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Definition
increase cGMP, vasodilates arteries > veins, afterload reduction Severe HTN, CHF. With methyldopa for HTN in pregnancy. With b-blocker to prevent reflex tachycardia. Compensatory tachycardia, fluid retention (reflex renin release), nausea, headache, angina. Drug-induced lupus. |
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Definition
Peripheral edema, flushing, dizziness, constipation *"Nifedipine is similar to Nitrates in effect" |
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Definition
Non-dihydropyridine CCN block voltage-dependent Ca channels on cardiac and smooth muscle Non-DHPs: heart > vascular effect HTN, angina, arrhythmias, Prinzmetal angina, Raynauds Constipation, gingival hyperplasia. Cardiac depression, AV block, peripheral edema, flushing, dizziness. |
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Definition
Non-dihydropyridine CCN block voltage-dependent Ca channels on cardiac and smooth muscle Non-DHPs: heart > vascular effect HTN, angina, arrhythmias, Prinzmetal angina, Raynauds Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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Nitroglycerin Mech? Use? Tox? |
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Definition
NO release, increase cGMP, smooth muscle dilation Veins >> arteries, decrease preload Angina, pulmonary edema, erection enhancer Reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial exposure |
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Isosorbide dinitrate Mech? Use? Tox? |
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Definition
NO release, increase cGMP, smooth muscle dilation Veins >> arteries, decrease preload Angina, pulmonary edema, erection enhancer Reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial exposure. *NB: isorboside mononitrate is active metabolite, has 100% bioavail - dinitrate is hepatic glucoronidated. |
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Nitroprusside Mech? Use? Tox? Antidote? |
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Definition
NO release, increase cGMP, smooth muscle dilation Short acting, for malignant HTN cyanide toxicity - thiosulfate to bind CN |
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Definition
D1 receptor agonist, relaxes renal smooth muscle. Only agent that improves renal perfusion as it lowers blood pressure. malignant hypertension |
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Definition
K+ channel opener - hyperpolarizes then relaxes smooth muscle. Malignant hypertension. Hyperglycemia (prevents insulin release) |
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Definition
HMG-CoA reductase inhibition, lower mavalonate. Compensatory increase in LDL uptake to make bile. Lowers LDL, triglycerides, slight raise in HDL Hepatotoxicity, rhabdomyolysis |
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Definition
Inhibits lipolysis in adipose tissue, reduces liver VLDL secretion raises HDL, lowers LDL, lowers triglycerides. *Also has vasodilatory effects Flushing (block with ASA), hyperglycemia, hyperuricemia |
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Cholestyramine, Colestipol, Colesevelam Mech? Use? Tox? |
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Definition
Bile acid resins, prevent reabsorption of bile acids, liver uses cholesterol to make more. Lowers LDL, slight HDL increase, slight triglyceride increase Tastes bad, GI discomfort, fat-soluble vitamin def., cholesterol gallstones |
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Definition
Prevent cholesterol reabsorption at brush border Lowers LDL Rare hepatotoxicity |
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Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate Mech? Use? Tox? |
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Definition
Fibrates; upregulate LPL, increase TG clearance large triglyceride reduction, lower LDL, raise HDL Myositis, hepatotoxic, *cholesterol gallstones. |
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Digoxin Mech? Use? Tox? Antidote? |
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Definition
Direct inhibition of Na/K ATPase, indirect increase in Ca, positive inotropy. Stimulates vagus nerve, decreases AV conductivity, SA node activity. CHF, atrial fibrillation. Cholinergic: N/V, diarrhea, blurry yellow vision. ECG: increased PR, decreased QT, T-wave inversion, ventricular tachyarrythmia, hyperkalemia. Worse with renal failure (excretion), hypokalemia (competes for binding), quinidine (protein binding displacement). Slowly normalize K+, lidocaine, anti-dig Fab, Mg++ |
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Definition
Class IA antiarrhythmic: Na channel blocker. Decrease slope of depolarization, prolong cardiac action potential duration (prolong QRS), prolong QT interval. Atrial and ventricular arrhythmias, esp. SVT, reentrant, V-tach. Cinchonism, thrombocytopenia, torsades de pointes. Increased toxicity with hyperkalemia. |
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Procainamide Mech? Use? Tox? |
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Definition
Class IA antiarrhythmic: Na channel blocker. Decrease slope of depolarization (prolong QRS), prolong cardiac action potential duration, prolong QT interval. Atrial and ventricular arrhythmias, esp. SVT, reentrant, V-tach. Drug-induced lupus, thrombocytopenia, torsades de pointes. Increased toxicity with hyperkalemia. |
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Disopyramide Mech? Use? Tox? |
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Definition
Class IA antiarrhythmic: Na channel blocker. Decrease slope of depolarization (prolong QRS), prolong cardiac action potential duration, prolong QT interval. Atrial and ventricular arrhythmias, esp. SVT, reentrant, V-tach. Thrombocytopenia, torsades de pointes. Increased toxicity with hyperkalemia. |
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Definition
Class IB antiarrhythmic: Na channel blocker Decrease slope of depolarization (prolong QRS), shorten cardiac action potential. Preferentially affect ischemic or depolarized tissue. Acute ventricular arrythmias (MI), digitalis-induced arrhytmias. Local anesthetic, CNS stimlation/depression, CV depression. Increased toxicity with hyperkalemia. |
