Cardiology - Pharmacology Flashcards
Hyperlipidemia Drug Classes (5) + Sample Drug
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
HMG-CoA Reductase Inhibitors - Names (3) + Mechanism + Toxicity (4)
Names - Lovastatin + Atorvastatin + Simvastatin
Mechanism - Inhibits cholesterol genesis - Increases LDL Receptor Expression
Toxicity - Pregnancy/Breast Feeding + Heptotoxicity (Check ALTs) + Myopathy + CYP450 Interactions
Niacin - Mechanism + Toxicity (3)
Mechanism - Inhibits lipolysis and reduces VLDL Synthesis –> Increases HDL
Toxicity - Facial Flushing (PGE Synthesis) + Heptatotoxicity + Hyperuricemia
Bile Acid Resins - Names (2) + Mechanism + Toxicity (5)
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
Cholesterol Absorption Block - Names (1) + Mechanism + Toxicity (2)
Names - Ezetimibe
Mechanism - Prevents cholesterol absorption
Toxicity - Diarrhea + Increased LFTs
Fibrates - Names (2) + Mechanism + Toxicity (3)
Names - Gemifibrozil + Fenofibrate
Mechanism - Increases LDL/TG Clarence - Good for when VLDL is the primary issue
Toxicity - Renal and Liver (LFTs) + Gallstones
Lovastatin - Class
HMG-CoA Reductase Inhibitor
Colestipol - Class
Bile Acid Resin
Cholestramine - Class
Bile Acid Resin
Ezetimibe - Class
Cholesterol Absorption Inhibitor
Geifibrozil - Class
Fibrate
Fenofibrate - Class
Fibrate
Liver LDL Uptake - 3 Results
1) Lowers HMG (No new LDL)
2) Increase ACAT (Increase LDL Breakdown)
3) Decrease LDL Receptors
Familial Hypercholesterolemia
Failure of the LDL Receptor - No Liver Uptake - None of the 3 Turn-Down Mechanisms Uses (HMG Inhibition + ACAT increase)
Classes of Anti-Arrhythmia Therapy + Mechanism + Prototype Drug (6)
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
Class IA Anti-Arrhythmia Drugs - Name (3) + Mechanism + Use + Toxicity (5)
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
Class IB Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (2)
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)
Class IC Anti-Arrhythmia Drugs - Name (2) + Mechanism (1) + Use + Toxicity
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
Class II Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (2)
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
Class III Anti-Arrhythmia Drugs - Name (3) + Mechanism + Use + Toxicity (3)
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)
Class IV Anti-Arrhythmia Drugs - Name (2) + Mechanism + Use + Toxicity (4)
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
Adenosine - Mechanism + Use + Toxicity (3)
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
Verapamil - Arrhythmia Class + Mechanism
Class - IV
Mechanism - Ca Channel Blocker
Diltiazem - Arrhythmia Class + Mechanism
Class - IV
Mechanism - Ca Channel Blocker
Sotalol - Arrhythmia Class + Mechanism
Class - III
Mechanism - K Channel Blocker
Ibutilide - Arrhythmia Class + Mechanism
Class - III
Mechanism - K Channel Blocker
Amiodarone - Arrhythmia Class + Mechanism + Special Features
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)
Esmolol - Arrhythmia Class + Mechanism
Class - II
Mechanism - Rapid Beta Blocker
Propranolol - Arrhythmia Class + Mechanism
Class - II
Mechanism - Beta Blocker
Flecainide - Arrhythmia Class + Mechanism
Class - IC
Mechanism - Slow Na Channel Blocker
Lidocaine - Arrhythmia Class + Mechanism
Class - IB
Mechanism - Rapid Na Channel Blocker
Mexiletine - Arrhythmia Class + Mechanism
Class - IB
Mechanism - Rapid Na Channel Blocker
Quinidine - Arrhythmia Class + Mechanism
Class - IA
Mechanism - Intermediate Na Channel Blocker with Long Action Potential
