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Cardio Exam 1 physiology and chem

Total questions: 89

Worksheet time: 48mins

Name
Class
Date
1.

which of the following of function groups are less stable

a)

Esters

b)

amides

2.

which of the following agents belong to sub class 1

a)

flecainide, propafenone

b)

lidocaine , mexiletine phenytoin

c)

disopyramide , procainamide, quinidine

3.

match description to the class of drugs

a)

flecainide, propafenone

b)

lidocaine , mexiletine phenytoin

c)

disopyramide , procainamide, quinidine

4.

match description to the class of drugs

a)

flecainide, propafenone

b)

lidocaine , mexiletine phenytoin

c)

disopyramide , procainamide, quinidine

5.

match description to the class of drugs:

a)

flecainide, propafenone

b)

lidocaine , mexiletine, phenytoin

c)

disopyramide , procainamide, quinidine

6.

which of the following drug is not effective for atrial arrhythmias due to very short action potentials ( Na+ channel inactive stage is brief)

a)

mexiletine

b)

lidocaine

c)

phenytoin

7.

match description to the class of drugs

a)

flecainide, propafenone

b)

lidocaine , mexiletine phenytoin

c)

disopyramide , procainamide, quinidine

8.

which of the following agents belong to sub class 2

a)

flecainide, propafenone

b)

lidocaine , mexiletine ,phenytoin

c)

disopyramide , procainamide, quinidine

9.

which of the following agents belong to sub class 3

a)

flecainide, propafenone

b)

lidocaine , mexiletine ,phenytoin

c)

disopyramide , procainamide, quinidine

10.

class 1 Na+ channel blockers( fast), will decrease the following

a)

slope of Phase 0 in cardiomyocytes(non-nodal cells)

b)

conduction velocity of AP

c)

QRS( conduction in ventricles)

d)

induced abnormal automaticity

11.

class 1 Na+ channel blockers( fast), will actually INCREASE the following

a)

slope of Phase 0 in cardiomyocytes(non-nodal cells)

b)

conduction velocity of AP

c)

QRS( conduction in ventricles)

d)

induced abnormal automaticity

12.

class 1 Na+ channel blockers( fast), can also decrease phase .......diastolic Na currents which increases threshold to action potential leading to decreased automaticity of abnormal pacemaker activity in cardiomyocytes that depends on Na+ channels

a)

3

b)

2

c)

4

13.

class 1 Na+ channel blockers decrease phase........and phase...........currents.

a)

3

b)

2

c)

4

d)

0

14.

transition between states depends on

a)

Heart rate

b)

membrane potential

c)

both

15.

in Tacycardia most of the channels are in the

a)

active state

b)

inactive state

c)

both

16.

Class 1 drugs decrease Na+ currents which leads to an/a............in the Effective recovery period

( ERP)

a)

decrease

b)

increase

17.

Drugs with a ..........recovery have a greater affect

a)

fast

b)

slow

18.

procanamide, quinidine, and disopyramide have a greater affinity for

a)

open state with intermediate recovery

b)

inactivated state with rapid recovery

c)

open state and a very slow recovery

19.

flecainide and propafenone have a greater affinity for

a)

open state with intermediate recovery

b)

inactivated state with rapid recovery

c)

open state and a very slow recovery

20.

Lidocaine and mexiletine have a greater affinity for

a)

open state with intermediate recovery

b)

inactivated state with rapid recovery

c)

open state and a very slow recovery

21.

Ester was changed t o amide to

a)

slow metabolism and increase half life for the orally active compound

b)

increase metabolism

c)

make more hydrophilic

d)

make more lipophilic

22.

metabolites P-aminobenzoic acid and N-acetylprocainamide are the metabolites. the acetylated one is

a)

active as antiarrythimics

b)

inactive

23.

this drug is available as a racemic mixture. the Tertiary amide can be converted into

a)

alcohol

b)

salt to improve water solubility

c)

acetate

d)

ATP

24.

name this drug

a)

procanamide

b)

lidocaine

25.

lidocaine has a rapid onset when administered

a)

IV

b)

orally

26.

lidocaine is a weak with a pKa = 8

a)

acid

b)

base

27.

the ether in mexiletine is .......stable than the amide of lidocaine because it is more resistant to hydrolysis. ( 1 chiral center)

a)

less

b)

more

28.

mexiletine undergoes fist pass metabolism

a)

minimal

b)

severe

29.

this drug is primary ...............in the stomach

a)

ionized ( hydrophilic)

b)

unionized(lipophilic)

30.

this drug is primary ...............in the intestines

a)

ionized ( hydrophilic)

b)

unionized(lipophilic)

31.

this drug is administered for V-fib

a)

IV

b)

Orally( 80-90 % bioavaility)

32.

which drug is this?

a)

lidocaine

b)

disopyramide

c)

flecainide

d)

propafenone

33.

flecainide is used to slow down rapid ventricular rates in V-fib. the amide is usually the .......basic moiety of the drug

a)

least

b)

most

34.

in disopyramine, the tirtiary amine is ......than the aromatich amine

a)

more basic

b)

less basic

35.

the S-isomer is mainly responsible for

a)

B1- blocking properties

b)

chirality

c)

basicity

36.

the secondary amine group is a weak base, and can easily be converted to

a)

a hydrochloride salt

b)

phosphate salt

37.

in cardiomyocytes class 1 drugs block

a)

Mg++

b)

Na+

c)

Ca++

d)

K+

38.

