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Pharmacology 514 > Cardiac Drugs > Flashcards

Cardiac Drugs Flashcards

1
Q

What is the mechanism of action of Digoxin?

A

Inhibits sodium-potassium ATP pump in cardiac muscle cells, results in increased intracellular calcium

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2
Q

What are some of the cardiac effects of Digoxin?

A 
Increased inotropy
Decreased left ventricular preload, afterload, wall tension, and oxygen consumption
Increased stroke volume
Decreased heart size
Increases automaticity
Decreases AV conduction
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3
Q

What happens to the Frank-Starling curve in a patient taking Digoxin?

A

Shifts to the left

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4
Q

How is Digoxin eliminated?

A

Primarily by kidneys with 35% excreted daily

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5
Q

Where is a tissue reservoir site for Digoxin?

A

Skeletal muscles - elderly have increased likelihood of elevated plasma levels due to decreased muscle mass

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6
Q

What is the MOA of Theophyline?

A

Nonselective PDE inhibitor that inhibits all fractions of PDE isoenzymes

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7
Q

How is Theophyline metabolized and excreted?

A

Metabolized by liver and excreted by kidneys

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8
Q

What is the MOA of milrinone?

A

Inhibition of PDEIII (phosphodiesterase enzyme III) that leads to increased intracellular concentrations of cAMP and cGMP that ultimately cause inward movement of calcium ions

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9
Q

What are the primary effects of milrinone?

A

Positive inotropy with vascular and airway smooth muscle relaxation

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10
Q

What are some clinical signs of digitalis toxicity?

A 
Anorexia
Nausea
Vomiting
Transitory amblyopia and scotomata
Pain simulating trigeminal neuralgia
Extremity pain
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11
Q

What is the normal plasma concentration for Digoxin?

A

0.5-2.5 ng/mL, >3 ng/mL indicates toxicity

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12
Q

How does hyperkalemia affect Digoxin?

A

reduces enzyme-inhibiting actions of glycosides and reduces the effects of Digoxin

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13
Q

What is the mechanism of action of class 1 antirhythmics?

A

sodium channel blockers, prolongs phase 0

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14
Q

What is the mechanism of action of class 2 antirhythmics?

A

beta blockers, decreases phase 4 slope

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15
Q

What is the mechanism of action of class 3 antirhythmics?

A

potassium channel blockers, elongates phase 3 and increases effective refractory period

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16
Q

What is the mechanism of action of class 4 antirhythmics?

A

calcium channel blockers, prolongs phase 0

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17
Q

What class of antirhythmic is Procainamide?

A

Class 1A

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18
Q

What is the mechanism of action of Procainamide?

A

blocks sodium channels and prolongs upstroke of the action potential, slows conduction, and prolongs the WRS duration on ECG

also prolongs APD by nonspecific blockade of potassium channels

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19
Q

What property of Procainamide causes hypotension?

A

Ganglion-blocking properties that reduces peripheral vascular resistance

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20
Q

What are Procainamide’s toxic effects?

A

excessive action potential prolongation, QT-interval prolongation, and induction of Torsades and syncope

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21
Q

What are some side effects of Procainamide?

A 
Lupus-like symptoms
Hypotension
Nausea
Diarrhea
Rash
Rarely - pleuritis, pericarditis, agranulocytosis, hepatitis
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22
Q

How is Procainamide metabolized?

A

metabolite metabolized hepatically

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23
Q

What is a metabolite of Procainamide and what is its significance?

A

NAPA, can cause Torsades if accumulated

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24
Q

How is Procainamide eliminated and what is its half-life?

A

Kidneys, half life of 3-4 hours

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25
Q

What are the clinical indications of using peripheral vasodilators

A

treat hypertensive crises, produce controlled hypotension, and facilitate LV forward stroke volume

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26
Q

Does SNP dilate veins, arteries, or both?

A

Both; decreases preload and after load

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27
Q

What is a molecule of SNP made of?

A

1 nitro group and 5 cyanide molecules

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28
Q

How is SNP metabolized

A

hemoglobin

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29
Q

How are the cyanide molecules generally eliminated?

A

Rodinase enzyme causes the cyanide to be attached to Vit B12 ( thiocyanate) which is then excreted by the kidneys

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30
Q

What is the onset of SNP?

A

immediate

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31
Q

What is the DOA of SNP?

