Cardiovascular Module Drug Lists

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blakegoodman08
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116345
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Cardiovascular Module Drug Lists
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2011-11-21 22:08:00
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Ross University Med Medical School s3 s3m3 pharmacology cardiovascular
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All the drug lists for the Cardiovascular module and important facts about individual drugs on those lists. Use for name recognition.
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  1. 6 classes of Diuretics and their sites of action
    • Carbonic Anhydrase Inhibitors: proximal tubule
    • Osmotic Diuretics: thin descending loop of Henle
    • Loop Diuretics: thin ascending loop of Henle
    • Thiazides and Congeners: early distal tubule
    • Potassium-Sparing Diuretics: late distal tubule and cortical collecting duct
    • Vasopressin/ADH Antagonists: medullary collecting duct
  2. Two Carbonic Anhydrase inhibitors (diuretics)
    • Acetazolamide: PO, IV; 90% tubular secretion
    • Dorzolamide: topical eye drops; binds CA in RBCs and eliminated over 5 months
    • both drugs bind carbonic anhydrase, preventing bicarb breakdown in the tubule and alkalizing urine
  3. 1 Osmotic diuretic
    Mannitol: freely filtered, not reabsorbed; osmotically draws water out in TDL and PCT
  4. 2 Loop Diuretics
    • Furosemide: can give IM in emergencies, 60% bioavailable
    • Ethacrynic acid: NOT a sulfonamide; 100% bioavailable
    • Both inhibit Na/K/Cl symporter, inhibit macula densa detection of ions; cause alkalosis
  5. 2 Thiazides/cogeners (diuretics)
    • Hydrochlorothiazide: 70% available, T1/2 6-15hr, 100% excreted in urine
    • Indapamide: 93% available, T1/2 16hr, completely metabolized
    • Cause alkalosis; inhibit Na/Cl symporter (NCC) in the DCT; also weak carbonic anhydrase inhibitors (alkaline urine)
  6. 3 Potassium-sparing Diuretics
    • Triamterene: blocks epithelial sodium channel (ENaC) in late DCT and CCT
    • Amiloride: same as triamterene, but lower oral availablility and longer T1/2
    • Spironolactone: aldosterone receptor antagonist; canrenone active metabolite; blocks production of ENaCs and Na/K-ATPases
    • All cause NaCl wasting while sparing K reabsorption; can lead to hyperkalemia, slight acidosis
  7. 2 Vasopressin/ADH antagonists (diuretics)
    • Conivaptan: IV, also hits V1a, helping diuresis
    • Tolvaptan: PO, slightly longer T1/2
    • Both target basolateral V2 receptor in principle cells, downregulating insertion of aquaporin channels
  8. Four classes of Antihypertensives
    • Diuretics: reduce volume, reduce pressure
    • Sympatholytics: regulate sANS signaling (α/β blockers)
    • Vasodilators: lower peripheral resistance
    • Inhibitors/antagonists of Renin-Angiotensin system: block end-effects of angiotensin (ups peripheral resistance, lowers diuresis, vascular/cardiac remodeling)
  9. 4 Diuretics for hypertension
    • Hydrochlorothiazide: 1st line drug, hits biporter
    • Indapamide: 1st line drug, thiazide drug
    • Furosemide: preferred only in malignant hypertension, concomitant chronic kidney disease (loop diuretic)
    • Spironolactone: combine with thiazides to prevent hypokalemia; tx hypertension of hyperaldosteronism
  10. 6 Sympatholytics for hypertension
    • Clonidine: α2 and imidozoline receptor agonist; centrally acting (NTS, rostral ventrolateral medulla)
    • Methyldopa: indirect adrenergic agonist (pre-synaptic neuron metabolizes to α2 agonist)
    • Prazosin: α1 antagonist in resistance and capacitance vessels
    • Propanolol: selective β-block; decrease HR, CO
    • Labetalol: α/β-block; decrease TPR, venous tone
    • Esmolol: similar to labetalol
  11. 8 Vasodilators for hypertension
    • Hydralazine: uncertain MOA,
    • Nitroprusside:
    • Minoxidil: opens arteriole smooth muscle K+ channel, hyperpolarizing membrane
    • Diazoxide: K+ channel opener similar to minoxidil
    • Nifedipine: dihydropyridine Ca2+ channel blocker; see anti-arrythmics
    • Verapamil: class IV Ca2+ channel blocker; see anti-angina
    • Diltiazem: class IV Ca2+ channel blocker; see anti-angina
    • Fenoldopam: D1-dopamine receptor agonist; renal and mesenteric vessel dilator
  12. 4 antihypertensive Renin/Angiotensin modifiers
    • Aliskiren: competitive inhibitor of renin, prevents angiotensinI conversion (rate-limiting step)
    • Captopril: ACE inhibitor; prevents angiotensinI -> angiotensinII conversion
