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98 Cards in this Set
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Mannitol
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Osmotic Diuretic
MOA: Inhibits water reabsorption throughout the tubule. It is a sugar alcohol that cannot be transported back into the system. It attracts water, allowing for excretion. Works at proximal tubule. Use: Decrease IOP in glaucoma, decrease intracerebral pressure, oliguric states, rhabdomyolysis SE: Acute hypovolemia |
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Acetazolamide
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Carbonic Anhydrase Inhibitor
-Diuretic MOA: Decreases H+ formation inside proximal tubule cell --> decreases Na/H antiport --> increases Na and HCO3 in lumen Uses: Glaucoma, acute mountain sickness (treats edema and respiratory alkalosis), and metabolic alkalosis SE: Bicarbonaturia and acidosis (loss of buffering capacity), hypokalemia, hyperchloremia (body adapts and absorbs Cl with Na), parethesia, renal stones, sulfonamide hypersensitivity |
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Hydrochlorothiazide
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Thiazide
-Diuretic -Antihypertensive MOA: Inhibits Na/Cl transporter in distal tubule, causes increased luminal Na and Cl in DCT --> diuresis. Uses: HTN, CHF, Nephrolithiasis (Ca stones), nephrogenic diabetes insipidus SE: Hypokalemia/alkalosis, *hypercalcemia (increased Ca absorption). Causes decreased insulin release from pancreas --> hyperuricemia, hyperglycemia, hyperlipidemia |
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Furosemide
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Loop Diuretic
-Antihypertensive MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased reabsorption of Ca and Mg --> Increased diuresis Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state SE: Sulfonamide hypersensitivity, *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity Drug Interactions: Digoxin |
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Ethacrynic acid
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Loop Diuretic
-Antihypertensive MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased back diffusion of K, decreased positive potential, decreased reabsorption of Ca and Mg. Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state SE: ***NO Sulfonamide hypersensitivity (use for pts with sulfa hypersensitivity), *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity Drug Interactions: Digoxin |
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Torsemide
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Loop Diuretic
-Antihypertensive MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased back diffusion of K, decreased positive potential, decreased reabsorption of Ca and Mg. Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state SE: Sulfonamide hypersensitivity, *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity Drug Interactions: Digoxin |
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Triamterine
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Diuretic - K+ Sparing
-Antihypertensive MOA: Blocks Na/K antiport in collecting duct SE: Hyperkalemia and acideosis |
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Spironolactone
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Diuretic - K+ Sparing
-Antihypertensive MOA: Aldosterone-receptor antagonist. Works at collecting duct principal cell. Uses: Hyperaldosteronic state (elevated in CHF), corrects hypokalemic state, antiandrogenic uses (female hirsutism) because it blocks steroid receptors, CHF SE: *Hyperkalemia and acidosis, antiandrogen |
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Amiloride
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Diuretic - K+ Sparing
-Antihypertensive MOA: Blocks Na/K antiport in collecting duct SE: Hyperkalemia and acideosis |
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Verapamil
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Antiarrhythmic: Type IV: Calcium Channel Blocker
MOA: Blocks slow cardiac Ca channels & blood vessels , decreases SA/AV nodal activity. Decreases CO and TPR. Uses: Supraventricular tachycardia (Does NOT work on the Ca channels of blood vessels) SE: *Peripheral edema, constipation, dizziness, flushing, hypotension, AV block |
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Diltiazem
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Calcium Channel Blocker
MOA: Blocks slow cardiac Ca channels & blood vessels, decreases SA/AV nodal activity. Decreases CO and TPR. Uses: Supraventricular tachycardia (Does NOT work on the Ca channels of blood vessels) SE: Dizziness, flushing, hypotension, AV block |
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Nifedipine
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Calcium Channel Blocker
-Antihypertensive -Antianginal MOA: Blocks slow Ca channels in blood vessels. Causes decreased intracellular Ca. Decreases TPR (mostly works on blood vessels). Antianginal - Important for vasospastic angina SE: Reflex tachycardia, *gingival hyperplasia |
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Amlodipine
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Calcium Channel Blocker
MOA: Blocks L-type Ca channels in heart and blood vessels. Causes decreased intracellular Ca. Decreases TPR Uses: HTN, angina SE: Reflex tachycardia, *gingival hyperplasia |
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Captopril
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ACE Inhibitor
-CHF -Antihypertensive MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation. Uses: HTN, protective of diabetic nephropathy, CHF SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema |
