Cardiology - Pharmacology Flashcards

1
Q

Hyperlipidemia Drug Classes (5) + Sample Drug

A

1) HMG-CoA Reductase Inhibitors - Statins
2) Resins - Bile Acid Binding - Colestipol + Cholestramine
3) Niacin (B3)
4) Fibric Acid Derivatives - Gemifiozil + Fenofibrate
5) Cholesterol Absorption Blockers - Ezetimibe

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2
Q

HMG-CoA Reductase Inhibitors - Names (3) + Mechanism + Toxicity (4)

A

Names - Lovastatin + Atorvastatin + Simvastatin
Mechanism - Inhibits cholesterol genesis - Increases LDL Receptor Expression
Toxicity - Pregnancy/Breast Feeding + Heptotoxicity (Check ALTs) + Myopathy + CYP450 Interactions

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3
Q

Niacin - Mechanism + Toxicity (3)

A

Mechanism - Inhibits lipolysis and reduces VLDL Synthesis –> Increases HDL
Toxicity - Facial Flushing (PGE Synthesis) + Heptatotoxicity + Hyperuricemia

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4
Q

Bile Acid Resins - Names (2) + Mechanism + Toxicity (5)

A

Names - Colestipol + Cholestramine
Mechanism - Bind bile acid in intestine + decrease re-absorption (cholesterol must be made to make new bile acids) over time effect wanes - Give with statin to preserve effect
Toxicity - Bad Taste + Teratogen + Interferes with intestinal absorption especially of other drugs/vitamins + constipation + bloating

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5
Q

Cholesterol Absorption Block - Names (1) + Mechanism + Toxicity (2)

A

Names - Ezetimibe
Mechanism - Prevents cholesterol absorption
Toxicity - Diarrhea + Increased LFTs

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6
Q

Fibrates - Names (2) + Mechanism + Toxicity (3)

A

Names - Gemifibrozil + Fenofibrate
Mechanism - Increases LDL/TG Clarence - Good for when VLDL is the primary issue
Toxicity - Renal and Liver (LFTs) + Gallstones

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7
Q

Lovastatin - Class

A

HMG-CoA Reductase Inhibitor

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8
Q

Colestipol - Class

A

Bile Acid Resin

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9
Q

Cholestramine - Class

A

Bile Acid Resin

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10
Q

Ezetimibe - Class

A

Cholesterol Absorption Inhibitor

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11
Q

Geifibrozil - Class

A

Fibrate

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12
Q

Fenofibrate - Class

A

Fibrate

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13
Q

Liver LDL Uptake - 3 Results

A

1) Lowers HMG (No new LDL)
2) Increase ACAT (Increase LDL Breakdown)
3) Decrease LDL Receptors

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14
Q

Familial Hypercholesterolemia

A

Failure of the LDL Receptor - No Liver Uptake - None of the 3 Turn-Down Mechanisms Uses (HMG Inhibition + ACAT increase)

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15
Q

Classes of Anti-Arrhythmia Therapy + Mechanism + Prototype Drug (6)

A

1A - Na Channel Blocker - Procainamide
IB - Na Channel Blocker - Lidocaine
IC - Na Channel Blocker - Flecainide
II - Beta Blocker - Propanolol
III - K Channel Blocker - Sotalol + Ibutilide + Amiodarone
IV - Ca-Channel Blocker - Verapamil + Diltiazem

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16
Q

Class IA Anti-Arrhythmia Drugs - Name (3) + Mechanism + Use + Toxicity (5)

A

Name - Procainamide + Disopyramide + Quinidine
Mechanism - Na Channel Blocker - Slows uptake + Increases Action Potential Duration/QT Interval - Intermediate Kinetics
Use - Atrial + Ventricular Arrhythmia - Re-Entry = Key
Toxicity - Reduced Peripheral Resistance + Hypotension + Increased Risk for Early Afterdepolarizations + SLE Like Syndrome
Disopyramide/Quinidine = Anti-Muscarinic

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17
Q

Class IB Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (2)

A

Name - Lidocaine + Mexiletine
Mechanism - Blocks Na Channel - Rapid + Use Dependent = Preferential for Ischemia Tissue - Decreases AP Duration
Use - Acute Ventricular Arrhythmia + Post MI
Toxicity - Low Toxicity (Cardio and Neuro)

