

e)

•Lactones represents pharmacophore

20.

↑ LDL levels: Generally treated with statins Other drugs may be added as needed

a)

true

b)

false

21.

Hypertriglyceridemia which true

a)

 Usually responds well to niacin, gemfibrozil, and fenofibrate;

b)

high-dose niacin should be used cautiously in diabetics because of worsening glycemic control.

22.

↓ HDL-C which is true

a)

Niacin, gemfibrozil and fenofibrate are also useful

b)

lifestyle modifications such as smoking cessation and increased exercise

23.

which are Anti-hyperlipoproteinemics combination product

a)

Simvastatin + Ezetimibe  Vytorin

b)

Simvastatin + Niacin

ER   Simcor

c)

Lovastatin + Niacin

ER  Advicor

d)

Atorvastatin + Amlodipine  Caduet

24.

Which of the following are potential side effects observed with niacin? [Select all that apply]

a)

Gout like symptoms

b)

Hepatotoxicity

c)

Facial flushing

d)

Worsening of glycemic control in diabetics

25.

Exercise

PJ is a 4.5-year-old boy. At his checkup, the pediatrician notices cutaneous xanthomas and orders a lipid panel. Repeated measures confirm that the patient’s serum cholesterol levels are high (936 mg/dL). Further testing confirms a diagnosis of homozygous familial hypercholesterolemia. Which of the following interventions will be least effective in this patient?

a)

Atorvastatin

b)

Mipomersen

c)

Lomitapide

d)

Ezetimibe

e)

Niacin

26.

Ring A: •is Essential for anchoring the compound to enzyme active site.

a)

Two cyclohexene rings

b)

Hydroxyl group at R1

c)

Methyl substitution at R2

27.

•Ring A: ↑ hydrophilicity and may provide some cellular specificity

a)

•Two cyclohexene rings

b)

Hydroxyl group at R1

c)

Methyl substitution at R2

28.

•↑ activity

a)

Two cyclohexene rings

b)

•Hydroxyl group at R1

c)

Methyl substitution at R2

29.

•Simvastatin (R2 = methyl) are less potent than lovastatin (R2 = Hydrogen)

a)

True

b)

False

30.

Ring A : Essential for anchoring the compound to enzyme active site.

a)

Two cyclohexene rings

b)

Hydroxyl group at R1

c)

Methyl substitution at R2

31.

Ring A: ↑ hydrophilicity and may provide some cellular specificity

a)

Two cyclohexene rings

b)

Hydroxyl group at R1

c)

Methyl substitution at R2

32.

Ring A: ↑ activity

a)

Two cyclohexene rings

b)

Hydroxyl group at R1

c)

Methyl substitution at R2

33.

Simvastatin (R2 = methyl) less potent than lovastatin (R2 = Hydrogen)

a)

true

b)

false

34.

Ring A are : Generally less lipophilic , with shorter duration of action than ring B

a)

true

b)

false

35.

Ring B: Generally lipophilic

a)

5-6 member heterocyclic ring attached with floro-phenyl

b)

R = Aryl groups/hydrocarbon chains/amides/SO2NH2

36.

Ring B : ↑ Activity

a)

5-6 member heterocyclic ring attached with floro-phenyl

b)

R = Aryl groups/hydrocarbon chains/amides/SO2NH2

37.

Ring B: Generally more lipophilic, longer DOA and more potent

a)

true

b)

false

38.

Examples: Lova- and simava-

a)

•Further metabolized in liver (CYP3A4)

•Active metabolite is the acid form

b)

•Excreted mainly in feces (80-85%)

c)

•Extensive first-pass metabolism (F~5%)

d)

Shorter duration of action, <2h (RingA) Clinical significance?

e)

•Lactone derivatives (prodrugs), NEUTRAL, lipophilic Converts to the acid form (active) after absorption

39.

which is tru Example: Prava-

a)

Acidic and hydrophilic statin (Ring A)

b)

• Extensive first-pass metabolism F~15-20%

c)

•Metabolized into active metabolite (less activity): Cyp3A4 substrate-Minor

d)

•Less muscle penetration

e)

basic and hydrophilic statin (Ring B)

40.

which is true for: Atorva-

a)

Acidic, most lipophilic statin

b)

Longer duration of action (Ring B)

c)

Metabolized to an equipotent metabolite (CYP3A4) Increased half-life of metabolite

Mainly excreted in bile (less by kidneys)

d)

