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ACEM part 1 pharmacology > cardio drugs > Flashcards

cardio drugs Flashcards

1
Q
  1. Which of the following is a irreversible alpha-receptor antagonist?
    a. phentolamine
    b. dibenamine
    c. prazosin
    d. terazosin
A
  1. Answer is dibenamine- analog of phenoxybenzamine B page 150-151
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2
Q

Regarding secondary intracellular messenger which is true for prazosin?

a. decreases IP3 and DAG levels in the cell
b. increases IP3 and DAG levels in the cell
c. decreases cAMP levels in the cell
d. increases cAMP levels in the cell

A
  1. Answer is a see table 9.1 page 129
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3
Q

Regarding clonidine which is false?

a. clonidine has greater alpha 1 affinity than alpha 2 affinity
b. reduces cAMP levels intracellularly
c. is used for hypertension
d. is available via oral and transdermal fomulation

A
  1. Answer is A page 129-130
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4
Q

Terazosin

a. is an irreversible apha-1 antagonist
b. is primarily excreted in the urine
c. it has a long half life of 22 hours
d. is extensively metabolised in the liver

A

d

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5
Q

Regarding doxazosin which is false?

a. is useful in treating BPH and hypertension
b. it is removed from the body mainly by excretion in urine
c. is extensively metbolised in the liver
d. its half life is around 20 hours.

A

b

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6
Q

Beneficial effects of nitrates in treatment of angina include all of the following except:
a. Decreased ventricular volume b. Decreased arterial pressure c. Decreased ejection time d. Increased collateral flow e. Reflex increase in contractility

A

e

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7
Q
  1. Glycerl trinitrate
    a. Acts by effecting adenylyl cyclase b. Acts by effecting nitric oxide c. Has high oral bioavailability d. Has significant effects on cardiac muscle e. Has no effect on pulmonary vascular pressure
A

b

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8
Q
  1. Verapamil
    a. Increases myocardial contractility b. Is a positive inotrope c. Causes skeletal muscle weakness d. Blocks active and inactive Ca2+ channels
A

d

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9
Q
  1. Regarding nitrates, they do not

a. Increase collateral coronary blood flow b. Demonstrate tachyphylaxis/tolerance c. Demonstrate physical dependence

A

c

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10
Q
  1. Coronary artery dilation occurs with

a. Adenosine b. High K+ c. Propranolol d. Enalapril e. None of the above

A

a

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11
Q
  1. With regard to verapamil, which of the following is NOT true?
    a. It significantly increases serum digoxin levels via a pharmacokinetic interaction b. Alpha blockade contributes to peripheral vasodilation c. At therapeutic levels end systolic volume is decreased d. Vasospastic angina is an indication for its use e. Combination with a beta blocker may cause atrioventricular block
A

c

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12
Q
  1. Nitrates, either directly or via reflexes, cause all of the following EXCEPT:
    a. Tachycardia b. Decrease in contractility c. Increase in venous capacitance d. Decrease in myocardial fibre tension e. Decrease in afterload
A

b

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13
Q
  1. With regards to calcium channel blockers, which is NOT a characteristic feature?
    a. They have a high first pass effect b. They are highly plasma protein bound c. They are extensively metabolized d. They act primarily at T type voltage gated calcium channels e. They bind more effectively to channels in depolarized membranes
A

d

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14
Q
  1. Regarding calcium channel blockers:
    a. Verapamil blocks only activated calcium channels b. They act from the inner side of the membrane c. The degree of block is unaffected by plasma concentration of calcium d. They predominantly affect the T-type calcium channels in cardiac muscle e. They do not affect AV nodal conduction velocity
A

b

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15
Q
  1. Verapamil
    a. Binds more effectively to calcium channels in depolarized membranes b. Increases the contractility of the heart c. Decreases the calcium available in skeletal muscle causing weakness d. Lessens ankle oedema in congestive cardiac failure e. Is a weak alpha adrenergic agonist
A

a

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16
Q
  1. Verapamil

a. Is a positive inotrope b. ? c. inhibits activated and inactivated sodium channels d. is a dihydropyridine

