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116 Cards in this Set
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Mechanism: Bind bile ← excrete in stool ← increase hepatic bile synthesis ← reduce LDL from blood
Response: ↓LDL (25%), ↑TG, ↑HDL (5%) |
Bile-Acid Binding Resins
Cholestyramine, Colestipol |
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Use: Hypercholesterolemia from LDLs
Effects: bloating, constipation Other: Effect offset by the increase of LDL creation; administration of statins makes it more effective |
Bile-Acid Binding Resins
Cholestyramine, Colestipol |
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Mechanism: Inhibit HMG-CoA reductase (rate-limiting step) in cholesterol synthesis; liver takes up LDLs
Response: ↓LDL (55%), ↓TG (45%), ↑HDL (10%) |
Statins
Atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin |
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Use: Coronary artery disease (CAD)
Effects: myopathy, hepatotoxicity Other: ↑ endothelial cell function, ↑ plaque stability, ↓inflammation |
Statins
Atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin |
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Mechanism: Inhibits transportation in jejunum (NPC1L1), increased synthesis in liver, LDL uptake
Response: ↓LDL (20%), ↓TG (5%), ↑HDL (2%) |
Cholesterol Absorption Blocker
Ezetimibe |
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Use: Adjunct w/ statins
Effects: Allergic reactions Other: Should NOT be used in conjunction w/ bile-acid binding resins |
Cholesterol Absorption Blocker
Ezetimibe |
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Mechanism: Inhibits lypolysis of TG ← stops transport of FFA into liver. Inhibits esterification of FA.
Response: ↓VLDL , ↓LDL (25%), ↓TG (50%), ↑HDL (40%) |
Niacin
Niacin (Nicotinic Acid) |
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Use: Hypertriglyceremia and w/ low HDL levels
Effects: flushing, heptatoxicity, insulin-resistance, gout Other: Niacin + Statins = myopathy. Sustained-release is best for pt. |
Niacin
Niacin (Nicotinic Acid) |
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Mechanism: Bind to PPARα ← reduces TG by stimulation of FA oxidation, ↑lipoprotein lipase synthesis, ↓apoC-III. HDL increase due to stimulation of apoA-I and apoA-II.
Response: ↓LDL (20%), ↓TG (50%), ↑HDL (10%) |
Fibrates
Fenofibrate, Gemfibrozil, Clofibrate |
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Use: Severe hypertriglyceridemia, ↑TG w/ ↓HDLs (assoc. w/ metabolic syndrome [Type II diabetes])
Effects: GI, hair loss Other: Fibrates + Statins = Myopathy. Increase LDL in some pt. |
Fibrates
Fenofibrate, Gemfibrozil, Clofibrate |
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Mechanism: Releases NO → activates guanylate cyclase → ↑cGMP → vasorelaxation; inhibit platelet aggregation
Response: ↓ venous/artery constriction (primary action in stable angina), ↓ arterial contraction, ↑ myocardial O2 supply, ↓O2 demand |
Nitrates
Nitroglycerin, Isosobide dinitrate, isosorbide 5-mononitrate Angina |
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Use: sublingual/IV/inhalation – fast - stop angina. Oral/patch/ointment – slow - prophylaxis
Effects: headache, hypotension Other: sildenafil (ED drugs) enhance effect of nitrates, tolerance ← MAJOR problem |
Nitrates
Nitroglycerin, Isosobide dinitrate, isosorbide 5-mononitrate Angina |
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Mechanism: Block β-receptors
Response: ↓HR/contractility/blood pressure/O2 demand, ↑O2 supply, coronary a. flow |
β-adrenergic blockers
atenolol, metoprolol, nadolol, propranolol Angina |
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Use: Chronic prophylaxis in stable angina
Effects: cardiac, bronchoconstriction, lethargy, fatigue, depression, nightmares, hypoglycemia Other: Careful w/ cardiac conduction issues, COPD. Withdrawal can cause angina |
β-adrenergic blockers
atenolol, metoprolol, nadolol, propranolol Angina |
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Mechanism: NON-competitively inhibit Ca++ through voltage-senstive L-type channels; slow channel recovery time (V/D)