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18
Q

Class IC Anti-Arrhythmia Drugs - Name (2) + Mechanism (1) + Use + Toxicity

A

Name - Flecainide + Propafenone
Mechanism - Na Blocker = Long Acting + Prolongs AV Node Refractory Period
Use - SVT + Wolf-Parkinson-White
Toxicity - Slow Refractory Period = High likelihood of producing a new arrhythmia

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19
Q

Class II Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (2)

A

Name - Propranolol + Esmolol
Mechanism - Beta Blockers (Esmolol = Rapid) - Slow Conduction + Supress Abnormal Pacemakers (Slower/Weaker Contractions)
Use - SVT + Slowing Ventricular Rate (Especially effective in AV Node) + Decreased Reentry
Toxicity - Impotence + Exacerbation of COPD/Asthma

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20
Q

Class III Anti-Arrhythmia Drugs - Name (3) + Mechanism + Use + Toxicity (3)

A

Name - Sotalol + Ibutilide + Amiondarone
Mechanism - Block IKr - Increase Action Potential Duration - Longer refractory period decreases reentry
Use - Afib/Flutter + Ventricular Tachycardia
Toxicity - Torsades + Excessive Beta-Blockade
Amiodarone = Special = Decreases Phase 4 Slope - Less Torsades Risk but high risk of pumonary firbosis + thyroid disfunction + hepatotoxicity (monitor LFTs)

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21
Q

Class IV Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (4)

A

Name - Verapamil + Diltiazem (Not NIfedepine)
Mechanism - Block Ca Channels = Shorter AP = Decreased Reentry = Decreased conduction velocity + longer refractory period
Use - Nodal Arrhythmia + AFib
Toxicity - Constipation + Flushing + Edema + AV Block

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22
Q

Adenosine - Mechanism + Use + Toxicity (3)

A

Mechanism - Inhibits AV Node Conduction by activating inward K+ Channels + Inhibiting Ca Channels (Hyperpolarizes)
Use - Super Rapid (10s) with high efficacy)
Toxicity - Flushing + Hypotension + Chest Pain

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23
Q

Verapamil - Arrhythmia Class + Mechanism

A

Class - IV

Mechanism - Ca Channel Blocker

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24
Q

Diltiazem - Arrhythmia Class + Mechanism

A

Class - IV

Mechanism - Ca Channel Blocker

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25
Q

Sotalol - Arrhythmia Class + Mechanism

A

Class - III

Mechanism - K Channel Blocker

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26
Q

Ibutilide - Arrhythmia Class + Mechanism

A

Class - III

Mechanism - K Channel Blocker

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27
Q

Amiodarone - Arrhythmia Class + Mechanism + Special Features

A

Class - III
Mechanism - K Channel Blocker
Special Feature - Decreases Phase 4 Slope - Less Torsades Risk but high risk of pumonary firbosis + thyroid disfunction + hepatotoxicity (monitor LFTs)

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28
Q

Esmolol - Arrhythmia Class + Mechanism

A

Class - II

Mechanism - Rapid Beta Blocker

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29
Q

Propranolol - Arrhythmia Class + Mechanism

A

Class - II

Mechanism - Beta Blocker

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30
Q

Flecainide - Arrhythmia Class + Mechanism

A

Class - IC

Mechanism - Slow Na Channel Blocker

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31
Q

Lidocaine - Arrhythmia Class + Mechanism

A

Class - IB

Mechanism - Rapid Na Channel Blocker

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32
Q

Mexiletine - Arrhythmia Class + Mechanism

A

Class - IB

Mechanism - Rapid Na Channel Blocker

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33
Q

Quinidine - Arrhythmia Class + Mechanism

A

Class - IA
Mechanism - Intermediate Na Channel Blocker with Long Action Potential
Also - Special Anti-Muscarinic AEs

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34
Q

Disopyramide - Arrhythmia Class + Mechanism

A

Class - IA
Mechanism - Intermediate Na Channel Blocker with Long Action Potential
Also - Special Anti-Muscarinic AEs