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Enalaprilat
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ACE Inhibitor
-CHF -Antihypertensive Prodrug = Enalapril MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation. Uses: HTN, protective of diabetic nephropathy, CHF SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema |
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Lisinopril
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CHF - ACE Inhibitor
MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation. Uses: HTN, protective of diabetic nephropathy, CHF SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema |
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Benazepril
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CHF - ACE Inhibitor
MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation. Uses: HTN, protective of diabetic nephropathy, CHF SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema |
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Losartan
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Angiotensin I Receptor ANT (ARB)
-CHF -Antihypertensive MOA: Blocks AT1 R's on adrenal cortex and blood vessels. Uses: HTN, protective of diabetic nephropathy, CHF SE: Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema |
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Digoxin
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CHF: Cardiotonic Agent - Cardiac Glycoside
MOA: Inhibits cardiac Na/K ATPase --> Increases intracellular Ca --> Increases contractile force. Also inhibits neuronal Na/K ATPase, causes increased vagal and sympathetic stimulation Pharmacokinetics: Long half life, requires loading dose. Large Vd (tissue protein binding) - Displacement by other drugs Uses: CHF, Supraventricular tachycardia SE: Early signs are GI - Anorexia, nausea, ECG and late signs are CNS - disorientation, visual effects. Toxic doses - Cardiac arrhythmias Drug interactions - Quinidine and verapamil displace from tissue binding site Similar to digitoxin, but longer-lasting effects |
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Amrinone
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CHF: PDE Inhibitor
MOA: Increases cAMP in heart muscle, causing increased inotropy. Increases cAMP in smooth muscle, results in decreased TPR |
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Milrinone
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CHF: PDE Inhibitor
MOA: Increases cAMP in heart muscle, causing increased inotropy. Increases cAMP in smooth muscle, results in decreased TPR |
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Propranolol
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Beta Blocker (Non-selective)
-Antiarrhythmic: Class II -CHF -Antihypertensive -Antianginal MOA: Decreases HR, SV, CO. Also decreases renin release and aqueous humor production. Use: Prophylaxis post-MI and supraventricular tachyarrhythmias SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs Caution: Asthma, vasospastic disorder, diabetes |
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Sotalol
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Beta Blocker
-Antiarrhythmic: Class II -CHF MOA: Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR. Also a K-channel blocker Use: Life-threatening ventricular arrhythmia SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs Caution: Asthma, vasospastic disorder, diabetes |
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Carvediolol
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Beta Blocker and Alpha Blocker
-CHF |
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Quinidine
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Na Channel blocker
- Antiarrhythmic: Class I MOA: Antiarrhythmic - Block fast Na channels, preferentially in the open/activated state. Increases AP duration and effective refractory period. Also blocks K+ channel. Also causes muscarinic receptor blockade, which can increase HR and AV conduction. SE: *Cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation), hypotension, prolongation of QRS and increased QT interval associated with syncope (torsades) |
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Procainamide
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Na Channel blocker
- Antiarrhythmic: Class I MOA: Antiarrhythmic - Block fast Na channels, preferentially in the open/activated state. Increases AP duration and effective refractory period. Also blocks K+ channel. SE: SLE-like syndrome (more likely with slow-acetylators), hematotoxicity, CV effects (torsades) |
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Lidocaine
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Na Channel blocker
- Antiarrhythmic: Class I MOA: Antiarrhythmic - Block fast Na channels, preferentially for tissues partly depolarized (slow conduction in hypoxic and ischemic tissues). Decreases APD due to block of the slow Na window currents, but this increases diastole and extends the time for recovery. Used for post-MI & open-heart surgery. SE: CNS (seizures), LEAST cardiotoxic |
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Phenyloin
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Na Channel blocker
- Antiarrhythmic: Class I MOA: Antiarrhythmic - Block fast Na channels, preferentially for tissues partly depolarized (slow conduction in hypoxic and ischemic tissues). Decreases APD due to block of the slow Na window currents, but this increases diastole and extends the time for recovery. *Class Ib antiarrythmic, but usually used as an antiepileptic |
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Esmolol
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Beta Blocker (Cardioselective, B1)
