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Cardiovascular > Drugs > Flashcards

Drugs Flashcards

1
Q

Procainamide

A
  • Ia
  • Blocks INa and partially blocks IKr, slowing the action potential upstroke and prolonging the action potential duration
  • Termination of sustained ventricular tachycardia (not first line). Ventricular tachycardia after MI (rarely used for this).
  • Drug-induced lupus, only during long term oral use (not available PO in USA). Fever. Agranulocytosis
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2
Q

Quinidine

A
  • Ia
  • Blocks INa and partially blocks IKr, slowing the action potential upstroke and prolonging the action potential duration. Also binds the M2 muscarinic receptor for vagolytic effects
  • Converts atrial fibrillation or flutter to sinus rhythm (rarely used for this). Maintain sinus rhythm in patients with atrial fibrillation (but can raise mortality)
  • Cinchonism (CNS toxicity: tinnitus, hearing loss, delirium, and psychosis). Nausea, vomiting, diarrhea
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3
Q

Disopyramide

A
  • Ia
  • Blocks INa and blocks IKr, slowing the action potential upstroke and prolonging the action potential duration. Also binds the M2 muscarinic receptor for vagolytic effects (stronger than quinidine)
  • Hypertrophic obstructive cardiomyopathy (but not commonly used)
  • Antimuscarinic side effects (urinary retention, constipation, blurred vision, dry mouth, closed-angle glaucoma)
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4
Q

Lidocaine

A
  • Ib
  • Binds INa+ channel in active and inactive states, but not in the resting state. So it has little effect in normal tissue, but does exert effects in sick (ischemic) tissue.
  • Ventricular arrhythmias, particular post-MI
  • CNS toxicity: confusion, delirium, paresthesias, grand mal seizures
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5
Q

Mexiletine

A
  • Ib
  • Binds INa+ channel in active and inactive states, but not in the resting state. So it has little effect in normal tissue, but does exert effects in sick (ischemic) tissue.
  • Chronic suppression of ventricular arrhythmias (not first line, but sometimes)
  • Nausea, vomiting
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6
Q

Flecainide

A
  • Ic
  • Sodium channel blocker, prolongs conduction time. Has negative inotropic effects
  • Acute conversion of atrial fibrillation to sinus rhythm. Maintenance of sinus rhythm in atrial fibrillation. Suppression of premature ventricular contractions (rarely used for this, raises mortality).
  • Confusion, irritabilityIcSodium channel blocker, prolongs conduction time. Has negative inotropic effects
  • Acute conversion of atrial fibrillation to sinus rhythm. Maintenance of sinus rhythm in atrial fibrillation. Suppression of premature ventricular contractions (rarely used for this, raises mortality).Confusion, irritability
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7
Q

Propafenone

A
  • Ic
  • Sodium channel blocker, some β-blocking activity, negative inotropic effects
  • Acute conversion of atrial fibrillation to sinus rhythm. Maintenance of sinus rhythm in atrial fibrillation. Suppression of premature ventricular contractions (rarely used for this, raises mortality).
  • Can exacerbate bronchospasm (β-blocker…)
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8
Q

Beta-blockers

A
  • II
  • Decrease slope of phase 4 in the SA node, and decrease the upstroke velocity in the SA and AV node, slowing conduction
  • Slowing of ventricular response in atrial fibrillation. Disrupting reentrant arrhythmias. Suppressing premature ventricular contractions or atrial premature beats
  • Bronchospasm, depression, cognitive impairment, hypotension
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9
Q

Amiodarone

A
  • III
  • Blocks potassium channels, increases action potential duration and effective refractory period. Also blocks Na+ channels, β receptors, and Ca2+ channels (class I, II, and IV-like effects). Most effective, but has significant side effects.
  • Suppression of ventricular tachycardia (defibrillators more effective). Maintenance of sinus rhythm in atrial fibrillation/flutter. Acute conversion from atrial fibrillation to sinus rhythm.
  • Hyperthyroidism and hypothyroidism. Pulmonary fibrosis, liver toxicity, photodermatitis (grayish-blue skin discoloration). Dronedarone, a congener, has fewer side effects.
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10
Q