Response: ↓HR/contractility (V/D), ↓arterial/coronary artery contraction, ↓myocardial O2 demand, ↑O2 supply |
Ca++ channel blockers
Dihydropuridines [Nifedipine/SR, nicardipine, amlopdipine, nisoldipine], dilitaizem/SR, verapamil/SR Angina |
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Use: Chronic prophylaxis of stable/variant angina
Effects: Headache, hypotension, leg edema, constipation Other: Careful w/ cardiac conduction issues; do NOT use w/ β-blockers (V/D) |
Ca++ channel blockers
Dihydropuridines [Nifedipine/SR, nicardipine, amlopdipine, nisoldipine], dilitaizem/SR, verapamil/SR Angina |
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Mechanism: Na+ channel blocker “late” ←no increase in intracellular Na+/Ca++. Inhibits FA oxidation
Response: NO change to BP/HR. ↑exercise tolerance, ↓wall tension (cell swelling) |
Ranolazine
Angina |
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Use: Chronic prophylaxis of stable angina, used in combination w/ anything
Effects: Dizziness, headache, constipation Other: Unaffected by age/other conditions |
Ranolazine
Angina |
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Mechanism: Irreversibly binds COX-1, blocking synthesis of TxA2 → ↓platelet aggregation (7-10 days)
Response: >50% decrease in death or MI |
Aspirin
Anti-Platelet Drug Unstable Angina |
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Use: LOW doses preferred
Effects: Bleeding, allergic response Other: 5-8% show resistance ← pt. more likely to have poor prognosis |
Aspirin
Anti-Platelet Drug Unstable Angina |
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Mechanism: Inhibits ADP binding to platelets ← ↓platelet aggregation/activation
Response: 35% reduction in death or MI |
ADP inhibitors
Clopidogrel, ticlopidine ← both PRO-drugs Anti-Platelet Drugs Unstable Angina |
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Use: Slow onset of effect; 4-8 day effect ← used in conjunction w/ aspirin
Effects: neutropenia, thrombotic thrombocytopenic purpura, bleeding Other: Clopidogrel better/faster/less side effects than ticlopidine, HOWEVER there is some resistance |
ADP inhibitors
Clopidogrel, ticlopidine ← both PRO-drugs Anti-Platelet Drugs Unstable Angina |
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Mechanism: prevents fibrinogen crosslinking ← ↓aggregation
Response: ↓MI (9%), early treatment ← better outcomes |
Glycoprotein (GP) IIb/IIIa receptor inhibitors
Abciximab, eptifibatide, tirofiban Anti-Platelet Drugs Unstable Angina |
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Use: IV only; short half-life, used w/ aspirin/heparin/ADP inhibitors
Effects: thrombocytopenia Other: Best used prior to percutaneous coronary interventions |
Glycoprotein (GP) IIb/IIIa receptor inhibitors
Abciximab, eptifibatide, tirofiban Anti-Platelet Drugs Unstable Angina |
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Mechanism: Inhibits coagulation proteases by antithrombin (intrinsic/common pathway factors Xa/IXa). LMWH acts on factor Xa
Response: ↓MI/death – heparin (33%), LMWH (66%) |
Heparin
Unfractionated heparin, low molecular weight heparin, enoxaparin Anitcoagulant |
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Use: Heparin – IV. LMWH – SubQ. LMWH is better
Effects: Risk of bleeding/thrombocytopenia Other: resistance to heparin |
Heparin
Unfractionated heparin, low molecular weight heparin, enoxaparin Anitcoagulant |
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Mechanism: Sulfated pentasaccharide; binds to antithrombin and does selective inhibition of factor Xa
Response: Efficacy similar to heparin |
Fondaparinux
Anitcoagulant |
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Use: SubQ; long half-life/100% bioavailability ← no need for monitoring of clotting time
Effects: Bleeding; reduced compared to heparin ←thus better for long term use Other: More cost effective than enoxaparin |
Fondaparinux
Anitcoagulant |
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Mechanism: Bind to catalytic site of thrombin and stop substrate binding
Response: Produce anti-coagulation, but efficacy unknown |
Direct Thrombin inhibition