-Antiarrhythmic: Class II MOA: Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR Use: Prophylaxis post-MI and supraventricular tachyarrhythmias *Used as IV, used in acute SVTs SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs Caution: Vasospastic disorder, diabetes |
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Acebutolol
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Beta Blocker (Cardioselective, B1)
-Antiarrhythmic: Class II MOA: Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR Use: Prophylaxis post-MI and supraventricular tachyarrhythmias SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs Caution: Asthma, vasospastic disorder, diabetes |
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Bretyllium
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K+ Channel Blocker (AP Prolongation)
-Antiarrhythmic: Class III MOA: Blocks K+ Channel, slows repolarization of AP. Increases APD and ERP, especially in ventricular and Purkinje diseases |
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Amiodarone
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K+ Channel Blocker (AP Prolongation)
-Antiarrhythmic: Class III MOA: Blocks K+ Channel, slows repolarization of AP. Increases APD and ERP, especially in ventricular and Purkinje diseases *Mimics classes I, II, III, IV - Increases APD and ERP in ALL cardiac tissues. Used for all arrhythmias. *LONG half-life - binds extensively to all tissues, large Vd SE: Pulmonary fibrosis, blue pigmentation of skin (smurf), phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfunction |
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Adenosine
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Antiarrhythmic
MOA: Activates adenosine receptors to cause Gi-coupled decrease in cAMP - Decreases HR. Decreases SA and AV nodal activity DOC: aroxysmal supraventricular tachycardias and AV nodal arrhythmias SE: Flushing, sedation, dyspnea |
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Clonidine
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alpha-2 Agonist
-Antihypertensive MOA: Decreases sympathetic stimulation (negative feedback, decreases release of NE, decreases alpha1 and beta1 activation). Decreases TPR AND HR Use: HTN, Opiate withdrawal SE: CNS depression, edema |
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a-methyldopa
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alpha-2 Agonist
-Antihypertensive MOA: Decreases sympathetic stimulation (binds to alpha2 presynaptic R's and decreases release of NE, decreases alpha1 and beta1 activation). Decreases TPR AND HR Use: HTN and HTN-management in pregnancy SE: *Hemolytic anemia, CNS depression, edema |
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Reserpine
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Antihypertensive: Interferes with storage vesicles (NE)
MOA: Prevents storage in vesicles (NE) - Decreases CO and TPR, decreases release of catecholamines SE: *Severe depression, edema, increases GI secretions (PNS) |
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Guanethidine
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Antihypertensive - Inhibits NE Release
MOA: Binds NE vesicles and inhibits NE release SE: Diarrhea, edema |
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Prazosin
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alpha-1 Blocker
-Antihypertensive MOA: Arteriolar and venous vasodilation to decrease BP. Also inhibits SM contraction in prostate Use: HTN, BPH SE: Reflex tachycardia, "first-dose" syncope, *orthostatic hypotension, urinary incontinence (increases PNS) |
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Hydralazine
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Antihypertensive: Direct-Acting Vasodilator - Nitric Oxide
MOA: Decreases TPR through arteriolar dilation SE: SLE-like syndrome and slow acetylators, edema, reflex tachycardia |
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Nitroprusside
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Antihypertensive: Direct-Acting Vasodilator - Nitric Oxide
MOA: Decreases TPR through dilation of both arterioles and venues Use: DOC for hypertensive emergencies, IV SE: Cyanide toxicity - co-administer with nitrites and thiosulfate |
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Inamrinone
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CHF: Cardiotonic Agent - PDE inhibitor
MOA: Increases cAMP in heart cells (increases inotrophy) and SM cells (decreases TPR) |
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Milrinone
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CHF: Cardiotonic Agent - PDE inhibitor
MOA: Increases cAMP in heart cells (increases inotrophy) and SM cells (decreases TPR) |
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Nitroglycerine
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NO Precursor
-Antianginal MOA: Pro-drug of NO. Venodilation decreases preload, which decreases O2 requirement. Nitrates decrease infarct size and post-MI mortality. SE: Flushing, headache, orthostatic hypotension. Reflex tachycardia & fluid retention. Methemoglobinemia. *Don't use with sildenafil (viagra) |
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Isosorbide dinitrate
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NO Precursor
-Antianginal MOA: Pro-drug of NO. Venodilation decreases preload, which decreases O2 requirement. Nitrates decrease infarct size and post-MI mortality. SE: Flushing, headache, orthostatic hypotension. Reflex tachycardia & fluid retention. Methemoglobinemia. *Don't use with sildenafil (viagra) |
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Atorvastatin
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Statin