Mainly excreted in bile (less by kidneys)

e)

Significant interactions with drugs affecting CYP3A4, PgP and OATP1B1

41.

which is true about Example: Fluva-

a)

•Acidic, lipophilic statin (ring B)

b)

• Strong affinity for CYP2C9

c)

• Extensive first-pass metabolism

d)

• Racemic mixture

e)

Strong affinity for CYP 3A4

42.

which is true about Example: Rosuva-

a)

•Hydrophilic statin

b)

•Longer half-life (~20h) (Ring B)

c)

•Not extensive first-pass metabolism (F~20%)

d)

•Excreted unchanged (~ 90%) in feces Some metabolism by Cyp2C9 (~10%)

43.

which is tru about Example: Pitava-

a)

Acidic, intermediate-long half-life (~11h) (Ring B)

b)

Least first-pass metabolism.

Less metabolism issues

c)

Majorly metabolized by UDP-glucuronosyltransferase (UGT1A3 & UGT2B7)

d)

ess likely to interact with drugs metabolized by 3A4, good in geriatric patients

e)

99% protein bound

Excreted in feces (~80%)

44.

Ring A characteristic low t1/2

a)

= Lova

b)

Prava

c)

Simva

d)

Fluva

45.

Ring B low t1/2

a)

Fluva

b)

lova

c)

silva

d)

prava

46.

Long DOA

a)

Rosuva

b)

Atorva

c)

Pitava

47.

intermed-long

a)

Pitava

b)

Rosuva

c)

Atorva

48.

Metabolism (major)

Cyp 3A4 = Simva, Lova, Atorva, Prava (minor)

Cyp2C9 = Fluva, Rosuva (10%), Atorva

Glucorinadation = Pitava

All can nteract with OAT1B1 in hepatocytes

a)

true

b)

false

49.

Any time of the day

a)

Prava

b)

Atorva

c)

Rosuva

d)

Pitava

50.

All drugs undergo extensive FPM Exceptions: Pitava and Rosuva

a)

true

b)

false

51.

hyroxylated metabolites same activity as parent drug

a)

Atorva

b)

Pitava

c)

Rosuva

52.

statins DDIs OATP1B1 inhibitors

a)

Gemfibrozil

b)

cyclosporin

c)

atorva-

d)

simva-

53.

Cyp3A4 inhibitors

a)

Macrolide antibiotics

b)

HIV protease inhibitors

c)

Azole antifungals like ketoconazole

d)

DDI with atorva-, simva-, lova-  (-statins)

54.

the most lipophilic is

a)

Atorvastatin

b)

Rosuvastatin

55.

Most hydrophilic (sulfonamide)

a)

Atorvastatin

b)

Rosuvastatin

56.

Severe muscle pain and even rhabdomyolysis

More common with lipophilic ones like Atorva-, lova-, simva-

a)

true

b)

false

57.

statins are less Known for hepatotoxicity and myopathy

a)

true

b)

false

58.

LDL lowering potency which is true

a)

mas potente Rosuvastatin> Atorvastatin>Pitavastatin>Simvastatin>Lovastatin>Pravastatin

>Fluvastatin menos potente

b)

menos potente Rosuvastatin<Atorvastatin<Pitavastatin<Simvastatin<Lovastatin<Pravastatin

<Fluvastatin mas potente

59.

which is true about Bempedoic acid (Nexletol®)

a)

PO, Approved 2/21/20

b)

To treat adults with heterozygous familial hypercholesterolemia or established atherosclerotic cardiovascular disease who require additional lowering of LDL-C

c)

SE: Myopathy, GI upset,

d)

Increases serum conc of simvastatin and pravastatin (also increasing myopathy): Avoid these statins at high dose

60.

Bile Acid Sequestrants: Cholestyramine

a)

Not orally absorbed

b)

Copolymer consisting primarily of polystyrene, with a small amount of divinylbenzene as the cross-linking agent.

c)

Contains approximately 4 mEq of fixed quaternary ammonium groups (4o amine) per gram of dry resin

d)

Prevalite

e)

Questra

61.

bile sequestrate Examples: Colestipol

a)

functional group are basic secondary and tertiary amines (2o and 3o amines)

b)

Less adsorption capacity as compared to cholestyramine

c)

more adsorption capacity as compared to cholestyramine

d)

Functional anion-exchange capacity of the resin depends on intestinal pH

e)

Functional anion-exchange capacity of the resin independs on intestinal pH

62.