Lepiridun, bivalirudin, argatroban Anitcoagulant |
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Use: IV
Effects: Bleeding Other: Unknown efficacy at this time |
Direct Thrombin inhibition
Lepiridun, bivalirudin, argatroban Anitcoagulant |
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Mechanism: Binds to fibrin and readily activates BOUND plasminogen ← activation of lytic cycle
Response: restores coronary flow; improves myocardial function/survival (18%) |
Fibrinolytics
alteplase, reteplase, tenecteplase Treating MI |
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Use: IV; best when given <2 hrs after onset of symptoms
Effects: bleeding; stroke ← DO NOT give heparin! Other: good results in diabetic patients. Poor results in elderly or those with HTN. |
Fibrinolytics
alteplase, reteplase, tenecteplase Treating MI |
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Mechanism: Stimulate μ-type opioid receptors in brain/spinal cord
Response: Reduce pain/anxiety/autonomic activity. ↓venous/arterial contraction, ↓cardiac O2 demand |
Analgesics
Morphine, meperidine, pentazocine Treating MI |
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Use: IV to reduce pain; sometimes LARGE doses are necessary
Effects: hypotension, ↓respiration, vomiting Other: Used in unstable angina |
Analgesics
Morphine, meperidine, pentazocine Treating MI |
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Mechanism: Inhibit ACE (ACEI); block angiotensin’s access to the AT-1 receptor (ARB)
Response: ↓venous/arterial contraction, ↓sympathetic activity, ↑renal Na+/H2O excretion, reduce ventricular remodeling |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) Treating MI |
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Use: administered after aspirin/β-blockers, etc…
Effects: hypotension, cough (ACEI), angioedema (ACEI) Other: Good for elderly or those w/ previous MI/COPD |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) Treating MI |
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Mechanism: stop vit. K activation ← stop activation of factors II, VII, IX, X (to help remember; 2+7=9; 10)
Response: ↓growth of existing thrombi; stop new thrombi |
Oral anticoagulants
Warfarin, etc… Post-MI Prevention |
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Use: Anticoagulation; check effect by monitoring prothrombin time
Effects: Bleeding (7%), skin necrosis, MANY drug interactions Other: liver disease increases warfarin effect; ↑vit. K intake →↓warfarin effect |
Oral anticoagulants
Warfarin, etc… Post-MI Prevention |
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_________ Dysfunction
Impaired contractility (in ventricles) ← due to myocardial ischemia (primarily) MAJOR cause is ischemia overall decrease in EF (>55% → 20%) |
Systolic Dysfunction
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_________ Dysfunction
Most common drugs to use: diuretics, renin-angiotensin system inhibitors, β-blockers, aldosterone antagonists Used to treat ‘acute’ issues: diuretics, nitrates, β-agonists, phosphodiesterase inhibitors |
Systolic Dysfunction
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________ Dysfunction
Decreased compliance (ability to stretch/expand) and pumping efficiency MAJOR cause is HTN/diabetes |
Diastolic Dysfunction
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________ Dysfunction
More difficult to treat Heart failure symptoms ← fatigue, exercise intolerance, exertional dyspnea, pulmonary/systemic edema ← due to increased filling pressures in the heart Sudden worsening of heart failure ← called ‘acute decompensation’ |
Diastolic Dysfunction
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Mechanism: Reversibly inhibit Na+-K+-2CL- transporter in thick ascending loop of Henle
Response: ↑excretion of Na+/H2O/K+/Ca++/Mg++/Cl-/H+; ↑venous capacity ← BOTH ↓preload/edema |
Loop Diuretics ← MOST efficacious of ALL diuretics
Furosemide (Lasik), bumetanide, torsemide, ethacrynic acid - Survival |
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Use: Diuretics!; used for both acute (IV) and chronic cases (oral); survival increase?!
