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36 Cards in this Set
- Front
- Back
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Digoxin
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Class: Digitalis Glycosides
Use: CHF Mechanism: increase myocardial contraction (+ inotrope) - decrease HR - diuretic action Side Fx: - GI - Cardiac (arrhythmias, brady/tachycardia, most serious - v. tach / v. fib.) - CNS (disorientation, delirium) - Vision (blurry, halos, dark spots) - high Ca increases digitalis toxicity (synergistic) - low K+ increases toxicity (& vice versa)...K+ used to treat toxicity - treatment: - discontinue glycoside & diuretic, then can give KCl orally or i.v. - lidocaine & propranolol for arrhythmias Other:- Quinidine - increases levels of it - antacids, sulfasalazine, bile acid binding resins - decrease levels - renal dx & hypothyroid increase half life - orally "digitalized" to get up to proper dose |
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Dobutamine
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Class: Non-Glycoside Inotropic Agent
Use: severe, refractory CHF Mechanism: β1-adrenergic agonist - causes increased CO (+ inotrope) Side Fx: tolerance, - some tachycardia, arrhythmia Other: given i.v. |
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Dopamine
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Class: Non-Glycoside Inotropic Agent
Use: severe, refractory CHF Mechanism: endogenous catecholamine (+ inotrope) - activates β1-adrenergic receptors - can increase renal blood flow ---> enhances Na & H20 excretion Side Fx: - more tachycardia than dobutamine - tolerance Other: given i.v. |
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Captopril
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Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: CHF - decrease preload & afterload - increase CO & exercise capacity - decrease pulmonary/peripheral congestion Mechanism: inhibit angiotensin converting enzyme --> blocks effects of A-II like vasoconstriction, release of aldosterone (retention of Na & H20) - blocks A-II production in myocardium ----> inhibits A-II mediated hypertrophy in CHF Side Fx:- non-productive cough (via higher levels of bradykinin normally degraded in absence of drug) - too much reduction in BP possible when combined w/ diuretics & other antihypertensives Other: |
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Enalapril
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Class: Angiotensin Converting Enzyme (ACE) Inhibitors
Use: CHF - decrease preload & afterload - increase CO & exercise capacity - decrease pulmonary/peripheral congestion Mechanism: inhibit angiotensin converting enzyme --> blocks effects of A-II like vasoconstriction, release of aldosterone (retention of Na & H20) - blocks A-II production in myocardium ----> inhibits A-II mediated hypertrophy in CHF Side Fx: - non-productive cough (via higher levels of bradykinin normally degraded in absence of drug) - too much reduction in BP possible when combined w/ diuretics & other antihypertensives Other: prodrug - activated by liver ...congested in CHF |
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Losartan
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Class: Angiotensin-II Receptor Blocker
Use: CHF - decrease preload & afterload - increase CO & exercise capacity - decrease pulmonary/peripheral congestion Mechanism: competitive antagonists of A-II - therapeutic fx same as ACE inhibitors - better for inhibiting A-II mediated hypertrophy in CHF (some occurs via ACE-independent pathways) Side Fx: - too much reduction in BP possible when combined w/ diuretics & other antihypertensives - don't cause cough |
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Hydrochlorothiazide
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Class: Thiazide Diuretic
Use: CHF, HTN Mechanism: A) inhibits Na+-Cl- symporter in distal convoluted tubule = NaCl excretion, water diuresis B) action independent of pt's acid-base balance C) ^ excretion of Na+, Cl- K+, H+; decreased excretion of Ca++ - reduce ECF volume & preload - relieve pulmonary congestion & peripheral edema Side Fx: (A) hypokalemia & metabolic alkalosis (increased excretion of K+ & H+ in late distal tubule & collecting duct) B) Gout C) sulfonamide allergy D) Stevens-Johnson syndrome E) hyperglycemia F) increase plasma LDL & total cholesterol, triglycerides G) fatal hyponatremia H) lithium toxicity Other: - thiazides are 1st choice for CHF pts |