-Anti-atherosclerotic MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity *Cytochrome P450 inhibitors enhance toxicity of statins |
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Simvastatin
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Statin
-Anti-atherosclerotic MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity *Cytochrome P450 inhibitors enhance toxicity of statins |
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Lovastatin
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Statin
-Anti-atherosclerotic MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity *Cytochrome P450 inhibitors enhance toxicity of statins |
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Pravastatin
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Statin
-Anti-atherosclerotic MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity *Cytochrome P450 inhibitors enhance toxicity of statins |
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Gemfibrozil
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Fibric Acid Derivatives
-Antiatherosclerotic Agent MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia SE: Hepatotoxicity |
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Fenofibrate
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Fibric Acid Derivatives
-Antiatherosclerotic Agent MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia SE: Hepatotoxicity |
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Clofibrate
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Fibric Acid Derivatives
-Antiatherosclerotic Agent MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia SE: Hepatotoxicity |
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Cholestyramine
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Bile Acid Sequestrant
-Antiatherosclerotic MOA: Complex bile salts in gut. Causes decreased enterohepatic recirculation of bile salts, increased synthesis of new bile, decreased liver cholesterol, increased LDL-R expression, decreased blood LDL SE: Increased VLDL and triglycerides, GI disturbances, malabsorption of lipid-soluble vitamins |
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Colestipol
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Bile Acid Sequestrant
-Antiatherosclerotic MOA: Complex bile salts in gut. Causes decreased enterohepatic recirculation of bile salts, increased synthesis of new bile, decreased liver cholesterol, increased LDL-R expression, decreased blood LDL SE: Increased VLDL and triglycerides, GI disturbances, malabsorption of lipid-soluble vitamins |
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Niacin (Nicotinic acid)
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Antiatherosclerotic
MOA: Inhibition of VLDL synthesis, causing decreased plasma VLDL and LDL and **increased plasma HDL. SE: Flushing, hyperglycemia |
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Ezetimibe
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Antiatherosclerotic
MOA: Prevents intestinal absorption of cholesterol, decreases LDL SE: GI distress |
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Pilocarpine
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Muscarinic Agonist
MOA: Ophthalmic effects predominate - Contraction of sphincter muscle of the iris (miosis) and enhances tone of trabecular network. Contraction of ciliary muscle --> Accommodation. Use: Glaucoma, dry mouth (Sjogren's) SE: Topical - stinging & local irritation. Oral - Sweating and worsens asthma/COPD symptoms. |
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Bethanecol
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Muscarinic Agonist
MOA: Mostly works on smooth muscles. GU - Increases detrusor tone and decreases resistance of internal sphincter. GI - Increases motility and secretion Use: Gastric atony (increases motility) and urinary retention SE: Bronchoconstriction, GI (nausea, vomiting, diarrhea), Miosis |
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Carbachol
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Muscarinic Agonist
MOA: Non-selective cholinergic agonist Use: Topically for glaucoma, increases aqueous humor outflow into the canal of Schlemm |
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Physostigmine
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Anticholinesterase
MOA: Inhibits AChE. Readily crosses BBB. Use: Antidote for anticholinergic delirium (from atropine overdose). |
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Neostigmine
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Anticholinesterase
MOA: Inhibits AChE, increases accumulation of acetylcholine at neuromuscular junctions and synapses. Skel muscle - Reverses neuromuscular blockade. GU - Increased tone, motility and relaxation of sphincters. Heart - Decreased HR, contractility, and conduction velocity. Use: Reverse nondepolarizing neuromusclar blockade (ex: coming out of surgical anasthesia), Myasthenia gravis. |
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Pyridostigmine
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Anticholinesterase
MOA: Inhibits AChE, increases accumulation of acetylcholine at neuromuscular junctions and synapses. Skel muscle - Reverses neuromuscular blockade. GU - Increased tone, motility and relaxation of sphincters. Heart - Decreased HR, contractility, and conduction velocity. Use: Myasthenia gravis. |
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Edrophonium
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Anticholinesterase
MOA: Inhibits AChE Use: Used to diagnose myasthenia gravis: Tensilon test - Increased ACh in NM junction able to overcome ACh receptor Abs leads to sudden improvement then decreased muscle strength. Also used to differentiate between cholinergic crisis (overmedication) and worsening myasthenia. |