Effects: K+ depletion; metabolic alkalosis Other: Resistance in heart failure pts. ← add thiazide to overcome. Potentiated w/ renin-angio inhib. |
Loop Diuretics ← MOST efficacious of ALL diuretics
Furosemide (Lasik), bumetanide, torsemide, ethacrynic acid - Survival |
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Mechanism: Inhibit Na+/Cl- transporter on luminal part of distal convoluted tubule
Response: ↑excretion of Na+/H2O/K+/ Mg++/Cl-/H+ BUT ↓Ca++ ; ↓preload/edema |
Thiazide diuretics
hydrocholorothiazide, metolazone, chlorthalidone, etc. - Survival |
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Use: ONLY for chronic heart failure
Effects: K+ depletion, ↑uric acid/glucose Other: Potentiated by renin-angiotensin inhibitors |
Thiazide diuretics
hydrocholorothiazide, metolazone, chlorthalidone, etc. - Survival |
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Mechanism: Block luminal Na+ channels in distal tubule/collecting duct
Response: ↑excretion of Na+/H2O/ Cl-, BUT ↓Ca++/K+/ Mg++/ H+ |
Potassium sparing diuretics
Amiloride, triamterene - Survival |
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Use: W/ other diuretics to prevent K+ loss
Effects: hyperkalemia, GI Other: DO NOT confuse w/ aldosterone antagonists (which also K+-sparing diuretics) |
Potassium sparing diuretics
Amiloride, triamterene - Survival |
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Mechanism: Block EXPRESSION of luminal Na+ channels; competitive antagonist of aldosterone receptor in kidney
Response: ↑excretion of Na+/H2O/ Cl-, BUT ↓Ca++/K+/ Mg++/ H+ ; ↓ventricular remodeling |
Aldosterone Antagonists
Spironolactone, eplerenone + Survival + |
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Use: ↑survival (25%) for pt. w/ severe HF
Effects: hyperkalemia, gynecomastia, impotence/menstrual irregularities (spir.) Other: -- |
Aldosterone Antagonists
Spironolactone, eplerenone + Survival + |
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Mechanism: Inhibit ACE (ACEI); block angiotensin’s access to the AT-1 receptor (ARB)
Response: ↓venous/arterial contraction, ↓sympathetic activity, ↑renal Na+/H2O excretion, reduce ventricular remodeling |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) + Survival + |
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Use: administered after aspirin/β-blockers, etc…
Effects: hypotension, cough (ACEI), angioedema (ACEI) Other: Good for elderly or those w/ previous MI/COPD |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) + Survival + |
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Mechanism: Competitively block β-receptors; carvedilol ← direct vasodilator
Response: ↓vectricular remodeling; ↓arrhythmias; ↓ cardiac work ← ↓HR |
β-adrenergic blockers
metoprolol, carvedilol, bisprolol + Survival + |
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Use: Start w/ LOW doses; ↑survival (35%); chronic failure ONLY
Effects: cardiac, bronchoconstriction, lethargy, fatigue, depression, nightmares, hypoglycemia Other: Careful w/ cardiac conduction issues, COPD. Withdrawal can cause angina |
β-adrenergic blockers
metoprolol, carvedilol, bisprolol + Survival + |
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Mechanism: Unknown
Response: ↓arteriolar contraction → ↓afterload → ↓cardiac work |
Direct arterial vasodilators
Hydralazine + Survival + w/Nitrates |
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Use: ↑survival when used w/ isosorbide dinitrate
Effects: headache, tachycardia, edema Other: hydralazine + isosorbide dinitrate = better than ACEI/ARB for African Americans |
Direct arterial vasodilators
Hydralazine + Survival + w/Nitrates |
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Mechanism: Releases NO → activates guanylate cyclase → ↑cGMP → vasorelaxation; inhibit platelet aggregation