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Furosemide
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Class: Loop Diuretic
Use: CHF, HTN Mechanism: (see HTN card) - reduce ECF volume & preload - relieve pulmonary congestion & peripheral edema Side Fx: (see HTN card) Other: |
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Spironolactone
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Class: K+ sparing Diuretic
Use: - aldosterone is high in CHF pts --> causes fluid retention & myocardial fibrosis --> these aldosterone antagonists have dual effect in CHF (also HTN) Mechanism: (see HTN card) - reduce ECF volume & preload - relieve pulmonary congestion & peripheral edema Side Fx: (see HTN card) Other: |
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Hydralazine
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Class: Direct Vasodilators
Use: - pts. w/ severe CHF refractory to other therapies - pts. right after acute MI who had preexisting chronic CHF - HTN Mechanism: primarily afterload reduction - directly dilates arterioles (unknown mechanism) Side Fx: A) alone cause massive dilation of arterioles...increased capillary hyd. pressure = edema B) renal retention of Na+ & water C) drop in BP activates SNS = increased renin, NE, E = greater retention of Na+ & water (tachycardia, edema, loss of efficacy) D) Lupus-like rxn Other: - can be combined w/ Nitrate (increases survival in CHF pts) |
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Nitroprusside
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Class: Direct Vasodilators
Use: - pts. w/ severe CHF refractory to other therapies - pts. right after acute MI who had preexisting chronic CHF Mechanism: - preload & afterload reduction Side Fx: Other: - only i.v (intensive care) |
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Nitroglycerin
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Class: Direct Vasodilators
Use: - pts. w/ severe CHF refractory to other therapies - pts. right after acute MI who had preexisting chronic CHF Mechanism: - primarily preload reduction Side Fx: - tolerance can develop |
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Nesiritide
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Class: Direct Vasodilators
Use: - pts. w/ severe CHF refractory to other therapies - pts. right after acute MI who had preexisting chronic CHF Mechanism: - vasodilator & diuretic - increases cGMP ---> decreases arterial & venous smooth m. tone Side Fx: Other: - only i.v (intensive care) |
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Bisoprolol
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Class: Beta-Blockers
Use: less severe CHF pts. Mechanism: - prevent down regulation of β-adrenergic receptors in myocardium (which prevents CO from going too low) - also prevent tachycardia & arrhythmias - also inhibit renin release from kidney Side Fx: Other: |
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Carvedilol
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Class: Beta-Blockers
Use: less severe CHF pts. Mechanism: - prevent down regulation of β-adrenergic receptors in myocardium (which prevents CO from going too low) - also prevent tachycardia & arrhythmias - also inhibit renin release from kidney Side Fx: Other: - antioxidant & α-blocker as well |
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Nitroglycerin
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Class: Antianginal Drugs - Organic Nitrates
Use: A) can be used to treat all 3 forms of angina: atherosclerotic (stable), Prinzmetal's, vasospastic (unstable) angina B) sublingual tablet - for after start of acute anginal pain Mechanism: A) rapidly release NO in presence of smooth m. cells = increase in cGMP = smooth m. relaxation (esp. venous smooth m.) B) this causes peripheral vascular dilation = reduced preload (low dose) & reduced afterload (high doses) C) reduces myocardial cell oxygen demand (in atherosclerotic angina) Side Fx: A) orthostatic hypotension B) headache C) reflex increase in HR & contractility D) systemic Na+ & water retention E) tolerance F) fatal hypotensive interaction w/ Viagra (& other PDE-5 inhibitors) Other: A) rapidly denitrated in liver...high 1st pass effect |
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Isosorbide Dinitrate
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Class: Antianginal Drugs -Organic Nitrates