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35
Q

Procainamide - Arrhythmia Class + Mechanism

A

Class - IA

Mechanism - Intermediate Na Channel Blocker with Long Action Potential

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36
Q

Anti-Arrhythmia Drugs that Increase Action Potential Duration (2) + Impact

A

IA (Procainamide)
III (Amiodarone + Sotalol)
Increased Risk of Early Afterdepolarization and Torsades

37
Q

Major HTN Treatment Classes (6)

M2 Only

A

1) Diuretics
2) Direct Oral Vasodilators (Hydralazine + Minoxidil)
3) Alpha-1 Blockers
4) CNS Symp. Inhibitors (Clonidine)
5) Calcium Channel Blockers
6) RAAS Inhibitors

38
Q

2 Key M2 HTN Points

M2 Only

A

Never Give RAAS Inhibitors in Pregnancy

Verapamil causes Constipation

39
Q

HTN Treatment in Heart Failure (4)

A

Diuretics + RAAS Inhibition + B-Blockers (Be Careful) + Aldosterone Antagonists

40
Q

HTN Treatment after an MI (3)

A

B-Blockers + ACE Inhibitors + ARBs

41
Q

HTN Treatment with Diabetes (4)

A

RAAS Inhibitors + Ca Channel Blockers + Diuretics

42
Q

Direct Oral Vasodilators for HTN (2) + Adverse Effects

M2 Only

A

Hydralazine + Minoxidil - For Resistant HTN

Toxicity - Tachycardia + Increased Na/H2O Retention (Vasodilation Activates the RAAS System)

43
Q

Anti-Arrhythmia Treatment - Wolfe-Parkson-White Review

M2 Only

A

Beta-Blockers + Ca Channel Blockers Alone - Only Slow AV Node Fast Pathway
Must Add IC to Slow the Accessory Pathway

44
Q

Heart Failure Drugs - 3 Major Mechanisms

M2 Only

A

1) Positive Inotropic + 2) Vasodilators (Both Elevate Frank Starling Curve
3) Diuretics - Move you back on the curve

45
Q

Major Classes of Heart Failure Drugs (7)

M2 Only

A

1) Diuretics
2) RAAS Inhibitors
3) Cardiac Glycosides
4) Sympathomimetics
5) Bipyramides
6) Beta Blockers
7) Special Vasodilators

46
Q

3 Major Cardiac Diuretic Classes + Mechanism + Drug Name

M2 Only

A

1) Loop Diuretics (Furosimide)
2) Thiazides (HTCZ + Metolazone + Indaparmid
3) K Sparing Diruetics (Amiloride + Spironolactone)

47
Q

Furosemide - Class + Mechanism + Use + Toxicity (3)

A

Class - Loop Diuretic
Mechanism - Inhibits Na/H2O Reabsorption
Use - Primarily for Edema + Pulmonary Congestion in HTN + HF
Toxicity - Hypokalemia + Metabolic Acidosis + Ototoxicity

48
Q

HTCZ - Class + Mechanism + Use + Toxicity

A

Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia

49
Q

Metolazone - Class + Mechanism + Use + Toxicity

A

Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia

50
Q

Indaparmid - Class + Mechanism + Use + Toxicity

A

Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia

51
Q

Amiloride - Class + Mechanism + Use + Toxicity

A

Class - K Sparing Diuretic (Aldosterone Inhibitor)
Mechanism - Save K + Water - Prevents Aldosterone Remodeling in Heart
Use - K Sparing + Anti-Aldosterone
Toxicity - Hyperkalemia + High AII + Metabolic Acidosis + Gynocomastia

52
Q

Spironolactone - Class + Mechanism + Use + Toxicity

A

Class - K Sparing Diuretic (Aldosterone Inhibitor)
Mechanism - Save K + Water - Prevents Aldosterone Remodeling in Heart
Use - K Sparing + Anti-Aldosterone
Toxicity - Hyperkalemia + High AII + Metabolic Acidosis + Gynocomastia

53
Q

Low Renin HTN Treatment

M2 Only

A

Diuretics = Key = African American HTN

54
Q

ACE Inhibitors - Name (2) Mechanism + Use + Toxicity (3)