Response: ↓ venous/artery constriction ← ↓preload (primary action in stable angina), ↓ arterial contraction (↓afterload), ↓pulmonary/systemic edema, ↑ myocardial O2 supply, ↓O2 demand |
Nitrates
Nitroglycerin, Isosobide dinitrate, isosorbide 5-mononitrate + Survival + w/ Hydralazine |
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Use: sublingual/IV/inhalation – fast - stop angina. Oral/patch/ointment – slow - prophylaxis
Effects: headache, hypotension Other: sildenafil (ED drugs) enhance effect of nitrates, tolerance ← MAJOR problem |
Nitrates
Nitroglycerin, Isosobide dinitrate, isosorbide 5-mononitrate + Survival + w/ Hydralazine |
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Mechanism: Binds to α-subunit of Na+-K+-ATPase ← inhibits sodium transport out of cell ← ↑intracellular Na+ ← reduces Na+-Ca++ exchanger ← ↑intracellular Ca++ ← ↑cardiac contractility
Response: ↑cardiac output, ↓filling pressures; ↑exercise tolerance, ↓edema; ↓sym/↑parasym |
Digoxin
- Survival |
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Use: SEVERE HF or atrial fib.; no increase in survival
Effects: anorexia, vomiting, blurred vision, arrhythmias Other: MANY drug interactions; K+/digoxin antibodies used to treat overdose |
Digoxin
- Survival |
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Mechanism: activate β-receptors ← ↑cardiac contractility, ↑renal blood flow; stimulate α-adrenergic
Response: ↑cardiac output; ↓filling pressures |
β-adrenergic agonists
dopamine, dobutamine - Survival |
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Use: ACUTE failure only; maintains circulatory stability
Effects: tachycardia, arrhythmias Other: Dobutamine infused for DAYS in severe cases |
β-adrenergic agonists
dopamine, dobutamine - Survival |
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Mechanism: Inhibit phosphodiesterase type IIIa → ↑cAMP → ↑intracellular Ca++
Response: ↑cardiac contractility/reate of relaxation; ↑cardiac output; ↓filling pressure; ↓venous/arterial contraction |
Phosphodiesterase inhibitors
Amrinone, milrinone, enoximone |
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Use: ACUTE HF; maintains circulatory stability
Effects: Hypotension, arrhythmias Other: Drug of choice for those on β-blockers; chronic therapy DECREASED survival! |
Phosphodiesterase inhibitors
Amrinone, milrinone, enoximone |
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Mechanism: recombinant human B-type natriuretic peptide
Response: ↓venous/arterial contraction; ↑cardiac output; ↓filling pressures |
Nesiritide
- Survival |
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Use: ACUTE HF; maintains circulatory stability
Effects: hypotension, increased plasma creatinine Other: ↑mortality/renal failure |
Nesiritide
- Survival |
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Class ___
Block Na+ and K+ channels ↓ conduction, ↑ refractoriness, ↓ automaticity |
Class IA Anti-Arrhythmic Drugs
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Class ___
Block Na+ channels ↓ conduction, ↓ automaticity |
Class IB Anti-Arrhythmic Drugs
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Class ___
STRONGLY Block Na+ channel ↓↓ conduction, ↓ automaticity |
Class IC Anti-Arrhythmic Drugs
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Class ___
Blockage of β-receptors ↓ AV conduction, ↓ automaticity |
Class II Anti-Arrhythmic Drugs
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Class ___
Blockage of K+ channels ↑ refractoriness |
Class III Anti-Arrhythmic Drugs
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Class ___
Blockage of Ca++ channels ↓ AV conduction, ↓ triggered activity |
Class IV Anti-Arrhythmic Drugs
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Block Na+/K+-ATPase
↓ AV conduction |
Digoxin Anti-Arrhythmic
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Increase K+ channel opening
↓ AV conduction |
Adenosine Anti-Arrhythmic
