Cardio Drugs Exam 1

Front 1

Very irritating to the gastrointestinal system

Back 1

Quinidine

Front 2

Alleviated by concurrent use of aluminum hydroxide or diphenoxylate

Back 2

Quinidine

Front 3

Cinchonism (Tinnitus, headache, dizziness, and/or blurred vision) with
elevated levels (Also, reported after single doses)

Back 3

Quinidine

Front 4

Thrombocytopenia, hepatitis, and drug fever

Back 4

Quinidine

Front 5

Extremely hypotensive with intravenous administration

Back 5

Quinidine

Front 6

Different salts contain different amounts

Back 6

Quinidine

Front 7

Elevates digoxin concentrations; May enhance warfarin
effect; Concentrations are elevated by amiodarone

Back 7

Quinidine

Front 8

Half-life: 6-8 hours

Back 8

Quinidine

Front 9

Primary elimination route of Quinidine

Back 9

hepatic

Front 10

Extremely short half-life

Back 10

Procainamide

Front 11

unabsorbed wax matrix found in stool

Back 11

Procainamide

Front 12

50% metabolized by liver; mostly to active metabolite known as NAPA

Back 12

Procainamide

Front 13

behaves like a Type III antiarrhythmic agent and is renally excreted

Back 13

NAPA

Front 14

50-80% of patients develop a positive ANA while receiving

Back 14

Procainamide

Front 15

pleural or
pericardial pain rather than a rash

Back 15

Symptoms of procainamide-induced SLE

Front 16

GI, neutropenia, or (rarely) agranulocytosis

Back 16

Procainamide

Front 17

Concentrations elevated by cimetidine and amiodarone

Back 17

Procainamide

Front 18

Many patients cannot tolerate drug due to anticholinergic adverse effects

Back 18

Disopyramide

Front 19

Protein binding is concentration-dependent

Back 19

Disopyramide

Front 20

Metabolism increased by phenytoin

Back 20

Disopyramide, Mexiletine

Front 21

Disopyramide elimination

Back 21

50% renal, 50% hepatic

Front 22

Only available for intravenous administration

Back 22

Lidocaine

Front 23

Only useful in the treatment of ventricular arrhythmias

Back 23

Lidocaine

Front 24

slows down its own metabolism

Back 24

Lidocaine

Front 25

Adverse effects tend to be CNS in nature

Back 25

Lidocaine

Front 26

Metabolism decreased by β-blockers and cimetidine

Back 26

Lidocaine

Front 27

Extremely GI irritating (take with food)

Back 27

Mexiletine

Front 28

Very proarrhythmic; May be unresponsive to cardioversion

Back 28

Flecainide

Front 29

Concentrations may be elevated by amiodarone

Back 29

Flecainide

Front 30

Combined Type IC and β-blocker antiarrhythmic

Back 30

Propafenone

Front 31

should be used cautiously in patients who would normally not be
receiving β-blockers

Back 31

Propafenone

Front 32

non-linear “first-pass” effect and non-linear elimination

Back 32

Propafenone

Front 33

Metabolized to active compounds present at levels < 20% of the parent compound

Back 33

Propafenone

Front 34

Concentrations may be
elevated by quinidine

Back 34

Propafenone

Front 35

Elevates digoxin and liver-metabolized β-blocker
concentrations and enhances warfarin activity

Back 35

Propafenone

Front 36

Oral loads of 600 mg have been used for acute conversion of atrial fibrillation

Back 36

Propafenone

Front 37

Useful in ventricular fibrillation; Not very useful in ventricular tachycardia

Back 37

Bretylium

Front 38

Causes an initial rapid hypertension followed by a more chronic hypotension

Back 38

Bretylium

Front 39

Induces emesis

Back 39

Bretylium

Front 40

Demonstrates pharmacology of Types IA, IB, and IC

Back 40

Moricizine

Front 41

Phenothiazine-like structure

Back 41

Moricizine

Front 42

Auto-enzyme inducer

Back 42

Moricizine

Front 43

Lowers theophylline concentrations

Back 43

Moricizine

Front 44

Moricizine elimination

Back 44

liver metabolism

Front 45

Currently, the most effective antiarrhythmic for ventricular arrhythmias

Back 45

Amiodarone

Front 46

Half-life ranges from 35-110 days

Back 46

Amiodarone

Front 47

Cannot give a full loading dose at once (due to slow distribution)