Sotalol

A
  • III
  • Blocks K+ channels with some β-blocking activity
  • Maintenance of sinus rhythm in atrial fibrillation/flutter. Prevention of AVNRT, AVRT. Ventricular tachyarrhythmias.
  • Similar side effects to β-blockers: bronchospasm, depression, hypotension, cognitive impairment
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11
Q

Dofetilide

A
  • III
  • Blocks K+ channels, and some Na+ channel blocking activity
  • Maintenance of sinus rhythm in atrial fibrillation/flutter
  • Headaches, GI complaints
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12
Q

Ibutilide

A
  • III
  • K+ channel blocker
  • Acute termination of atrial fibrillation and atrial flutter
  • Few extracardiac effects other than GI complaints
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13
Q

Verapamil

A
  • IV
  • Ca2+ channel blockers, block L-type channels and prolong conduction time and refractory periods in the AV node
  • Heart rate control in atrial fibrillation/flutter. Can be used to terminate supraventricular tachycardias.
  • Constipation and peripheral edema (from smooth muscle interference in gut and vasodilation, respectively), hypotension
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14
Q

Adenosine

A
  • Unclassified
  • Interacts directly with A1 adenosine receptors in the heart, activating K+ channel, indirectly decreasing L-type Ca2+ channel activity and the funny current, If. Causes marked hyperpolarization and transient elective heart block.
  • Diagnosis and termination of supraventricular tachycardias by producing transient heart block. Effective in terminating reentrant rhythms (acts as a reset button).
  • Transient flushing, chest pressure, and chest burning
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15
Q

Digoxin

A
  • Unclassified
  • Complicated mechanism: direct membrane effects (mediated by blocking Na+/K+ ATPase), and indirect effects (vagomimetic). Slows conduction, mainly in the SA node, atria, and AV node.
  • Control of ventricular response in atrial fibrillation/flutter (usually with a β-blocker or Ca2+ channel blocker)
  • Yellow vision, anorexia, nausea, vomiting, disorientation, hallucination. Toxicity treated with anti-digoxin antibody fragments
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16
Q

Aspirin

A
  • Platelet aggregation inhibitor
  • Acetylates cyclooxygenase, irreversibly inhibiting it. Prevents production of ThromboxaneA2 (platelet activator)
  • Function returns to normal after 7-10 days when new platelets appear in circulation.
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17
Q

NSAIDs

A
  • Platelet aggregation inhibitor
  • Reversibly inhibits cyclooxygenase, function returns when drug concentration falls.
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18
Q

Clopidogrel

A
  • Platelet aggregation inhibitor
  • P2Y12 ADP receptor blocking agent, can be used with aspirin. Needs to be activate, some people resistant.
  • Trade name: Plavix
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19
Q

Ticlopidine

A
  • Platelet aggregation inhibitor
  • ADP receptor blocking agent
  • Trade name: Ticlid, use is associated with increased incidence of Thrombotic Thrombocytopenic Purpura (TTP) in 1:2000-4000 patients
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20
Q

Prasugrel

A
  • Platelet aggregation inhibitor
  • ADP receptor blocking agent, used in patients resistant to clopidogrel
  • Trade name: Efient
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21
Q

Ticagrelor

A
  • Platelet aggregation inhibitor
  • ADP receptor blocking agent, used in patients resistant to clopidogrel
  • Trade name: Brilinta
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22
Q

Abciximab

A
  • Platelet aggregation inhibitor
  • Humanized murine Fab monoclonal antibody binds to and inhibits GP IIb/IIIa function
  • Trade name: ReoPro
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23
Q

Dipyridamole

A
  • Platelet aggregation inhibitor
  • Inhibits adenosine uptake, acts on PLA2, causes increased platelet cAMP, leading to inhibition
  • Trade name: Persantine
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24
Q

Warfarin

A
  • Vitamin K Antagonist
  • Inhibits vitamin K epoxide reductase (VKORC1)Anticoagulant
  • Trade name: Coumadin
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25
Q

