Antiarrhythmic Drugs

Question 1

Management of afib without CHF

Answer 1

beta-blocker
CCB
Digoxin

Question 2

Management of afib with CHF

Answer 2

beta blockers
Digoxin (Increase cardiac output)

(never CCB)

Question 3

Thyroxine

Answer 3

will enhance the renal clearance (CLr) of digoxin when used to treat CHF and control ventricular rate

Question 4

Drugs that enhance digoxin toxicity

Answer 4

quinidine, amiodarone, captopril, verapamil, diltiazem, cyclosporin

decreases renal clearance and/or volume distribution

Question 5

Drugs that reduce digoxin toxicity

Answer 5

thyroxine (increase clearance)
cholestyramine (decrease GI absorption)

Hypothyroidism decreases renal clearance

Question 6

ECG changes relates to the BENEFICAL effects of digoxin on rate control

Answer 6

pro-longed P-R interval

Question 7

Sites of action of Digoxin

Answer 7

AV node - prolonged refractory period = slowed conduction = prolonged PR interval

Ventricle
- accelerated repolarization = shortened Q-T interval
- changes in phase 2 or 3, or in direction of repolarization = depressed S-T segment or inverted T-wave

Question 8

appropriate drugs to use in combination for the treatment of a 59-year-old woman during the EARLY stages of chronic heart failure (CHF)

Answer 8

Furosemide + captopril + metoprolol

Question 9

3-step treatment of CHF

Answer 9

step 1: initiate ACE inhibitor to reduce workload. add beta blocker if stable systolic dysfunction
step 2: persistent symptoms add aldosterone antagonist
step 3: still persistent add digoxin, ARB

**for african-american patients add hydralazine/isosorbide dinitrate (bidil)

Question 10

Ivabradine

Answer 10

slows rate without affecting force of contraction

selective and specific inhibitor of the hyperpolarization activated cyclic nucleotide-gated channels (If channels; funny current) - inhibition of If ion current flow prolongs diastolic depolarization, slows firing in the SA node.

CYP3A4

Question 11

Lidocaine

Answer 11

Must be given intravenously d/t high first pass

Question 12

Class IA

Answer 12

Quinidine, Procainamide
Moderate blockers - prolong repolarization = increased refractory period = cells in re-entry cycle cannot depolarize

sodium and potassium channels

Question 13

Class IB

Answer 13

Lidocaine, Mexiletine

Mild blockers = shorten repolarization

Question 14

Class 1A, 1B, 1C

Answer 14

all block sodium channels

1A also blocks potassium channels

Question 15

antiarrhythmic agents most likes to produce drug-induced thrombocytopenia

Answer 15

Quinidine

Question 16

Lupus-like syndrome produced by

Answer 16

procainamide

Question 17

Antimuscarinic actions

Answer 17

quinidine, disopyramide&raquo_space; procainamide

Question 18

Increase plasma digoxin, thrombocytopenia, alpha bock, cinchonism

Answer 18

Quinidine

Question 19

first line treatment for drug induced torsade’s de pointes

Answer 19

magnesium

Question 20

Antiarrhythmics and potassium

Answer 20

hypokalemia - producing ectopic pacemaker activity especially during digoxin treatment

Question 21

REDUCES serum cholesterol, LDL, VLDL, and triglycerides and INCREASES HDL cholesterol, in part, by DECREASING hepatic triglyceride synthesis and INCREASING lipoprotein lipase activity. This drug is also noted for causing an annoying flushing and pruritus.

Answer 21

Niacin

Question 22

Niacin

Answer 22

decrease adipose lipase activity
decrease LDL, triglycerides, and increase HDL

nicotinic acid, Vit B3

Question 23

Fibric Acid

Answer 23

activate hepatic PPAR-a
decrease triglycerides, LDL
increase HDL

Question 24

Bile Resins

Answer 24

prevent bile acid reabsorption
decrease LDL

Question 25

Ezetimibe

Answer 25

inhibit intestinal cholesterol absorption
decrease LDL

Question 26

Hypolipidemic drugs

Answer 26

HMG-CoA reductase inhibitors “Statins”
Niacin
Fibric Acid Derivatives
Bile Acid binding resins
intestinal sterol absorption inhibitor
PCSK9 Inhibitors

Question 27

HMG-CoA reductase inhibitors

Answer 27

atrovastatin
fluvastatin
lovastatin
pravastatin
rosuvastatin
simvastatin
pitavastatin

Question 28

Fibric Acid Derivatives

Answer 28

Gemfibrozil
fenofibrate

act as ligand for the nuclear transcription factor PPAR-a
activation of hepatic PPAR-a = decreases plasma triglycerides, VLDL, and LDL
increases HDL

tx for hypertriglyceridemia

toxic effects: potentiate anticoags and increase risk of gallstones

Question 29

Bile Acid-Binding Resins

Answer 29

Colestipol
Cholestyramine
Colesevelam

all block absorption of bile acids

Question 30

Intestinal Sterol Absorption Inhibitor

Answer 30

Ezetimibe

block absorption of cholesterol

Question 31

PCSK9 Inhibitors

Answer 31

Evolocumab
alirocumab

Question 32

Statin Toxicity

Answer 32

increased CK acitivity indicates skeletal muscle toxicity = rhabdomyolysis

measure aminotransferase and CK before treatment and every 6-12 mos