Use: A) can be used to treat all 3 forms of angina: atherosclerotic (stable), Prinzmetal's, vasospastic (unstable) angina B) sublingual tablet - for after start of acute anginal pain Mechanism: A) rapidly release NO in presence of smooth m. cells = increase in cGMP = smooth m. relaxation (esp. venous smooth m.) B) this causes peripheral vascular dilation = reduced preload (low dose) & reduced afterload (high doses) C) reduces myocardial cell oxygen demand (in atherosclerotic angina) Side Fx: A) orthostatic hypotension B) headache C) reflex increase in HR & contractility D) systemic Na+ & water retention E) tolerance F) fatal hypotensive interaction w/ Viagra (& other PDE-5 inhibitors) |
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Verapamil
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Class: Antianginal Drugs - Calcium Channel Blockers
Use: A) HTN B) angina (preventative) Mechanism: A) decreases Ca2+ entry through L-type Ca2+ channels in heart ...lowers ventricular contractility = lowers CO Side Fx: Other: |
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Diltiazem
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Class: Antianginal Drugs - Calcium Channel Blockers
Use: A) HTN B) angina (preventative) Mechanism: A) decreases Ca2+ entry through L-type Ca2+ channels in heart ...lowers ventricular contractility = lowers CO Side Fx: A) suppresses HR & A-V conduction (weaker effect than w/ verapamil) B) nausea, headache |
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Nifedipine
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Class: Antianginal Drugs - Calcium Channel Blockers
Use: A) effective in all types of HTN, esp. elderly & African Americans B) work well in pts. w/ high Na+ intake (irrespective of degree of Na+ sensitivity C) primary pulmonary HTN (unique) D) angina (preventative & treatment of acute attacks) Mechanism: A) decreases Ca2+ entry through arterial L-type Ca2+ channels into vascular smooth m. cells = reduction in arterial vascular tone = drop in TPR B) inherent natriuretic capability Side Fx: A) reflex tachycardia (due to peripheral vasodilation) B) nausea, headache C) postural hypotension D) ankle edema Other: |
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Cholestyramine
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Class: Bile Acid Binding Resins
Use: A) high LDL hyperlipoproteinemias (along w/ dietary control & other drugs) MOA: A) exchange Cl- for bile acids in intestine...bile acid-resin complex can't be reabsorbed B) increase in hepatic LDL receptors (b/c liver tries to replace lost bile acids)...plasma [LDL] decreases C) slight increase in HDLs SFx: A) VLDLs may initially rise (prolonged rise in pts. w/ preexisting high VLDLs) B) can cause systemic toxicity (b/c resins not absorbed) C) GI distress D) not very palatable E) resins can sequester, inhibit absorption of other drugs (thiazide diuretics, antibiotics, barbiturates, Ezetimibe)...take at separate times F) interfere w/ fat soluble vitamin & iron absorption G) wt. loss by malabsorption (high dose) PK: A) ion-exchange capacity B) not digested or absorbed from intestinal lumen |
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Colestipol
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Class: Bile Acid Binding Resins
Use: A) high LDL hyperlipoproteinemias (along w/ dietary control & other drugs) MOA: A) exchange Cl- for bile acids in intestine...bile acid-resin complex can't be reabsorbed B) increase in hepatic LDL receptors (b/c liver tries to replace lost bile acids)...plasma [LDL] decreases C) slight increase in HDLs SFx: A) VLDLs may initially rise (prolonged rise in pts. w/ preexisting high VLDLs) B) can cause systemic toxicity (b/c resins not absorbed) C) GI distress D) not very palatable E) resins can sequester, inhibit absorption of other drugs (thiazide diuretics, antibiotics, barbiturates, Ezetimibe)...take at separate times F) interfere w/ fat soluble vitamin & iron absorption G) wt. loss by malabsorption (high dose) PK: A) ion-exchange capacity B) not digested or absorbed from intestinal lumen |
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Lovastatin
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Class: HMG-CoA Reductase Inhibitors