ADR of disopyramide include

a)

dry mouth

b)

urinary retention

c)

constipation

d)

headache

39.

which of the following Class 1C drugs have extensive and poor metabolizers( genetically determined)

a)

flecainide

b)

Propafenone

40.

which of the folollowing drugs are not associated with Torsades de pointes ( no significant affect on QT )

a)

flecainide and propafenone

b)

dofetilide and ibutilide

c)

procainamide and quinidine

41.

Class 1A: match the ADRs to the drug

a)

quinidine

b)

procainamide

c)

procainamide and quinidine

42.

Class 1A: match the ADRs to the drug

a)

quinidine

b)

procainamide

43.

Class 1B: match the ADRs to the drug

a)

mexiletine

b)

lidocaine

44.

Class 1B: match the ADRs to the drug

a)

mexiletine

b)

lidocaine

45.

Class 1C: match the ADRs to the drug

a)

profenone

b)

flecainide

46.

match the drugs to the indication:

a)

atrial and ventricular arrhythmias

b)

local anesthetic and ventricular arrythmias

c)

atrial and ventricular arrhythmias

high risk of proarrythmias in patients with congestive heart failure and coronary artery disease

47.

match the drugs to the indication:

a)

atrial and ventricular arrhythmias

b)

local anesthetic and ventricular arrythmias

c)

atrial and ventricular arrhythmias

high risk of proarrythmias in patients with congestive heart failure and coronary artery disease

48.

match the drugs to the indication:

a)

atrial and ventricular arrhythmias

b)

local anesthetic and ventricular arrythmias

c)

atrial and ventricular arrhythmias

high risk of proarrythmias in patients with congestive heart failure and coronary artery disease

49.

this drug specifically inhibits slow Na+ channels in pacemaker cells, decreases phase 4 spontaneous depolarization , FDA use for CHF and sinus tachycardia & HF. ADRs include bradycardia, AV block, vision changes, and QT prolongation

a)

flecainide

b)

ivabradine

c)

propafenone

50.

propanolol, timolol, and sotalol are

a)

selective betablockers

b)

nonselective betablockers

51.

atenolol, esmolol, metoprolol are

a)

selective betablockers( B1>B2)

b)

nonselective betablockers

52.

carvedilol, labetalol are

a)

selective third generation beta blockers( B1>B2)

b)

nonselective third generation beta blocker

53.

betaxolol and nebivolol are

a)

selective third generation beta blockers( B1>B2)

b)

nonselective third generation beta blocker

54.

acebutolol, penbutolol, pindolol are selective beta blockers, but not used clinically for arrythmias due to

a)

Intrinsic sympathomimetic activity(ISA)

b)

bioavalability

c)

interactions with other drugs

55.

selective B-blocker drugs are less likely to produce

a)

vasodilation

b)

broncoconstriction

56.

what is the primary affect of b-blockers in pacemaker cells?

a)

all the above

b)

decrease automaticity in SA node, decrease slope of phase 4 & HR,

c)

decrease Na+ and Ca2+ currents

d)

Increase AV conduction time and refractory period

57.

what is the primary affect of b-blockers in cardiomyocytes( fast response cells)?

a)

increase force of contraction

b)

decrease force of contraction ( activity of Ca2+)

58.

according to the diagram, b-blockers ............cAMP and decrease rate of conduction & force of contraction

a)

increase

b)

decrease

59.

which of the following are severe/rare sideeffects of B-blockers

a)

hypotension, bradycardia

b)

heart block, DAD, EAD , bronchoconstriction

c)

dizziness, fatigue

d)

lethargy

60.

what is the structural difference between beta-Agonists and antagonist ? Beta antagonists have

a)

b)

61.

B-selectivity ...........with increasing size of the R-group

a)

increases

b)

decreases

62.

match drug to description

a)

more lipophilic, undergoes exensive hepatic metabolism, lower dose for hepatic impaired

b)

more hydrophilic, no hepatic metabolism, excreted unchanged in urine, low dose for renal impairement

63.

match drug to description

a)

more lipophilic, undergoes exensive hepatic metabolism, lower dose for hepatic impaired

b)

more hydrophilic, no hepatic metabolism, excreted unchanged in urine, low dose for renal impairement

64.

