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
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
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)
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
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
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
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…)
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
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.
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
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
12
Q
Ibutilide
A
- III
- K+ channel blocker
- Acute termination of atrial fibrillation and atrial flutter
- Few extracardiac effects other than GI complaints
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
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
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
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.
17
Q
NSAIDs
A
- Platelet aggregation inhibitor
- Reversibly inhibits cyclooxygenase, function returns when drug concentration falls.
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
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
20
Q
Prasugrel
A
- Platelet aggregation inhibitor
- ADP receptor blocking agent, used in patients resistant to clopidogrel
- Trade name: Efient
21
Q
Ticagrelor
A
- Platelet aggregation inhibitor
- ADP receptor blocking agent, used in patients resistant to clopidogrel
- Trade name: Brilinta
22
Q
Abciximab
A
- Platelet aggregation inhibitor
- Humanized murine Fab monoclonal antibody binds to and inhibits GP IIb/IIIa function
- Trade name: ReoPro
23
Q
Dipyridamole
A
- Platelet aggregation inhibitor
- Inhibits adenosine uptake, acts on PLA2, causes increased platelet cAMP, leading to inhibition
- Trade name: Persantine
24
Q
Warfarin
A
- Vitamin K Antagonist
- Inhibits vitamin K epoxide reductase (VKORC1)Anticoagulant
- Trade name: Coumadin
25
Low Molecular Weight Heparin
* 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.
26
Heparin
* 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.
27
Fondaparinux
* 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.
28
Rivaroxaban
* Direct Factor Xa Inhibitor
* Small molecule inhibitor of factor Xa (free and bound)
* Anticoagulant
* Trade name: Xarelto, monitoring not required
29
Apixiban
* Direct Factor Xa Inhibitor
* Small molecule inhibitor of factor Xa (free and bound)
* Anticoagulant
* Trade name: Eliquis, monitoring not required
30
Hirudin
* 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
31
Bivalirudin
* 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
32
Argatroban
* Direct Thrombin Inhibitor
* Binds only the active site pocket on thrombin
* Anticoagulant
* Need to test APTT at 2 hours, avoid in liver failure
33
Dabigatran
* 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
34
Lepirudin
* Direct Thrombin Inhibitor
* Binds only the active site pocket on thrombin
* Anticoagulant
* Need to test APTT at 2 hours, avoid in renal failure
35
Atorvastatin
* 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
36
Rosuvastatin
* 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
37
Pravastatin
* Statin
* Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
* Moderate intensity (40 mg/day)
* Not metabolized by CYPs
38
Simvastatin
* Statin
* Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
* Moderate intensity (40 mg/day)CYP3A4
39
Fluvastatin
* Statin
* Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
* Moderate intensity (40/80XL mg/day)
* CYP2C9
40
Pitavastatin
* 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
Lovastatin
* Statin
* Inhibits HMG CoA Reductase, decreasing cholesterol synthesis. Leads to increased LDL receptors
* Moderate intensity
42
Cholestryamine
* 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
Colestipol
* Bile Acid Binding Sequestrant (resin)
* Lower LDL ~20%
* Very safe, non-systemic, but cannot be used if triglycerides \>250
44
Colesevelam
* Bile Acid Binding Sequestrant (gel)
* Lower LDL ~20%
* Very safe, non-systemic, but cannot be used if triglycerides \>250
45
Ezetimibe
* 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
Stanol ester
* Plant Stanol/Sterol Ester
* Inhibit micellar cholesterol absorption
* Lower LDL 10-14%
47
Niacin
* 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
Gemfibrozil
* 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
Fenofibrate
* 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
Omega 3 Fatty Acids
* 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
Furosemide
* 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
Torsemide
* 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
Ethycrinic Acid
* 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
Hydrochlorothiazide (HCTZ)
* 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
Chlorthalidone
* 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
Chlorthiazide, metolazone
* 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
Trimterene
* 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
Spironolactone
* 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
Eplerenone
* 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
Amiloride
* 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
Nitroglycerin
* IV Vasodilator
* Primarily a venodilator
62
Nitroprusside
* 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
Nesiritide
* IV Vasodilator
* Primarily an arteriolar dilator
64
Minoxidil
* 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
Hydralzaine
* 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
Nitrates
* Oral Vasodilator
* Pure venodilator
* Can cause reflex tachycardia
67
ACE inhibitors (-opril/-april/-epril/-ipril)
* 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
Angiotensin receptor blocker (-artan)
* Oral Vasodilator
* Block the angiotensin II receptor (AT1), decreasing sympathetic activation, relaxing smooth muscles, and causing diuresis
* Hyperkalemia, renal failure, teratogenic!
69
Dobutamine
* Inotrope
* Beta I and B2 agonist
70
Dopamine
* Inotrope
* B1 agonist
71
Norepinephrine
* Inotrope
* B1 agonist
72
Milrinone
* Inotrope
* Phsophodiesterase inhibitor
73
Digoxin
* 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
Atenolol
* 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
Metoprolol
* 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
Propanolol
* 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
Timolol
* 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
Methyldopa
* 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
Clonidine
* 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
a1 blockers (-zosin)
* a1 blocker
* Blocks the a1 receptor (postsynaptic), causing vasodilation.
* Hypertension, decreases total peripheral resistance and BP
81
Verapamil
* 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
Diltiazem
* 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
Nifedipine
* 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
Amlodipine
* 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
PCSK9 Inhibitors
* Disinhibit LDLR
* Dec LDL
* Myalgias, Delerium, Dementia
86
Alteplase (tPa)
* Act plasminogenShort t1/2
* Higher fibrin specificity
* Direct plasminogen activation
87
Tenecteplase (TNK-tPa)
* Act plasminogen
* Higher fibrin specificity
* Direct plasminogen activation
88
Streptokinase
* Act plasminogen
* Antigenic
89
Ranolazine
* 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
Aliskiren
Inhibit renin
91
