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41 Cards in this Set
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- Back
- 3rd side (hint)
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Essential HTN
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Diuretics, ACE inhibitor, angiotensin II receptor blockers, calcium channel blockers
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CHF
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Diuretics, ACE inhbitors/ARBs. beta blockers, K+ sparing diuretics
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beta blockers are contra-indicated in decompensated heart failure
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DM
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ACEi/ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers
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ACEi protect against diabetic neuropathy
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Hydralazine
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increase cGMP leading to smooth muscle relaxation in the arterioles more than the veins
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Use: sever hypertension, CHF, HTN in pregnancy, with methyldopa. beta blockers prevent reflex tachycardia
Toxicity: compensatory tachycardia (not for angina), fluid retention, nausea, H/A, angina. Lupus-like syndrome |
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Calcium channel blocker
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Nifedipine, verapmil, dilitizaem
block voltage gated L type channels in cardiac and smooth muscle Vascuaturel: nifedipine> dilitiazem>verapmil Heart: verapmil>dilitiazem > nifedipine |
Use: HTN, angina, arrythmias (not nifedipine), Prinzmetal's angina, Raynaud's
Toxicity: Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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Nitroglycerin, isosorbide dintrate
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vasodilation by releasing NO in smooth muscle causing increase in cGMP; dilates veins more than arteries
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Use: angina, pulmonary edema; erection enhancer
Toxicity: reflex tach, hypotension, flushing H/A, Monday disease in industrial exposure (tolerance develops over work week and then weekend and then tachycardia dizziness and H/A on re-exposure) |
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Nitroprusside
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short acting: increase cGMP via direct release of NO
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Use: malignant htn
Toxicity: can cause cyanide toxicity |
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Fenoldopam
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D1 agonist, relazes renal vascular smooth muscle
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Use: malignant HTN
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Dizoxide
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K+ channel opener - hyperpolarizes and relaxes smooth muscle
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Use: malignant HTN
Toxicity: can cause hyperglycemia because it reduces insulin release |
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HMG CoA reductase
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inhibit cholesterol precursor
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effects: significantly lowers LDL, lowes triglycerides and increases HDL
Toxicity: hepatotoxicity, rhabdomyolysis |
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Niacin
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inhibits lypolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
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effects: significantly lowers and raises LDL and HDL, lowers triglycerides
Toxicity: red flushed face which is decreased with aspirin, hyperglycemia (acanthosis nigricans) hyperuricemia |
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Bile acid resins
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cholestyramine, colestipol, colesevelam prevent intestinal reabsorption of bile acids; liver must use cholesterolti make more
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effects: significantly lowers LDL and slightly raises HDL and triglycerides
Toxicity: tastes bad, causes GI discomfort and there is decreased absroption of fat soluble vitamins, also causes cholesterol gall stones |
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ezetimibe
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prevents cholesterol reabsorption at small intestine brush border
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effect: significantly decreases LDL
Toxicity: rare increase in LFTs |
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Fibrates
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gemfibrozil, clofibrate, benafibrate, fenofibrate. upregulate LPL and increase TG clearance
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effect: significant decrease triglycerides, increase HDL and decrease LDL
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digoxin
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75% bioavailability 20-40% protein bound, long half life with urinary excretion
direct inhibition of Na/K ATPase leads to increase in intracellular Ca through inhibition of Na/Ca antiport, stimulates vagus nerve |
Use: CHF, atrial fibrillation (decrease conduction at AV node and depression of SA node
Toxicity: Cholinergic - N/V/D blurry yellow vision; EKG - increase PR and decrease T, T wave incersion, arryhtmia, hyperkalemia; worsened by renal failure, hypokalemia (digoxin binds at K+ site), quinidine (decreases clearance) |
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Quinidine
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Class IA antiarrythmic; increase AP duration, increase effective regractory period, increase QT interval.affect both atrial and ventricular arrythmias, especially re-entrant and extopic supraventricular and v tach
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Toxicity: cinchonism -- h/a tinnitus); thrombocytopenia torsades de pointes due to increase QT interval,
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Procainamide
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Class IA antiarrythmic; increase AP duration, increase effective regractory period, increase QT interval.affect both atrial and ventricular arrythmias, especially re-entrant and extopic supraventricular and v tach
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Toxicity: SLE-like syndrome, thrombocytopenia torsades de pointes due to increase QT interval,
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Disopyramide
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Class IA antiarrythmic; increase AP duration, increase effective regractory period, increase QT interval.affect both atrial and ventricular arrythmias, especially re-entrant and extopic supraventricular and v tach
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Toxicity: thrombocytopenia torsades de pointes due to increase QT interval,
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Lidocine
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Class II anti-arrythmic, decrease AP duration,preferentially affect ischemicor deplarized Purkinje and ventricular tissue
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Use: post MI, acute centricular arrythmias, and in digitalis induced arrythmias
Toxicity: local anesthetic, CNS stimulation/depression, cardiovascular depression |
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Mexiletine
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Class II anti-arrythmic, decrease AP duration,preferentially affect ischemicor deplarized Purkinje and ventricular tissue
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Use: post MI, acute centricular arrythmias, and in digitalis induced arrythmias
Toxicity: local anesthetic, CNS stimulation/depression, cardiovascular depression |
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Tocainide
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Class II anti-arrythmic, decrease AP duration,preferentially affect ischemicor deplarized Purkinje and ventricular tissue