Use: A) reduction of elevated LDL cholesterol (alone or as adjunct w/ diet & other drugs) MOA: A) in liver, inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase (catalyzes conversion of HMG-CoA to mevolonate...rate limiting step in synthesis of cholesterol) B) reduce overall systemic cholesterol C) increased hepatic LDL receptors = more reduction of LDL cholesterol D) VLDLs & IDLs also reduced (statins are most potent LDL & non-LDL cholesterol lowering agents) E) may raise HDLs SFx: A) liver dysfunction (increased serum transaminase...liver function tests recommended) B) myopathy C) GI disturbances, HA, cramps, blurred vision (all mild) D) contraindicated in pregnancy PK: A) prototype drug of group B) oral C) extensive "first-pass" metabolism (inhibited by other drugs & lots of grapefruit juice) D) excreted in feces by secretion in bile E) prodrug...requires activation |
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Pravastatin
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Class: HMG-CoA Reductase Inhibitors
Use: A) reduction of elevated LDL cholesterol (alone or as adjunct w/ diet & other drugs) MOA: A) in liver, inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase (catalyzes conversion of HMG-CoA to mevolonate...rate limiting step in synthesis of cholesterol) B) reduce overall systemic cholesterol C) increased hepatic LDL receptors = more reduction of LDL cholesterol D) VLDLs & IDLs also reduced (statins are most potent LDL & non-LDL cholesterol lowering agents) E) may raise HDLs SFx: A) liver dysfunction (increased serum transaminase...liver function tests recommended) B) myopathy C) GI disturbances, HA, cramps, blurred vision (all mild) D) contraindicated in pregnancy A) oral B) extensive "first-pass" metabolism (inhibited by other drugs & lots of grapefruit juice) D) excreted in feces by secretion in bile E) active as ingested form |
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Simvastatin
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Class: HMG-CoA Reductase Inhibitors
Use: A) reduction of elevated LDL cholesterol (alone or as adjunct w/ diet & other drugs) MOA: A) in liver, inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase (catalyzes conversion of HMG-CoA to mevolonate...rate limiting step in synthesis of cholesterol) B) reduce overall systemic cholesterol C) increased hepatic LDL receptors = more reduction of LDL cholesterol D) VLDLs & IDLs also reduced (statins are most potent LDL & non-LDL cholesterol lowering agents) E) may raise HDLs SFx: A) liver dysfunction (increased serum transaminase...liver function tests recommended) B) myopathy C) GI disturbances, HA, cramps, blurred vision (all mild) D) contraindicated in pregnancy PK: A) oral B) extensive "first-pass" metabolism (inhibited by other drugs & lots of grapefruit juice) D) excreted in feces by secretion in bile |
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Gemfibrozil
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Class: Fibric Acid Analogues (Fibrates)
Use: A) 1° hyperlipidemia B) hypertriglyceridemia secondary to defect in apolipoprotein E MOA: A) increased PPAR-α (receptor) activity = increased lipoprotein lipase activity = increased clearance of VLDL B) increased oxidation of FFA in liver (less available for VLDLs) C) may increase HDLs SFx: A) gallstones (rare) B) GI upset, nausea (common) C) risk of myopathy (esp. combined w/ statin) PK: A) oral B) enterohepatic recycling |
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Fenofibrate
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Class: Fibric Acid Analogues (Fibrates)
Use: A) 1° hyperlipidemia B) hypertriglyceridemia secondary to defect in apolipoprotein E MOA: A) increased PPAR-α (receptor) activity = increased lipoprotein lipase activity = increased clearance of VLDL B) increased oxidation of FFA in liver (less available for VLDLs) C) may increase HDLs SFx: A) gallstones (rare) B) GI upset, nausea (common) C) risk of myopathy (esp. combined w/ statin) PK: A) oral |
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Niacin
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Class: Lipid Lowering Drugs - Other
Use: A) all types of 1° hyperlipidemias MOA: A) inhibits intracellular lipase activity in adipocytes...so inhibits lipolysis = less FFA sent to liver = reduced VLDL synthesis & plasma VLDL B) increases VLDL catabolism (via enhanced activity of extracellular lipoprotein lipase) C) big increased in HDL (most effective drug for this) SFx: A) flushing, itching, burning skin (due to dilation of skin vessels)...mediated by prostaglandin release...decreased w/ aspirin before niacin PK: A) oral B) metabolized to nicotinamide (vitamin) |
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Omega-3-Ethyl Esters
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Class: Lipid Lowering Drugs - Other