    • Enalapril/enalaprilat: prodrug/metabolite ACE inhibitor
    • Losartan: competitive, selective angiotensinII receptor antagonist
  13. 5 classes of Anti-Arrhythmic Drugs
    • Class I: 3 subclasses (abc), all Na+ channel blockers
    • Class II: β-adrenoreceptor blockers
    • Class III: K+ channel blockers
    • Class IV: Ca2+ channel blockers
    • Miscellaneous: different MOAs
  14. 2 Class Ia anti-arrhythmics
    • Quinidine: blocks activated Na+ channels, at high doses K+, Ca2+, and α1; a-flutter and fib, ectopic vent beats, recurrent suprav- and v-tach
    • Procainamide: Blocks activated Na+ channels, some K+ channels; WPW and arrhythmias when others are poorly tolerated
  15. 3 Class Ib anti-arrhythmics
    • Lidocaine: blocks inactivated > activated Na+ channels; least cardiotoxic; acute vent arrhythmia, digitalis arrhythmias
    • Mexiletine: oral lidocaine analogue for v-tach
    • Phenytoin: mainly inactivated Na+ channel block; digitalis-induced arrhythmias
  16. 1 Class Ic anti-arrhythmic
    Flecainide: blocks activated Na+, some K+ channels; rhythm control of a-flutter, fib, and chronic supravent arrhythmias
  17. 4 Class II anti-arrhythmics
    • Esmolol: used in ICU for short T1/2
    • Metoprolol
    • Sotalol
    • All are selective β1 blockers in cardiac tissue; depress contractility and slow HR; control a-flutter/fib, hypertrophic cardiomyopathy, prophylaxis of v-fib
  18. 3 Class III anti-arrhythmics
    • Amiodarone: K+ channel block, inactivated Na+ channels; most effective antiarrhythmic, used in chronic control, sustained v-tach, and hypertrophic cardiomyopathy; can lead to pulmonary fibrosis, many other toxicities
    • Sotalol: nonselective β-block and K+ channel block; supravent and vent arrhythmias
    • Ibutilide: blocks K+ and causes inward Na+; used only in a-flutter/fib
  19. 3 Class IV anti-arrhythmics
    • Verapamil: see anti-angina
    • Diltiazem: see anti-angina
    • both are activated and inactivated Ca2+ channel blockers used in acute tx of suprav-tach and acute tx, chronic control of a-flutter/fib
  20. 3 Miscellaneous anti-arrhythmics
    • Adenosine: hyperpolarization of SA and AV nodes, decreasing SA automaticity and AV conduction; 1st choice for paroxysmal supravent-tach
    • Magnesium Sulfate: unknown MoA, effective prevention of recurrent torsade de pointes and digitalis induced arrhythmias
    • Digoxin: see drugs for heart failure; useful in a-flutter/fib in cardiac failure where Ca2+ blockers could worsen situation
  21. 5 classes of Heart Failure Drugs
    • Inotropic Drugs: modulate contractility (inotropy) of the heart to affect preload/afterload
    • Renin-Angiotensin-Aldosterone modulators: reduce afterload (angiotensin) and preload (aldosterone); cornerstone tx in all stages of heart failure
    • Diuretics: prevent Na+ and H2O retention to stabilize hemodynamic decompensation
    • β-Blockers: unknown MoA, possibly dangerous due to negative inotropic effect
    • Vasodilators: reduce preload and afterload by reversing vasoconstriction associated with heart failure
  22. 4 Inotropic Drugs for heart failure
    • Digoxin: cardiac glycoside that blocks Na+/K+-ATPase; many actions, but primarily improves efficiency of myocyte contraction, reducing O2 demand in failure
    • Dobutamine: selective β1 agonist, very + inotropy (greater than digoxin) and + dromotropy (conduction velocity)
    • Dopamine: MoA dependent on dose; mid-dose gives + inotropic effects, in addition ot vasodilation from lower doses (D-1 and β1/2 agonist); especially useful in poor renal perfusion
    • Milrinone: inhibitor of specific cardiac phosphodiesterase; leads to + inotropy and peripheral vasodilation
  23. 4 Renin-Angiotensin-Aldosterone modulating drugs for heart failure
    • Captopril: ACE inhibitor (hypertension)
    • Enalaprilat: ACE inhibitor (hypertension)
    • Losartan: AngiotensinII receptor antagonist (hypertension)
    • Spironolactone: aldosterone receptor antagonist, stops ENaC insertion (diuretics); attenuate pathologic remodeling at sub-diuretic doses and synergistic with above 3
  24. 2 Diuretics for heart failure
    • Furosemide: triporter loop diuretic
    • Thiazides: Na/Cl biporter DCT diuretic
    • Main use for these is to prevent water and NaCl retention to reduce preload and edema
  25. 3 β-Blockers for heart failure
    • Metoprolol
    • Carvedilol
    • Bisoprolol
    • NOT A CLASS EFFECT. They decrease HR, reduce myocardial remodeling, inhibit renin secretion, and upreg β1 receptors otherwise downregulated in failure.