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Definition
Class IB antiarrhythmic: Na channel blocker Decrease slope of depolarization (prolongs QRS), shorten cardiac action potential. Preferentially affect ischemic or depolarized tissue. Acute ventricular arrythmias (MI), digitalis-induced arrhytmias. Local anesthetic, CNS stimlation/depression, CV depression. Increased toxicity with hyperkalemia. |
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Term
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Definition
Class IB antiarrhythmic: Na channel blocker Decrease slope of depolarization (prolongs QRS), shorten cardiac action potential. Preferentially affect ischemic or depolarized tissue. Acute ventricular arrythmias (MI), digitalis-induced arrhytmias. Local anesthetic, CNS stimlation/depression, CV depression. Increased toxicity with hyperkalemia. |
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Definition
Class IC antiarrythmic: Na channel blocker. Decrease slope of depolarization (prolongs QRS), no effect on cardiac action potential length. V-fib, intractable SVT. Last resort. CI: structural abnormalities (post-MI) Proarrythmic, esp. post-MI. AV node block. Increased toxicity with hyperkalemia. |
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Term
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Definition
Class IC antiarrythmic: Na channel blocker. Decrease slope of depolarization (prolongs QRS), no effect on cardiac action potential length. V-fib, intractable SVT. Last resort. CI: structural abnormalities (post-MI) Proarrythmic, esp. post-MI. AV node block. Increased toxicity with hyperkalemia. |
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Definition
Class IC antiarrythmic: Na channel blocker. Decrease slope of depolarization (prolong QRS), no effect on cardiac action potential length. V-fib, intractable SVT. Last resort. CI: structural abnormalities (post-MI) Proarrythmic, esp. post-MI. AV node block. Increased toxicity with hyperkalemia. |
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Class II anti-arrhythmics Mech? Use? Tox? Antidote? |
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Definition
= beta-blockers lower cAMP, lower Ca currents. Slower automaticity. Prolonged PR interval (AV node block). V-tach, SVT, atrial fibrillation and flutter. Asthma/COPD CI, CNS effects. Can decrease insulin release and mask effects of hypoglycemia. Glucagon. |
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Definition
B-SAID block K! Class III antiarrhythmics: K channel blockers Prolong action potential duration, prolong QT interval. Last resort! New arrhythmias, hypotension |
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Definition
B-SAID block K! Class III antiarrhythmics: K channel blockers (sotalol: beta-block and K channel block) Prolong action potential duration, prolong QT interval. Last resort! torsades de pointes, beta-block toxicity |
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Term
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Definition
B-SAID block K! Class III antiarrhythmics: K channel blockers Prolong action potential duration, prolong QT interval. Amiodarone effects lipid membrane, numerous effects. Last resort! **Pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism (PFTs/LFTs/TFTs). Corneal deposits, blue/grey skin discoloration, photosensitivity, neurologic effects, constipation, CV depression. |
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Definition
B-SAID block K! Class III antiarrhythmics: K channel blockers Prolong action potential duration, prolong QT interval. Last resort! Torsades de pointes |
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Definition
B-SAID block K! Class III antiarrhythmics: K channel blockers Prolong action potential duration, prolong QT interval. Last resort! Torsades de pointes |
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Class IV anti-arrhythmics Mech? Use? Tox? |
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Definition
= Non-DHP CCBs: Verapamil, Diltiazem Decrease conduction velocity, increase PR interval. SVT, nodal arrythmias Constipation, flushing, edema, CV depression |
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Adenosine Mech? Use? Tox? Antidote? |
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Definition
Inhibit adenylyl cyclase, hyperpolarize cells. Will abolish AV node re-entrant SVTs, use for Dx. Flushing, hypoTN, chest pain. Block with theophylline. |
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Definition
Adenosine deaminase inhibitor allows for accumulation of adenosine, same effects and uses. |
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Term
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Definition
dihydropyridine CCB (-dipines) block voltage gated Ca channels DHPs: vascular > cardiac HTN, Prinzmetal's angina, Raynauds. Not for typical angina, arrythmias - not cardioselective, reflex tachycardia. Peripheral edema, flushing, dizziness, constipation. |
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Term
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Definition
Phosphodiesterase inhibitor Increases cardiac contractility, decreases preload and afterload. IV only, short term therapy. |
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Steps to lower LDL? Steps to lower TG? Steps to raise HDL? |
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Definition
LDL: Diet & exercise -> Statin -> Ezetimibe. TG: Diet & exercise -> Fibrate -> Niacin HDL: Diet & exercise -> Niacin |
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Term
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Definition
Irreversibly bind presynaptic vesicles in adrenergic neurons. Blocks monoamine transport into vesicles, allowing them to be degraded by MAOs. Cheap anti-hypertensive, not used in developed world anymore due to AEs. Depression (anti-NE and 5HT effects), nasal congestion (anti-adrenergic), increased gastric acid secretion (anti-adrenergic). |
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