Low Molecular Weight Heparin

A
  • Heparin
  • Enhanced inactivation of factor Xa relative to heparin
  • Anticoagulant
  • Reduced incidence of heparin induced thrombocytopenia, and reduced risk of osteoporosis. Can also be self-administered.
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26
Q

Heparin

A
  • Heparin
  • Lower molecular weight inhibits Xa, higher molecular weight inhibits thrombin and binds platelets. All enhance antithrombin activity.
  • Anticoagulant
  • Can cause heparin induced thrombocytopenia, and osteoporosis (when used chronically), can be self administered.
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27
Q

Fondaparinux

A
  • Synthetic heparin analog
  • Enhances ability of antithrombin to inhibit factor Xa, but no anti-thrombin activity.
  • Anticoagulant
  • Trade name: Arixtra. No thrombocytopenia, but cannot be used in patients in renal failure.
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28
Q

Rivaroxaban

A
  • Direct Factor Xa Inhibitor
  • Small molecule inhibitor of factor Xa (free and bound)
  • Anticoagulant
  • Trade name: Xarelto, monitoring not required
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29
Q

Apixiban

A
  • Direct Factor Xa Inhibitor
  • Small molecule inhibitor of factor Xa (free and bound)
  • Anticoagulant
  • Trade name: Eliquis, monitoring not required
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30
Q

Hirudin

A
  • Direct Thrombin Inhibitor
  • Binds both the active pocket site and fibrinogen binding exosite on thrombin.
  • Anticoagulant
  • Originally derived from leeches, now made with recombinant DNA technology
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31
Q

Bivalirudin

A
  • Direct Thrombin Inhibitor
  • Binds both the active pocket site and fibrinogen binding exosite on thrombin, but is a truncated version of hirudin
  • Anticoagulant
  • Need to test activated clotting time at 45 minutes, avoid in renal failure
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32
Q

Argatroban

A
  • Direct Thrombin Inhibitor
  • Binds only the active site pocket on thrombin
  • Anticoagulant
  • Need to test APTT at 2 hours, avoid in liver failure
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33
Q

Dabigatran

A
  • Direct Thrombin Inhibitor
  • Binds only the active site pocket on thrombin
  • Anticoagulant
  • Dabigatran etexilate (trade name: Pradaxa) is a prodrug that is converted to dabigatran in the gut, does not need to be monitored
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34
Q

Lepirudin

A
  • Direct Thrombin Inhibitor
  • Binds only the active site pocket on thrombin
  • Anticoagulant
  • Need to test APTT at 2 hours, avoid in renal failure
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35
Q

Atorvastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • High intensity (40/80 mg/day), moderate intensity (10 mg/day)CYP3A4
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36
Q

Rosuvastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • High intensity (20/40 mg/day), moderate intensity (5/10 mg/day)
  • Minimally metabolized by CYP2C9
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37
Q

Pravastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • Moderate intensity (40 mg/day)
  • Not metabolized by CYPs
38
Q

Simvastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • Moderate intensity (40 mg/day)CYP3A4
39
Q

Fluvastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • Moderate intensity (40/80XL mg/day)
  • CYP2C9
40
Q

Pitavastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • Moderate intensity (2-4 mg/day)Longest half-life, tolerated in HIV patients, not well studied
41
Q

Lovastatin

A
  • Statin
  • Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
  • Moderate intensity
42
Q

Cholestryamine

A
  • Bile Acid Binding Sequestrant (resin)
  • Binds bile acids in the gut, causing depletion of hepatic cholesterol pools and increased production of LDL receptors. Lower LDL ~20%
  • Very safe, non-systemic, but cannot be used if triglycerides >250
43
Q

Colestipol

A
  • Bile Acid Binding Sequestrant (resin)
  • Lower LDL ~20%
  • Very safe, non-systemic, but cannot be used if triglycerides >250
44
Q

Colesevelam

A
  • Bile Acid Binding Sequestrant (gel)
  • Lower LDL ~20%
  • Very safe, non-systemic, but cannot be used if triglycerides >250
45
Q