    • CARBIME: mnemonic
  26. 3 Vasodilators for heart failure
    • Nitrates: very large reduction in preload/afterload
    • Hydralazine: direct vasodilator, unknown MoA
    • Nesiritide: ANF analogue (recomb brain natriuretic peptide); arteriolar and venous vasodilator
    • Arteriolar dilators preferred in 1* low CO
    • Venous dilators preferred in 1* pulmonary congestion
    • Losartan, Milrinone, and Captopril also considered vasodilators
  27. 5 classes of Anti-Hyperlipidemic drugs
    • HMG-CoA inhibitors: prevents mevalonic acid formation (rate-limiting step)
    • Bile Acid Binding Resins: increase excretion of bile acids by up to 10x
    • VLDL Secretion Inhibitors: prevent lipolysis in adipose tissue
    • Fibric Acid Derivatives: activate nuclear transcription receptor PPAR-α, increasing LPL synth and VLDL hydrolysis
    • Intestinal Sterol Absorption Inhibitors: selectively inhibits absorption of sterols at small intestine brush border
  28. 1 HMG-CoA Inhibitor for hyperlipidemia
    • Lovastatin: 20-55% drop of LDL, 10-35% drop of triglycerides, 5-10% increase in HDL
    • includes any drug with '-statin'
    • Good for high cholesterol or LDL, atherosclerosis, prevention of coronary artery disease and stroke
  29. 1 Bile-Acid Binding Resin for hyperlipidemia
    • Cholestyramine: 10-35% reduction of LDL; little effect on HDL, VLDL, or triglycerides
    • all resins basically just bind and remove cholesterol from the GI tract
    • Good for all isolated increases of LDL
  30. 1 VLDL Secretion Inhibitor for hyperlipidemia
    • Niacin: 15-25% drop of LDL, 15-40% drop of VLDL, 30-50% drop of triglycerides, and 15-30% bump of HDL
    • Strongly inhibits adipose lipolysis and reduces catabolism of apo-A1 from HDL
    • Good high VLDL, LDL, and low HDL
  31. 1 Fibric Acid Derivative for hyperlipidemia
    • Gemfibrozil: 30-60% drop of triglycerides, 20-30% drop of VLDL, 5-10% bump of HDL, and variable effect on LDL
    • Drug of choice for Hyperlipoproteinemia Type III
  32. 1 Intestinal Sterol Absorption Inhibitor for hyperlipidemia
    • Ezetimibe: 15-20% drop of LDL, 5-8% drop of triglycerides, 16% drop of Apo-B, little effect on HDL
    • Used for hyperlipidemias in conjunction with statins
  33. 3 classes of Anti-Anginal Drugs
    • Nitrates and Nitrites: marked relaxation of large veins and large arteries to lesser extent, decreasing preload and afterload respectively
    • Ca2+ Channel Blockers: cause vasodilation (decrease afterload), decrease conduction, automaticity, and contractility, and increase refractoriness
    • β-Adrenoreceptor Blockers: reduction in heart rate, contractility, and blood pressure lead to decreased O2 demand and increase subendocardial perfusion
  34. 3 Nitrates/Nitrites for angina
    • Amyl Nitrite: 3-5min duration
    • Nitroglycerin: many RoA with variant onset and duration
    • Isosorbide Mononitrate: oral RoA, 15-40min onset with 6-10hr duration
  35. 2 Subclasses of Ca2+ Channel Blockers for angina
    • Dihydropyridines: selectively block vessel Ca2+ channels (no direct cardiac action)
    • Others: block Ca2+ channels in heart and vessels (nonselective)
    • Also good for Raynaud's phenomenon
  36. 2 Dihydropyridines for angina
    • Nifedipine: high vascular selectivity
    • Nicardipine: very high vascular selectivity
    • Both Ca2+ channel blockers; decrease afterload; also dilate cerebral vessels, inhibiting delayed reactive vasospasm from subarachnoid hemorrhage
  37. 3 "other" Ca2+ channel blockers for angina
    • Verapamil: low vascular selectivity
    • Diltiazem: low vascular selectivity; improves diastolic compliance
    • Bepridil: no selectivity
    • All have cardiac effects in addition to vascular effects
  38. 3 β-Blockers for angina
    • Propanolol: nonselective β-blockade
    • Metoprolol: selective β1-blockade
    • Atenolol: selective β1-blockade

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