A

3-5 minutes

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32
Q

What is the standard dose of SNP?

A

0.3-10mcg/kg/min

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33
Q

What could be a detrimental effect of SNP?

A

reflex tachycardia, leading to increased O2 demand and potentially cause myocardial ischemia

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34
Q

SNP molecule is what percent cyanide?

A

44%

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35
Q

What is the purpose of controlled hypotension

A

operations that require a bloodless field and reduced blood loss

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36
Q

Why is SNP good to use for hypertensive emergencies?

A

ease of titration, rapid onset, short DOA, and efficacy

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37
Q

Which drug has a risk of causing cyanide toxicity

A

SNP

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38
Q

What are the effects of cyanide toxicity?

A

tissue hypoxia, anaerobic metabolism, and eventually death

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39
Q

What is the treatment for cyanide toxicity?

A

3% sodium nitrate, sodium thiosulfate, Vit B12, discontinue infusion, treat acidosis, administer 100% O2

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40
Q

Does hydralazine dilate veins, arteries, or both?

A

arteries; decreases after load

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41
Q

What is the standard dose of hydralazine?

A

2.5-10mg IV

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42
Q

What is the onset of hydralazine?

A

10-20 minutes

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43
Q

Metabolism/excretion of hydralazine?

A

liver/renal

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44
Q

Does hydralazine decrease SBP or DBP more?

A

DPB

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45
Q

What is the DOA of hydralazine?

A

unpredictable

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46
Q

Does nitroglycerin dilate veins, arteries, or both?

A

veins primarily; decreases preload; can cause arterial dilation at higher doses

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47
Q

Which vasodilator is most commonly used for angina

A

nitroglycerin

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48
Q

What is the MOA of nitroglycerin?

A

contains a nitro group which contributes to NO mediated vasodilation

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49
Q

What is the onset of nitroglycerin?

A

2-5 minutes

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50
Q

What is the DOA of nitroglycerin?

A

5-10 minutes

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51
Q

Which drug to people develop rapid tolerance to?

A

nitroglycerin

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52
Q

What can be done to reverse nitroglycerin tolerance?

A

a drug free interval of 12-14 hours

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53
Q

T/F: Nitroglycerin reduces myocardial ischemia primarily by dilating coronary arteries and increasing blood supply to the myocardium?

A

F: reduces ischemia primarily by reducing preload and therefore reducing myocardial oxygen consumption

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54
Q

What are SE of nitroglycerin?

A

Headache, flushing, decreased sensitivity to heparin

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55
Q

Which vasodilator is effective in reducing sphincter of Oddi spasm?

A

nitroglycerin

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56
Q

Is tachycardia more marked with A1 or A2 antagonists?

A

A2 because they increase NE release increasing B1 stimulation at the heart

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57
Q

Phentolamine has what effect at A1 and A2 receptors

A

A1=A2 antagonist

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58
Q

What are some adverse effects related to Phentolamine administration

A

cardiac stimulation, tachycardia, arrhythmias, myocardial ischemia

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59
Q

What are clinical uses of phentolamine

A

pheochromocytoma excision, HTN crisis, extravascular administration of sympathomimetic agents

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60
Q

What is dose of phentolamine?

A

30-70mcg/kg IV

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61
Q

What effect does prazosin have on a1 vs. a2 receptors?

A

a1»»»a2 antagonist

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62
Q

Why is prazosin’s reduced a2 activity beneficial

A

results in relative absence of tachycardia

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63
Q

What are the clinical uses of Prazosin?

A

preop prep for patients with pheo, essential HTN, decreasing after load in patients with heart failure, raynaud phenomenon

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64
Q

What are some EKG changes associated with Digoxin?

A

Scooped ST
Biphasic T wave
Shortened QT
Long PR

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65
Q

How long does it take to see effects of Digoxin administered IV?

A

5-30 minutes

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66
Q

If a patient has kidney disease, should the Digoxin dose be decreased? And if so, by how much?

A

Eliminated via kidneys so dose needs to be decreased by 75%

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67
Q

Does Digoxin have any effects on someone with normal cardiac function?

A

No

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68
Q

How can Digoxin be used in anesthesia?

A

Can be administered prophylactically to someone with limited cardiac reserve or in patients with CAD recovering from anesthesia (administered day before surgery and 0.25 mg given before induction)

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69
Q

What are the dosing recommendations for Digoxin?