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___ Complex
Direct association w/ conduction velocity Ex. INCREASED___ = general decreased conduction velocity |
QRS Complex
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___ Complex
Direct association w/ refractoriness Ex. INCREASED ___ = increased refractoriness |
QT Complex
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___ Complex
Direct association w/ delay at AV node Ex. INCREASED ___ = increased delay at AV node |
PR Complex
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Chronic ______ dysfunctions
NO DRUGS are proven to increase survival HOWEVER, drugs that reduce preload (anti-hypertensive) are used to slow progression |
Chronic Diastolic Dysfunctions
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Mechanism: Block Na+ and K+ channels
Response: ↓ conduction, ↑ refractoriness, ↓ automaticity EKG: ↑ QRS, ↑ QT |
Class IA
Quinidine, Procainamide, Disopyramide |
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Use: Wide-array of supraventricular or ventricular arrhythmias due to ectopic/reentry automaticity. Can stop atrial arrhythmias (flutter/fibrillation)
Other: Causes arrhythmias, decreases ventricular contractility, muscarinic antagonist |
Class IA
Quinidine, Procainamide, Disopyramide |
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Mechanism: Block Na+ channels (in ischemic or damaged tissue)
Response: ↓ conduction, ↓ automaticity |
Class IB
Lidocaine, Mexiletine, Phenytoin |
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EKG: ↓ QT
Use: Ventricular arrhythmias associated w/ re-entry/ectopic automaticity. Long QT syndrome. Digoxin induced arrhythmias Other: NO effect in normal hearts. Lidocaine administered parenterally |
Class IB
Lidocaine, Mexiletine, Phenytoin |
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Mechanism: Block Na+ channels STRONGLY (but slowly)
Response: ↓↓ conduction, ↓ automaticity |
Class IC
Flecainide, Moricizine, Porpafenone |
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EKG: ↑↑ QRS
Use: Major ventricular arrhythmias from re-entry. Atrial flutter/fibrillation, AV node re-entry tachycardia Other: Causes arrhythmias, decreases ventricular contractility |
Class IC
Flecainide, Moricizine, Porpafenone |
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Mechanism: Block β-receptors
Response: ↓ AV conduction, ↓ automaticity |
Class II
Propranolol, Acebutolol, Timolol, *-olol |
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EKG: ↑ PR
Use: Arrhythmias associated w/ sympathetic nerve drive (stress, exercise, surgery, etc…). Ventricular rate control w/ atrial flutter/fibrillation. Long QT syndrome Other: Decreased death after a MI. Will affect normal and damaged hearts |
Class II
Propranolol, Acebutolol, Timolol, *-olol |
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Mechanism: Block K+ channels
Response: ↑ refractoriness, ↓ automaticity |
Class III
Amiodarone, Bretylium, Sotalol, Ibutilide, *-ilide |
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EKG: ↑QT, ↓ PR
Use: Supraventricular/ventricular automaticity due to re-entry/ectopic. Can stop atrial fib./flutter. Used when treating ventricular arrhythmias associated w/ cardiac resuscitation. Good for pt. w/ heart failure Other: Amiodarone blocks α/β adrenergic receptor, and Ca++/Na+ channels. *-ilide drugs stop atrial fibrillation/flutter |
Class III
Amiodarone, Bretylium, Sotalol, Ibutilide, *-ilide |
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Mechanism: Block Ca++ channels
Response: ↓ AV conduction, ↓ automaticity |
Class IV
Verapamil, Diltiazem |
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EKG: ↑ PR
Use: AV node re-entry tachycardia. Ventricular rate control w/ atrial flutter/fibrillation |
Class IV
Verapamil, Diltiazem |
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Mechanism: Block Na+/K+ ATPase