Also - Special Anti-Muscarinic AEs
Disopyramide - Arrhythmia Class + Mechanism
Class - IA
Mechanism - Intermediate Na Channel Blocker with Long Action Potential
Also - Special Anti-Muscarinic AEs
Procainamide - Arrhythmia Class + Mechanism
Class - IA
Mechanism - Intermediate Na Channel Blocker with Long Action Potential
Anti-Arrhythmia Drugs that Increase Action Potential Duration (2) + Impact
IA (Procainamide)
III (Amiodarone + Sotalol)
Increased Risk of Early Afterdepolarization and Torsades
Major HTN Treatment Classes (6)
M2 Only
1) Diuretics
2) Direct Oral Vasodilators (Hydralazine + Minoxidil)
3) Alpha-1 Blockers
4) CNS Symp. Inhibitors (Clonidine)
5) Calcium Channel Blockers
6) RAAS Inhibitors
2 Key M2 HTN Points
M2 Only
Never Give RAAS Inhibitors in Pregnancy
Verapamil causes Constipation
HTN Treatment in Heart Failure (4)
Diuretics + RAAS Inhibition + B-Blockers (Be Careful) + Aldosterone Antagonists
HTN Treatment after an MI (3)
B-Blockers + ACE Inhibitors + ARBs
HTN Treatment with Diabetes (4)
RAAS Inhibitors + Ca Channel Blockers + Diuretics
Direct Oral Vasodilators for HTN (2) + Adverse Effects
M2 Only
Hydralazine + Minoxidil - For Resistant HTN
Toxicity - Tachycardia + Increased Na/H2O Retention (Vasodilation Activates the RAAS System)
Anti-Arrhythmia Treatment - Wolfe-Parkson-White Review
M2 Only
Beta-Blockers + Ca Channel Blockers Alone - Only Slow AV Node Fast Pathway
Must Add IC to Slow the Accessory Pathway
Heart Failure Drugs - 3 Major Mechanisms
M2 Only
1) Positive Inotropic + 2) Vasodilators (Both Elevate Frank Starling Curve
3) Diuretics - Move you back on the curve
Major Classes of Heart Failure Drugs (7)
M2 Only
1) Diuretics
2) RAAS Inhibitors
3) Cardiac Glycosides
4) Sympathomimetics
5) Bipyramides
6) Beta Blockers
7) Special Vasodilators
3 Major Cardiac Diuretic Classes + Mechanism + Drug Name
M2 Only
1) Loop Diuretics (Furosimide)
2) Thiazides (HTCZ + Metolazone + Indaparmid
3) K Sparing Diruetics (Amiloride + Spironolactone)
Furosemide - Class + Mechanism + Use + Toxicity (3)
Class - Loop Diuretic
Mechanism - Inhibits Na/H2O Reabsorption
Use - Primarily for Edema + Pulmonary Congestion in HTN + HF
Toxicity - Hypokalemia + Metabolic Acidosis + Ototoxicity
HTCZ - Class + Mechanism + Use + Toxicity
Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia
Metolazone - Class + Mechanism + Use + Toxicity
Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia
Indaparmid - Class + Mechanism + Use + Toxicity
Class - Thiazide Diuretic (Less Powerful)
Mechanism - Best for Na Reduction
Use - Anti-HTN + Reduce Afterload
Toxicity - Hypokalemia + Metabolic Acidosis + Hypercalemia
Amiloride - Class + Mechanism + Use + Toxicity
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
Spironolactone - Class + Mechanism + Use + Toxicity
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
Low Renin HTN Treatment
M2 Only
Diuretics = Key = African American HTN
ACE Inhibitors - Name (2) Mechanism + Use + Toxicity (3)
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)
Angiontensin Receptor Blocker - Name (1) Mechanism + Use + Toxicity (3)
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
Renin Blocker - Name (1) Mechanism + Use + Toxicity
M2 Only
Name - Aliskiren
Mechanism -Like ACE Inhibtor
Use - Experimental
Toxicity - Bradykinin Angioedema + Cough
Losartan - Class
ARB
Catopril - Class
ACE Inhibitor
Enalapril - Class
ACE Inhibitor
Aliskiren - Class
Renin Inhibitor
Cardiac Glycosides - Name (2) + Mechanism + Effects + Use + Toxicity (4)
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