A

0.125 - 0.25 mg/day

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70
Q

What can speed the metabolism of Theophylline?

A

Cigarettes

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71
Q

What is the loading/maintenance dose of Theophylline?

A

Loading dose of 5 mg/kg IV followed by infusion of 0.5 - 1 mg/kg/hr

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72
Q

What are some of the cardiac effects of Calcium?

A

Intense positive inotropy (lasts 10-20 minutes)
Increased stroke volume
Decreased left ventricular end-diastolic pressure
Decreased heart rate
Decreased systemic vascular resistance

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73
Q

When would it be ideal to administer Calcium during anesthesia?

A

At the end of cardiopulmonary bypass to improve contractility and stroke volume–patients usually hypocalcemic from cardioplegic solutions and citrated blood

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74
Q

Which contains more calcium: 10% calcium chloride or 10% calcium gluconate?

A

10% Calcium chloride (should only be administered via central line)

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75
Q

What are the dosing recommendations for calcium?

A

5 to 10 mg/kg IV (Stoelting)

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76
Q

What is the mechanism behind hypotension caused by Milrinone?

A

Inhibits PDEIII –> Increased cAMP –> EFFLUX of calcium from smooth muscle cells –> vasodilatation
(cAMP acts opposite in smooth muscle cells than cardiac muscle cells)

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77
Q

What are the dosing recommendations for Milrinone?

A

50 mcg/kg IV bolus followed by 0.5 mcg/kg/min

Stoelting and Nagelhout

78
Q

What is the treatment for Digitalis toxicity?

A

Correction of predisposing cause
Drugs to treat arrhythmias (Lidocaine or Atropine)
Insertion of temporary pacemaker if complete heart block present
Supplemental potassium (decreases binding of Digoxin)
Fab-fragments (antibodies to Digoxin)

79
Q

What drugs decrease GI absorption of cardiac glycosides?

A

Oral antacids

80
Q

What drugs can increase the likelihood of arrhythmias with Digoxin?

A

Sympathomimetics

Pancuronium

81
Q

What is the most common arrhythmia with Digitalis toxicity?

A

Atrial tachycardia (Stoelting)

82
Q

In patients with normal renal function, which drugs frequently cause Digitalis toxicity?

A

Diruetics that cause potassium depletion

83
Q

What effect does Phenoxybenzamine have on a1 vs. a2 receptors?

A

a1>a2; irreversible antagonist

84
Q

Method of action for ARB’s?

A

Produce antihypertensive effects by blocking vasoconstrictive effects of angiotensin-2 without affecting ACE activity

85
Q

What are the side effects of ACE Inhibitors?

A

C - Cough
A - Angioedema/ Agranulocytosis
P - Proteinurea/ Potassium excess
T - Taste change
O - Orthostatic hypotension - controversial
P - Pregnancy contraindication (fetal renal damage)
R - Renal artery stenosis contraindication
I - Increases renin
L - Leukopenia / liver toxicity

86
Q

What is the dose for phenoxybenzamine?

A

0.5-1.0mg/kg

87
Q

What is the pathophysiology behind angioedema?

A

Bradykinins associated with vasodilation and increased vascular permeability. Can be hereditary.

88
Q

When are alpha antagonist most beneficial in treating a hypertensive crisis

A

when it is due to excess circulating alpha agonists (pheo, overdose on sympathomimetic drugs, or clonidine withdrawal

89
Q

Method of action for ACE Inhibitors?

A

Prevent the conversion of angiotensin-1 to angiotensin-2

90
Q

Method of action for ARB’s?

A

Produce antihypertensive effects by blocking vasoconstrictive effects of angiotensin-2 without affecting ACE activity

91
Q

What complication may present when treating with vasopressin?

A

It can cause coronary vasospasm, which can induce MI.

92
Q

Which population has a greater risk of angioedema?

A

African American - 5 times greater

93
Q

What is the pathophysiology behind angioedema?

A

Bradykinins associated with vasodilation and increased vascular permeability. Can be hereditary

94
Q

What is responsible for the cough caused by ACE-I?

A

The accumulation of excess bradykinin, which is usually broken down by angiotensin converting enzyme (ACE).

95
Q

What intrinsic mechanisms are responsible for hemodynamic maintenance?

