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PHARMA > 2nd BLOCK Part 2 > Flashcards

2nd BLOCK Part 2 Flashcards

1
Q

A 66-year-old man had a myocardial infarct. Which one of the following would be appropriate prophylactic antiarrhythmic therapy?

A. Lidocaine.
B. Metoprolol.
C. Procainamide.
D. Quinidine.
E. Verapamil.
A

Metoprolol

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2
Q

A 58-year-old woman is being treated for chronic suppression of a ventricular arrhythmia. After 2 months of therapy, she complains about feeling tired all the time. Examination reveals a resting heart rate of 10 beats per minute lower than her previous rate. Her skin is cool and clammy. Laboratory test results indicate low thyroxin and elevated thyroid-stimulating hormone levels. Which of the following antiarrhythmic drugs is the likely cause of these signs and symptoms?

A. Amiodarone.
B. Procainamide.
C. Propranolol.
D. Quinidine

A

Amiodarone

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3
Q

Slow conduction in ischemic and depolarized cells and slow or abolish abnormal pacemakers wherever these processes depend on sodium channels.

A

GROUP 1 ANTIARRHYTHMICS

LOCAL ANESTHETICS

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4
Q

Slow the rate of rise of the action potential (thus slowing conduction), prolong the action potential, and increase the ventricular effective refractory period

A

Group A1 Drugs

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5
Q

Can be used in all types of arrhythmias: atrial and ventricular arrhythmias are most responsive and commonly used in arrhythmias during the acute phase of myocardial infarction.

A

Procainamide

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6
Q

Causes cinchonism (headache, vertigo, tinnitus); cardiac depression; gastrointestinal upset; and autoimmune reactions (eg, thrombocytopenic purpura).

A

Quinidine

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7
Q

May cause hypotension and a reversible syndrome similar to lupus erythematosus.

A

Procainamide

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8
Q

May cause hypotension and a reversible syndrome similar to lupus erythematosus.

A

Procainamide

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9
Q

Is particularly associated with quinidine and other drugs that prolong AP duration

A

Torsades de pointes

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10
Q

Usually exacerbates the cardiac toxicity of group1 drugs.

A

Hyperkalemia

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11
Q

An orally active 1B agent.

A

Mexiletine

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12
Q

Selectively affect ischemic or depolarized Purkinje and ventricular tissue and have little effect on atrial tissue

A

Group 1B Drugs

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13
Q

Because these agents have little effect on normal cardiac cells, they have little effect on the ECG

A

Group 1B Drugs

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14
Q

Useful in acute ischemic ventricular arrhythmias, for example, after myocardial infarction.

A

Lidocaine

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15
Q

Never given orally because it has a very high first-pass effect and its metabolites are potentially cardiotoxic in acute ischemic ventricular arythmias

A

Lidocaine

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16
Q

These drugs ocasionally cause typical local anesthetic toxicity (ie, central nervous system [CNS] stimulation, including convulsions); cardiovascular depression (usually minor); and allergy (usually rashes but may extend to anaphylaxis) except:

  • Lidocaine
  • mexiletine
  • Quinidine
  • Procainamide
A

Quinidine
Procainamide

Does: Lidocaine and mexiletine

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17
Q

These drugs have no effect on ventricular AP duration or the QT interval and they are powerful depressants of sodium current, however, and can markedly slow conduction velocity in atrial and ventricular cells

A

Group 1C Drugs

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18
Q

Is approved only for refractory ventricular tachycardias and for certain intractable supraventricular arrhythmias. They are also more likely than other antiarrhythmic drugs to exacerbate or precipitate arrhythmias (proarrhythmic effect).

A

Flecainide

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19
Q

Is primarily cardiac β-adrenoceptor blockade and reduction in cAMP, which results in the reduction of both sodium and calcium currents and the suppression of abnormal pacemakers.

A

GROUP 2 ANTIARRHYTHMICS

BETA BLOCKERS

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20
Q

Beta blockers diminish _________, thus depressing automaticity, prolonging AV conduction, and decreasing heart rate and contractility.

A

Phase 4 depolarization

21
Q

•Class II agents of these drugs are useful in treating tachyarrhythmias caused by increased sympathetic activity. They are also used for atrial flutter and fibrillation and for AV-nodal reentrant tachycardia.