Back 47

Amiodarone

Front 48

blue-gray skin (<10%),
photosensitivity (25-75%), corneal deposits (nearly 100%), optic neuritis (1%), hepatotoxicity (<3%); and bradycardia (5%) [check TFTs & LFTs every 6 mths]

Back 48

Amiodarone

Front 49

Pulmonary Fibrosis (10-15% incidence at 400 mg/day)

Back 49

Amiodarone

Front 50

check PFTs including DLCO at baseline; CXR q 12 mths to monitor for

Back 50

Pulmonary Fibrosis

Front 51

Elevates concentrations of warfarin, digoxin, quinidine,
procainamide, phenytoin, flecainide, and cyclosporin

Back 51

Amiodarone

Front 52

liver metabolized to desethylamiodarone

Back 52

Amiodarone

Front 53

Combined Type III and nonselective β-blocker antiarrhythmic

Back 53

Sotalol

Front 54

fatigue, bradycardia, dyspnea

Back 54

Sotalol

Front 55

Ibutilide elimination

Back 55

hepatically metabolized

Front 56

Sotalol elimination

Back 56

renal

Front 57

Antiarrhythmics with predominantly type III properties used to convert atrial
fibrillation/flutter to normal sinus rhythm

Back 57

Ibutilide (IV) & Dofetilide (po)

Front 58

Can cause torsade de pointes and other proarrhythmias

Back 58

Sotalol, Ibutilide (IV) & Dofetilide (po)

Front 59

Dofetilide elimination

Back 59

renal

Front 60

appears safe to use in patients with congestive heart failure

Back 60

Dofetilide

Front 61

Half-life is less than 10 seconds

Back 61

Adenosine

Front 62

Effects are potentiated by dipyridamole & CBZ and antagonized by methylxanthines

Back 62

Adenosine

Front 63

DO NOT use in patients with heart transplants

Back 63

Adenosine

Front 64

facial flushing, dyspnea, and chest pressure which
lasted less than 1 minute and were generally not severe

Back 64

Adenosine

Front 65

Short-term (<1 min) asystole may occur

Back 65

Adenosine

Front 66

Hypotension is generally not observed

Back 66

Adenosine

Front 67

Selective β-blocker with extremely short half-life

Back 67

Esmolol

Front 68

hypotension, cardiac failure, bronchospasm

Back 68

Esmolol

Front 69

May induce hypoglycemia and/or mask signs of hypoglycemia in diabetics

Back 69

Esmolol

Front 70

Rapid injection may cause vasoconstriction

Back 70

digoxin

Front 71

Elevated digoxin concentrations can cause

Back 71

hyperkalemia

Front 72

Long distribution phase; therefore, wait 6-12 hours after the administration of
a dose before measuring a concentration

Back 72

digoxin

Front 73

Some is eliminated hepatically; therefore, it is possible to use digoxin in anephric
patients.

Back 73

digoxin

Front 74

The half-life of digoxin in a patient with normal renal function is about

Back 74

1.5 days.

Front 75

7 days
minimum to reach steady-state

Back 75

digoxin

Front 76

verapamil, amiodarone, quinidine, propafenone, and carvedilol.

Back 76

reduce elimination of digoxin

Front 77

treatment of chronic hypokalemia in patient receiving digoxin

Back 77

potassium

Front 78

acute OD of digoxin causes

Back 78

hyperkalemia

Front 79

The best and most predictable absorption of digoxin is with the

Back 79

capsules