A

ADH (Vasopressin), RAAS, SNS

96
Q

When a patient, who took their ACE Inhibitor the morning of surgery, exhibits hypotension that does not respond to Phenylephrine or ephedrine, what is the next line drug?

A

Vasopressin

97
Q

What complication may present when treating with vasopressin?

A

It can cause coronary vasospasm, which can induce MI.

98
Q

Why is Procainamdie typically given as a 2nd or 3rd choice for atrial or ventricular arrhythmias?

A

Lupus symptoms and frequent dosing required

99
Q

What classification of antirhythmic is Lidocaine?

A

Class 1B

100
Q

What is the mechanism of action of Lidocaine?

A

Blocks activated and inactivated sodium channels

101
Q

How is Lidocaine administered?

A

Only IV, significant first pass effect taken PO

102
Q

Is Lidocaine the least or most toxic of the sodium channel blockers?

A

Least toxic

103
Q

What is a common side effect of Lidocaine?

A

Hypotension caused by suppression of myocardial contractility

104
Q

What are the dosing recommendations for Lidocaine?

A

150-200 mg over 15 minutes followed by infusion of 2-4 mg/min

105
Q

What is the mechanism of action of Verapamil?

A

Blocks inactivated and activated L-type calcium channels

106
Q

What are some side effects of Verapamil?

A

Constipation
Lassitude
Nervousness
Peripheral edema

107
Q

How is Verapamil metabolized?

A

Extensively by liver

108
Q

What is Verapamil used to treat?

A

SVT
Tachydysrhythmias
Premature uterine contractions

109
Q

What happens if you give someone Verapamil that’s in Vtach?

A

Causes Vfib and circulatory collapse

110
Q

Why would you not want to give Verapamil to someone who has AV nodal disease?

A

Can induce AV block, causes pronounced depression of AV nodal transmission

111
Q

What is the mechanism of action of Diltiazem?

A

Blocks calcium channels in the AV node

112
Q

In which classification of antirhythmic is Amiodarone?

A

Class 3, but blocks all other channels in other classes

113
Q

What is the mechanism of action of Amiodarone?

A

Prolongs action potential duration on QT interval by blockade of potassium channels in heart; also blocks sodium, calcium, and adrenergic receptors

114
Q

How is Amiodarone metabolized?

A

Hepatic metabolism

115
Q

How is Amiodarone eliminated?

A

Elimination complex with rapid component of 3-10 days and slower component of several weeks. Effects are maintained for 1-3 months after discontinuation

116
Q

What enzyme does Amiodarone interact with?

A

CYP3A4

117
Q

What are some side effects of Amiodarone?

A

Hypotension
Symptomatic bradycardia or heart block in patients with preexisting sinus or AV node disease
Dose-dependent pulmonary toxicity
Abnormal liver function tests and hypersenstivity hepatitis
Skin deposits resulting in photodermatitis and gray-blue skin discoloration in sun-exposed areas
Asymptomatic corneal deposits
Halos in peripheral visual fields

118
Q

How does Amiodarone affect T3 and T4?

A

Blocks peripheral conversion of T3 to T4 which can be a source of an accumulation of inorganic iodine or hyper/hypothyroidism

119
Q

What is the mechanism of action of Adenosine?

A

A1 adenosine receptor agonist, ionic mechanisms in AV node are unknown, activates adenosine-sensitive K+ channels in SA and atrial myocytes

Causes inward current of potassium to hyperpolarize cell and inhibits outward calcium current

120
Q

What is the half-life of Adenosine?

A

<10 seconds in the blood

121
Q

What are some side effects of Adenosine?

A 
Flushing
Shortness of breath
Chest burning
Afib
Headache
Hypotension
Nausea
Paresthesias
122
Q

What are the dosing recommendations for Adenosine?

A

6 mg followed by 12 mg dose if needed

123
Q

What does phase 0 of the cardio myocyte action potential consist of?

A

Rapid influx of sodium

124
Q

What does phase 1 of the cardiomyocyte action potential consist of?

A

Sodium gates close and potassium leaves cell

125
Q

What does phase 2 of the cardiomyocyte action potential consist of?

A

Calcium channels open while potassium channels are still open, equal balance of calcium coming into cell and potassium leaving the cell

126
Q

What does phase 3 of the cardiomyocyte action potential consist of?