Use: A) reduce very high plasma triglcerides MOA: A) inhibits hepatic synthesis of triglycerides from endogenous free fatty acids (via increased oxidation, decreased delivery, decreased synthesis) B) may increase HDL SFx: A) symptoms of flu B) mild GI distress |
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Ezetimibe
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Class: Cholesterol Absorption Inhibitors
Use: A) high LDL type hyperlipoproteinemias (alone or combined w/ others) MOA: A) inhibits intestinal absorption of dietary & biliary cholesterol (by inhibiting protein-mediated transport system) = less cholesterol delivered to liver (via chylomicrons) = induces increase in LDL receptors in hepatic cell membranes = increased hepatic uptake of LDLs = reduced plasma LDL conc. B) may increase HDLs SFx: A) few known if used alone B) Fibrates increase, bile acid binding resins decrease availability of Ezetimibe conc. PK: A) oral, 1x/day B) converted to active metabolite in small intestinal wall cells & liver...recycled back into intestine via enterohepatic circulation |
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Ranolazine
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Class: Fatty Acid Oxidation Inhibitor
Use: A) pts still suffering from chronic stable angina despite taking other agents (used in combination w/ other antianginal agents) MOA: A) may shift source of fuel used by myocardium from fatty acids to glucose (less oxygen demand) B) selective inhibition of pathologic increases in late Na+ current caused by myocardial ischemia (reduces ischemia-induced Ca overload & related O2 demand) SFx: A) dizziness, headache, nausea, constipation B) interacts w/ verapamil & diltiazem = increase in plasma conc. of ranolazine C) contraindicated in pts. w/ cardiac QT prolongation or taking QT-prolonging drugs PK: new oral agent, metabolized in liver |
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Propranolol
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Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonist at β1 & β2-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness E) high lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) all non-cardiac symptoms are less severe w/ cardioselective β-blockers |
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Nadolol
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Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A competitive antagonist at β1 & β2-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness E) low lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) all non-cardiac symptoms are less severe w/ cardioselective β -blockers |
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Timolol
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Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina, arrhythmia, migraine or other dx responsive to β-blockers C) treat "silent" ischemia MOA: A competitive antagonists at β1 & β2-receptors B) also inhibit renin release (from renal JG cells) C) however, inhibition of physiologic B2-mediated vasodilation limits antihypertensive effectiveness D) moderate lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) less severe non-cardiac side fx (b/c of ISA) |
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Atenolol
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Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) low lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) bronchoconstriction (pts. may require inhalable bronchodilator) E) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) F) hypertriglyceridemia, fall in HDLs G) less severe non-cardiac side fx |
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Metoprolol
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Class: β-Adrenergic Receptor Blocker
Use: A) HTN (alone, less effective in elderly & African-American pts) B) best if HTN is associated w/ tachycardia & high CO, or accompanied by angina (preventative esp. for exercise-induced), arrhythmia, migraine C) treat "silent" ischemia MOA: A) competitive antagonists at β1-receptors B) no ISA, so lower BP mainly by reducing CO (contractility, HR) C) also inhibit renin release (from renal JG cells) D) moderate lipid solubility SFx: A) bradycardia (reduced exercise tolerance) B) cardiac arrest (in pts. susceptible to A-V block) C) rebound HTN (w/ sudden withdrawal) D) may exacerbate & mask symptoms of insulin-induced hypoglycemia in diabetics (e.g. tachycardia...but don't block sweating) E) hypertriglyceridemia, fall in HDLs |