Ezetimibe

A
  • Cholesterol absorption inhibitor
  • Absorbed, glucuronidated, and then localizes to the intestinal villi, preventing absorption of cholesterol
  • Lower LDL ~20%
  • Useful in combination with a moderate intensity statin
46
Q

Stanol ester

A
  • Plant Stanol/Sterol Ester
  • Inhibit micellar cholesterol absorption
  • Lower LDL 10-14%
47
Q

Niacin

A
  • Vitamin B3
  • Potent inhibitor of adipose tissue lipolysis by activating GPR109A (a GPCR). This decreases flux of free fatty acids to the liver for VLDL production
  • Lowers LDL and VLDL, raises HDL
  • No measurable benefit when added to a statin. Take aspirin before niacin to avoid cutaneous vasodilation and flushing.
48
Q

Gemfibrozil

A
  • Fibrate
  • Doubt we need, he cited a paper
  • Lowers LDL if LDL is high alone. LDL elevated if not high already. Increases HDL if baseline levels are low.
  • Can cause cholelithiasis and mild GI symptoms
49
Q

Fenofibrate

A
  • Fibrate
  • Doubt we need, he cited a paper
  • Lowers LDL if LDL is high alone. LDL elevated if not high already. Increases HDL if baseline levels are low.
  • Can cause cholelithiasis and mild GI symptoms
50
Q

Omega 3 Fatty Acids

A
  • Inhibit hepatic production and utilization of triglyceride rich particles
  • Lower TG in a dose-dependent fashion (up to 50% in pt with very high TG). Slightly increase HDL, do nothing for LDL.
  • No consistent evidence in RCT
51
Q

Furosemide

A
  • Loop Diuretic
  • Inhibit the Na-K-2Cl symporter in the thick ascending loop of Henle
  • Rapid diuresis, HTN in CKD
  • Hypokalemia, hypocalcemia, hypomagnesemia, increased LDL and triglycerides, hyperglycemia
52
Q

Torsemide

A
  • Loop Diuretic
  • Inhibit the Na-K-2Cl symporter in the thick ascending loop of Henle
  • Rapid diuresis, HTN in CKD
  • Hypokalemia, hypocalcemia, hypomagnesemia, increased LDL and triglycerides, hyperglycemia
53
Q

Ethycrinic Acid

A
  • Loop Diuretic
  • Inhibit the Na-K-2Cl symporter in the thick ascending loop of Henle
  • Rapid diuresis, HTN in CKD
  • Ototoxicity, hypokalemia, hypocalcemia, hypomagnesemia, increased LDL and triglycerides, hyperglycemia
54
Q

Hydrochlorothiazide (HCTZ)

A
  • Thiazide Diuretic
  • Inhibit the Na-Cl symporter in the distal convoluted tubule
  • First line hypertension
  • Hypokalemia, hyponatremia, hypercalcemia, impotence, impaired glucose tolerance, increased cholesterol
55
Q

Chlorthalidone

A
  • Thiazide Diuretic
  • Inhibit the Na-Cl symporter in the distal convoluted tubule
  • First line hypertension
  • Hypokalemia, hyponatremia, hypercalcemia, impotence, impaired glucose tolerance, increased cholesterol
56
Q

Chlorthiazide, metolazone

A
  • Thiazide Diuretic
  • Inhibit the Na-Cl symporter in the distal convoluted tubule
  • First line hypertension
  • Hypokalemia, hyponatremia, hypercalcemia, impotence, impaired glucose tolerance, increased cholesterol
57
Q

Trimterene

A
  • Potassium Sparing Diuretic
  • Inhibits renal epithelial Na channels in the late distal tubule and collecting duct
  • Diuretic, generally an add-on therapy with another diuretic class
  • Hyperkalemia, nausea, vomiting
58
Q

Spironolactone

A
  • Potassium Sparing Diuretic
  • Antagonizes the mineralcorticoid (aldosterone) receptor on epithelial cells in the late distal tubule and cortical collecting duct
  • Diuretic, generally an add-on therapy with another diuretic class
  • Hyperkalemia, gynecomastia
59
Q