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Isoflurophate (DFP)
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Anticholinesterase
MOA: Organophosphate "nerve gas" - Suicide inhibitor of AChE. Accumulation of ACh at NM junctions and neuronal synapses. Clinical: CNS - Coma, resp depression, seizures. Muscarinic - BRADYCARDIA. Nicotinic - Muscle twitching, fasiculations, weakness & flaccid paralysis. |
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Pralidoxime (2-PAM)
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Antidote to Cholinesterase Inhibitor
MOA: Cholinesterase regenerator to organophosphate toxicity. ACh R blocker to decrease muscarinic hyperactivity that would otherwise cause potentially fatal bradycardia. Regeneration is due to pralidoxime's higher affinity for phosphorus. |
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Atropine
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Muscarinic Antagonist
Use: Antidote for physostigmine overdose SE: "Red as a beet, blind as a bat, dry as a bone, hot as a hare, and mad as a hatter." - flush, blurred vision, decreased secretions, hyperthermia, delirium, hallucinations |
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Scopolamine
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Muscarinic Antagonist
Use: Motion sickness prophylaxis. SE: "Red as a beet, blind as a bat, dry as a bone, hot as a hare, and mad as a hatter." - flush, blurred vision, decreased secretions, hyperthermia, delirium, hallucinations |
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Ipratropium
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Muscarinic Antagonist
MOA: Decreased bronchoconstriction and bronchial secretions. Use: COPD!! and asthma SE: Dry mouth & sedation |
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Norepinephrine
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Alpha Adrenergic Agonist
MOA: Peripheral vasoconstriction and increased BP. Use: Severe hypotension (used in ICU) SE: Reflex bradycardia |
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Epinephrine
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MOA: Stimulates a1, a2, B1 and B2 R's. B is predominant at low doses and alpha at high doses. Net effect is equivalment to sympathetic stimulation.
Use: Cardiac arrest, cardiogenic shock, severe HTN SE: Can precipitate MI or arrhythmias. |
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Dopamine
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MOA: Precursor to NE, stimulates D1>B1>a1. Low doses - D1 predominates - Renal and splanchnic vasodilation. Medium dose - B1 predominates, Increased CO.
Use: Decompensated CHF - Treat with medium doses SE: Arrhythmias |
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Dobutamine
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Beta Adrenergic Agonist
-Stimulates B1>>B2 -CHF MOA: Increases cardiac contractility and CO. Use: Decompensated congestive heart failure SE: Arrhythmias |
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Amphetamine
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alpha=B
MOA: Causes release of endogenous NE after presynaptic uptake Use: ADHD SE: Restlessness, dependence |
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Ephedrine
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B>alpha
MOA: Stimulates release of NE from sympathetic neurons. Net effect is to increase HR and Co, and variably increase TPR to increase BP. Use: Nasal decongestant SE: HTN |
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Cocaine
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Indirect Agents Affecting Adrenergic NTs
MOA: Blocks reuptake of catecholamines (potentiates NE > Epi). CNS stimulation --> depression. CV (moderate doses) --> tachycardia, arrhythmia & MI. SE: Myocardial ischemia |
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Phenylephrine
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alpha1 Agonist
MOA: Reduces mucosal blood flow by causing vasoconstriction of superficial blood vessels, causing the fluid in the interstitial space draining through the veins, reducing edema. Use: *Vasopressor, nasal decongestant SE: Reflex bradycardia and *hypertension |
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Methoxamine
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alpha1 Agonist
MOA: Vasoconstriction of skin and splanchnic vessels. Increases TPR. Use: Hypotension. Also used to treat tachycardia (due to reflex bradycardia) SE: Reflex bradycardia via baroreceptors |
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Metaraminol
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Alpha Adrenergic Agonist
a1 >> B1 Use: Hypotension, particularly as a complication of anesthesia. Used for priapism. |
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Tetrahydrozoline
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alpha1 Agonist
MOA: Decreases redness by limiting blood flow to eye surface Use: VISINE |
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Clonidine
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alpha2 Agonist
MOA: Works to suppress sympathetic outflow. Use: HTN and drug withdrawal SE: Sedation, dry mouth, *rebound hypertension |
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Phenoxybenzamine
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Non-selective alpha blocker
MOA: IRREVERSIBLE antagonist. Alpha blockade causes dilation of vascular SM, decreases BP. Also inhibits neuronal extraneuronal NE reuptake. Use: HTN, specifically pts with *pheochromocytoma SE: Orthostatic hypotension, reflex tachycardia |
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Tolazoline
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Alpha Antagonist