A

Repolarization, calcium channels close and potassium continues to leave cell

127
Q

What does phase 4 of the cardiomyocyte action potential consist of?

A

Baseline or resting membrane potential

128
Q

What phases make up the effective refractory period?

A

Phases 0-3

129
Q

Which phases are involved in the nodal cell action potential?

A

Phase 0, 3, and 4

130
Q

What antiarrhythmic classification does Diltiazem fall into?

A

Class 4

131
Q

What are the electrophysiological effects of Adenosine?

A

Decreases phase 4 depolarization of SA node pacemaker cells

Hyperpolarizes and suppression of calcium dependent myocytes

132
Q

What are the prototype osmotic diuretics?

A

Mannitol and urea

133
Q

What is the mechanism of action of osmotic diuretics?

A

Alter the osmolarity of the plasma, glomerular filtrate, and renal tubular fluid resulting in osmotic diuresis–water is absorbed from the proximal renal tubules and the loops of Henle

134
Q

What are some clinical uses for osmotic diuretics?

A

Prophylaxis against acute renal failure
Differential diagnosis of acute oliguria
Treatment of increases in ICP, mannitol may also decrease formation of ICP
Decreasing IOP

135
Q

Do osmotic diuretics alter the elimination rate of long-acting nondepolarizing neuromuscular blocking drugs?

A

No, glomerular filtration is not altered by Mannitol

136
Q

What is the mechanism of action of potassium-sparing diuretics?

A

Acts in the distal convoluted tubules independent of aldosterone to produce diuresis, they cause an increase in the urinary excretion of sodium, chloride, and bicarb

137
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibits sodium reabsorption of sodium and chloride ions in the cortical portions of the ascending loops of Henle and to a lesser extent in the proximal renal tubules and distal renal tubules

138
Q

What is the primary reason for Thiazide use?

A

Essential hypertension when diuresis, natriuresis, and vasodilation are synergistic

139
Q

Are the Thiazide diuretic effects independent or dependent of acid-base balance?

A

Independent

140
Q

What are common side effects of Thiazide diuretics?

A

Hypokalemia, hypochloremia, and metabolic alkalosis

Can also cause hyperglycemia and aggravate diabetes mellitus

141
Q

What is the prototype loop diuretic?

A

Furosemide

142
Q

What is the mechanism of action of loop diuretics?

A

Inhibits reabsorption of sodium and chloride primarily in medullary portions of the ascending limb of loop of Henle

143
Q

How does Furosemide affect renal physiology?

A

Evokes renal production of prostaglandins resulting in renal vasodilation and increased renal blood flow

144
Q

What drug can attenuate the diuretic effect of Furosemide?

A

NSAIDS

145
Q

What are some clinical uses of Furosemide?

A

Mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction
Treatment of increased intracranial pressure
Inhibition of cellular uptake of calcium for hypercalcemia
Differential diagnosis of acute oliguria
Little use in the chronic treatment of essential hypertension

146
Q

What is the most common side effect of Furosemide?

A

Electrolyte abnormalities

147
Q

What is the prototype carbonic anhydrase inhibitor?

A

Acetazolamide

148
Q

What is the primary site of action of carbonic anhydrase inhibitors in the kidney?

A

proximal renal tubules

149
Q

What is the mechanism of action of carbonic anhydrase inhibitors?

A

Inhibits enzyme, carbonic anhydrase, activity that diminishes secretion of H+ ions and increases

150
Q

What is the prototype for beta blockers?

A

Propanolol

151
Q

What is the mechanism of action of Propanolol?

A

Beta 1 and Beta 2 antagonist

152
Q

What is the mechanism of action of Metropolol?

A

Beta 1 selective antagonist

153
Q

Which patient population would benefit from Metropolol or Atenolol?

A

Asthmatics or diabetics because of the little antagonism of beta 2 receptors

154
Q

What is the mechanism of action of Atenolol?

A

Selective beta 1 antagonist

155
Q

What is the mechanism of action of Labetalol?

A

Beta and alpha 1 antagonist

156
Q

What is the mechanism of action of Esmolol?

A

Ultra short-acting beta 1 antagonist

157
Q

What are some clinical applications for Propanolol?

A 
HTN
Angina
Arrhythmias
Migraines
Hyperthyroidism
158
Q

What effects does Propanolol have on HR and BP?