Response: ↓ AV conduction |
Digoxin
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EKG: ↑ PR
Use: Ventricular rate control w/ heart failure, and atrial fibrillation Other: High risk of arrhythmia induction. Increased cell contractility. ↓ sympathetic activity and ↑ parasympathetic activity |
Digoxin
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Mechanism: Increase K+ channel opening, adenylate cyclase inhibitor
Response: ↓ AV conduction, ↓ sinus node rate, ↓ intracellular cAMP |
Adenosine
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EKG: ↑ PR
Use: AV nodal re-entry tachycardia ← may present as an anxiety attack Other: VERY SHORT duration. IV administration. |
Adenosine
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Mechanism: Reversibly inhibit Na+/Cl- transporter on luminal part of distal convoluted tubule
Response: ↑excretion of Na+/H2O/K+/ Mg++/Cl-/H+ BUT ↓Ca++ ; ↓plasma volume/extracellular fluid/CO. Activates renin-angiotensin system ← this offsets the overall effect |
Thiazide Diuretics ← FIRST step in HTN (except those w/ other pre-existing conditions)
hydrocholorothiazide, metolazone, chlorthalidone, etc. HTN |
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Use: Initial mono-therapy. Blacks/eldery respond best.
Effects: K+ depletion, Mg++ loss, ↑uric acid/glucose Other: Potentiated by renin-angiotensin inhibitors |
Thiazide Diuretics ← FIRST step in HTN (except those w/ other pre-existing conditions)
hydrocholorothiazide, metolazone, chlorthalidone, etc. HTN |
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Mechanism: Reversibly inhibit Na+-K+-2CL- transporter in thick ascending loop of Henle
Response: ↑excretion of Na+/H2O/K+/Ca++/Mg++/Cl-/H+; plasma volume/extracellular fluid/CO. Activates renin-angiotensin system ← this offsets the overall effect |
Loop Diuretics
Furosemide (Lasik), bumetanide, torsemide, ethacrynic acid HTN |
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Use: Most effective diuretics, but NOT AS GOOD for lowering BP
Effects: K+ depletion; metabolic alkalosis Other: Resistance in heart failure pts. ← add thiazide to overcome. Potentiated w/ renin-angio inhib. |
Loop Diuretics
Furosemide (Lasik), bumetanide, torsemide, ethacrynic acid HTN |
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Mechanism: Block luminal Na+ channels in distal tubule/collecting duct
Response: ↑excretion of Na+/H2O/ Cl-, BUT ↓Ca++/K+/ Mg++/ H+ |
Potassium sparing diuretics
Amiloride, triamterene HTN |
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Use: W/ other diuretics to prevent K+ loss
Effects: hyperkalemia, GI Other: DO NOT confuse w/ aldosterone antagonists (which also K+-sparing diuretics) |
Potassium sparing diuretics
Amiloride, triamterene HTN |
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Mechanism: Block EXPRESSION of luminal Na+ channels; competitive antagonist of aldosterone receptor in kidney
Response: ↑excretion of Na+/H2O/ Cl-, BUT ↓Ca++/K+/ Mg++/ H+ |
Aldosterone Antagonists
Spironolactone, eplerenone HTN |
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Use: In combination w/ other diuretics due to low efficacy; or those w/ resistant HTN
Effects: hyperkalemia, gynecomastia, impotence/menstrual irregularities (spir.) Other: eplerone better at lowering BP; more adverse effects than K+-sparing diuretics |
Aldosterone Antagonists
Spironolactone, eplerenone HTN |
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Mechanism: Competitively block β-receptors; carvedilol ← direct vasodilator
Response: ↓CO/renin release; ↓sympathetic nervous system →↓ BP |
β-adrenergic blockers
metoprolol, carvedilol, bisprolol HTN |
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Use: Start w/ LOW doses; young/middle-aged people, especially non-black
Effects: cardiac, bronchoconstriction, lethargy, fatigue, depression, nightmares, hypoglycemia Other: Careful w/ cardiac conduction issues, COPD. Withdrawal can cause angina. Helpful also in cases such as migraine headaches/anxiety, etc… |