A

Beta blockers

22
Q

A very short-acting β blocker for intravenous administration, is used exclusively in acute arrhythmias.

A

Esmolol

23
Q

Are commonly used as prophylactic drugs in patients who have had a myocardial infarction except

Propranolol
Metoprolol
Sotalol
Timolol

A

Sotalol

24
Q

These agents prolong the duration of the action potential without altering Phase 0 of depolarization or the resting membrane potential instead, they prolong the effective refractory period.

A

GROUP 3 ANTIARRHYTHMICS

POTASSIUM IK CHANNEL BLOCKERS

25
Q

Is usually classified as a group 3 drug because it blocks the same K channels and markedly prolongs AP duration as well as blocking sodium channels.

A

Amiodarone

26
Q

Is a new drug, similar to amiodarone but less efficacious and less toxic.

A

DRONEDARONE

27
Q

The hallmark of group 3 drugs (IK CHANNEL BLOCKERS)

A

prolongation of the AP duration

28
Q

Has antianginal as well as antiarrhythmic activity.

A

Amiodarone

29
Q

Is effective in the treatment of severe refractory supraventricular and ventricular tachyarrhythmias. Despite its side-effect profile, it is the most commonly employed antiarrhythmic.

A

Amiodarone

30
Q

COMMON EFFECTS

  • interstitial pulmonary fibrosis
  • gastrointestinal tract intolerance
  • tremor, ataxia, dizziness
  • hyper- or hypothyroidism
  • liver toxicity
  • Photosensitivity
  • Neuropathy
  • muscle weakness
  • blue skin & corneal discoloration caused by iodine accumulation
A

Amiodarone

31
Q

They decrease the inward current carried by calcium, resulting in a decreased rate of Phase 4 spontaneous depolarization. They also slow conduction in tissues that are dependent on calcium currents, such as the AV node. Although voltage-sensitive calcium channels occur in many different tissues, the major effect of calcium-channel blockers is on vascular smooth muscle and the heart.

A

GROUP 4 ANTIARRHYTHMICS

CALCIUM L-TYPE CHANNEL BLOCKERS

32
Q

Their major use is in the prevention of these nodal arrhythmias in patients prone to recurrence. The most important toxicity of these drugs is excessive depression of cardiac contractility, AV conduction, and blood pressure. These agents should be avoided in ventricular tachycardias.

A

GROUP 4 ANTIARRHYTHMICS

CALCIUM L-TYPE CHANNEL BLOCKERS

33
Q

Use and state-dependent block of I Na channels. They are slowed conduction velocity and pacemaker activity and have prolonged action potential duration and refractory period

A

Procainamide

34
Q

Highly selective use and state dependent it has minimal effdct in normal tissue and no eefect on I k

A

Lidocaine

35
Q

Similar to lidocaine but oral activity and longer duration of action and also used in neuropathic pain

A

Mexilletine

36
Q

Block of Beta receptors and has slowed pacemaker activity

A

Propranolol

37
Q

Similar to propranolol but beta 1 selective

A

Metoprolol

38
Q

Used in perioperative and thyrotoxicosis arrythmias

A

Esmolol

39
Q

Increase in diastolic I K of AV node and causes marked hyperpolarozation and conductiom block

A

Adenosine

40
Q

Increase in all K currents, decreased automaticity, decreased digitalis toxicity

A

Potassium ion

41
Q

I K block and Betal adrenoceptor block

A

Sotalol

42
Q

Selective I K block-prolonged action potential and QT interval

A

Ibutilide

43
Q

Used for ventricular arrhythmias post-myocardial infarction and digitalis-induced arryhtmias

A

Lidocaine

44
Q

Used for postmyocardial infarction as prophylaxis against sudden death ventricular fibrilation and for thyrotoxicosis

A

Propranolol

45
Q

Treatment of acute atrial fibrilation

A

Ibutilide

46
Q

Rate control in atrial fibrilation

A

Diltiazem

47
Q

Used for acute nodal tachycardias

A

Adenosine

48
Q

Used for digitalis toxicity and other arrhythmias if serum K is low

A

Potassium Ions

PHARMA (26 decks)

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