A

c

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17
Q
  1. The calcium channel blocker with the most rapid onset of action when given orally is
    a. Diltiazem b. Nifedipine c. Verapamil d. Felodipine e. nicardipine
A

b

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18
Q
  1. Antiarrythmic drugs may work in any of the following ways EXCEPT:
    a. Reducing ectopic pacemaker activity b. Modifying conduction in reentrant circuits c. Sodium channel blockade d. Calcium channel blockade e. Reducing the effective refractory period
A

e

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19
Q
  1. Lignocaine
    a. Has poor oral bioavailability b. Blocks sodium channels not inactivated channels c. Is effective in AF d. Exacerbates VT in 30% e. Suppresses electrical activity of normal and arrythmogenic tissue equally
A

a

20
Q
  1. Flecainide
    a. Has poor oral bioavailability b. Is safe in ischaemia induced arrythmias c. May be used in reentry tachycardias d. Is a class Ia antiarrythmic e. Reduces mortality in post MI PVCs
A

c

21
Q
  1. adenosine
    a. has a half life of 2 minutes b. increases AV nodal conduction c. predominantly inhibits sinoatrial nodal function d. directly inhibits AV nodal conduction e. is more effective in the presence of theophylline or caffeine
A

d

22
Q
  1. adenosine
    a. has a half life of 30 seconds b. is the drug of choice for ventricular tachyarrythmias c. works by directly inhibiting the sinoatrial node with only mild effect on the atrioventricular node d. causes flushing in over 50% of patients e. is less effective in the presence of caffeine and theophylline
A

e

23
Q
  1. regarding antiarrythmics
    a. adenosine alters QRS duration b. amiodarone has a short half life c. lignocaine is also useful in supraventricular arrythmias d. flecainide is unsafe in people with ischaemic heart disease e. quinidine has no effect on QRS duration
A

d

24
Q
  1. amiodarone
    a. has a short half life b. stimulates Na channels c. is only effective against ventricular arrythmias d. has antianginal effects e. can cause emphysema in 5-15% of people
A

d

25
Q
  1. In the Vaughan-Williams classification
    a. Class 1 drugs affect potassium channels b. Class II drugs affect calcium channels c. Class II drugs affect sodium channels d. Class III drugs affect potassium channels e. Class IV drugs affect chloride channels
A

d

26
Q
  1. In therapeutic doses, adenosine:
    a. Acts by affecting sodium channels b. Is administered as a sloq IV push c. Is metabolized in the liver d. Produces a bradycardia by vagal stimulation e. Affects adenosine receptors at the AV node
A

e

27
Q
  1. adenosine
    a. closes K+ channels b. opens Cl- channels c. half life of 10min d. profoundly blocks SA node e. blocks Ca2+ dependent action potential
A

e

28
Q
  1. regarding adenosine
    a. its receptors are ion channels b. it increases AV nodal conduction c. it enhances K+ conductance d. it is the drug of choice in VF e. it has a half life of 2 minutes
A

c

29
Q
  1. which doesn’t prolong the refractory peiod in normal cells?
    a. Amiodarone b. Lignocaine c. Sotalol d. Quinine e. Procainamide
A

b

30
Q
  1. amiodarone
    a. is only effective in suppression of ventricular arrythmias b. causes peripheral vasodilation via alpha-adrenergic effects c. commonly causes corneal opacification d. increases warfarin clearance e. decreases AV donal refractory period
A

b

31
Q
  1. lignocaine displays all of the following EXCEPT:
    a. increased action potential duration b. binding to both activated and inactivated sodium channels c. predominant metabolism d. decreased clearance associated with concomitant propranolol administration e. ineefectiveness against arrythmias in normally polarize tissues
A

a

32
Q
  1. which of the following does NOT prolong the effective refractory period in the atrioventricular node?
    a. Propranolol b. Amiodarone c. Flecainide d. Verapamil
A