A

lowers HR and BP

159
Q

What effects does Metropolol and Atenolol have on HR and BP?

A

Lowers HR and BP

160
Q

What effects does Labetalol have on HR and BP?

A

Lowers BP with limited HR increase

161
Q

What is a clinical application to use Labetalol?

A

HTN

162
Q

What are some clinical applications for Metropolol and Atenolol?

A

Angina
HTN
Arrhythmias

163
Q

What is a clinical application for Carvedilol?

A

Heart failure

164
Q

What are clinical applications for Esmolol?

A 
Rapid control of BP and arrhythmias
Pheochromocytoma
Cocaine toxicity?
Thyrotoxicosis
Myocardial ischemia intraoperatively
165
Q

What is withdrawal hypersenstivity?

A

Acute discontinuation of beta antagonist therapy that results in excess SNS activity due to upregulation of beta receptors that manifests in 24-48 hours

166
Q

What is the most common adverse effect of beta blockers?

A

bradycardia

167
Q

What are some effects of beta blocker toxicity?

A

Bradycardia
Airway obstruction/constriction
Cardiac decompensation in patients with compensated heart failure because their cardiac output is dependent on sympathetic drive

168
Q

Which beta blocker is only available IV?

A

Esmolol

169
Q

What is the onset of action and duration of Esmolol?

A

Full effect evident within 5 minutes and action ceases within 10-30 minutes

170
Q

What does long-term use of Phenoxybenzamine cause?

A

Decrease in hematocrit. It constricts peripheral vessels and shunts blood to vital organs and overly perfuses kidneys

171
Q

What route can you administer Phenoxybenzamine?

A

PO

172
Q

Which has a longer half-life, Labetalol or Metropolol?

A

Labetalol - 1/2 life 5 hrs (Metropolol 3-4 hours), need to keep this in mind when administering beta blocker to patient that is going home

173
Q

What is the 1/2 life of Esmolol?

A

10 minutes

174
Q

What are some concerns with patients who have been treated chronically with Propanolol?

A

Decreased clearance of local anesthetics
Decreased pulmonary clearance of fentanyl
(both are basic lipophilic amines)

175
Q

Which beta blocker is the most selective to beta 1?

A

Atenolol

176
Q

In whom would it be advantageous to give Atenolol?

A

Those who need beta 2 receptor activity: COPD/asthma, and severe CAD

177
Q

What is the half-life of Atenolol?

A

6-9 hours (long-lasting anti-hypertensive drug therefore only given once a day PO)

178
Q

How is Esmolol metabolized?

A

plasma esterases

179
Q

Does Esmolol cross the BBB or placenta?

A

No, poor lipid solubility

180
Q

Which beta blocker is the “go to” for someone that’s never had a beta blocker?

A

Esmolol

181
Q

What is the beta to alpha ratio of Labetalol?

A

7:1

182
Q

What is Labetalol’s affinity for alpha 1 receptors in comparison to phentolamine?

A

1/10th affinity

183
Q

What is Labetalol’s affinity for beta receptors in comparison to Propanolol?

A

1/3rd affinity

184
Q

What is the dose of Verapamil?

A

75-150 mcg/kg IV

185
Q

What are some of the pharmacokinetic properties of Verapamil?

A

Highly protein bound
Active metabolites
Elimination 1/2 time 3-7 hours

186
Q

What drug has greater coronary and peripheral vasodilatory effects than Verapamil?

A

Nifedipine

187
Q

What are some effects of Nifedipine?

A

Decreased BP - used PO to treat HTN
Baroreceptor-mediated increase in HR
Little to no effect on SA and AV node activity
Little effect on myocardial contractility

188
Q

At what dose do you start a Nicardipine gtt?

A

5 mg/hr

189
Q

How much can you increase a Nicardipine gtt every 5 minutes if needed?

A

2.5 mg/hr

190
Q

What is the maximum dose of a Nicardipine gtt?

A

15 mg/hr

191
Q

What is Diltiazem useful to treat?

A

HTN
SVTs
A-fib
Migraine headaches

192
Q

What are some of the effects of Nicardipine?

A

Lacks SA and AV nodal effects
Has little effect on myocardial contractility
Has the greatest vasodilation effects
Very useful in short-term treatment of HTN

Pharmacology 514 (7 decks)

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