Eplerenone

A
  • Potassium Sparing Diuretic
  • Antagonizes the mineralcorticoid receptor (aldosterone) on epithelial cells in the late distal tubule and cortical collecting duct
  • Diuretic, generally an add-on therapy with another diuretic class
60
Q

Amiloride

A
  • Potassium Sparing Diuretic
  • Inhibits renal epithelial Na channels in the late distal tubule and collecting duct
  • Diuretic, generally an add-on therapy with another diuretic class
  • Hyperkalemia, nausea, vomiting
61
Q

Nitroglycerin

A
  • IV Vasodilator
  • Primarily a venodilator
62
Q

Nitroprusside

A
  • IV Vasodilator
  • Metabolized by blood vessels to nitric oxide, causing vasodilation.
  • Lower blood pressure in difficult patients or emergencies. Mixed venous and arterial vasodilator
  • Hypotension, cyanide and thiocyanate toxicity. IV only
63
Q

Nesiritide

A
  • IV Vasodilator
  • Primarily an arteriolar dilator
64
Q

Minoxidil

A
  • Peripheral vasodilator
  • Activates a potassium channel in vascular smooth muscle, causing K efflux. This hyperpolarizes the cell and relaxes it.
  • Lower blood pressure in difficult patients
  • Water and sodium retention, tachycardia/angina/heart failure, hypertrichosis, effusions
65
Q

Hydralzaine

A
  • Oral Vasodilator
  • Causes arteriolar smooth muscle to relax
  • Lower blood pressure in difficult patients or emergencies. Pure arterial vasodilator
  • Headache, nausea, flushing, dizziness, angina, edema. Can cause reflex tachycardia. Drug induced lupus. IV or oral
66
Q

Nitrates

A
  • Oral Vasodilator
  • Pure venodilator
  • Can cause reflex tachycardia
67
Q

ACE inhibitors (-opril/-april/-epril/-ipril)

A
  • Oral Vasodilator
  • Block conversion of angiotensin I to angiotensin II, decreasing sympathetic activation, relaxing smooth muscles, causing diuresis, and increasing bradykinin (vasodilation)
  • Cough, hyperkalemia, renal failure, angioedema, teratogenic!
68
Q

Angiotensin receptor blocker (-artan)

A
  • Oral Vasodilator
  • Block the angiotensin II receptor (AT1), decreasing sympathetic activation, relaxing smooth muscles, and causing diuresis
  • Hyperkalemia, renal failure, teratogenic!
69
Q

Dobutamine

A
  • Inotrope
  • Beta I and B2 agonist
70
Q

Dopamine

A
  • Inotrope
  • B1 agonist
71
Q

Norepinephrine

A
  • Inotrope
  • B1 agonist
72
Q

Milrinone

A
  • Inotrope
  • Phsophodiesterase inhibitor
73
Q

Digoxin

A
  • Inotrope
  • Complicated mechanism: direct membrane effects (mediated by blocking Na+/K+ ATPase), and indirect effects (vagomimetic). Slows conduction, mainly in the SA node, atria, and AV node.
  • Control of ventricular response in atrial fibrillation/flutter (usually with a β-blocker or Ca2+ channel blocker)
  • Yellow vision, anorexia, nausea, vomiting, disorientation, hallucination. Toxicity treated with anti-digoxin antibody fragments
74
Q

Atenolol

A
  • Beta blocker
  • Cardioselective, blocks the B1 receptor
  • Basically, decrease CO. Decreasing HR, decreased contractility, and decreased renin release. Used in patients with CAD, and for hypertension (but not as the sole agent)
  • Bradycardia, hyperkalemia, fatigue, cold extremeties, bronchospasm.
75
Q

Metoprolol

A
  • Beta blocker
  • Cardioselective, blocks the B1 receptor
  • Basically, decrease CO. Decreasing HR, decreased contractility, and decreased renin release. Used in patients with CAD, and for hypertension (but not as the sole agent)
  • Bradycardia, hyperkalemia, fatigue, cold extremeties, bronchospasm.
76
Q