c

33
Q
  1. adenosine
    a. is effective in converting atrial flutter b. depresses conduction through the AV node c. requires reduction of dose in patients with hepatic failure d. has a half life of 30-60 seconds e. is safe in sick sinus syndrome
A

b

34
Q
  1. regarding amiodarone
    a. it has no alpha adrenergic effects b. it has no beta adrenergic effects c. it has low affinity for activated sodium channels d. it increases warfarin clearance e. it enhances conduction through accessory pathways
A

c

35
Q
  1. amiodarone
    a. has a low affinity for activated sodium channels b. is associated with thyroid dysfunction in 50% of patients c. has a half-life of 8-20 days d. increases clearance of warfarin e. commonly causes peripheral vasoconstriction
A

a

36
Q
  1. which does not prolong the refractory period of normal cells
    a. amiodarone b. lignocaine c. quinidine d. sotalol e. procainamide
A

b

37
Q
  1. the most common adverse effect of procainamide is

a. bradycardia b. pulmonary infiltrates c. fever d. hypotension e. anaphylaxis

A

d

38
Q
  1. Digoxin
    a. Causes a decrease in intracellular sodium b. Causes hypokalaemia in overdose c. Has a half life of 40 hours in a normal patient d. Decreases cardiac output e. Has no role in the treatment of heart failure
A

c

39
Q
  1. Digoxin
    a. Does not cross the blood brain barrier b. Hypokalaemia decreases efficacy of digoxin c. Hypomagnesaemia decreases efficacy of digoxin d. Antibiotics have effects on digoxin
A

d

40
Q
  1. Digoxin
    a. Is not very lipid soluble and has a low volume of distribution b. Is extensively metabolized prior to its excretion c. Is highly protein bound d. Has a half-life of 100 hours, thus allowing for once daily dosing e. None of the above are correct
A

a

41
Q
  1. The electrical effects of digoxin in therapeutic concentrations include:
    a. The ability to revert atrial fibrillation to normal sinus rhythm in >60% of patients <12 hours b. No indirect effect (ie. Vagal) upon the Purkinje fibres in the ventricles c. Increased refractory period at the atrioventricular node d. Increased rate of firing of the sinoatrial node e. ST segment elevation in the inferolateral segments of the ECG
A

c

42
Q
  1. Which of the following drugs has no significant interaction with digoxin?
    a. Quinidine b. Amlodipine c. Verapamil d. Warfarin e. Thiazide diuretics
A

d

43
Q
  1. Digoxin exerts its effects upon myocardial muscle at a cellular level by
    a. Increasing intracellular calcium b. Inducing Na+/K+/ATPase at the cell membrane c. Acting as a second messenger for G proteins d. Acting directly upon actin and myosin filaments to promote contractility e. Sub-contracting non-union labour and threatening legal action via the high court if the cell doesn’t give into its demands!
A

a

44
Q
  1. Digoxin Fab antibodies
    a. Are used routinely in the management of digoxin toxicity b. Decreases the serum digoxin level in the circulation c. Are commonly associated with tachyarrythmias after administration d. Take approximately 12 hours to have an effect e. Are metabolized in the liver
A

b

45
Q
  1. The primary mechanism of action of digoxin involves:
    a. An increase in action potential amplitude b. An increase in ATP synthesis c. Modification of the actin molecule d. An increase in intracellular Ca2+ levels e. Block of the Na+/Ca2+ exchange
A

d

46
Q
  1. Regarding pharmacokinetics of digoxin
    a. It is poorly absorbed with oral administration b. Its renal clearance is increased with renal disesase c. 40% of individuals have enteric bacteria inactivating it d. two thirds of digoxin is excreted by the kidneys e. the enterohepatic circulation contributes to the short half-life
A

d

47
Q
  1. All of the following may increase the effect of digoxin EXCEPT:
    a. Amiodarone b. Frusemide c. Carbamazepine d. verapamil e. quinidine
A

c

ACEM part 1 pharmacology (4 decks)

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