β-adrenergic blockers
metoprolol, carvedilol, bisprolol HTN |
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Mechanism: NON-competitively inhibit Ca++ through voltage-senstive L-type channels; slow channel recovery time (V/D)
Response: ↓arteriolar contraction → ↓TPR; mild diuretic effects |
Ca++ channel blockers
Dihydropuridines [Nifedipine/SR, nicardipine, amlopdipine, nisoldipine] ← these used predominately; dilitaizem/SR, verapamil/SR HTN |
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Use: All ages/races; better for stroke prevention than MI
Effects: Headache, hypotension, leg edema, constipation; vasodilation effects less significant in V/D Other: MOST antihypertensive drugs have reduced efficacy for those on NSAIDs, not so for these |
Ca++ channel blockers
Dihydropuridines [Nifedipine/SR, nicardipine, amlopdipine, nisoldipine] ← these used predominately; dilitaizem/SR, verapamil/SR HTN |
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Mechanism: Inhibit ACE (ACEI); block angiotensin’s access to the AT-1 receptor (ARB)
Response: ↓actions of angiotensin II; ↓a/v contraction; ↓SNS → ↓TPR; ↑sodium/H2O excretion |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) HTN |
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Use: Less effective in blacks/elderly; potentiated w/ use of a diuretic; protective against neuropathy/coronary artery disease and HF
Effects: well-tolerated; hypotension, cough (ACEI), angioedema (ACEI) Other: No effect in combining ACEI and ARB ← fewest side effects |
Renin angiotensin inhibitors
ACE inhibitors (ACEI) (enalapril, lisinopril, etc.); angitension receptor blockers (ARBs) (valsartan, candesartan, losartan) HTN |
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Mechanism: Block angiotensin I and II formation; AND inhibit activity of renin
Response: ↓actions of angiotensin II; ↓a/v contraction; ↓SNS → ↓TPR; ↑sodium/H2O excretion |
Renin angiotensin inhibitors (part 2)
Aliskeren HTN |
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Use: Less effective in blacks. Potentiated by diuretics. Positive effects w/ ACEI/ARBs.
Effects: Diarrhea; allergic reactions ← require withdrawal. DO NOT use in pregnant women! Other: Expensive! |
Renin angiotensin inhibitors (part 2)
Aliskeren HTN |
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Mechanism: Block α1-adrenergic receptors
Response: ↓arterial/venous contraction in response to NE/E → ↓TPR |
α-adrenergic blockers
doxazosin, terazosin HTN |
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Use: TOLERANCE!; restrict to a multi-drug therapy or men w/ BPH
Effects: Hypotension, headache Other: Fluid retention ← USE with a diuretic |
α-adrenergic blockers
doxazosin, terazosin HTN |
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Mechanism: activate α2-adrenergic receptors in brainstem
Response: ↓SNS tone → ↓CO/TPR |
Centrally acting sympatholytics
clonidine, methyldopa, guanabenz, guanfacine HTN |
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Use: Limited to resistant hypertension
Effects: Sedation, dry mouth, bradycardia Other: Discontinuation can cause rebound hypertension; methyldopa ← OK w/ pregnancy |
Centrally acting sympatholytics
clonidine, methyldopa, guanabenz, guanfacine HTN |
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Mechanism: Minoxidil is a K+-channel opener (agonist)
Response: ↓arterioloar contraction → ↓TPR; ↑SNS/RAS/Na+ retention |
Direct acting vasodilators
hydralazine, minoxidil HTN |
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Use: Minoxidil ← used for severe refractory hyertension
Effects: headache, tachycardia, edema, hair growth (rogaine w/ MINOXIDIL!) Other: given w/ a diuretic and β-blocker |
Direct acting vasodilators
hydralazine, minoxidil HTN |