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Use: post MI, acute centricular arrythmias, and in digitalis induced arrythmias
Toxicity: local anesthetic, CNS stimulation/depression, cardiovascular depression |
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Flecainide
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Class III anti-arrythmic, no effect on AP duration, useful in V Tach that progresses to V fib and in intractable SVT
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Use: last resort in refractory tachyarryhtmias, not for pts with structural abnormaliites
Toxicity: pro-arryhtmic, especially post MI, significnat prolons refractory period in AV node |
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Encainide
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Class III anti-arrythmic, no effect on AP duration, useful in V Tach that progresses to V fib and in intractable SVT
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Use: last resort in refractory tachyarryhtmias, not for pts with structural abnormaliites
Toxicity: pro-arryhtmic, especially post MI, significnat prolons refractory period in AV node |
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Propafenone
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Class III anti-arrythmic, no effect on AP duration, useful in V Tach that progresses to V fib and in intractable SVT
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Use: last resort in refractory tachyarryhtmias, not for pts with structural abnormaliites
Toxicity: pro-arryhtmic, especially post MI, significnat prolons refractory period in AV node |
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Class I antiarrythmics
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local anesthetics, slow or block conduction in depolarized cells. decrease slope of phase 0 and increase threshold for diring in abnoraml pacemaker cells. state dependent fro tissue that is frequently depolarized
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sodium channel blockers
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Class II antiarrythmics
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beta blockers
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beta blockers
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propanol
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decrease cAMP, and Ca currents. suppress abnormal pace makers by decreasing slope of phase 4, AV node is particualr sensitive to increased PR interval
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se: V tach, SVT, sloweing ventricular rtes during a Fib and flutter
Toxicity: impotence, exacerbation of asthma, CV effects - bradycardia, AV block, CHF, CNS effects - sedation, sleep alteration. may mask signs of hypoglycemia |
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esmolol
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decrease cAMP, and Ca currents. suppress abnormal pace makers by decreasing slope of phase 4, AV node is particualr sensitive to increased PR interval
short acting |
se: V tach, SVT, sloweing ventricular rtes during a Fib and flutter
Toxicity: impotence, exacerbation of asthma, CV effects - bradycardia, AV block, CHF, CNS effects - sedation, sleep alteration. may mask signs of hypoglycemia |
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metoprolol
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decrease cAMP, and Ca currents. suppress abnormal pace makers by decreasing slope of phase 4, AV node is particualr sensitive to increased PR interval
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se: V tach, SVT, sloweing ventricular rtes during a Fib and flutter
Toxicity: impotence, exacerbation of asthma, CV effects - bradycardia, AV block, CHF, CNS effects - sedation, sleep alteration. may mask signs of hypoglycemia can cause hyperlipidemia |
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atenolol
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decrease cAMP, and Ca currents. suppress abnormal pace makers by decreasing slope of phase 4, AV node is particualr sensitive to increased PR interval
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se: V tach, SVT, sloweing ventricular rtes during a Fib and flutter
Toxicity: impotence, exacerbation of asthma, CV effects - bradycardia, AV block, CHF, CNS effects - sedation, sleep alteration. may mask signs of hypoglycemia |
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timolol
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decrease cAMP, and Ca currents. suppress abnormal pace makers by decreasing slope of phase 4, AV node is particualr sensitive to increased PR interval
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se: V tach, SVT, sloweing ventricular rtes during a Fib and flutter
Toxicity: impotence, exacerbation of asthma, CV effects - bradycardia, AV block, CHF, CNS effects - sedation, sleep alteration. may mask signs of hypoglycemia |
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sotalol
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increase AP duration, increase effective refractory period, used when other anti-arrythmics fail, increase QT interval
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torsades de pointes, excessive beta block
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ibutilide
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class III, increase AP duration, increase effective refractory period, used when other anti-arrythmics fail, increase QT interval
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torsades de pointes
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bretylium
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class III, increase AP duration, increase effective refractory period, used when other anti-arrythmics fail, increase QT interval
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new arrythmias, hypotension
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dofetilide
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class III, increase AP duration, increase effective refractory period, used when other anti-arrythmics fail, increase QT interval
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amidoarone
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Class III, increase AP duration, increase effective refractory period, used when other anti-arrythmics fail, increase QT interval
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pulmonary fibrosis, hepatotoxicity, hypothyroidism/hypertheyroidism, corneal deposits, skin deposits resulting in phtodermatitis, neurologic effects, constipation, CV effects - bradycardia, heart block, CHF
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verapamil
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decrease conduction velocity, increase ERP and PR interval
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Use: prevention of nodal arrythmias (like SVT)
Toxicity: constipation, flushing, edema, CV effects - CHF AV block, sinus node depression |
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dilitiazem
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decrease conduction velocity, increase ERP and PR interval
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Use: prevention of nodal arrythmias (like SVT)
Toxicity: constipation, flushing, edema, CV effects - CHF AV block, sinus node depression |
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adenosine
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increase potassium out of cells hyperpolarizes cell and decreases ca current
very short acting |
Use: dxing abolishing supraventricular tachycardia
Toxicity: flushing, hypotension, chest pain, blocked by theophylline |
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potassium
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depress ectopic pacemakers in hypokalemia
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Use: digoxin toxicity
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magnesium
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effective in torsades de pointes and digoxin toxicity
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