Contains four basic amino functional groups

Fragment A is a primary amine (1o amine)

Fragment B is an alkylated amine attached to a quaternary ammonium group

Fragment C is a pair of secondary amines (2o amine)

Fragment D is a secondary amine(2o amine)

a)

Colesevelam- Welchol®

b)

Cholestyramine- Questran®

c)

colestipol- colestipol®

63.

Biles sequestrate site ADRs

a)

Bloating

Constipation

b)

Impaired absorption of drugs

Fat soluble vitamins and

Other drugs (eg, thiazide diuretics, warfarin, pravastatin, fluvastatin

c)

An unpleasant gritty taste

d)

diarrhea

64.

Which of the following drugs is most likely to increase this patient’s triglyceride and VLDL cholesterol concentrations when used as monotherapy?

a)

Atorvastatin

b)

Niacin

c)

Gemfibrozil

d)

Ezetimibe

e)

Cholestyramine

65.

Bile Acid Sequestrants:

↓ cholesterol in liver ↓ LDL receptors on the liver (↑ blood clearance)

↑ fatty acid absorption

a)

↑ their fecal excretion

↑ bile acid elimination

b)

↑ the hepatic conversion of cholesterol to bile acids thus

c)

↓ cholesterol in liver

d)

↑ LDL receptors on the liver (↑ blood clearance)↓ fatty acid absorption

e)

↓ cholesterol in liver ↓ LDL receptors on the liver (↑ blood clearance)

↑ fatty acid absorption

66.

PPARα Activators

a)

gemfibrozil

b)

fenofibrate

c)

fenifibric

67.

•Active form = basic e.g. Gemfibrozil, fenofibric aci

a)

true

b)

false

68.

• Ester =  prodrug e.g. Fenofibrate

a)

true

b)

false

69.

Gemfibrozil

a)

• Significant interactions with statins

b)

Skin rashes common

c)

Skin rashes less common

d)

•Inhibitor of CYP2C8, CYP2C9, CYP2C19

• Inhibitor of OATP1B1

e)

• Acidic,  lipophilic compound

70.

Fenofibrate

a)

Prodrug, very lipophilic, micronized formulations available

b)

Bioactivated by esterases to the free carboxylic acid form

Half life (20h) =  ~ 7 times more than gemfibrozil

c)

Absorption: Increased when taken with meals

71.

PPARα Activators toxicity

a)

Risk of gallstone formation (cholelithiasis)

b)

↑ Risk of myopathy if combined with statins

c)

Nausea is most common

d)

↓ white blood count

Can potentiate action of anticoagulants

72.

Lipolysis inhibitors :Niacin: Mechanism of Action

a)

↓ Free fatty acids in blood

↓ mobilization of FFAs

b)

↓ TG synthesis

c)

↓ VLDL

↓ LDL

d)

Niacin or nicotinic acid or vit B3 (Niaspan®)

MOA-Inhibits lipase in the adipose tissue (Inhibition of lipolysis)

e)

Blocks breakdown of fats

73.

Lipolysis inhibitors: Usefulness in the treatmenthypercholesterolemia, hypertriglyceridemia, and low levels of HDL

a)

true

b)

false

74.

lipolysis inhibitor cause

a)

hepatotoxicity

b)

Cutaneous flushing (common)

c)

Hyperuricemia

d)

Can worsen glycemic control in diabetics

75.

Omega-3 fatty acids

a)

Lovaza® (purified form): 38% EPA, 47% DHA, 17% other

b)

Lovaza® (purified form): 38% DHA, 47% EPA, 17% other

76.

What is the difference between dietary and Rx strength omega-3-Fas?

a)

Lovaza have 85% of DHA and EPA

b)

Dietary ones have 13-63% fish oils

c)

Dietary ones have 85% fish oils

d)

Lovaza have 13-63% of DHA and EPA

77.

If a patient is pregnant, which of the following drugs should be avoided because of a risk of harming the fetus?

a)

Cholestyramine

b)

Pravastatin

c)

Niacin

d)

Fenofibrate

e)

Ezetimibe

78.

Agonists of PPARα

a)

↓ cholesterol levels

↓TG synthesis

↑ fatty acid oxidation

↑HDL

b)

↑ cholesterol levels

↑TG synthesis

↑ fatty acid oxidation

↑HDL

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