Impact of K+ On Digoxin
Low K+ Increases Digoxin Effect
High K+ Decreases Digoxin Effect
Important due to small digoxin therapeutic window
Digoxin - Class
Cardiac Glycoside
Levosimendan - Class
Cardiac Glycoside
Bipyrimidiens - Name (2) + Mechanism + Use + Toxicity (3)
M2 Only
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)
Milrinone - Class + Special Feature
M2 Only
Class - Bipyrimidien
Special Feature - More Arrhythmia but less bone marrow thrombocytopenia
Inamrione - Class + Special Feature
M2 Only
Class - Bipyrimidien
Special Feature - More bone marrow thrombocytopenai but less arrhythmias
General Order of CHF Treatment (5)
M2 Only
1) Diuretics
2) ACE/ARB
3) B-Blocker
4) Aldosterone Antagonist + Digoxin if Severe
5) Transplant
Special Case Vasodilators for CHF - Name + Use (3)
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
Nitroprusside - Class + Use
Class - Emergency Vasodilator
Use - Rapid + Powerful vasodilaterl for Acute Severe Hypotension - SE = Cyanosis
Hydralazine - Class + Use
Class - Emergency Vasodilator
Use - Chronic Failure/HTN in African Americans - SE = Headache
Nesiritide - Class + Use
Class - Emergency Vasodilator
Use - Atrial Peptide Vasodilator - Acute Failure but can cause hypotension
Vasodilators (Angina Treatment) - Approaches (3)
M2 Only
1) Increase Myocardial Perfusion/Oxygenation
2) Decrease Heart Work Rate + O2 Demand (Major Therapy Goal)
3) Increase O2 Extraction from Blood (Not Possible)
Nitroglycerin - Mechanism + Types (3) + Use + Toxicity (5)
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
Oral/Sublingual Nitroglycerin - Use + Effects
Use - Instant Angina Vasodilation
Effects - Reduces Pulm. Resistance with no impact on peripheral systemic resistance
High Dose Nitroglycerin - Use + Effects
Use - Long Acting + Oral Angina Vasodilation
Effects - Impacts both pulm. systemic resistance (vs. just pulm. in sublingual) + More reflex cardiac stimulation + AEs
Sildinafil - Class + Mechanism + Interactions
Class - Phosphodiesterase (PDE5) Inhibitor
Mechanism - Vasodilation via cGMP in the penis
Interactions - Increases NO and can interact with vasodilators
Calcium Channel Blocker - Mechanism + Classes (2) + Names (2 Each)
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
Dihydropyridine Blockers - Names (2) + Mechanism + Use + Adverse Effects (6)
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
Non-Dihydropyridine Blockers - Names (2) + Mechanism + Use + Adverse Effects (5)
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)
Variant Angina Treament - 2 Methods + 1 Failed Method
M2 Only
Responds to Nitrates + Ca Channel Blockers
No Response to Beta Blockers
Anti-Angina Therapy - 2 Major Class
1) Nitrates = Affect Preload - Nifedipine (Dihydropyrimidines Blocker) = Similar
2) B-Blcokers = Affect Afterlod - Verapamil (Non-Dihydropyrimidines Blocker) = Similar
Nitrate Angina Therapy Response - First Aid - 4 Points
Affects Preload - Nifedipine = Similar
1) Decrease EDV + BP
2) Reflex Increase in Contractility + HR
3) Decrease Ejection time + Mycoardial O2 Demand
B-Blocker Angina Therapy Response - First Aid - 4 Points
Affects Afterload - Verapamil = Similar
1) Increase EDV + Ejection Time
2) Lowers BP + Contractility + HR
3) Lowers Myocardial O2 Demand
Verapamil - Class
Non-Dihydropyrimidines - Open L-Type Calcium Channel Blocker
Diltiazem - Class
Non-Dihydropyrimidines - Open L-Type Calcium Channel Blocker
Nifedipine - Class
Dihydropyrimidines - Closed L-Type Calcium Channel Blocker
Amlodipine - Class
Dihydropyrimidines - Closed L-Type Calcium Channel Blocker