A

Name - Catopril + Enalapril (april)
Mechanism - Decrease AI to AII Conversion - Decreases AIII + Increases Bradykinin
Use - Stage II-IV CHF to support diuretics by inhibiting cardiac remodeling + decrease symp. activity
Toxicity - Teratogenic + Hyperkalemia + Cough and Angioneurotic Edema (From Bradykinin)

55
Q

Angiontensin Receptor Blocker - Name (1) Mechanism + Use + Toxicity (3)

A

Name - Losartan (sartans)
Mechanism -Block AT1 Receptor
Use - Alternative to ACE in patients who develop bradykinin cough (no bradykinin effects) - Less Effective
Toxicity Teratogenic + Hypokaemia - No Bradykinin Cough

56
Q

Renin Blocker - Name (1) Mechanism + Use + Toxicity

M2 Only

A

Name - Aliskiren
Mechanism -Like ACE Inhibtor
Use - Experimental
Toxicity - Bradykinin Angioedema + Cough

57
Q

Losartan - Class

A

ARB

58
Q

Catopril - Class

A

ACE Inhibitor

59
Q

Enalapril - Class

A

ACE Inhibitor

60
Q

Aliskiren - Class

A

Renin Inhibitor

61
Q

Cardiac Glycosides - Name (2) + Mechanism + Effects + Use + Toxicity (4)

A

Name - Digoxin + Levosimendan
Mechanism - Inhibits the Na/K ATPase –> Causes a Na Build-Up in the cell –> Inhibits the NCX from getting Ca out of the cell (no Na gradient in)
Effects - Stronger Contraction + Enhances Vagal Tone + Slows AV Conduction
Use - CHF (Increase Contractility) + Afib (Slows AV Node Conduction)
Toxicity - AV Node Block + Nausea, Vomit + Visual Loss

62
Q

Impact of K+ On Digoxin

A

Low K+ Increases Digoxin Effect
High K+ Decreases Digoxin Effect
Important due to small digoxin therapeutic window

63
Q

Digoxin - Class

A

Cardiac Glycoside

64
Q

Levosimendan - Class

A

Cardiac Glycoside

65
Q

Bipyrimidiens - Name (2) + Mechanism + Use + Toxicity (3)

M2 Only

A

Name - Milrinone + Inamrinone
Mechanism - Prevent cAMP Breakdown - Increase Contractility
Use - CHF - Increase Symp. Activity
Toxicity - Bone Marrow Damage (Worst in Inamrinone) + Arrhythmia (Worse in Milrinone) + Liver Toxicity (Both)

66
Q

Milrinone - Class + Special Feature

M2 Only

A

Class - Bipyrimidien

Special Feature - More Arrhythmia but less bone marrow thrombocytopenia

67
Q

Inamrione - Class + Special Feature

M2 Only

A

Class - Bipyrimidien

Special Feature - More bone marrow thrombocytopenai but less arrhythmias

68
Q

General Order of CHF Treatment (5)

M2 Only

A

1) Diuretics
2) ACE/ARB
3) B-Blocker
4) Aldosterone Antagonist + Digoxin if Severe
5) Transplant

69
Q

Special Case Vasodilators for CHF - Name + Use (3)

A

Nitroprusside - Rapid + Powerful vasodilaterl for Acute Severe Hypotension - SE = Cyanosis
Hydalazine - Chronic Failure/HTN in African Americans - SE = Headache
Nesiritide - Atrial Peptide Vasodilator - Acute Failure but can cause hypotension

70
Q

Nitroprusside - Class + Use

A

Class - Emergency Vasodilator

Use - Rapid + Powerful vasodilaterl for Acute Severe Hypotension - SE = Cyanosis

71
Q

Hydralazine - Class + Use

A

Class - Emergency Vasodilator

Use - Chronic Failure/HTN in African Americans - SE = Headache

72
Q

Nesiritide - Class + Use

A

Class - Emergency Vasodilator

Use - Atrial Peptide Vasodilator - Acute Failure but can cause hypotension

73
Q

Vasodilators (Angina Treatment) - Approaches (3)

M2 Only

A

1) Increase Myocardial Perfusion/Oxygenation
2) Decrease Heart Work Rate + O2 Demand (Major Therapy Goal)
3) Increase O2 Extraction from Blood (Not Possible)

74
Q

Nitroglycerin - Mechanism + Types (3) + Use + Toxicity (5)