Used in vet medicine... -_- |
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Phentolamine
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Non-selective alpha blocker
MOA: Competitive antagonist. Alpha blockade causes dilation of vascular SM, decreases BP Use: HTN, pheochromacytoma SE: Orthostatic hypotension, reflex tachycardia |
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Isoproterenol
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Beta Agonist - B1-B2
MOA: Stimulates Beta R's - B1 increases HR & inotropy. B2 causes vascular SM relaxation. Net effect is increased HR and CO. Use: Bradycardia, heart block and arrhythmias. SE: Arrhythmias, flushing, angina |
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Albuterol
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Beta Agonist - B2 >> B1
MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation Use: Bronchospasm in asthma, bronchitis, and COPD SE: Tremor. Sinus tachycardia |
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Terbutaline
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Beta Agonist - B2 >> B1
MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation Use: IV for treatment of status asthmatics. Also used to suppress premature labor |
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Metaproterenol
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B2 >> B1
MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation Use: Bronchospasm in asthma, bronchitis, and COPD SE: Tremor. Sinus tachycardia |
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Metoprolol
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Beta Blocker
-HTN MOA: Selectively inhibits B1 R's. Decreases HR (acts as a Class II antiarrhythmic). Also decreases inotropy. Overall decreases O2 demand Use: Ischemic heart disease, HTN, arrhythmias SE: Bradycardia |
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Nadolol
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Beta Blocker - Non-selective
MOA: Selectively inhibits B1 R's. Decreases HR (acts as a Class II antiarrhythmic). Also decreases inotropy. Overall decreases O2 demand Use: Ischemic heart disease, HTN, arrhythmias, portal HTN, thyrotoxicosis, migraine prevention. SE: Bradycardia, *bronchospasm |
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Timolol
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Beta Blocker - Non-selective
-HTN MOA: Decreases HR, SV, CO. Also decreases renin release and *aqueous humor production (can be used as eye drops) Use: Glaucoma |
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Carvediol
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Beta blocker (also alpha1) - Non-selective
-CHF MOA: Decreases HR, SV, CO & TPR. Vasodilatory due to alpha1 blockade. Use: Compensated heart failure (Improves symptoms, ejection fraction and survival) SE: Hypotension, bradychardia. |
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Labetalol
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Beta blocker (also alpha1) - Non-selective
MOA: Decreases HR, SV, CO & TPR. Vasodilatory due to alpha1 blockade. Use: HTN |
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Nicotine
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Depolarizing Ganglionic Blocker
MOA: Agonist for nicotinic ACh R's. Nm causes skeletal muscle contract. Nn stimulates both SNS and PNS. Epinephrine release, increase HR, peripheral vasoconstriction, Increased gut motility and secretion, increased respiratory rate. Use: Aid smoking cessation SE: Dependence |
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Hexamethonium
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Depolarizing Ganglionic Blocker
MOA: Competitive antagonist of Nn receptors at PNS and SNS ganglia. Use: Hypertensive crises - no longer used because of the many side effects that result from loss of all autonomic tone. |
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Tubocurarine
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Competitive Neuromuscular Blocker
Use: Muscle paralysis during surgery or intubation MOA: Antagonize receptor at neuromuscular endplate, inhibiting muscle contraction |
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Pancuronium
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Competitive Neuromuscular Blocker
MOA: Nondepolarizing blockade causes skeletal muscle paralysis that can be overcome by stimulation or administration of cholinesterase inhibitor Use: Induce paralysis (surgery) SE: Histamine causes flushing, edema, erythema, hypotension, tachycardia. Increased HR and CO. |
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Vecuronium
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Competitive Neuromuscular Blocker
MOA: Nondepolarizing blockade causes skeletal muscle paralysis that can be overcome by stimulation or administration of cholinesterase inhibitor Use: Induce paralysis (surgery) SE: Histamine causes flushing, edema, erythema, hypotension, tachycardia. Increased HR and CO. |
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Succinylcholine
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Depolarizing Neuromuscular Blocker
MOA: Binds nicotinic (Nm) Ach R's, causing depolarization of membrane. Drug is NOT inactivated by acetylcholinesterase - prolonged depolarization. Causes depolarizing blockade that cannot be overcome. Use: Paralysis for surgical procedures SE: Malignant hyperthermia |
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Trimethaphan
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Competitive Ganglionic Blocker
Use: Muscle paralysis during surgery or intubation MOA: Antagonize receptor at neuromuscular endplate, inhibiting muscle contraction |