Propanolol

A
  • Beta blocker
  • Blocks the B1 and B2 receptors
  • Basically decrease CO. Decreasing HR, decreased contractility, and decreased renin release. Also causes vasoconstriction and a slight increase in PVR. Used in patients with CAD, and for hypertension (but not as the sole agent)
  • Bradycardia, hyperkalemia, fatigue, cold extremeties, bronchospasm.
77
Q

Timolol

A
  • Beta blocker
  • Blocks the B1 and B2 receptors
  • Basically decrease CO. Decreasing HR, decreased contractility, and decreased renin release. Also causes vasoconstriction and a slight increase in PVR. Used in patients with CAD, and for hypertension (but not as the sole agent)
  • Bradycardia, hyperkalemia, fatigue, cold extremeties, bronchospasm.
78
Q

Methyldopa

A
  • Centrally acting agent
  • Replaces norepinephrine in secretory vesicles in adrenergic neurons. Acts centrally on the brain to inhibit central adrenergic outflow.
  • Useful for hypertension in pregnancy, but many side effects
  • Sedation, dry mouth, fatigue, depression, liver toxicity
79
Q

Clonidine

A
  • Centrally acting agent
  • Stimulates a2 receptors in the brain, decreasing PVR to lower BP
  • Used adjunctively due to side effects, has few interactions with other drugs
  • Sedation, dry mouth, sleepiness, bradycardia, fatigue, depression, liver toxicity. Can get withdrawal symptoms if stopped suddenly.
80
Q

a1 blockers (-zosin)

A
  • a1 blocker
  • Blocks the a1 receptor (postsynaptic), causing vasodilation.
  • Hypertension, decreases total peripheral resistance and BP
81
Q

Verapamil

A
  • Calcium channel blocker (phenylalkylamine)
  • Block the L-type calcium channel (mostly cardiac), relaxing smooth muscle
  • Hypertension, greatly reduces PVR. Good in patients with diabetes, renal insufficiency, lipid problems, and asthma.Constipation, dizziness, nausea, bradycardia
82
Q

Diltiazem

A
  • Calcium channel blocker (Benzothiazepine)
  • Block the L-type calcium channel (vascular and cardiac), relaxing smooth muscle
  • Hypertension, decreases cardiac output and PVR. Good in patients with diabetes, renal insufficiency, lipid problems, and asthma.
  • Edema, headache, nausea, dizziness, diarrhea, bradycardia
83
Q

Nifedipine

A
  • Calcium channel blocker (Dihydropyridine)
  • Block the L-type calcium channel (primarily in smooth muscle), relaxing smooth muscle
  • Hypertension, decreases cardiac output and PVR. Good in patients with diabetes, renal insufficiency, lipid problems, and asthma.
  • Peripheral edema, headaches, flushing, dizziness, GERD, constipation
84
Q

Amlodipine

A
  • Calcium channel blocker (Dihydropyridine)
  • Block the L-type calcium channel (primarily in smooth muscle), relaxing smooth muscle
  • Hypertension, decreases cardiac output and PVR. Good in patients with diabetes, renal insufficiency, lipid problems, and asthma.
  • Peripheral edema, headaches, flushing, dizziness, GERD, constipation
85
Q

PCSK9 Inhibitors

A
  • Disinhibit LDLR
  • Dec LDL
  • Myalgias, Delerium, Dementia
86
Q

Alteplase (tPa)

A
  • Act plasminogenShort t1/2
  • Higher fibrin specificity
  • Direct plasminogen activation
87
Q

Tenecteplase (TNK-tPa)

A
  • Act plasminogen
  • Higher fibrin specificity
  • Direct plasminogen activation
88
Q

Streptokinase

A
  • Act plasminogen
  • Antigenic
89
Q

Ranolazine

A
  • Inhibit late, inward Na current -> less Na/Ca exchange in ischemic tissue -> less Ca overload
  • Safe with other anti-ischemic drugs and if low HR/BP
90
Q

Aliskiren

A

Inhibit renin

91
Q
A

Cardiovascular (39 decks)

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