A

Mechanism - Increases NO Release with increase smooth muscle cGMP and relaxation
Use - Decreae Heart Size and Wall tension during systole (with reflex symp. activation)
Types - Short Acting + Long Acting + Sildinafil
Toxicity - Flushing + Ortho HTN + Hypotension + Tachycardia + Headache

75
Q

Oral/Sublingual Nitroglycerin - Use + Effects

A

Use - Instant Angina Vasodilation

Effects - Reduces Pulm. Resistance with no impact on peripheral systemic resistance

76
Q

High Dose Nitroglycerin - Use + Effects

A

Use - Long Acting + Oral Angina Vasodilation

Effects - Impacts both pulm. systemic resistance (vs. just pulm. in sublingual) + More reflex cardiac stimulation + AEs

77
Q

Sildinafil - Class + Mechanism + Interactions

A

Class - Phosphodiesterase (PDE5) Inhibitor
Mechanism - Vasodilation via cGMP in the penis
Interactions - Increases NO and can interact with vasodilators

78
Q

Calcium Channel Blocker - Mechanism + Classes (2) + Names (2 Each)

A

Mechanism - Block L-Type Calcium Channels - Inhibit Ca Influx in Cardiac + Smooth Muscle
Class 1 - DMechanism - Blocks Closed Calcium Channels - Impacts Smooth Muscle more than Cardiac
Use - Angina + HTN + Raynouds
AE - Less than Non-Dihydro - Flushing + Dizziness + Peripheral Edema + Constipation/Cardiac Depression (But Less) + Reflexive Effects ihydropyridine = = Block Closed Channels
Class 2 - Non-Dihydropyridine = Verapamil + Diltiazem = Block Open Channels

79
Q

Dihydropyridine Blockers - Names (2) + Mechanism + Use + Adverse Effects (6)

A

Names - Nifedipine + Amlodipine
Mechanism - Blocks Closed L-Type Calcium Channels - Impacts Smooth Muscle more than Cardiac
Use - Angina + HTN + Raynouds
AE - Less than Non-Dihydro - Flushing + Dizziness + Peripheral Edema + Constipation/Cardiac Depression (But Less) + Reflexive Effects

80
Q

Non-Dihydropyridine Blockers - Names (2) + Mechanism + Use + Adverse Effects (5)

A

Names - Verapamil + Diltiazem
Mechanism - Blocks Open L-Type Calcium Channels - Impacts Smooth Muscle and Cardiac equally (more cardiac impact than dihydropyridine)
Use - AV Nodal Arrhythmia (Afib/Flutter) + Angina + HTN + Migraines
AE - More Pronounced - Constipation + Flushing + Dizziness + Peripheral Edema + Cardiac Depression/Hypotension (High Dose)

81
Q

Variant Angina Treament - 2 Methods + 1 Failed Method

M2 Only

A

Responds to Nitrates + Ca Channel Blockers

No Response to Beta Blockers

82
Q

Anti-Angina Therapy - 2 Major Class

A

1) Nitrates = Affect Preload - Nifedipine (Dihydropyrimidines Blocker) = Similar
2) B-Blcokers = Affect Afterlod - Verapamil (Non-Dihydropyrimidines Blocker) = Similar

83
Q

Nitrate Angina Therapy Response - First Aid - 4 Points

A

Affects Preload - Nifedipine = Similar

1) Decrease EDV + BP
2) Reflex Increase in Contractility + HR
3) Decrease Ejection time + Mycoardial O2 Demand

84
Q

B-Blocker Angina Therapy Response - First Aid - 4 Points

A

Affects Afterload - Verapamil = Similar

1) Increase EDV + Ejection Time
2) Lowers BP + Contractility + HR
3) Lowers Myocardial O2 Demand

85
Q

Verapamil - Class

A

Non-Dihydropyrimidines - Open L-Type Calcium Channel Blocker

86
Q

Diltiazem - Class

A

Non-Dihydropyrimidines - Open L-Type Calcium Channel Blocker

87
Q

Nifedipine - Class

A

Dihydropyrimidines - Closed L-Type Calcium Channel Blocker

88
Q

Amlodipine - Class

A

Dihydropyrimidines - Closed L-Type Calcium Channel Blocker