Amiodarone, ibutilde and dofetiled are

a)

Class 1 drugs

b)

class 2 drugs

c)

class 3 drugs

d)

class 4 drugs

65.

What is the MOA of of amiodarone or dofetilde?

a)

block Na+ and Ca+ from entering cell and therefore increasing refractory period

b)

block b1 and b2 receptors

c)

block K+ channels( pahse 3 of action potential) prolonging it and inhibiting repolarization increasing refractory period

66.

what is a disadvantage of amiadorone

a)

it has a matebolite that is potent and they both last in body for long time even after discontinuation

b)

it has many matebolites

c)

it does not have Iodine

67.

dronedarone is an anologue of amiadarone. the removal of Iodine in dronedarone makes the drug

a)

more hydrophilic

b)

more lipophilic

c)

shortens halflife

d)

decreases toxicitity

68.

Dofetilide is......... selective compared to amiodarone

a)

less

b)

highly more

69.

Class 3 MOA

a)

block Ca2+ in phase 2

b)

block Na influx in phase 0

c)

block K+ channels from Repolarization in phase3

d)

block K+ rectifier in phase 4

70.

which of the following drugs are Class 3 drugs?

a)

Amiodarone

b)

quinidine

c)

ibutilide

d)

dofetilide

e)

procainamide

71.

which of the following drugs are Class 3 drugs?

a)

ibutilide

b)

mexiletine

c)

dronedarone

d)

flecainide

e)

disopyramide

72.

of the following drugs , they both have a sulfonamide group, which one has a methanesulfonamide

a)

sotalol

b)

ibutilide

c)

dofetilide

73.

Class 3 drugs block

a)

delay rectifier K+ in phase 3

b)

K+ in phase 4( diastolic current or T1 transient K+)

74.

an issue with class 3 drugs is that they may cause

a)

EAD

b)

torsade the point

c)

both

75.

if a patient has a QTC > 440msc we should not give them

a)

quinidine

b)

dofetilide, ibutilide

76.

which of the following class 3 drugs block multiple channels?

a)

quinidine

b)

dofetilide, ibutilide

c)

amiadarone, dronedarone, sotalol

77.

which of the following class 3 drugs have class 1,2,3,4 activity( Na,K,Ca++, and beta blocker activity)?

a)

dronedarone

b)

dofetilide, ibutilide

c)

amiadarone

d)

sotalol

78.

which of the following drugs belong to class 4: blocking activated and inactivated L-type Ca2+ channels in cardiac cells

a)

Diltiazem

b)

dofetilide, ibutilide

c)

amiadarone

d)

verapamil

79.

which of the following class 3 drugs have class 2 and 3 activities ?

a)

dronedarone

b)

dofetilide, ibutilide

c)

amiadarone

d)

sotalol

80.

which of the following class 3 drugs are known to cause Hyperthyroidism due to IOdine hypersensitiyty, Vision problems, blue ray skin pigmentation, torsades, brady cardia etc ( NASTY drug)

a)

dronedarone

b)

dofetilide, ibutilide

c)

amiadarone

d)

sotalol

81.

verapamil and diltiazem have their greatest effect in : increasing threshold and slowing depolarization( decreasing SA rate, AV conduction, slowing reentry arrhythmias involving AV node)

a)

pacemaker cells

b)

myocardium

82.

verapamil and diltiazem block Ca++ in phase 2 plateu, shorten action potential , prevents DAD + EAD in

a)

pacemaker cells( slow response cell)

b)

myocardium( fast response cell)

83.

verapamil and diltiazem may block Ca++ in later phase 4 and in phase 0, this results in a decrease in

a)

HR

b)

SA rate

c)

AV conduction rate

d)

all the above

84.

Diltiazem and verapamil will

a)

improve heart failure

b)

worsen heart failure

85.

match MOA to drug: Activates Ach-sensitive K+ channels leading to hyper polarization( SA,AV, atrium), decreasing Ca++ current( decreasing cAMP that occur with sympathetic activation)

a)

adenosine

b)

digoxin

86.

match MOA to drug: usually used for arrhythmias: increases vagal tone( indirect action = actiovation of ACh-sensitive K+ channels in atrium( hyperpolorization), shortening APD which decreases Ca++ currents in AV node and increases Effective refractory period

a)

adenosine

b)

digoxin

87.

match MOA to drug: usually used for arrhythmias: increases vagal tone( indirect action = actiovation of ACh-sensitive K+ channels in atrium( hyperpolorization), shortening APD which decreases Ca++ currents in AV node and increases Effective refractory period

a)

adenosine

b)

digoxin

88.

this drug is a glycoside

a)

adenosine

b)

digoxin

89.

common side effects of digoxin include

a)

nausea, anorexia

b)

blurred or yellow vision

c)

DADs, AV block

d)

atrial tachycardia